Principles and Practices in Cutaneous Laser Surgery (Basic and Clinical Dermatology)

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Author: Arielle Kauvar | George Hruza

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Boca Raton London New York Singapore

Published in 2005 by Taylor & Francis Group 6000 Broken Sound Parkway NW, Suite 300 Boca Raton, FL 33487-2742 © 2005 by Taylor & Francis Group, LLC No claim to original U.S. Government works Printed in the United States of America on acid-free paper 10 9 8 7 6 5 4 3 2 1 International Standard Book Number-10: 0-8247-5833-1 (Hardcover) International Standard Book Number-13: 978-0-8247-5833-2 (Hardcover) Library of Congress Card Number 2005041805 This book contains information obtained from authentic and highly regarded sources. Reprinted material is quoted with permission, and sources are indicated. A wide variety of references are listed. Reasonable efforts have been made to publish reliable data and information, but the author and the publisher cannot assume responsibility for the validity of all materials or for the consequences of their use. No part of this book may be reprinted, reproduced, transmitted, or utilized in any form by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying, microfilming, and recording, or in any information storage or retrieval system, without written permission from the publishers. For permission to photocopy or use material electronically from this work, please access www.copyright.com (http://www.copyright.com/) or contact the Copyright Clearance Center, Inc. (CCC) 222 Rosewood Drive, Danvers, MA 01923, 978-750-8400. CCC is a not-for-profit organization that provides licenses and registration for a variety of users. For organizations that have been granted a photocopy license by the CCC, a separate system of payment has been arranged. Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe. Library of Congress Cataloging-in-Publication Data Principles and practices in cutaneous laser surgery / editor, Arielle N.B. Kauvar ; associate editor, George J. Hruza. p. ; cm. – (Basic and clinical dermatology ; 33) Includes bibliographical references and index. ISBN 0-8247-5833-1 1. Skin—Laser surgery. I. Kauvar, Arielle N. B. II. Hruza, George J. [DNLM: 1. Laser Surgery—methods. 2. Skin Diseases—surgery. WR 650 P9566 2005] RL120.L37P75 2005 617.4’770598—dc22

Taylor & Francis Group is the Academic Division of T&F Informa plc.

2005041805

Visit the Taylor & Francis Web site at http://www.taylorandfrancis.com

Dedication

To my husband, David R. Kauvar And my three wonderful sons, Ellery, Darien and Hadley Kauvar, For filling my life with love and happiness To my parents, Berta and Harry Bienenstock, For their enduring affection and steadfast guidance Arielle N.B. Kauvar

To my children Stephanie and Paul Hruza For giving my life joy and fulfillment To my parents Judita and Zdenek Hruza For their unwavering support and love George Hruza

Foreword

Almost all clinical texts on skin therapy with lasers and other non-invasive energy sources are in some way out of date, because this fascinating field is prone to making progress (which is discussed a bit more, below). So, read this excellent book as soon as possible. Part of it will be passe´ within a few years, although I don’t know exactly which part. In 25 years, however, this book will still be worth reading. Basic principles inherent in the science and art of medicine do not fade away, and nothing is ever “un-invented”. Indeed, our best stuff is not really new. Arielle Kauvar and George Hruza have given us something built to last, written by colleagues with clinical acumen based on a wealth of ideas and experience. This text should be fun for anyone who wields or thinks about wielding therapeutic photons. I plan to keep it handy for my own use, for residents and students, and for those stunningly inquisitive patients who seem to abound in Boston. Medical professionals have used light to treat skin problems for at least 3000 years. Thermal treatments of skin have been around on a fee-for-service basis for at least twice that long. The recent “explosion” of lasers, intense pulsed light (IPL) sources, lightactivated drugs (photodynamic therapy, PDT), ultrasound, and advanced radiofrequency treatments has occurred during ,1% of this long history, for good reasons. Laser skin surgery is undeniably “high-tech,” and new technology is neat stuff. Lasers are far smaller, more reliable, versatile, efficient, long-lived, and controllable. The recent optical telecommunications “bubble” created many new fiber-based lasers, amplifiers, scanners and detectors that are just beginning to trickle down into medicine. However, new technology is merely a stimulus, and not the primary reason for progress in this field. Very soon after the first laser was invented in 1960—a flashlamp-pumped, longpulsed ruby laser—Leon Goldman, MD and other admirable pioneers widely explored its potential for laser skin surgery. More than 30 years later, the same laser was used to create the “breakthrough” of permanent laser hair removal, which is now available around the world using other lasers and more recently, intense pulsed light sources. Why did it take so long? Intense pulsed light sources were invented long before lasers; why did they appear much more recently than lasers in dermatology? IPLs are xenon flashlamps with optical filters, which have been around for about 60 years. So, if IPLs are a great leap backward—why not keep going? Any sophomore at MIT could show that focused, filtered sunlight can achieve about the same spectrum and brightness as an IPL, because the surface of the sun is a plasma at the same temperature as that in our IPLs. Unless someone in the esthetic device industry with a death-wish does it first, v

vi

Foreword

I hope some day to enjoy making a scanned, focused, solar “photorejuvenator,” just for fun. How ironic it would be to use sunlight for treating skin damage caused by itself. So, if new technology is not the primary limitation to progress in this high-tech corner of medicine—what is? The answer is a humble one, pertinent to this book: we lack the understanding necessary for progress. I do not mean a basic physical or biological science understanding. What we lack most is the ability to pose clinical connections with existing science and technologies. The readership of this book (yes, you!) is in a position to contribute something to that kind of understanding. As a group of biomedical professionals we are no more or less intelligent, and no more or less naı¨ve, than those before us during millennia of using light to treat skin disease. Oddly enough, it is probably the most recent info in this book that runs the greatest risk of early obsolescence. The trick, apparently, is to do something both new and long-lasting. I like this book because it brings the attentive reader to the brink of our lack of understanding. Bon appetit! R. Rox Anderson, MD Prof. of Dermatology Director, Wellman Center for Photomedicine Harvard Medical School

Preface

Lasers have become integral to the modern practice of medicine in the fields of dermatology, plastic surgery, otolaryngology, and phlebology. With the skin being the most accessible organ in the body, many cutaneous disorders and conditions are ideally suited to treatment by laser technology. Lasers are safely used to destroy or alter epidermal and dermal processes and lesions comprising blood vessels or pigment. With the development of the principles of “selective photothermolysis” by Drs. R. Rox Anderson and John Parrish in the 1980s, selective site-specific destruction of skin lesions became a reality. The appropriate combination of laser wavelength and exposure time enabled the removal of blood vessels and pigment without affecting the surrounding tissue. For the first time in medical history, port wine stains were gradually lightened with a series of noninvasive treatments leaving these patients with normalappearing skin. Similarly, tattoos and melanocytic lesions could be targeted by pigmentabsorbing lasers without altering the normal skin pigmentation. The same basic principles have been used to create lasers that selectively damage leg veins and hair follicles. More recently, new technology has led to the development of skin resurfacing lasers and to the development of a whole new approach to facial rejuvenation and the treatment of wrinkles, photodamage, and scars. Dramatic clinical results and a low incidence of adverse side effects have generated much enthusiasm among physicians and patients for these procedures. Laser technology and its application to the treatment of skin disorders has developed at a rapid pace in recent years. Multiple types of laser systems are now available to treat a wide variety of cutaneous lesions, including vascular and pigmented lesions, tattoos, hair, leg veins, scars, and wrinkles. Clinicians using lasers as well as residents and fellows in training are faced with a perplexing array of technology with few resources for obtaining background knowledge and practical information necessary to perform these treatments. The purpose of this text is to provide an up-to-date, comprehensive yet straight-forward approach to understanding lasers and performing laser treatment for cutaneous disorders. The book is intended for use by practicing physicians. For convenience and clarity, information is readily available about each laser system as well as specific treatment indications. Section I provides the fundamentals for understanding laser instrumentation and physics. A comprehensive review of each laser system, its interaction with tissue and treatment indications are presented in Section II of the book. Existing technologies are compared and the details of operation are reviewed. Section III offers a step-by-step approach to laser treatment of specific skin disorders, with an emphasis on the selection vii

viii

Preface

of the appropriate laser for each clinical situation, treatment guidelines, and possible pitfalls. In Section IV, a guide to patient selection, appropriate education, and credentialing, as well as establishing a laser surgical unit is provided for clinicians new to the practice of laser surgery. The comprehensive scope of this text with its in-depth analysis yet practical approach make it a useful reference and teaching tool for both the novice and the experienced laser surgeon in the fields of dermatology, plastic surgery, otolaryngology, and phlebology. Arielle N. B. Kauvar

Acknowledgment

We are grateful to our many colleagues and friends whose hard work and dedication helped make this book a reality. This project would not have been possible without the patience, understanding, and support of our families and office staff. We sincerely appreciate the invaluable assistance and guidance of Sandra Beberman and the support staff at Marcel Dekker and Taylor & Francis. Arielle N.B. Kauvar and George J. Hruza

ix

Contents

Foreword . . . . . . . Preface . . . . . . . . . Acknowledgment . . List of Contributors

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1. Cutaneous Laser Surgery: Historical Perspectives . . . . . . . . . . . . . . . . . . . . . Gary J. Brauner

3

Section I: Understanding Lasers

2. An Introduction to Lasers and Laser –Tissue Interactions in Dermatology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . J. Stuart Nelson 3. Laser Safety Measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Christie Travelute Ammirati and George J. Hruza

59

79

Section II: Laser Science and Instrumentation 4. Continuous Wave Lasers: Argon, Dye, KTP, Copper Vapor, Krypton . . . . . . 105 Thomas O. McMeekin 5. Continuous Wave and Pulsed CO2 Lasers E. Victor Ross

. . . . . . . . . . . . . . . . . . . . . . . . . . 129

6. Er:YAG Lasers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 181 Ulrich Hohenleutner and Michael Landthaler 7. Pulsed Dye Lasers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 199 Kristen A. Richards and Jerome M. Garden 8. Clinical Uses of the Long Pulse Duration Pulsed Dye Laser . . . . . . . . . . . . . 219 Eric F. Bernstein 9. Pulsed KTP and Diode (532 nm) Lasers . . . . . . . . . . . . . . . . . . . . . . . . . . . . 245 Robert M. Adrian, Emil Tanghetti, and Arielle N. B. Kauvar xi

xii

10. Q-Switched Ruby Laser Vic A. Narurkar

Contents

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 259

11. The Q-Switched Nd:YAG (1064 þ 532 nm) Laser . . . . . . . . . . . . . . . . . . . . 265 Suzanne L. Kilmer, Macrene R. Alexiades-Armenakas, Vicki J. Levine, and Robin Ashinoff 12. Q-Switched Alexandrite Lasers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 285 Christopher A. Nanni 13. Long-Pulsed Alexandrite Laser . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 297 Cathy A. Slater, John B. Newman, and David H. McDaniel 14. Diode Lasers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 317 Murad Alam, David A. Wrone, and Beatrice Berkes 15. Long-Pulsed Nd:YAG (1064 nm) Lasers Neil Sadick and Arielle N. B. Kauvar

. . . . . . . . . . . . . . . . . . . . . . . . . . . 337

16. Noncoherent Light Source . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 355 Robert A. Weiss and Margaret A. Weiss 17. Excimer Lasers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 375 James M. Spencer 18. Photodynamic Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 387 Shirley Jean-Baptiste, David A. Wrone, and Murad Alam 19. Skin Cooling in Laser Dermatology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 403 Kristen M. Kelly and J. Stuart Nelson 20. Reflectance Confocal Microscopy for Basic and Clinical Dermatology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 415 Salvador Gonza´lez, Robert H. Webb, R. Rox Anderson, and Milind Rajadhyaksha

Section III: Lasers Treatment of Cutaneous Disorders 21. Laser Treatment of Port Wine Stains . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 441 Arielle N. B. Kauvar 22. Lasers and the Treatment of Hemangiomas Milton Waner and Jay Kincannon

. . . . . . . . . . . . . . . . . . . . . . . . . 461

23. Laser Treatment of Acquired Vascular Lesions Tina B. West

. . . . . . . . . . . . . . . . . . . . . . 475

24. Lasers in the Treatment of Pigmented Lesions . . . . . . . . . . . . . . . . . . . . . . . 489 Jeffrey S. Dover, Kenneth A. Arndt, and Richard J. Ort

Contents

xiii

25. Laser Treatment of Tattoos . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 505 Suzanne L. Kilmer 26. Carbon Dioxide Laser Treatment of Epidermal and Dermal Lesions in Principles and Practices in Cutaneous Laser Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 519 Leslie C. Lucchina and Suzanne M. Olbricht 27. Skin Resurfacing with CO2 Lasers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 535 Richard E. Fitzpatrick and Elizabeth Rostan 28. Skin Resurfacing with Erbium:YAG Lasers . . . . . . . . . . . . . . . . . . . . . . . . . 553 Kucy Pon, Vivek Iyengar, and Thomas Rohrer 29. Combined Laser Resurfacing Techniques . . . . . . . . . . . . . . . . . . . . . . . . . . . 569 Mitchel P. Goldman and Elizabeth Roston 30. Combining Laser Resurfacing with Facial Surgery . . . . . . . . . . . . . . . . . . . . 589 Cynthia Weinstein 31. Laser Treatment of Scars and Striae . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 619 Tina S. Alster and H. L. Greenberg 32. Nonablative Skin Rejuvenation and Acne Therapy . . . . . . . . . . . . . . . . . . . . 637 David J. Goldberg and Arielle N. B. Kauvar 33. Laser Treatment of Leg Veins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 653 Arielle N. B. Kauvar 34. Laser Hair Removal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 677 Christine C. Dierickx 35. Laser Assisted Hair Transplantation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 703 Marc R. Avram 36. Treatment of Nonwhite Skin with Lasers . . . . . . . . . . . . . . . . . . . . . . . . . . . 717 Woraphong Manuskiatti and Mitchel P. Goldman Section IV: Considerations in the Practice of Laser Surgery 37. Legal Considerations in Laser Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 749 David J. Goldberg 38. Establishing a Laser Unit Elizabeth I. McBurney

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 757

39. Anesthesia Options for Laser Surgery John A. Carucci and David J. Leffell Index

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 775

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 789

List of Contributors

Robert M. Adrian, M.D., F.A.C.P. Murad Alam, M.D. Illinois, USA

Center for Laser Surgery, Washington, DC, USA

Department of Dermatology, Northwestern University, Chicago,

Macrene R. Alexiades-Armenakas, M.D., Ph.D. New York, USA

Private Practice, New York,

Tina S. Alster, M.D. Dermatology and Pediatrics, Georgetown University Medical Center, Washington Institute of Dermatologic Laser Surgery, Washington, DC, USA Christie Travelute Ammirati, M.D. Division of Dermatology, Penn State University College of Medicine, Pennsylvania, USA R. Rox Anderson, M.D. Department of Dermatology, Wellman Laboratories of Photomedicine, Massachusetts General Hospital, Massachusetts, USA Kenneth A. Arndt, M.D. SkinCare Physicians of Chestnut Hill, Chestnut Hill and Clinical Professor of Dermatology, Harvard Medical School, Massachusetts, and Clinical Professor of Dermatology, Yale University School of Medicine, Connecticut, USA Robin Ashinoff, M.D. Department of Dermatology, Hackensack University, Hackensack, New Jersey, USA Marc R. Avram, M.D. Department of Dermatology, Weill-Cornell Medical Center, New York, New York, USA Beatrice Berkes, M.D. California, USA

Department of Dermatology, Loma Linda University,

Eric F. Bernstein, M.D. Laser Surgery and Cosmetic Dermatology Centers, Marlton, New Jersey, USA; University of Pennsylvania, Pennsylvania, USA Gary J. Brauner, M.D. Department of Dermatology, Mount Sinai School of Medicine, New York, New York, USA John A. Carucci, M.D., Ph.D. Medicine, Connecticut, USA

Department of Dermatology, Yale University School of xv

xvi


Christine C. Dierickx, M.D. Wellman Laboratories of Photomedicine, Massachusetts General Hospital, Massachusetts, USA; Department of Dermatology, University of Ghent, Belgium Jeffery S. Dover, M.D. F.R.C.P.C. SkinCare Physicians of Chestnut Hill, Chestnut Hill, Massachusetts and Associate Clinical Professor of Dermatology, Yale University School of Medicine, Connecticut, USA Richard E. Fitzpatrick, M.D. San Diego, California, USA

Dermatology Associates of San Diego County, Inc.,

Jerome M. Garden, M.D. Department of Dermatology, Northwestern University Medical School and Divisions of Dermatology and Plastic Surgery, Children’s Memorial Hospital, Chicago, Illinois, USA David J. Goldberg, M.D., J.D. Department of Dermatology, Mount Sinai School of Medicine, New York, New York, USA Mitchel P. Goldman, M.D. Cosmetic Laser Associates of La Jolla, Inc., La Jolla and University of California, San Diego, California, USA Salvador Gonza´lez, M.D., Ph.D. Massachusetts General Hospital, Harvard Medical School and Department of Dermatology, Wellman Laboratories of Photomedicine, Massachusetts General Hospital, Massachusetts, USA Washington Institute of Dermatologic Laser Surgery,

H. L. Greenberg, M.D. Washington, DC, USA Ulrich Hohenleutner, M.D. Regensburg, Germany George J. Hruza, M.D. Medicine, Missouri, USA Vivek Iyengar, M.D.

Department of Dermatology, University of Regensburg,

Division of Dermatology, St. Louis University School of

SkinCare Physicians of Chestnut Hill, Massachusetts, USA

Shirley Jean-Baptiste, M.D.

Northwestern University, Chicago, Illinois, USA

Arielle N. B. Kauvar, M.D. New York Laser & Skin Care, Department of Dermatology, New York University School of Medicine and Department of Dermatology, SUNY Downstate Medical Center, New York, New York, USA Kristen M. Kelly, M.D. Department of Dermatology and Surgery, Beckman Laser Institute, University of California, California, USA Suzanne L. Kilmer, M.D. Laser & Skin Surgery Center of Northern California, Sacramento, California, USA Jay Kincannon, M.D. Department of Dermatology and Pediatrics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA Michael Landthaler, M.D. Regensburg, Germany David J. Leffel, M.D. cine, Connecticut, USA

Department of Dermatology, University of Regensburg,

Department of Dermatology, Yale University School of Medi-

Vicki J. Levine, M.D. Department of Dermatology, New York University School of Medicine, New York, New York, USA


xvii

Leslie C. Lucchina, M.D. Department of Dermatology, Brigham and Women’s Hospital and Department of Dermatology, Harvard Medical School, Massachusetts, USA Woraphong Manuskiatti, M.D. Department of Dermatology, Siriraj Hospital, Mahidol University, Bangkok, Thailand Elizabeth I. McBurney, M.D. Department of Dermatology, Lousiana State University School of Medicine, Tulane University School of Medicine, Lousiana, USA David H. McDaniel, M.D. Laser Skin & Vein Center of Virginia, Virginia Beach, Virginia and Eastern Virginia Medical School, Norfolk, Virginia, USA Thomas O. McMeekin, M.D. Department of Dermatology and Pediatrics, University of Rochester and Department of Dermatology, State University of New York at Buffalo, New York, New York, USA Christopher A. Nanni, M.D.

Private Practice, Glendore, California, USA

Vic A. Narurkar, M.D. Bay Area Laser Institute and Department of Dermatology, University of California at Davis, California, USA J. Stuart Nelson, M.D., Ph.D. Department of Surgery, Dermatology and Biomedical Engineering, Beckman Laser Institute, University of California, California, USA John B. Newman, M.D. Laser Skin & Vein Center of Virginia, Virginia Beach, Virginia and Department of General Surgery, Naval Medical Center Portsmouth, Portsmouth, Virginia, USA Suzanne M. Olbricht, M.D. Department of Dermatology, Lahey Clinic and Department of Dermatology, Harvard Medical School, Massachusetts, USA Richard J. Ort, M.D. SkinCare Physicians of Chestnut Hill and Department of Dermatology, Beth Israel Deaconess Medical Center, Massachusetts, USA Kucy Pon, M.D.

SkinCare Physicians of Chestnut Hill, Massachusetts, USA

Milind Rajadhyaksha, Ph.D. Department of Dermatology, Wellman Laboratories of Photomedicine, Massachusetts General Hospital, Harvard Medical School, Massachusetts, USA; Lucid, Inc., New York, New York, USA Kristen A. Richards, M.D.

Scripps Memorial Hospital, California, USA

Thomas Rohrer, M.D. SkinCare Physicians of Chestnut Hill, Chestnut Hill and Associate Clinical Professor of Dermatology, Boston University School of Medicine, Massachusetts, USA E. Victor Ross, M.D., C.D.R., M.C., U.S.N. Dermatology Department, Naval Medical Center San Diego and Division of Dermatology, University of California, San Diego, California, USA Elizabeth Rostan, M.D. California, USA

Dermatology Associates of San Diego County, Inc., San Diego,

Neil S. Sadick, M.D., F.A.C.P., F.A.A.C.S. Department of Dermatology, Weil Medical College of Cornell University, New York, New York, USA Cathy A. Slater, M.D., M.P.H. Laser Skin & Vein Center of Virginia, Virginia Beach, Virginia and Boice-Willis Clinic, Rock Mount, North Carolina, USA

xviii


James M. Spencer, M.D., M.S. Department of Dermatology, Mount Sinai School of Medicine, New York, New York, USA Emil Tanghetti, M.D.

Private Practice, Sacramento, California, USA

Milton Waner, M.D., F.C.S. Department of Otolaryngology, St. Lukes—Roosevelt Hospital, New York, New York, USA Robert H. Webb, Ph.D. Department of Dermatology, Wellman Laboratories of Photomedicine, Massachusetts General Hospital, Massachusetts, USA Cynthia Weinstein, M.B.B.S., F.A.C.D., F.R.A.C.P. Australia.

Private Practice, Melbourne,

Margaret A. Weiss, M.D. Department of Dermatology, Johns Hopkins University School of Medicine, Maryland, USA Robert A. Weiss, M.D. Department of Dermatology, Johns Hopkins University School of Medicine, Maryland, USA Tina B. West, M.D.

Private Practice, Chevy Chase, Maryland, USA

David A. Wrone, M.D. Chicago, Illinois, USA

Department of Dermatology, Northwestern University,

Section I: Understanding Lasers

1 Cutaneous Laser Surgery: Historical Perspectives Gary J. Brauner Mount Sinai School of Medicine, New York, New York, USA

1. 2. 3. 4.

5.

6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19.

Finding the Right Thread in the Cloak It Takes a Nobel Prize Winner to Think of it Ruby Other New Lasers 4.1. Argon Laser 4.2. CO2 Laser Multidisciplinary Societies 5.1. Laser Institute of America 5.2. International Society for Laser Medicine and Surgery 5.3. American Society for Laser Medicine and Surgery Laser safety—The American National Standards Institute Personnel and Patient Safety—Plume Patient Safety—SCAR Postoperative Wound Care Selective Photothermolysis Wellman Lab and Beckman Lab Nd:YAG LASER 12.1. Q-switching Pigment Lasers Serendipity Resurfacing Laser-Assisted Hair Transplantation Pulsed Light Sources Laser Hair Removal Chilling and Wrinkles

4 4 9 9 9 12 15 15 15 15 16 17 17 22 23 24 25 25 26 27 28 30 31 31 33 3

4

Brauner

20. Biostimulation 21. Photodynamic Therapy 22. Return of the Scientific Method—The Charge for the Future References

1.

34 35 36 39

FINDING THE RIGHT THREAD IN THE CLOAK

A proper history of lasers in dermatologic surgery requires not just a chronological recitation (1 – 3) of what we know as published fact by the sequential appearance of peer-reviewed and dated articles and Congress presentations but also an attempt to find the thread of true progress weaving through the fabric of the “cloak of magical claims.” The use of light and its many colors, both visible and invisible, for the treatment and healing of cutaneous disease is a true analog of Joseph’s multicolored cloak. How does the laser-surgeon-turned-historian achieve a sense of perspective over the laser miracles of the past 40 years while sitting in the midst of them? Is he/she woven too tightly into the woof and warp to see above it? This author’s selection of a few articles and concepts as seminal ones will trace this thread but it does not negate the importance of many other legitimate contributions in our cloak (Table 1.1). There is a sense and a nonsense to our history. The relentless march of technical, industrial, and military genius in developing new lasers after 1960 was at first random and certainly unrelated to dermatologic surgery at least until 1983 (4). But there were clearly identifiable and critical seminal events which brought about the flowering of cutaneous laser surgery. These events define the thread this author will trace—they span theoretical physics, inventive genius of laser manufacture, optical modeling schema of the skin and its chromophores to direct development of appropriate lasers to treat cutaneous disease (4–13), accidental discoveries, the advertising kingdom, the medical–industrial complex, and ethics of the marketplace and of the practice of medicine. All of these elements and events must be elaborated and reflected upon before a full though pro tem view of the evolution of cutaneous laser surgery is understood and hopefully utilized to direct its future. For spatial considerations the ever-expanding spectrum of laser technology for medical communication by fiberoptic networks, holographic reconstructions, or laser microsurgical manipulations of subcellular organelles or genes will not be reviewed.

2.

IT TAKES A NOBEL PRIZE WINNER TO THINK OF IT

Albert Einstein (Fig. 1.1) (14 –18), Time Magazine’s outstanding persona of the 20th century, also had the first insight into what has become our 21st century world of lasers. He elaborated the concept of stimulated emission of radiation in 1917 (19,20) wherein he postulated that if an electron were in an already excited state and were hit by a photon of the proper energy, instead of rising to a still higher energy level, it would fall to a lower level and emit a second photon of precisely the same wavelength as the initial photon, and the initial photon would also continue on without having been absorbed. Theoretically, one could then have a stream of unique and uniform photons arising in an incremental but massive exponential cascade (21). Laboratory experiments in the 1920s confirmed this postulate of stimulated emission but even in the experiments spontaneous emission of radiation and not stimulated emission predominated (21). According to Itzkan and Drake (22) Dirac’s theory of quantum electrodynamics in the

Cutaneous Laser Surgery: Historical Perspectives

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Table 1.1 Seminal Events and Personae Albert Einstein Schawlow and Townes Theodore Maiman Leon Goldman, MD Argon laser-D Apfelberg, K. Arndt “Nonsense” science CO2 Laser Hyperbole and unreproducible results Interdisciplinary societies: LIA, ISLMS, ASLMSa Laser safety: ANSI standards Personnel and patient safety: plume Patient safety: scar Minimal dose: B. Cosman, scanners Chilling: C. Chess Postoperative wound care: G. Brauner, A. Schliftman Photothermolysis: R. Anderson, J. Parrish Wellman Lab and Beckman Lab Hyperbole? Corruption of scientific method Pigment lasers Q-switched lasers Serendipity: scars: T. Alster Resurfacing: R. Fitzpatrick, R. Kaufmann, A. Kauvar, J. Dover, R. Adrian Serendipity redux and hair removal: R. Anderson, M. Grossman Thermokinetics: J. Nelson, R. Anderson Biostimulation and “cool” lasers Real scientific method: side-by-side studies; Report of complications Nonphysician use of medical lasers a

LIA, Laser Institute of America; ISLMS, International Society for Laser Medicine and Surgery; ASLMS, American Society for Laser Medicine and Surgery.

1920s established the nature of coherence whereby the stimulated photons would not only have the same frequency as the inciting photon but phase and direction as well. In order to have a scenario where stimulated emission predominated, a population inversion of more excited atoms or molecules than unexcited ones had to be produced. Charles H. Townes (Fig. 1.2) was the first to manufacture such a functioning prototype which produced microwaves, thus the first MASER microwave amplified stimulated emission of radiation. He had been involved with radar in World War II and became interested in microwaves (21). Townes had first thought of the mechanism for amplification of the radiation on a park bench in Franklin Park in Washington in April 1951 (21,23). Also, in 1951 the Russian physicist V. A. Fabrikant applied for a Soviet patent on amplifying stimulated emission but it was not published until 1959 and did not influence the course of American laser physics (21). In the USA in 1953 Joseph Weber was the first to propose stimulated emission. Townes’ research group recognized in 1953 (23 – 25) that ammonia molecules in the ground state would be attracted by an electrical field and those in an excited state would be repelled and thus these researchers could separate out excited ammonia molecules and force them through a small hole into a cavity into a true population inversion. In their doing so, stimulated emission of 1.25 cm microwaves

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Figure 1.1 Albert Einstein in 1905 in the Swiss patent office in Berne (Lucien Chavan). (Courtesy, The Albert Einstein Archives, The Jewish National and University Library, The Hebrew University of Jerusalem, Israel.)

spontaneously occurred. In 1957 Schawlow (Fig. 1.3) and Townes (26,27) first elaborated their concept of an optical resonator which could amplify stimulated emission in a chamber with parallel opposing reflective mirrors and thus produce waves coherent in space, all in phase and of uniform frequency (and thus wavelength) (21). Townes and Schawlow thought that the first practical “optical maser” (i.e., “laser”) would be an electric

Figure 1.2 Charles Townes, coinventor of the maser. (Courtesy, Bell Labs/Lucent Technologies.)


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Figure 1.3 Theodore Schawlow, coinventor of the maser with the ruby optical maser (i.e., laser). (Courtesy, Bell Labs/Lucent Technologies.)

current pumping or energizing a gas but the first effective laser was made in Hughes Labs by Maiman (Fig. 1.4) in 1960 by surrounding a 4 cm long ruby crystal rod with a spiral flashlamp, which excited the chromium in the ruby crystal when it absorbed blue-green light and produced a chromium population inversion.

Figure 1.4 Theodore Maiman, inventor of the first laser, the ruby. (Courtesy, Hughes Research— Labs HRL.)

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The development of lasers 50 years after Einstein’s’ first conceptualization was of such importance to the scientific community that Townes as well as the Russian physicists Nikolai Basov and Aleksander Prokhorov received the Nobel Prize in 1964. Shawlow, who had collaborated in 1958 with Townes to obtain the first laser patents (27), shared the 1981 Nobel Prize for using lasers to study the nature of atoms and molecules (21). Hecht and Teresi provide a fascinating blow-by-blow account of the 20-year patent controversy between Gordon Gould and Townes and Schawlow and the race to produce the first laser in the late 1950s—the first of many laser controversies. Interestingly, Maiman’s seminal contribution, announced on July 7, 1960, in a brief four-paragraph article—the very first laser—was refused publication in the prestigious Physical Review Letters but was finally presented in Nature (28,29). Although “LASER,” as used now, is an acronym for light amplified stimulated emission of radiation, Orazio Svelto, an Italian professor of quantum electronics and laser pioneer (30) reflected on an ancient (1st century AD) but apparently timeless reference from Pliny the Elder in “Natural History XXII,” 49 that “the laser is numbered among the most miraculous gifts of nature and lends itself to a variety of applications.” Pliny was not prescient or more brilliant than Einstein or Townes and Schawlow; however, his “laser” was a celebrated, commercially important, but extinct since the 2nd century, plant raised in North Africa and used as a culinary dressing but more importantly also as a cure for a variety of diseases, even injuries such as scorpion stings or arrow wounds. A 1960s timeline (21) shows that rapid progress in laser research began around 1962 in scientific laboratories and commercial manufacture of lasers began at about the same time. The US military had a significant interest in laser development very early on; in fact, this interest and its associated elements of secrecy led to much of Gould’s problems with others’ recognition of his early contributions since he was under contract with the government. The first gas laser was also invented in 1960 but by 1965 laser activity had been found in gases in over 1000 different wavelengths. In the early 1960s Dr. Leon Goldman (Fig. 1.5), a Cincinnati dermatologist, started a center for medical laser research at the University of Cincinnati where he, also Chief of Dermatology, often used himself as the first human guinea pig at which to aim a newly developed laser and became thereby the father of laser medicine and surgery—another seminal event. He had originally been given a grant in 1961 to study the safety of lasers by the National Institute of Health and Occupational Medicine and so opened the laboratory to study the ruby laser. It was Leon Goldman who first realized the possibilities of therapeutic uses of lasers as medical instruments but he was unable to interest the Surgeon General in funding his research. The John A. Hartford Foundation did come up with support for him, enabling him to run a multidisciplinary laboratory of biologists, safety engineers, and physicians from other surgical disciplines (31) from 1961 to 1976. It was only because of the ingenuity and persistence of this one man that lasers finally were made applicable to the treatment of human malformation and disease and degenerative changes (32). Since the ruby laser was the only one available, it was that which he turned on himself, laboratory animals, and other humans (33). Goldman first exposed normal white and black skin and also white and black human skin covered with various black dyes to the ruby laser (34) and then attempted to treat cutaneous lesions such as seborrheic keratoses and superficial hemangiomas (33,35,36) and tattoos (37). Histologically, nonspecific thermal destruction of the cutaneous target occurred; clinically, there was long-lasting oozing and crusting, usually resulting in scarring, which was fortunately only rarely hypertrophic. By

He also experimented artistically and performed laser sculpting on a variety of media, which he exhibited at dermatologic meetings.


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Figure 1.5 Leon Goldman, MD, “father” of laser medicine and surgery. (Courtesy, American Society for Laser Medicine and Surgery.)

1967 (38) he had concluded that both long-pulsed ruby and “neodymium” (?Nd:YAG) laser were specifically absorbed more by colored tattoo pigments than by the surrounding normal skin and this distinguished laser surgery from techniques such as electrosurgery, which produced nonspecific coagulation necrosis. His first experiment with a Q-switched ruby laser in 1964 showed craters on normal and tattooed skin for focused beams as he had obtained with the normal mode ruby laser. With nonfocused impacts he noted a selective difference with no damage to normal skin but transient whitening of the tattooed area without significant damage to the skin but with only edema and spongiosis apparent (37). His contributions were the first to suggest the concept of selective targeting by lasers. 3.

RUBY

The ruby laser was first used on the eye by Zweng et al. (39) in 1962. It was the principal laser studied by Dr. Leon Goldman in his earliest work (40–48). Almost 15 years passed before others took up Goldman’s mantle and began in earnest to perform cutaneous laser surgery. Ohshiro’s extensive work with normal mode ruby laser and nevi and other dyschromias including port-wine stains (49) did not begin until 1975. Studies of Q-switched ruby lasers for treatment of tattoos took a full 20 years and FDA approval, still another decade. 4.

OTHER NEW LASERS

Javan developed the first gas laser, He–Ne, in 1961 (50). Johnson produced an infrared laser beam from a Nd-doped yttrium–aluminum–garnet rod (Nd:YAG) also in 1961 (51). By 1964 Goldman was using this laser for experiments on tattoos and normal skin (37,52). 4.1.

Argon Laser

Bennett et al. (53) invented the blue-green argon laser in 1962. It was first used on the eye by L’Esperance (54) in 1967. This laser became commercially available in 1971 (55) and

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was the first laser to be widely used for treatment of cutaneous disease once the initial excitement, and unfortunately concurrent disappointment, with the ruby laser had passed, which had proven to be uncontrollably too destructive for skin disease in its original industrial format. Reports by Apfelberg and coworkers (56 – 60) begining in 1976 about their experiences with the argon laser since 1972 were the stimulus and seminal event for the upsurge in interest by dermatologists and plastic surgeons, though Leon Goldman’s group (61 – 65) had earlier published data on its usefulness. The mid- to late-1970s, after now a second decade, were the formative years for cutaneous laser surgery. Numerous dermatologists and plastic surgeons began to use the argon laser (66) and a flood of laser-related papers began. Arndt and Noe and their coworkers in Boston (67) in a series of papers began the first formal introduction to the dermatologic readership of laser terminology and to the histologic, clinical, and spectrophotometric analysis of what argon lasers could perform on a variety of vascular lesions (68 –70). By the late 1970s and early 1980s these reports as well as thermal models to help understand the dynamics of laser –port-wine stain interaction were formulated in rapid succession. Concurrently, the carbon dioxide laser appeared in the cutaneous surgeon’s armentarium and the American Society for Laser Medicine and Surgery (ASLMS) was founded. What the argon laser allowed for the first time was a therapy for widespread telangiectasia that was sensible in that destruction proceeded from the vessel outward rather than from the surface of the skin inward as by electrodesiccation or electrofulguration, then the standard treatment. In practice, with early argon laser surgical techniques there was thin second-degree burn injury involving the papillary dermis and the entire epidermis. Still, since the maximal energy dissipation was in the vessel itself rather than on the surface of the skin it seemed more reliable particularly for more deeply situated and resistant spider angiomas and for treating networks of fine vessels extending over large areas of the cheeks as in extensive rosacea. For congenital port-wine stain this treatment was miraculous. Ten percent of patients could expect entire clearance of their vascular malformation and 75% of the remaining patients would have dramatic and long-lasting or permanent and significant lightening with only one treatment. With further treatments the stains continued to lighten further (71,72). Alternatives prior to laser included mutilating procedures such as cryosurgery in which nonspecific and unquantifiable damage led to improvement with scarring, or tattooing with skin-colored pigments which only lightened the areas slightly in an artificial-appearing manner, superficial radiation (Fig. 1.6) with progressively worsening radiation dermatitis and development of skin cancer, or excision with grafting (Fig. 1.7) which was often more of a technical than a cosmetic triumph. There were several historically relevant adverse sequelae that began with this instrument. The first was a seminal event whose importance took almost 20 years to gain recognition, the use of nonphysicians, in this instance, nurses, to perform argon laser surgery. In the “reproducible” or “sense” technique—which meant using a standard protocol of power setting, spot size, pulse duration, and prechilling (Gilchrest) or postchilling, and postoperative wound care appropriate for a second-degree burn injury, or one that could be repeated reliably from patient to patient and physician to physician and also could be quantifiably studied and reported in a series of patients treated with the same or precise but differing parameters—intense monotony was the rule. Imagine 5000 bursts of laser energy clicking off second by second for 1 h merely to cover a 2 by 3 in. square of port-wine stain! To some laser surgeons it seemed more appropriate to use one’s trained skills for “real surgery” whereas a trained assistant could hold a handpiece when given standard parameters and perform “laser surgery.” This time-saving assistance


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Figure 1.6 Port-wine stain, years after radiotherapy.

was used by Apfelberg (56 –60,73) but he also reported an acknowledged incidence of hypertrophic postoperative scarring of 16%, which was 3 –15 times higher than the experience of other laser surgeons (68,70,74 – 77). The question of nonphysicians performing laser surgery (vide infra) became a major issue by 1998 (78,79). Monotony of this technique and its slowness in covering large areas had many more aggressive laser surgeons using the nonreproducible or nonsense technique—passing the laser in a continuous beam rapidly by hand or “air-brushing” over the area to be treated.

Figure 1.7 Port-wine stain, after split thickness skin grafting.

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This could be a masterful and quick way of treating a port-wine stain without requiring multiple return visits but as a nonreproducible technique it was not universally reliable—not from patient to patient, not teachable and usable from physician to physician (certainly not from a printed article) and not even in the same patient in the same area since hand speed varied especially on turning corners. This was only surgical artistry at work. Avoiding excessive thermal damage and excessive flat or hypertrophic scarring required great skill. In addition, the lack of standard postoperative wound care consistent with the known care of burn injury in this technique made understanding literature and clinical abstracts a frustrating quest. Laser surgical interpretation was muddled by tremendously differing techniques and incomparability of results and style. The art of laser surgery flourished but the science lagged behind. A price was paid by patients for the lack of rigorous “reproducible” literature and the seeds of discord and controversy were laid down. Because of misinterpretation of the literature (70,74,76) only few laser surgeons (71,72,77,80) would treat children by argon laser; some would treat none under age 8, some arbitrarily none under age 12, assuming, in error, a 38% risk of scar, thus denying therapy to the age group in which the greatest emotional impact of having a port-wine stain was occurring (81 –85). A third adverse sequel of argon laser surgery reflected, in retrospect, poor judgment by the underreporting of scarring. The definition of only cosmetically unacceptable hypertrophic scar as “scar” was too limiting but was almost uniformly applied by cutaneous laser surgeons, who wished to focus instead on the dramatic overall beneficial results of argon laser surgery. 4.2.

CO2 Laser

The CO2 laser was invented by Patel (86 – 88) (Fig. 1.8) of Bell Labs in 1964, but the first surgical CO2 laser was developed by Polanyi et al. (89) in 1965 and was first exhibited in 1967. Jako (90) noted that the earliest laser work in otolaryngology was by Stahle and Hoegberg (91) in 1965, using a pulsed laser for inner ear irradiation, Conti and Bergomi (92) in 1966 for the posterior labyrinth, and Sataloff (93) in 1967 for otosclerotic stapes. About the same time in 1965 he first began studies with Polanyi on cadaveric vocal cords with the pulsed Nd:YAG laser hoping to find that the laser could be used to cut tissue, but it was able to produce only small lesions. By 1967 Jako and Polanyi

Figure 1.8 C.K.N. Patel, inventor of the CO2 laser. (Courtesy, Bell Labs/Lucent Technologies.)


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were examining the absorption of CO2 laser by human cadaveric vocal cords; they developed an endoscopic delivery system in 1968. Soon after, Strong, Jako, and Polanyi (94 –98) initiated laser laryngeal surgery. Jako (90) performed vocal cord nodule removal in a dog soon thereafter and first operated on a human in 1970. Jako described the “precision of the CO2 laser beam and good wound healing subsequent to its impacts” (94). Hall et al. (99) described incisional surgery by laser in 1971. For gynecologists serendipity (or better, foresight) initiated the specialty into laser surgery when Joseph Bellina (100 – 102), the father of the gynecologic laser, realized the potential of this instrument in treating neoplasia of the cervix when he observed CO2 laser surgery used to remove laryngeal lesions (103). Despite work by others such as Kaplan and coworkers (104 – 106), who in 1973 first used the CO2 laser on the cervix (104 – 106). Fischer claims that Bellina had great difficulty convincing other American surgeons to perform such surgery. The Gynecologic Laser Society was founded in 1979 and thereafter authors such as Dorsey and Diggs (107) and Baggish and coworkers (108,109) began to publish prolific studies on cervical, vaginal, and vulvar diseases. Cerullo and Burke (110) noted that experiments with laser on neural tissue began as early as 1964 but the laser was too destructive for the meticulous surgery required in neurosurgery; only when microsurgery also matured by the late 1970s did laser neurosurgery begin. Heppner and Ascher (111) initiated CO2 laser neurosurgery in 1976. The laser was ready and waiting but the rest of the technology for appropriate delivery was not. A similar hiatus between the development of lasers and their practical use in gastroenterology had occurred while the field waited for the development of appropriate fiberoptic technology for laser delivery—for such lasers as argon, Nd:YAG, and tunable dye (112 –116). Nd:YAG was first used for GI disease with fiberoptics in 1973 (112,113); Keifhaber et al. (113) reported its first use in GI bleeding in 1975. It was the early 1970s before cutaneous applications of CO2 laser began in studies by Goldman et al. (31,117,118) on skin cancer. Kaplan helped to develop the commercial Sharplan laser in 1972, which became a standard mass-produced surgical device. Among the early authors, Frishman et al. (119) and Kaplan and coworkers (105,106,120) also published on skin cancer, Kaplan et al. (121) on other plastic surgical applications, and, Stellar et al. on decubitus ulcers (122) and on excision of third-degree burns (123,124). Among dermatologists McBurney (125,126) pioneered its use in 1978, also after a hiatus of almost a decade, as a vaporizing instrument for the treatment of warts and tattoos. Adams and Price (127) decribed its use in treating basal cell carcinoma in 1979. Bailin’s group (128 –132) at the Cleveland Clinic authored numerous early anecdotal reports on tattoos and a variety of epidermal tumors and port-wine stains. Interestingly, Reid , a gynecologist, and Muller (133,134) were the first to use the CO2 laser on a large series of tattoo patients and the first to suggest that this laser had to be used in multiple stages with incomplete treatment in each stage since a .16% risk of hypertrophic scarring arose in their patients if the tattoo had been removed by laser in one visit. These observations were compatible with what was by then long known about removal of tattoos in multiple sessions by dermabrasion. Nevertheless, the authors exhibited an experience contrary to the innovative but conservative wisdom of Leon Goldman who advised repeatedly, and even framed a placard on his wall for emphasis, “If you don’t need the laser, you don’t use it” (31,135,136). Overzealous use of laser on cutaneous lesions here reflected the worst practice of experimenting with a new device merely because it was new and high-tech but without a total understanding of the nature of the destruction which would ensue (Fig. 1.9).

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Figure 1.9 Severe hypertrophic scars after CO2 laser surgery for port-wine stain by inexperienced laser surgeon.

A singular, but fortunately nonscarring, abuse of Goldman’s maxim took place in the early evolution of podiatric laser surgery where fees of thousands of dollars were charged for laser debridement of diseased nails (i.e., an expensive laser analog of a nail clipper), giving patients a sour taste about the ethics of laser surgeons. Another adverse side of this laser’s history is that it was the first cutaneous laser about which unreproducible results were first reported in the literature and heated controversy first began to appear at laser meetings, particularly with claims made for healing of keloids. Though initial reports were overwhelmingly enthusiastic (131,137), claiming almost universal and persistent clearing with laser alone subsequent authors found a significant recurrence rate even with adjunctive therapy (138 – 141). Also, the laser’s “basic advantages” were subject to hyperbole and were promoted as 1. 2. 3. 4. 5. 6. 7. 8.

Noncontact surgery Dry-field, almost bloodless surgery Highly sterile surgery Highly localized and precise microsurgery Clear field of view and easy access in confined areas Prompt healing with minimal postoperative swelling and scarring Apparent reduction in postoperative pain No electromagnetic interference with monitoring instrumentation (120)

The number of times the same Kodachrome of this table was shown by dozens of laser lecturers became countless and laser dogma with little or no basis in critical anecdotal or peer-reviewed science became well instilled early in cutaneous CO2 laser surgery. This instrument was wonderful in that it was noncontact surgery and could be


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used as a vaporizing or excisional tool in patients wearing electronic devices or on anticoagulants. However, it could not stop freely running blood from vessels greater than 0.5 mm in diameter. In fact, hemostasis was often better in wart surgery with topical application of hemostatic Monsel’s solution than by laser charring and overburning the base of the wart. On digits a tourniquet or digital compression could produce equal hemostasis without the need for the laser. The field was not necessarily sterile, particularly at low fluences when less that 500 W/cm2 was applied. With high fluences it was found useful to sterilize wound bases in decubitus ulcers, synergistic gangrene, burns, and osteomyelitis (120,142– 144). Healing was not prompt; in fact, it was slower than traditional cold steel surgery or dermabrasion (145,146). Furthermore, the subsequent re-epithelialized area of a vaporization site was often fragile for months, capable of producing spontaneous bullae and hypertrophic scarring if that new surface had broken down. Pain was not reduced since nerve endings were not neatly sealed (147). When employed appropriately (148) the CO2 laser can safely and effectively treat dozens of cutaneous conditions, often better than older techniques including vaporization of actinic cheilitis and actinic keratoses, adenoma sebaceum, angiokeratomas, appendageal tumors, Bowenoid papulosis, condyloma acuminata, digital mucous cysts, epidermal nevi, Hailey –Hailey disease, ingrown nails, lichen myxedematosus, lichen sclerosus, lymphangioma circumscriptum, neurofibromas, nodular amyloidosis, pyogenic granulomas, rhinophyma, rhytids, sebaceous hyperplasia, xanthelasma, as well as cosmetic applications of resurfacing. Excisional applications for blepharoplasty or for patients compromised by anticoagulation or electronic devices such as pacemakers are widely employed.

5. 5.1.

MULTIDISCIPLINARY SOCIETIES Laser Institute of America

In 1968, partly at the instigation of Arthur Shawlow, a group of laser researchers in California founded the Laser Institute of America. This first meeting was attended by 75 members and now has grown to 200 corporate and almost 2000 individual members. Based now in Orlando, Florida (www.LaserInstitute.org) this group focuses mostly on laser science and safety and credentialling standards. It also is the secretariat and publisher of the ANSI standards, the latest of which is Z136.3 last revised in 1996. It sponsors a variety of courses and both the annual International Congress on Applications of Lasers and Electro-Optics (ICALEO) and the biennial International Laser Safety Conference (ILSC). 5.2.

International Society for Laser Medicine and Surgery

In 1975 Israeli surgeon, Dr. Isaac Kaplan, and others founded the first major interdisciplinary medical-surgical laser society, the International Society for Laser Medicine and Surgery (ISLMS), and held the First International Symposium on Laser Surgery in Jerusalem in November 1975. 5.3.

American Society for Laser Medicine and Surgery

In March 1979 in the USA, Drs. Ellet Drake and Leon Goldman set about establishing a multidisciplinary group of physicians and scientists who might be interested in exchanging

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knowledge and exploring uses for lasers in medicine and surgery and invited 280 renowned scientists from around the world, of whom about half attended, to an organizational meeting in San Diego in January 1981, where the ASLMS was founded. This seed organization (Fig. 1.10) has blossomed into one with now over 3000 physicians, veterinarians, nurses, industrial innovators, and laser researchers, and is the largest of its type in the world. This group (www.aslms.org) has met annually since then, running several full-day single-subject symposia as well as providing the largest forum for presentation of original abstracts on laser medicine and surgery in the USA. It sponsors the journal Lasers in Surgery and Medicine, the sixth “most cited” surgical journal, and has established ethical standards for the use of lasers and also formulated general guidelines for hospitals to use in credentialling laser surgeons. The happy concurrence of publications of unique results of argon laser surgery, the availability of the CO2 laser, and now a society dedicated to promoting laser use and widespread education produced the first tidal wave of interest in lasers by cutaneous surgeons.

6.

LASER SAFETY—THE AMERICAN NATIONAL STANDARDS INSTITUTE

Although Leon Goldman had initiated studies on laser–tissue interaction in 1961 as a means of exploring laser hazards and safety precautions, it was not until 1975 that the FDA established a performance standard for laser products as a supplement to the Radiation Control for Health and Safety Act of 1969 (102). Four classes of risk (I through IV) were established. Safety features and labels required for each of these classes of lasers were outlined in the Federal Register (149) and are best summarized and explained in the manual from the American National Standards Institute (ANSI). Interestingly, hazards were concerned with the work environment and accidental human exposure—relative risks of accidental damage to the eye and skin defined the classification schema (150–153). Hazards and

Figure 1.10 American Society for Laser Medicine and Surgery group photograph of the second annual meeting, 1982. (L. Goldman, first row center; G. Brauner, third row, center.)


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controls cited by ANSI in document Z136.3 include engineering controls, administrative controls, procedural controls, and protective equipment (154,155). Strict protocols were formulated by hospital laser safety committees for patient and personnel safety. They reviewed electrical hazards, eye and skin burn hazards, protective eyewear of specific optical density and absorbance of the appropriate wavelength, protective clothing and absorbent wet drapings of flame-resistant materials, nonreflective instruments and anesthesia ventilation systems, and the ready presence of fire extinguishers (156,157). Communication patterns between the laser-operating technician and the surgeon for on– off and standby modes were formalized. Laser-specific in-servicing for nurses and technicians were made compulsory. Treatment of pathologic processes in a patient and hazards of incorrect or inappropriate use were not addressed and to this day have still not been written into law (vide infra).

7.

PERSONNEL AND PATIENT SAFETY—PLUME

Since lasers used in cutaneous surgery until the most recent thermally “cool” devices essentially generate much focal heat or mechanico-acoustic waves, either splatter debris or smoke are often generated. The presence of acrid smoke generated from boiling and charred skin by the CO2 laser and the need to remove such obvious pollution (158 –161) led to seminal discoveries of the nature of operative-generated smoke and splatter debris (162). Even though electrosurgical apparatuses used for decades produced visible smoke it had been tolerated without comment. This was clearly not so with the laser. Laser smoke or debris may contain tumor cells (163,164), blood, blood-borne pathogens such as papilloma virus or HIV (165 – 169), bacteria (170,171), particulates as small as 0.1 mm in diameter, and toxic gases including benzene, formaldehyde, and acrolein (154,158,160). For slower-moving particulates, such as those generated by CO2 laser, not only masks which filtered less than 0.3 – 0.1 mm (167,172,173) but also vacuum evacuators held within 1 cm of the target area became necessary (161). For faster-moving particulates such as those generated by the immensely energetic Q-switched lasers the value of suction and the speed required have not been ascertained since the velocity of ablated material is 10,000 m/s (174); physical obstructions and traps such as plastic cylinders attached to ruby or Nd:YAG handpieces or clear membranes applied directly to the skin surface and shot through have been used. Jako (164) notes that various pioneering researchers including himself who had first experimented with the Nd:YAG laser on tissue in the mid-1960s found that it exploded tissue and that scattered cells and tissue fragments were found in the operative area. Nevertheless, Fader and Ratner (173), citing several authors such as Gloster and Roenigk (175), who suggested that CO2 laser surgeons should have had a larger incidence of wart contamination, and Hughes (176) and Hughes who could not find human papilloma viral DNA in Er:YAG wart plume, de-emphasize the inherent risk of plume infection.

8.

PATIENT SAFETY—SCAR

The argon laser had not been developed specifically for the treatment of cutaneous disease but was used mostly for spectroscopy. Most manufacturers were supplying instruments with 1 or 2 mm spot sizes with 0.1 s being the shortest pulse duration (shutter speed). Even with the “minimal dose” technique of Cosman (71,72), wherein one selected the

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lowest power setting to produce a visible whitening of the skin after laser impact, one had to depend on this visual signal which reflected not vascular obliteration alone but that plus coagulation of the dermis and perhaps even the epidermis with a change in light reflectance, so-called “blanching.” Thus, an inside-out second-degree burn injury was produced. The necrotic collagen as well as the obliterated vessel had to be replaced by new collagen, which might end up as transparent as normal collagen or which frequently, even without excess elevation, became dense enough so that the area became opacified and lighter than normal skin color. For at least its first 12 years Leon Goldman’s laboratory deemed the desirable end point of treating PWS by long-pulsed ruby laser treatment (136) as an improvement by “producing collagen damage with superficial fibrosis [to] . . . change the optical quality of tissue.” In other words the end point was production of scar tissue but it was not ever called so except by Brauner (75) and Schliftman concerning argon laser, who also recognized the similarity of this “opacification” to the appearance of an opaque collagen skin test in transparent skin (Figs. 1.11 –1.13). Such opacification was later cited as an adverse effect by Geronemus (177) but was mistakenly thought to be hypopigmentation. It was not a reflection of total and permanent destruction of melanocytes by the argon laser since these areas did tan in sunlight and even hyperpigmented without sun but represented a true scar. As a typical example, in a large review as late as 1986, Apfelberg and McBurney (60) cited a 14% incidence of “scarring” in port-wine stains treated by argon laser with a variety of parameters and a 35% risk in strawberry hemangiomas. Nevertheless, photodocumentation of their results, even those reported as good results, clearly showed scars, but these were mischaracterized as not only “no change in sebaceous skin” but also exhibiting mild scarring in nasal telangiectases, “flattening and blanching . . . of strawberry mark” but with a densely opaque and hypertrophic lip scar, “lightening” but with a dense slightly hypertrophic scar on a treated tattoo, “without scarring” of a pyogenic granuloma which does have a small hypertrophic scar, “resolution of trichoepithelioma”

Figure 1.11

Flat opaque scars after argon laser surgery and appropriate dressing.


Figure 1.12

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Almost invisible opacification of an argon laser test area.

without mention of an opaque atrophic hairless patch on the lip. The results were so good in many authors’ experience as compared to their prior attempts at improvement that small amounts of scarring were similarly overlooked and certainly underreported by most laser surgeons who reserved the term “scarring” to mean real hypertrophic scarring. The reader of a paper or the audience of a lecture was led to believe that this instrument was not only wonderfully effective—which it was—but that it was also not as problematic as it really

Figure 1.13 Same area after stretching, exhibiting flat opacification and not true hypopigmentation.

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turned out to be. Time and time again, even with photographic documentation showing scarring, authors mentioned only improvement of the primary lesion and left it up to the reader to deduce that scarring was more prevalent than reported. A variety of methods were attempted to minimize hypertrophic scarring. Apfelberg tried to treat only small areas assuming that a larger second-degree burn injury would be more likely to hypertrophy. He spaced his treated areas with parallel untreated areas in a “banded” or “striped” pattern but eventually discarded the technique since scars continued to appear (73,178,179) (Fig. 1.14). Cosman tried to minimize the amount of thermal damage by using the lowest possible power setting to be effective. Unfortunately, the visible end point used in port-wine stains without magnification was not watching the vessel disappear or coagulate but watching the dermis and epidermis coagulate. With this minimal dose technique, Cosman used the lowest power setting to produce discrete whiteness of the epidermis after laser impact for each individual patient and used that dose uniquely for the patient with 0.2 s bursts. Many surgeons, including Cosman, used the dot-by-dot intermittent technique with slight or no overlap of the 1 or 2 mm bursts to produce uniform as well as reproducible injury. Scheibner and Wheeland (180,181) used the continuous wave tunable dye laser tuned to 577 nm with magnification by 8-power optical loupes to trace out vessels and observe them constrict and coagulate as the visual end point. Tracing was done in a continuous fashion but with the surgeon’s hand moving quickly. This meticulous and incredibly laborious method was thus more sparing of the epidermis and the dermis surrounding the vessels. Since the minimal achievable pulse duration was 50– 100 ms scanners were developed (182) which could move a beam so quickly over an area that the effective time of injury was 1 ms and much more focal to the vessel (183,184). Scanners were also developed for use in gynecologic surgery and by 1982 for the cutaneous CO2 laser with a microslad coupled to the Sharplan 733 laser (Fig. 1.15) and later a Sharplan 777 scanner; these scanners were not used primarily for vascular lesions but for more precise vaporization of large areas such as tattoos and for resurfacing of scarring from acne, varicella, or trauma and other contour defects such as rhytids. Robotized hexagonal scanners were introduced by Rottoleur et al. (185) in 1988 initially for use with the argon laser, but later they were used with continuous wave dye and copper vapor lasers (Fig. 1.16) which had appeared commercially. The release of pulsed dye lasers for vascular and pigmented lesions dimmed the aura and popularity of hexagonal scanners (186) but scanners appeared again in the mid-1990s as adjuncts for laser resurfacing with carbon dioxide and Er:YAG lasers.

Figure 1.14 Hypertrophic scarring after argon laser “stripe” technique and an undressed wound.


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Figure 1.15 Sharplan microslad scanner for CO2 laser cutaneous resurfacing and tattoo ablation. (Courtesy, Am J Cosmet Surg.)

Chilling heat-injured skin was long known to diminish the extent of overall burn injury so that postlaser cooling of the treated area became a common afterthought. Perhaps more importantly, if local anesthesia had not been used, it would have helped relieve the symptomatic burning pain. Preoperative chilling was attempted (187) to

Figure 1.16 Hexascan scanner, the first American application by Alan Schliftman, MD, of the most widely used scanner for continuous or quasi-continuous lasers (argon, continuous dye, copper vapor, copper bromide) for vascular and pigmented lesions. (Courtesy, Am J Cosmet Surg.)

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slow down and pool targeted erythrocytes in port-wine stains and not to diminish burn injury. Unfortunately, no pooling was statistically demonstrable and the main “benefit” was a lower incidence of atrophic scarring, scarring which could just as well have been caused by lack of closed dressings. Even intraoperative chilling (188 – 191) was attempted in the hope of preserving the epidermis so that there would be no open wound to become potentially infected and to preserve the upper papillary dermis. Since an inside-out thermal injury was produced by the laser, a lower set temperature point for the epidermis meant that the temperature rise from spread of heat from the injured vessel would still be below a necrosis threshold of 708C (9). Chess (190,191) has promulgated for years the importance of intraoperative chilling for a variety of lasers and invented the first practical “icing” device. Landthaler (189) had used an ice cube to chill the epidermis as he moved his deeply burning continuous Nd:YAG for hemangiomas. Leon Goldman (188) had toyed with a variety of unusual chilling implements in his laboratory. A deeper understanding of the thermokinetics of laser injury has led to resurgent interest in chilling in the late 1990s for maximal thermal injury to targets such as deeper or larger telangiectases (192) and venules, deeper or resistant port-wine stains (193 –202), and the hair follicle. A concurrent approach to greater selectivity of the laser for its target in the mid- to late-1980s centered on the greater relative absorption by oxyhemoglobin than melanin of yellow wavelengths (203). The argon-laser-pumped continuous tunable dye laser tuned to 577 nm (204), the quasi-continuous copper vapor laser (205 –210) at 578 nm, and the pulsed dye laser at 577 nm, had better absorption and deeper penetration so that theoretically deeper vessels could be targeted and more energy could be delivered to destroy vessels with less or no epidermal injury. The continuous dye and copper vapor were both found to be somewhat more effective than the blue-green argon but their clinical thermal effect was essentially unchanged from the argon experience (206) whether made freehand or by scanner. They were followed shortly in the cutaneous surgical marketplace by the quasi-continuous copper bromide laser (211,212) and the quasi-continuous krypton laser (7). Interestingly, the pulsed dye laser was shifted to 585 nm, which is less well absorbed than 577 nm, and now is also used at 595 nm (213).

9.

POSTOPERATIVE WOUND CARE

As noted before, interpretation of adverse events when continuous wave lasers were employed for cutaneous laser surgery and epidermal necrosis ensued became obscured by the fact that scarring was underreported or redefined and postoperative care was not standardized, not mentioned in the literature or in lectures, and sometimes not given. Second-degree thermal wounds all scar and it is likely that the absence of postoperative dressings over the necrotic wound in early argon laser surgery was responsible for much of the incidence of hypertrophic scars. With proper postoperative dressings and antibacterial ointment the incidence of such scarring dropped to less than 1% (75,77) from a range of 3 –16% or more (60,68,71,73,74,178,214,215) (Figs. 1.11 and 1.17). Brauner and Schliftman were early proponents of scrupulous postoperative wound care. Unfortunately, there was an accompanying and unexpected large incidence of contact dermatitis to bacitracin with large areas of coverage (216 –218). Though the need for scrupulous postoperative care is now well established for this type of laser induced wound, the most appropriate type of dressing has been controversial in the past half-decade as facial resurfacing became the leading example of cutaneous laser surgery (218 – 227).


Figure 1.17

10.

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Hypertrophic scars after argon laser surgery and an undressed wound.

SELECTIVE PHOTOTHERMOLYSIS

Leon Goldman was seminal in beginning and motivating the use of medical and surgical lasers but the direction of laser use was related to the industrial lasers provided to us. Micromanipulators, fiberoptics, scanners, and microscopic couplers were all cleverly invented accessories for the main item but the main item was never designed from the ground up for altering specific pathogenic targets, that is, not until 1983. The second most remarkable seminal event for laser surgery was the optical construct, which allowed us to understand the nature of the amount of thermal or acoustic alteration that was minimally necessary to produce our biologic result. Not only could we select a target and an appropriate laser using the target’s relative absorption characteristics but we could also construct a laser putting out a burst of light corresponding in its duration to the thermal relaxation time of the target. This combination of selection by absorption and by size became the theory of selective photothermolysis as elaborated by Anderson and Parrish (4,5) (Fig. 1.18). It was the first of many modeling constructs around which medical lasers would be manufactured. The courtship of laser industry and laser surgeons, which had begun after the institution of ASLMS, was now ready for the full-fledged partnership of marriage. Now laser surgeons could request industry machines capable of specific tasks. The pulsed dye laser for vascular lesions was the first of these many instruments (228 –235). Though shifted from its original experimental format of 577 nm (236,237), 360 ms pulses, and 5 mm spot size to 585 nm (235,238 – 244) and 450 ms and now up to 600 nm and 20 ms pulses with 5, 7, and 10 mm spot sizes, it allowed for rapid treatment of large areas—perhaps 100 times faster than the argon laser had been. Pain was usually not severe enough to require anesthesia except in children. There was almost no thermal damage to the epidermis except mild crusting by days 3– 4 postoperative and thus no second-degree burn injury and essentially no risk of either hypertrophic or flat opaque scar. In the mid- to late 1980s it very quickly became the vascular laser of choice despite the simultaneous appearance of other quasicontinuous yellow lasers (205 – 207,245 –248). Because of its greater safety and specificity it was widely offered to children who for the most part (74,76,77,80,241,249,250) had been denied continuous or quasi-continuous laser treatments. The dramatic impact of a laser able to treat deformed children without scarring and with a “100% cure rate” (240) was earth-shaking.

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Figure 1.18 R. Rox Anderson, MD, conceptualizer of “selective photothermolysis.” (Courtesy, Wellman Laboratories of Photomedicine.)

What actually happened was unfortunate as this drama had an adverse side as well. Tan et al.’s enthusiastic report in the widely publicized New England Journal of Medicine had the public convinced that the laser was painless and 100% effective, thus putting all cutaneous laser surgeons on the spot trying to re-explain that neither scenario was true. This laser has been documented to clear PWS in only 40% of patient populations (251) with repeated treatments, though the remainder of patients are very significantly improved. As initially with the carbon dioxide laser, hyperbole was fashioning unrealistic public demand. The second adverse sequel was that this industry –surgeon marriage meant that there was an increasingly important role that the medical – industrial complex would play, not just in the delivery of care, but also in its cost since the new lasers represented hundreds of thousands of dollars in investment to be paid off by the laser surgeon. There was, as well, the possible perversion of scientific methodology and reporting by not-so-subtle conflicts of interest such as special deals in pricing of lasers, free or loaned lasers, research grants, surgeons acting as spokespersons in advertising routines for companies; these same laser surgeons would then be called upon to present or publish new data in what the audience was supposed to think represented no conflict of interest. For the first time it would not be egos or ideas under attack by skeptical laser audiences but the very ethics and truthfulness of the presenters. This was a nasty and unexpected challenge to honest scientific methodology; vocal controversy and insult became an unfortunate coparticipant at laser meetings as evidenced by chairmen’s forewarning to their panelists at the 1998 ASLMS about personal (ad hominem) attacks.

11.

WELLMAN LAB AND BECKMAN LAB

Although Rox Anderson first immersed himself in lasers as an undergraduate student in 1976, in the Wellman Labs of Photomedicine (www.wellman.mgh.harvard.edu), of


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which he is now the research director, had opened at Massachusetts General Hospital (MGH) in Boston in 1974 as a multidisciplinary research laboratory devoted to basic and applied research in human photobiology. It is now the world’s largest biomedical laser research facility as well. In 1988 a laser applications research laboratory to develop specific medical laser applications was formalized. In 1992 the MGH laser center, a hospital-wide multispecialty center to deliver care by laser therapy to a variety of patients, was established in coordination with the Wellman Labs. In 1982 the Beckman Lab (www.bli.uci.edu) was founded by Drs. Michael Berns and Hugh Beckman, both bioengineering scientists. This institute is now part of the University of California, Irvine, and houses multidisciplinary basic research groups, as well as having a clinical laser surgical center for patient care. It, along with the Wellman Lab, are unique facilities in the USA for fundamental laser research. The rest of laser progress has essentially been the fruit of individual practicing laser surgeons or research grantees in concert with clever industrial invention.

12.

Nd:YAG LASER

The Nd:YAG laser was first used by Goldman in studies on tattoos shortly after its invention in 1961. Though used primarily in endoscopic gastrointestinal laser surgery, particularly for bleeding, since it had such deeply penetrating nonselective thermal necrosis of almost 4 mm when used in normal mode, Landthaler et al. (189) in Germany in the mid-1980s first advanced its use for therapy of large vascular cutaneous tumors. These cavernous hemangiomas (252–258) or large blebs of port-wine stains (52,215) were too thick to be affected by the available argon laser or even the pulsed dye laser when it appeared. Intraoperative chilling by moving an ice cube quickly over the skin just prior to single or a group of widely spaced bursts was necessary to attempt to preserve epidermal integrity. David and coworkers (253) noted that the scarred resultant area might then be excised in a secondary procedure with minimal bleeding for an even better cosmetic result. Apfelberg et al. (254,256,257) and Waner and coworkers (259,260) promoted the use of the Nd:YAG laser in the USA with both noncontact and contact surgery with a sapphire tip, (261,262). The laser heated the tip, which then acted as a hot hemostatic scalpel (254). With Q-switching (vide infra) this laser became widely employed worldwide for treatment of tattoos and pigmented lesions in the 1990s. Adaptation of the normal mode Nd:YAG laser by doubling its frequency and thus halving its wavelength to 532 nm makes it particularly applicable for the treatment of vascular lesions with a similar therapeutic profile compared to other continuous wave lasers such as argon (263). Only recently, in the late 1990s, when combined with a chill-tip, has its use been expanded again for the treatment of vascular lesions but now without epidermal thermal damage and mostly without purpura (vide infra). 12.1. Q-switching In 1967 Leon Goldman (38) published his 3-year experience with the long-pulsed 1.8 ms ruby laser and the neodymium laser to treat tattoos, producing nonspecific histologic necrosis and subsequent fibrosis with decreased pigment. In 1964 Goldman had already first compared the normal mode and the “new” Q-switched ruby laser (37) on tattoos. By increasing the power density, he was able to show permanent tattoo pigment removal with the Q-switched ruby laser by 1967 (38). In 1967, a full 15 years before Reid, Laub and coworkers (264) showed that Q-switched ruby laser with 10 ns pulses

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and 5.4 mm spot sizes with 2 – 4 J output could destroy tattoo pigment without epidermal damage (265). Kitzmiller (136) in 1974, reviewing Goldman’s Cincinnati experience, also claimed that Q-switched ruby laser in nanosecond bursts had been found to be more effective than normal mode ruby laser in tattoo removal. In 1983, Reid et al. (266,267) described the first series of patients treated successfully with Q-switched ruby laser without scarring. Another historical laser hiatus occurred, this time almost a decade before American publications on tattoo removal (268,269) and Polla et al. (270) and Dover et al. (271) on melanocyte destruction followed by FDA approval in 1989 (3), which allowed American use of commercial Q-switched ruby lasers for hyperpigmentation and tattoos, 25 years after Leon Goldman first used it. Q-switching is compatible with the principle of selective photothermolysis since the thermal relaxation time of targeted melanosomes or tattoo pigment granules are within the nanosecond range emitted by a Q-switched device. Soon after the appearance of the “new” Q-switched ruby laser, the Q-switched Nd:YAG laser emitting at both 1064 and 532 nm (272 – 274) and the Q-switched alexandrite (275 – 277) lasers were marketed in the early 1990s for treating similar conditions (Fig. 1.19). A non-Q-switched but nanosecond pulse flashlamp-excited dye laser (PLDL) for hyperpigmentation also appeared; its wavelength of 510 nm was close to the most effective wavelength for melanosome destruction (514 nm) (278,279).

13.

PIGMENT LASERS

The high prevalence of unsightly pigmented lesions such as solar lentigines, flat seborrheic keratoses, cafe´ au lait macules, and even nevi offered a large spectrum of potentially treatable lesions and spurred the boom in the use of pigment-targeting lasers. Q-switching was not essential for melanocyte destruction but allowed for more intense focal melanosome injury and lesser risk of scarring, but continuous wave green argon, KTP, krypton, and copper vapor lasers had been widely used in the 1970s through the early 2000s for benign pigmented lesions with acceptable results (280 – 283). Hyperbole reigned here too. Initial reports of very high success rates (284,285) for cafe´ au lait macules were tempered by frequent recurrences reported by subsequent investigators (276,279,286 – 288). Even the use of progressively deeper penetrating red alexandrite or ruby lasers seemed no more permanently effective than the more shallow-penetrating green lasers.

Figure 1.19 First observation of dermal holes immediately after tattoo pigment explosion in minipigs produced by alexandrite laser by Gary Brauner, MD, and Alan Schliftman, MD.


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“Nonsense” science also played a role when these lasers were used to treat lentigo maligna. Arndt’s initial anecdotal case report of success with the shallowly penetrating argon laser for lentigo maligna had to be retracted 2 years later by the recurrence of the melanoma since it was too deep to be entirely eradicated (289,290). Such nonsense application of laser was potentially life-threatening since obliteration of only the superficial component of a lentigo maligna allows deeper melanoma to metastasize (J. Spencer, personal communication). Treatment of tattoos and nevus of Ota (291) temporarily but inadequately moved the focus of laser – tissue interaction from merely the physics of light absorption by skin and adnexae to the equally pertinent subsequent biologic behavior of the injured tissue. These two conditions continued to improve and recede long after therapy—the rush to treat them as quickly as possible and maintain patient satisfaction undermined proper side-by-side studies to ascertain biologically appropriate treatment intervals. Unfortunate counterpoints in the 1990s were the unsettling discoveries of unanticipated very delayed (months) opacification of CO2-resurfaced areas or even of pulsed dye or continuous dye laser-treated poikiloderma of Civatte (292) as well as the fortuitous discovery of beneficial tightening of rhytids seen after CO2 resurfacing. Treatment of nevocellular nevi by lasers has reached no consensus or historical conclusion. Some of Leon Goldman’s first attempts with laser were centered on the treatment of melanoma (41,47). Much of Ohshiro’s early work in Japan in the late 1970s involved destruction of nevi by long-pulsed ruby lasers (49). Brauner and Schliftman (286) first raised the question of the “angry melanocyte” in discussing idiosyncratic hyperpigmentation of a cafe´ au lait patch as a result of the first use of the pulsed 510 nm PLDL laser for treating hyperpigmentation. Postinflammatory hyperpigmentation (293) was by then long known to occur after CO2 , argon, copper vapor, and now after Q-switched Nd:YAG (288), 1320 Nd:YAG (294), Q-switched ruby, and long-pulsed ruby hair removal lasers. Brauner’s was the first clinical recapitulation of Dover et al.’s (271) first experiments with pigmented guinea pig skin showing that guinea pigs treated at less than a “threshold” of 0.3 J/cm2 developed hyperpigmentation and Hruza et al.’s (295) 1991 electronmicroscopic studies of normal human skin showing subthreshold stimulation of melanogenesis, which was precisely the opposite of what was intended. Attempts to debulk congenital nevocellular nevi, which can be very unsightly, may be of a size or location where a mutilating scar might be left after excision, and among which the giant ones are considered potentially premalignant seemed reasonable. Multiple treatments with well-absorbed Q-switched alexandrite or ruby lasers are required for debulking and a significant though nonpigmented residue of dermal melanocytes may still be histologically present (296 –298). If these melanocytes retain latent subthreshold stimulation precisely what risks are latent?

14.

SERENDIPITY

In the early 1990s within a decade of the marriage of surgeon and industry serendipity reminded us that not all laser developments are predetermined rationally. In 1993, Alster reported that, when treating hypertrophic, persistently red scars for the erythema with a pulsed dye laser, she obtained not just improvement of the erythema but a distinct textural improvement, so much so that the scars flattened, occasionally dramatically, after several sessions (299). At first argon laser induced scars, then hypertrophic scars of other cause, facial acne scars, and even keloidal sternotomy scars responded. When Alster considered atrophic scars she found a similar result. The scar texture improved to the eye.

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The scar became less depressed and the surface was demonstrably changed on skin surface topographic textural analysis by optical profilometry, erythema reflectance spectrometry, scar height measurements, and pliability scores (300 – 306). The pulsed dye laser rapidly became an instrument widely used for scar treatment or as adjunctive therapy. McDaniel reported in 1995 and 1996 (307,308) his results with striae distensae, which are in some ways histologic equivalents of atrophic scars. Use of the pulsed dye laser with a 10 mm spot size and a low energy fluence of 3 J/cm2 showed clinical improvement and measurable improvement of skin texture by optical profilometry. These results are reproducible in some capable hands (306) but not in others (309,310). Since striae are not made to disappear but only contract slightly, hyperbole by the lay press played a prominent and unnecessary role.

15.

RESURFACING

Focal laser ablation of acne scars was one of the earliest procedures performed by cutaneous laser surgeons in the early 1980s. Although the freehand airbrush technique could be performed on tattoos and still leave a cosmetically acceptable scar on the trunk and extremities, the artistry required made laser resurfacing of large areas of acne scarring or rhytids on the face potentially more hazardous than dermabrasion. It was especially worrisome because the latter healed within a 2-week time frame while laser wound healing was prolonged often beyond the 2-week window of healing after which unsightly scars could develop. Though scanners had been coupled earlier to the CO2 laser for gynecologic cervical ablation, only in 1982 did Brauner and Schliftman first introduce to the USA the Sharplan microslad scanner (182) which allowed precise controllable movement of the beam in an X –Y grid pattern with uniform though Gaussian ablation. Such uniformity not only led to better results in tattoo removal but also allowed for more controlled ablation for resurfacing the face for acne scarring. Although this was the first mechanically assisted laser resurfacing, it did not gain widespread popularity for rhytid removal because the healing time still was slower than that for dermabrasion, presumably because of residual thermal damage. Focal laser resurfacing was done for treatment of rhinophyma since 1980 (132,311) and for actinic cheilitis for much of the 1980s (312 – 314). In 1989 David et al. (315) presented the first report of 4 years’ experience on “laser resurfacing” for facial wrinkles by a CO2 laser with clinical and histologic improvement. Their technique really represented a 50% trichloroacetic acid peel supplemented by focal epidermal and upper dermal coagulation without visible vaporization of the deeper rhytids by the defocused 0.1 s gated hand-held laser. Healing took 5– 14 days. Studies on superpulse CO2 laser had been done in the late 1980s (316,317), but in 1993 Fitzpatrick (318) presented studies showing that the principles of selective photothermolysis could be applied to the CO2 laser, that a re-engineered “ultrapulse” laser delivering up to 500 mJ in a single pulse with a pulse duration of less than 1 ms, which is the calculated thermal relaxation time of skin, would produce the most precise vaporization and leave the smallest possible thermal damage of 50 – 100 mm. With such a small residue, more rapid tissue healing could be expected and the collagen to be laid down would more likely be thinner and less likely opaque. Whereas more traditional CO2 laser resurfacing could take 2 or even 3 weeks to re-epithelialize and even David et al.’s combined trichloroacetic acid (TCA) –laser process took up to 2 weeks to heal this, new laser allowed for healing after two or three passes in about 10 days. Traditional dogma of wound healing had indicated that a wound taking longer than 2 weeks to heal


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was much more likely to result in a visible or even unsightly scar. Since Fitzpatrick’s technique was used alone to treat entire faces, it was the seminal event in laser resurfacing (319,320). The appearance commercially of both the scanner-driven SilkTouch laser by Sharplan (with much more precise ablation than its older-generation scanning microslad device) and the Coherent UltraPulse laser which provided individual ultrashort pulses and the clinical and histologic reports of Kauvar and coworkers (321 – 324), David et al. (325), Dover and Hruza (326,327), Cotton et al. (328), Ross et al. (329,330), Chernoff et al. (331,332), Lowe et al. (333), and Lask et al. (334) led to an unprecedented avalanche of cosmetic surgeons beginning to perform laser surgery mostly for actinic damage and rhytids but also for acne scarring (335). Although chemical peeling and dermabrasion were long-established and safe techniques for the treatment of wrinkles, the ability to easily remove wrinkles to a precise and uniform depth (unlike peels), to remove the need for artistry (unlike dermabrasion and peels), to remove the risk of exposure to sprayed blood (unlike dermabrasion) and the high-tech appeal of the laser instrumentation compounded interest in the laser (227). Serendipity gave a coup-de-grace to the older techniques when it was soon noted that improvement in laser-treated wrinkling continued as the healed areas tightened and contracted over a period of months (319). Competing claims of efficacy of scanned vs. Ultrapulse lasers in numerous anecdotal reports were based on experience with one or other laser. Comparative studies of side-by-side treatments, not just randomized or anecdotal surveys, were needed and were much delayed by the costs involved in having more than one equivalent laser. These competing claims were laid to rest by studies such as those by Burns (336) on half-faces and by Alster et al. (337) with four randomized CO2 lasers for quarter-face resurfacing. The perception by industry of the huge potential market spurred on marketing and advertising unprecedented with other lasers. The whole direction of cutaneous laser surgery shifted dramatically from a medical –scientific discipline to a medical – industrial commercial one (338). Courses were now driven not by medical interest in academic settings but by almost weekly promotional courses directly by laser companies using guest laser lecturers. Roving laser rental companies first appeared with a “have laser (and technician), will travel” motto. In-hospital laser peer credentialling became a practical though not a moral irrelevancy. The early 1990s saw a new federal administration with health care as its priority and fostering HMOs as its club to beat down costs. In 1992 Medicare law drastically cut physician reimbursements. With the appearance of safe cosmetic laser surgery as an alternative for diminished income, not only traditional cutaneous surgeons (dermatologists, otolaryngologists, and plastic surgeons) but even family practitioners, dentists, oral surgeons, and gynecologists began to perform cosmetic cutaneous laser surgery. A sudden influx of large numbers of cosmetic surgeons into ASLMS changed its balanced multidisciplinary format to a predominantly cutaneous surgical forum. Preceding the explosion of interest in laser resurfacing in the USA, Kaufmann and coworkers (339 – 343) in Ulm, Germany, had been studying since 1988 (almost a full decade earlier) the erbium:YAG laser, which held the potential for much more precise cutaneous ablation since its absorption by water was an order of magnitude greater than that of CO2 . It had been first researched in the USA in the mid-1980s for ophthalmologic use (344,345). Walsh and coworkers (346,347) published the first American cutaneous studies showing the markedly diminished zone of residual thermal dermal damage after erbium:YAG pulses. Kaufmann’s initial studies were not followed by American cutaneous laser surgeons until 1997 when Teikemeier (also German) and Goldberg published the first preliminary study on 20 patients (348). Immediately, the laser pendulum began to swing away from the CO2 laser (which had been so heavily touted as safer and more efficacious

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than all prior resurfacing modalities) to the erbium; the CO2 laser was suddenly no longer viewed as such a “safe” instrument. The precision of the Er:YAG laser and the much smaller demonstrable degree of thermal damage left behind was hyped by industry and speaker alike. The simultaneous discovery that delayed opacification, misconstrued as hypopigmentation (349,350), could occur with some frequency in CO2-resurfaced patients helped accelerate the swing. The faster healing and decreased postoperative erythema of the Er:YAG laser was considered powerful evidence of its effectiveness and safety but at the same time laser surgeons also reported that results did not seem as good with this laser (351 – 354). Qualified statements about its use for shallow rhytids rather than significant ones now had to be employed to explain the poorer results. The lack of controlled side-by-side studies permitted the hyperbole to sweep away much interest in the CO2 laser and dozens of manufacturers got on the Er:YAG bandwagon. Hyperbole was again marching at a much faster pace than true science. Authors such as Alster and Adrian with systematic side-by-side studies brought order to the scene. Alster (355) reviewed laser resurfacing by six randomized Er:YAG lasers in her patients. Adrian (351,352) in his seminal histologic studies had earlier admonished other laser surgeons using the CO2 laser for resurfacing that they had misunderstood the nature of vaporization and thermal damage, that with the parameters of UtraPulse 500 microsecond pulses, unlike older traditional CO2 laser vaporization, dermal ablation was limited to the upper reticular dermis and further applications of the CO2 laser only produced more thermal damage and increased the risk of scarring. With the waters muddied by conflicting claims of Er:YAG’s efficacy vs. CO2 , it was again Adrian who showed with his careful histologic studies that equally deep destruction by Er:YAG and CO2 lasers would produce equal clinical results with equal healing times and equal erythema. He clearly unmasked the errors of the initial excitement as due to the laser surgeon’s not truly understanding the nature of the the two types of injury and basically not performing equivalent surgery with each laser. Commercial adaptations, including variable pulse durations, of the Er:YAG laser, to more closely resemble the CO2, have evolved over the past 4 years (356 –358). Combination therapies (359) relying on the virtues of each of these lasers were employed, producing faster ablation and leaving less residue by using CO2 first then erbium or more precise ablation but better hemostasis by using erbium first then CO2 (360) or even using both lasers through the same handpiece in the same laser device (361,362). Even the variable-pulse Er:YAG followed by shortpulse Er:YAG has been tried and seems to work even better than CO2 followed by short Er:YAG (360).

16.

LASER-ASSISTED HAIR TRANSPLANTATION

Concurrent with resurfacing technology was the suggestion that a narrow band of thermally damaged tissue should be hemostatic and might allow for rapid and bloodless hair transplantation by insertion of thin slits of hair-bearing skin or individual follicular units into slits or holes made by one of these lasers. Although with the CO2 laser a bloodless wound can be produced by either an UltraPulse laser or laser with rapid scanning, the amount of oxygen diffusion through this area and the rapidity of establishment of a vascular supply to the hair matrix was questionable and so, yet another controversy (363 –366) began in the mid-1990s. Walter Unger (367 –370), a prominent hair transplant surgeon, first reported his experience in 1994 with the UltraPulse laser. He thought that laser-recipient sites had good hair growth but that it was delayed compared to control cold steel grafts. Fitzpatrick


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(371) found that the laser-assisted procedure was 50% faster than control cold steel grafting but healing was slower and graft take was not as good. Ho et al. (372) claimed that slit placement with the UltraPulse laser was 50% faster than cold steel and thought growth in lased slits was good. Grevelink and coworkers (373,374) first reported on the use of a CO2 laser with the Sharplan SilkTouch scanner to develop recipient sites. Smithdeal (375) in 1997 employed the Sharplan scanner with good results and Tsai et al. (376) using a similar scanner said that his patients thought the laser-prepared sites looked more natural and had better density than cold steel sites. Neidel et al. (377) recently reported a single case of Er:YAG laser-assisted transplantation with a good results. A small number of physicians are still promoting laser methodology (366,368,370,372, 376,378) but cold-steel surgery is still the predominant method of graft recipient design (365).

17.

PULSED LIGHT SOURCES

Though not true lasers, intense broad-band pulsed light sources with a wavelength range of 590 – 1200 nm have recently found widespread use as epilating devices (379 – 383). The first generation of these machines with 550 –1200 nm bandwidth have been used for the treatment of vascular lesions since M. Goldman’s work (384 –387) in 1994. Since these devices were also approved by the FDA in a different category from lasers, they have been a focus of controversy, especially when marketed and administered by lay personnel (78). Bitter’s (388) seminal article on “Fotofacials” by intense pulsed light treatments launched the huge demand for nonablative techniques for cosmetic facial improvement by lasers or light sources. He claimed “wrinkling, skin coarseness, irregular pigmentation, pore size and telangiectases showed visible improvement in more than 90% of subjects.” His optimistic observations were matched by some (389,390) but met with skepticism from many others. While most laser surgeons now agree that dyschromias are readily improved by this technique it is not clear that significant clinical improvement in wrinkling is effected (391) despite evidence of new papillary dermal collagen formation histologically (392).

18.

LASER HAIR REMOVAL

When Q-switched ruby lasers were employed in large numbers in cutaneous laser surgery another serendipitous enlightenment occurred. The immensely powerful though short bursts of energy generated to fragment tattoo particles were noted not only to vaporize darkly pigmented hairs but also to bleach them below their follicular exit and even to inhibit their reappearance. Studies by Dover et al. (271) in 1989 had shown selective pigment cell damage in follicles from this laser, which caused the leukotrichia. It seemed that laser energy had reached a portion of the pigmented hair bulb and disrupted it enough so that it might act also as a depilatory, or better still, a nonscarring permanent or epilatory instrument. The financial appeal of entering the 6 billion dollar-a-year industry of cosmetic hair removal was too enticing for laser manufacturers to avoid. Truly medical applications such as treating disfiguring hirsutism in women or pseudofolliculitis barbae in men (and rarely women) were an additional potential benefit. Thermally nonselective but effective destruction of hair follicles in hair-bearing grafts, or for trichiasis, had been reported as early as the 1970s (393 – 396) but hair

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removal by thermal damage confined to the hair follicle governed by the principle of selective photothermolysis had not been attempted. The first FDA-approved laser for hair removal did not depend on the pigmented hair as a target but instead a patented mineral oil lotion was used containing carbon-based material, which was presumed to seep into the follicles after waxing immediately prior to massaging of the lotion and thus provide a target for the laser. Presumably, the mechanico-acoustic wave appearing after the laser impact would then disrupt the base of the follicle so that the loosened hair would fall out and the damaged follicle would no longer produce hair. In 1995 Goldberg and coworkers (397,398) presented the first studies showing very short-term efficacy. Hyperbole from the mass media was unfortunately not countered immediately; neither the short 12 week duration of the study nor the low 25% hair loss at that time was widely publicized. The hairs grew back, in fact most of them by 3 months, although more slowly in lased sites, and all of them grew back (399) by 6 months. Nanni and Alster (399) also demonstrated that the scientific principle behind this laser was flawed in that the carbon suspension was not required for hair removal since, at 1 month, waxing plus laser alone was equivalent to carbon-assisted laser removal. Nevertheless, these flawed data became a public mantra that laser removes hair. The public was led to believe by the mass media that this was permanent hair removal done quickly, painlessly, and without potential for scarring, all unlike traditional electrolysis. The public again had unrealistic expectations driven by laser hyperbole and many patients became dissatisfied with this very expensive and temporary procedure. When educated properly about the relative long-lasting effects and the apparent diminution of caliber of hair, most of the treated public was content. Also in 1995, Grossman et al. (400) reported their preliminary results with normal mode ruby laser in black-haired dog skin and found that this laser with a pulse duration of 0.297 ms, shorter than the estimated thermal relaxation time for a 200– 300 mm hair follicle of 40 –100 ms (401), could produce selective thermal damage to the hair follicle. They soon followed this abstract with a published report on 13 patients treated only once with normal mode ruby laser (402), noting that four of them had less than 50% regrowth after 6 months. They also claimed that “selective thermal injury to follicles was observed.” Unfortunately, only horizontal sections of the upper follicle were shown. It was years before any investigator presented vertical sections exhibiting the nature of damage to the hair bulb and still no one has shown the numbers of scarred or atretic follicles on vertical section. Controversy again reigned because of the claims of “permanent” hair loss by these and other authors and the lack of both clinical and histologic proof (403). In mouse studies the Wellman Lab showed in 1998 that only anagen hairs were affected by ruby laser. This suggests that at least for mice the pigmented bulb and not the stemcell-containing bulge was the ruby laser’s target (404). Only one of Grossman et al.’s original 13 patients had lost all hair at 2 years’ follow-up and the four with diminished hair had no decrease in actual hair counts; histology showed hair follicles but with evidence of some miniaturization with vellus hairs replacing terminal hairs (405). Subsequent studies demonstrated long-term hair reduction with several long-pulse lasers, though patients required a series of treatments. The long-pulsed ruby, alexandrite, diode (810 nm), and Nd:YAG (1064 nm) are widely used for long-term hair reduction (406). In 1999 the word “permanent” was redefined in an Orwellian fashion by the FDA to no longer mean “forever” but, for the hair follicle, to mean absence of a visible hair for a period longer than one estimated anagen–telogen growth cycle for a particular body region. Such language manipulation served as a marketing ploy that only confused the public more. One positive redirection concurrent with attempts to make hair removal safer was a renewed interest in thermokinetics and protection of tissues not by selectivity of


33

absorption and nonabsorption but protection even in the face of absorption by both the target and the nontarget. Because the thermal relaxation time of the pigmented epidermis is estimated at 3 – 10 ms, the epidermis is also a target for the ruby laser and with high fluences of 20 J/cm2 or more required for hair removal, significant destruction of the epidermis would occur if simultaneous cooling devices were not used. If two tissues shared too many common absorbents but were either physically different in size or were separated by some distance in the skin one could select pulse durations intermediate between each tissue’s estimated thermal relaxation time. One could preferentially heat smaller targets faster and larger targets slower to spare inversely their corresponding larger or smaller coabsorbers. One type of thermokinetically set alexandrite hair removal laser was manufactured which lengthened its pulse duration in order to deliver its energy over a longer period to the hair bulb and follicle and over too long a period to appreciably affect epidermal melanin in light-complexioned patients. Unfortunately, this theoretical enhancement did not provide a marked clinical difference (407). Such selectivity of longer pulse durations for larger targets to also protect smaller targets has more recently been employed for long-pulsed diode hair removal lasers for very darkly pigmented patients (408).

19.

CHILLING AND WRINKLES

Laser technologies seem to have a knack for recapitulating. Just as the ruby laser reappeared in the late 1980s after a 20-year hiatus, so renewed interest in green lasers for vascular lesions and a renewed understanding of the importance of chilling reappeared in the mid- to late 1990s, particularly by Wellman Lab (199,200) and Beckman Lab. Part of the interest in chilling was fostered by the large amounts of energy required to destroy or alter hair follicles and the need to protect the epidermis even better than theoretical thermokinetics alone. In 1994 Nelson’s group (193) at the Beckman Institute began a series of theoretical (194) and clinical (193,195 – 198,409) studies and first described the use of a spray cooling device using 20 – 80 ms bursts of a cryogen to cool and protect the epidermis during port-wine stain therapy. They saw no blistering appear after even 20 –36 J/cm2 with cooling spray but both blistering and necrosis without it. With this apparatus they could not only diminish intraoperative pain (197) and diminish epidermal injury with the 585 nm pulsed dye laser and with the 532 nm solid state laser (202) but, with the continuous Nd:YAG laser applied for thick vascular lesions in a cockscomb model (410), they could produce deep thermal effects to 6 mm without epidermal injury. Such dynamic cooling was adapted also for long-pulsed alexandrite hair removal systems. In the late 1990s, doubled-frequency 532 nm Nd:YAG laser with intermediate pulse widths of 2 – 10 ms and coupled with a sapphire water-cooled chill tip was introduced for treatment of vascular lesions without purpura. The chill tip was able to protect the epidermal integrity by keeping epidermal temperature at 5 – 5.58C and fluences of 9.5 –15 J were employed (190). Chill tips were consolidated with various long-pulsed ruby and diode lasers for hair removal also. Chilling by spray can be used just prior to, during, or even after the laser burst as a type of “thermal quenching.” Despite the dramatic and novel benefit of laser resurfacing, public demand has been driven by market forces as fast as development of the Web. Yesterday’s technology even for laser surgery rapidly and unjustifiably really becomes considered yesterday’s practice. Marketing forces the public to search for newer and quicker medical “fixes,” hence the appearance of the “lunchtime peel,” the “lunchtime microdermabrasion” and ultimately the lunchtime (i.e., no “downtime”) laser resurfacing by nonablative lasers (411,412).

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The public is confused into believing that these techniques all produce the same results as a true wounding resurfacing and without any hazard. Kelly et al. (294) in 1999 and Nelson et al. (409) showed that a small but statistically evident improvement in rhytids could be safely achieved with a 1320 nm Nd:YAG and dynamic cooling; there was rare blistering and hyperpigmentation and rarer pitted scarring. However, Ross et al. (413) thought that this process is too variable and prone to deep dermal collagen injury with resultant granulomatous inflammation, fibrosis, and pitted scarring. Muccini et al. (414) reported 18% shrinkage of collagen and new collagen synthesis without epidermal destruction in treating rhytids with a 980 nm diode laser with a spherical optical handpiece that focused the energy into the dermis. Goldberg and Whitworth (415) discovered subtle yet visible improvement of rhytids after slight epidermal ablation with uncooled Q-switched Nd:YAG laser, and Goldberg and Cutler (416) found that intense pulsed light sources with a precooled light guide did the same without epidermal ablation. Patients treated with pulsed dye laser for vascular lesions also report improved skin textures as have those treated for atrophic and hypertrophic scars. Nonablative skin remodeling has ballyhooed the promise of reduction of wrinkles, pore size, and oiliness, improvement of skin texture, and removal of pigmentary dyschromias, both brown and red, with no epidermal damage, no downtime from work, and no morbidity (417). Amazingly, the lasers and light sources touted to produce these changes have included the entire spectrum from 532 to 1540 nm—clinical improvement or histologic evidence of procollagen, new collagen synthesis or deposition was noted for 532 nm, 2 ms laser (418), 585 nm, 450 ms pulsed dye laser (419), low-fluence 595 nm long-pulse chilled pulsed dye laser (420), 585 nm, 360 ms pulsed dye laser (421), chilled 1320 nm Nd:YAG laser (422, 423), and chilled 1540 nm Er:glass laser (424). Similar claims were made for intense pulsed light (389,392). More realistic assessments of improvement indicated that though most subjects showed some improvement, it was at most minimal—only 18% by grading in Rostan’s study (420)—and could lead to patient dissatisfaction as for 80% of Trelles patients (423) even though they had histologic evidence of new collagen.

20.

BIOSTIMULATION

Numerous European authors, most prominently E. Mester in Hungary, have studied biostimulatory effects of lasers on cutaneous tissues in vivo and in vitro since the mid-1960s (425 –428). Beginning with the long-pulse ruby, then the He – Ne and argon lasers, he performed studies on 15 different biologic systems, such as Erlich’s ascites tumor cells, hair growth in mice, rat marrow hemoglobin synthesis, human fibroblast RNA and DNA protein synthesis, and wound healing, first reporting his results in 1968 (425). In general, he found that lower-intensity lasers produced biostimulatory effects while higher doses were inhibitory. In the mid-1980s a short burst of interest by American authors Abergel, Castro, and coworkers (429 – 437) showed that Nd:YAG laser could inhibit or stimulate fibroblast collagen production without destruction of the cells and without thermal effect and that He – Ne and Ga – As lasers could stimulate collagen production in vivo and in vitro. The Nd:YAG laser was also shown to inhibit keloidal fibroblasts in culture and to clinically shrink keloids. For the most part though, the American cutaneous surgical community did not follow Mester’s lead perhaps because of very few pertinent English language articles, or more likely the great difficulty of performing controlled clinical trials when the strict definition of biostimulation meant that no measurable immediate tissue changes (i.e., thermal) took effect. As a further


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example, although ASLMS annual meetings have always had a section on biostimulation, the papers presented most recently invariably are not from the USA. In the 1980s the gallium –arsenide laser was removed from cutaneous study protocols by the FDA. The He – Ne laser attained unfortunate notoriety at the same time when it was fraudulently promoted by lay practitioners and some chiropractors as a laser nonsurgical facelift. Ultimately, renewed interest in minimal thermal or acoustic damage inciting fibroblastic repair will undoubtedly spill over into biostimulation as well and, hopefully, more American literature will be forthcoming.

21.

PHOTODYNAMIC THERAPY

Photochemotherapy depends on an external light source activating an exogenous photosensitizer. This process has been employed to treat disease for over 3000 years, first used for vitiligo with plant extracts containing psoralens acting as the sensitizers. Modern studies of photosensitizers began with Raab (438) and his professor, von Tappeiner (439) just 100 years ago, who found that acridine and other dyes would kill paramecia when exposed to light. von Tappeiner (440) published the first text on the subject in 1907 and named the process photodynamic action. Interestingly, one of the first therapeutic applications he published was with the dermatologist Jesionek (441) on the use of eosin as a photosensitizer to treat cutaneous diseases including skin cancer (442). In 1942 Auler and Banzer (443) first exhibited the retention of hematoporphyrin by rat tumor tissue and the tumor’s selective destruction by subsequent quartz lamp radiation. Diamond et al. (444) in 1972, Dougherty (445) in 1974, and Tomson et al. (446) in 1974 started the modern era of photodynamic therapy, Diamond with hematoporphyrin derivative (HpD) and rat gliomas, Dougherty with fluorescein and mouse mammary carcinomas, and Tomson with acridine orange and mouse epithelial tissue where argon laser was the illuminating source. Dougherty’s report in 1975 of HpD injected intraperitoneally in animal models with application of deeply penetrating red light initiated intense study of HpD (441,447 –452). Both noncoherent light sources and lasers have been employed in the past several decades, although the laser’s monochromaticity and coherence would seem to make it a preferable choice. Since HpD and its purified product Photofrin (porfimer sodium) have been the most widely studied compounds, red light sources have been their complement. The continuous wave tunable dye laser tuned to red wavelengths from 630 to 690 nm and the quasi-continuous gold vapor laser at 628 nm were the lasers of choice. Photofrin and laser technique was approved for general use by the FDA (451,453) in 1995 but with limitations to pulmonary, gastrointestinal, and urologic malignancies. Only a few select experimental centers such as Dougherty’s in Buffalo were able to continue to provide information on applications for cutaneous carcinoma. Thus, 25 years of American studies of these photosensitizers and benzoporphyrin derivative, tin ethyl etiopurpurin, and monoaspartyl chlorin e6 have been retarded. Allison et al.’s (454) recent literature review and their own data showed enticing remission rates with clinical cures of up to 100% claimed by various authors (Table 1.2). Topical 5-aminolevulinic acid (with a nonlaser blue light source) has been approved in 2000 in the USA for cutaneous premalignancies (455). Bissonette and Lui’s (453) review showed that complete response of actinic keratoses ranged from 81% to 100%, which bodes well for a promising future for photodynamic therapy and skin disease.

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Table 1.2 Photodynamic Therapy of Cancer Involving the Skin Photodynamic therapy

Complete remission

Basal cell carcinoma Wilson, 151 BCC (125 primary, 26 recurring) Wilson, 588 lesions in Gorlin’s syndrome Warloe lesions ,2 mm thick lesions .2 mm thick

IV PDT 88% IV Photofrin 95% Topical ALA 90% Topical ALA 45%

Squamous cell carcinoma Hernnijton, 32 lesions Robinson, 500 lesions Jones, 6 Bowen’s

IV PDT 81% IV Photofrin 100% IV Photofrin 100%

Kaposi’s sarcoma Bernstein Allison, 121 lesions

IV Photofrin 33% IV SnET2 75%

Breast adenocarcinoma metastasis Allison, 86 lesions

IV SnET2 92%

Source: Adapted from Allison et al. (454).

However, when it comes to invasive cancer, another picture emerges. Warloe and coworkers (456 –458) obtained mediocre results with topical therapy of even thin 2 mm tumors; only with combined aggressive approaches were cure rates comparable to those of traditional therapy. Sacchini et al.’s (459) experience with topical TPPS in azone and 630 nm light in 14 cases of basal cell carcinoma (BCC) evidenced biopsy-proven complete remission in all tumors less than 2 mm thick but also only partial remission in those more than 2 mm thick. Biel’s (452) review of his own and others’ experience found poor results from systemic photodynamic therapy uniformly for tumors more than 5 mm thick.

22.

RETURN OF THE SCIENTIFIC METHOD—THE CHARGE FOR THE FUTURE

Industrial hyperbole and the seeming need by many cutaneous laser surgeons to be the first “kid on the block” by presenting anecdotal evidence for a new use of a particular laser (148), whether justifiable biologically or financially for the patient, swung the pendulum of laser activity and continues to do so at a violent pace toward the nonsense pole antithetical to Leon Goldman’s maxim. In recently reviewing laser skin resurfacing, Kauvar (324) bemoaned and warned that “rapid development of novel instrumentation is outpacing our ability to study fully their biological effects in tissue.” The immense cost of purchasing several similar lasers to compare their efficacy and the unlikely provision of loaned or free competing lasers by a laser manufacturer (anxious to market a new product) complicated interpretation of new data and even made those presented for one laser system only suspect and continued to foster divisiveness and antagonism even in the public arena. Even with panels of experts presenting their data, too often listeners would query, “Well, which of these very expensive instruments should I purchase?” Fortunately, a number of laser surgeons could occasionally swing the pendulum back toward “sense” science by doing side-by-side or randomized comparisons (Fig. 1.20) (186,192,197,205,207,208,329,337,352 –356,415,459,460). For example, Schliftman and


37

Figure 1.20 Two comparative side-by-side studies of argon, copper vapor, and continuous dye lasers on a port-wine stain by Drs. Schliftman and Brauner.

Brauner (205,207) in 1990 showed that equivalently dosed copper vapor laser was more effective than continuous wave dye laser or argon laser on side-by-side test areas of port-wine stain after one treatment. In 1993 Waner et al. (208) compared two yellow lasers, the copper vapor and pulsed dye, for facial telangiectases. Upon side-by-side comparison the former laser healed more quickly and was more cosmetically acceptable to the patients but both gave equivalent clinical improvement. In 1995 Dover et al. (186) compared port-wine stains treated with hexascan-assisted continuous dye laser with those treated with matched side-by-side pulsed dye laser and found both lasers effective, with the pulsed dye more so. A minimal and equivalent side effect profile for both sites was shown. Waldorf et al. (197) compared dynamically cooled sites with uncooled sites on pulsed dye laser-treated paired sites in port-wine stains, illustrating the epidermal sparing and pain relief effects of this device. Adrian and Tanghetti (192) paired pulsed dye laser and sapphire-tip-chilled 532 nm Nd:YAG laser for facial telangiectasia. Leuenberger et al. (460) had better results with Q-switched ruby laser on black tattoos than sideby-side Q-switched Nd:YAG and Q-switched alexandrite, although all worked well. McDaniel et al. (356) compared CO2 laser for perioral rhytid resurfacing to combined sequential CO2 and then Er:YAG resurfacing and found no significant clinical differences. Alster et al. (337) found no significant clinical differences in four randomized simultaneous CO2 resurfacing lasers and in a second study (355), in six randomized Er:YAG resurfacing systems. Khatri et al. (353) found quicker recovery but lesser therapeutic effect in Er:YAG than in CO2-laser-resurfaced areas. Goldberg and Whitworth (415) compared side-by-side char-free CO2 lasers and QS Nd:YAG laser for periorbital rhytid removal. Grossman et al. (461) studied side-by side flashlamp-pulsed light source, two types of long-pulsed ruby laser, long-pulsed alexandrite, and long-pulsed diode lasers for hair removal. Determining optimal intervals for therapies requiring multiple treatments (as mentioned previously concerning pigmented lesion removal) requires paired side-byside comparisons as well, but the rush to publication and for rapid treatment obscured the need for understanding the biology of laser healing and tissue restoration. The emergence of on-line Internet laser discussion groups and even journals such as lasernews.net (http://lasernews.net) and Dermatology Online Journal (http://matrix. ucdavis.edu/DOJdesk/desk.html) fosters rapid communication and helps disseminates more quickly new insights and possible complications but accelerates the speed of what we think is laser “science” perhaps faster than the biology of healing and repair is willing to provide us with correct information. Time tempers judgment but accelerated internet time may only interfere with a cautious laser surgeon’s perspective.

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In a similar vein, hyperbole (308 –338) masked the true incidence of complications. Some cautious but perhaps courageous laser surgeons did report side effects and preached thoughtful reflection and methodology (222,319,349,355,462 – 469). This author raised the question of underreporting of scarring and the role of wound dressings in preventing hypertrophic scarring in 1984 (75). In a 1987 review Olbricht et al. (463) surveyed laser surgeons, 69% of whom had seen at least one case of hypertrophic scarring after argon laser and 64% after CO2 laser surgery, but no true incidence of scarring was tabulated. Lent and David (464) noted hyperpigmentation in 16% of laser-resurfaced patients postoperatively and Fitzpatrick et al. (319), 25%. Nanni and Alster (466) found a 37% incidence, more common in darker patients (up to 100% of Fitzpatrick type IV and V patients) (355,466), but this is reversible particularly with postoperative hydroquinones. Bernstein et al. (349) first made known the previously unreported late onset of hypopigmentation with CO2-laser-resurfaced patients, which may have represented both melanocyte destruction and delayed opacification. This delayed side effect, which seemed to correlate with prolonged erythema, was largely responsible for the shift to Er:YAG laser resurfacing systems. Rendon-Pellerano et al. (467) reviewed the rare but expectable early and late complications seen after laser resurfacing but reported four worrisome unpredictable outcomes, disseminated herpes simplex without prior clinical history of herpes, delayed wound healing with spontaneous breakdown of previously healed skin and protracted healing with scarring thereafter, granulomatous response of the lip margins, and a case of staphylococcal parapharyngeal abscess. Our past history, short as it has been in cutaneous laser surgery, has been one of brilliance, bringing unimaginable benefits to our patients with deformity, as well as convenience and safety for cosmetic surgery. Our future will undoubtedly continue in a similar vein. In an era of high technology we can only expect more extraordinary technical innovations and new seminal events. Hopefully, as physicians first, we will be mindful of the cautions laid down by Leon Goldman and by our sense of honest scientific inquiry and our ethos of “primum non nocere.” Hopefully, we will continue to view the potential of cutaneous laser surgery with the same excitement and joy that Leon Goldman did at laser’s very inception in 1960 as a potential for healing. Hopefully, future historians of cutaneous laser surgery will not record how our professionalism was swept away by a tidal wave of marketing hyperbole. Timeline of the Development of Cutaneous Laser Surgery Early 20th century 1906– 1917 1920s 1951 1957

Einstein’s conceptualization of stimulated emission of radiation Theory of coherence—Dirac Theory of amplification—Townes (USA), V. A. Fabrikant (USSR) Optical resonator—Schawlow and Townes

1960s 1960 1961 1961 1961 1961 1962 1962 1962 1962

First Laser, ruby—Maiman First gas laser, He-Ne, at Bell Labs Nd:YAG laser—Johnson and Naussau Ruby laser used on port-wine stain—Leon Goldman Nd:YAG laser for tattoos—Goldman Microscope coupled with ruby laser—Bessis and Coll Ruby laser used on eye by Zweng Argon laser invented First commercial production of lasers

Cutaneous Laser Surgery: Historical Perspectives 1962 1963 1964 1964 1964 1965 1966 1967 1967 1968 1970s 1970 Early 1970s Early 1970s 1971 1972 1974 1974 Late 1970s Late 1970s

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Laser research laboratories founded Low-power lasers and wound healing—Endre Mester First article on laser surgery of the skin—Leon Goldman Q-switched ruby laser on tattoo—Goldman CO2 laser invented—Patel Nd:YAG to cut human tissue—Jako First surgical CO2 laser—Polanyi First commercial CO2 laser—American Optical Co. Argon laser used on eye—L’Esperance First CO2 laser use in urology—Mulvaney and Beck CO2 laser on human larynx—Jako Fiberoptics developed for lasers Photodynamic therapy of malignancy—Dougherty First commercial argon laser First use of CO2 laser for disease of cervix—Kaplan CO2 laser on vaginal tissue, cervical dysplasia, condylomas—Bellina Wellman Lab founded Argon laser for cutaneous disease—Apfelberg, Arndt, Noe, and others CO2 laser for cutaneous disease—McBurney and others

1980s Early 1980s Early 1980s 1981 1981 1982 1983 Mid 1980s Late 1980s to early 1990s 1988 1989

Intraoperative and postoperative wound care Mechanized scanners American Society of Laser Medicine and Surgery founded Q-switched ruby laser for tattoos—Reid Beckman Lab founded Theory of selective photothermolysis—Anderson and Parrish Continuous Nd:YAG laser for cutaneous vascular tumors “Yellow lasers”: pulsed dye, continuous wave dye, copper vapor, copper bromide, krypton Er:YAG for resurfacing—Kaufmann First commercial American Q-switched ruby laser for tattoos

1990s Early 1990s 1993 1993 1993 1994 1995 1997 1999 1999

Q-switched Nd:YAG, Q-switched alexandrite Pulsed dye laser treatment of scars Ultrapulse and high-speed-scanned CO2 laser resurfacing Pulsed light sources for vascular lesions Q-switched Nd:YAG laser-assisted hair removal Long-pulse ruby laser for hair removal First American Er:YAG laser for resurfacing Long-pulse diode laser for hair removal Long-pulse 1320 nm Nd:YAG laser for thermal remodeling

Source: Adapted partially from “The Development of Laser Medicine” (monograph, American Society for Laser Medicine and Surgery, 1987), Hecht and Teresi (21), and Bellina et al. (102).

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Brauner Goldman M. Leg veins and laser. Lasers Surg Med 1994; (suppl 6):48. Schroeter C, Neumann H. An intense light source. The photoderm VL-flashlamp as a new treatment possibility for vascular skin lesions. Dermatol Surg 1998; 24:743 – 748. Dover J, Sadick N, Goldman M. The role of lasers and light sources in the treatment of leg veins. Dermatol Surg 1999; 25:328 – 336. Raulin C, Schroeter C, Weiss R et al. Treatment of port-wine stains with a noncoherent pulsed light source: a retrospective study. Arch Dermatol 1999; 135:679 – 683. Bitter P. Noninvasive rejuvenation of photodamaged skin using serial, full-face intense pulsed light treatments. Dermatol Surg 2000; 26:835 – 842, discussion 843. Hernandez-Perez E, Ibiett E. Gross and microscopic findings in patients submitted to nonablative full-face resurfacing using intense pulsed light: a preliminary study. Dermatol Surg 2002; 28:651 –655. Negishi K, Tezuka Y, Kushikata N et al. Photorejuvenation for Asian skin by intense pulsed light. Dermatol Surg 2001; 27:627 – 631, discussion 632. Goldberg D, Cutler K. Nonablative treatment of rhytids with intense pulsed light. Lasers Surg Med 2000; 26:196– 200. Goldberg D. New collagen formation after dermal remodeling with an intense pulsed light source. J Cutan Laser Ther 2000; 2:49– 61. Berry J. Recurrent trichiasis: treatment with laser photocoagulation Ophthalmic Surg 1979; 10:36 – 38. Kuriloff D, Finn D, Kimmelman C. Pharyngoesophageal hair growth: the role of laser epilation. Otolaryngol Head Neck Surg 1988; 98:342– 345. Finkelstein L, Blatstein L. Epilation of hair-bearing urethral grafts using the neodymium: YAG surgical laser. J Urol 1991; 146:840 – 842. Gossman M, Yung R, Berlin A et al. Prospective evaluation of the argon laser in the treatment of trichiasis. Ophthalmic Surg 1992; 23:183 – 187. Goldberg D. Topical solution—assisted laser hair removal. Lasers Surg Med 1995; 7S:47. Goldberg D, Littler C, Wheeland R. Topical suspension-assisted Q-switched Nd:YAG laser hair removal. Dermatol Surg 1997; 23:741 –745. Nanni C, Alster T. Optimizing treatment parameters for hair removal using a topical carbonbased solution and 1064-nm Q-switched neodymium:YAG laser energy. Arch Dermatol 1997; 133:1546 – 1549. Grossman M, Farinelli W, Flotte T et al. Laser targeted at hair follicles. Lasers Surg Med 1995; S7:47. Wheeland R. Laser-assisted hair removal Dermatol Clin 1997; 15:469– 477. Grossman M, Dierickx C, Farinelli W et al. Damage to hair follicles by normal-mode ruby laser pulses. J Am Acad Dermatol 1996; 35:889– 894. Anderson R, Burns A, Garden J et al. Multicenter study of long-pulse ruby laser hair removal. Lasers Surg Med suppl 1999; 11:56. (Abstracts.) Lin T, Manuskiatti W, Dierickx C et al. Hair growth cycle affects hair follicle destruction by ruby laser pulses. J Invest Dermatol 1998; 111:107 – 113. Dierickx C, Grossman M, Farinelli W et al. Permanent hair removal by normal-mode ruby laser. Arch Dermatol 1998; 134:837 –842. Nanni C, Alster T. A practical review of laser assisted hair removal using the Q-switched Nd:YAG, long-pulsed ruby and long-pulsed alexandrite lasers. Dermatol Surg 1998; 24:1399 – 1405. Goldberg D, Ahkami R. Evaluation comparing multiple treatments with a 2-msec and 10-msec alexandrite laser for hair removal. Lasers Surg Med 1999; 25:223– 228. Battle E. Hypertrichosis [treatment modalities for dark skin types]. American Academy of Dermatology Annual Meeting, San Francisco, CA, Mar 14, 2000. Nelson J, Milner T, Dave D et al. Clinical study of non-ablative laser treatment of facial rhytides. Lasers Surg Med 1997; 95:32– 33. Hoffman W, Anvari B, Said S et al. Cryogen spray cooling during Nd:YAG laser treatment of hemangiomas. A preliminary animal model study. Dermatol Surg 1997; 23:635– 641.

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Goldman M. Non-ablative laser treatment of wrinkles. Cosmet Dermatol 2000; 13:17 – 20. Menaker G, Wrone D, Williams R et al. Treatment of facial rhytids with a non-ablative laser: a clinical and histologic study. Dermatol Surg 1999; 25:440– 444. Ross E, Sajben F, Hsia J et al. Nonablative skin remodeling: selective dermal heating with a mid-infrared laser and contact cooling combination. Lasers Surg Med 2000; 26:186 – 195. Muccini J, O’Donnell F, Fuller T et al. Rapid report; laser treatment of solar elastosis with epithelial preservation. Lasers Surg Med 1998; 23:121– 127. Goldberg D, Whitworth J. Laser skin resurfacing with the Q-switched Nd:YAG laser. Dermatol Surg 1997; 23:903 –906, discussion 906 – 907. Goldberg D, Cutler K, Nonablative treatment of rhytids with intense pulsed light. Lasers Surg Med 2000; 26:196 – 200. Hardaway C, Ross EV. Nonablative laser skin remodeling. Dermatol Clin 2000; 20:97 – 111,ix. Bernstein E, Ferreira M, Anderson D. A pilot investigation to subjectively measure treatment effect and side-effect profile of non-ablative skin remodeling using a 532 nm, 2 ms pulseduration laser. J Cosmet Laser Ther 2001; 3:137– 141. Zelickson B, Kilmer S, Bernstein E et al. Pulsed dye laser therapy for sun damaged skin. Lasers Surg Med 1999; 25:229 – 236. Rostan E, Bowes L, Iyer S et al. A double-blind, side-by-side comparison study of low fluence long pulse dye laser to coolant treatment for wrinkling of the cheeks. J Cosmet Laser Ther 2001; 3:129 – 136. Bjerring P, Clement M, Heickendorff L et al. Selective non-ablative wrinkle reduction by laser. J Cutan Laser Ther 2000; 2:9– 15. Goldberg D. Non-ablative subsurface remodeling: clinical and histologic evaluation of a 1320-nm Nd:YAG laser. J Cutan Laser Ther 1999; 3:153– 157. Trelles M, Allones I, Luna R. Facial rejuvenation with a nonablative 1320 nm Nd:YAG laser: a preliminary clinical and histologic evaluation. Dermatol Surg 2001; 27:111– 116. Fournier N, Dahan S, Barneon G et al. Nonablative remodeling: clinical, histologic, ultrasound imaging, and profilometric evaluation of a 1540 nm Er:glass laser. Dermatol Surg 2001; 27:799 –806. Mester E et al. Laserstrahlenwirkung auf das Wachstum des Erlichsen Ascitestumor. Arch Geschwultsforsch 1968; 32:201. Mester E et al. Stimulation of wound healing by laser rays. Acta Chir Acad Sci Hung 1972; 13:315. Mester E, Mester A, Mester A. The biomedical effects of laser application. Lasers Surg Med 1985; 5:31 – 39. Wheeland R. Lasers for the stimulation or inhibition of wound healing. J Dermatol Surg Oncol 1993; 19:747 –752. Castro D, Abergel R, Meeker C et al. Effects of the Nd:YAG laser on DNA synthesis and collagen production in human skin fibroblast cultures. Ann Plast Surg 1983; 11:214 – 222. Abergel R, Meeker C, Dwyer R et al. Nonthermal effects of Nd:YAG laser on biological functions of human skin fibroblasts in culture. Lasers Surg Med 1984; 3:279– 284. Abergel R, Dwyer R, Meeker C et al. Laser treatment of keloids. Lasers Surg Med 1984; 4:291 – 295. Abergel R, Meeker C, Lam T et al. Control of connective tissue metabolism by lasers; recent developments and future prospects. J Am Acad Dermatol 1984; 11:1142– 1150. Castro D, Saxton R, Fetterman H et al. Biostimulative effects of Nd:YAG Q-switch dye on normal human fibroblast cultures: study of a new chemosensitizing agent for the Nd:YAG laser. Laryngoscope 1987; 97:1454 – 1459. Abergel R, Lyons R, Castel J et al. Biostimulation of wound healing by lasers: experimental approaches in animal models and in fibroblast cultures. J Dermatol Surg Oncol 1987; 13:127–133. Lyons R, Abergel R, White R et al. Biostimulation of wound healing in vivo by a helium-neon laser. Ann Plast Surg 1987; 18:47 – 50.

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Brauner Castro D, Saxton R, Fetterman H et al. Bioinhibition of human fibroblast cultures sensitized to Q-switch II dye and treated with the Nd:YAG laser: a new technique of photodynamic therapy with lasers. Laryngoscope 1989; 99:421 – 428. Saxton R, Haghighat S, Plant D et al. Dose response of human tumor cells to rhodamine 123 and laser phototherapy. Laryngoscope 1994; 104:1013 – 1018. Raab O. Uber die Wirkung fluorescierendes stoffe und Infusorien. Z Biol 1900; 39:524. Tappeiner H. Uber die Wirkung fluorescierender Stoffe auf Infusorien nach versuchen von O. Raab. Munch Med Wochenschr 1900; 47:5. Tappeiner H, Jodlbauer A. Die sensibilisierende Wirkung fluorescierender Substanzen. In: Vogel F, ed. Gesammelte Untersuchungen uber die photodynamische Erscheinung. Leipzig, 1907. Jesionek A, Tappeiner H. Zur Behandlung der Hautcarcinome nmit fluorescierenden Stoffen. Arch Klin Med 1905; 82:223. Straight R. Photodynamic therapy in laser surgery and medicine. In: Dixon J, ed. Surgical Application of Lasers. 2nd ed. Chicago: Yearbook Medical Publishers, 1987:310 – 349. Auler H, Banzer G. Untersucheungen uber die Rolle der Porphyrine bei geschwulstkranken Menschen und Tieren. Z Krebsforsch 1942; 53:65. Diamond I, McDonagh A, Wilson C et al. Photodynamic therapy of malignant tumors. Lancet 1972; II:1175 – 1177. Dougherty T. Activated dyes as antitumor agents. J Natl Cancer Inst 1974; 52:1333 – 1336. Tomson S, Emmett E, Fox S. Photodestruction of mouse epithelial tumors after acridine orange and argon laser. Cancer Res 1974; 34:3124 – 3127. Dougherty T, Grindey G, Fiel R et al. Photoradiation therapy. II. Cure of animal tumors with hematoporphyrin and light. J Natl Cancer Inst 1975; 55:115– 121. Dougherty T. Photoradiation therapy for cutaneous and subcutaneous malignancies. J Invest Dermatol 1981; 77:122 – 124. Dougherty T. Hematoporphyrin as a photosensitizer of tumors. Photochem Photobiol 1983; 38:377 – 379. Daniell M, Hill J. A history of photodynamic therapy. Aust NZ J Surg 1991; 61:340 – 348. Lui H, Anderson R. Photodynamic therapy in dermatology: recent developments. Dermatol Clin 1993; 11:1 – 13. Biel M. Photodynamic therapy and the treatment of head and neck cancers. J Clin Laser Med Surg 1996; 14:239 –244. Bissonette R, Lui H. Current status of photodynamic therapy in dermatology. Dermatol Clin 1997; 15:507 – 519. Allison R, Mang T, Wilson B. Photodynamic therapy for the treatment of nonmelanomatous cutaneous malignancies. Semin Cutan Med Surg 1998; 17:153 – 163. Henney J. First drug device to treat actinic keratoses. J Am Med Assoc 2000; 283:596. Peng Q, Warloe T, Moan J et al. Distribution of 5-aminolevulinic acid-induced porphyrins in noduloulcerative basal cell carcinoma. Photochem Photobiol 1995; 62:906 – 913. Peng Q, Warloe T, Berg K et al. 5-Aminolevulinic acid-based photodynamic therapy. Clinical research and future challenges. Cancer 1997; 79:2282– 2308. Soler A, Warloe T, Tausjo J et al. Photodynamic therapy by topical aminolevulinic acid, dimethylsulphoxide and curettage in nodular basal cell carcinoma: a one-year follow-up study. Acta Dermatol Venereol 1999; 79:204 – 206. Sacchini V, Melloni E, Marchesini R et al. Preliminary clinical studies with PDT by topical TPPS administration in neoplastic skin lesions. Lasers Surg Med 1987; 7:6– 11. Leuenberger M, Mulas M, Hata T et al. Comparison of the Q-switched alexandrite, Nd:YAG, and ruby lasers in treating blue-black tattoos. Dermatol Surg 1999; 25:10 – 14. Grossman M, Lou W, Kauvar A et al. Comparison of different lasers and light sources hair removal. Lasers Surg Med 1999; (suppl 11):14. (Abstracts.) Fried M, Kelly J, Strome M. Complications of Laser Surgery of the Head and Neck. Chicago: Yearbook Medical Publishers, 1986. Olbricht S, Stern R, Tang S et al. Complications of cutaneous laser surgery. A survey. Arch Dermatol 1987; 123:345 – 349.

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Lent W, David L. Laser resurfacing: a safe and predictable method of skin resurfacing. J Cutan Laser Ther 1999; 1:87 – 94. Nanni C. Complications of laser surgery. Dermatol Clin 1997; 15:521 – 534. Nanni C, Alster T. Complications of carbon dioxide laser resurfacing. An evaluation of 500 patients. Dermatol Surg 1998; 24:315 – 322. Rendon-Pellerano M, Lentini J, Eaglstein W et al. Laser resurfacing: usual and unusual complications. Dermatol Surg 1999; 25:360 – 367. Anderson R, Geronemus R, Kilmer S et al. Cosmetic tattoo ink darkening: a complication of Q-switched and pulsed laser treatment. Arch Dermatol 1993; 129:1010 – 1014. Nanni C, Alster T. Laser-assisted hair removal: side effects of Q-switched Nd:YAG, long-pulsed ruby, and alexandrite lasers. J Am Acad Dermatol 1999; 41:165– 171.

2 An Introduction to Lasers and Laser –Tissue Interactions in Dermatology J. Stuart Nelson Beckman Laser Institute, University of California, Irvine, California, USA

1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Introduction Electromagnetic Radiation Light Bulb vs. a Laser Basic Laser Principles Lasers in Dermatology Continuous Wave vs. Pulsed Lasers Q-Switching Laser Delivery Dosimetry Basic Laser – Tissue Interactions: Reflection, Scattering, Transmission, and Absorption 11. The Process of Absorption 12. Chromophores in Human Skin 13. Heat 14. Ablation of Human Skin 15. Selective Photothermolysis 16. Selective Photothermolysis of Cutaneous Blood Vessels 17. Selective Photothermolysis of Tattoos 18. Selective Photothermolysis of Pigmented Lesions 19. Selective Photothermolysis and Laser Assisted Hair Removal 20. Skin Cooling 21. Photochemistry and Photodynamic Therapy 22. Fluorescence 23. Conclusion References

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INTRODUCTION

Dermatologic laser surgery is regarded as one of the fastest growing areas in the emerging fields of photomedicine and biomedical optics. The unique properties of lasers create an enormous potential for specific therapy of skin diseases. As with any device, the most efficacious and appropriate use requires an understanding of the basic photobiological and photophysical principles of laser –tissue interaction as well as the properties of the laser itself. Modifications of current lasers and innovative advances in biomedical laser instrumentation may eventually allow the physician to match optimally the laser and treatment procedure with the lesion. This chapter provides a brief description of the nature of the laser, how it works, and the fundamental mechanisms of its interaction with human skin.

2.

ELECTROMAGNETIC RADIATION

Electromagnetic radiation is a fundamental form of energy that exhibits both wave properties, because of alternating electric and magnetic fields, and particle properties, comprising packets of energy called photons. A relationship exists between the energy of the photon (E) and the speed of light (c), and frequency (n) and wavelength (l) of the radiation. The constant of proportionality (h) is Planck’s constant. E ¼ hn and E ¼ hc=l

n ¼ c=l

(2:1) (2:2)

These equations show that the energy of an electromagnetic wave is proportional to its frequency and inversely proportional to wavelength. Long-wavelength photons carry less energy than short-wavelength photons as expressed by Planck’s law. The electromagnetic spectrum is portrayed in Fig. 2.1. It can be seen that visible light lasers

Figure 2.1 The spectrum of electromagnetic radiation.

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occupy a relatively small region of the entire spectrum. However, with the continued development of the free-electron laser, the region occupied by lasers eventually might be extended into the near-X-ray part of the spectrum with wavelengths as short as 10 nm.

3.

LIGHT BULB

VS .

A LASER

Photons are the fundamental units of light, and they are the same whether produced by a light bulb or a laser (Fig. 2.2). The laser and the light bulb differ in how their photons are organized. Light from a light bulb radiates in all directions, and there is a direct mathematical relationship between the loss of light intensity and the distance one moves away from the bulb. In the laser, photons are emitted parallel (or nearly parallel) to, and in phase with, each other as they travel toward infinity. This property is known as coherence and explains why the light intensity of a laser does not decrease very much with distance. Another feature of light from a light bulb is that it is white or yellow-white in color because it contains all the different colors and wavelengths in the visual portion of the electromagnetic spectrum and, hence, is polychromatic. A glass prism placed in front of a light bulb refracts the different wavelengths and allows the constituent colors to be seen. With the laser, the prism produces light of one wavelength and one color. The light from the laser is therefore pure or monochromatic. This property, under some circumstances, allows for selective absorption of laser energy by a targeted chromophore within human skin—structures with high absorption at a laser wavelength can be selectively altered or destroyed. Another difference between the two light sources is their intensity. The number of photons per unit area of emission produced by the laser is much greater than for any

Figure 2.2 Characteristics of light from a conventional light bulb and from a laser.

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other light source. In fact, millions more photons are emitted by a laser than by a comparable surface area of the sun. For example, peak powers of 1012 W can be obtained with certain short-pulsed lasers. Laser power can also be varied over a wide range to achieve quite different tissue effects. For example, a low-power laser may be used to heat gently a tissue, with perhaps the only change being an increase in metabolic rate. A high-power pulsed laser may be used to achieve nonlinear optical effects (e.g., optical breakdown) causing explosions within the tissue (1). As a result of these three basic differences—coherence, monochromaticity, and intensity—the laser produces a highly unique form of electromagnetic radiation. Otherwise, photons from the light bulb and the laser obey the same basic laws and principles governing their interaction with human skin.

4.

BASIC LASER PRINCIPLES

The word laser is an acronym derived from light amplification by the stimulated emission of radiation. The amplification of the stimulated emission of radiation is the actual physical process that goes on within the laser device (2 – 5). Figure 2.3 illustrates the process of lasing: the stimulated emission of one photon by the action of another photon. To understand the acronym, it is necessary to examine some basic atomic physics. Figure 2.3(a) illustrates two atoms existing in what is termed the ground state, the lowest possible energy level. If by some mechanism the electrons of these atoms are excited from the ground state by the input of energy, they move to a higher energy level called the excited singlet state [Fig. 2.3(b)]. The source of this energy or “pumping system” can be electrical, chemical, radiofrequency waves, or light from a flashlamp or another laser. When these atoms are in the excited singlet state, they very quickly drop down to an in-between, long-lived energy level called the metastable state [Fig. 2.3(c)]. This state may last as long as a few seconds, as compared

Figure 2.3 Energy transitions characteristic of atoms in stimulated emissions. (a) Two groundstate atoms (1,2). (b) Excitation to the singlet state by input of energy (black arrows). (c) Transition to the metastable state. (d) Atom 1 spontaneously drops to the ground state, emitting a photon that stimulates atom 2 also to drop to the ground state. Both photons (yellow arrows) from atoms 1 and 2 have the same wavelength and travel parallel to each other and in phase.


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with 1026 – 1029 s for most excited states. This explains why some materials can go through the lasing process and others cannot. Only atoms and molecules with a metastable state in their energy structure can achieve what is called a population inversion and undergo stimulated emission. What happens next is a spontaneous event. Those atoms existing in the metastable state spontaneously, and by random action, return to the ground state with the loss of some energy. This loss of energy occurs in the form of light—the release of a photon [Fig. 2.3(d)]. If the photon is in close proximity to another atom still in the metastable state (recall that the metastable state is long-lived so that there are going to be many atoms still at that energy level at a given moment), it collides (interacts) with that atom. This interaction stimulates the second atom to return to its ground state and, in the process, emit another photon of light. This phenomenon is termed stimulated emission of radiation. It is a basic principle of physics that since both photons come from identical energy levels, they are of the same wavelength (color) and are moving parallel and in phase with each other (the property of coherence). The first laser built in 1960 used synthetic red ruby, which is an aluminum trioxide crystal doped with chromium atoms. It was the chromium atoms inside the aluminum trioxide crystal that underwent the lasing process to produce red light. Figure 2.4 presents the foregoing on a much grander scale. Here, the atoms in the lasing medium in the ground state are represented by violet circles and those in the metastable state, by red circles [Fig. 2.4(a)]. Most of the atoms initially are in the ground state and are subsequently excited to the singlet state by a flash of light. They rapidly drop

Figure 2.4 Schematic of laser action illustrating photon cascade. (a) Unstimulated crystal; a few atoms (red circles) are spontaneously in the singlet or metastable state, but most are in the ground state (violet circles). (b) Energy input excites ground-state atoms to the singlet state whence they drop down to the metastable state. (c) Stimulated emission of excited atoms by photons of stimulated emitting atoms. (d) Photon cascade is produced by reflection at reflecting ends of the laser cavity; stimulated emission continues. (e) Further photon cascade occurs and laser light passes out the partially reflective end of the laser cavity.

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down to the metastable state [Fig. 2.4(b)]. Following this event, spontaneous emission occurs as described previously. The two emitted photons strike other atoms in the metastable state causing them to emit photons in parallel and in phase with those already present [Fig. 2.4(c)]. All this occurs within a fraction of a second creating an intense buildup of many photons, or a photon cascade. If the laser cavity has opposing reflective surfaces, the photons are oscillated through the medium at the speed of light, stimulating the emission of more photons [Fig. 2.4(d)]. This buildup of intensity by oscillation between two reflecting surfaces results in the final process in lasing: amplification. By permitting the release of some photons through a partially reflective surface at one end of the cavity, the result is a bright, intense monochromatic beam of light: a laser beam [Fig. 2.4(e)].

5.

LASERS IN DERMATOLOGY

Different kinds of lasers (Fig. 2.5) are identified by the type of material that undergoes the lasing process (e.g., the argon laser has argon gas as the lasing medium) inside the device. There are four types of lasing materials: solid, gas, liquid, or semiconductor. It is possible to obtain lasing action from any of these types of lasing materials provided that their atomic structures have metastable states that permit the stimulated emission process to occur. Examples of solid-state lasers are the ruby, alexandrite, and neodymium yttrium –aluminum – garnet (Nd:YAG) lasers. Examples of gas lasers are the excimer, argon, and carbon dioxide lasers. An example of a liquid laser is the pulsed dye laser. Liquid lasers employ complex organic dyes, such as rhodamine or coumarin, in solution or suspension. Diode lasers use two layers of a semiconductor material, such as gallium arsenide. Some diode lasers are tuneable over a broad wavelength range. They can be operated on battery power and, due to their small size which provides for efficient packaging, are useful for remote operation.

Figure 2.5 Identification of different types of medical lasers.


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Generally and by convention, a medical laser is referred to in terms of its wavelength in either nanometers (nm) or micrometers (mm). There are also ways to modify the wavelengths obtainable from lasers. The simplest of these is frequency doubling or harmonic generation, where high-intensity light propagating through a nonlinear, asymmetric crystal generates laser light at twice the input frequency (Fig. 2.6). For example, light from high-power Nd:YAG lasers can be doubled in frequency by placing a KTP (potassium-titanyl-phosphate) crystal inside the laser cavity itself and focusing the beam into the crystal. Since the frequency of light is inversely proportional to wavelength, the result is light emitted from the crystal with twice the frequency or half the wavelength of the incident light. In practice, invisible near-infrared 1064 nm wavelength light is passed through a KTP crystal producing green visible light at a wavelength of 532 nm. The resulting laser is sometimes referred to as a KTP laser. Similar complicated physical processes can be used to double, triple, or quadruple the wavelengths from the primary laser source. Dye lasers contain a tube filled with flowing dye solution that is excited within the laser cavity. The output wavelength may be “tuned” from 400 to 1000 nm as desired by changing the dye. Precise wavelength tuning is controlled by the individual dye’s fluorescence, typically in the 30 –100 nm range, and is accomplished through the use of prisms, diffraction gratings, or birefringent filters placed within the cavity. By choosing different dyes, laser light of virtually any wavelength in the visible spectrum can be produced. Unfortunately, all of the dye lasers must contend with photoinduced dye disintegration, necessitating frequent changes of the dye after a certain number of pulses. In summary, there are a wide range of lasers available for clinical use. The dye lasers, and in the future the free-electron laser, can be precisely tuned to emit photons at wavelengths that match absorption peaks of tissue chromophores, thus permitting their selective destruction and subsequent tissue ablation.

6.

CONTINUOUS WAVE vs. PULSED LASERS

A continuous wave (CW) laser may be differentiated from a pulsed laser, which provides bursts of energy. In the CW mode, the laser delivers a continuous beam of light with little or no variation in power output over time In CW operation, laser output is controlled by the physician, typically by depressing a foot pedal. A pulsed laser delivers its energy in the form of a single pulse or a train of pulses. The frequency or pulse repetition rate is the number of pulses emitted in 1 s (Hertz).

Figure 2.6 Frequency doubling by passing an Nd:YAG laser beam through an asymmetric potassium-titanyl-phosphate (KTP) crystal.

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The duration of the pulse, or pulse width, is defined as the total time required for the pulse to rise from zero intensity, build to a maximum, and then return to zero intensity. An alternative definition for pulse width (used for short pulses) is the time between the 50% points on the pulse curve. This is called full width at half maximum. “Superpulse” is a term specific to some carbon dioxide lasers that have been modified to produce very short pulses with high peak powers in a repetitive fashion, commonly several hundred pulses per second. From the physician’s point of view, superpulse is most useful for incisional surgery with a focused beam. High peak power maximizes tissue vaporization, and short pulse duration minimizes adjacent thermal injury.

7.

Q-SWITCHING

Q-switching of lasers is a mechanism often used to control the light output by concentrating all the energy into a single, intense pulse with a duration on the order of nanoseconds and an energy of 10 J or more. With Q-switching (the Q-factor stands for “quality factor,” used in electronics theory terminology), a fast electromagnetic switch (Pockel’s cell) in the laser cavity causes excitation of the active medium to buildup far in excess of the level of the medium when the shutter is open. In operation, the flashlamp is turned on and the population inversion gradually grows. Lasing is prevented by the shutter. When the population inversion is at a maximum, the shutter is opened so that lasing occurs and a large burst of energy is emitted as the cavity rapidly depletes the population inversion. The net result is an extremely high peak power (greater than 106 W) nanosecond duration pulse or series of pulses. Several methods are available to create laser pulses with pulse widths on the order of femtoseconds (10215 s). Because the techniques can be quite complicated, especially for producing very short pulse widths, they are not discussed here.

8.

LASER DELIVERY

Transmission of laser energy from the laser cavity to the tissue is provided by one of three devices: articulated arms, optical fibers, or micromanipulators. Articulated arms direct laser energy from the laser cavity to the desired location through a series of hollow, rigid tubes with reflecting mirrors at each connection. The series of mirrors is chosen to be reflective of the laser wavelength being transmitted so that coherence and power are maintained, allowing the fine focusing of the exiting beam. A hand piece at the end of the arm contains a lens that focuses the beam to various spot sizes with uniform light intensity. Several limitations remain in articulated arm systems. Despite recent advances to improve their mobility, articulated arms are somewhat cumbersome to use in a clinical setting. The mirrors are easily misaligned when either the laser device or the articulated arm is disturbed. Despite the aforementioned limitations, carbon dioxide or Er:YAG lasers almost exclusively utilize articulated arms because their infrared wavelengths are not transmissible along currently available optical fibers. The most common and convenient way of delivering laser energy to the skin is through flexible optical fibers. Most visible light can be transmitted along optical fibers which are composed of two or more concentrically arranged optical materials and light is carried through the fiber by total internal reflection. Most optical fibers contain a quartz core surrounded by a silicone rubber cladding. Optical fibers can be hand-held or coupled to a hand piece with a focusing lens for cutaneous applications.


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Both articulated arms and optical fibers can be coupled through a microscope with a micromanipulator which provides a controlled means of moving the laser beam across the surface of human skin. The micromanipulator can also be coupled with a computer for completely preprogrammed and precise skin irradiation. 9.

DOSIMETRY

Laser light is a form of energy that is subject to certain fundamental physical laws defined by a set of equations. An understanding of these relationships is required in order to properly use the laser as a medical device (6). Laser light emitted from the customized medical device is generally characterized in terms of power, measured in watts. The energy (stated in Joules) is defined as the power times the time interval during which light is emitted: Energy (J) ¼ power (W) time (s)

(2:3)

The power density or irradiance is then defined as the power applied per unit area of target tissue: Power density ¼ power (W)=p r 2 (cm2 )

(2:4)

Fluence is defined as the energy applied to an area of target tissue: Fluence (J=cm2 ) ¼ power density (W=cm2 ) time (s)

(2:5)

It can readily be appreciated that the effect of the laser beam on human skin can be affected by any of three variables: power, time, and spot size. The effects of power and time are proportional whereas that of spot size (radius) is an inverse square. If either the power or time is doubled, fluence increases by a factor of 2. However, if the spot size is decreased by a factor of 2, fluence increases by a factor of 4. Doubling the spot size results in a fourfold reduction in fluence. 10.

BASIC LASER – TISSUE INTERACTIONS: REFLECTION, SCATTERING, TRANSMISSION, AND ABSORPTION

How can this intense, pure beam of light be used in the clinical management of patients? The successful applications of lasers to dermatologic surgery rely upon an adequate appreciation of the principles of light interactions with human skin. It is important to recognize that these interactions are complex phenomena influenced not only by laser parameters, such as power, spot size, pulse duration, repetition rate, and wavelength, but also by properties of the tissue itself. If a laser beam is directed at the skin, light may be reflected back to the source or to another undesired surface. Reflection occurs as a result of changes in the indices of refraction at the air – skin interface. When light strikes the skin surface, approximately 5% is reflected. Since tissues reflect light, their reflectance properties are important considerations. Instruments in the operative field may also reflect the light, creating potential health hazards for the patient and attending medical personnel. If reflectance is adequately controlled and light enters human skin, the ultimate determinant affecting that tissue is the absorption of light. However, two things can happen other than absorption. Light can scatter from particles and structures in the skin to places where it is not wanted. Scattered energy is a major reason for the spread of tissue damage around the focused spot because it changes the direction of the incident

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beam. In human skin, collagen fibers are particularly important scattering structures. The degree of scatter is heavily dependent on the wavelength of the light and the composition of the tissue. Light scattering in human skin is greater and more random at shorter wavelengths. Light scattering at longer wavelengths is less and more forward directed. Finally, light might be transmitted through the tissue with only a minimal amount being absorbed. Since every tissue has reflective, scattering, and transmissive properties, understanding these tissue characteristics is an important aspect of knowing how to use the laser. 11.

THE PROCESS OF ABSORPTION

When photons enter the tissue, those that are not reflected, scattered, or transmitted are absorbed. Without absorption, there is no response. Absorption is the key to effective laser use (Fig. 2.7). Absorption refers to a process that occurs when energy supplied by electromagnetic radiation (e.g., light) is transferred to an absorbing molecule, M, so that a more energetic, excited-state species, M , is produced. This excitation can be depicted by the equation: M þ hn ! M

(2:6)

where hv represents the amount of energy absorbed. Within 1026 –1029 s following excitation, the energy is lost, most often as heat, and the species relaxes to its former state: M ! M þ heat

(2:7)

Relaxation may also result from decomposition of M to form a new species; such a process is called photochemical decomposition (see section on Photochemistry and Photodynamic Therapy). Alternatively, relaxation may involve fluorescent or phosphorescent re-emission of a photon (see section on Fluorescence). It is important to

Figure 2.7 Laser –tissue interactions.


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note that the lifetime of M is so short that its concentration at any instant is ordinarily negligible. All molecules contain a unique energy level structure. In order to have light energy absorbed, the energy level structure of the absorbing molecules in the tissue must correspond to the energy of the incident radiation (light). These energy-absorbing molecules in human skin are generally referred to as chromophores. When light is absorbed by a chromophore, energy is transferred from the incoming photon to the chromophore in the skin that is to be altered or changed. Once this energy is absorbed, the energy has to go somewhere, and this is really the key to producing the changes seen in human skin after laser irradiation. Normally, we think of lasers as producing heat, and most laser dermatologic procedures initiate a local thermal event. Radiation, from high-energy sources such as X-rays and gamma rays, ionizes molecules in the tissue and results in relatively nondiscriminant tissue damage. The nonionizing wavelengths, which include visible light electromagnetic radiation, can cause electronic excitations in specific atoms or molecules in the skin which permit selective targeting of chromophores with specific wavelengths of light. Although not demonstrating the same degree of target specificity as visible energy, infrared energy excites vibrational modes in certain tissue molecules that result in a generalized heating of human skin.

12.

CHROMOPHORES IN HUMAN SKIN

Hemoglobin has significant light absorption in the violet, blue/green, and yellow portions of the spectrum (7,8). This absorption starts to decline in the red region. These absorption features permit the scattering and transmission of red light thus causing hemoglobin to appear red in color. In the case of laser treatment of cutaneous blood vessels, the wavelengths suitable for consideration are the hemoglobin Soret absorption band at 418 nm and the absorption bands at 542 and 577 –595 nm (Fig. 2.8). Despite the higher extinction coefficient of the Soret band, this wavelength can be rejected for clinical use because penetration of photons into the dermis in insufficient. However, if one takes advantage of the longer-wavelength hemoglobin absorption band at 577 – 595 nm, where tissue penetration is increased and melanin absorption is reduced, less heating of the epidermis should occur and more incident light energy is transmitted to the blood vessels. For these reasons, the pulsed dye laser (577 – 595 nm) has been the mainstay of treatment for multiple cutaneous vascular lesions. The yellow light is absorbed by hemoglobin in these lesions causing thermal damage and thrombosis of targeted vessels. Melanosomes are the fundamental sites for melanin synthesis and occur as organelles within melanocytes. Absorption is the dominant process by epidermal melanin. Although highest in the ultraviolet portion of the spectrum, melanin absorption is also significant in the visible and near-infrared wavelengths. For these reasons, Q-switched green (KTP), red (ruby, alexandrite), and near-infrared wavelengths have been utilized for the treatment of certain epidermal and dermal pigmented lesions. Water has no light energy absorption in the visible portion of the spectrum and very minimal absorption in the near-infrared portion. However, further out in the infrared (beyond 2 mm), water in the tissue has significant absorption. The Er:YAG and carbon dioxide lasers are currently the most frequently used surgical lasers. Since human skin contains water as a major constituent, the Er:YAG (2.94 mm) and carbon dioxide (10.6 mm) lasers producing infrared photons that are specifically absorbed by water can have a direct effect on the epidermis and dermis. If used properly, the

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Figure 2.8

Nelson

Chromophores in human skin—absorption spectra of hemoglobin, melanin, and water.

Er:YAG and carbon dioxide lasers are clinically equivalent to dermabrasion because the laser gradually removes cell layer after cell layer through volatilization of water present in human skin. Photons emitted by the Nd:YAG laser (at a wavelength of 1.06 mm), on the other hand, are very poorly absorbed by hemoglobin, melanin, water, and other chromophores in human skin. Light penetration into skin is very deep (4 – 6 mm) resulting in a large volume of coagulated tissue—substantially larger than that created by either the Er:YAG or the carbon dioxide laser. Because of the extensive penetration of the Nd:YAG laser into skin, its use in the continuous mode is somewhat limited in cutaneous surgery. For example, the Nd:YAG laser cannot be used to ablate superficial lesions like the Er:YAG or carbon dioxide laser. Recently, however, Nd:YAG lasers pulsed in the millisecond domain have been used to target telangiectasia and reticular veins of the legs. These lasers take advantage of the small peak in the hemoglobin absorption curve, with relatively no competition from melanin or water. Wavelengths suitable for nonablative laser skin rejuvenation must have low melanin absorption, which favors the choice of longer wavelengths (i.e., near- and mid-infrared) over visible light (9). Therefore, most attempts at nonablative laser skin regeneration have used wavelengths with low (650 – 1100 nm) or intermediate tissue water absorption to deposit laser energy nonselectively in the upper (100 – 400 mm) dermis. Wavelengths from 1.3 to 1.8 mm meet this need, which currently limits the selection of light sources to the 1.32 and 1.44 mm Nd:YAG lasers, the 1.45 mm diode laser, and the 1.54 mm Er:glass laser. Because deposited heat is redistributed within the skin by heat diffusion, the ultimate depth of thermal injury is affected not only by the optical penetration of the selected wavelength but also by a multitude of other variables beyond the scope of this chapter.


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In summary, selection of the correct laser for a particular clinical procedure requires an understanding of the absorptive as well as the reflective, scattering, and transmissive properties of the target tissue. 13.

HEAT

Given that one goal of laser therapy is the precise control of thermal energy, a thorough understanding of the sequelae of tissue heating is required. Ideally, from the clinical point of view, the physician should be able to confine the heating process to produce the desired result. Physicians experienced in laser therapy acquire the ability to discern these tissue changes visually so that the heating process can be stopped at the desired point. It is therefore important that physicians planning to use lasers take a basic course in laser theory and clinical management and complete a preceptorship with an experienced instructor who can help them develop the requisite skills. Figure 2.9 shows the effect of a rise in temperature in human skin during laser irradiation. As the tissue is heated and the temperature rises to between 378C and 608C, the skin starts to retract and conformational changes occur. At a temperature above 608C, there is protein denaturization and coagulation. From 908C to 1008C, drying and shrinkage of the skin occur. Above 1008C, the skin is carbonized and subsequently vaporized and ablated.

14.

ABLATION OF HUMAN SKIN

The Er:YAG and carbon dioxide lasers are currently the lasers of choice for human skin ablation. Since light is absorbed so intensely by water, penetration depths are only a few micrometers. Absorption of many photons in such a small volume of tissue produces a

Figure 2.9 Thermal interaction of laser irradiation with human skin.

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rapid rise in skin temperature. As energy is added, the temperature of water is raised to its boiling point. Internal vapor pressure builds up until a microexplosion occurs. The rapid expansion created by this excitation give rise to the actual ejection of microscopic tissue fragments at high velocities. Since most of the energy of the laser pulse goes into the thermal phase change associated with tissue vaporization, ablated fragments ejected from the skin surface carry most of the energy with them, leaving little energy in the form of heat to damage surrounding tissue. Because vaporization is such a rapid process, thermal damage to adjacent tissue, although varying with the duration of exposure, is usually limited to a zone of 100–200 mm (carbon dioxide) or less (Er:YAG) in human skin.

15.

SELECTIVE PHOTOTHERMOLYSIS

The laser has many inherent properties that contribute to its ability to effect a specific biological outcome. Most important, from a clinical point of view, are the properties of emitted wavelength and pulse duration. If the clinical objective is to cause selective destruction of a specific chromophore, the wavelength chosen should match the highest absorption of the targeted chromophore relative to other optically absorbing molecules. Given that one goal of treatment is the precise control of thermal energy, the pulse duration of laser irradiation is just as important as optical and tissue factors. One way to maximize the spatial confinement of heat is to use a laser with a pulse duration on the order of the thermal relaxation time (Tr) of the target chromophore (10). Tr is defined as the time required for the heat generated by the absorbed light energy within the target chromophore to cool to half of the original value immediately after the laser pulse. During a lengthy laser exposure, most of the heat produced diffuses away despite its origin in the target structure. The target does not become appreciably warmer than its surroundings because the absorbed energy is invested almost uniformly in heating of the tissue during exposure. As a result, longer pulse durations offer a more generalized heating and, therefore, less spatial selectivity resulting in nonspecific thermal damage to adjacent structures regardless of how carefully one has chosen a wavelength. However, if the laser pulse is suitably brief, its energy is invested in the target chromophore before much heat is lost by thermal diffusion out of the exposure field. A transient maximum temperature differential between the target and adjacent structures is then achieved. Shorter pulse durations confine the laser energy to progressively smaller targets with more spatial selectivity. The transition from specific to nonspecific thermal damage occurs as the laser exposure equals and then exceeds Tr . Therefore, selective target damage depends on delivering a pulse of light of shorter duration than Tr , which can be estimated because the latter is directly proportional to the square of the diameter of the target and inversely proportional to the thermal diffusivity of the tissue (Table 2.1). A laser emitting at a Table 2.1 Relationship of Target Chromophore Diameters and Their Thermal Relaxation Times (Tr) Target Microvessel Blood vessel Tattoo pigment Melanosome Melanocyte

Diameter (mm)

Tr

50 150 0.5 – 100 0.5– 1.0 7

1.4 ms 12.8 ms 20 ns – 3 ms 20– 40 ns 1 ms


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selectively absorbed wavelength with a pulse duration less than Tr can be expected to cause highly selective target damage (Fig. 2.10). This process, termed selective photothermolysis, was introduced in 1983 as a means of achieving target chromophore destruction by careful selection of wavelength and pulse duration.

16.

SELECTIVE PHOTOTHERMOLYSIS OF CUTANEOUS BLOOD VESSELS

The pulsed dye lasers at 577 – 595 nm, wavelengths well absorbed by the targeted hemoglobin molecule relative to other optically absorbing structures, cause selective thermal damage to dermal blood vessels while minimizing epidermal melanin absorption. Furthermore, because the Tr for cutaneous blood vessels 50 –150 mm in diameter is between 1.4 and 12.8 ms, the 0.45– 50 ms pulse duration produced by these lasers matches the Tr for dermal blood vessels, thus confining the laser energy to the targeted vessel before much heat is lost by thermal diffusion out of the exposure field (11). Patients with a wide range of vascular abnormalities, such as port wine stains, hemangiomas, telangiectasias, angiomas, venous lakes, poikiloderma of Civatte, and angiokeratomas, have benefited from pulsed dye laser therapy (12). The green light (532 nm) produced by the frequency-doubled Nd:YAG laser (KTP laser) is also preferentially absorbed by hemoglobin. Although melanin absorption is higher and light penetration into human skin is less at this shorter wavelength, the KTP laser has been approved by the FDA for many of the same procedures as the pulsed dye laser.

Figure 2.10 Selective photothermolysis. With relatively long laser exposure times, selective target damage is followed by thermal diffusion and damage to adjacent structures. Selective thermal damage can be confined to the tissue target by choosing a pulse duration that is shorter than Tr .

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SELECTIVE PHOTOTHERMOLYSIS OF TATTOOS

Amorphous carbon, graphite, India ink, and organometallic dyes, typically found in dark blue-black amateur and professional tattoos, have a broad absorption in the visible and near-infrared portions of the spectrum. At visible wavelengths longer than 600 nm, hemoglobin and melanin light absorption is minimized and tattoo dyes can be targeted selectively (13). The pigment granules characteristically found in tattoos have diameters of 0.5– 100 mm, which correspond to Tr of 20 ns to 3 ms. With the development of the Q-switched ruby (694 nm), alexandrite (755 nm), and Nd:YAG (1.06 mm) lasers, tattoo removal without scarring can be achieved. The frequency-doubled, Q-switched Nd:YAG laser (KTP laser) emits at a wavelength of 532 nm, which provides improved removal of red dye.

18.

SELECTIVE PHOTOTHERMOLYSIS OF PIGMENTED LESIONS

Although highest in the ultraviolet portion of the spectrum, melanin absorption is also significant in the visible and near-infrared wavelengths. The diameters of individual melanosomes (0.5 –1.0 mm) and melanocytes (7 mm) correspond to Tr of 20 –1000 ns. Therefore, Q-switched green, red, and near-infrared wavelengths have been utilized for this indication. Studies have shown that the effects of Q-switched lasers are melanosome dependent, and vacuolization of pigment-laden cells has been seen immediately after laser irradiation on examination by light and electron microscopy (14). Disruption of melanosomes at pulse widths less than Tr presumably resulted from a shock wave or cavitation induced by thermal expansion or by the temperature gradient generated across the pigmented cells. Q-switched lasers have been used successfully to treat a wide variety of pigmented lesions including lentigines, ephelides, and nevus of Ota (12).

19.

SELECTIVE PHOTOTHERMOLYSIS AND LASER ASSISTED HAIR REMOVAL

The human hair follicle is a complex structure derived from both epidermal and dermal components. The target chromophores, primarily melanin-rich hair shafts, are located deep in human skin (bulge around 1.5 mm and bulb at 2 –7 mm). At this depth, only red and near-infrared wavelengths are useful (690 –900 nm). The follicular structure responsible for regeneration has not been conclusively identified and, therefore, current systems target the entire follicle. As a result, long pulse widths on the order of milliseconds and high fluences capable of heating large volumes of tissue are required (15). Millisecond-domain ruby, alexandrite, diode, and Nd:YAG lasers using high light doses can produce selective injury to human hair follicles resulting in prolonged growth delay and, in some cases, permanent hair loss after a single treatment.

20.

SKIN COOLING

The clinical objective of laser therapy is to maximize thermal damage to target chromophores while minimizing injury to overlying skin. Unfortunately, for many skin types, the threshold light dosage for epidermal injury due to melanin absorption can be very close to


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that for permanent removal of target chromophores. A valuable method to overcome this problem is to cool selectively the superficial layers of the skin during laser therapy which prevents thermal injury despite some melanin absorption. Rapid and spatially selective epidermal cooling can be achieved by active skin cooling (16). The first and intuitively simple objective of skin cooling is to decrease epidermal damage. So long as the epidermis is prevented from reaching a temperature in response to laser exposure that is above its threshold for denaturation (60 – 658C), the epidermis and upper dermis can be preserved. The second objective is to permit the use of higher light dosages for treatment of laser resistant lesions. The third objective is the treatment of patients with all skin types. For patients with darker skin types (types IV – VI), it is not possible to treat lesions without cooling due to epidermal damage with a sufficiently high light dosage. The fourth objective is reduction of pain and posttreatment swelling or edema. Several different methods have been developed for cooling human skin in conjunction with laser therapy. All methods utilize a precooled medium brought in contact with the skin surface. Deeper skin layers are cooled by heat diffusion toward the cooled surface with subsequent transfer to the cooling medium. The rate of heat transfer across the interface between the skin and the cooling medium depends primarily on the temperature difference between the two adjacent materials, as well as other parameters, specific to each cooling method. Therefore, cooling efficiency using any method can be adequately characterized by the proportionality constant, termed heat transfer coefficient (h), regardless of the physical mechanisms involved. Contact cooling (CC) of human skin is achieved by heat conduction into an adjacent precooled solid body, usually an optically transparent plate, kept at constant temperature (210 to 48C) by a cooling system. Laser exposure is delivered through the plate, which is pressed against the patient’s skin. CC can be very efficient especially when a highly conductive material, such as sapphire, is used for the cooling plate. However, in practice, the thermal resistance at the interface of the intervening layer between the skin and the plate inevitably impairs the rate of heat extraction with CC. Air, bubbles, hair, or other substances may impede the direct contact between the skin surface and the cooling plate. Human skin can also be cooled by air precooled (AC) and blown onto or across the surface at temperatures as low as 2308C. Despite the low air temperature used, AC is characterized by the lowest cooling rate since the heat transfer coefficient for forced convection in gas is very low. As a result, long cooling times (on the order of several seconds) are necessary to induce significant temperature reductions in the basal layer. Therefore, the final outcome is inevitably general (“bulk”) cooling of the entire skin with minimal spatial selectivity. Rapid and spatially selective epidermal cooling can be achieved by active cooling using a cryogen spray (CSC) or dynamic cooling (17). Tetrafluoroethane (TFE) is the only cryogenic compound currently FDA approved for use in dermatologic laser surgery. TFE is a nonflammable, nontoxic, environmentally compatible freon substitute which does not deplete atmospheric ozone or contribute to global warming (18). CSC’s main cooling mechanism is rapid evaporation of cryogen, which extracts the necessary latent heat from the skin. Liquid cryogen is “atomized” into a fine spray and directed toward the skin surface. During flight, spray droplets cool rapidly due to cryogen evaporation. Therefore, the droplet temperature when impinging on the skin surface is typically between 2408C and 2608C. As a result, CSC provides a rapid, large, and spatially selective epidermal temperature reduction. A layer of liquid cryogen can remain on the skin surface after spurt termination. Consequently, cooling continues for a much longer time than the actual user-specified spurt duration. The presence of liquid

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cryogen on the skin surface after spurt termination constitutes de facto skin cooling during and after the laser exposure. Cryogen spurt duration and delay between spurt termination and the laser pulse can be controlled electronically, which results in predictable cooling with reproducible spatial selectivity. The development of skin cooling methodology has definite advantages for patients receiving laser therapy: (1) cooling permits safe and effective laser treatment by increasing the threshold for epidermal damage, (2) cooling permits the use of higher-incident light doses for treatment of resistant lesions, (3) cooling permits the treatment of patients with all skin types, and (4) for all patients, particularly children, pain and distress associated with laser therapy are significantly reduced.

21.

PHOTOCHEMISTRY AND PHOTODYNAMIC THERAPY

Photon energy may also be dissipated by photochemistry. The basic concept of photochemistry is that certain molecules (natural or applied) can function as photosensitizers. The presence of these photosensitizers in certain cells makes them vulnerable to light at wavelengths absorbed by the chromophore. The excited photosensitizer subsequently reacts (transfers its energy) with a molecular substrate, such as oxygen, to produce highly reactive singlet oxygen which causes irreversible oxidation of some essential cellular component. All of this occurs without the generation of heat. Although photodynamic therapy (PDT), using porphyrin derivatives and visible light, has primarily focused on the treatment of skin cancer, PDT is also being used for the clinical management of selected nonmalignant, dermatological indications, such as actinic keratosis, psoriasis, and PWS (19).

22.

FLUORESCENCE

Photon energy may be dissipated as the re-emission of light. If this happens within 1026 s after absorption, it is called fluorescence. The fluorescent photon is emitted as the excited atom returns to the ground state. However, because some energy is lost by collisions with other atoms in the excited state, the energy of the fluorescent photon is lower (and therefore the wavelength is longer) than that of the absorbed photon. It appears that many of the photosensitizing dyes used to induce photochemistry are also fluorescent. If in the case of porphyrins, 400 nm blue-violet light from a krypton laser is used with an appropriate filter and image intensifier, fluorescence can be observed (19). Clinical trials are now in progress in which the effectiveness of fluorescence for detection and localization of certain premalignant and malignant skin lesions is being evaluated.

23.

CONCLUSION

Since the laser was first developed in 1960, it has found many uses in dermatology. Moreover, lasers are now the treatment of choice for several clinical entities for which no reliable or effective modality was previously available. Research into increasing our understanding of the optical characteristics of skin has made it possible to concentrate not on the effects of any particular laser system but on the basic biological and physical principles of laser – tissue interaction. Modern technology allows us to manipulate the physical characteristics of lasers and design them for specific therapeutic purposes.


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REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.

12.

13. 14.

15. 16. 17.

18. 19.

Boulnois JL. Photophysical processes in recent medical laser developments. A review. Lasers Med Sci 1986; 1:47– 66. Elion HA. Laser Systems and Applications. New York: Pergamon Press, 1967. Hitz CB. Understanding Laser Technology. Tulsa, OK: PennWell Publishing, 1985. O’Shea DC, Callen WR, Rhodes WT. Introduction to Lasers and Their Applications. Menlo Park, CA: Addison-Wesley Publishing, 1978. Siegman AE. Lasers. Mill Valley, CA: University Science Books, 1986. Sliney D, Wolbarsht M. Safety with Laser and Other Optical Sources. New York: Plenum Press, 1985. Anderson RR, Parrish JA. Optical properties of skin. In: Regan JD, Parrish JA, eds. The Science of Photomedicine. New York: Plenum Press, 1982:147 – 194. Anderson RR, Parrish JA. The optics of human skin. J Invest Dermatol 1981; 77:13– 19. Kelly KM, Majaron B, Nelson JS. Nonablative laser and light rejuvenation. Arch Facial Plast Surg 2001; 3:230– 235. Anderson RR, Parrish JA. Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science 1983; 220:524 – 529. Dierickx CC, Casparian JM, Venugopalan V, Farinelli WA, Anderson RR. Thermal relaxation of port-wine stain vessels probed in vivo: the need for 1– 10 millisecond laser pulse treatment. J Invest Dermatol 1995; 105:709 – 714. Kelly KM, Nelson JS. Critical review of lasers in dermatology. Critical reviews of optical science and technology. In: Ryan TP, ed. Matching the Energy Source to the Clinical Need. Vol. CR75. Bellingham, WA: SPIE Optical Engineering Press, 2000:3 – 23. Cesario-Kelly KM, Nelson JS. Q-switched laser treatment of tattoos. Lasers Med Sci 1997; 12:89 – 98. Anderson RR, Margolis RJ, Watenabe S, Flotte T, Hruza GJ, Dover JS. Selective photothermolysis of cutaneous pigmentation by Q-switched Nd:YAG laser pulses at 1064, 532, and 355 nm. J Invest Dermatol 1989; 93:28– 32. Ross EV, Ladin Z, Kriendel M, Dierickx CC. Theoretical considerations in laser hair removal. Dermatol Clin 1999; 17:333 – 355. Nelson JS, Majaron B, Kelly KM. Active skin cooling in conjunction with laser dermatologic surgery. Semin Cutan Med Surg 2000; 19:253– 266. Nelson JS, Milner TE, Anvari B, Tanenbaum BS, Kimel S, Svaasand LO, Jacques SL. Dynamic epidermal cooling during pulsed laser treatment of port-wine stain. A new methodology with preliminary clinical evaluation. Arch Dermatol 1995; 131:695 – 700. Nelson JS, Kimel S. Safety of cryogen spray cooling during pulsed laser treatment of selected dermatoses. Lasers Surg Med 2000; 26:2 – 3. Nelson JS, McCullough JL, Berns MW. Principles and applications of photodynamic therapy in dermatology. In: Arndt KA, Dover JS, Olbricht SM, eds. Lasers in Cutaneous and Aesthetic Surgery. Philadelphia, PA: Lippincott-Raven Publishers, 1997:349 – 382.

3 Laser Safety Measures Christie Travelute Ammirati Penn State University College of Medicine, Hershey, Pennsylvania, USA

George J. Hruza St. Louis University School of Medicine, St. Louis, Missouri, USA

1. Introduction 2. Laser Safety Organizations and Regulations 2.1. American National Standards Institute 2.2. The Center for Devices and Radiological Health 2.3. Occupational Safety and Health Administration 2.4. The National Institute for Occupational Safety and Health 3. Laser Hazard Classification 4. Eye Hazards 4.1. Eye Anatomy 4.2. Electromagnetic Spectrum 4.3. Retinal Injury 4.4. Corneal Injury 4.5. Lenticular Injury 5. Eye Protection 5.1. Patient Protection 5.2. Medical Surveillance 6. Skin Hazards 7. Teeth Hazards 8. Fire Hazards 8.1. Fire Prevention 8.2. Fire Containment 9. Electrical and Mechanical Hazards 9.1. Controlled Access 10. Chemical Hazards 10.1. Chemical Protection 11. Accoustic Hazards

80 80 80 82 82 82 82 83 84 85 87 87 88 88 90 90 91 91 91 91 92 93 93 95 95 95 79

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12. Laser Plume Hazards 12.1. Organic Compounds 12.2. Particulate Debris 12.3. Pathogenicity 12.4. Protection and Evacuation 12.5. Smoke Evacuators 12.6. Laser Masks References

1.

95 95 96 96 97 97 98 98

INTRODUCTION

Lasers produce intense monochromatic, collimated, and coherent light. These properties, which allow for the highly selective destruction of target chromophores, also carry significant safety concerns. There are an ever-increasing number of cutaneous lasers available today and it can prove challenging to remain current with the unique safety issues of each system. Overall, surgical lasers have a good safety record but their potential hazards can cause significant injury and even death (1). This chapter provides an overview of laser safety issues as they apply to the patient, laser surgeon, and staff. It augments, but cannot hope to replace, formal instruction.

2.

LASER SAFETY ORGANIZATIONS AND REGULATIONS

There are several organizations that concern themselves with laser safety. In the USA these organizations include the American National Standards Institute (ANSI), the Center for Devices and Radiological Health (CDRH), the Occupational Health and Safety Administration (OSHA), and the National Institute for Occupational Safety and Health (NIOSH). Many of these organizations publish laser safety manuals that are available free of charge (see Table 3.1).

2.1.

American National Standards Institute

The ANSI is a consensus group of industry, university, and government laser experts who developed the ANSI-Z136 series. This set of standards provides recommendations for the safe use of lasers and laser systems. There is no inherent requirement for adherence to their guidelines and compliance is voluntary unless mandated by an employer or organization. The American National Standard for Safe Use of Lasers (ANSI-Z136.1) and the American National Standard for Safe Use of Lasers in Health Care Facilities (ANSI-Z136.3) are the expected standards of care in the USA and are often cited in litigation. OSHA and the Joint Commission for Accreditation of Healthcare Organizations (JCAHO) reference these standards when evaluating laser-related occupational safety issues. The ANSI-Z136 series provides information on laser classification, safety calculations, and control measures. These standards of care apply to all laser operators, regardless of the clinical application or practice setting. Specifically, private office-based laser centers are expected to have training policies and safety protocols similar to those used in hospitals.

Laser Safety Measures

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Table 3.1 Laser Safety Resources Laser safety source University of Waterloo “Laser Manual” OSHA Technical Manual Section III: Chapter 6 “Laser Hazards” OSHA PUB 8-1.7 “Guidelines for Laser Safety and Hazard Assessment” Berkely Lab Health and Safety Manual Chapter 16 “Lasers” NIOSH Hazard Control “Control of Smoke from Laser/Electrosurgical Procedures” LaserFX “Basic Laser Safety” Rockwell Laser Institute “Statistical Data for Laser Accidents” Laser Institute of America “Laser Generated Air Contaminants (LGAC)” Laser Institute of America “Laser Safety Information Bulletin” American Society for Lasers in Medicine and Surgery “Smoking Guns” Lawrence Livermore National Laboratory “Environment, Safety and Health Manual” Center for Devices and Radiological Health “21CFR 1040.10 and 1040.11” University of Illinois “UIUC Laser Safety Tutorial” Navy Laser Safety Page U.S. Army Laser/Optical Radiation Program Oklahoma State University Optical Radiation Branch (AFRL/HEDO) Air Force Canadian Centre for Occupational Health & Safety (CCOHS) “Lasers in Health Care” University of Pennsylvania Laser Safety

Website www.adm.uwaterloo.ca/infohs/lasermanual/documents www.osha-slc.gov/dts/osta/otm_iii/otm_iii_6.html

www.osha-slc.gov/OshDoc/Directive_data/PUB_8-1_7.html

ehssun.lbl.gov/ehsdiv/pub3000/CH16.html

www.cdc.gov/niosh/hc11.html

www.laserfx.com/sci4.html www.iac.net/rli/accidents/stat_dat.html

www.rli.com/lgac.html

www.laserinstitute.org/safety_bulletin

www.aslms.org/general-smokegunsl.html

www.llnl.gov/es_and_h/hsm/chapter_28

www.fda.gov/cdrh/index.html

phantom.ehs.uiuc.edu/rad/laser/laser.html www.nswc.navy.mil/safety/laser chppm-www.apgea.army.mil/laser/laser.html www.pp.okstate.edu/ehs/links/laser.html www.brooks.af.mil/AFRL/HED/HEDO www.ccohs.ca/oshanswers/phys_agents/lasers.html

www.oehs.upenn.edu/laser/laser_manual.html

Note: There are many laser safety resources available on the Internet. Many have safety manuals that can be downloaded free of charge.

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The Center for Devices and Radiological Health

The CDRH U.S. Federal Laser Product Performance Standard (FLPPS) regulates the manufacture of commercial lasers. Under guidelines 21 CFR Part 1040.10 and 1040.11, the manufacturer is required by federal law to classify and appropriately label a laser with its hazard class. These regulations are designed to insure product safety and do not pertain to or regulate laser use once they have been purchased. 2.3.

Occupational Safety and Health Administration

OSHA is a federal regulatory agency concerned with safety and health conditions in the workplace. While it does not have a comprehensive standard for medical lasers, it has issued several regulations that pertain to laser safety. The Eye and Face Protection Standard (29CFR 1926.102) and Personal Protective Equipment Standard (29CFR 1910.132-138) mandate that employees who are exposed to laser beams by occupation or assignment be provided with appropriate laser-specific eye protection. The BloodBorne Pathogen Standard (29CFR 1910.1030) addresses employee protection from potentially infectious exposures and has been extrapolated to include laser-generated debris (2). The OSHA Technical Manual and, Guidelines for Laser Safety and Hazard Assessment are available free of charge from OSHA (see Table 3.1). These manuals provide an excellent overview of laser safety and are highly recommended. 2.4.

The National Institute for Occupational Safety and Health

NIOSH is a federal agency responsible for conducting research and making recommendations for preventing work-related illness and injury. In 1996, NIOSH published Control of Smoke from Laser/Electric Surgical Procedures (HC11). This hazard control discusses the rationale for controlling the smoke from laser or electrosurgical procedures and makes recommendations for optimal smoke evacuation. 3.

LASER HAZARD CLASSIFICATION

In general, lasers are classified according to their relative hazards. The basis for this classification scheme is the ability of the laser beam to cause unintended injury to the eye or skin (2). The ANSI classification, which is the most commonly cited standard, stratifies risk from I to IV (Table 3.2). Class I lasers are very low-power lasers that do not emit hazardous radiation (typically ,0.4 mW) and are considered to be safe for continued viewing. Few lasers function at this very low level and most Class I lasers are in this category by virtue of an enclosure that prevents access to their radiation (embedded). An example of an embedded laser would be a laser printer. Class I lasers are exempt from control measures or warning labels. The Class IIa subclassification was developed for bar-code scanners, which emit visible light and are not intended for viewing. They have an upper power limit of 4 mW and are considered safe unless viewed directly for .1000 s. Class IIa lasers are required to carry the label, “Avoid Long-Term Viewing of Direct Laser Radiation” but are exempt from other hazard controls. Class II lasers emit ,1 mW of visible (400–760 nm) light. The human eye will blink and look away within 250 ms when exposed to a bright visible light. This is known as the blink reflex or aversion response and it is usually sufficient to protect the eye from Class II laser injury (4). With intentionally prolonged viewing (.250 ms), these lasers are capable of damaging the eye (5). Alignment beams or low-power helium–neon laser pointers are


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Table 3.2 ANSI Classification of Risk Class

Energy (mW)

Exposure limits

I IIa II

,0.0004 ,0.004 ,1

IIIa

1 –5

Hazardous in ,0.25 s when viewed with collecting optics

IIIb

5– 500

IV

.500

Direct beam or specular reflection hazardous in ,0.25 s Direct beam, specular or diffuse reflection hazardous in ,0.25 s

None Safe for ,1000 s Safe for ,0.25 s

Comments Safe for viewing Not intended for direct viewing Do not purposely stare into the beam Do not view through collecting optics without protective eyewear Do not view direct beam or specular reflection without protective eyewear Do not view direct beam, specular or diffuse reflection without protective eyewear; skin and fire hazard as well

Source: Refs. (2,3).

examples of Class II lasers. They require a “CAUTION” warning with the phrase, “LASER RADIATION—DO NOT STARE INTO BEAM.” Class III lasers, which include ultraviolet (UV), visible, and infrared lasers are divided into subclasses IIIa and IIIb. Class IIIa lasers, such as diode aiming beams, emit 1–5 mW of energy (6). These lasers are safe for brief viewing (,250 ms) but can be hazardous when viewed through collecting optics (i.e., microscope or endoscope). All Class IIIa lasers require a “CAUTION” warning with the phrase, “LASER RADIATION—DO NOT STARE INTO BEAM OR VIEW DIRECTLY WITH OPTICAL INSTRUMENTS.” (Note: Prescription eyewear is not considered to be a collecting optic.) Class IIIb lasers, such as retinal photocoagulators, produce 5– 500 mW and exposure to their direct or reflected beam can cause eye and skin damage (7). Class IIIb lasers are not considered to be fire hazards but they are subjected to all other control measures outlined in this chapter. They require a “DANGER” warning with the phrase, “LASER RADIATION—AVOID DIRECT EXPOSURE TO THE BEAM.” Almost all medical lasers are designated as Class IV and have power levels greater than 500 mW (continuous wave) or generate more than 10 J/cm2 in 250 ms (pulsed system). Even brief exposures to their direct, reflected, or scattered emissions pose eye, skin, and fire hazards. These lasers require a “DANGER” warning with the phrase, “LASER RADIATION—AVOID EYE OR SKIN EXPOSURE TO DIRECT OR SCATTERED RADIATION.”

4.

EYE HAZARDS . . . I was not wearing protective goggles at the time, although they were available in the laboratory. When the beam struck my eye, I heard a distinct popping sound, caused by a laser-induced explosion at the back of my eyeball. My vision was obscured almost immediately by streams of blood floating in the vitreous humor. It was like viewing the world through a round fish bowl full of glycerol into which a quart of blood and a handful of black pepper have been partially mixed. Decker, CD. Laser accident victim’s view. Laser Focus August 1977.

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The above account was written by a researcher who suffered permanent eye damage from a 1064 nm Nd:YAG laser beam. The eye is an intricate and complex organ, comprising several structures, each with their own absorption spectrum. As with all laser – tissue interactions, photon energy must be absorbed to have an effect (Grothus –Draper Law) and the ocular structure at risk will vary with the wavelength in use (8). To understand how this selective injury can occur, eye anatomy and basic principles of optical physics should be reviewed.

4.1.

Eye Anatomy

The cornea is the main focusing element for vision and is protected from the environment by its tear film and numerous sensory receptors (9) (Fig. 3.1). The cellular turnover of the outer corneal layers is approximately 48 h and allows most of the superficial injury to heal without residual damage. Permanent corneal scarring will occur if the damage extends to the deeper layers. The lens performs fine focusing of images onto the retina. Normally, the lens is transparent but changes in its proteins can produce a cataract. The space between the cornea and lens is filled with the aqueous humor and the interior of the eyeball is filled with the gelatinous vitreous humor. The cornea and lens, along with the aqueous and vitreous humors, comprise the anterior segment of the eyeball. The retina is divided into two major components. The pigmented monolayer is called the retinal pigmented epithelium and the multilayered neural component is called the neural retina. The rods and cones, which function as photoreceptors, are located adjacent to the neural retina. Rods are mainly concerned with low light vision and are found predominantly in the periphery of the retina. Cones are responsible for color perception and visual acuity. They are concentrated centrally within the macula. The fovea is in the center of the macula and is responsible for fine focusing activities such as

Figure 3.1 Anatomic structures of the human eye.


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reading. The retina, which is rich in photoreceptors, does not contain pain receptors. The choroid is a vascular layer that is separated from the retina by Bruch’s membrane.

4.2.

Electromagnetic Spectrum

The divisions between the different portions of the electromagnetic spectrum (EMS) are somewhat arbitrary and the regions tend to overlap (10) (Fig. 3.2). The EMS includes radiation that extends from cosmic rays to radiowaves. The UV spectrum includes radiation from 100 to 400 nm and is divided into four subdivisions: vacuum UV (100 –200 nm), UV-C (200 –290 nm), UV-B (290 – 315 nm), and UV-A (315 –400 nm). The visible

Figure 3.2 Diagrammatic representation of the electromagnetic spectrum and the specific sites of laser-induced ocular damage. The optical spectra used for cutaneous lasers are expanded to present more detail. [Adapted from Refs. (8,10,11,13– 15).]

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spectrum is often referred to as visible light and extends from 400 to 760 nm. The infrared (IR) spectrum spans from 760 to 106 nm and has three subdivisions: near-IR (760 – 1400 nm), mid-IR (1400 – 3000 nm), and far-IR (3000 –106 nm). The term specular describes mirror-like reflections, which can reflect close to 100% of incident light (11). Specular reflection by a flat surface will not change a fixed beam’s diameter, only its direction (Fig. 3.3). Convex surfaces will cause beam divergence and concave surfaces will make the beam converge. Diffuse reflections result when surface irregularities scatter light in all directions. Whether the reflection is specular or diffuse will depend on the wavelength of light that strikes the surface (12). A given surface, which will diffuse visible light, may produce specular reflections when struck by longer IR wavelengths. Although oversimplified, wavelengths in the UV, mid- and far-IR regions are primarily absorbed by the anterior segment while the posterior segment absorbs the majority of visible and near-IR wavelengths. There are two transition zones in which both segments of the eye may be damaged. These zones are found at the transition from UV to visible light and where near-IR light becomes mid-IR (2). An example would be the Nd:YAG laser at 1340 nm, which can simultaneously damage the cornea, lens, and retina (13).

Figure 3.3 Diagrammatic representation of reflections by various specular and anodized surfaces. Convex specular surfaces cause beam convergence. Concave specular surfaces cause beam divergence. Flat specular surfaces change a fixed beam’s direction but not its diameter. Anodized, brushed or matte surfaces cause beam diffusion. [Adapted from Refs. (11,12,16).]


4.3.

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Retinal Injury

Light of 400– 1400 nm wavelength poses the most serious risk to the retina and is known as the retinal hazard zone (8). For Class IV lasers, the blink reflex is not protective, as by the time it can engage, the damage has already occurred. The human eye can focus collimated laser light down to a 10– 20 mm spot (11). The law of the conservation of energy applies to this convergence and the energy density will increase geometrically as the spot diameter decreases. Thus, normal focusing by the eye results in a 100,000-fold increase in energy fluence. This can be likened to a magnifying lens focusing sunlight onto paper and causing it to burn. The eye focuses and intensifies the laser beam in a similar fashion onto the retina. Visible and near-IR lasers can produce retinal injury via thermal and photoacoustic mechanisms (8). Thermal injury may remain confined to the dimensions of the laser spot or if the energy is excessive, heat may extend the damage peripherally. Q-switched lasers produce powerful nanosecond pulses that create shock waves (photoacoustic effects) within the retina. This type of mechanical damage forcibly expels burned debris into the vitreous and due to its global effect on the retina often produces more destruction than thermal damage alone (17,18). The location and extent of the damage within the retina determines the degree of perceived visual loss. A small lesion, at the periphery of the fundus, may go unnoticed while damage to even the smallest portion of the fovea will produce a decrease in visual acuity and color perception. Since retinal tissue does not regenerate, any damage will be permanent. Unprotected eye exposure to visible (400 – 760 nm) laser light produces an intense flash of colored light followed by an after-image. Exposure to near-IR (760 –1400 nm) laser light may not be initially apparent because wavelengths much longer than 760 nm are invisible to the human eye (14). Since there are no pain receptors in the retina and the beam is invisible, accidental exposure to a near-IR beam may go unnoticed until the damage is severe. By far, the most common laser associated with retinal injury is the 1064 nm Nd:YAG laser (19). Symptoms from Nd:YAG laser injury can range from a headache to the audible “pop” and appearance of “floaters” as described by Decker (20). Treatment for laser-induced retinal injury is largely anecdotal but the majority of the literature supports observation or the use of corticosteroids (21,22). Apparently, as long as the fovea is not damaged, the potential for spontaneous recovery of vision is favorable (23,24).

4.4.

Corneal Injury

The cornea is susceptible to damage from radiation within the UV spectrum and above 1400 nm (13,15). As with all laser – tissue interactions, the extent of injury will depend on the wavelength, energy, and duration of exposure. Since amplification by the lens is not involved, injury thresholds for the cornea are significantly higher than those that cause retinal injury (11). Corneal injury from wavelengths beyond 2800 nm (i.e., 2940 nm Er:YAG and 10,600 nm CO2 lasers) is usually confined to the superficial layers, which are capable of regeneration (25). While superficial corneal burns can be intensely painful, they usually resolve in 2–3 days without sequelae. Both lasers are capable, with sufficient energy, of producing deeper injury with scarring and corneal opacification (25). Treatment of superficial corneal injury consists of topical antibiotics and an eye patch. There is no effective medical treatment for deeper injury and corneal transplantation may be the only hope for restoring vision. Surgical preparations used before laser surgery can also injure the cornea. Chlorhexidine, apart from being flammable, can cause severe keratitis with permanent opacification

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if allowed to come in contact with the cornea (26,27). Regardless of the treatment location, chlorhexidine should not be used before laser surgery since it could be potentially aerosolized in the laser plume. This vapor could injure the eyes of the patient, laser operator, or assistant if adequate laser smoke evacuation is not in use. 4.5.

Lenticular Injury

The human lens strongly absorbs UV-A and to a lesser extent visible and near-IR (760 –1400 nm) light (13,15). Visible and near-IR light is thought to damage the lens by conductive heating of the iris. If the energy is sufficient, acute exposure can produce an immediate burn. More commonly, the exposure is chronic and it can take years for the cataract to become evident. 5.

EYE PROTECTION

If there is any possibility of viewing a Class IIIb or Class IV laser beam, appropriate eye protection must be provided for all personnel and patients within the laser control area. OSHA’s Eye and Face Protection Standard [29CFR 1926.102 (b)(2)] addresses the safety of employees who work with lasers. An employer’s obligation to provide and pay for personal protective equipment is outlined in OSHA’s Personal Protective Equipment Standard (29CFR 1910.132 –138). To better understand eye protection requirements, the maximum permissible exposure (MPE) and the nominal hazard zone (NHZ) should be defined (2). MPE is the level of laser radiation to which a person may be exposed without damage to the eye or skin. The MPE will vary with laser wavelength, duration of exposure and pulse repetition and is expressed in joules per square centimeter or watts per square centimeter. ANSI Z-136.1 tables A3(a) and (b) list the MPE for specific wavelengths. Exposure to energy above these limits can result in tissue damage. The NHZ is the distance from the laser at which the level of direct, reflected, or scattered radiation exceeds the MPE. As such, it defines the space in which control measures are required. The NHZ is a function of the laser settings in use such as spot size, energy, and pulse duration. These parameters are often changed during a procedure and continual calculation of the NHZ would be unrealistic. To simplify this situation, the NHZ for Class IV lasers is defined as the entire surgery room. Laser protective eyewear (LPE) provides the primary means to guard against ocular injury and must be worn whenever the laser is enabled. To be effective, the LPE must be wavelength specific and have sufficient optical density (OD) for the laser in use. OD is a logarithmic function that defines the ability of a protective lens to absorb a specific wavelength: OD ¼ log10

incident light (in J=cm2 or W=cm2 ) transmitted light (in J=cm2 or W=cm2 )

For example, an OD of 4 allows 1/104 of the laser energy to be transmitted. Cutaneous lasers range from 308 to 10,600 nm and there is no single lens filter that will provide protection throughout this range of wavelengths without being opaque. A higher OD does not always mean improved safety (28). Lenses with higher OD values are often dark in color, which can limit color discrimination and visualization of the treatment area (29). Clearly, there must be a balance between maximal eye protection and visibility because compliance will be low if eyewear is difficult to see through.


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There are a variety of reflective and absorbent optical filters available. A reflective filter allows the transmission of as much of the remaining visible spectrum as possible but may create potentially hazardous reflections. Other disadvantages of glass reflective filters are that they are heavy and if the coating is scratched, radiation may reach the eye. Absorbent filters molecularly convert, rather than reflect, laser energy. They can be made from polymeric materials, which weigh less, are easily molded into comfortable shapes, and are not affected by surface scratches (30). Their disadvantage is that they are easily cracked and can melt with sufficient heat. Any damage to the optical filter, be it reflective or absorptive, can lower the OD value in an unpredictable manner (31). Therefore, LPE should be handled carefully and examined prior to each use for cracks, scratches, or loose-fitting lenses. Do not rely on the color of the lens or style of the LPE to identify the level of protection, as this can be misleading. Different types of LPE often look alike and it is important to check the wavelength and OD prior to relying on them for protection. Some laser facilities have more than one laser in each room. In that case, color coded tape can be applied to the laser handpiece and matching LPE to minimize confusion. There are several styles of LPE available. Goggles can be worn over prescription glasses but must fit snugly if they are to be effective. The disadvantages of this style are that they may be cumbersome and can produce a tunnel vision effect. Spectacles resemble eyeglasses with side shields (Fig. 3.4). Wraps consist of a single lens, which is usually made from lightweight plastic and wraps across the eyes from temple to temple. While it is true that optical glass will filter wavelengths below 300 nm and above 2700 nm, prescription eyeglasses do not have side shields and therefore do not confer adequate protection (16). Class IV laser beams may be reflected by specular surfaces in the surgical field and still maintain sufficient energy to cause thermal damage. Metallic surfaces that appear dull and nonreflective may be specular to 10,600 nm CO2 light (12). Therefore, all jewelry should be removed from the field and the laser should not be aimed at any metallic or shiny surface. Metallic instruments or items that are needed in the field during treatment should be anodized (have a brushed or matte finish) to decrease the reflectivity of the beam. A black coating (ebonizing) augments anodizing but does not provide sufficient beam diffusion when used alone. Plastic devices can melt and should only be used if they are known to be laser-resistant.

Figure 3.4 Wavelength-specific laser eye protection. Note the side shields and prominently labeled optical density. These can be manufactured with prescription corrective lenses as well.

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5.1.

Ammirati and Hruza

Patient Protection

Ideally, nonsedated patients should be offered the same eye protection as that worn by the operating staff. This allows them to see the actions taking place in the room and can reduce unnecessary anxiety. Nonsedated patients can also wear opaque mini goggles, with a few caveats. This type of LPE is often stiff and the elastic strap must be tightened until there is a lightproof seal around the eyes. The strap itself can be flammable and should be maneuvered away from the treatment area or “strapless” goggles can be taped into place. For infants and children, it may be necessary to cut the goggles at the nosepiece and individually tape them over the eyelids. Moistened gauze or Telfaw can be placed over the closed lids and under the mini goggles to add a second level of protection (32). Laser treatment on or near the eyelids requires corneal eyeshields (Fig. 3.5). After topical anesthetic drops (e.g., 0.5% tetracaine HCl ophthalmic solution) have been instilled onto the conjunctiva, the eyeshield concavity is lubricated with a water-based lubricant (e.g., Lacri-lubew) and carefully placed under the eyelid against the eyeball. Studies investigating the thermal response curves and rates of warming for various types of eyeshields have shown them to be variable (33). Metallic eyeshields provide the best protection from transmitted light and heat but can be highly reflective. To decrease the risk of beam reflection, the convex surface should be anodized. Plastic eyeshields, especially those of darker color, should be avoided since they tend to melt when struck with sufficient laser energy (34). Well-intentioned family members, present for emotional support, are also at risk for injury. Their lack of laser safety training further increases their risk and whenever possible they should be discouraged from staying for the procedure.

5.2.

Medical Surveillance

ANSI-Z136.1 requires preassignment medical surveillance exams for all laser personnel who will be exposed to Class IIIb or IV laser energy. This examination must be documented before participation in laser surgery and establishes the baseline ocular history, visual acuity, peripheral fields, and color vision. Any abnormal finding would warrant a dilated

Figure 3.5 Corneal eye shields. Note the anodized convex exterior surface to decrease specular reflection.


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ophthalmologic exam and other tests as deemed appropriate. A second rationale for preassignment examinations is to identify certain personnel who may be at increased risk from laser exposure. This includes workers who use photosensitizing medications, which have been shown to lower the threshold for laser damage to the eye (35). Periodic examinations are not required for asymptomatic personnel but ANSI does require an examination after any suspected laser injury has occurred. At his/her discretion, an employer may elect to obtain an examination when employment is terminated to provide legal protection against future claims of injury.

6.

SKIN HAZARDS

Although the skin is more likely to be exposed to laser injury, it is not usually given the same priority as eye protection. This is because there is a vast difference in the magnitude of injury produced by a laser strike to the eye as compared to the skin. Depending on the energy and wavelength in use, lasers can produce cutaneous burns that range from superficial erythema to extensive blistering and charring. However, most skin injuries are relatively minor because an alert person will quickly remove the exposed skin from the path of the laser beam. A sedated patient, however, can suffer more severe skin burns since they will not reflexively withdraw from the laser impact. As a rule, when treating anesthetized patients, it is good practice to protect the surrounding skin with wet towels.

7.

TEETH HAZARDS

Dental enamel absorption is high in the UV and IR regions (36). When lasers are used around the lips and in the oral cavity, care must be taken that a stray laser beam does not damage or discolor tooth enamel or dental prosthetics (37,38). A moistened gauze or dental roll can be used as protection if the teeth are near the treatment field.

8.

FIRE HAZARDS

Class IV lasers can cause flash fires or electrical fires. A flash fire can result if the laser beam strikes a flammable material within the surgical field. An electrical fire would be one that occurs within the laser unit itself. To limit injury, each of these emergent situations requires an immediate response and personnel must be familiar with all safety protocols. 8.1.

Fire Prevention

A flash fire can occur if a direct or reflected beam ignites gauze, hair, cosmetics, or drapes within the surgical field (Fig. 3.6) (34). Nylon or rayon fabrics are especially hazardous since they can melt and adhere to the skin. To avoid this risk, all unnecessary material should be removed from the treatment site. Makeup is also flammable and must be removed before treatment begins. Drapes and gauze pads used in the field should be wet or nonflammable. If wet gauze or drapes are used, they should be periodically checked to make sure that they have maintained their moisture. One study found Telfaw pads to be more flame-resistant than gauze and their preferential use might be warranted (32). For small treatment areas, hair can be positioned away from the field with water-soluble lubricating gel (i.e., K-Yw Jelly). For larger areas, a wet towel should be used.

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Figure 3.6 Ignition of dry gauze by the continuous wave argon laser. (Ignition occurred within seconds.)

Alcohol readily ignites when exposed to the heat of a laser impact (39). Hair sprays and gels often contain alcohol, as do topical preparations such as chlorhexidine surgical scrub and some lidocaine gels. Iodophors may also ignite at high temperatures, especially if they accumulate near the operative field (40). The use of any potentially flammable preparation should be discouraged. If its use is absolutely necessary, it should be washed completely from the site before treatment begins. Methane release, during laser treatment of the anogenital area, also poses a fire hazard. A moist rectal tampon can be used to decrease this risk. Medical grade silicone can ignite when exposed to CO2 laser energy. This was first discovered during CO2 laser vaporization of silicone deposits in breast tissue (41). This “silicone flash” has now been experimentally produced by microdroplet silicone, which is the form used for dermal augmentation on the face (42). Even tiny fractions of silicone produced a visible flare with a flame extending as far as an inch from the experimental test site. This presents a theoretical concern and although it has not been shown in practice, it is unclear whether a history of silicone facial augmentation should be considered a relative contraindication to CO2 resurfacing. There have been several reports of ignition during the use of the pulsed dye laser treatment when supplemental oxygen was in use (32,39,43). Oxygen greatly increases the combustion potential of any flammable material, even those that are saturated with water (32,43). If possible, supplemental oxygen should be momentarily discontinued when any surgical laser is in use. Alternatively, spontaneous respiration with a laryngeal mask airway can be used (44). 8.2.

Fire Containment

During treatment, a bowl of water should be within reach of the laser operator at all times since an immediate response could limit the potential damage to the patient. A separate safety protocol is required if an electrical fire occurs within the laser unit itself. These situations require extreme caution and the staff should be trained to handle this emergency as well. It should be stressed that water must never be used on an electrical fire as this could lead to electrocution. A fire extinguisher should be available in each laser treatment room


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or it can be attached to the side of the laser itself. The extinguisher of choice, for a laser unit electrical fire, is a halon fire extinguisher (45). Common dry chemical extinguishers emit a fine dust, which can damage laser optics or circuitry, and should not be used.

9.

ELECTRICAL AND MECHANICAL HAZARDS

The most lethal hazard associated with lasers is the high voltage that powers them. Most medical lasers operate on 220 or higher AC voltage. This is typically doubled or tripled by the laser exciter (power supply). Several deaths have occurred when persons working with the high-voltage portions of laser systems did not follow safety practices (2). Untrained personnel should never manipulate or access the laser power supply. If an emergent situation arises and it is absolutely necessary to access the power supply, first insure that the main power has been disconnected. Second, call for assistance and do not attempt repairs alone. In the event of high-voltage injury, a second person will be needed to call for emergency medical personnel and administer cardiopulmonary resuscitation until they arrive. Cutaneous lasers are designed to be portable but a significant jolt to the unit can result in misalignment of the laser head or optical fiber. Prior to beginning laser surgery the operator should verify the alignment of the laser beam and the integrity of the spot size. The Baggish 1 J test can be used for focused-beam CO2 lasers (46). To perform this test, the laser power is set to 10 W with an exposure duration of 100 ms. At these settings, 1 J of energy should be produced. A well-focused 1 J CO2 laser beam should penetrate through a standard wooden tongue depressor. If the beam does not penetrate, calibration is indicated. Visible and near-IR laser alignment can be checked by firing at an appropriately colored photopaper (i.e., red photopaper for 585 nm pulsed dye laser). The resultant laser spot on the photopaper should match exactly with the location of the alignment beam. The spot should also be of the appropriate diameter with its edges sharply defined and its center without “hotspots” (uneven burn patterns).

9.1.

Controlled Access

OSHA regulations state that access to the laser and entrance to the surgery room must be strictly controlled (47). The CDRH mandates that Class IIIb and IV lasers incorporate a key activated control switch (3). The laser must be rendered inoperable if the key is not in place. When the laser is not in use, the key should be removed from the control panel and stored in a secure location. The ANSI standards recommend that a door interlock system be used during laser procedures (2,48). While this may be effective in nonmedical settings, its use is impractical for most medical laser procedures. An interlock system would disengage the laser if the door to the laser room were opened. While this would provide safety for the person entering the room, it could compromise patient care since the operator may be at a critical point in the procedure. It is far better to post warning signs on the door when the laser is in use and train personnel to limit all nonessential entrance. Wavelength-specific eyewear can be hung next to the sign if unplanned entrance is necessary (Fig. 3.7). Laser warning signs should be promptly removed when the procedure is completed or their significance may be forgotten. Windows, doorways, and open portals, through which laser light might escape, must be adequately covered or shielded. Visible and near-IR laser wavelengths readily penetrate

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Figure 3.7 A laser warning sign should be prominently displayed on the door leading into the surgical suite. The sign should be removable and taken down when treatment has been completed. Laser-specific eye protection should be hung next to the sign to allow safe entrance once treatment has commenced.

window glass. If the windows are at eye level, opaque, laser-resistant coverings will be needed. To prevent accidental discharge of the laser, foot pedals are designed with protective housing (Fig. 3.8). To engage the laser, the foot must be purposely placed within the device and the pedal depressed. To limit any confusion, the smoke evacuator foot pedal is placed near the assistant, who is usually on the other side of the patient. When it is not in use, the laser should be placed in stand-by mode. This provides a second line of defense against accidental discharge.

Figure 3.8 Laser foot pedal on the left equipped with protective housing. This is compared to the unprotected smoke evacuator foot pedal on the right. The protective housing on the laser foot pedal decreases any risk for laser misfire.


10.

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CHEMICAL HAZARDS

Some laser systems use toxic gases, organic dyes, and solvents that can be hazardous if not properly handled. Excimer lasers, which are not routinely used for cutaneous surgery, may contain toxic halogens mixed with an inert gas and special training is required to service these units (49). Dye lasers use a lasing medium that consists of a complex organic dye dissolved in an organic solvent. Limited animal studies have shown some laser dyes to be toxic, mutagenic (Ames/Salmonella assay), and possibly carcinogenic (50 – 52). Since specific data are limited, all dyes should be treated as hazardous chemicals. 10.1. Chemical Protection Impervious gloves and protective eyewear are to be used when handling laser dye and quencher solutions. If skin contact occurs, the area should be washed immediately with soap and water. Eye contact is a medical emergency and requires copious irrigation with water and prompt medical attention. In the case of accidental ingestion, the local poison control center should be contacted. Prolonged inhalation is also not recommended and persistent symptoms will require medical attention. OSHA’s Employee Right to Know Act of 1988 requires that employees who work with potentially hazardous materials have certain rights. This includes access to the material safety data sheet that accompanies each dye laser. This sheet will supply appropriate information pertaining to toxicity, personal protective equipment, and the storage of chemicals.

11.

ACCOUSTIC HAZARDS

The noise level of certain lasers, such as the Er:YAG, may be of sufficient intensity to warrant hearing protection during their use.

12.

LASER PLUME HAZARDS

A plume, consisting of smoke, vapor, and particulate debris, is generated whenever a laser ablates tissue. Depending on the type of medical procedure, the laser plume may contain carcinogens, mutagens, irritants, tissue fragments, potentially infectious viral particles, and bacteria (2). The hazard potential of this plume has been the subject of understandable concern as well as debate. In 1992, the EUREKA international project STILMED (Safety Technology in Laser Medicine) began systematic investigations of the chemical, particulate, and microbiological hazards of laser plume (53). Their final results were summarized and are available from SPIE—The International Society of Optical Engineering (see Table 3.1). 12.1. Organic Compounds The laser plume’s smell is nauseating and its particulate matter can cause eye, nose, and throat irritation. Chemical analysis of continuous wave CO2 and Nd:YAG laser plumes identified carbon monoxide, hydrogen cyanide, ammonia and more than 150 volatile organic compounds, including benzene, formaldehyde, and toluene (54 – 56). Extreme

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laser-generated temperatures split tissue molecules into free radicals, which catalyze the generation of these toxic compounds. If an oxygen donor, such as aerosolized water, is available, then the formation of free radicals and other harmful laser plume substances can be reduced (57). Wiping away charred tissue, prior to continued lasing, will also reduce the emission of toxic compounds (58). The particulate aerosol of the laser plume is known to have in vitro mutagenic, genotoxic, and clastogenic (disruption or breakage of chromosomes) potential (59,60). Laser-generated carcinogens are similar to those found in cigarette smoke and vaporization of 1 g of tissue produces the same amount of mutagenic smoke as smoking three to six cigarettes (60). While there is no epidemiologic evidence of increased malignancies in personnel chronically exposed to laser smoke, safe levels of ambient mutagens remain to be determined and unnecessary exposure should be avoided (61). 12.2.

Particulate Debris

The majority of CO2 laser-generated particles range from 0.1 to 0.8 mm in diameter (62). Particles of this size are easily deposited in the lower respiratory tract and can cause parenchymal damage (63). Experimental rats, when forced to breathe CO2 laser smoke for prolonged periods, developed congestive interstitial pneumonia, bronchiolitis, and emphysema (64). Similar experimental changes have been induced by the continuous wave 1064 nm Nd:YAG laser plume (65,66). 12.3.

Pathogenicity

The infectious potential of laser-generated cellular debris has been the focus of understandable concern. Early studies with the Nd:YAG and CO2 lasers failed to culture laser plume debris and it was hoped that the extreme temperatures generated by these lasers would sterilize any debris (67 –69). Recent findings, however, have been to the contrary (70 – 73), which may be due to different collection techniques as well as variations in the laser settings used (62,74). Transmission of human papilloma virus (HPV) from laser ablation of infected tissue remains a serious concern among laser surgeons. Infectious bovine papilloma virions and intact DNA from HPV have been recovered from the CO2 laser plume (75,76). The degree of risk that these findings represent in actual practice is not completely known. A comparative study of CO2 laser surgeons, who frequently treated HPV-infected lesions, failed to find an increased incidence of common warts (77). However, when grouped by anatomic site, CO2 laser surgeons were found to have a higher risk of acquiring nasopharyngeal papillomas. This is due to the ability of HPV types 6 and 11, which cause genital condyloma acuminata through contact, to induce nasopharyngeal papillomas after inhalation (78 –80). These findings also imply that there is a true infectious hazard, albeit small, from laser ablation of HPV-infected tissue and that strict adherence to protective measures is indicated. Transmission of human immunodeficiency virus (HIV) or hepatitis via the laser plume represents a serious potential hazard, but studies thus far have been limited (81 –84). Proviral HIV DNA and HIV p24 protein from CO2 laser smoke were detectable in culture at 14 days but were not sustained at 28 days (81). Examination of the Er:YAG laser plume, which failed to reveal HPV DNA (85), did recover infectious retrovirus (86). Hepatitis B virus, which can survive for 72 h outside the body, poses a theoretical risk during laser procedures but has not been studied. To date, there have been no cases of HIV or hepatitis transmission from a patient to a physician via laser plume. However,


97

since the degree of risk has not been clearly delineated and the consequences of infection are so severe, protective measures are a must. Additional concern surrounds the tissue debris that is ejected at supersonic speed by Q-switched lasers, such as the alexandrite, ruby, and Nd:YAG. Q-switched lasers cause a heat-induced explosion within tissue cells, which can liberate viable surface cells into the air at supersonic speeds. These ejection speeds are beyond the capture of a smoke evacuator and different protective measures will be needed (87). 12.4. Protection and Evacuation In 1996, NIOSH issued the Health Hazard Control, Control of Smoke from Laser/Electric Surgical Procedures (HC-11). This was the first federal statement calling for the evacuation of smoke generated by lasers and electrosurgery. In HC-11, NIOSH clearly identifies laser and electrosurgery smoke as a health hazard and provides guidelines for optimal evacuation. 12.5. Smoke Evacuators Smoke evacuation provides the first line of defense against laser plume hazards and there are several methods available. In-line wall suction filters have been used for small amounts of laser plume evacuation but are not recommended. They clog easily and the plume is exhausted elsewhere in the facility, usually without adequate filtration, and creates an airborne hazard (66). A high-efficiency laser smoke evacuator is a more reliable unit that consists of a vacuum, charcoal filter, high-efficiency particulate air (HEPA) filter, and ultra-low particulate air (ULPA) filter. The activated charcoal filter serves to trap toxic chemicals and noxious vapors. The HEPA filter traps particles as small as 0.3 mm in diameter with .99% efficiency. The ULPA filter captures 0.1 mm particles and this additional efficiency has a significant clinical impact. Recall that rats, when forced to inhale CO2 laser smoke, developed microscopic pulmonary changes (64). When laser smoke was filtered through an HEPA filter, prior to being inhaled, the rats developed similar but less severe pulmonary lesions. After a ULPA filter was added to the filtration system, no pathologic lung changes were observed (88). A high-efficiency smoke evacuator will only be effective when the nozzle is kept within 2 in. of the treatment site (89). Evacuation efficiency is dramatically reduced when the tube is held farther away (90). The vacuum tubing is changed after each patient and treated as biohazardous waste (81). Any lingering odor or smoke in the air suggests that the filter should be inspected and changed if necessary. Currently, there are two types of filter monitor systems available on laser smoke evacuators, pressure drop monitors, and time-based monitors (83). Pressure monitors measure the drop in pressure across the filter. When a critical pressure is reached, an indicator light signals that the filter should be changed. A time-based monitor will signal the need for a filter change after a preset period of use. Its signal may be premature if the vacuum has been left running while the laser was not engaged. To limit exposure to Q-switched laser-generated debris, a collecting cone or shield can be placed over the handpiece during use. The laser can also be fired through a transparent membrane, such as Cling Filmw or Vigilonw to reduce the ejection of particulate matter into the air (Fig. 3.9). Comparative studies with the Q-switched Nd:YAG laser found Cling Filmw to be superior to Tegadermw, Opsitew, or 2nd Skinw (91). Collecting cones and transparent membranes may reduce the ejected debris but not reliably eliminate it. Additional protective equipment such as gloves and laser masks are recommended.

98

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Figure 3.9 Ejected cellular debris trapped by a clear membrane. The Q-switched Nd:YAG laser was fired through acetate sheeting during laser treatment of a tattoo.

12.6.

Laser Masks

Laser plume particles 0.1 –0.8 mm in size are too small to be effectively filtered by a standard surgical mask (92). Specially designed laser masks trap particles down to 0.1 mm. To be effective, they must fit snugly and have a moldable nosepiece and flexible side panels. It is recommended that laser masks be changed after each case or if they become wet during the procedure. To achieve 0.1 mm particle filtration, laser masks use electrostatically charged synthetic fibers. Moisture can eliminate the electrostatic charge and compromise the filtration capacity of the mask (88).

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Dierkesmann R, Huzly A. Side effects of endobronchial laser treatment. Endoscopy 1985; 17:49 – 53. American National Standards Institute. American National Standard for the Safe Use of Lasers. Orlando, FL: Laser Institute of America, 1993. US Department of Health and Human Services. Title 21 CFR, Subchapter J. Part 1040.10 Performance Standards for Laser Products. Sliney D, Trokel S. Safety standards and laser exposure limits. In: Sliney D, Trokel S, eds. Medical Lasers and Their Safe Use. New York: Springer-Verlag, 1993:87 – 94. Luttrull JK, Hallisey J. Laser pointer-induced macular injury. Am J Ophthalmol 1999; 127:95–96. Marshall J. The safety of laser pointers: myths and realities. Br J Ophthalmol 1998; 82:1335 – 1338. McHugh JD, Marshall J, Ffytche TJ, Hamilton AM, Raven A, Keeler CR. Initial clinical experience using a diode laser in the treatment of retinal vascular disease. Eye 1989; 3:516 – 527. Marshall J. Structural aspects of laser-induced damage and their functional implications. Health Phys 1989; 56:617 –624. World Health Organization. Lasers and Optical Radiation. Geneva: World Health Organization Press, 1982.

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Ammirati and Hruza Pogrel MA, Muff DF, Marshall GW. Structural changes in dental enamel induced by high energy continuous wave carbon dioxide laser. Lasers Surg Med 1993; 13:89– 96. Shariati S, Pogrel MA, Marshall GW Jr, White JM. Structural changes in dentin induced by high energy, continuous wave carbon dioxide laser. Lasers Surg Med 1993; 13:543 – 547. Bean AK, Ceilley RI. Reducing fire risks of the flashlamp pumped 585-nm pulse dye laser. J Dermatol Surg Oncol 1994; 20:224. Rosio T. Basic laser safety. In: Roenigk R, Roenigk H, eds. Roenigk and Roenigk’s Dermatologic Surgery: Principles and Practice. New York: Marcel Dekker, Inc., 1996. Becker DW Jr. Laser silicone flash. Plast Reconstr Surg 1988; 81:600. Zager W, Huang J, McCue P, Reiter D. Laser resurfacing of silicone-injected skin: the “silicone flash” revisited. Arch Otolaryngol 2001; 127:418 – 421. Fretzin S, Beeson WH, Hanke CW. Ignition potential of the 585-nm pulsed-dye laser. Review of the literature and safety recommendations. Dermatol Surg 1996; 22:699 – 702. Epstein RH, Halmi BH. Oxygen leakage around the laryngeal mask airway during laser treatment of port-wine stains in children. Anesth Analg 1994; 78:486 –489. Ball K. Lasers: The Perioperative Challenge. 2nd ed. St. Louis, MO: Mosby, 1991. Sliney D, Trokel S. Laser checkout and demonstration procedures. In: Sliney D, Trokel S, eds. Medical Lasers and Their Safe Use. New York: Springer-Verlag, 1993. US Department of Labor. Guidelines for Laser Safety and Hazard Assessment: OSHA Instructional PUB 8-1.7, 1991. American National Standards Institute. American National Standards for the Safe Use of Lasers in the Health Care Environment. Orlando, FL: Laser Institute of America, 1996. Lorenz A. Gas handling safety for laser makers and users. Lasers Appl 1987; 6:69– 73. Mosovsky JA. Laser Dye Toxicity, Hazards and Recommended Controls. Livermore, CA: Lawrence Livermore National Laboratory, 1983. Kues H, Lutty G. Dyes can be deadly. Laser Focus 1975; 11:58 – 60. Anonymous. Lasers. In: Health & Safety Manual. California, CA: Lawrence Livermore National Laboratory, 1995:1 – 20. Woellmer W. Results of EUREKA project STILMED: transfer to standards. Proceedings APIE Laser-Tissue Interaction and Tissue Optics II, Vol. 2923, Bellingham, WA, 1996:189 – 193. Kokosa JM, Benedetto MD. Probing plume protection problems in the health care environment. Laser J Appl 1992; 4:39 – 43. Ott D. Smoke production and smoke reduction in endoscopic surgery: preliminary report. Endosc Surg Allied Technol 1993; 1:230– 232. Albrecht H, Hagemann R, Waesche W, Wagner G, Mueller G. Volatile organic components in laser and electrosurgery plume. Proceedings SPIE Laser Interaction with Hard and Soft Tissue, Vol. 2077, Bellingham, WA, 1994:310 – 317. Lademann J, Weigmann H, Meffert H, Sterry W. Radical formation during laser-tissue interaction. Proceedings SPIE Laser-Tissue Interaction and Tissue Optics II, Vol. 2923, Bellingham, WA, 1996:156 –163. Weigmann H, Lademann J, Meffert H, Sterry W. Permanent gases and highly volatile organic compounds in laser plume. Proceedings SPIE Laser-Tissue Interaction and Tissue Optics, Vol. 2923, Bellingham, WA, 1996:164 – 167. Plappert UG, Stocker B, Helbig R, Fliedner TM, Seidel HJ. Laser pyrolysis products— genotoxic, clastogenic and mutagenic effects of the particulate aerosol fractions. Mutat Res 1999; 441:29 – 41. Tomita Y, Mihashi S, Nagata K, Ueda S, Fujiki M, Hirano M, Hirohata T. Mutagenicity of smoke condensates induced by CO2-laser irradiation and electrocauterization. Mutat Res 1981; 89:145 – 149. Hunter JG. Laser smoke evacuator: effective removal of mutagenic cautery smoke. Aesthetic Plast Surg 1996; 20:177 – 178. Nezhat C, Winer WK, Nezhat F, Forrest D, Reeves WG. Smoke from laser surgery: is there a health hazard? Lasers Surg Med 1987; 7:376– 382.

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Section II: Laser Science and Instrumentation

4 Continuous Wave Lasers: Argon, Dye, KTP, Copper Vapor, Krypton Thomas O. McMeekin University of Rochester and State University of New York at Buffalo, Rochester, New York, USA

1. Continuous Wave Argon Laser 1.1. Laser Parameters 1.2. Indications—Port-Wine Stains 1.3. Perioperative Considerations 1.4. Telangiectasias 1.5. Other Vascular Lesions 1.6. Hemangiomas 1.7. Pigmented Lesions 2. Continuous and Quasicontinuous Argon-Pumped Tunable Dye Laser 2.1. Laser Parameters 2.2. Indications—Port-Wine Stains 2.3. Perioperative Considerations 2.4. Facial Telangiectasias 2.5. Argon-Pumped Tunable Dye Laser Pigmented Lesions 3. Copper Vapor Lasers/Copper Bromide Lasers 3.1. Laser Parameters 3.2. Indications—Port-Wine Stains 3.3. Perioperative Considerations 3.4. Facial Telangiectasia 3.5. Other Vascular Lesions 3.6. Pigmented Lesions 4. KTP Lasers 4.1. Laser Parameters 4.2. Indications—Port-Wine Stains/Telangiectasias 4.3. Perioperative Considerations 4.4. Hemangioma 5. Krypton Laser 5.1. Laser Parameters

106 106 106 108 109 110 110 112 112 112 112 113 113 114 114 114 116 117 117 117 118 119 119 120 121 121 123 123 105

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5.2. Indications—Telangiectasia 5.3. Operative Considerations References

1. 1.1.

123 124 124

CONTINUOUS WAVE ARGON LASER Laser Parameters

Although the argon laser emits at six wavelengths from 457.9 to 514.5 nm, 80% of the total emissions occur at 488 and 514 nm. A filter can be used to limit the wavelength to green light at 514 nm, or all the blue-green light can be delivered by a fiber optic cable in a continuous beam. The fiber optic delivery cable comes with spot sizes of 0.1–1.0 mm, with a fluence range of 0–2.0 W. A scanner is available, but no cooling is built into the system. Optional cooling with ice pretreatment or using a commercial cooling chamber is available. The light can penetrate into tissue up to 1 mm, however, thermal injury in port wine stains is seen at ,0.5 mm. Argon light is well absorbed by both melanin and oxyhemoglobin. The argon laser is no longer manufactured, but an ophthalmic argon laser is made by Lumenis Laser Corporation (Palo Alto, CA).

1.2.

Indications—Port-Wine Stains

The argon laser was developed in the 1970s for the treatment of vascular lesions. Although the ruby laser and the CO2 laser antedated the argon laser, neither was greeted with the enthusiasm that heralded the first results published in 1976 in port-wine stains (1,2). This enthusiasm was partially due to the poor treatment options for port-wine stains which included radiation, cryosurgery, excisional surgery with grafting, tattooing with skin-colored pigments, dermabrasion, and electrosurgery. The optimism was also heightened by the now disproved theory that the blue-green light was specific for the chromophore oxyhemoglobin and would penetrate the necessary depth to coagulate the ectatic vessels in the vascular malformation. A trial-and-error approach characterized the experience over the first 5 years. Few attempts were initially made to study the histology and correlate the successes that were observed with prognostic factors or treatment parameters. The results of argon laser treatment of port-wine stains were essentially that 60– 75% of cases showed good to excellent results, only 10% showed complete disappearance, and 10% showed no response or only slight fading [see Fig. 4.1(a) and (b)] (3 –5). The risk of scarring varied from a low of 4% (6), to .50% (6), and with a survey of patient perceptions as high as 86%, when skin texture changes were included (7). Hypopigmentation was also common because of the high absorption of melanin at 514 nm (7). Particularly disturbing was the high incidence of scarring noted in children (7,8). The predictive values of age, color of the port-wine stain, and biopsy were helpful in defining prognostic parameters (8). Those patients over age 37, with purple-colored lesions, and a large target (large mean vascular area filled with erythrocytes) responded favorably (8). Darkly pigmented patients responded less than lighter skinned patients due to competitive absorption by melanin. A variety of manipulations to improve results included: prechilling the port-wine stain (9), using mechanical shutters and lower fluences (10), recommending test sites and observing for 2–4 months to predict outcome (11) and altering the treatment technique.

Continuous Wave Lasers

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Figure 4.1 (a) Preoperative argon laser treatment of port-wine stain lip. (b) Postoperative argon laser treatment of port-wine stain lip.

Four treatment techniques were used to treat port-wine stains. A point-by-point or continuous technique with adjacent, but not overlapping spots (2), a striping technique utilizing parallel strokes that leaves a zebra look to the lesion while trying to minimize collateral heat damage (12), a dot or pointillistic technique delivering spots separated by 1 –2 mm (13), and, finally, a microspot tracing technique using a spot size equal to the blood vessel being photocoagulated (14). This latter technique proved to be tedious and time-consuming so that only small areas could be treated in a single session (15). Despite the attempts to improve clinical results, the argon laser was limited by the small spot sizes, the long pulse durations, and the short wave lengths (488 – 514 nm), which did not reach the depth necessary to coagulate the deeper vessels of port-wine stains (16). Histologic studies confirmed that the clinical finding observed with the argon lasertreated port-wine stains was the result of nonspecific coagulative necrosis of the superficial dermal ectatic blood vessels with subsequent fibrosis and small vascular channels replacing the superficial part of the lesion (16 – 18). The diffusion of heat collaterally caused nonspecific thermal damage leading to the potential of epidermal atrophy, depigmentation, dermal fibrosis, and scarring (19). The scarring was also more prominent in difficult areas such as the upper lip, nasolabial fold, angle of the jaw, and neck. The trunk responded less well than the face, the arms less well than the trunk, and the lower extremities responded poorly.

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The role of argon laser therapy in the treatment of port-wine stains diminished with the development of lasers capable of selective photothermolysis (20) and the development of computerized robotized scanning devices (see section “Argon-Pumped Tunable Dye Laser”). The current role of argon laser treatment is for the treatment of nodules of hypertrophic port-wine stains in adults (Table 4.3). 1.3.

Perioperative Considerations

Preoperatively, laser patients should avoid sunlight for several weeks prior to argon irradiation or use total sunblocks such as zinc oxide or titanium dioxide. A representative consent form for laser surgery is included in Table 4.1. Topical anesthetics such as EMLA or lidocaine cream 30% can be used prior to intralesional anesthesia. Large lesions require either field blocks or intralesional lidocaine 1%. The use of epinephrine is not felt to alter the result of laser therapy of vascular lesions, and will prolong the duration of anesthesia. Toxicity with large quantities of topical or intralesional lidocaine must be avoided (21). Buffered lidocaine reduces the pain of injection and is recommended for larger areas. For the treatment of port-wine stains, a 1.0 mm spot is used with the handpiece held perpendicular to the skin at its focal length and 0.5– 0.8 W power. It is moved slowly enough to produce a white to grey response which represents thermal coagulation of tissue proteins and is the endpoint for port-wine stains. A continuous back-and-forth airbrushing method, either vertical, horizontal, or in concentric circles, is used. Solitary

Table 4.1 Consent Form for Laser Treatment of Vascular Lesions I certify that I have been informed by Dr. ________________ of the following: 1. The outcome of ________ laser therapy. 2. No guarantee of results has been made. 3. Possible side effects include hypopigmentation, hyperpigmentation, scarring, infection, and incomplete removal of lesion, discomfort, swelling, prolonged wound healing. 4. Alternative treatment methods including no treatment. 5. Treatment protocol, anesthesia requirements, laser safety and precautions necessary with laser goggles during procedure. For the treatment of _______________________________________. To minimize the chances of side effects and complications it is important that I follow all postoperative instructions carefully. I understand it may take multiple treatments to clear some lesions and no guarantee as to exact number of treatments has been made to me. I authorize the taking of photographs throughout the course of my laser treatment. These photographs may be used for the purpose of medical publication, education, and treatment decisions. I have been given the opportunity to ask questions, and have received satisfactory answers. I have read the contents of this consent and fully understand them before signing my name below. _______________________________________ Patient Signature

___________________ Date

_______________________________________ Witness Signature

___________________ Date

I have explained the above statements to the patient and answered all questions. _______________________________________ Physician Signature

___________________ Date


109

nodules can be coagulated, then the coagulum wiped away between subsequent passes until they flatten. If test sites are performed, an area representative of the entire lesion in the least conspicuous area is chosen. A 1 –2 cm area should be used for each fluence tested. Immediate postlaser irradiation, a topical antibiotic ointment or a bland healing ointment such as Aquaphor should be applied (Table 4.2). A semiocclusive dressing such as Opsite or Vigilon will speed wound healing and provide protection to the wound which takes several days to re-epithelialize. The patient may wash with soap and water twice daily and reapply the dressings until full healing occurs. Sunblocks are recommended for 2 months postoperatively to avoid hyperpigmentation. 1.4.

Telangiectasias

Telangiectasia treated with the argon laser lesions often results in complete disappearance of the vessels without significant sequelae [Fig. 4.2(a) and (b)] (22,23). Excellent results in linear ectatic vessels of the nose [Fig. 4.3(a) and (b)] (23), diffuse telangiectasia of rosacea (24), nevus araneus (25), and telangiectasia from scleroderma and radiation (23,24) were reported frequently with only one or two treatment sessions. Postrhinoplasty “red nose syndrome” has also been reported to respond to argon laser treatment, especially if superficial ectatic vessels were present (26). Although the success rate has been high in 65– 99% of patients with telangiectasia (2,24), the same problems with hypopigmentation, hyperpigmentation, recurrence of vessels, and depressed scars has been reported (27). To minimize these side effects, a small beam size and 50 ms shuttering has been recommended (15,28). With these caveats, the treatment of telangiectasia has been successful in the hands of skilled laser surgeons, making this application one of the remaining indications for argon laser therapy (Table 4.3). Higher power outputs are required for the shuttered method of treating linear telangiectasia. For a vessel 0.5 mm in diameter a laser spot of 0.5 mm should be used with a pulse duration of 0.03 s and 1 –3 W of power output or just enough to cause disappearance of the vessel without skin whitening. The vessels are traced with the handpiece perpendicular to the skin at the correct focal length.

Table 4.2 Patient Care Sheet for Post-Laser Treatment of Vascular Lesions 1. Wash twice daily with soap and water. Apply a topical antibiotic (Polysporin Ointment) or Aquaphor healing ointment. 2. Apply a semi-occlusive dressing after the ointment (Telfa or Vigilan) until the wound has healed (1 – 4 days). 3. If swelling occurs elevated use ice bag compresses several times daily for the first few days. 4. Take a nonaspirin analgesic such as Tylenol as needed should you experience any pain or discomfort. 5. Avoid direct sunlight for 2 months following laser treatment. 6. A sunscreen of 45 or higher (Solbar 50 or UVA Guard 45) or a titanium dioxide sunblock (PreSun for Sensitive Skin) should be used before sun exposure once the wound has healed. Sun-protective clothing and hats should be used when appropriate. 7. Avoid trauma to the area including contact sports until healing is complete. 8. Makeups are allowed immediately to camouflage the treated area, but care should be taken to avoid rubbing and irritation when removing. 9. Please call your physician if you have any questions or concerns regarding your postoperative care.

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Figure 4.2 (a) Preoperative argon laser treatment of telangiectasias cheek. (b) Postoperative argon laser treatment of telangiectasias cheek.

Despite the success in facial telangiectasia, the treatment of lower extremity spider veins has been uniformly disappointing with worsening or no change in more than 49% of patients (29). 1.5.

Other Vascular Lesions

Many other benign lesions can be treated with the argon laser if they are vascular or have a vascular component. Cherry angioma (23), angiokeratoma (30), and venous lakes (24,31) all respond to continuous wave argon therapy, but may require several treatment sessions. Coagulation of the vascular lesion is the endpoint. Retraction or shrinkage of the lesion and superficial whitening of the epidermis occurs. Adenoma sebaceum (32,33), angiolymphoid hyperplasia (34), granuloma faciale (23), and Kaposi’s sarcoma (35) have also been treated with mixed results and a risk of scarring. 1.6.

Hemangiomas

Hemangiomas are the most common tumor of infancy and most commonly involve the head and neck. They usually develop after birth and undergo a rapid proliferative phase, followed by involution and regression. Many lesions leave fibro-fatty tissue and atrophy with telangiectasia as they resolve. Reconstructive surgery or treatment with


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Figure 4.3 (a) Preoperative argon laser treatment of linear ectatic vessels nose. (b) Postoperative argon laser treatment of linear ectatic vessels nose.

the flashlamp pulsed dye laser at this late stage may lead to further improvement (35). Argon laser therapy has been used to treat these proliferative hemangiomas (36 – 39). The risks of scarring, inability to prevent the deeper component from continuing to proliferate, and the lack of depth of penetration (,1 mm) outweigh the potential benefit of treatment by argon laser (40). The treatment of choice for most hemangiomas that are superficial remains the flashlamp pulsed dye laser.

Table 4.3 Current Clinical Indications for Argon Laser Therapy 1. Nodules in mature port wine stains 2. Large linear telangiectasias of nose and face 3. Small vascular lesions: Angiokeratoma Cherry angioma Venous lakes 4. Small lesions with a vascular component: Angiolymphoid hyperplasia Adenoma sebaceum Granuloma faciale

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Pigmented Lesions

The majority of epidermal and dermal pigmented lesions can now be treated more selectively with Q-switched lasers (Chapters 10 – 13). A high complication rate of hypopigmentation and texture change accompanied the treatment of lentigines, cafe´ au lait, junctional nevi, seborrheic keratoses and nevus of Ota (41). Failure was noted in larger lesions of Becker’s nevi and cafe´ au lait (35). Tattoos are no longer treated with the argon laser due to the scarring noted and the new lasers (Chapter 24) capable of selective photothermolysis (42).

2. 2.1.

CONTINUOUS AND QUASICONTINUOUS ARGON-PUMPED TUNABLE DYE LASER Laser Parameters

The argon laser provides the power to an organic dye rhodamine, which can emit wavelengths from 488 to 638 nm. Most typically, the wavelength is tuned to 577 or 585 nm, where the absorption of oxyhemoglobin is maximal (20). Other wavelengths such as 540 nm have also been used to treat port-wine stains (43). The chromophores of melanin and oxyhemoglobin absorb the emitted light in varying degrees based on the selected wavelength. At 585 nm, the penetration of the light is approximately 1.0 mm. Spot sizes of 100 mm to 1.0 mm are available for fiber optic cable delivery. The beam can be delivered either in a continuous wave form, or mechanically shuttered to produce pulse durations from 20 ms to 2.0 s. Scanners are available with the Hexascan used the most extensively (44,45). Cooling is not available with the scanners, but a commercial cooling chamber can be adapted (cool laser optics, Westborough, MA). The argon-pumped tunable dye laser previously was manufactured by CoherentLihtan, but is no longer available. 2.2.


The development of the argon-pumped tunable dye laser paralleled the publication of the theory of selective thermolysis (20). Disappointment with argon laser therapy of port-wine stains was growing because of the high rate of scarring and the relative nonspecific coagulative necrosis observed (16). Early histologic studies of vessel damage at longer wavelengths (577 nm) showed more selective damage to vessels was feasible (46 –48). Two methods were developed to minimize collateral damage from the argon pumped tunable dye laser. The first was the use of low power, a small spot size, and a tracing technique previously described (section “Perioperative Considerations Under Continuous Wave Argon Laser”) (14,15). The second was a computerized scanner which gave precise control of dosimetry and allowed placement of small, 1 mm diameter treatment spots in nonadjacent locations in a grid. Using the tracing method, the early results published showed a good response in older patients with port-wine stains in over two-thirds [Figs. 4.4(a) and (b) and 4.5(a) and (b)], but a continued risk of hypopigmentation (15%), atrophic scarring (15%), and hypertrophic scarring (5%) (49). Other studies showed the argon pumped tunable dye laser to be as good as the argon laser in treating port-wine stains (50), or more effective (51). Children have also responded to this tracing method, but the average total treatment time per patient was 3 21 h (52). The use of scanners shortened the treatment times, but the development of more selective flash lamp pumped pulse dye lasers (PDLs) became the treatment of choice


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Figure 4.4 (a) Preoperative argon pumped tunable dye laser treatment of port-wine stain cheek. (b) Postoperative argon pumped tunable dye laser treatment of port-wine stain cheek.

for children and adults (Chapters 7 and 23). Comparison studies of port-wine stains treated with a hexascan and the argon-pumped tunable dye laser at 585 nm vs. the PDL at 585 nm show greater lightening with the PDL in 40% after one treatment, with less hypopigmentation and hyperpigmentation (53).

2.3.


The preoperative planning and postoperative care are similar to the argon laser (see section “Continuous Wave Argon Laser”). For the tracing method, the argon-pumped tunable dye laser set at 577 nm is used with a 100 mm beam and power settings of 0.08–0.5 W. Using loupes of 8–10 power magnification vessels of 30–300 mm are traced using increasing power until the vessel disappears completely. The vessels are traced outward in concentric circles from a control point, with treatment sessions of 45–60 min, and areas covered averaging 1–2 in.2 (15). Retreatment can be performed after several months. With a hexascan, the suggested treatment parameters are 585 nm wavelength, 18–24 J/cm2 (depending on area, age of patient and vessel size) with 1–2 mm overlapping fields to prevent geometric patterning (45).

2.4.

Facial Telangiectasias

Comparison studies have also been done for facial telangiectasia (54,55). Using the tracing method and shuttered pulses, the flashlamp PDL had excellent results in 11 of 14 patients vs. just 4 of 14 with the tunable dye laser [Fig. 4.6(a) and (b)]. The purpura was a problem to 6 of 13 who preferred the tunable dye laser despite the poorer results (55). The same conclusions were reached in another study of facial telangiectasia using a robotized scanner and a tunable dye laser vs. the PDL. All patients in the pulsed dye laser treatment had 100% excellent results vs. 47% in the tunable dye group. Likewise, half the

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Figure 4.5 (a) Preoperative argon pumped tunable dye laser treatment of port-wine stain neck. (b) Postoperative argon pumped tunable dye laser treatment of port-wine stain neck.

patients preferred the tunable dye due to the lower incidence of hyperpigmentation and lack of bruising (54). 2.5.

Argon-Pumped Tunable Dye Laser Pigmented Lesions

The results for pigmented lesions are similar to those of the argon laser. The use of the hexascan with the green light (514 nm) speeds up the treatment and clears lentigines in one or two treatments, and allows treatment of cafe´ au lait macules, nevus spilus, and Becker’s nevi (45). The longer pulse durations of 30 ms and the small relative spot size of 1 mm may limit the effectiveness in larger lesions. More selective wavelengths, and short pulse durations that approximate the thermal relaxation time of melanin makes the further use of this laser in pigmented lesions questionable (Chapter 26).

3. 3.1.

COPPER VAPOR LASERS/COPPER BROMIDE LASERS Laser Parameters

Both copper laser systems produce yellow light at 578 nm and green light at 511 nm by heating elemental copper or copper salts in the optical cavity. They differ only in the


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Figure 4.6 (a) Preoperative argon pumped tunable dye laser treatment of telangiectasias nose. (b) Postoperative argon pumped tunable dye laser treatment of telangiectasias nose.

efficiency [1% copper bromide laser (CBL) vs. 0.5% copper vapor laser (CVL)] in energy conversion, the temperature at which they operate (6008C CBL and 16008C CVL) and the power output (CBL watts vs. CVL milliwatts). The light emitted is a train of 20 –40 ns high-energy pulses with pulse intervals of 63 ms and a frequency of 10– 16 kHz, with a peak power of 4 kW per pulse. Because the pulse intervals are too short for the targeted tissue (blood vessels) to thermally cool, the physiologic effect is a quasicontinuous pulse. The power output is generally measured as an average of the train of pulses. This quasicontinuous pulse train may be mechanically shuttered, used with a scanning device (see previous section) or used in a quasicontinuous mode to trace vessels. The light is delivered to a handpiece with spot sizes of 100 mm to 1.0 mm via a flexible quartz fiber. The chromophores for halide lasers are the same as argon, and argon PDLs, with absorption by melanin and oxyhemoglobin. The green band at 511 nm is used to target melanin, but the exposure times are longer than the thermal relaxation time of melanin. Q-switched lasers have since replaced the benign pigmented lesion applications of this laser. There were two manufacturers for the CVL: 1. 2.

Aesculap Meditec North America (Irvine, CA). Continuum Biomedical, Inc. [Livermore, CA (CBL)].

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At 578 nm, copper vapor laser light is mostly absorbed by oxyhemoglobin, and penetrates deeper than the argon laser. With melanin absorbing maximally at 300 –500 nm, the energy is less well absorbed by melanin. Histologically, the effects of this quasicontinuous laser on vessels is similar to other continuous wave lasers when used to trace vessels or treat port-wine stains freehand (56). More selective histology showing specific necrotic endothelial cells of ectatic vessels without rupture or hemorrhage while sparing epidermal and adjacent dermal structures was reported using a robotized scanner (57) and by mechanically shuttering the beam (58). Results comparing the argon laser to the copper vapor in treatment of port-wine stains are equivalent with the copper laser producing better fading (59). Thicker and darker port-wine stains with the so-called large vessels have been reported to respond well [Fig. 4.7(a) and (b)] (60). For subsequent treatments, the more selective pulsed dye lasers can be used to finish the smaller vessels. Excellent results were reported in 24% of 25 patients using the CVL with a hexascan and fluences of 12– 15 J/cm2. There was no response in 20% and adverse sequelae of hypopigmentation and scarring in 11 of 25 (60). The risk of hypopigmentation, especially in Fitzpatrick Type V skin, has been reported by several studies (61,62). CVL treatment of port-wine stains is not as selective in brown skin as compared to white skin. When treating brown skin, selection of minimal pulse widths and maximum power outputs are recommended (62). Two studies compared the CVL with a Hexascan and the flashlamp PDL in treatment of port-wine stains (63,64). The first found better fading of macular blanchable port-wine stains in the flashlamp PDL group without a significant difference in adverse reactions (63). An edge in clearing with the flashlamp PDL was also seen in the second study, but more adverse side effects such as hyperpigmentation were noted (64). It is generally felt that the PDL is safer, more effective and has an acceptable rate of side

Figure 4.7 (a) Preoperative copper vapor laser treatment of port-wine stain cheek. (b) Postoperative copper vapor laser treatment of port-wine stain cheek.


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effects. It is noteworthy that copper vapor has been supplemented with PDL for port-wine stains except for port-wine stain nodules. 3.3.


The treatment of small lesions with the yellow light (578 nm) may not require anesthesia, but larger lesions or children require topical and/or field block anesthesia to minimize pain. The patient should avoid tanning preoperatively and caution should be used in Fitzpatrick skin types III –VI. Postoperatively, the wounds may occasionally blister or be edematous for several days. Ice packs, cool compresses, and topical antibiotic ointments are recommended routinely. Sun avoidance or sunblocks are advised for 2 months postoperatively. With magnifying loupes, the laser can be operated in a continuous tracing technique delivering 15,000 pulses per second with vessel disappearance at the end point. The actual dosimetry will depend on hand speed, the spot size, and average power settings. Typical port-wine stain settings for a 100 mm spot size would be 90 –140 mW for children under age 12; 120 – 180 mW for children age 12– 18; and 180 –260 mW for adults (65). For a field blanch or spot-by-spot method an entire contiguous area is treated using spot-byspot placement. Higher powers (25 – 50%) are required for the shuttered technique. Typically, a common setting is 0.2 s on and 0.2 s off. The endpoint again is vessel blanch or disappearance. Vessels are traced with treatment sessions varying from 5 –60 min (66). Typical settings for a CVL with a 150 mm spot size and a 600 mm optical fiber, using the above shuttering (0.2 s on, 0.2 s off ) were the lowest power (300 – 600 mW ) to achieve the end point (67). 3.4.

Facial Telangiectasia

One of the best indications for the CVL has been the treatment of facial telangiectasias [Fig. 4.8(a) and (b)]. The lack of purpura is a major factor in the success this treatment has enjoyed. Using the free-hand technique, one study of 20 patients showed good clearing in 18 of 20, with punctate scabbing seen in 50% and temporary hyperpigmentation in 15% [Fig. 4.9(a) and (b)] (67). The only nonresponders were the fine diffuse telangiectasias of rosacea, which respond better to PDL. Another study of 33 patients with telangiectasias had good to excellent results in two-thirds and only 19% with poor results (60). They also used the shuttered method with a 1 mm spot and pulse duration of 50– 200 ms. The nose and nasolabial fold were the most difficult areas with 7 of 33 showing atrophic scarring (60). Transient edema on the cheeks and eyelids lasting 1– 3 days was also observed. Similar transient edema has been reported in a study of 180 patients with almost 50% developing hypopigmentation (68). Good results were seen in 47% with further improvement to 86% seen in patients with combined CVL treatment and sclerotherapy of facial vessels (68). 3.5.


Cherry angioma, venous lakes, and pyogenic granuloma have been reported to respond well to CVL treatment [Fig. 4.10(a) and (b)] (65). An advantage of quasicontinuous

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Figure 4.8 (a) Preoperative copper vapor laser treatment of telangiectasias nose. (b) Postoperative copper vapor laser treatment of telangiectasias nose.

wave lasers such as the copper vapor in treating larger diameter vessels in venous malformations, as well as hypertrophic nodular port-wine stains, has been reported (69). Hemangiomas in the early proliferative phase have been treated with the CVL successfully with less than 1% risk of scarring (70). It is hypothesized that a photothermal reaction which provides a vasoconstrictive effect deeper than photothermolysis is responsible for some of the improvement (70). Other lasers such as the long-pulsed (1.5 ms) dye laser are more selective and have supplanted the CVL for the treatment of hemangioma as well as port-wine stains (Chapter 7). 3.6.

Pigmented Lesions

The green light band (511 nm) of the CVL may be used to treat benign pigmented lesions such as lentigines, freckles, dermatosis papulosa nigra, and seborrheic keratoses (71). Excellent results with few side effects were reported (71). A variable response is seen with larger lesions such as cafe´ au lait, Becker’s nevus, and melasma (72). Transient hyperpigmentation may be seen in up to 10%, which clears with hydroquinones (71). Other types of hyperpigmentation such as seen after sclerotherapy may respond in up to 69% of patients after one session with the CVL (73). The newer Q-switched lasers have replaced the copper vapor in treating pigmented lesions today.


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Figure 4.9 (a) Preoperative copper vapor laser treatment of linear ectatic vessels nose. (b) Postoperative copper vapor laser treatment of linear ectatic vessels nose.

4. 4.1.

KTP LASERS Laser Parameters

The KTP laser is a frequency doubled Nd:YAG laser that produces a train of pulses at a frequency of 25,000 Hz at 532 nm wavelength. The 1064 nm light is converted to 532 nm

Figure 4.10 (a) Preoperative copper vapor laser treatment of hemangioma lip. (b) Postoperative copper vapor laser treatment of hemangioma lip.

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with a KTP crystal (potassium titanyl phosphate). The Nd:YAG laser is continually pumped laser with a krypton arc lamp that is a switched type, producing nanosecond pulses. The light is delivered to the tissue via a fiberoptic cable (0.2 – 0.6 mm) with 1, 2, and 4 mm spot sizes. A scanner (Smartscan) is available, as is a cooling chamber. The quasicontinuous wave KTP laser, manufactured by Lasercope (San Jose, CA), has a modulated arc lamp that produces a greater average power (160 W) and can produce single pulses of 1 –50 ms, each composed of multiple nanosecond pulse trains. The 532 nm wavelength is near to one of oxyhemoglobin’s absorption peaks at 540 nm, and can be used to treat a variety of vascular cutaneous lesions.

4.2.

Indications—Port-Wine Stains/Telangiectasias

Histologically, the results from KTP laser are similar to argon laser, with obliteration of vessels in the upper dermis, dermal fibrosis, and normal re-epithelialization (74). Clinically, the results for port-wine stains are equivalent to CVL or the argon pumped tunable dye laser (75,76). The results on telangiectasia and port-wine stains have been good, producing vessel clearing with little to no purpura [see Figs. 4.11(a) and (b) and 4.12(a) and (b)] (77,78). Further comparison studies with the newer long PDLs and long pulse KTP lasers are needed (Chapters 7 and 9).

Figure 4.11 (a) Preoperative KTP laser treatment of telangiectasias nose/cheeks. (b) Postoperative KTP laser treatment of telangiectasias nose/cheeks.


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Figure 4.12 (a) Preoperative KTP laser treatment of spider veins legs. (b) Postoperative KTP laser treatment of spider veins legs.

4.3.


The pre/postoperative considerations are similar to the argon and CVLs (see sections under “Continuous Wave Argon Lasers” and “Copper Vapor Lasers/Copper Bromide Lasers”). The treatment techniques vary. Using a 0.6 mm bore fiber passed directly into an hemangioma via a 20 gauge needle and 15 J of energy, hemangiomas can be treated. Using a 1 –4 mm spot at 5 W and 0.1 –1.0 s pulses with 0.2 s pulse duration generating a fluence of 127 J/cm2, nodular or adult port-wine stains can be treated. Finally, using a hexascan with fluences between 10 and 20 J/cm2 and pulse widths of 3 –5 ms, port-wine stains can be treated. A tracing technique similar to the copper vapor (see section under “Copper Vapor Lasers/Copper Bromide Lasers”) can be used for telangiectasia. 4.4.

Hemangioma

Intralesional bore fiber treatment of hemangiomas has been reported until shrinkage is seen or overlying heat is felt (79). About 92% of 12 patients had a greater than 50% reduction of hemangioma size, but only 8% maintaining this reduction at 6 months. Since one-third ulcerated after therapy and ulceration is associated with scar formation, this technique should be used with caution (40).

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Figure 4.13 (a) Preoperative Krypton laser treatment of diffuse telangiectasia cheeks. (b) Postoperative Krypton laser treatment of diffuse telangiectasia cheeks.

Figure 4.14 (a) Preoperative Krypton laser treatment of matted telangiectasia cheeks. (b) Postoperative Krypton laser treatment of matted telangiectasia cheeks.


5. 5.1.

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KRYPTON LASER Laser Parameters

Although the krypton laser has been used extensively in ophthalmology, it has more recently been introduced to dermatology. The krypton laser is a gas medium laser producing green light at 520 and 530 nm and yellow light at 568 nm. It is a continuous wave laser that can be shuttered to 50 ms pulses with pulse trains of 0.2– 10 s. It has two watts of green power and 1.0 W of yellow power in the HGM K1 Krypton Laser (HGM, Salt Lake City, UT). Selecting appropriate filters one can produce either yellow light at 568 nm, or green light with all three wavelengths. With all three wavelengths and a 1.0 mm spot, a fluence of 16 J/cm2 can be attained, which is enough to produce an endpoint of vessel disappearance. A digital autoscan is available. No external cooling chamber or spray are available. The chromophores are identical to the copper vapor previously discussed. 5.2.

Indications—Telangiectasia

Clinical studies using this laser are minimal. A retrospective questionnaire surveying 200 patients treated with the krypton laser in conjunction with microsclerotherapy found similar results to a CVL study by the same author (80). Sixty-four percent of patients had significant to total reduction in areas of their telangiectatic lesions, with 94% of

Figure 4.15 (a) Preoperative Krypton laser treatment of venous lake lip. (b) Postoperative Krypton laser treatment of venous lake lip.

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patients reporting a better to much better appearance [Fig. 4.13(a) and (b)]. However, 11% of patients reported atrophic scarring. A second article describing the treatment technique for spider nevi [Figs. 4.14(a) and (b) and 4.15(a) and (b)], reported that a small scar is almost inevitable from krypton laser photocoagulation of these vessels, but was acceptable to the patients (81). Since PDLs rarely leave any scars, they remain the gold standard for the treatment of telangiectasias. Further study on the krypton lasers’ safety and efficacy in dermatology are needed. 5.3.

Operative Considerations

The preoperative and postoperative patient directions are similar to the other continuous wave lasers. The operative pain is less than with the CVL and only 13% require a local anesthetic (80). The technique for facial telangiectasia is to use the 1.0 mm spot and 50 ms pulse duration with exposure times of 0.1–0.2 s when treating central feeding arterioles of spider telangiectasia, or 0.2–0.4 s when used to treat linear telangiectasias, with powers of 1.8–2.5 W. Generally, all three wavelengths are used together to get sufficient energy to photocoagulate the vessels (80). Blanching of the epidermis is avoided and a visual and audible popping of the central vessel is an endpoint on spider telangiectasia (81).

REFERENCES 1. 2. 3. 4. 5. 6. 7. 8.

9. 10. 11. 12.

13.

Goldman L, Dfreffer R, Rockwell JR Jr, Perry E. Treatment of port wine marks by an argon laser. J Dermatol Surg 1976; 2:385 –388. Apfelberg DB, Maser MR, Lash H. Argon laser management of cutaneous vascular deformities. A preliminary report. West J Med 1976; 124:99 – 101. Touquet VL, Carruth JA. Review of the treatment of port wine stains with the argon laser. Lasers Surg Med 1984; 4:191 – 199. Silver L. Argon laser photocoagulation of the port wine stain haemangiomas. Lasers Surg Med 1986; 6:24 – 28, 52– 55. Dixon JA, Gilbertson JJ. Argon and neodynium YAG laser therapy of dark nodular port wine stains in older patients. Lasers Surg Med 1986; 6:5– 11. Masser MR, Sammut DP, Jones SG, Saxby PJ. Argon laser therapy of port wine stains— prediction of the effect by transcutaneous microscopy. Lasers Med Sci 1989; 4:237– 240. Dixon JA, Huether S, Rotering R. Hypertrophic scarring in argon laser treatment of port wine stains. Plast Reconstr Surg 1984; 73:771– 780. Noe JM, Barsky SH, Geer DE, Rosen S. Port wine stains and the response to argon laser therapy: successful treatment and the predictive role of color, age, and biopsy. Plast Reconstr Surg 65:130– 136. Gilchrest BA, Rosen S, Noe JM. Chilling port wine stains improves the response to argon laser therapy. Plast Reconstr Surg 1982; 69:278 – 283. Brauner G, Schliftman A, Cosman B. Evaluation of argon laser surgery in children under 13 years of age. Plast Reconstr Surg 1991; 87:37 – 43. Cosman B. Experience in argon laser therapy of port wine stains. Plast Reconstr Surg 1980; 65:119 – 129. Apfelberg DB, Flores JT, Maser MR, Lash H. Analysis of complications of argon laser treatment for port wine hemangiomas with reference to striped technique. Lasers Surg Med 1983; 2:357 – 371. Apfelberg DB, Smith T, Maser MR, Lash H. Dot or pointillistic method for improvement in results of hypertrophic scarring in the argon laser treatment of port wine hemangiomas. Lasers Surg Med 1987; 6:552 – 558.

Continuous Wave Lasers 14.

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Schreibner A, McCarthy WH. An improved method of removal of port wine stains, venule and capillary flares using an argon laser with minimal power, small spot and longer duration exposure. Lasers Surg Med 1984; 3:368– 371. Scheibner A, Wheeland RG. Argon-pumped tunable dye laser for facial port stain hemangiomas in adults—new technique using a small spot size and minimal power. J Dermatol Surg Oncol 1989; 15:277– 282. Tan OT, Carney JM, Margoli R, Seki Y, Bell J, Anderson RR, Parrish JA. Histologic responses of port-wine stains treated by argon, carbon dioxide, and tunable dye lasers. A preliminary report. Arch Dermatol 1986; 122:1016 –1022. Finley JL, Barsky SH, Geer DE, Kamat BR, Noe JM, Rosen S. Healing of port-wine stains after argon laser therapy. Arch Dermatol 1981; 117:486 – 489. Finley JL, Arndt KA, Noe J, Rosen S. Argon laser –port-wine stain interaction. Immediate effects. Arch Dermatol 1984; 120:613– 619. Greenwald J, Rosen S, Anderson RR, Harrist T, MacFarland F, Noe J, Parrish JA. Comparative histologic studies of the tunable dye (at 577 nm) laser and argon laser: the specific vascular effects of the dye laser. J Invest Dermatol 1981; 77:305 – 310. Anderson RR, Parrish JR. Selective photothermolysis precise microsurgery by selective absorption of pulsed radiation. Science 1983; 220:524 – 527. Goodwin D, McMeekin T. A case of lidocaine cream absorption from topical administration of 40% lidocaine cream. J Am Acad Dermatol 1999; 41:280– 281. Apfelberg DB, Maser MR, Lash H, Rivers JL. Progress report on extended clinical use of the argon laser for cutaneous lesions. Lasers Surg Med 1980; 1:71– 83. Arndt KA. Argon laser therapy of small cutaneous vascular lesions. Arch Dermatol 1982; 118:220 – 224. Achauer BM, Vanderkam VM. Argon laser treatment of telangiectasia of the face and neck: 5 years experience. Lasers Surg Med 1987; 7:495 –498. Tan OT, Gilchrest BA. Laser therapy for selected cutaneous vascular lesions in the pediatric population: A review. Pediatrics 1988; 82:652 –662. Noe JM, Finley J, Rosen S, Arndt KA. Postrhinoplasty “red nose”: differential diagnosis and treatment by laser. Plast Reconst Surg 1981; 67:661 – 664. Dolsky RL. Argon laser surgery. Surg Clin N Am 1984; 64:861 – 879. Cosman B. Role of retreatment in minimal-power argon laser therapy for port wine stains. Laser Surg Med 1982; 2:43 – 57. Apfelberg DB, Maser MR, Lash H, White DN, Flores JT. Use of the argon and carbon dioxide lasers for treatment of superficial venous varicosities of the lower extremity. Lasers Surg Med 1984; 4:221 – 231. Flores JT, Apfelberg DB, Maser MR, Lash H, White D. Angiokeratoma of fordyce: successful treatment with the argon laser. Plast Reconstr Surg 1984; 74:835– 838. Landthaler M, Haina D, Waidelich W, Braun-Falco O. Laser therapy of venous lakes (BeonWalsh) and telangiectasias. Plast Reconstr Surg 1984; 73:78 – 83. Janniger CK, Goldberg DJ. Angiofibromas in tuberous sclerosis: comparison of treatment by carbon dioxide and argon laser. J Dermatol Surg Oncol 1990; 16:317– 320. Arndt KA. Adenoma sebaceum: successful treatment with the argon laser. Plast Reconstr Surg 1982; 70:91 – 93. Cheney ML, Googe P, Bhatt S, Hibbard PL. Angiolymphoid hyperplasia with eosinophilia (histiocytoid hemangioma): evaluation of treatment options. Ann Otol Rhinol Laryngol 1993; 102:303 – 308. Dover JS, Arndt KA, Geronemus RG, Alora MBT. Illustrated Cutaneous and Aesthetic Laser Surgery. 2nd ed. Stamford, CT: Appleton and Lange, 2000:147 – 181. Apfelberg DB, Greene RA, Maser MR, Lash H, Rivers JL, Laub DR. Results of argon laser exposure of capillary hemangiomas of infancy—preliminary report. Plast Reconstr Surg 1981; 67:188 – 193. Hobby LW. Further evaluation of the potential of the argon laser in the treatment of strawberry hemangiomas. Plast Reconstr Surg 1993; 71:481 – 489.

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McMeekin Achauer BM, Vanderkam VM. Argon laser treatment of strawberry hemangioma in infancy. West J Med 1984; 143:628– 632. Hobby LW. Visible light CW and quasi-CW laser treatment of superficial vascular lesions in children. Lasers Surg Med 1986; 6:16– 19. Goldman MP, Fitzpatrick RE. Cutaneous Laser Surgery. 2nd ed. St. Louis, MO: Mosby, 1999: 19– 178. McBurney EI. Clinical usefulness of the argon laser for the 1990s. J Dermatol Surg Oncol 1993; 19:359 – 362. Spicer MS, Goldberg DJ. Lasers in dermatology. J Am Acad Dermatol 1996; 34:1– 25. Hulsbergen-Henning JP, VanGemert MS. Port wine stain coagulation experiments with a 540-nm continuous wave dye laser. Lasers Surg Med 1983; 2:205– 210. Mondon S, Rotteleur G, Brunetaud JM, Apfelberg DB. Rationale for automatic scanners in laser treatment of port wine stains. Lasers Surg Med 1993; 13:113 – 123. McDaniel DH. Clinical usefulness of the hexascan. J Dermatol Surg Oncol 1993; 19:312 – 319. Anderson RR, Parrish JA. Microvasculature can be selectively damaged using dye lasers: a basic theory and experimental evidence in human skin. Lasers Surg Med 1981; 1:263 – 276. Anderson RR, Jaenicke KF, Parrish JA. Mechanisms of selective vascular changes caused by dye lasers. Lasers Surg Med 1983; 3:211 – 215. Greenwold J, Rosen S, Anderson RR, Harrist T, MacFarland F, Noe J, Parrish J. Comparative histological studies of the tunable dye (at 577 nm) laser and argon laser: the specific vascular effects of the dye laser. J Invest Dermatol 1981; 77:305 – 310. Lanigan SW, Cartwright P, Cotterill JA. Continuous wave dye laser therapy of port wine stains. Br J Dermatol 1989; 121:345 – 352. Malm M, Rigler R, Jurell G. Continuous wave (CW ) dye laser vs CW argon laser treatment of port wine stain (PWS). Scand J Plastic Reconstr Surg Hand Surg 1988; 22:241 – 244. Bandol Y, Yanai A, Tsuzuki K. Dye laser treatment of port-wine stains. Aesthetic Plast Surg 1990; 14:287 – 291. Scheibner A, Wheeland RG. Use of the argon-pumped tunable dye laser for port wine stains in children. J Dermatol Surg Oncol 1991; 17:735 – 739. Dover JS, Geronemus R, Stern RS, O’Hare D, Arndt KA. Dye laser treatment of port-wine stains: comparison of the continuous-wave dye laser with a robotized scanning device and the pulsed dye laser. J Am Acad Dermatol 1995; 32:237 –240. Ross M, Watcher MA, Goodman MM. Comparison of the flashlamp pulsed dye laser with the argon tunable dye laser with robotized handpiece for facial telangiectasia. Lasers Surg Med 1993; 13:374 – 378. Broska N, Martinho E, Goodman M. Comparison of the argon tunable dye laser in treatment of facial telangiectasia. J Dermatol Surg Oncol 1994; 20:749– 753. Tan OT, Stafford TJ, Murray S, Kurban AK. Histologic comparison of the pulsed dye laser and copper vapor laser effects on pig skin. Lasers Surg Med 1990; 10:552– 558. Neumann RA, Knobler RM, Leonhartsberger H, Gebhart W. Comparative histochemistry of port wine stains after copper vapor laser (578 nm) and argon laser treatment. J Invest Dermatol 1992; 99:160 – 167. Walker EP, Butler PH, Pickering JW, Day WA, Fraser R, Van Halewyn CN. Histology of port wine stains after copper vapor laser treatment. Br J Dermatol 1989; 121:217 – 223. Sheehan-Dare RA, Cotterill JA. Copper vapour laser treatment of port wine stains: clinical evaluation and comparison with conventional argon laser therapy. Br J Dermatol 1993; 128:546 – 549. Neumann RA, Leonhartsberger H, Bohler-sommeregger K, Knebler R, Kokoschka EM, Honigsmann H. Results and tissue healing after copper-vapour laser (at 578 nm) treatment of port wine stains and facial telangiectases. Br J Dermatol 1993; 128:306– 312. Haedersdal M, Wolf HC. Risk assessment of side effects from copper vapor and argon laser treatment: the importance of skin pigmentation. Lasers Surg Med 1997; 20:84 –89.

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5 Continuous Wave and Pulsed CO2 Lasers E. Victor Ross Naval Medical Center and University of California, San Diego, California, USA

1. Background 1.1. Physical Properties 1.2. Beam Profiles 1.3. Mechanically Shuttered Pulses and Superpulsing 1.4. Laser Spot Size 1.5. Delivery Systems 1.6. General Operating Principles 2. Laser – Tissue Interactions 2.1. Physics 2.2. Residual Thermal Damage 2.3. Clinical Examples of Laser – Tissue Interactions 2.3.1. High PD, Short Exposure Time 2.3.2. Long Exposures in CW Low –Medium PD Defocused Mode 2.3.3. Very Low PDs and Short Exposures 2.3.4. High PDs with Small Spots (0.1 – 0.3 mm), Used in Incisions 3. Comparison of the Resurfacing Lasers 3.1. UltraPulse 3.2. The SilkLaser 3.3. The NovaPulse 3.4. Nidek Unipulse 3.5. TruPulse 3.6. Summary of Resurfacing Systems 4. Wound Healing after CO2 Laser 5. Ultrastructure after CO2 LSR 6. Applications 6.1. Applications Where the Laser Performs Better Than Most Other Modalities 6.1.1. Trichoepitheliomas 6.1.2. Adenoma Sebaceum 6.1.3. Common Warts

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6.1.4. Condyloma Acuminata 6.1.5. Nail Matrixectomy 6.1.6. Earlobe Keloids 6.1.7. Larger Keloids and Nonearlobe Keloids 6.2. Acne Keloidalis Nuchae 6.2.1. Pyogenic Granuloma 6.2.2. Actinic Cheilitis 6.2.3. Sebaceous Hyperplasia 6.2.4. Epidermal Nevi 6.2.5. Syringoma 6.2.6. Xanthelasma 7. Lesions that Might Be Treated Equally Well with Other Modalities 7.1. Seborrheic Keratoses 7.2. Dermatosis Papulosis Nigra 7.3. Neurofibromas 7.4. Steatocystomas 7.5. Pearly Penile Papules 7.6. Basal Cell Carcinoma 7.7. Bowen’s Disease 7.8. Hidradenitis Suppurativa 7.9. Scar Revisions 7.10. Chondrodermatitis Nodularis Helicus 7.11. Lymphangioma Circumscriptum 7.12. Nevus Sebaceous 7.13. Hydrocystoma 7.14. Histiocytoma or Xanthoma Disseminatum 7.15. Hailey – Hailey and Darier’s Disease 7.16. Kaposi’s Sarcoma 7.17. Tattoos 7.18. Disseminated Superficial Actinic Porokeratosis 7.19. Actinic Keratosis 8. Laser Sterilization 9. Technique Pearls 9.1. CW Vaporization 9.2. Cutting 10. Laser Safety Issues Specific to the CO2 Laser 11. New Developments 12. Pre- and Postoperative Considerations 12.1. Preoperative Considerations 12.1.1. Relative Contraindications 12.1.2. Preoperative Regimen 12.1.3. Postoperative Care 13. Conclusions References Appendix I: Sample Operative Note Appendix II: Consent Form Appendix III: Sample Postoperative Instructions Appendix IV: Patient Information Handout

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BACKGROUND

The CO2 laser was one of the first lasers to be used surgically. Since its invention by Patel in 1964, the laser’s strength is linked to its high absorption by water at 10.6 mm. The first published studies using the CO2 laser emphasized the device as a cutting tool with improved hemostatic capabilities over scalpel surgery, and typically the laser was used with a tightly focused beam (1). Subsequently, especially in dermatology, the laser has been used more as a defocused vaporizing or controlled heating tool. With the CO2 laser, one can simultaneously hold a coagulator, scalpel, and vaporizer, depending on the power density (2). 1.1.

Physical Properties

CO2 lasers are pumped electrically, that is, the laser cavity is excited by electrical discharges. All but one of the CO2 lasers presently used in cutaneous surgery are longitudinally excited, meaning that the pumping occurs at the ends of the sealed tube. One laser, the TruPulse (Tissue Technologies, Albuquerque, NM) is transversally excited, meaning that the electrical discharge occurs across the tube. Carbon dioxide lasers use a mixture of CO2 , N2 , and helium as the lasing medium. Doping of the CO2 gas with other elements, particularly nitrogen, increases the laser’s efficiency. There are multiple energy transitions for the CO2 laser, so that 10.6 mm is not the only possible emitted wavelength. The 10.6 mm photons are created when CO2 molecules drop from a higher-energy asymmetric stretching mode to a lower-energy stretching or bending mode. The wavelengths are longer than those in visible light lasers because the transitions are of the rotational/vibrational type, whereas the ruby laser, for example, involves moving electrons into higher and lower stages (electronic transitions) (3 – 8). The overall efficiency (5 –20% from the wall plug) of CO2 lasers is among the highest of all lasers. This efficiency is one reason why a room with a CO2 laser tends to get less hot than a room with a solid state laser, where the efficiency is less than 1%, and much of the remainder of the energy is wasted as heat (6). CO2 lasers are capable of a large range of powers. In medicine the range is usually 10 – 100 W continuous wave (CW) power, and up to 10,000 W peak power for pulsed applications. Conventional medical CO2 lasers develop about 50 W average power per meter length of the tube, so that a taller laser tower (the upright part of the laser) is associated with more power (6). 1.2.

Beam Profiles

Most CO2 laser beam profiles are Gaussian (TEM 00), which is a function of the way the beam is created in the laser cavity. The Gaussian beam profile is bell shaped, and because it tends to be stable and easy to propagate through an articulated arm, it is a desirable beam profile to have from an engineering perspective. However, the Gaussian beam profile also creates nonuniform local fluences at the skin surface (4,9,10). These nonuniformities, however, are typically mitigated by (1) the delivery device, (2) the user’s choice of fluences, and (3) the skin lesion itself. For example, scanners can be configured to deliver various degrees of overlap that decrease the effects of the “wings” of the Gaussian profile, creating a more uniform surface fluence. Also, the user can choose lower fluences (at or near the ablation threshold) in resurfacing that allow for fairly uniform heating across the spot. Finally, many skin lesions are bell-shaped, which naturally accommodates the bell-shaped beam profile if one is trying to ablate an exophytic lesion such as a verruca or an adnexal tumor.

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The TruPulse laser runs multimode, so that it has a flatter beam profile. However, multimode beam profiles usually have a larger beam waist and are more difficult to focus to a uniform spot. Like the TruPulse, the Novapulse laser (Lumenis, Norwood, MA) beam profile is more flat-topped than Gaussian. In this case, the flatter beam profile is the result of mode mixing as the beam bounces along the inside walls of the hollow waveguide delivery device (11). Top hat profiles have been described as ideal, but it is the specific application and the skill of the physician that determines the “idealness” of a beam profile.

1.3.

Mechanically Shuttered Pulses and Superpulsing

Older CO2 lasers were either truly CW or operated at such a high frequency that the laser tissue interaction was, for all intents and purposes, CW. Early attempts to control laser exposure times involved the use of mechanical shutters to “chop” the pulse. The shortest possible exposures available with these devices were typically 50 –100 ms. Because the peak powers were low (the same as the average power, or 10– 30 W), the power densities were often subablative or marginally supra-ablative, and the only advantage was confinement of thermal injury to a level not observed with longer exposures (and higher fluences). The next generation of CO2 lasers used so-called “superpulsed (SP) technology”. Pulses were on the order of 50– 200 mJ and were delivered with varying repetition rates (50 –500 Hz). Sometimes they were delivered as couplets spaced very close together temporally. Unlike gated or mechanically shuttered pulses, however, these laser emissions were truly pulsed, that is, they were generated at the electrical source as pulsed exposures. These lasers delivered average powers similar to CW lasers, but the lasers were not “on” all of the time (Fig. 5.1). The older SP lasers only performed at very high repetition rates [so-called rapid superpulsed mode (RSP)], because of engineering limitations. The laser used a train of pulses, as few as 12, in trains of 50 ms or more. Even some newer SP lasers run only at repetition rates of 300 Hz, so that single-pulse ablation/heating is not

Figure 5.1 Differences between CW, mechanically shuttered, and RSP modes.


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possible. Most SP lasers have a nonconstant pulse profile, so that the tail of the micropulse has a lower irradiance than the initial portion of the micropulse. This characteristic, and the rapid repetition rate, has contributed to levels of thermal damage not much lower than those of CW lasers. To minimize residual thermal damage (RTD) with RSP lasers, duty cycles should be low, or the repetition rate will be too high and thermal damage will accumulate (12 –14). Even though thermal damage was reduced somewhat by RSP lasers (typically by 10 – 30% using the same average power and fluence as in comparable CW applications) (15,16), it was not until the introduction of high-energy pulsed lasers with low repetition rates (single-pulse effects) and scanners that the full advantages of SP CO2 lasers were realized for defocused ablative and near-ablative applications (17,18). The term “UltraPulse,” used by a leading manufacturer, refers to a subset of superpulsed lasers with a rectangular pulse profile, capability of low repetition rates, and higher peak powers than older first-generation SP lasers. In a pulsed CO2 laser, there is a capacitor network that stores charge across the cavity electrode. Pulsed CO2 lasers can be excited by either direct current (DC) or radiofrequency (RF) power supplies. The RF laser develops high peak powers more easily than DC lasers, as RF excitation achieves and maintains the population inversion more efficiently within the cavity (see Chapter 2). Analogous to the ideal beam profile (top hat), the ideal temporal pulse shape should be rectangular, that is, the pulse is instantaneously turned on or off. The RF laser is the most capable of producing these “rectangular pulses” with a minimal tail. Most CO2 lasers in medicine are excited by a DC. The exceptions are the UP and Novapulse lasers, which are RF excited (11,13). For the remainder of the chapter, we will describe exposures as RSP mode, UltraPulse (UP) mode, or CW mode. We will refer to “mechanically shuttered” pulses simply as shorter exposures in CW mode.

1.4.

Laser Spot Size

Spot size can be estimated by irradiating a tongue blade for a brief period. However, these simple spot size measurements are sometimes deceptive, because they depend partly on the damage threshold of the target. For example, if one takes the UltraPulse laser and uses the 3 mm spot with very low pulse energy, only the center of the spot will be heated sufficiently, and the operator might mistakenly underestimate the spot size. Rigorous spot size measurements are made by profiling the beam by either moving a pinhole, using a knife edge, or using a dedicated beam profiler. The method allows one to see the point where the local power density is 14% of that at the center, which has arbitrarily been defined as the edge of the spot for a Gaussian beam.

1.5.

Delivery Systems

Usually, CO2 lasers work with a rigid articulated arm. The arm preserves the profile of the beam but sometimes results in cumbersome positioning between the operator and target. Arms may be fragile and mirrors may be knocked out of alignment during movement of the laser, making it imperative to test the laser on a tongue depressor prior to each use. Solid fiber delivery systems presently are impractical for IR radiation, as the materials are hygroscopic and not durable enough for pulsed laser systems (8,11). Hollow waveguide delivery devices will be discussed later.

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General Operating Principles

In general, when the CO2 laser runs in CW mode, a footswitch or mechanical shutter controls the total time on tissue. In CW mode the operator is using the laser in either a defocused or a focused manner. This is dependent on the distance between the skin and the handpiece. Most lasers have a focusing handpiece whose focal length is roughly 100 mm. The focal length is the distance from the end of the spatula tip to the lens. Normally, the focal plane is at the end of the tip. Longer focal lengths are usually associated with larger spots and greater depths of field. The depth of field is how much one can move the handpiece to and from the target and skin without significantly altering the spot size. The lens in the handpiece, which one can see by peering into the proximal portion of the handpiece, is usually made of zinc selenide, as standard glass absorbs CO2 energy. The lens focuses a somewhat collimated 7– 12 mm beam that has propagated from “knuckle to knuckle” to the distal end of the articulated arm. The operator can rapidly switch from a vaporizing to a heating mode (or vice versa) by moving the handpiece away from or toward the skin. As one pulls back from the skin, the beam is defocused. In this way, one can vary the power density according to the individual goals of the application. Some manufacturers provide handpieces with lenses that produce collimated beams, such as the TruSpot by Coherent. These allow the physician to work at varying distances from the skin surface with constant spot sizes. Regardless of the handpiece, one will see the greatest power density (PD) at the middle of the spot for Gaussian beams. The power density at the beam center is two times that of the average power density across the spot (12,19). It follows that one sees the greatest ablation at the center of the spot, and normally charring at the periphery.

2. 2.1.

LASER – TISSUE INTERACTIONS Physics

There are four important components in the CO2 laser – tissue interaction (20,21): 1. The propagation of the beam in tissue: When the CO2 laser beam impacts the skin surface, attenuation of the beam is guided by Beer’s law, which describes an exponential reduction in beam strength. Optical absorption and scattering determine the optical penetration depth (OPD) of the laser beam in the skin. The beam is rapidly attenuated (by about 85% within 40 mm) due to the high water content of the epidermis and dermis. This implies that if there is no ablation, the depth of the thermal effect will only be about 20 –40 mm if there is perfect thermal confinement (see Chapter 2) (22 –24). One might ask, if the beam is attenuated so much after only 20 –40 mm, why is there thermal damage and vaporization hundreds of micrometers and even millimeters into the skin? The reason is that Beer’s law describes only the optical attenuation of the beam. However, ablation and tissue heating during the pulse as well as postpulse heat conduction, result in deeper tissue injury. If there is significant ablation, the front (or boundary of the laser – tissue interaction) is constantly changing. In other words, the beam impact point is starting at increasing depths in the skin but still maintaining 20 – 40 mm of optical penetration beyond the front. 2. The instantaneous absorption of laser energy: The next step in laser – tissue interaction is conversion of laser irradiation to heat, which is instantaneous within the optical field. For all lasers, except ultra-SP lasers and the excimer laser, the major means of destroying tissue is the conversion of light to heat. The resulting heat deposition results


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in either ablation or coagulation at the local level, depending mostly on the PD, or the time rate of energy delivery (W/cm2). Interestingly, the original PD ranges for CO2 lasers were chosen somewhat arbitra1 rily, but loosely based on the principle that it required 2.5 J over 10 s to convert 1 mm3 of water to steam. This required about 25 W average power (1). The threshold for tissue vaporization with the CO2 laser is about 100 –150 W/cm2, but at this low power density, there is much wasted heat with as much as 55% of the energy not used in ablation (12). It follows that the highest PD possible should be used that allows for control of the depth of injury. With standard CW lasers, the surgeon was forced to use a lower PD for control of vaporization depth, thereby increasing collateral thermal damage, or a higher PD for minimal RTD, but with more difficulty controlling the amount of removed tissue. One can think of the CO2 laser with high PD as delivering energy in such a rapid way that vaporization predominates over heating. In contrast, at lower irradiances of ,1000 W/cm2, heating predominates over vaporization (12,19). In both cases, the level of tissue destruction, which is the sum of depth of ablation plus residual thermal damage, will increase with exposure time. In the former case, the damage will be by tissue heating, and in the latter, by tissue vaporization. 3. The conduction of heat outside the OPD: This occurs on a much slower time scale than the aforementioned instantaneous heating due to absorption of the beam by tissue water and collagen. There is some absorption of 10.6 mm photons by dry collagen, but it is very small compared to tissue water. Because skin possesses high density and specific heat much like that of water, thermal diffusivity is high, and subsequently heat conduction is relatively poor. The temperature profiles deep to the OPD depend largely on the PD. If the energy is deposited before there is time for heat diffusion, thermal damage will be minimized (20,22,25 – 28). 4. Local denaturation of tissue: Finally, thermal damage is predicted from models that predict protein denaturation based on time – temperature combinations. This denaturation is based on integral equations where the denaturation is linearly dependent on time and exponentially dependent on temperature. In other words, by raising the temperature only by 10 – 208C, one requires only 1/10 the exposure time for equal denaturation (29).

2.2.

Residual Thermal Damage

Venugopalan and others have critically examined the various parameters that affect RTD in ablative and nonablative laser applications and have found the following (26): 1. Effect of ablation: Supra-ablative fluences and power densities are generally considered to be associated with less thermal damage than laser –tissue interactions without ablation. Theory predicts that if the ablation front outpaces the speed of heat conduction, thermal damage will be minimized. While this is true in principle and practice for prolonged irradiation times of .0.25 s, there are instances where the lack of ablation is associated with less injury than in those applications with ablation. For example, if one uses 3 J/cm2, one will observe less RTD at the base of the wound than at 10 J/cm2. The reason is that the total energy dose is less. Also, there is always a tail end of the penetrating beam as it is attenuated by tissue water. This “tail” fluence will not achieve ablation threshold, and therefore there will always be some RTD at the base of the ablation crater. To achieve large zones of thermal damage without ablation requires either overlapped low-energy pulses, or a low PD beam applied for times of over 50 ms (Fig. 5.2). The threshold for ablation is variable, and tends to increase with pulse duration and the strength

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Figure 5.2 (a) Microscopic view of pigskin after a single 1 ms pulse at 8 J/cm2 laser with Gaussian beam profile. Note that there is less RTD at the edges of the wound due to lower energy at the beam edge. (b) In contrast, after 10 pulses at 1 Hz, there is ablation at the center of the wound, and the RTD has “built up” to be slightly greater at the wound edge. This sequence shows that subablative fluences only result in more RTD when the heating is cumulative. Ablation at the center of the crater limited the RTD to 80 mm.

of the tissue. The dermis has a higher threshold than the friable cellular epidermis (23,24,30). 2. Effect of pyrolysis: Pyrolysis refers to the thermal decomposition of organic compounds in the absence of O2 (31). The resulting char acts as a heat source for several seconds after laser exposure. As air is a better insulator than the underlying skin, heat tends to travel to deeper tissues. With continued heating of the char, one sees a flame or a bright spot at the surface (“flash” point 5008C) and smoke formation, as the gaseous molecules on the surface of the char undergo combustion. Simultaneously, continued heating of the solid char component can result in “white-hot” plasmas that are so bright that the surgeon will be tempted to turn his eyes away from the operative field. 3. Effect of a nonsquare pulse shape: With older SP lasers, the laser pulse typically had a sharp rise time, followed by a slow tail. Thus, the PD was not constant during the pulse, leading to more thermal damage than predicted. However, if the pulse is short-lived, and there is sufficient interpulse cooling, the tail should not be clinically important. 4. Effect of pulse duration: According to the literature the pulse duration should be shorter than the thermal relaxation time. Thermal damage will be minimized if the laser pulse is delivered faster than the time it takes a heated layer of water equal to the optical penetration depth to cool. This time is based on the geometry and dimensions of the target, which in this case is assumed to be a layer of water 30 mm thick. Although the thermal relaxation time is approximately 1 ms, this number is reported with widely different values, partly because different models are used to determine the time for cooling (32). Experimental data support this argument (Fig. 5.3), as Walsh et al. (28) showed that with longer pulses (50 vs. 0.6 ms), there was more RTD. However, Venugopalan et al. (25,26) argued that a more important contributor to the increase in RTD in Walsh’s study was the decrease in PD for the longer exposures. Furthermore, the increases in RTD observed by Walsh et al., were the result of up to 50 pulses (overlapping at 1 Hz); single-pulse effects would have most likely not shown such a dramatic difference in RTD as a function of pulse duration. In our own study, we showed that for single pulses over a range of 0.25– 10 ms, there were no significant increases in RTD for fluences of 1, 3, and 10 J/cm2 on the basis of pulse duration (30). However, this is only a 40-fold range of pulse durations. Studies with shorter pulsed lasers have shown (33), along with our on experiments, that with 60 – 120 ms pulses, thermal damage is reduced to about 30 –50 mm compared to the 70– 120 mm levels observed in


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Figure 5.3 (a) RTD in pigskin after defocused CW CO2 laser beam (8 W, 2 mm spot, 0.5 s exposure, 115 J/cm2). Damage extends 500 mm deep to surface. (b) RTD is only about 90 mm after a 7 J/cm2 exposure with a pulse duration of 1 ms. (H&E stain, original magnification 100).

millisecond domain lasers. Moreover, Littler (34) found RTD intermediate between millisecond CO2 and erbium:YAG lasers with 130 ns CO2 laser pulses. The primary advantage of shorter pulses is (1) spatial confinement of thermal injury and (2) lowering of the ablation threshold. In general, the RTD with a very short pulse is roughly equal to two times the OPD, whereas that of longer pulses scales as the square root of the pulse duration assuming fluences above the damage threshold for tissue (28). 5. Power density: If one examines the study of Schomaker et al. (35) of RTD in CO2 laser surgery, there was no systematic association between PD and RTD over a range of 360 to 740,000 W/cm2. However, over this PD range, theory predicts only a 33% increase for the lowest PD over the highest PD. Dobry et al. (36) found that RTD and scar increased with PD in rats from 141 to 849 W/cm2. They used the same 0.1 s application times in all their experiments. It follows that the doses of energy were not the same, so that this study actually showed that increasing the fluence caused more RTD by increasing the wound depth. In practical terms, one must remember that by increasing the power, one only linearly increases the PD over any focal point in the beam profile, but by decreasing the spot size, because the area of a circle varies with the square of its radius, there is a quadratic increase in the PD at the impact site. Hobbs et al. (12) summarized that wound edge necrosis is minimized for PD .20,000 W/cm2 and exposures of about 0.1 ms. 6. Repetition rate: Early estimates of the critical repetition rate for minimizing thermal damage were as high as 1000 Hz. These rates, based on the inverse of the thermal relaxation time, which is the time for the target to cool to 37% of the peak temperature for the CO2 laser, were too high, as tissue requires more than 100 ms to cool completely before the next pulse. This is also known as the thermal recovery time. As long as ablation occurs, 20 Hz is the maximum rate that will limit RTD to near the theoretical minimum (25). Without ablation, the rate decreases to 1 – 5 Hz with the CO2 laser (37,38). Older RSP lasers showed that with high repetition rates, RTD was only modestly decreased vs. CW lasers (16,39,40). For vaporizing applications, Fitzpatrick (41)

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noted that the RSP mode was most helpful when the total string of pulses was short (i.e., when the macropulse ,50 ms), regardless of the duty cycle and repetition rate. 7. Fluence: Kamat et al. (42,43) studied fluence effects and noted that there was increased RTD with increasing fluence. They found that the greatest effect was in the basal layer. Since heating should have been greatest at the upper epidermis, this was somewhat unexpected; however, the authors suggested that weaknesses in the lamina lucida might have played a role. They found selective epidermal damage for fluences of less than 10 J/cm2. In agreement with their results, we have experimentally found that for pulse durations ,10 ms fluence (and not power density or achievement of ablation) is a more important parameter in determining the extent of RTD; that is, lower fluences usually result in less RTD. 8. Plasmas: Plasmas have been observed with the CO2 laser (22,44,45) with fluences above 19 J/cm2 for 100 ns and 2 ms pulse durations. Plasmas are PD-dependent, generally requiring PD .107 W/cm2 in tissue, so that either increasing the fluence or decreasing the pulse duration will increase the likelihood of their formation. As plasmas absorb incoming energy and also create very high, although focal, surface temperatures of 10008C, they are generally undesirable. It follows that one should choose pulse duration/fluence combinations that avoid optical breakdown. 9. Temperature profiles in CO2 laser surgery: Choi et al. (46) measured the temperature profile at the surface with a pulsed CO2 laser and found experimentally that the thermal relaxation time was about 20– 40 ms (the time for the peak temperature to decay to 37% of the maximum). They found that temperatures increased from about 2208C (after one pulse) to 4008C after 15 pulses at 1 Hz and 3.5 J/cm2, without wiping. They noted carbonization after four pulses and a simultaneous sharp increase in temperature to 3508C. They also found tissue burning (combustion) after the 10th pulse. The high temperatures (.1008C) are due to water superheating and are not unexpected. They noted that the time for total tissue cooling (to baseline temperature) was about 150 ms. It should be noted that with continued low-PD charring, one might expect peak surface temperatures of about 10008C (47,48). 2.3.

Clinical Examples of Laser – Tissue Interactions

2.3.1. High PD, Short Exposure Time Laser resurfacing (LSR) is the best example of this scenario, where there is some vaporization (ablation) and a small residual zone of thermal damage. The zone of thermal damage is the result of both (1) subablative localized energy densities (at the base of the wound, as the beam is rapidly attenuated) and (2) heat conduction during and after the pulse. For typical fluences used in LSR, the following cascade of events, corroborated by both human and animal histologies, occurs with each pass. After the first pass, the entire epidermis, for fluences of 5 – 8 J/cm2 with a 1 ms domain laser is heated plus about 10 – 40 mm of the dermis. With lower fluences or with treatment with the ultra-short pulse Tru-pulse laser, thermal damage can be reduced to lower levels (10,30,49 – 52). At this point, the epidermis is normally wiped away with wet gauze, and the papillary dermis is exposed. However, there is a case to be made for not wiping. If one knows the extent of the injury after one pass and is confident that this level of injury will successfully reverse the skin pathology, wiping only serves to increase patient discomfort and prolong healing. More importantly, there appears to be a level of dermal thermal injury beyond which long-term hypopigmentation is almost inevitable in selected patients, especially appearing along the lateral cheeks and extending to the jawline. Thus,


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one can titrate the injury according to the level of desired injury with one pass if one reliably knows the laser end points. For example, with the UP at 300 mJ and a density of 6, if the scans are laid down accurately, one can rely on complete epidermal denaturation and about 20 mm of dermal thermal damage. Of course, this is somewhat anatomy dependent, as in the thinner skin of the eyelids, neck, and temples, the thermal damage will extend deeper into the dermis. Thus, the same total thermal damage will result regardless of the delivery location. However, the level of dermal injury will increase in areas with a thinner epidermis. With the CO2 laser, once the denatured friable epidermis is wiped off, it takes many pulses to ablate the residual acellular dermis (53). With the typical Gaussian beam of the CO2 laser, there will be some ablation at 7 J/cm2 average fluence at the center of the spot, but very little at the perimeter. Overall, using this average fluence, the ablation is about 10 – 15 mm per pass, much less than was reported in the early days of LSR. Of course, as the average fluences reach 10, 15, and 20 J/cm2, the relative ratio of ablation to tissue heating will increase. That is, roughly the same RTD will result, but the amount of ablation per pass will increase, Depending on the patient’s pathology and age, one sees different surface characteristics after wiping the denatured epidermis. For younger patients with modest photodamage, normally a pink to red dermis is exposed. For an older patient with severe solar elastosis, one sees yellowing immediately. If the patient has either actinic keratoses (AKs) or incipient dysplasia, there is usually hyperemia and sometimes frank bleeding upon wiping. Often, vigorous wiping is helpful in unmasking early AKs that might not have been obvious from the surface prior to laser surgery. In these cases, it is wise to proceed with additional passes until there is mild yellowing. The RTD at the base of these wounds is often enough to remove the remainder of the AK. Fulton et al. (54) recently reported that the CO2 laser was inferior to dermabrasion for AKs and used examples of AKs and basal cell carcinomas (BCCs) recurring in LSR sites not long after laser surgery. He referred to the penetration depth of the laser as being the main limiting feature of this technique. This is true if one makes only one pass and does not wipe, a technique I do not advise when treating AKs. Once the AK is uncovered by wiping, however, the remaining lesion can be vaporized or heated to achieve a complete cure. 2.3.2. Long Exposures in CW Low – Medium PD Defocused Mode This is the so-called vaporization mode, which is actually a combination of simultaneous heating and vaporization, and is used for treating warts and other exophytic lesions where some tissue heating at the base of the wound is tolerated. Usually, one will encounter vaporization at the center of the spot and charring at the periphery. To decrease char, one must move in a pirouetting motion so that the char is not continuously heated. When the CO2 laser burns a hole in the skin, the mechanism for ablation is the rapid conversion of water to steam (23,55 – 57). In the epidermis, the fragility of this layer provides for easy ablation, as the water vapor easily escapes the intracellular space, typically carrying with it a solid residue of exploded cells. This debris will continue to be heated as it is carried off, thus one sees “burning” or combustion. The onset of vaporization by CW irradiation in this PD regime is not completely characterized, but Verdaasdonk et al. (47) studied it intensively. They found the following sequence at the tissue surface. Initially, there was slight tissue discoloration. Coincident with a “pop,” the surface was lifted slightly, suggesting boiling bubbles underneath. The sound was due to the rapid ejection of air through the ablation front (nozzle effect), like bursting a balloon. Next, a small black spot was noted in the center of the beam,

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presumably from carbonization of the dehydrated tissue. Within a few tenths of a second, this charred zone expanded and a ring was formed. Next, the char underwent combustion, unveiling a new hydrated surface. Later, there were cyclical rings of carbonization and vaporization, following each other in rapid succession as a progressively deeper crater was formed. The temperature associated with the onset of ablation was around 150 – 2008C (48). In contrast to the above scenario, for lower PDs with long exposure times, the char is never “blown off” (either by vaporization of water below the char or by combustion), and there is deep heating beneath the skin surface, as temperatures .10008C may occur at the surface. Indeed, this can be observed occasionally in the treatment of warts and rhinophyma, where prolonged application times of .0.5 –1 s can result in a brownish color and finally deep blackening of the surface. With increased blackening, the char acts as a nearly perfect absorber, and the char becomes hotter and hotter. This is why using lower PDs for prolonged periods is usually not advisable, as it simply results in very deep “invisible” tissue heating. It is advisable in these cases to wipe the char, thus exposing hydrated tissue, so that additional vaporization can take place. 2.3.3. Very Low PDs and Short Exposures With this technique (also known as thermabrasion), the laser is used in low power mode at 1 – 5 W with a defocused beam with very short bursts of CW radiation of about 0.1 s, and a total fluence of 1 –5 J/cm2 (58). Although the thermal gradient is not steep, that is, the temperature decay as a function of depth is small, there is so little total heat that this is safe as long as one pass is made, and this application will typically restrict RTD to the epidermis and superficial papillary dermis. It is useful in lentigos and mild photodamage. The goal is to use short bursts of subablative PDs to heat a specific thickness of tissue. In the case of dermatosis papulosis nigra (DPN), for example, one can heat the tissue just to a level similar to that of the hyfercator of 0.5– 2 mm. The end point is slight whitening of the tissue. This technique is best reserved for those who do not have access to a pulsed CO2 laser (43,59). 2.3.4. High PDs with Small Spots (0.1 –0.3 mm), Used in Incisions Most skin surgeons do not use the CO2 laser in cutting mode, with the exception of eyelid surgery. In addition to the cumbersomeness of using the laser as a cutting tool including the need to work around the articulated arm, the need for a smoke evacuator, and the constant vigilance that is required not to inadvertently strike an innocent bystander target, the laser cannot be endorsed as a first choice for incisions because healing is delayed compared with scalpel incisions. It is therefore not recommended for most routine skin surgeries (60). The indications for using CO2 for cutting regardless of the mode, include: Bleeding disorders Where epinephrine is not indicated Vascular lesions (hemangiomas and scalp tumors) Infected surgical sites In patients with pacemakers or implanted defibrillators (58) The advantages, on the other hand, are ease of excision and a relatively bloodless field. The lack of perfect hemostasis is partly explained by the paucity of RTD in a standard excision with CO2 laser. Because the small spot sizes of 0.1– 0.3 mm allow for high PDs, thermal damage is minimal (61). Microscopically, one finds 90 mm of basophilic change and 100 – 500 mm of lateral glassy hypereosinophilic change on routine staining


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(62 –64). It follows that high-flow vessels larger than 500 mm are likely to bleed after CO2 transection. In contrast, without blood flow, vessels up to 2 mm have been coagulated (55,65 –72). Also, Kaplan (personal communication) has noted that in adults the maximum coagulated vessel diameter is about 0.5 mm, but in children it is greater at about 1 –1.5 mm. One should note that minimizing RTD and achieving hemostasis are antagonistic (4). Ideally, one should choose the laser parameters with the least RTD that still achieves adequate control of bleeding. The amount of bleeding vs. other modalities such as diathermy and scalpel has been compared, and it appears that the CO2 laser performs as well as a cutting electrosurgical current. In our experience, however, we have found that a blended electrosurgical current achieves better hemostasis than a well-focused laser beam. Defocusing only works to stop bleeding when the bleeding is mild. Mullins et al. (73) found that by using suction ahead of the beam they could achieve better hemostasis. Another purported advantage of the CO2 laser is that it seals nerve endings (74), which presumably results in less postoperative pain than in scalpel excision.

3.

COMPARISON OF THE RESURFACING LASERS

There are over 10 lasers with resurfacing capabilities (Table) of lasers would be helpful. I will discuss the ones more commonly used. Most of these devices are also capable of CW operation. Alster et al. compared (75) four resurfacing lasers and found that they were similar in histologic and clinical outcomes. The same was true for clinical studies comparing the Sharplan SilkTouch and UltraPulse lasers (76 – 78). In another study, the TruPulse and UltraPulse were compared (79,80). Although the RTD was greater with the UltraPulse, the final cosmetic outcomes were similar. Kauvar et al. (51) studied the histology of superpulsed, SilkTouch, and UltraPulse lasers in human skin and found that after three passes, the SP and SilkTouch RTDs were both 150 mm, the UltraPulse RTD was 70 mm, and the CW laser RTD (10 W and 0.2 s exposure) was 400 mm. Many investigators have compared the various levels of RTD after three passes in LSR: a summary is provided in Table 5.1 (30,76,77,79,81,82). Table 5.1 Lasers with Resurfacing Capabilities

Typical “settings” UltraPulse (Lumenis, Norwood, MA) NovaPulse (Lumenis, Norwood, MA) SilkLaser (SilkTouch mode/ FeatherTouch mode) (Lumenis, Norwood, MA) TruPulse (Tissue Technologies, Albuquerque, NM) Unipulse (Nidek, Freemont, CA)

Typical safe fluence (J/cm2)

Typical RTD after two to three passes (mm)

Density 6, 300 mJ

7.5

90 – 110

Computer scanner E16, 7 W 18 W/36 W (with 200 mm handpiece)

6–7

60– 80

15/8

110/70

500 mJ

16– 18 W/20% overlap

5

50

14

70

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3.1.

Ross

UltraPulse

The UltraPulse laser is one of the two most popular resurfacing systems (14,81,83–95). In its initial configuration, the laser was equipped with a 3 mm spot-size handpiece with a collimated beam (TruSpot). Typical pulse energies were 250–500 mJ giving a fluence of 3–7 J/cm2 in these first efforts at skin resurfacing with single short pulses of ,1 ms. With the addition of the computer pattern generator (CPG) in 1995, the laser became more popular and easier to use over larger surface areas. The CPG scans a 2.25 mm beam in an x–y fashion with varying user controllable degrees of overlap. The popularity of the system is borne out by the frequent reference in the literature to the proprietary laser settings as if everyone should know their significance. Frequently, one will see, for example, in the methods and materials of a paper, the laser settings referred to as 3–5–5, which refers to the pattern–size–density. The pattern is one of seven different geometric configurations including squares, triangles, circles, diamonds, and even a ring. The size refers to the number of spots laid down per scan, and does not represent an absolute dimensional value. For the square pattern the size is the square root of the number of spots in the scan. Thus, for a size 5, there are 25 spots in the scan. The density refers to the overlap between spots; for example, density 5 implies about 30% overlap, and is typically chosen because it allows for overlap of the wings of the Gaussian beam and thus a fairly uniform tissue effect across the scan. Density 9 is about 60% overlap and is usually only used for exophytic lesions where rapid ablation is required and the concern for thermal damage is minimal. The density is important in determining RTD. Ross et al. (37) showed that after three passes with 300 mJ with wiping between passes, the respective RTDs based on basophilic collagen changes were 70, 95, and 145 mm for densities of 3, 6, and 9, respectively. The UltraPulse can also be used in a quasicontinuous mode (CW on panel, 3000 Hz) for cutting with the 0.2 mm handpiece. A 1 mm handpiece can be used for treatment of small exophytic lesions such as syringomas either in UltraPulse or in CW mode.

3.2.

The SilkLaser

This is a CW laser coupled with a flashscanner that sweeps the beam over a microspot in approximately 1 ms in SilkTouch mode and 0.4 ms in FeatherTouch mode. The early models possessed only the SilkTouch mode. In this mode, the laser dwell time, that is, the time the microbeam is in contact with any local area of tissue, is about 1 ms. Arbitrarily, the device was used with a 125 mm (focal length) focusing handpiece which spiraled a 220 mm beam at the focal plane. Typical powers were 6– 7 W with a 3– 4 mm scan size and 0.2 s “on-time.” These settings resulted in fluences of 16 J/cm2 and RTD levels of about 80 – 120 mm after three passes. As this was slightly greater than that usually observed with the UltraPulse with a similar pass number, Sharplan introduced the FeatherTouch. The dwell time was reduced to 0.4 ms, and the thermal damage after three passes with FeatherTouch was reduced to about 50 –80 mm (96). The SilkLaser can be used with newer 200 and 260 mm focal length handpieces. These spiral 360 and 420 mm microbeams, respectively. Because of the larger beam, higher powers must be used to achieve the same local PDs as with the shorter handpiece. Typical recommended powers are 18 W in SilkTouch mode and 36 W in FeatherTouch mode. Modern versions of the scanner interface with the laser directly, so that once the user chooses the power and handpiece, the panel provides representative settings that have been found to be safe and effective in LSR. Overall, using the longer handpiece is preferable because the depth of focus is greater, that is although one still should hold the handpiece tip close to the skin, the


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microbeam size will not change as significantly as when one uses the 125 mm handpiece. With this shorter handpiece, even holding the tip 2 mm above the skin surface can result in a 70% reduction in PD due to rapid divergence of the beam past the focal plane. In SilkTouch mode the laser beam overlaps on itself. This was due to the nature of the early device, where the laser and the scanner were not synchronized. This necessitated an “in and out” spiral to ensure complete coverage of all areas within the scan. With the FeatherTouch mode, there is only one spiral per pass, and the tangential velocity of the laser increases by about 1.3, thus the dwell time overall is decreased by about 60%. More importantly, because there is no overlap, RTD is significantly reduced. With the newer synchronized system, the panel gives suggested settings for power for a given handpiece and mode. For example, with the 125 mm handpiece (220 mm spot), the suggested laser power is 7 W, and for a given scan size such as 5 mm, the scan on-time is programmed for 0.43 s. For FeatherTouch mode with the same handpiece, the suggested power is 14 W, and for a 5 mm scan, the on-time is reduced to about 0.12 s. We have examined multiple tongue depressor impressions made by the laser with an operating microscope, and have confirmed that the SilkTouch mode does overlap almost, if not directly, on itself. This undoubtedly has contributed to the increase in RTD vs. the FeatherTouch mode as well as the increased fluence and slower tangential velocity. 3.3.

The NovaPulse

The NovaPulse can be used in pulsed or CW mode (75,97,98). This is an RF excited laser with 20 W average CW power capability and peak powers of upto 50 W in RSP mode. We have used the NovaPulse system for resurfacing, in which case it is coupled with either a 3 mm handpiece or a scanner, and found it to be a capable laser. The overall treatment times are somewhat longer than with the UltraPulse due to lower average powers for the NovaPulse. The laser scans a very small spot of 0.8 mm with the scanner. The pulse duration for a single pulse ranges from 50 to 1400 ms, depending on the pulse energy of 20 – 45 mJ. In other words, the duty cycle and average power increase slightly with each increase in pulse energy. The Nova Scan system generates a 3 mm spot size in a daisy pattern. A motor rotates the fiber tip, the 0.8 mm microspot, at about 1000 rpm 12 times to cover a 3 mm macrospot. For example, with a 6 W average power setting, the laser generates 360 mJ over 60 ms with a series of submillisecond pulses of about 30 mJ. A larger scanner, Dermascan, is also available with similar patterns and densities as the UltraPulse CPG. Depending on the application, the laser is capable of a number of programmed settings in CW (P programs) and pulsed (A, P, E, and F programs) modes. The unique feature of the NovaPulse laser is the delivery device, which is a proprietary hollow waveguide. The waveguide is a tube with a highly reflective coating on the inside wall. The waveguide is made of dielectric coated molybdenum encased in a stainless steel jacket. The laser beam enters at one end, and propagates down the guide into the handpiece. One problem with waveguides is that the transmission decreases from a maximum of about 85% to less than 40% if they are bent more than the arc of a basketball. This potentially introduces an unwanted variable into treatment if care is not taken by the operator (99,100). 3.4.

Nidek Unipulse

In skin resurfacing, the Unipulse (Nidek, Freemont, CA) scans a 1 mm spot at 100 –300 Hz with pulse energy ranging from 30 to 100 mJ depending on the pulse duration with a range from 200 to 800 ms. Typical operating parameters are 18 W average power and 20%

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overlap between adjacent spots or about 60 mJ pulses for an average calculated fluence of 16 J/cm2. For younger, less photodamaged patients, the power can be reduced to 14– 16 W. The laser also offers an array of SP and CW modes that can be used with a range of focusing handpieces. Of the SP, Unipulse, modes, Mode I is a very high-duty cycle mode with relatively long on-times and short off-times. This mode is designed for coagulation. With increasing numbers (II –V), the duty cycle decreases and the peak powers increase. Also, there is more time for cooling between pulses. 3.5.

TruPulse

This laser is fundamentally different from the others in that it is transversally excited, meaning that the electrodes are placed across the tube. This allows for brief highenergy pulses of 60 –100 ms and pulse energies of up to 500 mJ (79,80,101,102). The laser only operates in pulsed mode: there is no CW availability. The laser produces a multimode beam called “mesa” mode or flat top beam. The beam size is roughly 2 2 mm with the scanning handpiece for resurfacing (103). A 0.2 mm handpiece is also available for cutting. Because of the short pulse duration, the laser produces peak powers of up to 10,000 W. 3.6.

Summary of Resurfacing Systems

All of the resurfacing systems above are capable of achieving a combination of ablation and RTD that is suitable for obtaining a good cosmetic outcome. The physician should become comfortable with one system and have another system as a backup. Each different laser system, and even different lasers of the same model type, usually has unique features and idiosyncrasies that should be mastered prior to use. One should always look closely at the skin surface during irradiation. I normally have the aiming beam turned off or dimmed during pulsing. If something seems odd, stop the procedure, go back to the tongue depressor, and recheck the beam. For example, a mirror in the articulated arm once deteriorated during a CO2 laser case and the only sign was that the skin surface showed a collage of crescents rather than circles with the UltraPulse CPG.

4.

WOUND HEALING AFTER CO2 LASER

Early studies of wound healing after CO2 laser treatment focused on incisional wounds (104 –106). These studies found a delay in epithelial migration at the wound surface and a delay in fibroblast migration. Presumably, the RTD associated with CO2 wounds produces the delayed inflammatory response that crescendoes somewhat later than scalpel wounds of similar depth (39,107– 115). Consistent with this delayed inflammatory response, and possibly the delayed deposition of new collagen, Pogrel et al. (114) showed that CO2 wounds were associated with greater amounts of hyaluronidase production vs. scalpel wounds after 3 weeks. Harmon et al. (116) studied erbium and CO2 wounds and showed more platelet cell adhesion molecule in the CO2 wounds 6 weeks after injury. All of these findings suggest that the initial thermal damage in CO2 laser injury modulates the healing response vs. wounds without thermal damage. Wound healing has been compared between CO2 laser, cautery, and scalpel surgery. Lunkenheimer et al. (106) examined minipig incisions and found that wounds that were left unsutured healed best after scalpel surgery, with fine scars after 16 days, whereas the laser wounds and cautery wounds tended to appear as oval dents “filled up” by


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pinkish scars. They identified a microscopic transition zone “in a fairly unchanged condition that was particularly engaged in the process of tissue restoration.” Sloughing occurred above and within the transition zone. Hall examined sutured CO2 incisions and scalpel wounds and found that sutured laser wounds were weaker than scalpel wounds in rats after 21 days, but that by 40 days the wounds showed similar tensile strength. The delay in healing was blamed on the shedding of the eschar, which occurred around the sixth to eighth postoperative days just deep to the zone of basophilic staining collagen. Kamat et al., examined both sutured and unsutured human skin wounds after CW laser irradiation. They found that inflammation was delayed in laser wounds and that there was sloughing collagen, beneath which a new epidermis was formed (42). However, in deeper sutured wounds, there was also some entrapment of denatured collagen that remained unchanged and mummified for as long as 10 weeks after surgery. This study and our own results suggest that damaged collagen is handled differently in the skin depending on the depth of the damage, where superficially damaged collagen is more likely to be rapidly degraded within 1–2 weeks even when re-epithelialization has occurred over the specimen. In brief, CO2 laser-induced open wounds heal differently from wounds of similar depth with less than 75 mm RTD. They show delayed re-epithelialization and a different pattern of wound contraction. The wound contracts immediately, relaxes to a degree, and then undergoes a second contraction vs. dermatome, dermabrasion, or erbium:YAG laser wounds, which show little or no immediate contraction, then a one-time contraction and subsequent relaxation beginning about 2 –5 days after injury. Also, there is more fibroplasia per micrometer depth of injury and different patterns of enzymatic and cytokine activity in CO2 laser-induced wounds (50).

5.

ULTRASTRUCTURE AFTER CO2 LSR

Zweig et al. (61) studied both routine histology and electron microscopy in laser excisions and divided the zones ultrastructurally into two zones: (1) coagulation zone, where collagen fibers lost their periodicity, and (2) a transition region, where the periodicity of collagen fibers was partly retained. He also correlated the collagen changes seen in laser excisions with collagen changes after exposure to various controlled temperatures in a hot bath. In the bath, the minimum coagulation temperature was 738C, and the transition zone minimum temperature was 578C. Unfortunately, the exposures in the hot bath were for 160 s, much longer than the brief laser exposures. Undoubtedly, the temperatures required for similar collagen changes during short laser exposures would be much higher. More recently, Kirsch et al. (117) and Collawn et al. (118) have published separate studies on the ultrastructure of CO2 LSR with millisecond domain CO2 lasers. Kirsh et al., described two zones of damage, where Zone 2 represented a transition zone and, as in Zweig’s study, in this zone collagen fibers showed an increased cross-sectional area consistent with linear shrinkage. Zone I represented the tissue surface with more severely damaged fibers whose ultrastructure showed no distinct fibrillar component. Collawn et al., suggested that loss of the extracellular matrix rather than collagen shrinkage was responsible for the skin tightening seen during LSR.

6.

APPLICATIONS

The appeal of the CO2 laser is largely based on its utility, which increases rapidly with increasing physician skill. Since water is the chromophore, almost every skin lesion is a

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potential target. However, one must examine the selectivity of the laser before deciding that it is a better choice than other wavelengths that either target discrete chromophores or allow for shallower tissue effects due to higher water absorption, such as the erbium:YAG laser. Unlike most of the other lasers in this book where selectivity is based on spatial confinement of injury to a discrete target the CO2 laser’s selectivity is based only on how precisely the block of ablated or heated tissue matches the dimensions of tolerability of the skin for scarring and dyspigmentation. As long as everything within the block of tissue vaporized or heated can be sacrificed without adverse side effects, the CO2 laser is an attractive “what you see is what you get laser.” Once the CO2 laser light impacts on the skin, there is immediate absorption, so that the injury is always top to bottom unless one irradiates the skin from the undersurface, which is a technique used by some physicians. For this reason, the CO2 laser demands a high level of operator practice and skill to achieve reliable results. It follows that with greater use, one finds that the laser is as good or nearly as good as some of the pigment selective or vascular selective lasers for particular lesions. In the ensuing discussion of applications, if not specified, wiping with either a H2O2 or a saline soaked gauze pad or applicator stick is done between serial passes with the CO2 laser. Also, in all applications using a defocused CW mode, the reader should assume that an “airbrush” technique was used for plaque-like lesions.

6.1.

Applications Where the Laser Performs Better Than Most Other Modalities (In Addition to Resurfacing—See Chapter 29)

Rhinophyma can be treated with excellent results with the CO2 laser in either the pulsed or the CW mode (Fig. 5.4). The author exclusively used the CW mode until recently.

Figure 5.4 (a) Rhinophyma preop. (b) Just after surgery, 8 – 20 W CW CO2 laser, 1 –4 mm spot, airbrush technique. (c) 12 Weeks after surgery note improved cosmesis and lack of scarring.


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The advantage of this mode is that one can combine heating and vaporization by varying the spot size and power. By decreasing the former and increasing the latter, vaporization is observed, and the nose can be sculpted to its original shape. My recently adopted technique is to initiate treatment with 15–25 W in the defocused mode, using a pirouetting motion to vaporize the nose to a roughly desirable contour, followed by fine tuning in the UltraPulse mode. By using the high-energy short pulse mode at the end of the case, charring can be avoided and more of a “what you see is what you get” result is observed. One should use older photographs of the patient to guide the final silhouette. Also, one should periodically view the nose from different positions to ensure that the contour is even. Finally, no matter what method is used, occasionally one will encounter bleeding, in which case either aluminum chloride may be used or the laser can be used in the defocused mode for coagulation. One treatment end point is achieving the final nasal contour and another is using the sebaceous glands as a guide to treatment. Normally, if one can squeeze sebum from the glands near the end of the procedure, the ablation plane is not too deep. Several investigators have reported their experience in treating rhinophyma with the CO2 laser. Wheeland et al. (119) used a combined laser excision and vaporization approach, employing a focused 0.2 mm spot for excision with 15 W and an irradiance of about 50,000 W/cm2. The nose was grossly reshaped in this manner by cutting off the excess tissue. Next, they defocused the beam to 2 mm and decreased the power to about 4–5 W. This was used to gently smooth the remaining surface irregularities. Karim and Streitmann (120) retrospectively analyzed 20 patients after treatment with 12 W CW, using a combination of 0.2 mm spots for excision and defocused beams for vaporization. Simo and Sharma (121) reported three cases with good results. They used 5 W CW and a 1 mm spot to mark the perimeter of the field, then 15 W with a 2 mm spot to vaporize excess tissue. El-Azhary et al. (122) treated 30 patients with a 0.1 mm spot to excise, followed by a defocused beam at 15–20 W. They reported one case of scar and one case of leukoderma. 6.1.1.

Trichoepitheliomas

Both CW and UltraPulse lasers have been used to treat these lesions (123–127). Generally, the end point has been destruction to a level just below the adjacent skin surface. Deeper ablation results in scarring and more superficial ablation results in early recurrence. The typical laser settings in CW mode include 1–3 mm spot sizes and powers of 2–5 W. We have been using the 1 mm spot size in UltraPulse mode at 200–250 mJ, defocusing and focusing the beam to accommodate the skin dimensions and the ratio of ablation to heating. 6.1.2.

Adenoma Sebaceum

We have used both pulsed and CW lasers for these papules (Fig. 5.5). One can use the CO2 laser with a low power of 2 – 3 W and 1 –2 mm spot size with short application times of 0.25 – 0.5 s to gently vaporize/heat the papules so that they shrink over the subsequent few weeks. Alternately, one can use the pulsed laser to vaporize the lesions, but we have found that the pulsed mode results in mild bleeding in some areas. Once the exophytic portion of the lesions has been removed, the base at a different session 4 – 6 weeks later undergoes vascular lesion laser treatment. Janniger and Goldberg (128) performed a comparison study of argon and CO2 lasers (5 W, 2 mm CW) in a single-patient side-by-side study and found overall that the CO2 laser showed superior cosmetic results. We have similarly found that the CO2 laser works better than a vascular specific laser, at least for the exophytic component of the lesions. Boixeda et al. (129) compared CO2 , argon, and pulsed dye laser (PDL) in 10 patients and concluded that the CO2 laser overall was a better therapeutic tool.

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Figure 5.5 (a) Tuberous sclerosis patient preop. (b) Six months after treatment of exophytic lesions with CW CO2 laser, 2 – 3 mm spot, 2– 4 W, 0.5– 1 s exposures.

6.1.3.

Common Warts

Even with the large armamentarium of available wart treatments, including interferon, 5-fluorouracil, imiquimod, as well as traditional therapies such as liquid nitrogen, some warts persist. Generally speaking, CO2 laser is not a first-line destructive therapy because the pain, while usually not severe, tends to be prolonged vs. cryosurgery. The healing time is prolonged, some scarring is very likely in most areas, and there is a requirement for injectable anesthesia. However, warts which have persisted over 1 year despite therapy, especially if they interfere with some aspect of the patient’s life (either functionally or through significant cosmetic disfigurement), are good candidates for CO2 laser treatment (Fig. 5.6). Advantages of CO2 laser therapy include precise control of the

Figure 5.6 (a) Periungal wart preop. (b) Immediately postop, note that the wound is carried out deep into the sulcus. (c) Four weeks postop there is no evidence of recurrence and the nailfold contour is returning to normal.


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depth of injury, usually adequate hemostasis, immediate gratification of having the wart removed, and good “cure” rates. Technique: If a wart is very exophytic, I use higher PDs of 15 –20 W and a 2 mm spot size first, to vaporize the wart to a slightly raised level. The goal is to move quickly so as to minimize char. Residual debris is wiped away with moist gauze. At this point, a curet is use to separate the denatured tissue from the dermis. If the heating plane at the dermal – epidermal (DE) junction is sufficient, the wart will separate without much difficulty and the underlying dermal base will be only slightly heated. If one undertreats, the unheated remaining epidermis will still be attached to and interdigitated with the underlying dermis. Another pass will then need to be made, as attempting to forcibly separate the wart with the curet will result in unnecessary bleeding. Once the denatured wart is separated, the base should be heated gently with a lower power of 3– 5 W. Also, a rim 2 –5 mm from the clinically obvious wart should be heated. The underlying dermis can be identified by the appearance of skin lines or the observation of slight tissue shrinkage. CO2 laser treatment is often complicated by previous aggressive CO2 laser or liquid nitrogen therapy, and foci of wart can be intermixed with scar. Normally this requires that the entire previous treatment area be vaporized away. Otherwise, the recurrence rate will approach 100%. Periungal warts (Fig. 5.7) must be removed down to the level of the sulcus of the lateral nail fold (130 – 132). This requires that the physician be fairly aggressive in curettage. It is easy to stop the treatment too soon, mistaking the “hard” wart tissue in the nailfold for normal dermis. When the warty tissue has been completely removed the surface should be smooth and resist further curettage. One caveat: One should be careful not to continue to heat the remaining dermis in the nailfold, as often it is only hundreds of micrometers thick. Occasionally, one will expose focal fatty globules, which is an indication of too deep treatment. Bleeding can be a problem in wart treatment with the CW laser, particularly in the periungal area. We have found that use of a tourniquet greatly aids in hemostasis. For lesions where a tourniquet is not possible, pressure at the periphery of the lesion will usually slow down the bleeding enough so that a defocused beam can be applied to achieve hemostasis. Ashinoff et al. (133) found human papillomavirus (HPV) in 60% of SCC in the periungal region, therefore if the lesion in the nailfold is longstanding, a biopsy is warranted in adults. The literature contains many reports of CO2 laser treated verrucae. In a study by Street et al. (134) of recalcitrant periungal lesions, there was a 71% cure rate after 1 year, where the cure end point was the return of dermatoglyphic skin lines. Overall, long-term remission rates in CO2 laser wart treatment are difficult to assess; studies

Figure 5.7 (a) Preop view of a wart on the little toe. (b) 12 Weeks postop, note excellent result. Wart is still clinically resolved 1 year later.

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have suggested 5-year cure rates of 50 – 80% (130,131,135 – 137). Patient satisfaction with CO2 laser treatment is good; Sloan et al. (138) found in a retrospective evaluation of resistant warts that 71% of patients would have the treatment again, with the major adverse effect being pain. If common verrucae are in a cosmetically compromising position, one can use interferon to complement the destructive effect of the laser (139). 6.1.4.

Condyloma Acuminata

The CO2 laser has been used extensively in the treatment of condylomata. Although the laser is effective in the removal of the clinical lesions, viral particles can be recovered after laser treatment in peripheral skin. The literature reports cure rates ranging from 31% to 95% (140 – 145), with higher recurrence rates with 16/18 vs. 6/11 HPV subtypes. Lassus et al. (146) reported good clinical clearing at 24 months of 50% of resistant condylomata in 38 males after three treatments (3– 5 W CW, 2 mm spot). However, only 26% of patients showed elimination of the HPV genome. They concluded that although CO2 laser is ineffective in eradicating the HPV genome from therapy-resistant penile warts, the treatment reduces the recurrence of atypical changes and visible warts. Ferenzcy et al. (147) found HPV as far away as 1.5 cm from the clinical lesion. Duus et al. (148) found higher rates of recurrence after CO2 laser vs. electrocautery in vulvar condylomata. Recently, it was reported (149) that in condylomata treated by CO2 laser, there was no change in T-cell subsets, that is, the ratio of suppressor to helper cells was not changed by clinical elimination of the wart by CO2 laser. The CO2 laser has been especially helpful in pediatric patients under general anesthesia. Johnson et al. (150) examined 17 children with condylomata in a retrospective analysis and found 4/17 with early recurrences (within 3 months) using RSP mode at 3 – 5 W and 2 mm spot. After retreatment of the four recurrences, only one recurred. Davis and Noble (151) treated multiple condylomata with CW CO2 laser and found that the recurrence rate was 9/20 with laser alone and only 3/14 with laser plus sublesional interferon alpha 2 beta. Technique: For multiple very small lesions, acetowhitening is performed just prior to the procedure. Next, the area is anesthetized with lidocaine. We use the laser in CW mode with powers from 3 to 8 W, using lower powers for smaller lesions (2 –3 mm papules) and higher powers for more extensive exophytic lesions. The gross raised portion of the lesion is vaporized using a defocused spot of 1 –3 mm. The beam is brushed over the wart until whitening occurs. Wiping with wet gauze should allow easy separation of the wart from the underlying dermis. Using magnification loupes, any residual wart can be vaporized, and the surface is rewiped; this series is repeated until slight shrinking of the surface is observed. Finally, a 5 –10 mm rim of clinically normal tissue is grayed with a low-power brushing technique. Some caveats: Bleeding can be a problem in the treatment of some larger lesions, especially in the perianal region. Stretching the skin surface during lasing will decrease the risk of bleeding. Gentle vs. vigorous wiping also tends to reduce the likelihood of disrupting the vessel walls. Finally, for some smaller lesions, with skill one can use one pass to eliminate the lesion, leaving the browned dome intact without wiping. This technique increases the recurrence rate, as a portion of the deeper wart might persist, but the cosmetic result is enhanced, particularly in pediatric patients, where making a second pass tends to result in scarring. 6.1.5. Nail Matrixectomy Like phenol and electrosurgical ablation, the CO2 laser can be used to eliminate the nail matrix conditions such as chronic ingrown nails (152).


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Technique: The portion of the ingrown nail is removed with a nail splitter and hemostat, and the matrix visualized. Next the proximal nailfold skin is retracted and the laser is used in 0.5 s gated pulses in the 3 –5 W CW mode with a 1 mm spot. The area is allowed to heal by secondary intention. Complete ablation of the matrix sometime requires additional treatments. 6.1.6. Earlobe Keloids Earlobe keloids are particularly well suited to treatment with the CO2 laser. As long as most of the keloid is vaporized and care is taken in the postoperative period, we have found a low rate of recurrence and a high degree of patient satisfaction. We generally use the 3 mm handpiece with the UltraPulse laser with maximum pulse energy and a high repetition rate of 20 –40 Hz. We vaporize the lesion down to a point where one feels and sees very little keloid at the base. This requires many passes, so many that we do not count how many times we have treated one area but rather continue to vaporize until the area is contoured to a good end point. We generally use our thumb to push the keloidal tissue toward the laser handpiece. After many passes, one will begin to feel mild heating on the finger as the keloidal tissue is vaporized. The pulsed mode allows for relatively char-free tissue removal. However, because we do not try to avoid pulse stacking, the thermal damage is probably hundreds of micrometers deep rather than the 60 – 100 mm after traditional CO2 LSR for nonexophytic lesions. One can easily see the coarse collagen fibers in the keloid as the lesion is vaporized away. Remarkably, even though a substantial amount of tissue may be removed, we have not encountered any major loss of contour of the lower earlobe. Also, except for some mild hypopigmentation at the center of the laser site, the lesions tend to repigment after several months. In one patient we treated one keloid with the CO2 laser and the other with standard excisional surgery by shelling out the keloid and using the overlying skin as a graft and found the results to be as good or better on the laser treated side, with the laser treatment taking about a quarter of the time. For dumbell keloids, we generally ablate from both sides, leaving only a big-sized keloid remnant at the center. Conejo-Mir et al. (153) have reported that CO2 laser ablation plus interferon alpha 2 beta has resulted in better clearing than CO2 laser alone. Perilesional and sublesional interferon injections were performed three times a week for 3 weeks. As expected, earlobe keloids responded better than other sites. Stern and Lucente (154) found no difference in recurrence rates after CO2 vs. scalpel excision of earlobe keloids. Kantor et al. (155) excised 16 keloids, many of the “dumbell” type, on the ear with CO2 laser and found no recurrence after 6 months. They used a focused beam (0.1 – 0.2 mm) and closed the lesion anteriorly if the excision resulted in a through and through lesion. Although there were four early hypertrophic scars, these resolved with one to two IL injections of 40 mg/mL Triamcinolone acetonide. Recently imiquimod cream has been advocated postoperative after keloid excision vaporization. 6.1.7.

Larger Keloids and Nonearlobe Keloids

The literature shows considerable variability in the success of the CO2 laser in the treatment of keloids. Different investigators have used various techniques and postoperative interventions, so that advice based on sound prospective studies is generally lacking. Also, keloids have been removed both by laser excision and laser vaporization, and with and without primary closure in the case of laser excision. Despite all of these variables, some useful information can be summarized. Overall, studies have shown

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that the CO2 laser probably offers little advantage over excisional surgery of keloids (156 –161), but in some cases the CO2 laser might represent the best option. Like most other laser surgeons, we have found that keloids in scalp and beard areas almost always recur if the lesions are merely vaporized to the level of the dermis. Stucker and Shaw (156) examined 37 patients with keloids that were excised with a 1 mm spot and 10 W. For nonearlobe keloids they found that with second-intention healing, 25/31 lesions recurred, usually at the edge of the wound, within 3– 4 weeks of treatment. They showed that aggressive early IL corticosteroid injections seemed to determine the final outcome more than the laser’s use as the excision modality. Lim and Tan (162) studied CO2 laser use for keloids and found that deltoid keloids allowed to granulate did no better with laser than after scalpel excision. Norris (159) followed 23 patients after laser excision of nonfacial keloids and likewise found a 100% recurrence rate after secondintention healing. He used 8– 14 W and a 0.75 mm spot and concluded that laser was no better than scalpel for recurrence. We have also treated some larger keloids with the CO2 laser, combining vaporization and excision with variable success. Typically, we have found that the keloids on the chest return, and have performed test sites on any patient where this treatment is entertained. In one patient, we removed several large keloids with postoperative radiation therapy (XRT), and after 1 year the keloid had not returned. One recently published study supports the use of the CO2 laser in some keloids. This is based on CO2 laser irradiation of cell cultures from normal and keloidal tissue (163). In this study, CO2 laser treatment was associated with higher levels of beta fibroblast growth factor (b-FGF) than untreated keloid controls. Because higher levels of b-FGF tend to inhibit excess collagen secretion, the authors felt that superpulsed CO2 laser exposure might be beneficial in the treatment of keloids. More recently, the same group has reported that in chest keloids, the laser tends to cause decreased b-FGF levels vs. untreated keloid controls whereas facial keloids showed the opposite pattern, suggesting that the lower b-FGF level might be responsible for the high rate of scar recurrence after CO2 laser treatment in the chest area (164). 6.2.

Acne Keloidalis Nuchae

We have treated the small papules of acne keloidalis nuchae with the CO2 laser, but have found that the recurrence rate is high unless the lesions are vaporized to the cutaneous fat and the hair follicles are destroyed. Unfortunately, at this level, blood vessels may be encountered that are larger than 0.5 mm and the lesions often bleed profusely, requiring electrosurgical coagulation. For larger plaques of acne keloidalis nuchae, we have used the CO2 laser as an excisional tool and found that bleeding was much better controlled by using a blended electrosurgical cutting device. Kantor et al. (165) treated eight patients with the CO2 laser and found that as long as the lesions were excised to the level of the fat, there were no recurrences. Lesions were allowed to heal by secondary intention. The primary advantage of the use of CO2 laser in acne keloidalis nuchae is hemostasis vs. cold steel. Related to the use for acne keloidalis nuchae, the CO2 laser has also been used to excise areas of dissecting cellulitis of the scalp, after which the wounds were allowed to heal by secondary intention (166). 6.2.1.

Pyogenic Granuloma

Pyogenic granulomas (PGs) (68,167 –169) respond well to CO2 laser vaporization, provided that the level of destruction is adequate (Fig. 5.8). The author has treated many PGs that have recurred after electrodesiccation and curettage (ED&C) and cryotherapy.


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Figure 5.8 (a) Pyogenic granuloma preop, lesion had failed two ED&C attempts and one CO2 laser attempt. (b) Note depth of vaporization with CW CO2 laser, 1 – 3 mm spot, 5– 8 W. (c) Six months postop there is no recurrence and there is excellent restoration of the distal digit contour.

In most cases, the lesions have responded to CO2 laser in CW mode after only one treatment (Fig. 5.8). There have been reports of satellite lesion formation after treatment of PG, but only one case after CO2 laser treatment, and this occurred after laser excision, not vaporization (169). Technique: After injectable anesthesia, the lesion is vaporized with 3 –5 W power and a 2– 4 mm spot. Once the lesion is grossly flush with the surrounding skin, the denatured friable surface is curetted. Normally, this reveals a central feeder vessel surrounded by dermis or fibro-fatty tissue. At this point the vessel is vaporized using a more focused spot that is just large enough to accommodate the diameter of the vessel and the surrounding tissue is lightly grayed with a defocused beam. The key to effective one-time treatment is the depth of destruction. Patients who have been referred after treatment failure have invariably noted that the initial treatment had been more superficial. 6.2.2.

Actinic Cheilitis

Until recently the CW mode was used almost exclusively for widespread actinic cheilitis. Powers from 3 to 8 W using defocused 2– 4 mm beams were typically employed (18,157,170 – 178). The end point after the first pass in CW mode is white bubbling of the surface (opalescence). Higher powers will result in charring unless the handpiece is moved very quickly. This is wiped away with saline-soaked gauze. In mildly damaged areas, a bright pink papillary dermis is exposed. However, in areas where there is severe actinic damage, one sees a yellow-gray surface. Normally, an additional pass is performed in this area with a very low power of about 2 W for 0.5– 1 s. The importance of moving the handpiece in a rapid brushing manner cannot be overstated. When using the CW mode, the hand becomes a scanner, limiting the dwell time in a somewhat primitive manner, but one that becomes increasingly precise and reliable with practice.

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Recently, Dufresne and Curlin (175) reviewed 140 patients in seven studies. They found 15 cases of scarring and an average of 21 days for healing. They found that there was a low failure rate and better results than with trichloroacetic acid peel. Clearly, there is much variability in the literature results, presumably at least partly due to variability in technique. Sexton (179) reported correctly that since actinic cheilitis is an epidermal lesion, the injury should be limited to this top layer of skin. Johnson et al. (180) used histology to correlate clinical and microscopic findings after laser treatment and found that there were three depth categories which could be matched to wound color. Superficial to deep, these colors were pink, white/gray, and white coarse. The authors advised remaining in the two most superficial planes. We have encountered the same planes. However, one can see various surface colors after even a first uniform “light” pass of the laser. It follows that the pretreatment variability in the depth of solar damage also determines the spectrum of surface colors. Accordingly, we suggest the whiter areas are those focal areas with the greatest clinical damage prior to treatment. Moreover, we suggest the lack of surface pinkness is not only due to deeper treatment, but also due to pre-existing fibrosis in these areas, as well as increased acanthosis and interdigitations between the lesion and the underlying dermis. Zelickson and Roegnik (171) treated 43 patients and found good results after one laser pass (3–5 W, CW, 2 mm spot). He encountered three small postoperative scars that resolved after treatment with IL triamcinolone acetonide. Robinson (172) found in a prospective study that the CO2 laser was a better choice than 5-fluorouracil or 50% trichloroacetic acid, with decreased recurrence rates vs. those modalities after 4 years. David (176) treated eight patients and found good results with a rapid laser sweep with 15 W and 3 mm spot. He wiped after one pass and then stopped unless there were persistent white areas. Fitzpatrick et al. (18) reported 35 patients treated with either RSP mode or CW mode. They found that if the length of the envelope of superpulses or the length of a mechanically shuttered CW “pulse” was limited to ,50 ms, there was no difference in outcomes between these two regimes. They also found that both CW and continuous SP modes resulted in the same incidence of side effects. Their conclusion was that the repetition rate of the RSP mode (250 Hz) was so high that there was insufficient time for interpulse cooling. More recently, we have used the UltraPulse laser in pulsed mode for actinic cheilitis. We do not feel the technique is necessarily better than our older CW technique, only more reproducible and safer. On the first pass, we use the 3 mm Tru-spot handpiece and a pulse energy of 350– 400 mJ. After wiping with wet gauze the epidermis is removed, after which a second pass is made with the pulse energy reduced to 250 mJ. Additional passes are made to areas with severe photodamage (Fig. 5.9). These areas are identified by a whitened surface. We have noted that H2O2 is useful in wiping after the first pass, as its application helps to identify residual epidermal fragments. In retrospect, we suspect that some of our early recurrences were due to incomplete removal of focal thickened epidermis when using saline-soaked gauze. With saline, the residual epidermis is more difficult to distinguish from the sometimes fibrotic dermis. The H2O2 causes the epidermis to whiten dramatically, and with gentle use of a curette, the epidermis can be separated from the dermis. 6.2.3.

Sebaceous Hyperplasia

This is one of the more rewarding lesions to treat. The 1 mm handpiece is used with the UltraPulse laser, and the distance between the skin and handpiece tip is varied to accommodate the size of the lesion, which is usually about 1 – 2 mm. A pulse energy of 200 mJ is used, and a few overlapping passes are made to expose the yellow fatty nodules. Once exposed, these punctate 0.5 mm lobules are treated with additional


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Figure 5.9 (a) Preop view of 40-year-old white female (WF) with actinic cheilitis. (b) Immediately after treatment with two UltraPulse laser passes at 350 mJ with 3 m spot. (c) Appearance 4 weeks after treatment; note smooth surface.

pulses until they are either extruded are heated. The final result is a slight dell that resolves uneventfully in 1– 3 months. 6.2.4.

Epidermal Nevi

Although the histology suggests an epidermal lesion, there are abnormalities of the dermis that result in rapid recurrence if only the epidermis is removed. We have used electrodesiccation, dermabrasion, and the erbium:YAG laser, and have found that the CO2 laser and erbium:YAG lasers result in the best combination of excellent cosmesis and long remission. We use the UltraPulse laser in the initial pass, usually with the 3 mm handpiece and a pulse energy of 450 – 500 mJ. This results in epidermal ablation at the center of the spot, and after carefully heating the epidermis, the denatured epithelium can be wiped away. With magnifying loupes, the remaining areas of altered dermis can then be visualized. Usually, one can see fine papillomatosis where the epidermal nevus remains. At this point, we change to the 1 mm handpiece and ablate the remaining areas with pulse energies ranging from 150 to 250 mJ. The handpiece can be focused or defocused to either heat or ablate. As the handpiece is moved closer to the lesion, one increases the fluence and a louder pop is heard. After a few passes, the papillomatosis disappears and the area is smooth. We do not try to achieve complete removal of this surface finding, but rather “yellow” it slightly with the CO2 laser. The RTD is usually sufficient to obtain long-term remissions without significant scaring or pigmentation changes. In a recent study Cohen et al. (181) compared the CW CO2 laser and UltraPulse and found no significant differences in the two with respect to cosmesis or side effects. Losee et al. (182) used the FeatherTouch mode (120 W with 200 mm handpiece) to remove a large epidermal nevus. Hohenleutner and Landthaler (183) treated a large epidermal

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nevus with 20– 25 W CW and a 2 – 3 mm spot with a good result. They used yellowing of the dermis and loss of papillations as an end point. Ratz et al. (184) treated 15 patients with epidermal nevi with 15 –20 W and a 2 mm spot and noted scarring on the torso. They subsequently decreased the power to 5 W and noted better results. 6.2.5.

Syringoma

Syringomas are another adnexal tumor that can be easily treated with the CO2 laser (Fig. 5.10). We have used both the CW mode at a low power of 1– 3 W, with 0.1 s mechanically shuttered “pulses,” as well as the UltraPulse mode with the 1 mm handpiece. We have found that the UltraPulse mode is more elegant in that one can ablate the lesions by 100– 200 mm increments. Our typical end point is removing about half to two-thirds of the whitish lesion. This results in a small dell in the skin that heals with minimal hypopigmentation and scarring. Dark-skinned patients should be warned that there will usually be some hyperpigmentation starting about 3 weeks after the procedure. This usually resolves within 2 –3 months with or without bleaching creams. We normally do a test site with one or two lesions prior to treating an entire area (185). Wang and Roenigk (186) treated multiple syringomas with the SilkTouch (5 W, 125 mm handpiece) laser with one to three passes with good results. Wheeland et al. (187) treated 25 patients using 5 W and 2 mm defocused mode. They used 0.1 s gated bursts for each lesion. Two to three passes were required to remove the glistening white tumor. Healing was complete within 7– 10 days. 6.2.6.

Xanthelasma

Xanthelasma has been treated with both the CW mode as well as the pulsed CO2 laser. Apfelberg et al. treated six patients with the superpulsed CO2 laser (188). They used magnification loupes and 10 W average power and focused the beam in the initial pass, followed by a defocused beam and curettage to remove any remaining yellow material. Alster and West (189) have reported treatment with the UltraPulse laser, and we have treated seven patients in the past 4 years with both erbium:YAG and pulsed CO2 lasers. Our approach is to use the 1 mm handpiece with the UltraPulse and defocus the beam in the initial pass to denature the epidermis, followed by a more focused beam to pick out the remaining yellow material. Typically, even when some material remains grossly, the subsequent fibrosis masks the yellow color well; furthermore, treatment to remove all of the pigment increases the risk of pitted scarring (Fig. 5.11).

Figure 5.10 (a) Syringomas preop in 25-year-old white male (WM). (b) Eight weeks after treatment. Some lesions were treated with the UltraPulse laser using 150 – 250 mJ pulses with 1 mm spot. Others were treated with CW CO2 laser at 2 W, 1 mm spot with 0.5– 1 s gated “pulses.”


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Figure 5.11 (a) Xanthelasma preop. (b) Just after treatment with the UltraPulse laser at 200 – 350 mJ and 1 – 3 mm spot. Note that some yellow material remains at the end of treatment. (c) After 6 weeks, note good cosmetic result.

7. 7.1.

LESIONS THAT MIGHT BE TREATED EQUALLY WELL WITH OTHER MODALITIES Seborrheic Keratoses

The CO2 laser is a reasonable choice for treatment. We have treated patients with both CW and UltraPulse modes and have found that the pulsed mode results in faster healing and easier identification of end points (Fig. 5.12). The lesion can be vaporized away after many passes of the UltraPulse CO2 laser with 500 mJ and 3 mm spot size. Care should be taken near the base of the lesion so that unnecessary heating and subsequent pigmentation changes and scarring do not occur. Fitzpatrick et al. (17,18) treated seborrheic keratoses in both CW and RSP modes and found only a slight advantage in the RSP mode, once again supporting the concept that rapid overlapping pulses offer little advantage in RTD vs. conventional CW vaporization. 7.2.

Dermatosis Papulosis Nigra

We treat DPN with the 1 mm spot size with the UltraPulse laser. For smaller lesions, usually one 100–150 mJ pulse will desiccate the lesion adequately enough so that it falls off after a few days. Alternatively, the CW mode can be used at 1–2 W for 100–150 ms. 7.3.

Neurofibromas

We have used the UltraPulse laser, 1 –3 mm spots with pulse energies ranging from 200 to 500 mJ, and found that, after exposure of the dermis, the remaining tumor, which has a rubbery consistency, can be manually expelled by gentle pressure around the wound.

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Figure 5.12 (a) A Seborrheic keratosis in the right infraorbital area preop. (b) Larger portion was treated with the UltraPulse laser at 400 mJ, 3 mm spot up, and three to five passes. The smaller portion, to the reader’s right, was treated with CW CO2 laser at 5 W and 2 –3 mm spot. (c) Both sites showed good results after 10 weeks.

Following this, additional passes of the laser vaporize the rubbery lesions, and the wounds are allowed to heal by secondary intention. The areas heal with slight hyperpigmentation, which resolves after 6 months. Roenigk and Ratz (190) used the CW CO2 laser with a 2 mm beam and power of 4– 6 W (160 W/cm2), in a similar manner. Becker (191) treated a patient with multiple pedunculated and sessile lesions. He used the cutting 0.2 mm spot to excise the stalks in the pedunculated lesions, and a defocused beam at 35 – 60 W CW while squeezing the rubber nodule outward to remove the sessile lesions. 7.4.

Steatocystomas

We have treated these tumors of the sebaceous glands by first piercing the central portion with the 1 mm spot in the UltraPulse mode, after which gentle pressure can be used to extrude the small wall, which can be vaporized with subsequent passes. The wounds are allowed to heal by second intention. Krahanbuhl et al. (192) treated a single patient in a similar fashion using the CW CO2 (1 mm spot and 5 W, 100 ms gated pulse) with good results. 7.5.

Pearly Penile Papules

We have treated two patients with this variant of angiofibromas. In one patient we used both UltraPulse and CW modes and found that the pulsed mode resulted in more bleeding and just as long a recovery period (193). As the additional thermal damage from CW application using low 1–3 W powers and short 0.25–0.5 s exposures did not result in a clinically relevant scar, we recommend this technique. Magid and Garden (194) also reported two cases treated successfully with CW laser (5 W, 0.1 s burst with a 1–2 mm spot).


7.6.

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Basal Cell Carcinoma

Basal cell carcinoma (BCC) has been treated with the CO2 laser and curettage. In early reports the pulsed or CW laser replaced the hyfercater. Because no large studies have been performed, the role of this technique is unclear, particularly since the thermal damage induced by the hyfercater might be one reason for the relatively good success of traditional electrodesiccation and curettage. Superficial BCCs logically should have the best outcome with this technique. Wheeland et al. (195) reported the use of CO2 laser with curettage in the treatment of BCC. In this study, the CW laser was used in 52 patients for superficial lesions. They used powers of 4 – 5 W and 1 – 2 mm spot size that yielded a PD of 160– 510 W/cm2. The technique resulted in light charring at the skin surface, after which removal with H2O2 gauze showed a whitish yellow base. The base was then curetted, and this was repeated with the laser until the wound base was uniformly firm and no friability was observed. They found good overall cosmetic results with a hypertrophic scar rate of only 5% and no recurrence over a mean follow-up of 19 months. More recently, Kilmer and Chozen (196) reported the use of the UltraPulse laser in the treatment of BCCs, excluding those with a known infiltrative or morpheaform pattern. They used 450 mJ pulses with the 3 mm spot after curettage. In some patients, second passes were made. In subsequently excised specimens no tumor was found after laser treatment, and lesions followed clinically also did not show visible recurrence. Humphreys et al. (197) reported their experience with high-energy pulsed CO2 treatment of BCC and Bowen’s disease. They treated 30 tumors and found that BCC responded better than Bowen’s disease, whose full depth was not vaporized in excised specimens. Curettage was not performed in this study. Grobbelaar et al. (198) treated six BCC nevus syndrome patients, with up to 110 lesions treated in one session with the SilkTouch laser. The end point was the absence of punctate bleeding. Multiple passes were made, with wiping between passes. After a mean follow-up of 20 months, no clinical or histologic evidence of recurrence was noted. 7.7.

Bowen’s Disease

We have treated one patient with erythroplasia of Queyrat of the penis with the CO2 laser in UltraPulse mode (300 mJ, 3 mm spot, two passes) with excellent results. The patient had a poor response to Efudex. As with electrodesiccation and curettage, there is no margin control with this technique, so close clinical follow-up is required. Gordon and Robinson (199) recently reported laser vaporization of the finger for Bowen’s disease (3 W CW, 2–3 mm spot) with multiple passes. A postoperative biopsy showed no recurrence. 7.8.

Hidradenitis Suppurativa

Finley and Ratz (200) reported the use of the CW CO2 laser to excise axillary and inguinal lesions in seven patients with a power of 40 W and 0. 2 mm spot. The base of the wounds was lightly coagulated in the defocused mode. Time to healing by second intention ranged from 4 to 11 weeks. Only one recurrence was noted after 10 –27 months of follow-up. 7.9.

Scar Revisions

CO2 lasers have been used to resurface scars, both at the time of the excision (201,202) as well as after traumatic wounds. Like dermabrasion, the de-epithelialization of the scarred region appears to improve the excision line. Alster et al. (203) examined the use of the

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UltraPulse CO2 laser alone vs. CO2 plus PDL in hypertrophic scars, and found that the addition of PDL helped in most cases. Grevelink and White (202) performed simultaneous LSR and punch excisions and found that the wounds healed well with minimal scarring. Their conclusion was that there was no need for the traditional 1 – 2 month delay between punch grafts/excisions and facial resurfacing. 7.10.

Chondrodermatitis Nodularis Helicus

Taylor (204) reported 11 patients treated with the CO2 laser in RSP mode. He vaporized the affected nodule and allowed the wounds to heal by secondary intention. He noted no recurrence after 2– 15 months. 7.11.

Lymphangioma Circumscriptum

Haas and Narurkar (205) recently reported the use of the UltraPulse laser where two to three passes were made or treatment was carried out until the point where no visible lymphatic drainage was observed. There was mild hypertrophic scarring but no recurrence in the same area after 2 years. Others have reported success with the CW CO2 laser for this condition (206). Because of the deep nature of the lesions, lesions usually recur regardless of the treatment modality. The author has treated two patients and has followed a patient treated with the CW CO2 laser. The CW treated patient had developed hypertrophic scarring; subsequent treatment with the UltraPulse laser (300 – 500 mJ) with multiple passes resulted in resolution of the majority of the nodules and only mild textural changes at the surface. As expected, at the periphery of the scarred areas and even within the scars, there were recurrences of the translucent nodules. 7.12.

Nevus Sebaceous

These usually broad-based plaques are vaporized with many passes to a level where most of the yellow papules embedded in the lesion are removed. The final result is a smooth pink surface. Healing is by secondary intention. Like epidermal nevi, attempts to ablate the lesion down to the reticular dermis will result in longer remission but also in a greater likelihood of scarring. Where resection is possible, because of the risk of BCC or BCC-like lesions developing in these lesions, excision should be strongly considered. Ashinoff (207) reported treatment of an extensive nevus sebaceous on the midface in a 10-year-old girl with 6 W CW power in the defocused mode in three separate sessions. The intention was to remove only the exophytic portion, as the case would have resulted in extensive scarring after surgery for definitive removal. 7.13.

Hydrocystoma

We have treated these with the UltraPulse laser with good results. Bickley et al. (208) reported a case treated with the CW CO2 laser (5 W, 2 mm spot). 7.14.

Histiocytoma or Xanthoma Disseminatum

Carpo et al. (209) reported treatment with an SP CO2 laser. We have also treated a case with the UltraPulse laser (Fig. 5.13). We used the 3 mm spot and 500 mJ pulse energy for lesions 3 mm in diameter. For smaller lesions, we used the 1 mm spot-size handpiece. This handpiece can be focused or defocused depending on the size of the lesion. Once the epidermis is removed, the yellow base of the lesions is seen. At this point the smaller


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Figure 5.13 (a) Preop view of eruptive histiocytomas. (b) Six months after treatment with the UltraPulse laser at 200–350 mJ, 1– 3 mm spot, and multiple passes.

spot is used to ablate the remaining lesion. This will leave a depression if the lesion is completely removed. We have found that leaving about 20% of the lesion at the base results in a very nice cosmetic result without recurrences. 7.15. Hailey – Hailey and Darier’s Disease The author has only used the erbium:YAG laser for Hailey – Hailey disease, and has never treated a patient with the CO2 or erbium laser for Darier’s disease. However, there are reports of treatment with the CW CO2 laser for both of these dyskeratotic processes (210 –213). In one report (212) the CO2 laser was used defocused (2 mm spot, 10 W) to vaporize to a level without apparent disease, usually after two passes. In the case series, there were varying disease-free periods. The authors noted that the papillary dermis probably must be removed for long-term remission. More recently, Kruppa et al. (214) treated two patients with the SilkTouch system with good results (6 W, three passes with 125 mm handpiece). Christian and Moy (210) treated Hailey – Hailey disease with a short-dwelltime CO2 laser and showed that more passes resulted in superior outcomes. Touma et al. (213) used the UltraPulse laser for treatment of active lesions with success, and also found that prophylactic treatment of inactive lesions led to prolonged remissions in the majority of the treated areas. They also reported some mild scarring on the chest. 7.16. Kaposi’s Sarcoma Chun et al. (215) used the SilkTouch laser with 7 W and 6 mm scan size with good results on the penis. Kaplan (55) had reported the use of a CW CO2 laser many years earlier. 7.17. Tattoos The CW CO2 laser has been used to treat tattoos, but offers only slight advantages over other nonselective means of tattoo removal. The author had treated one large cosmetic

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tattoo with the CW CO2 laser combined with urea paste, and found long-term erythema and mild textural change, along with incomplete pigment removal. Although sometimes very effective (2,216 –219), as a general rule, because of a 20 – 50% risk of hypertrophic scarring, the CO2 laser cannot be advocated as the treatment of choice, particularly if dedicated shorter-pulsed lasers are available (Q-switched lasers) in the patient’s geographic region. An exception is treating brown- and skin-colored tattoos. Often, these will darken after a test site treatment with a Q-switched laser (paradoxical ink darkening), in which case the CW or pulsed CO2 laser can be used to gently de-epithelialize the skin. The resulting extrusion of ink, particularly if repeated, can result in an excellent final cosmetic result (220). Use of the CO2 laser prior to Q-switched laser has been attempted (221). One study concluded that the disadvantages (textural changes, increased need for anesthesia, and infection) outweighed the modest improvement in tattoo lightening over Q-switched laser treatment alone. 7.18.

Disseminated Superficial Actinic Porokeratosis

We have treated one patient with extensive disseminated superficial actinic porokeratosis (DSAP) on the legs with the UltraPulse (400 mJ, 3 mm spot) with two passes. EMLA alone was used for anesthesia. After 3 months, there was no clinical evidences of recurrence and only mild hypopigmentation at the treatment site. 7.19.

Actinic Keratosis

Like DSAP, the lesions can be treated with an SP laser with multiple passes. Treatment should be aggressive enough so that the final surface is smooth, as we have observed two patients after full-face LSR who developed squamous cellcarcinoma in what appeared to be small actinic keratoses at the time of treatment. The squamous cellcarcinoma occurred within 12 weeks of LSR. 8.

LASER STERILIZATION

Laser wounds have been shown to support bacterial growth after treatment, that is, if implanted with bacteria, they show a higher rate of infection than similar scalpel wounds (222). In contrast, the CO2 laser has also been used to sterilize wounds. In these cases, the wound base is treated in the defocused mode, and this material is then excised by the laser, after which the wound is closed primarily. Wounds deliberately contaminated by Pseudomonas were shown in a rat study to be sterilized more completely than after an iodine scrub (223). Lee et al. (224) treated infected sterniotomy wounds with a CW CO2 laser, excised the eschar, and then closed the wounds with good results. Hinshaw et al. (225) reported the use of the CO2 laser to sterilize purulent wounds. They sterilized the base with a defocused beam, followed by laser excision and primary closure. Irrigation of the wound was an important contributor to the success of the procedure. 9. 9.1.

TECHNIQUE PEARLS CW Vaporization

In review of the CW applications described earlier, it becomes clear that most CO2 laser surgeons somewhat arbitrarily choose the power and pulse duration. Typically, the surgeon repeats the cycle of irradiation and inspection, continuing until almost or no


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lesional tissue remains. Fleiming and Brody (226) proposed a more logical approach to the treatment of lesions with the CW CO2 laser. They cited several limitations in the empirical techniques commonly employed in the many publications cited earlier. (1) In many cases, the surgeon’s dependence on visual differentiation of normal from lesional tissue leads to possible overtreatment and scar, or undertreatment and rapid recurrence. (2) This technique is slow, because the cycle is repeated for each lesion. This was cited as a major drawback in a publication comparing electrosection and CW CO2 in the treatment of trichoepitheliomas (227). In Fleming and Brody’s study, they used a constant power in plotting the depth of the resulting crater as a guide in planning treatments. They noted that crater depth depended on fluence for the powers used (5–18 W and 1 mm spot). They found that the application time determined the crater depth for constant power and spot size. Based on their data and our own data with SP lasers, one can calculate an ablation depth of roughly 2500 mm for a fluence of 2000 J/cm2, as long as the irradiance is .1000 W/cm2, for example, a 10 W pulse delivered with a 1 mm spot and application time of 1 s. 9.2.

Cutting

The reader should note that 15 – 25 W will give a cutting depth of 3– 5 mm with a hand movement rate of 1.5 mm/s with a 0.3 mm spot (228). Also, wet gauze should always be used as a backstop so that the beam does not injure unintended targets (229). 10.

LASER SAFETY ISSUES SPECIFIC TO THE CO2 LASER

A primary area of concern is the eye, where the cornea can be injured. In one case, the cornea was damaged during LSR and required corneal transplant to restore vision (230). Eyeshields with the CO2 laser should be metal, as Ries et al. (231) showed that plastic shields will burn with prolonged CW irradiation. In the case of LSR lasers, although nine passes were required for shield perforation, melting of the surface was noted as early as the first pass. Also, Rohrich et al. (232) noted that plastic corneal protectors melted by the third pass and produced significant heat in LSR. Black surfaces have been advocated for laser surgery, but these may deteriorate after many passes. Roughened instruments are most effective but may not always be available. Therefore, protection of the eye should include side shields to prevent corneal injury from a reflection. Wood et al. (233) found that with the exception of silver finish polish, the hazard distances for laser reflections usually extend only to the immediate area of the operative field. The teeth should be covered during resurfacing, as dentin charring and cracking have been reported (234,235). Another area of concern is fire (236). Rohrich et al. (232) noted that dry but not wet gauze produced a flame with UltraPulse and SilkTouch irradiation. Wald et al. (237) found that the UltraPulse did not start a fire in an animal study, even with supplemental 6 L/min O2 close by (at 0.5 cm separation). However, the authors caution the reader that this is only so long as combustion does not occur. Other hazards peculiar to the CO2 laser are related to the plume. There are carcinogenic nitrosamines, and some particles are either too small to be filtered by the upper airway or too large to be removed from the alveoli. These particles can cause pulmonary fibrosis. The particulate matter in the plume has a mean diameter of 0.3 mm (238). Baggish et al. (239) found that rats showed interstitial lung changes after prolonged exposure to a CO2 plume. These changes were reduced with the use of an ultra-low-penetration air filter. Smoke evacuation systems have been reported to protect animals if they can trap particles of 0.3 mm or less (239). The smoke evacuator

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should provide at least 40 CFM (cubic feet per minute) suction as the lower limit for efficient collection of debris. The nozzle should be ,1–2 cm from the treatment area (240). It has been shown that the CW laser plume contains viable bacterial spores at low irradiance (,500 W/cm2). Despite studies showing HIV in the laser plume, there appears to a low rate of infection transmission in experimental systems (241). Fader et al. (236) suggested that this is due to a low concentration of viral particles in the plume compared to a normal infective load, the use of adequate filtration and masks, or the fact that it is too early to tell. In Baggish et al.’s study (241), the PD was 500 W/cm2 and they studied DNA capture. This study showed that proviral HIV DNA was present in smoke. There was infection in cultured cells but the infection was not maintained. The study showed that most if not all of the potentially infectious debris was present in the plume. It is unclear whether HIV can be transmitted by inhalation. Garden et al. (242) found intact HPV DNA in the laser plume. Gloster and Roenigk (243) sent out a questionnaire and found that 5% of the respondents believed the plume had infected them. This percentage was not significantly different from the incidence of warts in the population. They did find a significantly higher incidence of nasopharyngeal lesions, which is consistent with the likelihood that inhalation is the primary means of transmission of the virus. They did not find a difference when a smoke evacuator was used, but admitted that the denominator was small for the unprotected group. Overall, they found that CO2 laser surgeons were no more likely to develop hand warts than their non-CO2 laser counterparts. Ideally, one should use a mask designed with a pore size no greater than 0.1 mm.

11.

NEW DEVELOPMENTS

At the time of writing, various strategies were being developed to reduce thermal damage with the CO2 laser, both in resurfacing and in incisional surgery. These strategies have included reducing the pulse duration, changing the repetition rate, employing computer scanners with temperature feedback (244), and using other wavelengths such as 9.6 mm (3). Also of current interest is the dependence of collagen shrinkage on wavelength. Presently, CO2 laser wavelengths have targeted water in the dermis and epidermis. However, using other wavelengths, one can target molecular bonds in the dermis. For example, Ellis et al. (245) found that 7.2 –7.4 mm was better than 10.6 mm in inducing collagen contraction, suggesting that selective protein absorption might provide a better clinical effect than water absorption. They also considered that collagen denaturation and contraction are not necessarily associated, so that collagen denaturation alone is not responsible for collagen shrinkage, or that collagen denaturation might look different with light microscopy at different wavelengths. Investigators are also studying metal templates that surround the incisional field. These devices conduct heat away from the site to reduce lateral thermal damage (246).

12.

PRE- AND POSTOPERATIVE CONSIDERATIONS

12.1. 12.1.1.

Preoperative Considerations Relative Contraindications

The ideal patient for treatment, regardless of disease, is either very dark or very light, as patients tend to return to their constitutive color after CO2 laser surgery. Bronzed patients with Type II and III skin are at high risk for permanent hypopigmentation with increasing depth of injury; this should be discussed with the patient within the context of likelihood


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for cosmetic improvement. Whether the hypopigmentation is relative (i.e., lighter than the surrounding tanned untreated skin) or an absolute leukoderma is probably irrelevant, because the end result is similar potential line of demarcation. Any patient with decreased adnexal structures from previous radiation therapy or even laser hair removal or electrolysis should probably receive at least a test site. This advice is controversial for laser hair reduction, as there are no reports of compromised healing in CO2 laser induced areas previously treated with hair reduction lasers. The recommended minimum time interval between isotretinoin treatment and resurfacing (and vice versa) ranges from 6 months to 2 years (247,248). Weinstein found that two out of four cases of severe scarring in a review of 1925 CO2 resurfacing patients had received isotretinoin within 2 years. 12.1.2.

Preoperative Regimen

For adnexal tumors, test sites, and small-scar abrasions, no systemic or topical medications are prescribed. We have found that topical retinoids and bleaching preparations do not appear to alter the postoperative course. 12.1.3.

Postoperative Care

With the exception of excised wounds, in which sutures should be left in 3– 5 days longer than in scalpel wounds, wounds are left to heal by secondary intention and will heal optimally when kept moist and clean. Dressings will speed healing if they are changed (at least every 2 days). We have used Silon TSR (Biomedsciences, Allentown, PA) and Second Skin (SPENCO, Waco, TX), all with good results. The most important postoperative intervention is the use of a truly effective sunscreen. Until recently, we observed an almost 100% incidence of hyperpigmentation in our Hispanic and Asian patients, undoubtedly largely due to the omnipresent sun in southern California. The increase in color typically appears around Days 13 – 19, and has been most severe in areas with slightly deeper ablation (i.e., at the edge of discrete acne scars). While some of this increased color might be due to mechanical rubbing in making second passes with the CO2 laser, we have also routinely encountered this phenomenon after the erbium:YAG laser, where absolutely no wiping with gauze was performed. Most recently, we have observed a dramatic decrease in postinflammatory hyperpigmentation with the use of Total Block Sunscreen (Total Block, Fallene Ltd., King of Prussia, PA). In patients who have used this block, starting just after re-epithelialization is complete, we have noted a significant reduction in hyperpigmentation. More disturbing than the almost always temporary, especially on the face, postinflammatory hyperpigmentation, is the delayed onset of hypopigmentation after the CO2 laser in some cases. Laws et al. (249) examined the histology of a patient after CO2-induced loss of pigment and found that there were a normal number of melanocytes, but that they were simply not making melanin. Stuzin et al. (250) examined CO2 and phenol wounds in human skin and found postoperatively that epidermal melanocytes appeared to function normally in laser treated wounds. In the CO2 laser wounds there was a more regular distribution of melanosomes. In both wound types, there were melanocytes. In the phenol wounds, there simply was no melanin.

13.

CONCLUSIONS

It is interesting that in review of the vast literature of CO2 laser in skin, the laser has not enjoyed even greater popularity in dermatology. Particularly in CW and RSP modes, the laser is a very versatile tool whose uses are only limited by the creativity of the physician.

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Becker DW Jr. Use of the carbon dioxide laser in treating multiple cutaneous neurofibromas. Ann Plast Surg 1991; 26(6):582– 586. Krahenbuhl A, Eichmann A, Pfaltz M. CO2 laser therapy for steatocystoma multiplex. Dermatologica 1991; 183(4):294– 296. McKinlay JR, Graham BS, Ross EV. The clinical superiority of continuous exposure versus short-pulsed carbon dioxide laser exposures for the treatment of pearly penile papules. Dermatol Surg 1999; 25(2):124– 126. Magid M, Garden JM. Pearly penile papules: treatment with the carbon dioxide laser. J Dermatol Surg Oncol 1989; 15(5):552– 554. Wheeland RG, Bailin PL, Ratz JL, Roenigk RK. Carbon dioxide laser vaporization and curettage in the treatment of large or multiple superficial basal cell carcinomas. J Dermatol Surg Oncol 1987; 13(2):119 –125. Kilmer S, Chozen V. Ultrapulse laser treatment of basal cell carcinomas (abstract). Lasers Surg Med 1996; 8(suppl):36. Humphreys TR, Malhotra R, Scharf MJ, Marcus SM, Starkus L, Calegari K. Treatment of superficial basal cell carcinoma and squamous cell carcinoma in situ with a high-energy pulsed carbon dioxide laser. Arch Dermatol 1998; 134(10):1247– 1252. Grobbelaar AO, Horlock N, Gault DT. Gorlin’s syndrome: the role of the carbon dioxide laser in patient management. Ann Plast Surg 1997; 39(4):366 – 373. Gordon KB, Robinson J. Carbon dioxide laser vaporization for Bowen’s disease of the finger. Arch Dermatol 1994; 130(10):1250– 1252. Finley E, Ratz J. Treatment of hidradenitis suppurativa with carbon dioxide laser excision and second-intention healing. J Am Acad Dermatol 1996; 34(3):465 – 469. Greenbaum S, Rubin M. Surgical pearl: the high-energy pulsed carbon dioxide laser for immediate scar resurfacing. J Am Acad Dermatol 1999; 40(6, Pt 1):988– 990. Grevelink JM, White VR. Concurrent use of laser skin resurfacing and punch excision in the treatment of facial acne scarring. Dermatol Surg 1998; 24(5):527 – 530. Alster TS, Lewis AB, Rosenbach A. Laser scar revision: comparison of CO2 laser vaporization with and without simultaneous pulsed dye laser treatment. Dermatol Surg 1998; 24(12):1299– 1302. Taylor MB. Chondrodermatitis nodularis chronica helicis. Successful treatment with the carbon dioxide laser. J Dermatol Surg Oncol 1991; 17(11):862– 864. Haas AF, Narurkar VA. Recalcitrant breast lymphangioma circumscriptum treated by UltraPulse carbon dioxide laser. Dermatol Surg 1998; 24(8):893 – 895. Bailin PL, Kantor GR, Wheeland RG. Carbon dioxide laser vaporization of lymphangioma circumscriptum. J Am Acad Dermatol 1986; 14(2, Pt 1):257– 262. Ashinoff R. Linear nevus sebaceus of Jadassohn treated with the carbon dioxide laser. Pediatr Dermatol 1993; 10(2):189– 191. Bickley LK, Goldberg DJ, Imaeda S, Lambert WC, Schwartz RA. Treatment of multiple apocrine hidrocystomas with the carbon dioxide (CO2) laser. J Dermatol Surg Oncol 1989; 15(6):599– 602. Carpo B, Grevelink SV, Brady S, Gellis S, Grevelink J. Treatment of cutaneous lesions of xanthoma disseminatum with a CO2 laser. Dermatol Surg 1999; 25(10):751– 754. Christian M, Moy R. Treatment of Hailey-Hailey disease (or benign familial pemphigus) using short pulsed and short dwell time carbon dioxide lasers. Dermatol Surg 1999; 25(8):661– 663. Kartamaa M, Reitamo S. Familial benign chronic pemphigus (Hailey-Hailey disease). Treatment with carbon dioxide laser vaporization. Arch Dermatol 1992; 128(5):646–648. McElroy JA, Mehregan DA, Roenigk RK. Carbon dioxide laser vaporization of recalcitrant symptomatic plaques of Hailey-Hailey disease and Darier’s disease. J Am Acad Dermatol 1990; 23(5, Pt 1):893 – 897. Touma DJ, Krauss M, Feingold DS, Kaminer MS. Benign familial pemphigus (Hailey-Hailey disease). Treatment with the pulsed carbon dioxide laser. Dermatol Surg 1998; 24(12):1411– 1414.

192. 193.

194. 195.

196. 197.

198. 199. 200. 201. 202. 203.

204. 205. 206. 207. 208.

209. 210.

211. 212.

213.

Continuous Wave and Pulsed CO2 Lasers 214.

215.

216. 217. 218. 219. 220. 221. 222.

223. 224. 225.

226. 227. 228.

229. 230. 231. 232. 233. 234.

235. 236. 237.

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Kruppa A, Korge B, Lasch J, Scharffetter-Kochanek K, Hunzelmann N. Successful treatment of Hailey-Hailey disease with a scanned carbon dioxide laser. Acta Dermatol Venereol 2000; 80(1):53– 54. Chun YS, Chang SN, Park WH. A case of classical Kaposi’s sarcoma of the penis showing a good response to high-energy pulsed carbon dioxide laser therapy. J Dermatol 1999; 26(4):240– 243. Apfelberg DB, Manchester GH. Decorative and traumatic tattoo biophysics and removal. Clin Plast Surg 1987; 14(2):243 –251. Apfelberg DB. Summary of carbon dioxide laser usage in plastic surgery. Scand J Plast Reconstr Surg 1986; 20(1):19– 24. Bailin PL, Ratz JL, Levine HL. Removal of tattoos by CO2 laser. J Dermatol Surg Oncol 1980; 6(12):997 –1001. Levine H, Bailin P. Carbon dioxide laser treatment of cutaneous hemangiomas and tattoos. Arch Otolaryngol 1982; 108(4):236 – 238. Herbich GJ. Ultrapulse carbon dioxide laser treatment of an iron oxide flesh-colored tattoo. Dermatol Surg 1997; 23(1):60– 61. Ort R, Anderson R, Arndt K, Dover J. CO2 laser resurfacing of tattoos prior to Q-switched laser treatment. 2000. Madden J, Edlich R, Custer J, Panek P, Thul J, Wangensteen O. Studies in the management of the contaminated wound. IV. Resistance to infection of surgical wounds made by knife, electrosurgery, and laser. Am J Surg 1970; 119(3):222– 224. al-Qattan MM, Stranc MF, Jarmuske M, Hoban DJ. Wound sterilization: CO2 laser versus iodine. Br J Plast Surg 1989; 42(4):380 – 384. Lee JS, Tarpley SK, Miller AS III. CO2 laser sterilization in the surgical treatment of infected median sternotomy wounds. South Med J 1999; 92(4):380 – 384. Hinshaw JR, Herrera HR, Lanzafame RJ, Pennino RP. The use of the carbon dioxide laser permits primary closure of contaminated and purulent lesions and wounds. Lasers Surg Med 1987; 6(6):581– 583. Fleming MG, Brody N. A new technique for laser treatment of cutaneous tumors. J Dermatol Surg Oncol 1986; 12(11):1170– 1175. Shaffelburg M, Miller R. Treatment of multiple trichoepithelioma with electrosurgery. Dermatol Surg 1998; 24(10):1154– 1156. Karbe E, Beck W, Englisch G, Konigsmann H, Kramer H, Peterson W, eds. Experimental Surgery with Neodymium, Holmium, CO, and CO2 Lasers. Jerusalem: Jerusalem Academic Press, 1975. Lee MS, Hunt M, Richards S. Wet gauze in CO2 laser resurfacing. Australas J Dermatol 1999; 40(4):230– 231. Widder RA, Severin M, Kirchhof B, Krieglstein GK. Corneal injury after carbon dioxide laser skin resurfacing. Am J Ophthalmol 1998; 125(3):392– 394. Ries WR, Clymer MA, Reinisch L. Laser safety features of eye shields. Lasers Surg Med 1996; 18(3):309 –315. Rohrich RJ, Gyimesi IM, Clark P, Burns AJ. CO2 laser safety considerations in facial skin resurfacing. Plast Reconstr Surg 1997; 100(5):1285 – 1290. Wood RL Jr, Sliney DH, Basye RA. Laser reflections from surgical instruments. Lasers Surg Med 1992; 12(6):675– 678. Anic I, Segovic S, Katanec D, Prskalo K, Najzar-Fleger D. Scanning electron microscopic study of dentin lased with argon, CO2 , and Nd:YAG laser. J Endod 1998; 24(2):77– 81. Lobene R, Bhussry B, Fine S. Interaction of carbon dioxide laser radiation with enamel and dentin. J Dent Res 1968; 47(2):311– 317. Fader DJ, Ratner D. Principles of CO2/erbium laser safety. Dermatol Surg 2000; 26(3):235– 239. Wald D, Michelow BJ, Guyuron B, Gibb AA. Fire hazards and CO2 laser resurfacing. Plast Reconstr Surg 1998; 101(1):185– 188.

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Nezhat C, Winer W, Nezhat F, Forrest D, Reeves W. Smoke from laser surgery: is there a health hazard? Lasers Surg Med 1987; 7(4):376 – 382. Baggish MS, Elbakry M. The effects of laser smoke on the lungs of rats. Am J Obstet Gynecol 1987; 156(5):1260 –1265. Smith JP, Moss CE, Bryant CJ, Fleeger AK. Evaluation of a smoke evacuator used for laser surgery. Lasers Surg Med 1989; 9(3):276–281. Baggish M, Poiesz B, Joret D, Williamson P, Refai A. Presence of human immunodeficiency virus DNA in laser smoke. Lasers Surg Med 1991; 11(3):197 – 203. Garden JM, MK OB, Shelnitz LS et al. Papillomavirus in the vapor of carbon dioxide lasertreated verrucae. J Am Med Assoc 1988; 259(8):1199– 1202. Gloster HJ, Roenigk R. Risk of acquiring human papillomavirus from the plume produced by the carbon dioxide laser in the treatment of warts. J Am Acad Dermatol 1995; 32(3):436– 441. Howard J, Arango P, Ossoff J, Ossoff RH, Reinisch L. Healing of laser incisions in rat dermis: comparisons of the carbon dioxide laser under manual and computer control and the scalpel. Lasers Surg Med 1997; 20(1):90 – 96. Ellis DL, Weisberg NK, Chen JS, Stricklin GP, Reinisch L. Free electron laser infrared wavelength specificity for cutaneous contraction. Lasers Surg Med 1999; 25(1):1 – 7. Spector N, Reinisch L, Spector J, Ellis DL. Free-electron laser and heat-conducting templates: a study of reducing cutaneous lateral thermal damage. Lasers Surg Med 2002; 30(2):117 – 122. Weinstein C, Ramirez OM, Pozner JN. Postoperative care following CO2 laser resurfacing: avoiding pitfalls. Plast Reconstr Surg 1997; 100(7):1855– 1866. Weinstein C. Carbon dioxide laser resurfacing. Long-term follow-up in 2123 patients. Clin Plast Surg 1998; 25(1):109 –130. Laws RA, Finley EM, McCollough ML, Grabski WJ. Alabaster skin after carbon dioxide laser resurfacing with histologic correlation. Dermatol Surg 1998; 24(6):633 – 636. Stuzin JM, Baker TJ, Baker TM, Kligman AM. Histologic effects of the high-energy pulsed CO2 laser on photoaged facial skin. Plast Reconstr Surg 1997; 99(7):2036 –2050, discussion 2051– 2055.

239. 240. 241. 242. 243.

244.

245. 246. 247. 248. 249. 250.

APPENDIX I: SAMPLE OPERATIVE NOTE Procedure: CO2 Laser Ablation (Removal) Indication: Adnexal tumor Location: Face Procedure: The patient was counseled regarding the risks and potential benefits of the procedure. After giving informed consent, the skin was hydrated with a wet towel for 10 min. Ninety minutes before surgery, a thick layer of EMLA cream was applied to the treatment site. The cream was removed just prior to surgery. Just before surgery, metal eye shields were placed after instillation of anesthetic eyedrops. The face was cleansed with Septisol solution to include a 2 cm perimeter of untreated skin. A Gentian violet pen was used to demarcate the nodules to be treated. The entire treatment area was surrounded with wet towels and the hair was wetted with sterile saline. Approximately 0.2 cm3 of 2% lidocaine with 1:1,000,000 epinephrine was injected intradermally just deep to each lesion. The lesions were treated with 175–250 mJ with the UltraPulse laser. The 1 mm spot size was used to ablate the lesion to a level where only stippled remnants of the base were observed. Bacitracin ointment was applied, and written and verbal postoperative instructions were provided. The patient will be followed up in 7–10 days. After treatment, the eye shields were removed, and postoperatively, antibiotic ointment was placed over the lesions. The patient was counseled regarding postoperative care and will return within 48 h for evaluation,


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dressing removal, and wound cleansing. The patient was discharged from the clinic in good condition.

APPENDIX II: CONSENT FORM Name I understand that Dr. will perform carbon dioxide laser surgery on my (specify location) . I understand laser surgery consists of removing a bump on my skin. I understand that despite the ability of the device to precisely remove skin, the following restrictions apply to the treatment: 1. 2.

3. 4. 5. 6.

The goal is improvement rather than perfection. There is no guarantee that the anticipated results will be achieved. There will be significant swelling, oozing, and crusting, which may last for 1 – 2 weeks. In some cases redness may persist for up to 1 year, particularly in hot weather or after exercising. Improvement may continue as time elapses after treatment. The final result may not be apparent for up to 1 year. If additional improvement is desired after this time, it may be possible to re-treat areas, at additional cost. Although pain management is a primary concern during treatment, some mild transient discomfort may occur, especially “stinging” after the procedure. Generally, the carbon dioxide laser results in skin improvement. However, there is no guarantee that the results will be permanent. In rare cases, the skin can even look worse than before treatment. This may or not be due to one of the complications or consequences of laser surgery. These are outlined below.

I understand that the following complications, although infrequent, can occur after CO2 laser treatment: 1.

2. 3. 4.

Scarring: This can occur in the form a raised or depressed red area with change in skin texture. Over time these may turn white. It is important that any prior history of abnormal scarring is reported. Infection: Despite preventive measures, infection may occur, and additional medications may be necessary for treatment. Color changes: There is a risk of temporary or permanent dark or light changes to the skin. The likelihood of side effects will be decreased by my strict adherence to written postoperative instructions. Besides caring for the wound, avoiding sunlight exposure is critical, especially in the first 12 weeks after surgery.

Alternatives to carbon dioxide laser treatment are: accepting the present skin condition, use of cosmetics, or application of other procedures, including dermabrasion, erbium laser treatment, or surgical excision (cutting the skin lesion out). I have read this form and have been given the opportunity to discuss any questions I may have regarding the nature and aims of this procedure. Patient Witness

Date Date

Surgeon

Date

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Ross

APPENDIX III: SAMPLE POSTOPERATIVE INSTRUCTIONS 1.

2. 3.

4. 5.

6.

7. 8.

Immediately after treatment, an antibiotic with or without a dressing will be applied. Any dressing will be removed 1 –2 days after treatment. The dressing should be left alone until your follow-up visit. Avoid strenuous exercise for 10 days. Walking before sunrise and after sundown is recommended. There may be swelling after treatment, especially around the eyes (they may even be closed shut for 1 day). This will resolve within 3 days. An ice pack may be placed over swollen sites once the dressing has been removed. This may be done as often as 5 –10 min every hour while awake. Sleeping with your head elevated may reduce swelling (use two pillows). For the next 1–3 days, the wound should be cleaned at home by applying a dilute vinegar solution (about one teaspoon vinegar in one cup water) with a cloth or gauze. After soaking with this for 10–15 min, any excess crusts can be gently removed by using a Q-tip. Cleaning should be done often enough to keep the face clear of cumulated debris. This may require three to five sessions per day for the first 3 days. Occasionally, pinpoint bleeding may occur; this can be stopped by applying gentle pressure for several minutes. After cleaning the wound, a petrolatum-type ointment or antibiotic ointment should be applied. You are encouraged to allow shower water to irrigate the wound. Hair can be washed at the same time, preferably only with baby shampoo until after 5 days. You should not apply soaps to the open skin. Once the skin is healed (no open areas), your normal soap may be resumed. Before cleaning your face, you should wash your hands with an antibacterial soap (e.g., Dial or Safeguard) to avoid contamination of the treatment area. We will normally want to see you for follow-up visits weekly for the first 3 weeks after treatment. Call the office immediately for any rash, fever, or severe pain. These may be early signs of infection.

After 1 Week 1. After 1 week normally, the skin will be healed enough for you to be able to venture outside. When outside, the face should be covered with a broadspectrum sunscreen (at least SPF 15) and the head covered with a broad-brim hat. Total block 60 (Fallene Ltd., King of Prussia, PA) is recommended. It is most important to avoid any sun exposure as long as the skin is pink. Even a brief trip across the parking lot without protection can result in dark brown splotches. 2. A green concealer can be used to neutralize residual redness. A flesh-tone foundation can then be applied to conceal the green tone. 3. A light moisturizer can be applied ad lib (Curel, Moisturel, or Purpose) 4. Apply a steroid cream every night if your doctor prescribes it for redness. APPENDIX IV: PATIENT INFORMATION HANDOUT The carbon dioxide laser has become a popular method for skin surgery. By precisely removing and gently heating skin wrinkles, for example, new healthier skin will appear during the healing period. Also, the contour of acne scars can be improved. Other benign skin bumps can also be removed with the carbon dioxide laser. The carbon


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dioxide laser has been the most popular machine used to peel the skin. Although it works well, the heat generated causes prolonged healing. Often, 10 days to 2 weeks are required before crusts completely resolve and you can comfortably return to work. Also, often red skin is noted up to 4 months after surgery. Sometimes only a cream application is required for skin numbing, but usually an injection (with a needle—like at the dentist’s office) will be required to make you comfortable during the laser surgery. At the consultative visit, you will be counseled about the risks and benefits of carbon dioxide laser surgery. Representative photographs will be shown. If you are interested in carbon dioxide laser treatment, a date will be scheduled for surgery and a handout specific for your skin condition type of surgery will be provided.

6 Er:YAG Lasers Ulrich Hohenleutner and Michael Landthaler University of Regensburg, Regensburg, Germany

1. Introduction 2. Laser – Tissue Interaction 2.1. Er:YAG Laser Physics 2.2. Laser – Tissue Interaction 2.3. Ablation Efficacy 2.4. Residual Thermal Damage 2.5. Laser Plume and Noise 3. Commercially Available Er:YAG Lasers 4. Er:YAG Laser Treatment 4.1. General Treatment Considerations and Contraindications 4.2. Treatment Techniques 4.3. Anesthesia 4.4. Pre- and Perioperative Care 4.5. Postoperative Care 4.6. Wound Healing and Side Effects 5. Treatment Results 5.1. Skin Resurfacing (Rhytides, Actinically Damaged Skin) 5.1.1. Er:YAG Lasers Alone 5.1.2. Comparisons/Combinations of Er:YAG and CO2 Laser 5.2. Pigmentory Abnormalities 5.3. Acne Scars 5.4. Other Skin Lesions 6. Conclusion References

1.

181 182 182 182 183 183 184 186 186 187 188 189 189 189 190 190 190 191 192 192 193 193 194 194

INTRODUCTION

The introduction of Er:YAG lasers has considerably broadened the therapeutic possibilities for skin disorders. Er:YAG lasers allow an extremely precise but superficial ablation of the skin with considerably faster healing and reduced side effects compared to the CO2 laser. 181

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Hohenleutner and Landthaler

Their ablative effect is comparable to mechanical dermabrasion, but the technique is simpler to perform without the risk of injury from the high-speed rotating fraises. In areas of loose or thin skin like lips or eyelids, where even pulsed CO2 lasers carry a considerable risk of scarring, Er:YAG lasers are safe and effective. This chapter will present an overview of the laser–tissue interaction of Er:YAG lasers, their clinical applicability, therapeutic indications, and results, and the general considerations in Er:YAG laser therapy.

2. 2.1.

LASER – TISSUE INTERACTION Er:YAG Laser Physics

Like neodymium:YAG lasers, Er:YAG lasers are solid state lasers that mostly are flash lamp pumped. The laser medium is a crystal rod consisting of yttrium aluminum garnet that is doped with erbium. Er:YAG lasers emit light at 2940 nm wavelength, which is in the near-infrared spectrum. Like Nd:YAG lasers, they can be Q-switched (1), but most Er:YAG lasers for clinical applications work in the so-called free-running mode. Typical pulse times are 250 ms (250–350 ms). During this macropulse, Er:YAG lasers emit a chain of highenergy, 1 ms short pulses, so-called spikes (1,2). For clinical applications, the light of the Er:YAG laser usually is transmitted to the operating field by mirror arms and focusing lens handpieces, rather than via the usual quartz fibres because they absorb the Er:YAG lasers’ wavelength. 2.2.

Laser – Tissue Interaction

At 2940 nm, water has an absorption maximum. The absorption coefficient of water at this wavelength is approximately 13,000 cm21 (3–5). Additionally, the wavelength of the Er:YAG laser is very close to an absorption maximum of collagen at 3030 nm (6). Therefore, skin containing 70– 80% water has an absorption coefficient of approximately 8000 – 9000 cm21 at 2940 nm (1,3,4). In comparison, at the wavelength of CO2 laser radiation (10,600 nm), the absorption coefficient of water is approximately 790 cm21 (5). This very high absorption of the Er:YAG laser radiation in skin directly explains the precise and effective ablation properties of Er:YAG lasers. The irradiated light is absorbed in very small tissue volumes that are maximally heated and explosively vaporized. The theoretical skin penetration depth of Er:YAG laser radiation is 1 mm (3 – 5), as stated before. This penetration depth cannot explain the highly effective tissue vaporization that is possible with these lasers. Experimental ablation efficacies in skin of up to 200 mm and more per pulse (at 80 J/cm2) (1) have been observed. These ablation depths, nevertheless, can be explained by the model of dynamic vaporization and by the changed optical properties of water at high temperatures and high pressures (1,3,4). During a high-irradiance laser pulse, small layer after small layer of skin is irradiated and maximally heated while the more superficial layers are vaporized (4). The high temperatures and high pressures in the thin tissue layers change the optical properties of water and, consecutively, of the tissue. The water absorption decreases by two orders of magnitude (3) and allows a higher penetration depth of the laser radiation, which increases the ablation efficacy. Additionally, water vapor is nearly transparent for Er:YAG laser radiation (1). Therefore, the ejected particles and the vapor that are in the laser beam during the ablating macropulse cannot significantly weaken the incident irradiation. Hence, tissue layer after tissue laser is effectively removed, the particles are ejected at supersonic speed (1), and a deep tissue ablation becomes possible.

Er:YAG Lasers

183

These dynamic optical properties of water during infrared laser ablation (3) also explain the typical residual thermal damage zones of 10– 50 mm that are seen with Er:YAG lasers. With static optical properties and a theoretical penetration depth of 1 mm, these residual thermal damage zones would be limited to exactly this penetration depth and not exceed 1 mm. 2.3.

Ablation Efficacy

The threshold for ablation of skin with Er:YAG lasers in free-running mode with a pulse time around 250 ms is 1.5 J/cm2 (0.7 – 1.7 J/cm2) (2,7 –9). At fluences up to 20 J/cm2, the ablation per pulse strongly increases with the irradiant fluence. This has been demonstrated in many in vitro studies using pig or human skin (3,8 –10). Above 20 J/cm2, the ablation efficacy increases more slowly, but still linearly with the fluence (3). Above 60 J/cm2, the additional ablation that is achievable by an increase of the fluence further decreases (3). The application of multiple consecutive pulses to the same spot of tissue (“pulse stacking”) leads to decreased ablation efficacy and increased thermal damage. Although Hibst and Kaufmann (8) could not observe this effect at repetition frequencies of 1 Hz and 1 mm spot size, in our own study with repetition rates of 7 – 10 Hz we could clearly demonstrate this effect for 3 –4 mm spot sizes (9). The thermal damage zone was clearly dependent on the number of pulses applied and increased from 25 mm with less than 10 pulses to 100 mm with 40 pulses. This effect was confirmed by Ross et al. (11), who observed a 12-fold increase of thermal necrosis due to pulse stacking. In clinical application, pulse stacking, as defined by 100% overlap of pulses, is prevented by the sweeping motion of the handpiece over the skin that is used for most indications. Even at higher repetition frequencies, 100% pulse overlap is improbable when using this technique, and even if two or three pulses should be applied on the same spot, the thermal coagulation depth is not yet increased (see later). The ablation efficacy of skin with Er:YAG lasers at above-threshold fluences is between 2.5 and 6 mm per pulse per 1 J/cm2 (1,8 – 10). For example, with 1 mm spot size at 5 J/cm2 the ablation is about 10 mm per pulse (1,9) and increases to 20 mm at 10 J/cm2 and to 60 mm at 20 J/cm2 (1). To estimate the ablation depth per pass (in mm) for clinical purposes, it is recommended to multiply the applied fluence by 4 (12). These high ablation rates result in a relatively fast and effective ablation of skin in vivo. With typical clinical settings of 5 J/cm2 and repetition rates of 10 Hz, 20 – 60 mm of tissue is vaporized with one to two passes; with three passes, the vaporization increases to 80– 120 mm (13). In contrast to CO2 lasers, an increased number of passes with Er:YAG lasers does not lead to a decreased ablation efficacy (14 –16). With CO2 lasers, after several passes the tissue becomes increasingly dehydrated due to the fluid sealing effect of the coagulation zones, which can amount to up to 200 mm (17 – 20). Due to the lack of water, the skin can no more be vaporized and is only heated, which further increases the coagulation damage (16). With Er:YAG lasers, due to the minimal coagulation zones, there is no dehydration of tissue, hence no limit to tissue vaporization (14 –16). 2.4.

Residual Thermal Damage

Compared to the CO2 laser, the main advantage of Er:YAG lasers is the minimal to almost absent residual thermal damage in the skin. Many studies, either in vitro or in vivo, have clearly demonstrated that with output parameters as they are used in clinical application

184


(fluences up to 25 J/cm2, spot sizes up to 6 mm, repetition frequencies up to 20 Hz), the zone of residual thermal damage as visualized by collagen denaturation is typically about 10 – 30 mm and does not exceed 50 mm (2,9,10,12,13,17,21 – 24). Even with up to 10 passes at fluences of 14 – 24 J/cm2, the thermal necrosis remains constant at 15– 40 mm (14). Compared to the CO2 laser, this dramatically reduced thermal damage leads to reduced healing times, reduced postlaser erythema, and a lower frequency of side effects. Nevertheless, for the clinical effect of wrinkle reduction, the reduced coagulation of collagen and elastic fibers is a disadvantage. Some studies directly comparing Er:YAG and CO2 lasers for rhytides showed that although the Er:YAG laser leads to faster healing and reduced side effects, wrinkle improvement was better and more prolonged with the CO2 laser (17,25 –29). For non-skin-resurfacing indications, the nearly complete absence of residual thermal damage makes the Er:YAG laser the more precise and safer tool. Nevertheless, this holds true only for relatively superficial and not strongly vascularized skin lesions. The main disadvantage of the Er:YAG lasers in skin ablation is their inability to stop bleeding. Due to the absence of coagulation, there is a profuse capillary bleeding as soon as the papillary dermis with its superficial vessel loops is reached (2,7). This bleeding considerably interferes with further ablation in a clinical setting. Further ablation is only possible when the bleeding has stopped, since the blood film on the tissue prevents any further vaporization. Therefore, the clinical applicability of Er:YAG lasers for deeper vaporization, cutting, or the treatment of highly vascularized skin lesions (e.g., common or genital warts) is limited. Some Er:YAG lasers provide subablative pulses at subthreshold energy densities or with longer pulse times which produce a coagulation effect similar to CO2 lasers and are hemostatic. With pulse lengths up to 700 ms, decreased bleeding was noted without increasing residual thermal damage (30). Other authors, nevertheless, found that with subthreshold, longer pulses (“heating pulses”) the thermal damage zones increase up to 80 mm (31) and 100 mm, respectively (32). In contrast to ablative (above-threshold) pulses, “pulse stacking” with subablative pulses leads to greatly increased residual thermal damage, which can reach 200 mm (33). These increased coagulation zones lead to more hemostasis in the operating field and also to prolonged healing times and increased side effects compared to the pure ablative mode. In the clinical setting, these subablative pulses, provided by some Er:YAG lasers (Table 6.1), are used to produce a larger zone of thermal damage, with CO2 laser like clinical effects. The resultant “collagen shrinkage” and “collagen remodeling” have improved the long-term efficacy of Er:YAG laser skin resurfacing (34,35).

2.5.

Laser Plume and Noise

Several studies have demonstrated that the CO2 laser plume may carry infectious particles and is hazardous for the lungs due to the particle size (36 – 40). Regarding the Er:YAG laser plume, only one study exists so far. Hughes and Hughes (41) could not demonstrate HPV-DNA in the Er:YAG laser plume when treating human warts. Possibly, the intensive fragmentation and heating that occur when tissue is explosively vaporized and the particles are ejected at supersonic speed (1) prevent the survival of infectious particles in the Er:YAG laser plume. Nevertheless, until further data are available, it is recommended that infectious patients (hepatitis B and C, HIV) should not be treated with ablative lasers including Er:YAG lasers (7) since the risk of disseminating the infection cannot be totally excluded.

TM

2

No

–15 Hz –15 Hz –50 Hz

250 ms 350 ms

–1.2 J/pulse

2 J/pulse

45 W 100 ms–200 ms (Nd:YAG) ND ND

0.1– 45 W (Nd:YAG) –2 J/pulse

–2 J/pulse

500 ms

ND

–20 Hz

–45 Hz

1– 4 Hz

a ND ¼ no data available. Note: This table may be incomplete and implies no recommendation for specific machines!

Wavelight GmbH BuraneTM, www.wavelight-laser.net Wavelight GmbH SuperbTM, www.wavelight-laser.net

Sciton ProfileTM, www.sciton.com

Yes

–15 Hz

100/300/750/ 1000 ms 250 ms

2 J/pulse

Laserscope VenusTM Laser System, www.laserscope.com Limmer Laser UNILAS 2940, www.limmermt.com Lynton Lasers Ltd. SkinlightTM, www.lyntlaz.demon.co.uk Lynton Lasers Ltd. Skinlight PlusTM, www.lyntlaz.demon.co.uk Sciton ContourTM, www.sciton.com

–1 J/pulse

No

–20 Hz

300 ms

0.8 J/pulse

Yes

Yes

ND

Yes

No

ND

ND

2.5–3.5–5 mm, focused

2, 3, 4, 6, 10 mm, focused

Collimated, 4 mm

Focused, 1.5– 7 mm



Collimated, 3/5/7 mm

Focused, –10 mm collimated and contact fibers also available Focused, 1–8 mm

IrradiaTM, www.irradia.se

Yes

1 J/pulse

Fotona FidelisTM, www.fotona.de –50 Hz

ND

Yes

ND

ND

–3 J/pulse 100, 300, 750, 1000 ms

Focused, 1–10 mm

No

–28 Hz

250 ms

0.8–1–1.2 mm and 1–10 mm focused ND

Focused, 1.5– 5 mm fiber

Handpiece and spot size

–2 J/pulse

No

No

Yes

Long pulses (subablative)

–15 Hz

–28 Hz

–20 Hz

Repetition rate

250 ms

250 ms

ND

a

Pulse length

–1.2 J/pulse

–2 J/pulse

4–40 J/cm

Output

Asclepion-Meditec MCL 29 DermablateTM, www.asclepion.com Asclepion-Meditec DermablateTM, www.asclepion.com Fotona NovalisTM, www.fotona.si

Asclepion-Meditec Derma Star , www.asclepion.com Asclepion-Meditec Dermablate HareTM, www.asclepion.com

Company, web address

Table 6.1 Commercially Available Nd:YAG Lasers

ND

ND

Available

Integrated

ND

ND

ND

Available

ND

ND

ND

Available

ND

Available

ND

Scanner

Built-in Nd:YAG/KTP laser at 532 nm Variable coagulation depths up to 100 mm Built-in Nd:YAG for hair and vascular lesions

Cutting handpiece available

Built-in ruby and KTP 532 nm lasers Desktop size

Smoke evacuation in handpiece Built-in ruby laser for hair removal

Additional handpiece for hair transplant holes

Specialities

Er:YAG Lasers 185

186


Safety considerations as well as the prevention of unpleasant odors make an effective smoke evacuation device absolutely necessary for Er:YAG laser as well as for CO2 laser treatment. Another problem that is specific to the Er:YAG laser is the typical cracking noise that is associated with the explosive skin vaporization. Especially with higher fluences and high repetition rates, the resulting hammering noise is not unlike machine gun fire and can be quite bothersome (7). Depending on the distance to the treatment field, the noise intensity can reach levels that can possibly damage the ears [at least with chronic exposure (42)]. Therefore, for extensive procedures, the use of ear protection is recommended or at least should be taken into consideration.

3.

COMMERCIALLY AVAILABLE Er:YAG LASERS

As solid state lasers, Er:YAG lasers normally are reliable machines without high running expenses. Due to internal cooling circulation systems, they are air cooled and run on 110 or 220 V. In contrast to CO2 lasers, where different pulse lengths and different scanners lead to significantly different laser – tissue interactions and coagulation zones, the various commercially available Er:YAG lasers, at least with respect to their ablative pulses, produce similar effects on skin. This has been shown in a study by Alster (13), who performed a clinical and histological evaluation of six different Er:YAG lasers for skin resurfacing. Nevertheless, the Er:YAG laser machines offer different options for subablative pulses. Subthreshold pulses are available alone or in (fixed) combination with ablative pulses, and the irradiation parameters can be chosen either directly as fluence and/or pulse length or as the desired depth of coagulation. Also, the machines are different regarding their technical equipment. Output energies up to 2 J per pulse, spot sizes up to 10 mm, and various repetition frequencies are available. There are handpieces using focusing lenses with distance holders and handpieces with collimated beams, the latter being independent of the handpiece – skin distance. Spot sizes can be selected by changing the lenses or the distance holders, or directly at the handpiece. Additionally, for various lasers there are automatic or computerized scanner systems available. These can produce different shapes and sizes of treatment areas, and the pulse overlap can be selected. In some lasers, the smoke evacuation system is integrated into the handpiece. Table 6.1 gives an alphabetical overview of the Er:YAG laser systems commercially available at present. It should be emphasized that the therapeutic results achievable are more or less identical with those of the different lasers available (13), even if some lasers can treat faster due to higher output or may be more comfortable due to convenient handling.

4.

Er:YAG LASER TREATMENT

There have been a large number of publications regarding the application of Er:YAG lasers to a variety of skin disorders. The main field of application of the Er:YAG lasers is in skin resurfacing. The precise and effective ablation properties of these lasers have made them useful for many other cutaneous applications (Table 6.2).

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Table 6.2 Possible Indications for Er:YAG Laser Therapy Pigmentation

Resurfacing Scars Epidermal lesions

Dermal lesions

Warts Inflammatory dermatoses Others

4.1.

Lentigines Melasma/chloasma Postinflammatory hyperpigmentation Wrinkles, rhytides Solar elastosis Acne scars Surgical/traumatic scars Seborrhoeic keratoses Actinic keratoses Actinic cheilitis Epidermal nevi (M. Bowen) (Superficial basal cell carcinoma) (Erythroplasia of Queyrat) Dermal nevi Fibromata Xanthelasma Plane xanthoma Syringoma Sebaceous gland hyperplasia Nevus sebaceus Osteoma cutis Plane warts Vulgar warts, palmoplantar warts Psoriatic plaques Zoon’s balanitis M. Darier M. Hailey – Hailey Rhinophyma Hole boring for hair transplantation

General Treatment Considerations and Contraindications

As with all lasers, appropriate safety precautions for eye protection are required. As mentioned previously, efficient plume evacuation systems are necessary, and ear protection should be taken into consideration at least for more extensive procedures. Since Er:YAG laser ablation is precise and the residual thermal damage is almost negligible, it is quite comparable to mechanical dermabrasion. The clinical end point of treatment is either the apparent removal of the target lesion or, in resurfacing procedures, as soon as the desired depth of ablation is reached. There are only a few absolute contraindications to Er:YAG laser therapy, which include, in our opinion, the treatment of patients with infectious diseases that are contagious by blood or lymph fluid (hepatitis B and C, HIV) (7). The relative contraindications include (7,16,43) – – –

concomitant systemic retinoid treatment (which may produce prolonged healing time and atypical scarring) skin with a reduced number of dermal appendages (e.g., following electroepilation, burns) history of a tendency toward keloidal scarring

188


– – –

4.2.

prior blepharoplasty or ectropion collagen vascular or immune disorder (16) increased bleeding tendency (coagulation disorders, anticoagulation, high-dose acetylsalicylic acid treatment).

Treatment Techniques

Small or exophytic lesions (seborrhoic keratoses, warts, xanthelasmata, etc.) are treated with an appropriate spot size and average repetition rates (up to 10 Hz) until they are removed. For flat lesions, average fluences of 5 – 10 J/cm2 are often sufficient. With more exophytic lesions, higher fluences, if available, are often desirable to accelerate the procedure. If bleeding occurs, it is necessary to wait until the bleeding stops, otherwise further ablation will be ineffective. For skin resurfacing or other indications requiring extensive ablation, most authors recommend fluences of 5 J/cm2 (13,16), but higher fluences up to 20 J/cm2 have been described, too (7). The handpiece is led across the treatment area in a sweeping motion with a velocity that depends on the repetition rate chosen (12). The pulses and lines of pulses should overlap about 30%, resulting in a uniform ablation without leaving untreated spots (7). Pulse stacking on one point of the skin should be avoided due to increasing residual thermal damage (9,12). After each pass, the superficial fluffy debris may be cautiously removed by wet gauze, but, unlike with CO2 lasers, this usually is unnecessary with Er:YAG lasers (12,16,44). The subsequent passes should be oriented perpendicular or at an angle to the preceding passes to further enhance the uniformity of the ablation (7,12,45). The margins of the treatment areas can be blended into the untreated skin by using pulses of lower fluence (6) or by defocusing the handpiece or scanner (7) (which, in effect decreases the fluence). Using this technique and fluences of 5 J/cm2, the following ablation depths are usually achieved: one pass, 20 –40 mm or down to the granular layer of the epidermis; two passes, up to 60 mm or down to the basal cell layer; three to four passes, 80 – 120 mm or down to the papillary dermis, and deeper into the papillary and superficial reticular dermis after five to six passes (13,21). Weinstein (24) describes the following ablation depths using a scanner of 20 Hz and 30% pulse overlap: 5 J/cm2, superficial epidermal injury (30 – 40 mm) with negligible thermal necrosis; 10 J/cm2, epidermal injury to the level of the basal layer (50 mm) with minimal thermal necrosis (5 mm); 15 J/cm2, full-thickness epidermal injury through the basement membrane, minimal ablation of the papillary dermis (20 mm), and a narrow band of thermal necrosis (10 –15 mm). These schematic histological ablation depths provide an approximation of the real ablation depth achievable with different fluences and numbers of passes, and should not be relied on in patient treatment. A distinct advantage of the Er:YAG lasers is that, as in mechanical dermabrasion, one can directly evaluate the achieved depth by inspecting the skin surface after careful removal of the debris. Since there is almost no coagulation zone, some clinical end points can be used as guidelines for the depth of ablation in tissue. These end points are best visualized with magnifying lenses, as defined by Weinstein (7): Epidermis: Resurfacing within the epidermis produces a yellowish brown appearance on the epidermis. Epidermo-dermal junction: Once the epidermis is removed, a pinkish appearance of the upper papillary dermis will be readily appreciated. The follicle openings look small and regular like a fine sponge.

Er:YAG Lasers

189

Lower papillary dermis: When proceeding into the papillary dermis, pinpoint bleeding and a transsudate develop, indicating injury to the small capillaries. The follicle openings become wider and begin to stand out from the surrounding dermis. Upper reticular dermis: When the upper reticular dermis is reached, bleeding increases and the transsudate becomes more profuse. Follicle openings become much wider and the collagen bands become coarser and more haphazard in orientation. At this point it is generally best to proceed no further. 4.3.

Anesthesia

With Er:YAG lasers, the type and amount of anesthesia needed depends on the depth of ablation or resurfacing and the fluences used. Very superficial ablation procedures or the removal of very small lesions mostly can be performed using topical anesthesia only (EMLATM cream, tetracaine or lidocaine preparations) or with no anesthesia at all. With higher fluences above 5 –10 J/cm2, in the treatment of extensive lesions or if deeper ablation is required, local anesthesia, nerve blocks, and/or intravenous sedation, even general anesthesia may become necessary. The kind of anesthesia required depends on the kind of procedure that is planned and the individual sensitivity of the patient (7,11,16,46).

4.4.

Pre- and Perioperative Care

For the treatment of small, circumscribed, or exophytic lesions with Er:YAG lasers, no special pre- or perioperative measures are necessary. For extensive procedures like full-face resurfacing procedure for photodamage or acne scars, the same pre- and perioperative prophylactic measures are applicable as with CO2 laser treatment (7,16,46). These include pre- and postoperative skin conditioning with topical retinoic acid, weak chemical peels or creams, glycolic acid, and bleaching agents like hydroquinone (46). Oral antiviral therapy is used for prophylaxis against herpes simplex virus (7,16,46), but there is some debate regarding the used for oral antibiotics (46). Topical or systemic steroids are recommended by some authors to prevent significant postoperative swelling. For details, see the “Guidelines of Care for Laser Surgery” (47), the appropriate review articles (46,48,49), or the chapters on resurfacing later in this book.

4.5.

Postoperative Care

For small lesions, we recommend topical antibiotic ointments or ointments specifically designed to accelerate wound healing (e.g., BepantholTM ointment). This should be used until complete re-epithelialization has occurred and prevents the formation of irritating crusts. For extensive lesions as in skin resurfacing, either the open technique (application of ointments several times a day, following irrigation with water or vinegar solutions) or the closed technique (application of various kinds of occlusive dressings for several days) can be used (12,46). Weinstein (7) prefers using the closed technique with occlusive dressings for the first 1 –2 days to provide sufficient fluid absorption capacities. Due to the absence of the coagulation zone, there is much more postoperative exudate after Er:YAG than after CO2 laser ablation.

190


There has been much controversey regarding the preferred method of postoperative care (46,48,49), but in our opinion, either technique leads to good results if performed properly by a cooperative and intelligent patient with close physician monitoring. In our clinic, we use an occlusive dressing (CutinovaTM thin) for 1 –2 days for treatment of small lesions followed by the application of BepantholTM ointment several times a day. For extensive resurfacing procedure for photodamage or scar treatment, we use a semiocclusive jelly dressing for 2 – 3 days, followed by the application of BepantholTM ointment several times a day until reepithelialization is complete. 4.6.

Wound Healing and Side Effects

Depending on the depth of ablation, complete epithelialization of the skin is typically achieved in 3 – 10 days (6,13,21,44,50). The postoperative side effects with the Er:YAG laser are significantly reduced compared to CO2 lasers (7,21), because of the limited thermal damage zones. Postoperative erythema is a temporary side effect and resolves after 2–6 weeks according to the depth of ablation (6,12,21,44,50,51). Hyperpigmentation of the treatment areas, which is also a common side effect with CO2 lasers, is significantly less frequent with the Er:YAG laser (7,17). In the largest published series of 625 patients treated with an automatic scanner Er:YAG laser, temporary hyperpigmentation occurred in 3.4% and was transient in nature (7). Other authors report comparably low rates of hyperpigmentation between 0% and 10% of patients (6,44,51,52), whereas frequencies of up to 25% are reported after deeper ablation (17) or after additional complications like dermatitis or superinfection (13). Late-onset (up to 6 months postop) permanent hypopigmentation, the most feared long-term complication of CO2 laser resurfacing, seems to occur with Er:YAG lasers only in very deep ablation procedures. Its frequency has been reported to be 4.0% in the Weinstein series of 625 patients (7), 5% by Khatri et al. (17), and 2% by Riedel et al. (51). Many authors, however, found no occurrence of hypopigmentation with Er:YAG laser therapy (6,44,50,52 – 55). Other side effects include herpes simplex, bacterial or fungal superinfection, exacerbation of acne, irritant or contact dermatitis, pruritus, acneiform pustules, and milia formation. Most of these side effects are temporary and can be managed by proper topical or systemic treatment (6,12,56). An observation made by most authors is that with increasingly deep ablation, by either high fluences or repeated passes, the frequency of side effects increases accordingly and becomes progressively similar to CO2 laser treatment, especially if subthreshold pulses are added to increase the collagen shrinking effect (28,46). Atrophic scarring, hypertrophic scarring, or even keloid formation can occur with Er:YAG lasers, as with CO2 lasers (7) if the ablation is to deep for the skin area that has been treated or if superinfection occurs (e.g., ulcerating herpes). Special caution with a reduced number of passes or reduced fluences should be used in the treatment of sensitive areas with thin skin, like the eyelids or neck (7,12,16,43,50,57).

5. 5.1.

TREATMENT RESULTS Skin Resurfacing (Rhytides, Actinically Damaged Skin)

Literature abounds with the description of treatment techniques for Er:YAG lasers used in skin resurfacing (7,12,16,46). For more information, see the chapter “Skin Resurfacing with Er:YAG Lasers” later in this book. Here, only a short overview will be given over

Er:YAG Lasers

191

the treatment results that are achievable with Er:YAG lasers, with or without additional CO2 laser treatment, in skin resurfacing. 5.1.1.

Er:YAG Lasers Alone

Weiss et al. (6) report an average good to excellent improvement of periorbital rhytides 1 year after Er:YAG laser treatment with two passes at 21.2 J/cm2 and one additional pass at 15 J/cm2 direct over the wrinkle line. Perez et al. (21) used up to seven passes at 4 – 5 J/cm2 and found marked improvement of classes I– II rhytides in 8 of 15 patients. Moderate improvement was seen in six patients. Riedel et al. (58) treated with one to three passes at 1.4– 1.5 J per pulse (spot size not given) and could achieve a good to very good effect in the improvement of small to medium rhytides. Deep rhytides mostly recurred after 3 months. In Asian patients, Polnikorn et al. (54) achieved an 80% improvement of wrinkles and a 70% improvement of photoaged skin 6 months after Er:YAG laser treatment with several passes at 0.8 –1 J per pulse at 3.5 or 5 mm spot size. Clinical improvement (without further classification) was seen in facial rhytides treated with 2.5 to 5 mm spot size and up to 800 mJ pulse energy 2 months after treatment by Teikemeier and Goldberg (50). Goldberg and Cutler (55) treated patients with deep, class III rhytides with four passes at 5 J/cm2. Three consecutive treatment sessions were performed at 3-month intervals. After the first treatment session, no improvement was seen. Six months after the third treatment, 14 patients showed mild, 4 moderate, and 2 excellent improvement. Goldman et al. (43) treated photoaged skin of the neck and reported an improvement between 28% and 48%, according to the treatment method used [for details see Ref. (43)]. Likewise, Goldberg and Meine (44) achieved at least 25% improvement of rhytides and 50% improvement of photodamage-induced discoloration of the neck of patients treated with 3– 4.5 J/cm2 (four passes with an additional three to four passes directly over the rhytides). Jimenez and Spencer (52) performed Er:YAG laser resurfacing of the hands, arms, and neck for photodamaged skin. They observed prolonged healing times of up to 3 weeks after two to three passes at 5 J/cm2 (one to two passes in the neck) and the cosmetic results were disappointing: only one patient of seven showed a fair improvement in the hands, and only one patient of five showed a good result in the neck. With the introduction of modulated Er:YAG lasers with subablative pulses that lead to more thermal damage and hence to more collagen shrinkage, the efficacy of the Er:YAG laser for skin resurfacing and wrinkle treatment has improved. Rostan et al. (34) found a similar degree of improvement in facial laser resurfacing in a side-by-side comparison of pulsed CO2 laser and long-pulse Er:YAG laser treatment, with accelerated healing and fewer side effects on the Er:YAG-side. Zachary (35), too, observed a comparable efficacy of modulated Er:YAG and pulsed CO2 lasers with less side effects with the Er:YAG laser. In contrast, Newman et al. (29), in a side-by-side comparison in lip resurfacing, found fewer side effects with the long-pulse Er:YAG laser but better clinical improvement with the CO2 laser. Most authors performing Er:YAG laser resurfacing agree that the ideal indications for Er:YAG laser resurfacing are relatively mild, class I –II rhytides and mild photodamage of the skin, even if the subablative pulses have somewhat improved its clinical efficacy. Severe actinic elastosis, pronounced actinic keratoses, and deep rhytides respond better to CO2 laser resurfacing or combined procedures (7,13,16,46,56).

192


5.1.2. Comparisons/Combinations of Er:YAG and CO2 Laser Although the Er:YAG laser has been shown to provide some amount of intraoperative and postoperative skin contraction (59), the CO2 lasers, due to their increased coagulation depth leading to collagen denaturation and skin contraction, show improved efficacy for treatment of severe wrinkling or severe photodamage. For the treatment of rhytides, we performed a side-by-side comparison of Er:YAG (5 J/cm2, four to five passes) and CO2 laser (SilkTouchTM, 3 mm/5 W or 5 mm/10 W, two to three passes) treatment (25). After 8 weeks, the CO2-treated side showed marked improvement in 73% and moderate improvement 27%, whereas in the Er:YAG-treated side, moderate improvement was seen in 43% and only slight improvement in 57%. These results remained stable for over 1 year (26). Likewise, Khatri et al. (17) compared a pulsed CO2 laser (up to 6.5 J/cm2, 800 ms pulse length, two to three passes) with Er:YAG laser treatment (5 – 8 J/cm2, three or more passes). They found that the CO2treated side had better wrinkle improvement when using an identical numbers of passes. With five or more passes of the Er:YAG laser, the improvement scores were no longer significantly different. The frequency of erythema was significantly lower with the Er:YAG laser at 2 weeks (67% vs. 95%) and 8 weeks (24% vs. 62%), and hypopigmentation occurred in 5% with the Er:YAG laser and in 43% with the CO2 laser. Nevertheless, in the more aggressively treated Er:YAG patients, the incidence of erythema increased to 100% and 78% (at 2 and 8 weeks, respectively). McDaniel et al. (53) treated patients with deep rhytides with the pulsed CO2 laser and added, on one side of the face, three passes with an Er:YAG laser at 5.2 J/cm2. They found that the addition of the Er:YAG laser reduced crusting from 7.4 to 6.5 days and itching from 4.5 to 4.8 days. Otherwise, the results were identical, the average improvement of rhytides being 70%. These results were confirmed by Goldman and Manuskiatti (60), who found a significant reduction of healing time and erythema with an additional two passes of Er:YAG laser after Ultrapulse CO2 laser resurfacing without changes in the clinical result. Millman and Mannor (61) performed eyelid resurfacing with two passes of the Er:YAG laser followed by one pass of the CO2 laser and compared the results with a historical group of CO2 laser therapy only. They found that the combination therapy shortened the re-epithelialization time and the duration of erythema with a similar, satisfying cosmetic outcome in both groups. Similar results were achieved by Trelles et al. (62) by a fixed combination of an ablative Er:YAG and a nonablative CO2 laser pulse. These results are explained by the histological examinations of Utley et al. (23), who found the following residual thermal damage zones after ablation with an Er:YAG and a pulsed CO2 laser (at 4.7 J/cm2 each): CO2 alone (four passes) 89 mm, Er:YAG (four passes) þ CO2 (two passes) 97 mm, Er:YAG alone (eight passes) 43 mm, and CO2 (two passes) þ Er:YAG (four passes) 56 mm. Accordingly, Collawn (56) proposes to use the CO2 laser for severe and deep rhytides, CO2 laser followed by Er:YAG laser for moderate rhytides, and Er:YAG laser alone for fine wrinkles and discolorations.

5.2.

Pigmentory Abnormalities

Weinstein (24) treated 87 patients with pigmentation due to sun damage or chloasma with the Er:YAG laser using a computerized scanner with 30% pulse overlap. Three passes were performed (at 14, 10, and 7.5 J/cm2). All patients were reported to have shown excellent results with the removal of superficial and deeper pigmentation without recurrences.

Er:YAG Lasers

193

Polnikorn et al. (54) reported an average 16% improvement in the treatment of melasma in Asian skin (5 – 15 J/cm2, number of passes not specified). Drnovsek-Olup and Vedlin (63) reported an 80% clearing in two patients with chloasma after one treatment with 1.3 –1.7 J/cm2 and two to five passes. Manaloto and Alster (64) treated 10 patients with refractory melasma with three passes at 5– 7.6 J/cm2. The early results after 6 weeks showed a good initial response, followed by the development of a severe postinflammatory hyperpigmentation that had to be treated by sun screens, azelaic acid cream, and glycolic acid peels. Six months after treatment, the melasma was clinically improved in all patients but this had required intensive medical treatment of the hyperpigmentation. The authors, therefore, recommend Er:YAG laser treatment only in severe cases of otherwise refractory melasma.

5.3.

Acne Scars

The standard Er:YAG-laser treatment technique for acne scars is to perform to two to three passes over the entire anatomical unit followed by ablation of the shoulders of the acne scars with higher fluences or smaller spot sizes (7). Using this technique, Riedel et al. (51) could achieve good to very good results in 10 patients with acne scars. In Asian patients, Polnikorn et al. (54) reported an average 55% improvement using comparable techniques. Weinstein (24) first flattened the shoulders of the scars by single spots at 8 J/cm2, two to five passes, followed by treatment of the entire anatomical unit with the computerized scanner at 15 J/cm2 and 30% pulse overlap with two to three passes. For deeper acne scars, she used the CO2 laser (SilkTouchTM scanning device, 30 –40 J/cm2) for the shoulders followed by the Er:YAG laser as described before. Using this technique, she achieved no excellent, seven good (70 –90% improvement), and three fair results (50 –70% improvement). The long-pulsed Er:YAG laser has also been used for this indication. Jeong and Kye (65) achieved excellent and good results in 36% and 57% of 35 patients, respectively, for the treatment of found acne scars.

5.4.

Other Skin Lesions

Good to excellent results using Er:YAG laser ablation have been reported for a variety of small, circumscribed, and mostly exophytic skin lesions like seborrhoic warts, lentigines, epidermal nevi, milia, xanthelasmata, plane xanthomas, hidradenoma, plane warts, and fibroepithelial papillomata (10,46,51,54,58,66 –68). The Er:YAG laser is used to vaporize the small exophytic lesions until they have resolved. Good results in rhinophyma ablation are possible with Er:YAG lasers (46,54,69), but profuse bleeding makes this a tedious procedure (7). Combined procedures with the CO2 laser or conventional scalpel/razor/dermabrasion sculpting should be considered. As reported for dermabrasion and CO2 laser, Er:YAG laser ablation can achieve good results in Darier’s disease and Hailey– Hailey disease (70). A very rare disease, miliary osteoma cutis, reportedly can be treated by Er:YAG lasers with satisfying results (71,72). The same holds true for treatment of multiple eruptive vellus hair cysts (73). As with the CO2 laser, single recalcitrant plaques of psoriasis vulgaris refractory to conventional therapy can be treated with good clinical results by Er:YAG laser

194


ablation (74). In a single case of Zoon’s balanitis, this dermatosis responded well to Er:YAG laser ablation (75). Er:YAG lasers have also been used in the preparation of an adequate graft recipient bed on vitiligo skin for the transplantation of cultured melanocytes into these vitiligo lesions. The Er:YAG laser with its exact ablation and no residual thermal damage is ideal for preparing transplantation beds in these often bizarre and geometrically complicated lesions (76,77). In hair transplantation, Er:YAG lasers may be used to “drill” holes for recipient sites. Even in scarring alopecia, modern Er:YAG lasers with high pulse energy can drill holes for hair transplants efficiently, with less bleeding than with punches, and with less tissue damage as with CO2 lasers, which is important for graft take (78). 6.

CONCLUSION

Er:YAG lasers have become useful tools for facial resurfacing of mild to moderate facial scars, rhytids, and photodamage. These lasers have a high ablative capacity and produce very thin zones of residual thermal damage. Faster healing times and fewer side effects are therefore observed compared to CO2 laser treatment. The degree of number or scar improvement and skin contraction, however, is less than with CO2 lasers. Er:YAG lasers are useful devices for the treatment of benign epidermal lesions, leaving rapidly re-epithelializing wounds and minimal erythema. There are also considerable advantages in combining CO2 laser treatment with Er:YAG laser treatment to decrease residual thermal damage and speed re-epithelializing without compromising the efficacy. REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9.

10. 11.

12.

Walsh JT, Deutsch TF. Er:YAG laser ablation of tissue: measurement of ablation rates. Lasers Surg Med 1989; 9:327 – 337. Kaufmann R, Hibst R. Pulsed 2.94-mm erbium-YAG laser skin ablation—experimental results and first clinical application. Clin Exp Dermatol 1990; 15:389– 393. Walsh JT, Cummings JP. Effect of the dynamic optical properties of water on midinfrared laser ablation. Lasers Surg Med 1994; 15:295 – 305. Berger JW. Erbium-YAG laser ablation: the myth of 1-micron penetration. Arch Ophthalmol 1998; 116:830 – 831. Walsh JT, Flotte TJ, Deutsch TF. Er:YAG laser ablation of tissue: effect of pulse duration and tissue type on thermal damage. Lasers Surg Med 1989; 9:314 – 326. Weiss RA, Harrington AC, Pfau RC, Weiss MA, Marwaha S. Periorbital skin resurfacing using high energy erbium:YAG laser: results in 50 patients. Lasers Surg Med 1999; 24:81 –86. Weinstein C. Erbium laser resurfacing: current concepts. Plast Reconstr Surg 1999; 103:602–616. Hibst R, Kaufmann R. Vergleich verschiedener Mittelinfrarot-Laser fu¨r die Ablation der Haut. Lasermedizin 1995; 11:19– 26. Hohenleutner U, Hohenleutner S, Ba¨umler W, Landthaler M. Fast and effective skin ablation with an Er:YAG Laser: determination of ablation rates and thermal damage zones. Lasers Surg Med 1997; 20:242– 247. Kaufmann R, Hibst R. Pulsed erbium:YAG laser ablation in cutaneous surgery. Lasers Surg Med 1996; 19:324– 330. Ross EV, Glatter RD, Duke D, Grevelink JM. Effects of pulse and scan stacking in CO2 laser skin resurfacing: a study of residual thermal damage, cell death and wound healing. Lasers Surg Med 1997; 20(suppl 9):42. Ratner D, Tse Y, Marchell N, Goldman MP, Fitzpatrick RE, Fader DJ. Cutaneous laser resurfacing. J Am Acad Dermatol 1999; 41:365 – 389.

Er:YAG Lasers 13. 14.

15.

16. 17. 18. 19.

20. 21. 22. 23.

24. 25.

26. 27. 28.

29.

30. 31.

32. 33. 34. 35.

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Alster TS. Clinical and histologic evaluation of six erbium:YAG lasers for cutaneous resurfacing. Lasers Surg Med 1999; 24:87– 92. Tse Y, Manuskiatti W, Detwiler SP, Fitzpatrick RE, Goldman MP. Tissue effects of the erbium:YAG laser with varying passes, energy and pulse overlap. Lasers Surg Med 1998; 22(suppl 10):70. Kauvar AN, Grossman MC, Bernstein LJ, Kovacs SQ, Quintana AT, Geronemus RG. Comparison of tissue effects of carbon dioxide, erbium:YAG and novel infrared lasers for skin resurfacing. Lasers Surg Med 1998; 22(suppl 10):37. Alster TS. Cutaneous resurfacing with CO2 and erbium:YAG lasers: preoperative, intraoperative, and postoperative considerations. Plast Reconstr Surg 1999; 103:619– 632. Khatri KA, Ross V, Grevelink JM, Magro CM, Anderson RR. Comparison of erbium:YAG and carbon dioxide lasers in resurfacing of facial rhytides. Arch Dermatol 1999; 135:391– 397. Alster TS, Kauvar AN, Geronemus RG. Histology of high-energy pulsed CO2 laser resurfacing. Semin Cutan Med Surg 1996; 15:189– 193. Cotton J, Hood AF, Gonin R, Beeson WH, Hanke CW. Histologic evaluation of preauricular and postauricular human skin after high-energy, short-pulse carbon dioxide laser. Arch Dermatol 1996; 132:425 – 428. Rubach BW. Comparison of chemical peel and dermabrasion to carbon dioxide (CO2) laser resurfacing. Oper Tech Otolaryngol Head Neck Surg 1997; 8:9 –14. Perez MI, Bank DE, Silvers D. Skin resurfacing of the face with the erbium:YAG laser. Dermatol Surg 1998; 24:653 –659. Kaufmann R, Hartmann A, Hibst R. Cutting and skin-ablative properties of pulsed midinfrared laser surgery. J Dermatol Surg Oncol 1994; 20:112 – 118. Utley DS, Koch RJ, Egbert BM. Histologic analysis of the thermal effect on epidermal and dermal structures following treatment with the superpulsed CO2 laser and the erbium:YAG laser: an in vivo study. Lasers Surg Med 1999; 24:93– 102. Weinstein C. Computerized scanning erbium:YAG laser for skin resurfacing. Dermatol Surg 1998; 24:83 – 89. Hohenleutner S, Hohenleutner U, Ba¨umler W, Landthaler M. Laser skin resurfacing— Er:YAG-Laser und cw-CO2 Laser mit Scannersystem im Seitenvergleich. Hautarzt 1998; 49:367 – 371. Hohenleutner S, Hohenleutner U, Landthaler M. Comparison of erbium:YAG and carbon dioxide laser for the treatment of facial rhytides. Arch Dermatol 1999; 135:1416– 1417. Fitzpatrick RE, Rostan EF, Marchell N. Collagen tightening induced by carbon dioxide laser versus erbium:YAG laser. Lasers Surg Med 2000; 27:395 – 403. Greene D, Egbert BM, Utley DS, Koch RJ. In vivo model of histologic changes after treatment with the superpulsed CO2 laser, erbium:YAG laser, and blended lasers: a 4- to 6-month prospective histologic and clinical study. Lasers Surg Med 2000; 27:362 – 372. Newman JB, Lord J, Ash K, McDaniel DH. Variable pulse erbium:YAG laser skin resurfacing of perioral rhytides and side-by-side comparison with carbon dioxide laser. Lasers Surg Med 2000; 26:208 – 214. Khatri KA. The effects of variable pulse width of Er:YAG laser on facial skin. Dermatol Surg 2001; 27:332 – 334. Ross EV, McKinlay JR, Sajben FP, Miller CH, Barnette DJ, Meehan KJ, Chhieng NP, Deavers MJ, Zelickson BD. Use of a novel erbium laser in a Yucatan minipig: a study of residual thermal damage, ablation, and wound healing as a function of pulse duration. Lasers Surg Med 2002; 30:93 – 100. Pozner JM, Goldberg DJ. Histologic effect of a variable pulsed Er:YAG laser. Dermatol Surg 2000; 26:733 – 736. Majaron B, Srinivas SM, Huang HL, Nelson JS. Deep coagulation of dermal collagen with repetitive Er:YAG laser irradiation. Lasers Surg Med 2000; 26:215 –222. Rostan EF, Fitzpatrick RE, Goldman MP. Laser resurfacing with a long pulse erbium: YAG laser compared to the 950 ms pulsed CO2 laser. Lasers Surg Med 2001; 29:136 – 141. Zachary CB. Modulating the Er:YAG laser. Lasers Surg Med 2000; 26:223 – 226.

196 36. 37.

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54. 55. 56. 57. 58. 59. 60. 61.

Hohenleutner and Landthaler Ediger MN, Matchette LS. In vitro production of viable bacteriophage in a laser plume. Lasers Surg Med 1989; 9:296 – 299. Mullarky MB, Norris CW, Goldberg ID. The efficacy of the CO2 laser in the sterilization of skin seeded with bacteria: survival at the skin surface and in the plume emissions. Laryngoscope 1985; 95:186 – 187. Baggish MS, Elbakry M. The effects of laser smoke on the lungs of rats. Am J Obstet Gynecol 1987; 156:1260 – 1265. Garden JM, O’Banion MK, Shelnitz LS, Pinski KS, Bakus AD, Reichmann ME, Sundberg JP. Papillomavirus in the smoke of carbon-dioxide laser treated verrucae. J Am Med Assoc 1988; 259:1199 – 1202. Nezhat C, Winer WK, Nezhat F, Forrest D, Reeves WG. Smoke from laser surgery: is there a health hazard? Lasers Surg Med 1987; 7:376– 382. Hughes PSH, Hughes PA. Absence of human papillomavirus DNA in the plume of erbium:YAG laser-treated warts. J Am Acad Dermatol 1998; 38:426 – 428. Kirkpatrick JJR, Mackay IR. Sound levels produced by Erbium YAG lasers: health and safety issues. Lasers Med Sci 2000; 15:263– 265. Goldman MP, Fitzpatrick RE, Manuskiatti W. Laser resurfacing of the neck with the erbium: YAG laser. Dermatol Surg 1999; 25:164 – 167. Goldberg DJ, Meine JG. Treatment of photoaged neck skin with the pulsed erbium:YAG laser. Dermatol Surg 1998; 24:619 –621. Goldman MP. Techniques for erbium:YAG skin resurfacing: initial pearls from the first 100 patients. Dermatol Surg 1997; 23:1219 – 1221. Dover JS. Roundtable discussion on laser skin resurfacing. Dermatol Surg 1999; 25:639 – 653. Dover JS, Arndt KA, Dinehart SM, Fitzpatrick RE, Gonzalez E. Guidelines of care for laser surgery. J Am Acad Dermatol 1999; 41:484– 495. Roenigk RK, Rigel DS, Glogau RG. Table talk: common questions about laser resurfacing. Dermatol Surg 1997; 24:121 –130. Duke D, Grevelink JM. Care before and after laser skin resurfacing. A survey and review of the literature. Dermatol Surg 1998; 24:201– 206. Teikemeier G, Goldberg DJ. Skin resurfacing with the erbium:YAG laser. Dermatol Surg 1997; 23:685 – 687. Riedel F, Bergler W, Baker SA, Stein E, Hormann K. Kontrollierte Feinstdermablation im Gesichtsbereich mit dem Erbium:YAG-Laser. HNO 1999; 47:101– 106. Jimenez G, Spencer JM. Erbium:YAG laser resurfacing of the hands, arms, and neck. Dermatol Surg 1999; 25:831 –835. McDaniel DH, Lord J, Ash K, Md JN. Combined CO2/erbium:YAG laser resurfacing of peri-oral rhytides and side-by-side comparison with carbon dioxide laser alone. Dermatol Surg 1999; 25:285 –293. Polnikorn N, Goldberg DJ, Suwanchinda A, Ng SW. Erbium:YAG laser resurfacing in Asians. Dermatol Surg 1998; 24:1303 –1307. Goldberg DJ, Cutler KB. The use of the erbium:YAG laser for the treatment of class III rhytids. Dermatol Surg 1999; 25:713 –715. Collawn SS. Combination therapy: utilization of CO2 and erbium:YAG lasers for skin resurfacing. Ann Plast Surg 1999; 42:21 –26. Stuzin JM, Baker TJ, Baker TM. CO2 and erbium:YAG laser resurfacing: current status and personal perspective. Plast Reconstr Surg 1999; 103:588– 591. Riedel F, Windberger J, Stein E, Hormann K. Behandlung periokula¨rer Hautvera¨nderungen mit dem Erbium:YAG-Laser. Ophthalmologe 1998; 95:771 –775. Hughes PSH. Skin contraction following erbium:YAG laser resurfacing. Dermatol Surg 1998; 24:109 – 111. Goldman MP, Manuskiatti W. Combined laser resurfacing with the 950-microsec pulsed CO2 þ Er:YAG lasers. Dermatol Surg 1999; 25:160– 163. Millman AL, Mannor GE. Histologic and clinical evaluation of combined eyelid erbium:YAG and CO2 laser resurfacing. Am J Ophthalmol 1999; 127:614 – 616.

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Trelles MA, Allones I, Luna R. One-pass resurfacing with a combined-mode erbium:YAG/ CO2 laser system: a study in 102 patients. Br J Dermatol 2002; 146:473 – 480. Drnovsek-Olup B, Vedlin B. Use of Er:YAG laser for benign skin disorders. Lasers Surg Med 1997; 21:13 – 19. Manaloto RM, Alster T. Erbium:YAG laser resurfacing for refractory melasma. Dermatol Surg 1999; 25:121 – 123. Jeong J-T, Kye J-C. Resurfacing of pitted facial acne scars with a long-pulsed Er:YAG laser. Dermatol Surg 2001; 27:107 –110. Lorenz S, Hohenleutner S, Hohenleutner U, Landthaler M. Treatment of diffuse plane xanthoma of the face with the Er:YAG laser. Arch Dermatol 2001; 137:1413– 1415. Kaufmann R, Beier C. Erbium:YAG laser therapy of skin lesions. Med Laser Appl 2001; 16:252 – 263. Xanthelasma palpebrarum: treatment with the erbium:YAG laser. Lasers Surg Med 2001; 29:260 – 264. Orenstein A, Haik J, Tamir J, Winkler E, Frand J, Zilinsky I, Kaplan H. Treatment of rhinophyma with Er:YAG laser. Lasers Surg Med 2001; 29:230 – 235. Beier C, Kaufmann R. Efficacy of erbium:YAG laser ablation in Darier disease and Hailey-Hailey disease. Arch Dermatol 1999; 135:423– 427. Ochsendorf FR, Kaufmann R. Erbium:YAG laser-assisted treatment of miliary osteoma cutis. Br J Dermatol 1998; 138:371 – 372. Hughes PS. Multiple miliary osteomas of the face ablated with the erbium:YAG laser. Arch Dermatol 1999; 135:378 – 380. Kageyama N, Tope WD. Treatment of multiple eruptive hair cysts with erbium:YAG laser. Dermatol Surg 1999; 25:819 –822. Boehncke WH, Ochsendorf F, Wolter M, Kaufmann R. Ablative techniques in psoriasis vulgaris resistant to conventional therapies. Dermatol Surg 1999; 25:618 – 621. Albertini JG, Holck DEE, Farley MF. Zoon’s balanitis treated with erbium:YAG laser ablation. Lasers Surg Med 2002; 30:123 – 126. Kaufmann R, Greiner D, Kippenberger S, Bernd A. Grafting of in vitro cultured melanocytes onto laser-ablated lesions in vitiligo. Acta Derm Venereol 1998; 78:136 –138. Yang JS, Kye YC. Treatment of vitiligo with autologous epidermal grafting by means of pulsed erbium:YAG laser. J Am Acad Dermatol 1998; 38:280 – 282. Podda M, Spieth K, Kaufmann R. Er:YAG laser-assisted hair transplantation in cicatricial alopecia. Dermatol Surg 2000; 26:1010 – 1014.

7 Pulsed Dye Lasers Kristen A. Richards Scripps Memorial Hospital, La Jolla, California, USA

Jerome M. Garden Northwestern University Medical School and Children’s Memorial Hospital, Chicago, Illinois, USA

1. Introduction 2. Basic Concepts 3. Safety 4. Laser Parameters 5. Clinical Effectiveness 6. Port-Wine Stains 7. Telangiectasias 8. Hemangiomas 9. Other Benign Vascular Disorders 10. Nonvascular Lesions 11. Rhytides 12. Pre- and Postoperative Considerations 13. Summary References

1.

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INTRODUCTION

The pulsed dye laser’s clinical applications are diverse including vascular and nonvascular lesions as well as its newer use as a nonablative resurfacing tool. The paucity of side effects associated with the development of the dye laser in a pulsed mode has allowed the practitioner to treat lesions in all age groups and anatomical sites. 2.

BASIC CONCEPTS

In order to understand the reasons for the therapeutic advancements, it is important to evaluate several basic laser parameters. All lasers emit at specific wavelengths depending 199

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upon the type of lasing medium in the optical cavity. As such, many different wavelengths can potentially be used as a source of lesional irradiation. For cutaneous blood vessel processes, such as port-wine stains (PWS), hemangiomas, spider angiomas, or telangiectasias, the main lesional chromophore is hemoglobin. It is assumed oxyhemoglobin is the major hemoglobin species which is present. It is an excellent target for laser emission, being located intravascularly and in high concentration. Oxyhemoglobin has major absorption peaks at 418, 542, and 577 nm (1,2). Although the strongest peak is at 418 nm, and, therefore, this wavelength would be most readily absorbed, the laser emission wavelength chosen for therapy centers around the 577 nm peak. The reasons for deciding on the weaker 577 nm absorption band are twofold. First, the major competing chromophore in the skin is melanin. Melanin absorbs very well in the ultraviolet range and has a diminishing absorption capacity throughout the visible range. Absorption of melanin at 418 nm is significantly greater than at 542 or 577 nm, with the latter wavelength having the least amount of absorption. The other reason is the penetration depth of laser emission. For the nonionizing, visible range of wavelengths, the longer the wavelength the deeper is the tissue penetration. Therefore, 577 nm has the advantage of coinciding with an oxyhemoglobin absorption band which has decreased melanin absorption and the advantage of increased tissue penetration (3). Recent evidence suggests that the use of longer wavelengths still maintains selective oxyhemoglobin absorption and vascular damage while increasing the depth of penetration over 577 nm (4 –6). Tissue response to laser emission is not only wavelength dependent but also time dependent. Since the effect of most cutaneous medical lasers is mainly through photothermal conversion, a longer tissue exposure results in a greater thermal response. Mathematical tissue modeling has been used to predict optimum laser time emissions to effect selective destruction of cutaneous blood vessels (2). An index used to assist in these computations is the thermal relaxation time. This is the time in which a heated container, such as the cutaneous blood vessel, loses about two-thirds of its maximum heat. Depending on blood vessel size, optimum pulse durations, at a specific wavelength, can be estimated through these formulae to produce the desired selectivity. The goal of these calculations is to find the amount of time necessary to heat and denature the vasculature while sparing the surrounding tissue (1). Dierickx et al. (7) found that pulse durations for ideal laser treatment are in the 1– 10 ms region for PWS and depend on vessel diameter. Selective heating of the targeted blood vessels can be best accomplished through the containment of high temperatures to the vessels, followed by the slow diffusion of cooler temperatures to the perivascular area. If the pulse duration produces vascular destruction and does not remain on long enough to allow diffusion of undesired high temperatures to the surrounding tissue, tissue sparing occurs. Clinical studies initially evaluated normal skin response, and subsequently, PWS response. Analysis of the 350 ns to 20 ms pulse duration range at 577 nm revealed vascular selective laser-induced damage (8 – 10), but these pulse durations were unable to produce PWS lightening (11). Although the confinement of thermal damage was vascular-specific with no apparent perivascular change, the vessels were able to repair sufficiently to effect no clinical change. When pulse durations were extended to the 20 – 450 ms range, at 577 nm, vascular selectivity remained (9). However, with these longer pulse durations, lesional lightening also occurred. Histological evaluation revealed an intravascular coagulum and not the extravasation of RBC seen at the shorter pulse durations (9,12). The longer pulse durations, especially those .200 ms, had an increased tendency to produce lesional lightening. Perivascular changes remained unremarkable with only a few areas of scattered focal epidermal spongiosis. The epidermal changes occurred most commonly adjacent to the

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areas of superficial blood vessels, which may have reflected direct thermal diffusion to the epidermis from these vessels. From these studies it appears that the time for the intravascular photothermal conversion must be long enough to cause significant endothelial damage and still short enough not to allow high temperatures to diffuse into the perivascular area. After analysis and selection of the appropriate wavelength and pulse duration for optimizing selective destruction of cutaneous blood vessels, another important laser parameter is the amount of energy delivered to the tissue (13). Based on mathematical projections at 577 nm and modeled for cutaneous blood vessels, energy fluences may be estimated which can elevate the core vessel temperature to 708C, producing the desired permanent endothelial denaturation (1). When initially studied in normal skin, the necessary energies for purpura and vessel damage were remarkably similar to these estimated values. Indeed, when much higher energy densities were tested in normal skin, there was significant perivascular damage with collagen denaturation. The data assisted the clinician in developing a therapeutic energy range for the PWS. On normal skin, the energy necessary to produce purpura at 577 nm and a 360 ms pulse duration with a 3 mm spot size was found to be 3.5 –4.25 J/cm2, depending on skin temperature (14,15) and color (16). Both of these factors influence laser –tissue interaction. The colder the tissue, the more is the energy fluence necessary to produce purpura. This is due either to vessel constriction and a decrease in target size or the need to heat the tissue over a greater temperature range. Also, epidermal melanin, acting as a shield or barrier to the incoming photons, necessitated using higher energies for darker skin types. The PWS, with its dilated vessels, requires a higher-energy fluence to produce lesional lightening. Again, the tissue factors of temperature and color play a similar role in lesional skin response as in normal skin (17). Another laser parameter that has been analyzed is the spot size. The spot size is the area of laser impact on the tissue during each pulse. Animal studies observed inconsistent laser tissue effects with a circular spot size of ,3 mm in diameter (18). It is believed that optical effects secondary to dermal scattering are important factors in the clinical outcome with changing spot size. Recent clinical work with a 2 mm spot size in the treatment of solitary telangiectatic vessels demonstrates the necessity for higher-energy fluences than used with 3 mm or greater spot sizes (19). Dinehart et al. (20) studied the beam profile of the flashlamp-pumped pulsed dye laser and found that 13% overlap of pulses could occur to better cover large vascular lesions without an increase in postoperative side effects. The selective thermal destruction of blood vessels with sparing of surrounding tissue using the above approach of optimizing laser and tissue parameters has been termed selective photothermolysis (21). It allows for the incorporation of laser light into tissues, targeted for specific structures, producing photothermal selective damage, without the need for structure-specific laser focusing. It is this approach which has produced an advancement in the desired clinical outcome. While the theoretical concepts were being developed, it was necessary to have a laser which could properly deliver the optimized laser parameters to the tissue. The flashlamp-pumped tunable pulsed dye laser was chosen because of its inherent flexibility. An emission in the 577 nm range was achieved by selecting the appropriate organic dye as the lasing medium and tuning to the desired wavelength with a filter. Recent modifications mix different organic dyes at set concentrations, producing the desired wavelength emission and forgoes the need of a filter. Also, the pulsed dye laser excited the dye long enough to achieve a pulse duration in the 400– 500 ms range, with sufficient energy to produce spot sizes of 3 mm and above.

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Other lasers available for the treatment of cutaneous lesions either do not emit at the desired wavelength (argon, CO2 , Nd:YAG, ruby, current diodes, alexandrite and KTP) or are unable to produce pulse durations in the desired time range (argon, CO2 , Nd:YAG, ruby, KTP, copper-vapor, krypton, and argon laser-pumped tunable dye laser). Although many of these lasers are used beneficially to treat cutaneous blood vessel lesions, the decrease in laser – tissue selectivity with these lasers has limited patient selection, increased the need for technical expertise and, most importantly, potentially increased the occurrence of undesired side effects (22,23).

3.

SAFETY

The greatest risk to the patient and to the treating staff is eye damage. Because of good absorption of 585 nm light by the pigmented and vascular portions of the retina, there is a great potential for significant retinal damage if the appropriate protective eyewear is not worn. Goggles made from didymium, which has a narrow band of absorption high in the 500 nm visible spectrum are ideal for eye protection while at the same time allowing the operator to see. The patient can either wear these protective goggles, opaque goggles, or their eyes may be covered with gauze, or in the case of periorbital treatment, with metallic eye shields. Other risks include flash fire with the use of ethyl chloride cryogen spray, supplemental oxygen, and green vinyl tubing (24,25).

4.

LASER PARAMETERS

Pulsed dye laser parameters vary widely and are largely dependent on the lesion being treated. Table 7.1 outlines the parameters for currently used pulsed dye laser systems. Table 7.1 Pulsed Dye Laser Systems

Brand name

Wavelength (nm)

Pulse duration (ms)

Spot size and fluence (Maximum)

Candela

ScleroPLUS-HP

585– 600

1.5

Candela

V beam

595

Cynosure

Photo-Genica VLS

585– 600

Cynosure

Photo-Genica V-Star

595

5 mm, 20 J/cm2 7 mm, 15 J/cm2 10 mm, 6.0 J/cm2 2 7 mm, 30 J/cm2 7 mm, 15 J/cm2 10 mm, 7.5 J/cm2 3 10 mm, 25 J/cm2 3 mm, 20 J/cm2 5 mm, 20 J/cm2 7 mm, 10 J/cm2 10 mm, 5 J/cm2 3 5 mm, 20 J/cm2 7 mm, 20 J/cm2 10 mm, 10 J/cm2 12 mm, 7 J/cm2 3 5 mm, 25 J/cm2

Manufacturer

0.5– 40

0.45– 1.5

0.5– 40

Cooling Cryogen spray

Cryogen spray Air-cooled

Air-cooled

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The clinical information below more precisely addresses the settings indicated for the treatment of specific lesions. 5.

CLINICAL EFFECTIVENESS

There are many types of cutaneous blood vessel lesions that have been successfully treated with the pulsed dye laser including PWS, capillary hemangioma, telangiectasia, spider and senile angioma, permanent erythema from rosacea or trauma, angioma serpiginosum, angiofibroma, venous ectasia, and minor varicosities. It appears that in any small-caliber vessel, superficial tissue process is amenable to pulsed dye laser therapy (26 – 28). The most data and experience have been accumulated with PWS. In addition, there are many nonvascular lesions that have also been effectively treated using the pulsed dye laser. 6.

PORT-WINE STAINS

The major laser parameter which is varied with this laser is the emitted energy. However, wavelengths from 585 to 600 nm and pulse durations from almost 0.5 –10 ms are being used (29,30). Pulse durations past 20 ms are also being evaluated for effectiveness. Therapeutic energy dosages for PWS range from 3.5 up to 12 J/cm2 when using epidermal sparing methods such as cryogen sprays prior to laser impact for the higher fluences. The spot size generally used in treating PWS is either 7 or 10 mm. Originally in the treatment of PWS, test sites were placed over the lesion using energies of 1.5– 2 times the purpura dose. This was defined as the least amount of energy necessary to cause normal, nonlesional skin, to become purpuric within a set amount of time after laser exposures. However, as experience developed threshold testing was found unnecessary and test site energies are now chosen based on age, anatomical area, lesional thickness, and color (31). When the laser light impacts the tissue, two events occur. The patient experiences discomfort, described by many as a hot pin-prick or an elastic band snapping the skin, and the tissue becomes purpuric. The sensation is generally well tolerated by the adult patient except over anatomical sites of increased sensitivity such as the upper lip or periorbital areas. Larger diameter spot sizes may increase the perceived sensation. Epidermal cooling through cryogen sprays or cold water chambers also reduces associated pain. Local anesthesia, topical or injected, is helpful (32). In the adolescent or pediatric patient, several local anesthetic formulations have been useful. Four percent lidocaine gel (available in Great Britain) was found to be significantly better than eutectic mixture of local anesthetics (EMLA) in reducing pain caused by laser treatment (33). Twenty-five percent lidocaine in 70% dimethyl sulfoxide – ethanol was found to provide significantly greater permeation than EMLA cream but only provided some degree of anesthesia (10 – 100%) in 8/14 pediatric patients (34). Studies of pain control during pulsed dye laser treatments have shown iontophoresis using lidocaine 4% or 5% with or without epinephrine significantly decreases discomfort (35,36). The older child may find nitrous oxide beneficial, while infants have been helped by chloral hydrate or other oral mild sedating agents. Many of the children need even deeper sedation, with outpatient intramuscular or intravascular anesthesia being necessary. Popular anesthetics include propofol and ketamine for early infancy. Halothane can also be administered with ease when desired without the need for intubation (37). A newer fast-acting inhalation anesthetic agent, Sevoflurane, is now used in most patients for mask induction (38).

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The purpura which occurs after laser impact, appears immediately or within a few minutes. It gradually darkens over the initial 24 h. Histologically, the purpura represents an intravascular coagulum (12). Within 24 h a leucocytoclastic vasculitis develops in treated vessels. Resorption of the vessel occurs over 4 weeks. The vessels are replaced by normal diameter vessels within a few months of treatment (39). Clinically, the purpura remains with the PWS patient for an average of 7 –14 days (40). During this time, the pediatric patient applies a topical antibiotic ointment as part of postoperative care. The adult patient, however, is allowed to place a cosmetic cover-up over the treated area immediately after therapy. Occasionally, there is some epidermal scaling or crusting at the higher energies used in the adult patient, which is treated with a topical antibiotic ointment. An atopic dermatitis-like reaction occasionally develops with PWS treatment which usually responds to treatment with mild topical corticosteroids (41). Test sites are placed over the PWS during the initial evaluation to judge clinical efficacy and optimal energy dosage. Multiple sites are generally placed using various parameters. Since the PWS is nonhomogeneous, different energies, wavelengths, or pulse durations may be needed to achieve the same clinical effect over various anatomical areas of the PWS. The goal is to use the least amount of energy to achieve the maximum acceptable outcome. There appears to be a dose-dependent clinical therapeutic window. Too little energy does not produce enough clinical lightening and too much energy may cause undesired pigmentary and texture changes with the potential of scarring. Although the PWS darkening that occurs with the laser impact generally resolves in 7 – 14 days, it may remain slightly longer with the 7 mm spotsize and higher fluences and shorter when using longer pulse durations and wavelengths. Eventual lesional lightening may take 2– 3 months (26 –28,40). In fact, after the darkening resolves, the lesion may appear redder or unchanged for several weeks. There is almost always a need to re-treat the same lesional area to enhance the PWS lightening. These retreatment sessions are repeated every 2 –3 months until a maximum degree of lesional clearing is achieved. It is not uncommon for the full lesion to undergo many treatment sessions. Lesional lightening may be achieved even after 20 treatment sessions. However, the percentage of lightening with each treatment continues to decrease and eventually it becomes appropriate to suspend therapy. Lesional lightening outcome can range from total clearing to very little perceptible change. It is assumed that a more superficial vessel having a smaller caliber will clear easier than a larger vessel situated deep in the dermis. Response to treatment also seems to vary based on two major patterns of vascular abnormality. Type 1 vessels composed of superficial, tortuous end capillary loops responded more effectively than Type 2 vessels composed of dilated, ectatic vessels in the superficial horizontal vascular plexus (42). Analysis of posttreatment vessels showed coagulated vessels to be superficially located (within 400 mm of the dermoepidermal junction) and of moderate size (38+19 mm) whereas lesions that showed poor blanching were significantly smaller (19+6.5 mm) or deeper (.800 mm from the dermoepidermal junction). In addition, red PWS predict a good response due to superficial location of the PWS whereas pink PWS predict a poor response due to the small vessel size and deep location (43). Since these lesions are composed of various caliber vessels with differing depths of involvement, inconsistent lightening occurs when comparing patient outcome, even within the same lesion. Analysis of lesional lightening reveals that 36 – 44% of adult PWS patients have 75% or greater color lightening and approximately 75% of the patients have at least 50% lightening after a total of four treatments (44,45). These results were based on a limited number of retreatments. It is likely that continued lightening would have occurred

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with more retreatment sessions [Fig. 7.1(a) and (b)]. The adult patients in which repeated treatments do not produce a substantial amount of lightening, fortunately account for ,10% of the total treated patients. Some of these patients possess the nodular and thickened PWS, which do not respond well to this laser. In patients who failed to achieve .75% lesional lightening within nine treatment sessions, significant improvement was seen after 10– 25 repetitive treatments (46). Very resistant PWS may respond better to continuous wave or quasicontinuous wave lasers, such as the argon, coppervapor, Nd:YAG, or krypton lasers, or intense pulsed noncoherent light sources which incorporate a greater degree of nonselective thermal energy necessary to decrease the soft tissue and vascular enlargements (22). Of interest are the PWS patients who do not respond well and have clinically identical lesions to other patients who do achieve an acceptable degree of lightening. Apparently, the clinical presentation of the lesion is not a consistent predictor as to therapeutic outcome with this laser. Anatomical areas respond differently to this laser, as with other types of lasers. Central cheeks and the upper lip areas are more resistant to therapy. V2 distributed PWS were found to clear ,25% after repeated laser treatments (47). The lower extremities and the distal upper extremities also are less responsive. The periorbital, lateral facial, neck, chest, and upper arm areas generally respond the best to the pulsed dye laser (48,49). Lesion size also plays a role in determining the response to the treatment. In one study, none of four adult patients with PWS .100 cm2 achieved 50% clearing following a mean of 17.2 + 5.7 treatments (50). In another study 15 (32%) of 47 patients with PWS ,20 cm2 at initial evaluation were totally cleared vs. 3 (8%) of 36 patients with PWS .20 cm2 (51). Even more significant than the degree of lesional lightening in the adult PWS patient has been the paucity of undesired adverse effects. A retrospective study of 701 patients with PWS treated with the pulsed dye laser showed hyperpigmentation as the most frequently observed adverse event in 9.1% of patients. Generally, this darkening slowly resolved over 6 – 12 months. Hypopigmentation was only seen in 1.4% of patients. Blistering and crusting were seen in 5.9% and 0.7% of patients, respectively. There was also a small but definite risk of scarring. Atrophic scarring occurred in 4.3% of patients with a predisposition for younger patients. Hypertrophic scarring was seen rarely in only 0.7% of patients and had a predisposition toward the neck (52). The clinical outcome in the pediatric PWS population using the pulsed dye laser has also been remarkable (28,53 – 57). Some studies affirm a greater ability to achieve lesional

Figure 7.1 (a) A 40-year-old female with right cheek PWS. (b) Same patient after 10 treatments with the pulsed dye laser. Photograph was taken 4 months after the last treatment (7 mm spot size, 7.25 J/cm2, 585 nm, 0.5 ms pulse duration).

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lightening in the child than in the adult. The range of reported PWS lightening in these pediatric patients is from 100% clearing in all treated patients (53,54), to .95% clearing in 18% with the rest achieving 65 –70% response (55), to 42% of patients achieving .75% clearing and 84% of patients .50% response (56) to finally, 87% of patients reaching 50% lightening (57). These studies had differing age ranges, number of treatment sessions (ranging from two to more than six), and laser parameters, which make direct comparison difficult. Another study examined 91 patients younger than 18 years of age with PWS and found that the most successful response was seen in patients ,1 year old with small PWS (,20 cm2) which were located over bony areas of the face such as the central forehead (58). Other studies support the concept that there is no difference in response rates according to age. Alster and Wilson (59) reported that the number of treatments necessary to clear PWS in children 9 –16 years of age and patients .16 years of age was not greater than the number required to treat PWS in infants 0 –2 years of age. Van der Horst et al. (60) also found that there were no significant differences in color diminution of PWS amongst 89 patients divided into four different age groups. The small vessel caliber of the pediatric PWS compared to the adult may be a factor. The natural clinical progression of the PWS is to appear pink to red in childhood and to gradually darken and thicken in adulthood. This is due to progressive widening of the vessels with age. Unfortunately, there are infants who present with deeply colored PWS which indeed may lighten with greater difficulty (54). It is still necessary to perform retreatment sessions of lesional sites in the pediatric population. Whether with pediatric or adult PWS, after therapy is completed, when there is residual lesion that does not continue to sufficiently respond to warrant further procedures, there is always the potential of the lesion darkening with time. Indeed, that already has occurred in several patients. One would anticipate this happening due to natural evolution of vessel dilatation with aging. It is hoped that these treated lesions will not revert back to their original presentation since many of the vessels after treatment are of normal caliber. However, should the underlying etiology of PWS be a defect in PWS vessel nerve innervation, a greater than expected recurrence may happen. A prospective study examined 102 patients of ages 1 month to 66 years, with PWS who had good to complete responses after treatment with the pulsed dye laser. The authors found that PWS showed a tendency to recur at a rate approaching 50% between 3 and 4 years after completion of treatment (61). The energy dosages necessary for treatment of the pediatric PWS patient is less than in the adult, with the therapeutic window being smaller. However, energies as low as 3.5 J/cm2 have been used successfully in some pediatric PWS in certain anatomic areas, such as the neck and chest, using the 10 mm spot size. The potential to produce textural changes are greater in the pediatric population. Even energies above 6.5 J/cm2 have a tendency to produce these cutaneous changes in the younger ages. It is appropriate to treat these lesions with a greater number of repeat sessions at lower energies. The introduction of epidermal sparing using cold water chambers and cryogen sprays have allowed for a significant increase in energy to be tolerated. At 595 nm, in some cases, energies of 10 J/cm2 or greater may be used with a 7 mm spot size (30). Overlapping of the individual circular pulses is recommended in an effort to prevent a honeycomb pattern of clearing. This not only improves the appearance of the PWS as it clears but it also reduces the total number of needed treatments. However, overlapping should be limited to 10 –15% of the spot size (62). This is especially true in pediatric PWS, where there may be an increased risk of scarring if too much overlap occurs. The size of the treatment area is mainly determined by the patients’ tolerance of the procedure.

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Although treatment with the pulsed dye laser is far less painful than with continuous wave lasers, each pulse does produce discomfort. As the number of pulses increases, the pain associated with the treatment increases. Thus, pain may become the limiting factor of treatment if appropriate anesthetic intervention, such as that described earlier, is not used. Several new methods have been developed recently that more effectively increase clearance of PWS while minimizing side effects. Four patients completed clearing of their PWS after three to five sessions using a “multilayer technique.” During the first pass, the wavelength ranged from 590 to 600 nm with a long pulse (1.5 ms) while the second pass was performed utilizing the classic short pulse (450 ms) and wavelength (585 nm). One patient was noted to have mild blistering that eventually healed without scarring (63). Cryogen spray used in conjunction with the pulsed dye laser has allowed the use of higher fluences and improved PWS clearance while minimizing epidermal damage. In addition to increased clinical efficacy, a reduction in pain was also noted, especially in patients with darker skin types (64 – 66).

7.

TELANGIECTASIAS

Cutaneous vascular lesions, other than PWS, also respond well to the pulsed dye laser. Face, neck, and trunk telangiectases can be treated generally using a 2 7 mm or 2 mm spot size. Textural changes and hypopigmentation have been reported following treatment of facial telangiectasias (67). Telangiectasias may arise from a variety of causes, including actinic damage, rosacea, connective tissue disease, progressive ascending telangiectasia, telangiectasia macularis eruptiva perstans, hepatic dysfunction, or posttrauma (68 – 72). Darkening of the treated area resolves faster than with the PWS, lasting 5 –10 days. However, the dark appearance posttherapy is still of concern to many patients. Fortunately, the smaller 2 mm spot size has significantly diminished the posttherapy bruised appearance as does the use of the 595 nm wavelength or those even longer. Longer pulse durations may also reduce or eliminate the posttherapy darkening. Patient discomfort is less with the smaller spot size. Test site placement is only occasionally necessary with telangiectatic processes. Energies higher than 7.0 J/cm2 are usually necessary when using the 2 mm spot size. Lesional lightening may occur immediately after the posttherapy darkening resolves or up to 4– 6 weeks later. Retreatment sessions may be necessary but less often than with the PWS. The final therapeutic outcome is usually excellent with a significant reduction of the telangiectasias with only rare cases of skin texture change and/or depression. Vessels on the face respond best [Fig. 7.2(a) and (b)]. A study of 182 patients undergoing pulsed dye laser treatment showed that vessels .0.2 mm in diameter required multiple treatments, while vessels .0.4 mm in diameter were poorly responsive to pulsed dye laser treatment (73). Although lower extremity telangiectasias do not respond as favorably, very small caliber red vessels can be effectively treated. The fine caliber “star-burst”-type vessels, those ,0.2 mm in diameter, which often develop as a consequence of sclerotherapy may respond well to pulsed dye laser therapy, in one or two treatment sessions. A combined approach using other therapeutic modalities, such as sclerotherapy, on the larger caliber vessels and the laser on the very small caliber vessels which are more difficult to inject, has been used effectively. Unfortunately, even with these very small caliber vessels, postlaser hyperpigmentation may persist for many months.

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Figure 7.2 (a) A 55-year-old female with perinasal telangiectasia. (b) Same patient after one treatment with the pulsed dye laser. Photograph was taken 8 months after the last treatment (37 mm spot size, 9.5 J/cm2, 585 nm, 0.5 ms pulse duration).

A study of 30 women with leg telangiectasias showed treatment to be most efficacious if vessels .0.2 mm in diameter were treated first with the pulsed dye laser at fluences between 7 and 8 J/cm2, followed by treatment of vessels 0.2 mm in size or less. Treatment results were not affected by the vessel location on the legs. Concomitant use of polidocanol in varying concentrations from 0.25% to 0.75% did not show increased efficacy of treatment (74). Studies using wavelengths up to 600 nm and pulse durations at 1.5 ms for the treatment of up to 1.0 mm lower extremity vessels have been promising. Elliptically shaped spot sizes at energies of 15 J/cm2 or greater have been shown to be effective at both 450 and 1.5 ms (75 – 79). Posttherapy hyperpigmentation even under these varying parameters remains an undesired sequela.

8.

HEMANGIOMAS

Capillary hemangiomas have responded well to pulsed dye laser therapy (80 – 83). However, only the superficial type of hemangioma appear to therapeutically benefit from laser therapy while the deep, cavernous type is unaffected [Fig. 7.3(a) and (b)]. It is in the early phase of clinical presentation, before or immediately at the onset of the proliferative stage, that the best outcome is achieved. The flatter, superficial lesions, those

Figure 7.3 (a) A 4-month-old female with a palmar capillary hemangioma. (b) Same patient after three treatments with the pulsed dye laser. Photograph was taken 1 month after the last treatment (5 mm spot size, 6.00 J/cm2, 585 nm, 0.5 ms pulse duration).

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which are 3 mm or less raised off the skin surface, respond to treatment with almost complete resolution. Low-energy doses are delivered every few weeks until the lesion flattens and resolves. If the lesion is raised .3 mm above the skin surface, it is more difficult to interrupt active proliferation and achieve total resolution. After completed therapy, some areas have developed texture changes of atrophy and hypopigmentation. There are criteria suggested in assisting the laser clinician in deciding when it is appropriate to use the laser for the treatment of capillary or mixed hemangiomas (Table 7.2). Ulcerated capillary hemangiomas and proliferative hemangiomas in areas causing functional impairment have also responded rapidly to pulsed dye laser treatment enabling the return of normal function (84,85).

9.

OTHER BENIGN VASCULAR DISORDERS

Areas of permanent cutaneous erythema and/or diffuse telangiectasia as occurs in rosacea, postrhinoplasty red-nose, postradiotherapy (86), poikiloderma of Civatte (87), keratosis pilaris, posttrauma, or with scars, respond to the pulsed dye laser. The therapeutic approach is similar to the PWS, using a 5 mm spot size or greater and treating a wide surface area. Outcome has been very favorable, with significant reduction and elimination of the underlying permanently dilated vessels and manifested erythema. Use of the 10 mm spot size using low energies which are immediately below the purpura threshold are encouraging. It may be possible to treat telangiectasias and permanent erythema while not inducing significant purpura with this large spot size or in using longer wavelength and/or pulse duration. Controversy exists surrounding the efficacy of the pulsed dye laser in the treatment of hypertrophic scars as well as the mechanism by which improvement seems to occur. One controlled study of 16 adult patients treated with the pulsed dye laser for keloid sternotomy scars showed significant improvement in erythema, scar height, skin surface texture, and pruritus (88). Another study examined histologic features before and after treatment of hypertrophic burn scars. The author showed laser-irradiated scars to have decreased numbers of fibroblasts with nonsclerotic dermal collagen and normal vascularity. These patients were found to have a reduction in scar erythema and pruritus and Table 7.2 Criteria for Consideration in the Use of Laser Therapy for Hemangiomasa 1. 2.

3.

a

Potential for functional impairment Risk of ulceration Rapid enlargement Recurrent trauma Moist area Cosmetic disfigurement Highly visible lesion Extensive surface area

Richards KA, Garden JM. The pulsed dye laser for cutaneous vascular and nonvascular lesions. In: Hruza GJ, ed. Seminars in Cutaneous Medicine and Surgery. Vol. 19, No. 4. Philadelphia: W.B. Saunders, 2000:276– 286.

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improved scar pliability and skin surface texture (89). A recent controlled study of pulsed dye laser vs. silicone gel sheeting treatment of hypertrophic scars showed no difference from controls in clinical appearance or symptoms for either modality. In addition, examination of five biopsy specimens taken at week 0 and week 40 after treatment showed no change in fibrosis, number of telangiectasias, or number of mast cells when compared with healthy skin controls (90). The diversity of opinions on the efficacy of the pulsed dye laser in treating hypertrophic scars as well as the lack of a firm mechanism for scar reduction, leaves the door open for further studies. Solitary vascular lesions such as venous lakes, spider or cherry angiomas, angioma serpiginosum, and angiolymphoid hyperplasia with eosinophilia also respond favorably (26 –28,91,92). However, as with the PWS and hemangioma, the thicker lesions do not respond as well. A study of 18 patients with pyogenic granulomas showed clinical and symptomatic clearing of the lesions in 16 out of 18 patients with excellent cosmetic results (93). However, enlarged pyogenic granulomas are especially difficult to treat, even with multiple, repetitive, high-energy pulses to the lesion.

10.

NONVASCULAR LESIONS

Other cutaneous clinical processes which have been treated with the pulsed dye laser and evaluated for efficacy include plaque-type psoriasis (94,95) and warts (96). Both appear to respond but only in a limited manner (97). Psoriatic lesions do flatten but generally incompletely and can recur. One study showed that psoriatic plaques with vertically oriented vessels and few horizontal vessels responded better to treatment than plaques with numerous tortuous vessels (98). Warts which are not located over the periungual or plantar surfaces and are flat may resolve readily with laser therapy. However, very keratotic lesions and/ or those over the periungual or plantar surfaces have a much greater initial failure and follow-up recurrence rate. In both disease processes it is assumed that the laser interaction with the underlying vasculature plays a beneficial but uncertain role [Fig. 7.4(a) and (b)]. Recent applications of the pulsed dye laser in the treatment of cutaneous lesions are almost too numerous to count. Successful treatment has occurred in stretch marks (99), molluscum contagiosum (100), facial acne scars (101), xanthelasma palpebrarum (102), sebaceous gland hyperplasia (103), acne fulminans-associated granulation tissue (104), focal dermal hypoplasia (105), linear porokeratosis (106), nodular amyloidosis (107), Kaposi’s sarcoma (108), and granuloma faciale (109).

Figure 7.4 (a) A 29-year-old female with a left plantar verruca. (b) Same patient after three treatments with the pulsed dye laser. Photograph was taken 1 year after the last treatment (5 mm spot size, 10.00 J/cm2, 585 nm, 0.5 ms pulse duration).

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RHYTIDES

It has been noted for sometime that pulsed dye laser treatment of vascular lesions incidentally improved the appearance of rhytides in treated skin. This observation has been evaluated for its potential use as a primary nonablative resurfacing modality (110 – 114). In one study by Zelickson et al. (112) 9 of 10 patients with mild to moderate rhytides showed at least 50% improvement 6– 14 months after one treatment with the pulsed dye laser and 4 of 10 patients with moderate to severe rhytids showed improvement ranging from 4% to 38%. Treatment fluences in this study ranged from 3.0 to 6.5 J/cm2 and both 7 and 10 mm spot sizes were used with 10– 15% overlap. Long-term follow-up of patients with moderate to severe rhytides showed some regression to baseline and a blinded panel was unable to differentiate between pre- and postoperative images. Side effects included purpura and swelling in all patients which lasted 1 –2 weeks and postinflammatory hyperpigmentation in two patients. Histopathology showed a thickened stratum spinosum, thickened collagen within the papillary dermis and increased mucin (112). Another ultrastructural study examining periorbital rhytids following pulsed dye laser analysis showed stimulation of fibroblast-mediated extracellular matrix remodeling (113). Bjerring and colleagues (114) examined the response of Fitzpatrick rhytides Classes I –III following pulsed dye laser in 30 patients. Parameters included a fluence of 2.4 J/cm2, pulse duration of 0.35 ms and a 5 mm spot size. Classes II and III rhytides demonstrated an improvement of 20% 6 months after a single treatment. Class I rhytides showed even less improvement. Using the same parameters, the same authors then compared single-pass sites to double-pass sites in a study examining the upper arms and forearms of 10 volunteers. Suction blisters were placed on each area as well as a control site following treatment with the pulsed dye laser and the blister fluid was then examined. A statistically significant increase was seen in the production of Type III procollagen in the single-pass sites compared with the control sites. The double-pass sites did not demonstrate a significant improvement (114). The authors speculated that the higher energy produced by the double-pass treatment had a suppressive effect on fibroblast collagen production. They also proposed that because only smaller vessels with a diameter of 15 mm or less trigger fibroblast activity, the short 0.35 ms pulse duration is essential to the pulsed dye laser’s photorejuvenation properties (114). Histopathologic analysis of scars treated with pulsed dye laser show an increase in dermal collagen as well as an increase in regional mast cells. Since mast cells release a variety of stimulatory cytokines, this may also explain the therapeutic improvement in appearance of the skin following pulsed dye laser treatment (111).

12.

PRE- AND POSTOPERATIVE CONSIDERATIONS

Since the majority of the treated cases do not develop significant crusting or erosions, it is not necessary to prophylactically prescribe antibacterials or antivirals. Postoperative care in the majority of cases ranges from none in those cases where the skin remains intact or antibacterial ointments for areas of scaling or erosions. Postoperative dressings are rarely placed, especially in the pediatric cases, where movement of adhesive dressings may injure the skin with removal.

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Sun exposure and tanning need to be minimized prior to therapy due to increased melanin content absorbing the laser light. Both decreased effectiveness and increased chance of hypopigmentation may occur with laser therapy. After treatment, several weeks should pass before any UV exposure over the treated site to reduce the potential of dyspigmentation.

13.

SUMMARY

As the variety of pulsed dye lasers continue to expand so do the number of clinical applications to both vascular and nonvascular lesions. New topical anesthetic options make using the pulsed dye laser in the pediatric population even more feasible. In general, most types of cutaneous blood vessel disease have responded favorably to pulsed dye laser therapy. The best response occurs with processes which are superficially located and have small caliber vessel involvement, while the other types of vascular lesions may achieve a beneficial outcome but with greater difficulty. Nonvascular lesions of many types have also proven to respond effectively to pulsed dye laser therapy. Photodamaged skin and wrinkles have been shown to improve modestly following pulsed dye laser nonablative treatment. Side effects are rare and often transitory (115), but have been reported to include hypertrophic (116) and keloidal (117) scarring, pigmentary changes (118), and atrophic blanche-type scarring (119). Often these side effects were found to occur after using higher fluences than indicated (24,116), excessively overlapping pulses (120), or during concomitant Accutane use (117). Limitations in its ability to treat all lesions consistently well places an incentive on improving its design and use. Research into the methods of optimizing wavelength, pulse duration, spot size, and energy for the treatment of specific lesions is continuing. REFERENCES 1. 2. 3. 4. 5. 6. 7.

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Alster TS, Wilson F. Treatment of port wine stains with the flashlamp pumped pulsed dye laser: extended clinical experience in children and adults. Ann Plast Surg 1994; 32:478 – 484. Van der Horst C, Koster PHL, DeBorgre CAJM et al. Effect of the timing of treatment of port wine stains with the flash-lamp-pumped pulsed dye laser. N Engl J Med 1998; 338:1028 – 1033. Orten SS, Warner M, Flock S. Port wine stains: an assessment of 5 years of treatment. Arch Otolaryngol Head Neck Surg 1996; 122:1174 – 1179. Dinehart SM, Flock S, Waner M. Beam profile of the flashlamp-pumped pulsed dye laser: support for overlap of exposure spots. Lasers Surg Med 1994; 15:277 – 280. Bencini PL. The multilayer technique: a new and fast approach for flashlamp-pumped pulsed dye laser treatment of port-wine stains. Dermatol Surg 1999; 25(10):786– 789. Walderf HA, Alster TS. Effect of dynamic cooling on 585 nm pulsed dye laser treatment of port-wine stain birthmarks. Dermatol Surg 1997; 23:657– 660. Nelson JS, Milner TE, Anvari B. Dynamic epidermal cooling during pulsed laser treatment of port-wine stain. Arch Dermatol 1995; 131:695 – 700. Chang CJ, Nelson JS. Cryogen spray cooling and higher fluence pulsed dye laser treatment improve port-wine stain clearance while minimizing epidermal damage. Dermatol Surg 1999; 25(10):767 –772. Swinehart JM. Textural change following treatment of facial telangiectasias with the tunable pulsed-dye laser. Arch Dermatol 1999; 135:472 – 473. Polla LL, Tan OT, Garden JM, Parrish JA. Tunable pulsed dye laser for the treatment of benign cutaneous vascular ectasia. Dermatologica 1987; 174:11– 17. Gonzalez E, Gange RW, Momtaz KT. Treatment of telangiectasias and other benign vascular lesions with the 577 nm pulsed dye laser. J Am Acad Dermatol 1992; 27:220 – 226. Lowe NJ, Behr KL, Fitzpatrick R, Goldman M, Ruiz-Esparza J. Flashlamp pumped dye laser for rosacea-associated telangiectasia and erythema. J Dermatol Surg Oncol 1991; 17:522 – 525. Perez B, Nunez M, Boixeda P et al. Progressive ascending telangiectasia treated with the 585 nm flashlamp-pumped pulsed dye laser. Lasers Surg Med 1997; 21:413– 416. Ellis DE. Treatment of telangiectasia macularis eruptiva perstans with the 585-nm flashlamppumped dye laser. Dermatol Surg 1996; 22:33 – 37. Ruiz-Esparza J, Goldman MP, Fitzpatrick RE et al. Flash lamp-pumped dye laser treatment of telangiectasia. J Dermatol Surg Oncol 1993; 19:1000 – 1003. Goldman MP, Fitzpatrick RE. Pulsed dye laser treatment of leg telangiectasia with or without simultaneous sclerotherapy. J Dermatol Surg Oncol 1990; 16:338 –344. Bernstein EF, Lee J, Lowery J, Brown DB, Geronemus R, Lask G, Hsia J. Treatment of spider veins with the 595 nm pulsed-dye laser. J Am Acad Dermatol 1998; 39:746 – 750. Hsia J, Lower JA, Zelickson B. Treatment of leg telangiectasia using a long-pulse dye laser at 595 nm. Lasers Surg Med 1997; 20:1– 5. Hohenleutner U, Walther T, Wenig M, Baumler W, Landthaler. Leg telangiectasia treatment with 1.5 ms pulsed dye laser, ice cube cooling of the skin and 595 vs 600 nm: preliminary results. Lasers Surg Med 1998; 23:72– 78. Alora MB, Seven RS, Arndt KA, Dover JS. Comparison of the 595 nm long-pulse (1.5 ms) and ultralong-pulse (4 ms) lasers in the treatment of leg veins. Dermatol Surg 1999; 25:445 – 449. Dover JS, Sadick NS, Goldman MP. The role of lasers and light sources in the treatment of leg veins. Dermatol Surg 1999; 25:328 – 336. Glassberg E, Lask G, Rabinowitz LG, Tunnessen WW. Capillary hemangiomas: case study of a novel laser treatment and a review of therapeutics options. J Dermatol Surg Oncol 1989; 15:1214 – 1223. Ashinoff R, Geronemus RG. Capillary hemangiomas and treatment with the flashlamp pumped dye laser. Arch Dermatol 1991; 127:202 – 205. Garden JM, Bakus AD, Paller AS. Treatment of cutaneous hemangiomas by the flashlamppumped pulsed dye laser: prospective analysis. J Pediatr 1992; 120:555 – 560.

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Morelli JG, Tan OT, West WL. Treatment of ulcerated hemangiomas with the pulsed tunable dye laser. Am J Dis Child 1991; 145:1062 – 1064. Lacour M, Syed S, Linward J et al. Role of the pulsed dye laser in the management of ulcerated capillary haemangiomas. Arch Dis Child 1996; 4:161 – 163. Barlow RJ, Walker NPJ, Markey AC. Treatment of proliferative haemangiomas with the 585 nm pulsed dye laser. Br J Dermatol 1996; 134:700 – 704. Ahmad M, Mirza S, Foo ITH. Pulsed dye laser treatment of telangiectasia after radiotherapy for breast carcinoma. Br J Plast Surg 1999; 52:236– 237. Geronemus RG. Poikiloderma of civatte. Arch Dermatol 1990; 126:547– 548. Alster TS, Williams CM. Treatment of keloid sternotomy scars with 585 nm flashlamppumped pulsed-dye laser. Lanolt 1995; 345:1198 – 1200. Alster TS, Nanin CA. Pulsed dye laser treatment of hypertrophic burn scars. Plast Reconstr Surg 1998; 102:2190 – 2198. Wittenberg GP, Fabian BG, Bogomilsky JL et al. Prospective, single-blind, randomized, controlled study to assess the efficacy of the 585 nm flashlamp-pumped pulsed dye laser and silicone gel sheeting in hypertrophic scar treatment. Arch Dermatol 1999; 135:1049 – 1055. Long CC, Lanigam SW. Treatment of angioma serpiginosum using a pulsed tunable dye laser. Br J Dermatol 1997; 136:631 – 632. Lertzman BH, McMeekin T, Gaspari AA. Pulsed dye laser treatment of angiolymphoid hyperplasia with eosinophilia lesions. Arch Dermatol 1997; 133:920 – 921. Gonzalez S, Vibnagool C, Folo LD et al. Treatment of pyogenic granulomas with the 585 nm pulsed dye laser. J Am Acad Dermatol 1996; 35:428 – 431. Hacker SM, Rasmussen JE. The effect of flashlamp-pulsed dye laser on psoriasis. Arch Dermatol 1992; 128:853 – 855. Ros AM, Garden JM, Bakus AD, Hedblad MA. Psoriasis response to the pulsed dye laser. Lasers Surg Med 1996; 19:331 – 335. Tan OT, Hurwitz RM, Stafford TJ. Pulsed dye laser treatment of recalcitrant verrucae: a preliminary report. Lasers Surg Med 1993; 13:127 –137. Ross BS, Levine VJ, Nehal K, Tse Y, Ashinoff R. Pulsed dye laser treatment of warts: an update. Dermatol Surg 1999; 25:377– 380. Zelickson BD, Mehregan DA, Wendelschfer-Crabb G et al. Clinical and histologic evaluation of psoriatic plaques treated with a flashlamp pulsed dye laser. J Am Acad Dermatol 1996; 35:64 – 68. McDaniel DH, Ash K, Zukowski M. Treatment of stretch marks with the 585 nm flashlamppumped pulsed dye laser. Dermatol Surg 1996; 22:332 – 337. Hughes PSH. Treatment of molluscum contagiosum with the 585 nm pulsed dye laser. Dermatol Surg 1998; 24:229 –230. Alster TS, McMeekin TO. Improvement of facial acne scars by the 585 nm flashlamppumped pulsed dye laser. J Am Acad Dermatol 1996; 35:79 – 81. Schonermark MP, Raulin C. Treatment of xanthelasma palpebrarum with the pulsed dye laser. Lasers Surg Med 1996; 19:336 –339. Gonzalez S, White WM, Rajadhyaksha M et al. Confocal imaging of sebaceous gland hyperplasia in vivo to assess efficacy and mechanism of pulsed dye laser treatment. Lasers Surg Med 1999; 25:8– 12. Wasner AM, Cunningham B. Effective treatment of acne fulminans-associated granulation tissue with the pulsed dye laser. Pediatr Dermatol 1998; 15(5):396 – 398. Alster TS, Wilson F. Focal dermal hypoplasia (Goltz’s syndrome). Arch Dermatol 1995; (13):143– 144. Alster TS, Nanni CA. Successful treatment of porokeratosis with 585 nm pulsed dye laser irradiation. Cutis 1999; 63:265 – 266. Alster TS, Manaloto RMP. Nodular amyloidosis treated with the pulsed dye laser. Dermatol Surg 1999; 25:133 –135. Marchell N, Alster TS. Successful treatment of cutaneous Kaposi’s sarcoma by the 585 nm pulsed dye laser. Dermatol Surg 1997; 23:973 – 975.

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Ammirati CT, Hruza GJ. Treatment of granuloma faciale with the 585 nm pulsed dye laser. Arch Dermatol 1999; 135:903 – 905. Tope WD, Kageyama N. New methods in cutaneous resurfacing. Adv Dermatol 2001; 17:301 – 323. Goldberg DJ. Nonablative resurfacing. Clin Plast Surg 2000; 27(2):287 – 292, xi. Zelickson BD, Kilmer SL, Bernstein E et al. Pulsed dye laser therapy for sun damaged skin. Lasers Surg Med 1999; 25:229 – 236. Zelickson BD, Kist DA. Pulsed dye laser and photoderm treatment stimulates production of type-I collagen and collagenase transcripts in papillary dermis fibroblasts. Lasers Surg Med 2001; 27:33S. Bjerring P, Clement M, Heickendorff L et al. Selective non-ablative wrinkle reduction by laser. J Cutan Laser Ther 2000; 2:9– 15. Boixeda P, Nunez M, Perez B et al. Complications of 585 nm pulsed dye laser therapy. Int J Dermatol 1997; 36:393 – 397. Gaston DA, Clark DP. Facial hypertrophic scarring from pulsed dye laser. Dermatol Surg 1998; 24:523 – 525. Bernstein LJ, Geronemus RG. Keloid formation with the 585-nm pulsed dye laser during isotretinoin treatment. Arch Dermatol 1997; 133:111 –112. Levine VJ, Geronemus RG. Adverse effects associated with the 577 and 585-nanometer pulsed dye laser in the treatment of cutaneous vascular lesions: a study of 500 patients. J Am Acad Dermatol 1995; 32:613 – 617. Sommer S, Sheehan-Dare RA. Atrophie blanche-like scarring after pulsed dye laser treatment. J Am Acad Dermatol 1999; 41:100 – 102. Buscaglia DA. Hypertrophic scarring from pulsed dye laser treatment. Dermatol Surg 1999; 25(1):75.

8 Clinical Uses of the Long Pulse Duration Pulsed Dye Laser Eric F. Bernstein Laser Surgery and Cosmetic Dermatology Centers, Marlton, New Jersey and University of Pennsylvania, Philadelphia, Pennsylvania, USA

1. Port-Wine Stains 2. Keloids and Hypertrophic Scars 3. Verrucae 4. Rosacea and Facial Telangiectasias 5. Lower-Extremity Telangiectasias 6. Lupus Erythematosis 7. Striae 8. Sebaceous Gland Hyperplasia 9. Psoriasis 10. Nonablative Skin Remodeling with the PDL 11. Future Developments in Long-Pulse PDL 12. Laser Physics: Suggested Parameters References

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Based on the original work by Anderson and Parrish (1,2), pulsed lasers have become the mainstay of treatment for an ever-expanding number of cutaneous conditions. The rapid proliferation in the number and types of lasers used to selectively heat target tissues is even more remarkable when considering that this evolution occurred during less than two decades. Anderson and Parrish used a predictive model to choose a laser that would selectively target blood vessels. They modeled the wavelength, duration of exposure, and energy density necessary to destroy blood vessels. Initially, they chose a wavelength of 577 nm due to the strong hemoglobin absorption at this wavelength. They estimated that the optimal pulse duration for targeting unwanted cutaneous vessels was approximately 1 ms, based on experimental estimates of thermal relaxation for microvessels in Caucasian skin (1 – 3). The laser they selected had a pulse duration of 0.3 ms, less than the 1 ms pulse 219

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duration that they estimated to be optimal for targeting of cutaneous vessels, but at the limits of what was technically achievable at the time (1). Previously, continuous nonpulsed vascular lasers had an unacceptable side effect profile, resulting in necrosis of skin overlying blood vessels (1 – 3). This necrosis often resulted in permanent scarring. Anderson and Parrish proposed that the pulsed dye laser (PDL) would prove useful for the treatment of vascular malformations such as port-wine stains (PWS), hemangiomas, and other vascular lesions, with a satisfactory side effect profile (1). Following their initial observations (1,3), Anderson and Parrish published their landmark manuscript describing the concept of selective photothermolysis, detailing the ability of pulsed lasers to selectively remove unwanted blood vessels, pigmented structures, cells, and organelles without significant collateral damage to surrounding tissues (4). Selective damage to microvessels in the skin as well as melanosomes contained within melanocytes was demonstrated using 577 and 351 nm pulsed lasers. Physiologic responses to these pulsed lasers were also described (4). Since these initial observations, the evolution of the PDL has made treatment of PWSs more efficacious, resulting in fewer treatments being necessary, as well reducing the pain and pigmentary alterations following treatment. The PDL evolved from having small spot sizes of 4 –5 mm and pulse durations in the 0.3 – 0.5 ms range, to spot sizes of 7 – 10 mm and pulse durations of 1.5 ms and beyond. Longer pulse durations and larger spot sizes often yield improved clinical results, most likely due to the greater penetration depths afforded by larger spot sizes and gentler heating of larger vessels with longer pulse durations. An even newer generation of PDLs has evolved that attempt to create pulse durations in the 10–50 ms domain. True continuous pulses in this range have not been reliably achieved with PDLs. The characteristics of the rhodamine dyes used in PDLs are such that they begin to break down at the high temperatures reached when attempting to generate these longer pulse durations. Current lasers claiming pulse durations in the 40 ms range actually generate pulses composed of three to four shorter pulses separated by “off” times of various intervals. These shorter pulses are spread over 10–40 ms, although the laser does not fire throughout the entire time interval. Although the clinical effects of these longer pulse duration lasers differ from those of traditional PDLs, they still do not have the characteristics of a truly continuous 10–40 ms pulse. Currently, solid state neodymium:yttrium, aluminum, and garnet (Nd:YAG) lasers are capable of generating true long pulses of up to 50 ms at the 532 nm green wavelength (5–7). Comparable lasers capable of delivering yellow/orange light at these pulse durations are still years away.

1.

PORT-WINE STAINS

Following the initial experimental evidence that blood vessels could be destroyed using pulsed yellow-light lasers, PWSs were among the first clinical conditions to be treated. Initial attempts were made using lasers in the microsecond domain with relatively small spot sizes. Vascular injury was documented as was a negative correlation between skin pigmentation and treatment effect, although significant clinical improvement was not demonstrated (8,9). The authors postulated the need for lasers with pulse durations in the millisecond domain. Despite the landmark discoveries by Anderson and Parrish, the replacement of older laser technologies with the PDL for the treatment of PWSs was occurring slowly. Gradually, the PDL began to emerge as the frontrunner, as opposed to previously available laser technologies for the treatment of PWSs (10). Initial reports using PDLs with a wavelength of 577 nm and pulse durations of 0.3–0.4 ms demonstrated favorable clinical results for the treatment of PWSs (11). These results were reported 6 years after

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the initial observations by Anderson and Parrish (1) that pulsed yellow light could effectively remove unwanted cutaneous vessels. At that time, the argon laser was still reported to be the laser of choice for most physicians treating PWSs, despite the relatively high incidence of scarring when using these lasers (12). Clinical use of PDLs was limited largely due to the constraints of the available technologies. PDLs with pulse durations approaching 0.3–0.4 ms were being developed and utilized for the treatment of PWSs, yielding superior results over previously available systems (13–15). Wavelengths longer than 577 nm were evaluated and found to be more effective, presumably due to the deeper penetration of longer wavelengths within target vessels (16,17). Patients previously treated for PWSs with a 577 nm PDL were subsequently treated with a 585 nm PDL and demonstrated further clearing of their PWSs (16). Deeper penetration of the 585 nm light was demonstrated as compared to 577 nm light (16). The 585 nm PDL proved quite effective for the treatment of PWSs. The safety and improved efficacy of the PDL enabled treatment of infants with PWSs, yielding improved clearance over previous modalities. Ashinoff and Geronemous (18) demonstrated 50% clearance in 10 of 12 treated children, after a mean of only 3.8 treatments. These results were achieved without any pigmentary alterations, textural change, or evidence of scarring, demonstrating the safety of the 585 nm PDL for treating PWSs. These authors also demonstrated the ability of this laser system to induce regression in capillary hemangiomas, with an overall 70% improvement (19). The 585 nm PDL also proved effective for improving ulcerations and associated bleeding in hemangiomas (20). Goldman and Fitzpatrick reported on the treatment of 46 PWSs in 43 patients using the 585 nm PDL, and demonstrated 50% clearance after the first treatment. Subsequent treatments resulted in an additional 10% clearing. Overall, 16% of patients demonstrated 95% or greater clearance after an average of approximately four treatments. The laser proved extremely safe, with no evidence of scarring (21). Alster and Wilson reported on 76 patients treated with the 585 nm, 0.45 ms pulse duration PDL, showing .90% improvement in approximately half the patients, after an average of nine treatments. The overall improvement was 79% after nine treatments (22). Although the rate of improvement of PWSs was significant with an extremely low side effect profile, a large number of treatments were still required for near complete clearance. Treatments extended over years, still with incomplete clearing in many patients. Although the initial results with the PDL for treating PWSs were remarkable as compared to previously available technologies, further improvements in the PDL were incremental for a relatively long period of time. The development of a PDL with a pulse duration of 1.5 ms was a major stride forward. The initial 1.5 ms pulse duration PDL offered an elliptical 2 7 mm spot and 595 and 600 nm wavelengths. This laser was primarily designed for the treatment of facial and lower extremity telangiectasias. Subsequently, a 7 mm spot was offered with this laser, enabling delivery of a maximum fluence of 10 J/cm2. Initial results with this system demonstrated improved clearing of PWSs that had stopped progressing with conventional 585 nm, 0.45 ms pulse duration PDL treatment (Fig. 8.1). Improvement was again incremental, with many lesions failing to progress after a number of treatments using the 595 nm wavelength, 1.5 ms pulse duration, and a maximum fluence of 10 J/cm2 (author’s unpublished results). The highest available energy of 10 J/cm2 was not near the maximum tolerated fluence at this wavelength and spot size; however, earlier machines were limited to this energy. Subsequently, the 585 nm wavelength was offered, in addition to 595 and 600 nm, with the 1.5 ms pulse duration. A maximum fluence of 10 J/cm2 was also available with the 585 nm wavelength, using a 7 mm spot size. This energy was close to the maximally tolerated fluence, as demonstrated clinically by crusting in certain areas of treated PWSs, in a number of patients during 1– 2 weeks following treatment. Crusting of the

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Figure 8.1 (a) A patient with a PWS prior to treatment with the PDL. (b) Treatment with the 595 nm, 1.5 ms pulse duration PDL using a 7 mm spot produced further clearing of the PWS than was possible using the short pulse duration (0.45 ms), 585 nm PDL. (c) After initial improvement using 595 nm, the PWS again failed to improve after a number of treatments with the 1.5 ms pulse duration PDL at 595 nm. During this patient’s course of treatment, 585 nm became available with the 1.5 ms pulse duration PDL. Treatment at this wavelength resulted in the further improvement shown here.

treated site is indicative of epidermal damage, and is not uncommon in isolated areas of a PWS in some patients. Although undesirable, crusting very rarely results in scarring. Initial clinical observations revealed the potential for improved clinical results using 585 nm and the longer 1.5 ms pulse duration [Fig. 8.1(a) and (b)]. To demonstrate the effect of a longer pulse duration alone, a patient previously treated seven times with the 585 nm, 0.45 ms pulse duration PDL was subsequently treated with the 585 nm, 1.5 ms


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pulse duration laser. This patient was treated with the identical fluence, wavelength, and spot size that were used with the 0.45 ms laser, with the only variable being the longer, 1.5 ms pulse duration. The response in this patient was quite dramatic, with complete clearing of his PWS at the sites of laser impact (Fig. 8.2). While subsequent patients

Figure 8.2 (a) A PWS as it appeared following seven treatments with the conventional 0.5 ms pulse duration PDL. The patient reported considerable lightening to the point shown, but failure to improve with subsequent treatments. (b) The PWS was treated using the identical fluence, spot size, and wavelength used the previous seven treatments, but using the 1.5 ms pulse duration PDL. The circles at the site of laser impact demonstrate complete clearing, illustrating the potential benefit of longer pulse durations for treating PWSs. (c) Close-up view of the treated areas. The upper region was treated 4 weeks prior to this photo, while the lower portion was treated 6 weeks before the photo. The lower portion demonstrates the further clearing that has occurred with two additional weeks of healing time.

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have demonstrated a range of improvement, these results have proven to be typical in a substantial percentage of patients (Fig. 8.3). This initial report and further clinical experience have stimulated a more comprehensive ongoing study of the role of pulse duration in PWS clearance. Interestingly, a 1.5 ms pulse duration approximates the optimal parameters suggested by Anderson and Parrish (1) almost two decades ago. Currently, this author uses the 1.5 ms pulse duration PDL (Sclerolaser; Candela Laser Corp., Wayland, MA) with a maximum fluence of 6 J/cm2 using a 10 mm spot size and 585 nm. For higher energy densities a 7 mm spot and up to 10 J/cm2 are used. When PWSs fail to continue improving at the 585 nm wavelength, this author then treats using 595 nm. Higher fluences may be tolerated with 595 nm as compared to 585 nm in the same PWS. PWSs with linear vessels visible to the naked eye often respond better to 595 nm, as do many thicker PWSs. Higher fluences than have been used with 585 nm are often used with 595 nm to achieve clearance. Care must be taken not to injure the epidermis, and gradually increasing doses should be tested in small areas in as cosmetically unimportant an area as possible. Specific fluences are not recommended here, since various PDLs may result in significantly different clinical effects despite administration of treatments with identical wavelengths, fluences, and spot sizes (23). Thus, clinicians must develop experience with their particular laser, initially erring on the side of undertreatment. Indicators of clinical response such as purpura can indicate that an adequate fluence is being administered. However, when using long pulse duration PDLs, purpura may take a few minutes to fully appear, as compared to PDLs with pulse durations approximating 0.5 ms, which result in almost immediate purpura. In addition, the melanin content of a patient’s epidermis can influence side effects. Melanin is a major chromophore in skin, and is an undesired target. Care should be taken when treating dark-skinned or tanned patients. Often, epidermal pigment may drop into the dermis resulting in longer-standing hyperpigmentation. In addition, hemosiderin from resolving PWSs can reside in the dermis for some time acting as an unwanted chromophore. Hemosiderin also stimulates inflammation resulting in epidermal melanin pigment incontinence. Re-treating too soon to allow for this pigment to resolve can result in skin injury and the possibility of scarring. The administration of topical alphahydroxy acids, such as glycolic acid or ammonium lactate lotions, can increase epidermal turnover and stimulate dermal inflammation resulting in more rapid pigment clearance. Future improvements in the PDL may yield even quicker resolution of PWSs, with more complete responses.

Figure 8.3 (a) A patient with a large lower-extremity PWS prior to (a) and after (b) a single treatment with the 1.5 ms pulse duration, 585 nm PDL demonstrating near complete clearance at the sites of laser impact after a single treatment session. PWSs in this location are often difficult to treat.


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The newer very long pulse duration PDLs have been used to treat PWSs as well. These lasers use a train of three to four shorter pulses to achieve pseudo-long pulses in the 1.5 –40 ms range. Initial treatment regimens for PWSs have demonstrated clearing at short (1.5 ms) and longer (up to 40 ms) pulse durations, but required higher fluences to achieve results with the longer pulse durations. Although these lasers were developed for treatment of vascular lesions without purpura, at least one investigator demonstrated that improvement of PWSs correlated with the development of purpura. Treatments at various pulse durations resulted in improved clearance as a function of the amount of purpura that developed. Clearance was achieved at numerous pulse durations provided the purpuric threshold was reached (24). Further studies are necessary to determine if these newer pseudo-long pulse duration lasers offer any improvement over previous generation lasers for the treatment of PWSs.

2.

KELOIDS AND HYPERTROPHIC SCARS

Hypertrophic scars and keloids are similar in appearance with the exception that keloids may persist for many years and extend beyond the original boundaries of the injury that caused them. Both are large, smooth, erythematous, and often hyperpigmented nodules and plaques at sites of cutaneous injury. Keloids and hypertrophic scars are composed of very large bundles of collagen fibers, often arranged parallel to the epidermis. The erythema, pruritus, and pain that often accompany keloids and hypertrophic scars are indicative of the inflammatory infiltrate that maintains or enlarges them. This erythema provides clinical evidence of the vascular and inflammatory components of these lesions, and gives an indication that treatment with the PDL may help improve them. Alster (25) and Williams demonstrated the efficacy of the PDL for the treatment of hypertrophic or keloidal sternotomy scars. Patients were treated for one-half of their sternotomy scar with a 585 nm PDL, and evaluated for changes in erythema, height of the scar, surface texture, and subjective assessment of pruritis. A significant improvement in these parameters was noted, and this improvement persisted for a minimum of 6 months. Dierickx et al. (26) reported improvement of erythematous, hypertrophic scars treated with the 585 nm PDL. Improvement was rated at 77% after an average of two treatments. They reported 100% improvement in 40% of their patients. Goldman and Fitzpatrick (27), treated 48 patients with erythematous, hypertrophic scars using the PDL, with or without intralesional triamcinolone. Scars present for less than 1 year had a greater rate of complete clearance than scars present for longer than 1 year. Facial scars resolved completely more often than those on other sites. Seventy-three percent of scars on the face less than 1 year cleared after approximately two treatments, as compared to only 20% of scars on the face present for over 1 year and treated over four times on average. Sheridan et al. (28) investigated the safety of treating hypertrophic burn scars in children. Purpura was seen in all patients. However no pain, ulceration, or worsening of the lesions was seen, demonstrating the safety of the PDL for treating burn scars in children. Alster and Nanni (29) also demonstrated improvement of hypertrophic burn scars following 585 nm PDL treatment. Patients’ pruritis or pain improved after a single treatment. Decreased erythema and improved texture and pliability were noted after an average of only 2.5 treatments. A decrease of dermal sclerosis was also measured by histopathologic examination. Patients who were restricted in their range of motion by scarring from burns or other trauma often reported an increase in their ability to move the affected part, and a decrease in the symptoms of pain or pruritis. This was in addition to any cosmetic improvement noted, due to a reduction in erythema and thickness of the hypertrophic

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scar or keloid. More recently, investigators have been studying the effect of early PDL treatment in prophylactically preventing the development of hypertrophic scarring. McCraw et al. (30) reported prophylactic laser scar reduction during the early phases of wound healing. They suggested that early PDL treatment alters the physiology of a healing wound in the early phases, thus preventing later hypertrophic scar formation. Shakespeare et al. (31) used the PDL to help prevent hypertrophic scar formation following breast reduction surgery. They found a disruption in the vessel pattern after PDL treatment of early healing scars on histopathologic evaluation. PDL treatment led to early maturation of scars following surgery. For the treatment of hypertrophic scars and keloids, many clinicians (this author included) always combine PDL treatments with intralesional corticosteroids. Fitzpatrick (32) reports the combination of PDL treatment with intralesional triamcinolone and also investigates the use of intralesional 5-flourouracial. He reports that the most effective treatment was the combination of intralesional agents and PDL treatment. Because intralesional corticosteroid administration (this author uses 40 mg/mL of triamcinolone in most cases) often results in neovascularization and an increase in erythema in treated scars, the PDL is an ideal modality to combine with intralesional corticosteroid use. Intralesional corticosteroids can often dramatically flatten even very large keloids or hypertrophic scars (Fig. 8.4). Of course, not all keloids or hypertrophic scars respond to intralesional injections. When administering intralesional corticosteroids, care must be taken to inject only within the keloid. Triamcinolone injected beyond the keloid into the surrounding normal skin at a concentration of 40 mg/mL can produce significant atrophy, hypopigmentation, and neovascularization. A clinician must have a degree of patience, since initially the firm dense collagen matrix of a keloid accepts very little triamcinolone. Once the keloid starts to soften, larger amounts of triamcinolone may be administered. It often requires a strong doctor –patient relationship to convince the patient to persist with monthly treatments beyond the initial treatment period when very little improvement is noted. A well-known side effect of corticosteroid administration is the development of atrophy, the desired effect in this case, along with telangiectasia, an unwanted side effect. Because some of the vessels in keloids may be as large as typical lower-extremity spider veins, this author uses the 1.5 ms pulse duration PDL with a wavelength of 595 nm to treat them (Fig. 8.5). The 595 nm wavelength is more efficacious than 585 nm for treating larger linear vessels. In addition, hyperpigmentation following treatment seems to be reduced with 595 nm as compared to 585 nm, using identical fluences (unpublished observations). Typically, for treating keloids or hypertrophic scars with

Figure 8.4 (a) A patient with a hypertrophic, traumatic scar on his left cheek, present for 3 years, was treated with the long pulse duration PDL combined with intralesional injection of triamcinolone 40 mg/mL. (b) After triamcinolone injection and subsequent treatment with the 595 nm, 1.5 ms pulse duration PDL on two occasions 6 weeks apart, followed by two treatments with the PDL alone.


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Figure 8.5 (a) A patient presented for treatment of a very large, keloid that initially resulted following development of a cyst, and further enlarged following excision. (b) The same keloid following eight sessions of intralesional injection of triamcinolone (40 mg/mL), followed on three occasions by PDL treatment using the 595 nm, 1.5 ms pulse duration PDL. The patient is continuing treatment at this time.

the long pulse duration PDL, this author uses a 7 or 10 mm spot and fluences lower than those used to treat PWSs, in the range of 5.5 –7.0 J/cm2. The fluence is lowered for darker-skinned individuals. If posttreatment hyperpigmentation is present, bleaching agents (such as hydroquinone, with retinoids or alpha-hydroxy acids and possibly topical corticosteroids) are used prior to administration of the next treatment. Treatment may be delayed until a significant amount of the pigmentation has resolved. The newer lasers offering pseudo-long pulse durations in the 3– 40 ms range are quite effective in improving erythematous scars. As with the shorter pulse duration PDLs, this author uses intralesional corticosteroids in conjunction with laser treatment of thick, hypertrophic scars or keloids. One of these lasers, the V-beam (Candela), offers only the 595 nm wavelength. This wavelength is ideal for treating hypertrophic scars or keloids, due to the common occurrence of larger linear vessels within these lesions. When keeping the parameters such as fluence, wavelength, pulse duration, and spot size equal, the longer pulse duration lasers can actually result in more purpura at the 1.5 ms pulse duration. This is because the longer pulse duration lasers, such as the V-beam, actually break their pulses up into three to four shorter pulses administered within the 1.5 ms time frame. Thus, as compared to the previous generation of lasers delivering a fixed 1.5 ms pulse (where the laser is “on” for the entire 1.5 ms), the newer generation of lasers deliver higher peak powers resulting in more purpura when all other parameters are equal. However, newer lasers like the V-beam have the option of spreading the three to four minipulses over a 40 ms time frame. This results in significantly less purpura, and remarkably selective targeting of erythematous scars, while sparing the surrounding skin from significant erythema or purpura.

3.

VERRUCAE

Tan et al. (33) reported on the ability to treat recalcitrant verrucae with the 585 nm, 0.45 ms pulse duration PDL using a 5 mm diameter spot. They treated 39 patients and found a 72% clearance rate using energies of 6.25–7.50 J/cm2 after an average of 1.7 treatments. A further 18% had 80–95% of their warts cleared after an average of 1.3 more treatments. After 3 months of follow-up only one of the 39 patients had a recurrence of their verrucae. Thus, it was established that the PDL is an effective treatment for verrucae. Human papilloma virus resides in the viable epidermis causing hypertrophy of the epidermis and

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the associated stratum corneum. This thickened epidermis relies solely on the underlying dermis for nutrients. Presumably to support this increased growth in the epidermis, new capillary loops emerge within elongated dermal papillae. The justification for laser treatment of verrucae rests on the belief that the laser will damage these underlying vessels. In addition, light absorbed by the stratum corneum and epidermis produces thermal damage that further injures the epidermis where the wart virus particles reside, and possibly stimulates growth factors that may cause involution of the verrucae. The inflammatory infiltrate may alert the immune system to the presence of the wart virus in the relatively immuneisolated epidermis. Kauvar et al. (34) treated 703 recalcitrant and 25 previously untreated warts in 142 patients with the PDL. Response rates were 99% for body, limb, and anogenital warts, 95% for warts on the hands, 84% for plantar warts, and 83% for periungual warts. Side effects in the study were limited and rare. Jacobson et al. (35) reported a slightly lower success rate, with 68% of recalcitrant warts responding to treatment. Other investigators showed an even lower clearance rate for recalcitrant verrucae, with 48% of verrucae responding to treatment (36). A recent study by Robson et al. (37) prospectively studied the efficacy of PDL therapy for verrucae as compared to conventional treatments. They found the PDL to be highly effective, but only as effective as conventional therapies. Response rates were 66 and 70%, for PDL treatment and conventional therapy, respectively. Thus, PDL treatment is efficacious for the treatment of verrucae, but due to its greater expense as compared to most other treatments, may be reserved for treatment of verrucae refractory to conventional therapy. Practitioners most commonly use pulses administered one immediately after the other (often referred to as stacking of pulses) to treat verrucae. This deposits additional energy at the treatment site, increasing the amount of thermal damage to the epidermis. Although this would normally be undesirable for treating most vascular lesions, the added energy may serve to destroy some of the wart-infected cells in the epidermis. In addition, PDLs with longer pulse durations are being increasingly used to treat verrucae as this new technology replaces older, more conventional PDLs. Although the more modern lasers may deliver less peak power at longer pulse durations, a significant advantage in reducing unwanted thermal side effects when treating most conditions with the PDL, this may have an undesirable effect on clearance of warts. Thus, shorter pulse durations may prove more efficacious for treating verrucae. Conversely, the longer pulse duration may be more ideally suited to damaging the larger vessels underlying verrucae, which are evident as black dots at their base. This author uses a 1.5 ms pulse duration PDL (Sclerolaser, Candela) with a wavelength of 585 nm, and the maximum available fluence of 10 J/cm2 with a 7 mm spot when treating larger verrucae, or a 5 mm spot and 11 J/cm2 for smaller lesions. From one to four pulses are delivered to each treatment site depending on the size of the wart and the location. Treatments are administered through a clear wound dressing to eliminate the plume that often accompanies treatment of warts at high fluences with stacking of pulses. Typically, the dressing reduces the amount of administered energy reaching the target by only 9% (38). Care should be taken to remove the plastic coverings on the front and back of the dressing to prevent further loss of laser energy due to the dressing.

4.

ROSACEA AND FACIAL TELANGIECTASIAS

Facial telangiectasias often develop on the cheeks due to chronic photodamage. Patients often have an asymmetric number of telangiectasias on one side of their faces, with the greater number being on the side adjacent to the car window when they are driving


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(left side) or riding as the passenger (right side). Thus, in patients with asymmetric photodamage, a physician can often accurately predict whether the patient is the driver or the passenger. Since window glass blocks UV-B radiation, this implies that UV-A radiation and longer wavelengths, possibly including infrared radiation, contribute to the development of telangiectasias. Therefore, use of broad-spectrum sunscreens is a crucial component in any plan to eradicate sun-induced telangiectasias. Non-sun-induced telangiectasias develop most commonly in women on the lateral aspects of the nose and the inferiorlateral portion of the cheeks. These linear telangiectasias respond extremely well to PDL treatment using 1.5 ms, 595 nm light administered with a 2 7 mm spot (39). The longer 595 nm wavelength is quite effective at removing linear telangiectasias, and the laser energy can be limited mainly to the target vessel by using an elliptical spot to deliver the laser energy along the target vessel. In patients with widespread telangiectasias or diffuse erythema, a 7–10 mm spot should be used to treat the entire affected area. In addition to sun exposure and a hereditary predisposition to the development of spider veins, rosacea is one of the more common causes of facial telangiectasias and erythema in adults. Individuals with rosacea have a predisposition to develop telangiectasias and erythema in response to sun exposure. These vessels become more prominent when rosacea patients are exposed to stimuli such as alcohol consumption, and warm foods or beverages. Lowe et al. (40) studied the ability of the 585 nm PDL to treat facial telangiectasias and erythema in rosacea patients. They treated 27 patients who had both telangiectasia and erythema associated with rosacea. They demonstrated a good to excellent response in 89% of patients receiving from one to three treatments. Of particular interest was the ability of PDL treatment to reduce both the papular and the pustular component of rosacea in 59% of patients. In addition, those with the most severe rosacea had the largest degree of improvement. Thus, the telangiectasias that form as a result of long-term rosacea may play a role in maintaining or exacerbating the more acneiform component of rosacea. Facial telangiectasias respond quite well to PDL treatment, much better than telangiectasias on the lower extremities. Because rosacea patients often have linear vessels superimposed upon a background of erythema, this author uses the 1.5 ms pulse duration PDL with a wavelength of 595 nm, because this wavelength has proven superior for treating linear vessels as compared to 585 nm (unpublished observations). In addition, 595 nm administered at lower fluences than those commonly used for PWSs is less likely to result in overtreatment of facial skin (Fig. 8.6). Overtreatment of rosacea patients, who tend to have naturally ruddy complexions, results in excessive blanching at the site of laser impact. This excessive blanching of the skin can create a visible waffle pattern on the face showing the sites of laser impacts. Numerous further treatments may then be required to remove this patterning, often leaving the patient with an excessively light appearance. Thus, the lowest effective fluence should be used with the largest available spot size when treating rosacea to avoid this unwanted result. This author finds fluences from 5.0 to 6.5 J/cm2 to be effective in the majority of patients using the 595 nm, 1.5 ms pulse duration PDL (Sclerolaser, Candela). Test spots are always necessary to determine the minimally effective fluence, and multiple treatments may be necessary. The PDL is extremely effective for reducing erythema in rosacea patients, and further investigation of the ability of this treatment to reduce the papular and pustular component of rosacea may increase its role in management of this chronic, and often difficult to treat, condition. The ultra-long pulse duration PDLs have been successful in treating facial erythema and telangiectasias with reduced purpura. Purpura is significant with the 1.5 ms pulse duration lasers, and is often a reason why patients decline treatment. Patients with smaller vessels or diffuse erythema respond best to the ultra-long pulse duration PDLs. This author uses pulse durations of 6– 10 ms with the Candela V-beam, and fluences in

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Figure 8.6 (a) A patient with a long-standing history of rosacea presents for PDL treatment of numerous telangiectasias, superimposed on a background of erythema. (b) Purpura is evident immediately after treatment. (c) Two months after two treatments, spaced 6 weeks apart, with the 595 nm, 1.5 ms pulse duration PDL using relatively low fluences.

the range of 6 J/cm2 with the 6 ms pulse duration and in the range of 8.5 J/cm2 with the 10 ms pulse duration. Rohrer has shown that pulse stacking improves the clinical response for rosacea associated telangiectasia when subpurpuric pulse durations are used. While increasing the fluence beyond a certain point can increase purpura, stacking lower fluence pulses can deliver the same result as a single higher energy pulse without purpura formation. The effective fluence is roughly approximated by the fourth root of the stacked fluences. Cumulative heating is produced with less trauma. In this way, telangiectasia that may not respond to one pass with a 6 –10 ms pulse will resolve following treatment when 2– 4 pulses are stacked using a 10 mm spot, 6– 10 ms pulses, a 30 ms cryogen spray and a fluence of 7.5 J/cm2 (Fig. 8.7) (41). During treatment one observes a transient purpuric response followed by erythema that usually lasts for a few hours. An urticarial response may last for a few days following treatment, and may be responsible for the improvement often seen in fine lines, wrinkles, and enlarged pores following treatment. Multiple treatments are often required to achieve vessel clearance.


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Figure 8.7 Before (a) and after treatment of facial erythema and telangiectasia with a 595 nm pulsed dye laser using a 10 mm spot, 10 ms pulse duration and fluence of 7.5 J/cm2. (Courtesy of Thomas Rohrer, M.D.)

5.

LOWER-EXTREMITY TELANGIECTASIAS

Sclerotherapy has been and remains the mainstay of treatment for lower-extremity telangiectasias. However, patients are increasingly looking for adjunctive therapy, either due to incomplete clearing of telangiectasias or due to the development of matt telangiectasias as a result of sclerotherapy. Matt telangiectasias are very small, red, often clustered vessels that can occur following sclerotherapy injections of larger veins. Further injection of matt telangiectasias once they develop may be technically difficult due to their small size, or may even lead to the development of more matt telangiectasias resulting from the subsequent injections. The incidence of matt telangiectasias following sclerotherapy is reported to be approximately 15–24% (42). Thus, a need exists for adjuvant therapy to treat lower-extremity spider veins. In properly selected patients, lasers may offer additional improvement of matt telangiectasias that occur following sclerotherapy. In addition to the substantial number of patients developing matt telangiectasias, those patients who refuse sclerotherapy due to an aversion to needles are potential candidates for primary laser treatment, as are those whose vessels fail to clear following sclerotherapy. Hsia et al. (43) reported on treatment of lower extremity telangiectasias using the 1.5 ms pulse duration 595 nm PDL. Earlier results suggested that 595 nm was more successful at removing linear telangiectasias than the conventionally used 585 nm. This improved efficacy using 595 nm was presumably due to the ability of 595 nm to penetrate through a relatively large vessel, as opposed to the typical vessels comprising PWSs, due to the decreased hemoglobin absorption at 595 nm as compared to 585 nm. They treated vessels ranging from 0.5 to 1.0 mm in diameter using fluences of 15 and 18 J/cm2. A 2 7 mm elliptical spot was used to focus laser energy along the desired target vessel. Clearance was .50% in over 40% of patients 6 weeks following a single treatment at both energies. Six months following treatment, over 50% of patients demonstrated .50% improvement. Further improvement was noted with longer follow-up without additional treatment. These authors report an acceptable complication rate and suggest that the long pulse duration PDL may have a role in treating lower-extremity telangiectasias. A subsequent study investigated the effect of three consecutive treatments administered

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Figure 8.8 (a) Spider veins on the lower leg prior to PDL treatment. (b) Resolution of the veins following three PDL treatments using a fluence of 20 J/cm2, a wavelength of 595 nm, a 2 7 mm elliptical spot, and a 1.5 ms pulse duration. Hyperpigmentation is present in the area of the treated veins. [From Bernstein et al. (38).]

6 weeks apart using fluences of 15 and 20 J/cm2, a wavelength of 595 nm, and a 2 7 mm elliptical spot. Only patients with Fitzpatrick skin types I and II were included in the study. Clearance rates were approximately 80% on average (Fig. 8.8). Treatments were well tolerated although hyperpigmentation occurred in 30% of subjects (38). As recent experience dictates, more hyperpigmentation would have been seen if patients with skin types darker than type II, or tanned patients, were included in the treatment group. The development of the dynamic cooling device subsequent to this study may reduce the incidence of hyperpigmentation following treatment. However, hyperpigmentation following treatment of lower-extremity telangiectasias with the PDL has continued to limit their use for this application. Kauvar demonstrated that she was able to achieve greater than 75% clearance of red vessels ,1 mm in diameter after one treatment session using an elliptical spot, a 1.5 ms pulse duration and fluences of 22 –23 J/cm2 and 30 ms of cryogen (44). Others have used the elliptical spot with a 20 ms pulse duration, a fluence of 15 J/cm2 and 30 ms of cryogen (Fig. 8.9). Further improvements in the PDL with the availability of adequate fluences at longer pulse durations, and methods for improved protection of the epidermis, may increase the value of PDLs for treating lower-extremity telangiectasias in the future. Although true long pulse duration lasers with pulse durations as long as 50 ms have been produced using the Nd:YAG crystal, such long pulse durations in the yellow or

Figure 8.9 Leg veins before (a) and after (b) 2 treatments with a 20 ms pulse and a fluence of 15 J/cm2 using cryogen spray cooling. (Courtesy of Craig Trigueiro, M.D.)


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orange wavelengths are not yet available. Current long pulse duration lasers in these wavelength ranges utilize “pulses” that are actually composed of trains of shorter pulses to achieve pulse durations longer than 1.5 ms. Thus, the current generation of long pulse duration PDLs do not deliver dramatically improved performance for treating leg veins over the previously available 1.5 ms devices. A true 40 – 50 ms pulse duration, 595 nm PDL (or solid state laser offering this wavelength) would represent a major leap over currently available technology. As yet, this technology is not available.

6.

LUPUS ERYTHEMATOSIS

Discoid lupus erythematosis (DLE) often presents as telangiectatic, atrophic plaques, while systemic lupus erythematosis (SLE) presents as the classic butterfly rash with more diffuse erythema and telangiectasia. Since lesions of lupus erythematosis have a significant vascular component, the PDL is a rational treatment alternative. This is especially true because many lesions of DLE are refractory to treatment. In addition, after resolution of DLE lesions, the vascular component may remain. Raulin et al. (45) treated 12 patients with cutaneous lupus erythematosis with the PDL. In 10 of the patients the cutaneous lesions were limited to the skin, while two had SLE and the associated cutaneous eruption. They reported a median clearance rate of 70% in 9 of their 12 patients. Two patients had symptomatic improvement of pain and pruritus, without visible improvement, and one patient failed to improve. Of interest is the long follow-up period ranging from 3 to 32 months, with a median of 7 months, in which only one of the patients who had had complete clearance demonstrated a small relapse. This study suggests that perhaps the vessels that develop in cutaneous lesions of DLE and SLE may serve as targets for sun-induced exacerbations of these conditions. PDL treatment of the telangiectatic component of lupus may also affect the other symptoms of the disease. This author has treated patients with lesions of DLE. One such patient was initially treated only on one side of her face at her request. The referring physician reported that upon going into the sun against medical advice, her skin would flare only in the untreated site with erythema and edema (Fig. 8.10). The treated site demonstrated no reaction to sun exposure (personal communication). Since the lesions of lupus erythematosis often contain visible telangiectasias, the longer pulse duration PDL using a 595 nm wavelength appears to yield superior results to the conventional 585 nm PDL. Even somewhat large vessels on the face are easily removed in a single treatment session. The potential for PDL treatment to improve DLE and even sun-induced flares of SLE should be further investigated, since as in rosacea, the cutaneous blood vessels may be participating in exacerbating and maintaining the overall disease as a target for sun exposure. However, care should be taken especially when treating patients with SLE. Flaring of cutaneous lesions of SLE has been observed following PDL treatment in some patients (personal communications). Limiting test spots to small areas and limiting treatment sizes during a single session to small areas are advisable when treating patients with lupus.

7.

STRIAE

Striae result from acquired defects in cutaneous elastic fibers and, despite their quite obvious clinical appearance, show very subtle changes under histopathologic examination. Elastic fibers are among the last components to appear in a healing wound, and many wounds fail to develop a normal elastic fiber network. Thus, generation of new elastic fibers in skin by

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Figure 8.10 A patient with DLE prior to treatment (the clear area on the superior-lateral aspect of the left cheek is from a previous PDL test site) (a) and 2 months after two PDL treatments to the left cheek, using 595 nm and a 1.5 ms pulse duration (b). The treated site reportedly did not flare with the rest of the face on excessive sun exposure.

exogenous stimulation, such as PDL treatment, is quite difficult. McDaniel et al. (46) reported improvement of striae following PDL treatment. Clinically, they evaluated striae as more resembling normal skin following treatment with the PDL. Shadow profilometry supported these observations, demonstrating reduced skin shadowing in striae following treatment. They also reported an apparent return to more normal dermal elastic fiber morphology under histopathologic examination. These authors used relatively low energy densities, and reported superior results using a large, 10 mm-diameter spot with only 3.0 J/cm2. The increased effectiveness of the larger-diameter spot size may be due to the deeper penetration afforded by large spot sizes. Although lasers do induce an inflammatory response that may lead to extracellular matrix deposition, results thus far in improving the textural component of striae have been somewhat disappointing, as compared to treatment of other conditions exploiting the ability of the PDL to induce dermal remodeling. However, removing the erythema often present in striae is fairly easily accomplished with the PDL. The 1.5 ms pulse duration PDL works well using 7–10 mm spot sizes, 595 nm, and relatively low fluences between 5.5 and 6.5 J/cm2. Low fluences and the 595 nm wavelength offer the advantage of less hyperpigmentation in darker-skinned or tanned individuals following treatment, as compared to 585 nm and higher-energy densities. The new ultra-long pulse duration PDLs offer similar results to earlier PDLs. These lasers also remove the erythema that typifies striae quite easily, while inducing variable amounts of dermal remodeling. The remodeling achievable by PDLs is still somewhat disappointing. As our understanding of striae and elastic fiber metabolism advances, improved strategies for treating these difficult lesions should emerge.

8.

SEBACEOUS GLAND HYPERPLASIA

Sebaceous gland hyperplasia is one of the many signs of cutaneous photodamage, and is also seen in association with acne and rosacea. Clinically, yellow papules, typically


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2 – 4 mm in size develop on the face, in sun-exposed sites or sites of active acne and rosacea. Schonermark et al. (47) presented an initial report of two patients with sebaceous gland hyperplasia treated with the short pulse duration, 585 nm PDL. Two patients were treated using 6.5 –8.0 J/cm2, 585 nm, and a pulse duration of 0.3– 0.45 ms. Sebaceous gland hyperplasia completely resolved in these patients following two to three consecutive treatments with the PDL, with no side effects. Confocal imaging of sebaceous gland hyperplasia demonstrates prominent dermal vasculature associated with the hyperplastic sebaceous glands, and the targeting of these vessels by the PDL (48). Aghassi et al. (49) reported on 10 patients with 29 lesions of sebaceous gland hyperplasia treated with PDL. They administered three PDL pulses in succession, using a wavelength of 585 nm, fluences of 7 –7.5 J/cm2, and a 5 mm spot. The great majority of lesions responded to a single treatment session, with 28% of lesions resolving completely, 66% decreasing in diameter, and 93% flattening. Because these authors stacked pulses with the PDL, they suggest that either temporary ischemia induced by selective vessel destruction or nonspecific thermal damage may be responsible for resolution of the lesions. A number of the patients treated in this study developed depressions in the treated sites before complete healing. This may be indicative of excessive thermal damage due to stacking of pulses. Although pulse stacking is commonly used to treat verrucae, this technique may not be well suited to the treatment of sebaceous gland hyperplasia. Perhaps a number of treatment sessions, with one pulse administered to each lesion per session, would decrease the incidence of this side effect. The long pulse duration PDL may prove even more effective for treatment of sebaceous gland hyperplasia. Longer pulse durations and wavelengths may better penetrate through the vessels supplying these lesions. Future studies should clarify whether the more advanced PDLs offer advantages for treatment of sebaceous gland hyperplasia, possibly negating the need for stacking of pulses in order to destroy these lesions.

9.

PSORIASIS

Psoriasis is a chronic inflammatory process clinically characterized by a greatly thickened epidermis and stratum corneum. To support this substantially thickened epidermis, dilated capillary loops emerge in elongated dermal papillae. Because of the significant vascular component underlying the epidermal component in lesions of psoriasis, as demonstrated by the Auspitz sign, vascular lasers have been used in an attempt to treat psoriasis. Zelickson et al. (50) demonstrated resolution of psoriatic plaques in response to PDL treatment. Both clinical and histopathologic evidence of resolution of psoriatic plaques was documented. Of particular interest was the long-lasting nature of remissions in treated areas. The remissions lasted for up to 13 months following treatment. Thus, the PDL, presumably due to its vascular specificity, can induce long-term remission of psoriatic plaques. To further characterize the PDL parameters that optimize treatment of psoriasis, Zelickson et al., examined variable pulse durations and wavelengths for the treatment of psoriatic plaques. They treated four patients with relatively short wavelengths of 585 and 578 nm, and longer wavelengths of 595 and 755 nm. In addition, shorter pulse durations of 0.15 and 0.45 ms were compared to longer pulse durations of 1.5 and 5 ms. Superior results were obtained with the shorter wavelengths and shorter pulse durations (Brian Zelickson, MD, personal communication). It is possible that disruption of smaller vessels optimally targeted by these parameters is the key to treating psoriasis with the PDL, or that heating of other targets including the epidermal keratinocytes stimulates an inflammatory response that causes involution of the psoriatic plaques. Preliminary

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evidence suggests that longer pulse duration lasers may not have a significant benefit over the previous generation of PDLs for the treatment of psoriasis.

10.

NONABLATIVE SKIN REMODELING WITH THE PDL

The clinical observation made by patients that facial skin treated with the PDL for telangiectasias looked not only vein free, but also generally improved in texture and appearance, led to investigation of the use of the PDL for skin rejuvenation. Although the development of the high-energy carbon dioxide laser for skin resurfacing has become a standard for the treatment of facial photoaging and acne scarring, the improvements come at a price. Ablative lasers remove the epidermis and a portion of the dermis, requiring significant healing time. In addition, risks such as infection and pigmentary alterations must be considered. Also, persistent erythema may last for months following treatment. Still, for patients with severe photodamage, carbon dioxide laser resurfacing is the mainstay of treatment. However for patients with minimal photodamage, the associated risks and downtime may not be worth the relative improvements offered by carbon dioxide laser resurfacing. For patients with minimal to moderate photodamage, nonablative wrinkle reduction may be ideal, especially as an adjunct to topical treatment regimens. In addition, improvements in hypotrophic acne scarring after carbon dioxide laser resurfacing have been less impressive than results following treatment of severely wrinkled patients. Nonablative facial resurfacing with vascular lasers such as the PDL is a desirable alternative for these patients as well. The newer generation PDLs result in significantly less purpura than previous generation lasers [Fig. 8.11(a) and (b)]. Although purpura is reduced with the longer pulse duration PDLs, a hive reaction is often present following treatment. This reaction may be indicative of activation of resident mast cells and may presage tissue remodeling. A hive response occurs following treatment with 585 or 595 nm at virtually any pulse duration provided a threshold fluence is administered. Lowering the administered fluence or increasing the pulse duration can limit or eliminate purpura, making treatments more cosmetically acceptable. Coupling patient observations with physician assessments led to a more formal investigation of the ability of the short pulse duration PDL to improve and remodel photodamaged skin. Zelickson et al. (51) evaluated 20 patients, half with mild to moderate photodamage and half with moderate to severe photodamage. Clinically observable improvement was noted in 90% of the patients with mild to moderate wrinkling, and 50% of the patients with moderate to severe wrinkling. Nine of 10 patients with mild to moderate wrinkling demonstrated 25% or more improvement with 3 out of the 10 showing 75% improvement. In the mild to moderately wrinkled group, all patients maintained their level of improvement for 6 months, and five of the six patients maintained their improvement 12– 14 months posttreatment. Of the patients with moderate to severe wrinkling, only three patients had clinically observable improvement 12 weeks after treatment. Side effects of this treatment regimen included purpura and some swelling, which occurred in all subjects and lasted for 1– 2 weeks. Two patients experienced postinflammatory hyperpigmentation, which subsequently cleared. Histopathologically, increased cellularity and glycosaminoglycan (GAG) deposition were noted in treated skin. Both short pulse duration and long pulse duration PDLs have been shown to improve photodamaged skin via nonablative dermal remodeling. The N-lite laser (ICN Pharmacauticals, Costa Mesa, CA) is a short pulse duration (,0.5 ms) 585 nm PDL used at low fluences for nonablative dermal remodeling. This device has been shown to improve fine lines and wrinkles, and to stimulate production of dermal procollagen.


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Figure 8.11 (a) A patient with telangiectasias before treatment with the conventional PDL, 6.75 J/cm2, 585 nm, and a pulse duration of 0.45 ms. (b) One day after treatment, substantial purpura is evident. (c) The opposite cheek of the same patient before treatment with the long pulse duration PDL. (d) One day after treatment with 8.4 J/cm2, 595 nm, and a pulse duration of 10 ms, demonstrating minimal purpura following treatment. (Photos courtesy of Steven J. Ugent, MD, and Candela Corporation, Wayland, MA.)

The long pulse duration 595 nm PDL has also been shown to improve rhytides and stimulate dermal remodeling. Eleven of 15 patients demonstrated improvement of rhytides following 4-monthly laser treatments, as compared to only 3 of 15 patients improving on the control side, which was treated with the cryogen spray alone without laser treatment. An 18.1% improvement in clinical grading of photodamage was measured. This clinical improvement correlated with an increase in procollagen staining as evaluated by immunohistochemical evaluation (52). Patients undergoing treatment of mild to moderate photodamage may be unwilling to endure purpura if multiple treatments are required or alternatives are available. Fluences below the purpura threshold may be required for widespread use of the PDL

PWS

Hypertrophic

Trunk, extremities

PWSs Facial Neck, head

Periorbital Wrinkles

Matting

7 7 10 7 10 7

5 10

7 10 3 10 3 10 7 7, 10

Nasal

Leg

7 10 3 10

Telangiectasia Facial

Lesion

Spot size (mm)

3, 6

3, 6 3, 6

6 1.5, 3, 6, 10

1.5, 3, 6, 10

0.45 6

6, 10 6, 10 10, 20 6, 10, 20 20 20, 30

3, 6, 10 6 10, 20, 30

Pulse (ms)

10– 15 8– 12 4– 7.5 6– 12 6– 7.5 10– 15

3– 5 6

Up to 11 7.5 8– 12 11– 22 10– 12 11– 15

7– 9 5.5– 7.5 11– 14

Energy fluence (J/cm2)

Table 8.1 Candela V-beam 595 nm Treatment Guidelines

30/30 30/10 –30 30/10 –30 30/10 –30 30/10 –30 40/10

30/10 20/30

30/20 –30 30/20 –30 30/20 –30 30 –40/20 30/10 –30 30/10

30/20 –30 30/20 –30 30/20 –30

DCDa spray/ delay

8 –12 8 –12 8 –12 8 –12 8 –12 8 –12

2 –4 4

4 –6 4 –6 4 –6 8 –12 8 –12 6 –10

4 –6 4 –6 4 –6

Interval (weeks)

Use lower fluences for infants Begin at longer pulse widths and move to shorter pulse widths as the treatment progresses; development of purpura is less with longer pulse widths, but may decrease clearance obtained Use lower fluence on neck and extremities If end point is purpura, it should be present on PWS vessels only and not on surrounding skin overlap or retreat at same session. Observe epidermal response carefully when treating at higher fluences. Ectatic vessels may be double-pulsed ( pulse stacking)

Treat patient in supine or prone position. Expect purpura regardless of pulse width Pulse stacking or double pulsing may induce blisters; higher fluences may induce blistering and hyperpigmentation; observe vessel for intravascular spasm Perform compression check for vessel patency Larger spot size may improve results Four treatments, one treatment every 4 weeks; shorter pulse widths and higher fluences may induce purpura

Higher fluences and shorter pulse widths will cause purpura, but clearance may be faster May double or triple pulse depending on the refill of the vessel Treating first with the round spot followed by the 3 10 may eliminate vessels that do not clear

Comments

238 Bernstein

1.5 1.5 0.45

7 10 7

4.5– 5 3.5– 4 4– 5

7– 9 4– 6 4– 7 3– 6 12– 15 7.5

7– 10 8– 11.5 5– 7 6.5– 7 5– 6

7– 10

8– 11 6– 7.5

30/10 30/10 30/20

30/10 30/10 30/10 30/10 0/0 0/0

30/10 20 –30/10 –20 20 –30/10 –20 30/10 30/10

30/10

30/10 –30 30/10 –30

8 8 2 –4

6 2 –3 2 –3

6 6 6

4 –6 4 –6 4 –6 4 –6 4 –6

2

4 –6 4 –6

Always do test spots laterally; when treating, apply pulses close to one another to minimize uneven pattern; “feather” edges to minimize sharp line of demarcation with untreated skin; several gentle treatments may be required Treat as soon as possible (2 weeks after suture removal) and avoid treating keloids Newer, more vascular striae may respond better than older, whiter striae May repeat treatment every 3 – 4 weeks When treating warts, 100 ms of cryogen may be sprayed pre- and postlaser pulse to wart to cool area and/or topical anesthetic may be applied prior to treatment; may triple pulse (pulse stacking) if tolerated; treat wart and at least a 1 cm ring of uninvolved skin, since wart virus has been biopsied out to 1 cm; use concurrent topical therapies at home Look for light purpura, which will require test spots at a variety pulse durations and fluences May require three to four treatments or more

Decreased fluence and longer pulse duration may cause less purpura Vessels may be pulsed two to three times to get transient intravascular purpura which disappears and becomes blush pink May use 10 mm spot to treat entire cosmetic unit, then re-treat remaining larger vessels with a smaller spot Use caution with neonates Treat every 2 weeks for proliferative hemangiomas; improper treatment may cause scars; refer to a specialist if not within your typical practice One to two treatments may be required Double pulse center of hemangioma first, then treat peripheral veins

Dynamic cooling device (DCD) parameters will vary based on lesion, location, and level of patient’s comfort.

a

Benign vascular Gynecological lesions Psoriasis

Warts (verruca)

Striae

1.5,3 3, 6, 10 10 10 1.5 1.5

7 10 7 10 7 10

Scars

1.5 10, 20 20 10, 20 1.5

1.5, 3

3, 6, 10 6, 10, 20

7 7 10 7 10

7

7 10

Venous lake Angioma/spider angioma Poikiloderma of Civatte

Hemangioma

Rosacea

Clinical Uses of the Long Pulse Duration PDL 239

7 mmþ Upto 7 mm 10 mmþ Up to 7 mm Up to 10 mm Elliptical 7 mm 10 mmþ Elliptical 7 mm 10 mmþ Up to 7 mm 7 mm

Up to 7 mm 10 mmþ 7 mm (Pediatric) 7 mm (Adult) 10 mm (Pediatric) Up to 7 mm 10 mmþ

7 mmþ

Up to 10 mm 10 mm Up to 10 mm 7 mmþ

6.5 – 7.5 5.0 – 7.0 3.0 – 3.5 5.5 – 6.0 3 7.0 – 7.5 4.0 – 5.0 3.0 – 3.5 7.0 – 7.5 4.0 – 5.0 3.0 – 3.5 6.5 – 7.0 7.0 – 9.0

2.0 – 4.5 (First pass) 4.0 – 5.0 3.5 – 4.0 4.5 – 6.0 5.0 – 6.5 3.0 – 4.5 5.5 – 6.5 3–5

5.5 – 6.0 2.0 – 4.0 5.0 – 8.0 2.5 – 6.0

Parameters 0.5 ms (J/cm2) (purpuric doses)

Not recommended 6– 8 5– 7 5– 7 3– 6 7– 9 7– 10 4– 7.5 7– 9 7– 9 6– 7.5 Not recommended 8– 12

5– 8.5 4– 8 4.5– 6.0 5.0– 6.5 3.0– 4.5 Not recommended

Not recommended

5.0– 6.0 Not known 4.0– 8.0 4– 9

Parameters 2 ms (J/cm2) (purpuric doses)

Not recommended 8– 11 6– 7.5 5– 8 3– 6 9– 20 7– 14 6– 10 9– 14 7– 12 7– 10 Not recommended Not recommended

11– 14 11– 14 10– 10.5 Not recommended

7– 9

Not recommended

5– 7 Not known 5– 9 7– 12

Parameters 20 ms (J/cm2)

Not recommended Not recommended

Not recommended 8 – 12 6.5 – 8 5 – 10 Not recommended 9 – 20 7 – 16 7 – 14 7 – 14 7 – 13

11– 14 11– 14 10– 10.5 Not recommended

5–9 5–8 6.0 – 12.0 Not recommended 8 – 10 (Second pass, for chromophore) 7–9

Parameters 40 ms (J/cm2)

8– 12

2– 3

3– 4

4– 6 3– 6 4– 6 4– 6

Tx interval (weeks)

4– 6 3

4– 6

3– 4 6– 24 4– 6

4 – 6 weeks (Salicylic acid for 1 week prior to treatment) 3– 4 3– 4

Note: Multipass (Not multipulse or pulse stacking) treatment may be used with lower fluences to achieve intravascular coagulation with minimal collateral purpura.

Venous lakes Warts

Telangiectasia, face

Spider angioma Striae Telangiectasia, leg

Pyogenic granuloma Rosacea

Psoriasis

Port-wine birthmark

Hemangioma

Angiokeratoma Acne vulgaris Cherry angioma Erythematous, hypertrophic, and keloid scars Facial rejuvenation

Lesion

Spot size

Table 8.2 Cynosure V-Star 595 nm Treatment Parameters

240 Bernstein


241

for nonablative skin remodeling. The long pulse duration PDL offers not only longer pulse durations, but also the potential to treat with longer wavelengths, such as 595 nm. As the pulse duration is increased for equivalent fluences, clinical purpura is usually reduced. Future studies comparing various pulse durations and wavelengths may shed light on the optimal PDL parameters for nonablative resurfacing. Because quantification of the improvement following nonablative resurfacing is difficult due to the subtle nature of the improvement, this issue may not be resolved for some time.

11.

FUTURE DEVELOPMENTS IN LONG-PULSE PDL

PDLs with increasingly longer pulse durations are being developed. The longer pulse durations are currently achieved by creating a series of pulses that can be separated by various off times. Advances in cooling of the epidermis should also optimize PDL treatment of a variety of conditions. Currently, a series of pulses are used to simulate a continuously longer pulse because current limitations in PDL technology prevent generation of single pulses in the 40 –50 ms range. Potential advantages of these systems are lessened purpura and the potential to more effectively treat larger vessels, such as lower-extremity telangiectasias (Fig. 8.11). However, at least some of the clinical response seen following PDL treatment correlates with the development of purpura. Generation of continuous pulses in the 40 – 50 ms second range still eludes laser developers. As longer pulse durations and higher energies are made available for the PDL, clinical experience should determine which conditions will benefit from these advances in technology.

12.

LASER PHYSICS: SUGGESTED PARAMETERS

Tables 8.1 and 8.2 document suggested parameters from the manufacturers for the newest available PDLs from the companies listed.

REFERENCES 1. 2. 3. 4. 5.

6. 7. 8.

Anderson RR, Parrish JA. Microvasculature can be selectively damaged using dye lasers: a basic theory and experimental evidence in human skin. Lasers Surg Med 1981; 1(3):263 – 276. Parrish JA, Anderson RR, Harrist T, Paul B, Murphy GF. Selective thermal effects with pulsed irradiation from lasers: from organ to organelle. J Invest Dermatol 1983; 80(suppl):75s– 80s. Anderson RR, Jaenicke KF, Parrish JA. Mechanisms of selective vascular changes caused by dye lasers. Lasers Surg Med 1983; 3(3):211– 215. Anderson RR, Parrish JA. Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science 1983; 220(4596):524 –527. Bernstein EF, Kornbluth S, Brown DB, Black J. Treatment of spider veins using a 10 millisecond pulse-duration frequency-doubled neodymium YAG laser. Dermatol Surg 1999; 25(4):316– 320. Adrian RM. Treatment of leg telangiectasias using a long-pulse frequency-doubled neodymium:YAG laser at 532 nm. Dermatol Surg 1998; 24(1):19 – 23. Kauvar AN, Frew KE, Friedman PM, Geronemus RG. Cooling gel improves pulsed KTP laser treatment of facial telangiectasia. Lasers Surg Med 2002; 30(2):149 – 153. Tan OT, Kerschmann R, Parrish JA. The effect of epidermal pigmentation on selective vascular effects of pulsed laser. Lasers Surg Med 1984; 4(4):365 –374.

242 9.

10.

11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22.

23. 24. 25. 26. 27. 28.

29. 30. 31.

32. 33.

Bernstein Hulsbergen Henning JP, van Gemert MJ, Lahaye CT. Clinical and histological evaluation of portwine stain treatment with a microsecond-pulsed dye-laser at 577 nm. Lasers Surg Med 1984; 4(4):375– 380. Tan OT, Carney JM, Margolis R, Seki Y, Boll J, Anderson RR et al. Histologic responses of port-wine stains treated by argon, carbon dioxide, and tunable dye lasers. A preliminary report. Arch Dermatol 1986; 122(9):1016– 1022. Garden JM, Tan OT, Parrish JA. The pulsed dye laser: its use at 577 nm wavelength. J Dermatol Surg Oncol 1987; 13(2):134– 138. van Gemert MJ, Welch AJ. Treatment of port-wine stains: analysis. Med Instrum 1987; 21(4):213– 217. Garden JM, Polla LL, Tan OT. The treatment of port-wine stains by the pulsed dye laser. Analysis of pulse duration and long-term therapy. Arch Dermatol 1988; 124(6):889– 896. Glassberg E, Lask GP, Tan EM, Uitto J. The flashlamp-pumped 577-nm pulsed tunable dye laser: clinical efficacy and in vitro studies. J Dermatol Surg Oncol 1988; 14(11):1200– 1208. Tan OT, Sherwood K, Gilchrest BA. Treatment of children with port-wine stains using the flashlamp-pulsed tunable dye laser. N Engl J Med 1989; 320(7):416 –421. Tan OT, Morrison P, Kurban AK. 585 nm for the treatment of port-wine stains. Plast Reconstr Surg 1990; 86(6):1112– 1117. Nelson JS, Applebaum J. Clinical management of port-wine stain in infants and young children using the flashlamp-pulsed dye laser. Clin Pediatr (Phila) 1990; 29(9):503–508, discussion 509. Ashinoff R, Geronemus RG. Flashlamp-pumped pulsed dye laser for port-wine stains in infancy: earlier versus later treatment. J Am Acad Dermatol 1991; 24(3):467 – 472. Ashinoff R, Geronemus RG. Capillary hemangiomas and treatment with the flash lamppumped pulsed dye laser. Arch Dermatol 1991; 127(2):202– 205. Morelli JG, Tan OT, Weston WL. Treatment of ulcerated hemangiomas with the pulsed tunable dye laser. Am J Dis Child 1991; 145(9):1062– 1064. Goldman MP, Fitzpatrick RE, Ruiz-Esparza J. Treatment of port-wine stains (capillary malformation) with the flashlamp-pumped pulsed dye laser. J Pediatr 1993; 122(1):71 – 77. Alster TS, Wilson F. Treatment of port-wine stains with the flashlamp-pumped pulsed dye laser: extended clinical experience in children and adults. Ann Plast Surg 1994; 32(5):478– 484. Jackson BA, Arndt KA, Dover JS. Are all 585 nm pulsed dye lasers equivalent? A prospective, comparative, photometric, and histologic study. J Am Acad Dermatol 1996; 34(6):1000– 1004. Lou WW, Geronemus RG. Treatment of port-wine stains by variable pulse width pulsed dye laser with cryogen spray: a preliminary study. Dermatol Surg 2001; 27(11):963 –965. Alster TS. Improvement of erythematous and hypertrophic scars by the 585-nm flashlamppumped pulsed dye laser. Ann Plast Surg 1994; 32(2):186 – 190. Dierickx C, Goldman MP, Fitzpatrick RE. Laser treatment of erythematous/hypertrophic and pigmented scars in 26 patients. Plast Reconstr Surg 1995; 95(1):84 – 90, discussion 91 – 92. Goldman MP, Fitzpatrick RE. Laser treatment of scars. Dermatol Surg 1995; 21(8):685 – 687. Sheridan RL, MacMillan K, Donelan M, Choucair R, Grevelink J, Petras L et al. Tunable dye laser neovessel ablation as an adjunct to the management of hypertrophic scarring in burned children: pilot trial to establish safety. J Burn Care Rehabil 1997; 18(4):317 – 320. Alster TS, Nanni CA. Pulsed dye laser treatment of hypertrophic burn scars. Plast Reconstr Surg 1998; 102(6):2190– 2195. McCraw JB, McCraw JA, McMellin A, Bettencourt N. Prevention of unfavorable scars using early pulse dye laser treatments: a preliminary report. Ann Plast Surg 1999; 42(1):7 – 14. Shakespeare PG, Tiernan E, Dewar AE, Hambleton J. Using the pulsed dye laser to influence scar formation after breast reduction surgery: a preliminary report. Ann Plast Surg 2000; 45(4):357– 368. Fitzpatrick RE. Treatment of inflamed hypertrophic scars using intralesional 5-FU. Dermatol Surg 1999; 25(3):224– 232. Tan OT, Hurwitz RM, Stafford TJ. Pulsed dye laser treatment of recalcitrant verrucae: a preliminary report. Lasers Surg Med 1993; 13(1):127 – 137.

Clinical Uses of the Long Pulse Duration PDL 34. 35. 36. 37.

38. 39. 40.

41. 42.

43. 44.

45. 46. 47. 48.

49.

50.

51. 52.

243

Kauvar AN, McDaniel DH, Geronemus RG. Pulsed dye laser treatment of warts. Arch Fam Med 1995; 4(12):1035– 1040. Jacobsen E, McGraw R, McCagh S. Pulsed dye laser efficacy as initial therapy for warts and against recalcitrant verrucae. Cutis 1997; 59(4):206 – 208. Ross BS, Levine VJ, Nehal K, Tse Y, Ashinoff R. Pulsed dye laser treatment of warts: an update. Dermatol Surg 1999; 25(5):377– 380. Robson KJ, Cunningham NM, Kruzan KL, Patel DS, Kreiter CD, O’Donnell MJ et al. Pulseddye laser versus conventional therapy in the treatment of warts: a prospective randomized trial. J Am Acad Dermatol 2000; 43(2, Pt 1):275 –280. Bernstein EF, Lee J, Lowery J, Brown DB, Geronemus R, Lask G et al. Treatment of spider veins with the 595 nm pulsed-dye laser. J Am Acad Dermatol 1998; 39(5, Pt 1):746– 750. West TB, Alster TS. Comparison of the long-pulse dye (590 – 595 nm) and KTP (532 nm) lasers in the treatment of facial and leg telangiectasias. Dermatol Surg 1998; 24(2):221 – 226. Lowe NJ, Behr KL, Fitzpatrick R, Goldman M, Ruiz-Esparza J. Flash lamp pumped dye laser for rosacea-associated telangiectasia and erythema. J Dermatol Surg Oncol 1991; 17(6):522– 525. Rohrer TE, Chatrath V, Iyengar V. Does pulse stacking improve the results of treatment with variable pulse pulsed dye lasers? Dermatol Surg 2004; 30(2 Pt 1):163 –167; discussion 167. Goldman MP, Sadick NS, Weiss RA. Cutaneous necrosis, telangiectatic matting, and hyperpigmentation following sclerotherapy. Etiology, prevention, and treatment. Dermatol Surg 1995; 21(1):19– 29, quiz 31– 32. Hsia J, Lowery JA, Zelickson B. Treatment of leg telangiectasia using a long-pulse dye laser at 595 nm. Lasers Surg Med 1997; 20(1):1 – 5. Kauvar ANB, Grossman MC, Bernstein LJ, Kovacs SO, Quintana AT, Geronemus RG. The effects of cryogen spray cooling on pulsed dye laser treatment of vascular lesions. Lasers Surg Med 1998; (suppl 10):211. Raulin C, Schmidt C, Hellwig S. Cutaneous lupus erythematosus-treatment with pulsed dye laser. Br J Dermatol 1999; 141(6):1046– 1050. McDaniel DH, Ash K, Zukowski M. Treatment of stretch marks with the 585-nm flashlamppumped pulsed dye laser. Dermatol Surg 1996; 22(4):332 – 337. Schonermark MP, Schmidt C, Raulin C. Treatment of sebaceous gland hyperplasia with the pulsed dye laser. Lasers Surg Med 1997; 21(4):313 – 316. Gonzalez S, White WM, Rajadhyaksha M, Anderson RR, Gonzalez E. Confocal imaging of sebaceous gland hyperplasia in vivo to assess efficacy and mechanism of pulsed dye laser treatment. Lasers Surg Med 1999; 25(1):8 – 12. Aghassi D, Gonzalez E, Anderson RR, Rajadhyaksha M, Gonzalez S. Elucidating the pulseddye laser treatment of sebaceous hyperplasia in vivo with real-time confocal scanning laser microscopy. J Am Acad Dermatol 2000; 43(1, Pt 1):49– 53. Zelickson BD, Mehregan DA, Wendelschfer-Crabb G, Ruppman D, Cook A, O’Connell P et al. Clinical and histologic evaluation of psoriatic plaques treated with a flashlamp pulsed dye laser. J Am Acad Dermatol 1996; 35(1):64– 68. Zelickson BD, Kilmer SL, Bernstein E, Chotzen VA, Dock J, Mehregan D et al. Pulsed dye laser therapy for sun damaged skin. Lasers Surg Med 1999; 25(3):229 –236. Rostan E, Bowes LE, Iyer S, Fitzpatrick RE. A double blind side-by-side comparison study of low fluence long pulse dye laser to coolant treatment for wrinkling of the cheeks. J Cosmet Laser Ther 2001; 3:129– 136.

9 Pulsed KTP (532 nm) Lasers Robert M. Adrian Center for Laser Surgery, Washington, DC, USA

Emil Tanghetti Private Practice, Sacramento, California, USA

Arielle N. B. Kauvar New York Laser and Skin Care, New York; New York University School of Medicine, New York; and Suny Downstate Medical Center, New York, New York, USA

1. 2. 3. 4.

Introduction Laser – Tissue Interaction Laser Physics Laser Techniques 4.1. Facial Telangiectasias 4.2. Leg Telangiectasias 4.3. Port-Wine Stains 4.4. Poikiloderma of Civatte 4.5. Hemangioma, Venous Lakes, Cherry Angioma, and Spider Telangiectasia 4.6 Lentigines, Freckles, Macular Seborrheic Keratoses 5. Summary References

1.

245 246 250 251 251 252 253 254 254 254 255 255

INTRODUCTION

Although numerous laser and nonlaser pulsed photothermal devices are currently available for the treatment of vascular lesions, no single system has proven uniformly effective in the treatment of the wide variety of disorders encountered in clinical practice (1). Over the past few years, multiple individual case reports and clinical studies have highlighted the fact that any single laser system can show some degree of efficacy in the treatment of vascular lesions. Argon at 488 and 514 nm (2–4), argon pumped dye at 577– 585 nm (5,6), potassium titanyl phosphate (KTP) at 532 nm (7,8), pulsed dye at 585 nm (9 – 11) and 595 nm (12), krypton at 530 nm (13), copper vapor at 578 nm (14 – 16), copper bromide at 578 nm (17), alexandrite at 755 nm (18), diode at 810 nm (19), neodymium 245

246

Adrian, Tanghetti, and Kauvar

YAG at 1064 nm (20 – 22), and carbon dioxide at 10,600 nm (23 – 26) lasers and intense pulsed light have all shown a variable efficacy in the treatment of vascular lesions. Anatomic location, vessel size, color, depth, and skin type (epidermal melanin) are all important factors which must be considered in the choice of a light source for the treatment of these conditions. In this chapter, we will discuss current concepts in the use of KTP and diode lasers emitting radiation at 532 nm and their role in the treatment of vascular lesions. 2.

LASER – TISSUE INTERACTION

Examination of the absorption curve of hemoglobin and melanin shows well-defined peaks of hemoglobin absorption at 532 nm (Fig. 9.1). The insertion of a frequencydoubling crystal in the path of 1064 nm radiation produced from a neodymium-YAG rod can produce 532 nm light and this provides the opportunity to develop a wide variety of pulsed 532 nm lasers for the treatment of blood vessel disorders. A variety of factors play a role in the response of a chromophore (target) to energy at any given wavelength. Early experience with using argon 488 and 514 nm showed that epidermal melanin competed with hemoglobin at these wavelengths (2 –4) (Fig. 9.1). Absorption by melanin and lack of specific vascular effects at 488 and 514 nm was associated with postoperative complications including pigment disturbances as well as atrophic and hypertropic scarring. Elegant modeling studies of port-wine stains by Van Gemert et al. (27) suggested that wavelength, pulse duration, irradiance, and spot size were deemed relevant in the treatment of these lesions. They argued that 532 nm radiation has an absorption coefficient for blood, which is .585 and 590 nm (Table 9.1). This may explain why green light radiation at 532 nm has proven quite useful in the treatment of facial blood vessels,

Figure 9.1 Absorption spectra of major skin pigments at concentrations for which they typically occur. Values shown are absorption coefficients (ma) for pure water, human hemoglobins at 11 g/dL, and dihydroxyphenylalanine (DOPA)-melanin, which has an absorption spectrum similar to pigmented epidermis at 15-mg/dL concentration to water. DOPA-melanin concentration shown is approximately equivalent to heavily pigmented human epidermis. Absorption coefficient of single melanosomes is unknown. Hb, Hemoglobin: HbO2, oxyhemoglobin. (From Anderson RR. Optics of the skin. In: Lim HW, Soter MA, eds. Clinical photomedicine. New York: Marcel Dekker, 1993.)

Pulsed KTP (532 nm) Lasers

247

Table 9.1 Depth of Penetration Dependence on Wavelength Wavelength (nm)

Absorption coefficient (mm21)

Scattering coefficients (mm21)

Anisotrophy factor

48.0 47.5 47.3 47.2 47.0 46.8 46.7 46.6 46.4

0.995 0.995 0.995 0.995 0.995 0.995 0.995 0.995 0.995

Blood 415 500 532 545 560 577 585 590 633

300.0 11.5 26.6 33.0 20.0 35.4 19.1 6.9 5.0

Source: Van Gemert MJC, Pickering JW, Welch AJ. Modeling laser treatment or port-wine stains. In: Tan OT, ed. Management and Treatment of Benign Cutaneous Vascular Lesions. Philadelphia: Lea & Febiger, 1992.

port-wine stains and certain lower extremity telangiectasis. Certain investigators have suggested that one of the major limitations of 532 nm light is its limited dermal penetration. A closer look at Van Gemert’s modeling data, however, predicts a depth of maximum vascular damage at 1.4 nm for 532 nm radiation (Table 9.1), which may explain deep vascular effects seen during the application of this wave band of light for leg veins. Histologic studies using a high energy pulsed frequency doubled Nd-YAG laser at 532 nm (Versapulsew, Lumenis) demonstrate the effects of 532 nm radiation on dermal vasculature. Twenty-eight patients with lower extremity telangiectasia were treated with 16 – 20 J/cm2 using contact cooling, 3 – 5 mm spot sizes, and pulse durations of 10– 50 ms. Biopsies obtained immediately after treatment showed swelling of the vessel walls with loss of endothelium and intravascular coagulation without the erythrocyte extravasation typical of pulsed dye lasers (Fig. 9.2). In certain biopsies, a cuff of perivascular collagen coagulation was noted surrounded by normal collagen indicating that specific vascular effects could be produced. Response to laser treatment at 5 –7 days showed vessel wall inflammatory cell infiltration and necrosis only to be replaced at 3 weeks by a fibrotic perivascular scar in the dermis. This damage occurred in the mid reticular dermis presumably in areas unreachable by 532 nm radiation. Although the exact mechanism whereby these specific vascular effects are achieved at 532 nm is debated, there is no doubt that they occur and are responsible for clinical improvement of facial blood vessels, port wine stains and legs veins in response to this wavelength (28 –31). Pulse duration plays a significant role in treatment of vascular lesions. Studies by Van Gemert et al. (27) and Dierickx et al. (32) have demonstrated the need for lasers with a 1– 10 ms pulse duration in the treatment of port-wine stains. Small visible vessels generally require pulse durations at least 10 ms for optimum treatment. Larger vessels may require still longer pulse duration for vascular destruction. Longer pulse can be used to effectively treat larger blood vessels. Our findings and current techniques support the earlier work of Dierickx et al. (32) and Tanghetti. Rather than destroying the targeted vessels in one pass with a single high-energy pulse with unwanted heating of epidermis and dermis, repeated lower-energy passes can accomplish this task with less damage to the surrounding tissues as well as a deeper depth of injury to target vessels. Spot size is an issue, which cuts a number of ways. For the most superficial blood vessels, matching the spot size to the vessels targeted, especially without cooling, has

248


Figure 9.2 Leg vein biopsy immediately post treatment with Versapulsew laser at 20 J/cm2, 50 ms pulse duration, and 5 mm spot. Source: Van Gemert MJC, Pickering JW, Welch AJ. Modeling laser treatment for port-wine stains. In: Tan OT, ed. Management and Treatment of Benign Cutaneous Vascular Lesions. Philadelphia: Lea & Febiger, 1992.

some merits. This will limit the damage to the epidermis, which cannot be protected by cooling while still treating the targeted vessels. The damage and subsequent crusting will generally be limited and minor. However, if deeper vessels are targeted, a spot size of at least 3 mm and preferably larger is ideal. The modeling studies of Van Gemert et al. (27) have suggested that the larger spot sizes are required for deeper penetration of laser light due to the scattering effects of the dermis. In clinical practice, we use the largest spot available matched with appropriate fluences combined with epidermal cooling. The Versapulse laser (Coherent/Lumenis) is no longer manufactured. The Diolite (Iridex) is a low power device with small spot sizes, and consequently can be only used to trace facial telangiectasia, but has no role in the treatment of broader vascular lesions such as facial erythema, poikiloderma, or port wine stains. The Aura (Laserscope) is a high powered pulsed KTP laser with a contact cooling sapphire tip, and can be used with spot sizes 1 – 5 mm, adjustable at 0.1 mm increments. The Gemini (Laserscope) is the newest pulsed KTP system, with almost twice the power of previously available


249

Figure 9.3 Laserscope Aura/Gemini Versastat handpiece with an adjustable 1 – 5 mm spot size.

systems, and is equipped with both an adjustable 1– 5 mm spot size (Fig. 9.3), as well as a 10 mm (Fig. 9.4), photon recycling handpiece that has a water cooled sapphire tip. Photon recycling is a concept developed by Dr. Rox Anderson of Wellman Laboratories that uses a reflector in the handpiece to redirect the back-scattered photons back into the tissue, and substantially increases the effective fluence. The large spot size enables deeper penetration of the photons (Fig. 9.5) and delivery of higher effective fluences. With the new 10 mm spot, broader lesions such as facial erythema, poikiloderma and port wine stains can be treated with a lower risk of reticulation and increased efficacy. Cutaneous cooling has been a major advance in laser surgery and plays an important role in the treatment of vascular lesions (33,34). In addition to affording increased patient comfort during the procedure, higher energy is able to be used with reduced epidermal damage. When multiple pulses are delivered to a given vessel, epidermal cooling is

Figure 9.4 Laserscope Gemini VersaStat 10 mm handpiece with photon recycling.

250


Figure 9.5 The optical penetration of the photons at 532 nm is greatly increased with a 10 mm compared to a 1 – 5 mm spot.

essential. Studies have shown that contact cooling using a sapphire chill tip can lower the temperature of the epidermis (100–120 nm) to 158C within 250 ms. Although cooling is beneficial in the treatment of vascular lesions, tanned and darker skinned individuals need to be approached with caution since melanin competes with hemoglobin at 532 nm. Treatment of tanned individuals may be associated with significant postoperative complications such as blistering, crusting, and prolonged hypopigmentation in treated sites.

3.

LASER PHYSICS

A number of 532 nm pulsed and quasi-continuous lasers are available through various laser manufacturers (Table 9.2). There are significant differences among these systems, which are important to clinical safety and efficacy. In general, laser systems with, large spot sizes and Table 9.2 Lasers of Wavelength 532 nm Manufacturer Laser Type Maximum power (W) Spot size (mm) Pulse rate (Hz) Pulse duration (ms) Contact cooling Other

Coherent Lumenis Versapulsew FD Nd:YAG Solid State 7.2 2 – 10 1 – 10 2 – 50 Yes No longer manufactured

Iridex Diolitew Diode Pumped FD Nd:YAG 3 0.2– 1.4 1 – 15 1 – 50 No

Laserscope Auraw FD Nd:YAG

Laserscope Geminiw FD Nd:YAG

60 1–5 1 – 10 1 – 50 Yes

275 1 – 5, 10 1–4 1 – 50 Yes


251

cooling capable of delivering high energy fluences provides greater safety and efficacy in the treatment of vascular lesions. Unfortunately, these systems are generally more expensive than those without these features. Cutaneous cooling allows the delivery of higher energy fluences with increased patient comfort, safety and efficacy. Depending on the laser system one uses, treatment technique will vary. A detailed discussion regarding the clinical use of the Versapulsew laser will serve as a guideline for current technique using 532 nm lasers in the treatment of vascular lesions.

4. 4.1.

LASER TECHNIQUES Facial Telangiectasias

Dilated facial blood vessels or telangiectasias are a common occurrence affecting millions of individuals (35,36). While genetic factors may play a role in the development of these lesions, they are most commonly seen in patients of skin types I– III and may be associated with acne rosacea, chronic actinic damage, collagen vascular diseases, estrogens, overuse of topical cortico steroids, and photodamage. Lasers of 532 nm wavelength have proven effective in the treatment of facial telangiectasias (7,29). The availability of large spot sizes with high fluence and contact cooling of the epidermis laser provides excellent efficacy and safety in the treatment of this condition (Fig. 9.6). Small pink and red vessels ,0.3 mm in diameter are treated with between 9 and 13 J/cm2 using a 4– 6 mm spot size and pulse duration ranging between 10 and 30 ms. Vessels are treated with single, slightly overlapping pulses in an attempt to achieve a clinical endpoint of vessel disappearance. If vessels refill or persist during the treatment session, another series of pulses may be delivered in order to produce disappearance of the vessel. Blood vessels .0.4 mm are treated in a similar fashion but often respond to longer pulse durations in the 30–50 ms range. Single, slightly overlapping pulses with the same clinical endpoint as seen with smaller blood vessels are used. Blood vessels .1 mm in diameter may not disappear at the time of laser therapy, but will often develop which appears as a darkening of the vessel. This can be used as an effective end point. The clotted vessel will generally disappear over 1–2 weeks. Ultrasound gel has been quite useful in the use of the KTP laser for the treatment of port-wine stain and telangiectasias (37). This agent allows rapid and smooth movement of the chill tip over the skin. It also provides close contact of the chill tip with the epidermis facilitating heat transfer away from the epidermis during pulse delivery as well as after the treatment. Ultrasound gel may also help by means of refractive index matching. Gel is also quite helpful in treating irregular surfaces such as the nasolabial folds with a contact chilling

Figure 9.6 Facial telangiectasia before (a) and 1 month after (b). Treatment with Versapulsew laser: 12 J/cm2, 5 mm spot, 30 ms pulse.

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device where direct contact to the skin surface can only be made by a thick layer of gel between the skin and chilling device. Patients who have tanned skin or Fitzpatrick types IV–VI may blister and develop hypopigmentation of a temporary nature using 532 nm radiation. Tanned skin represents a relative contraindication to 532 nm laser treatment and we routinely ask patients to return after their tan has faded. At the completion of treatment, patients apply cool compresses to the treated area for 10–20 min. Patients can be seen 4–6 weeks later and retreated if necessary. Complications from Versapulse laser treatment of facial telangiectasias are uncommon but most often result from lack of contact of the chill tip with the epidermis or use of excessive energy fluence. These problems may be seen during treatment as immediate greying or blistering of the skin. If this occurs one should re-examine their technique to be sure that there is proper contact of the chill tip to the skin and that appropriate energy fluences are being used. Occasionally, when treating a patient with significant facial telangiectasias of the face edema and swelling of the face and lower eyelids will be seen after a night’s rest. This can last 1–3 days and can be treated by head elevation when sleeping. Our experience in the treatment of over 1000 patients with facial telangiectasia indicate that 85–90% of patients achieve .75% improvement of their telangiectasias from one treatment sessions. Approximately 15–20% of patients require touch up treatment sessions to achieve optimal results. A great benefit in the use of longer pulse 532 nm lasers is that postoperatively patients do not experience the excessive purpura as seen during the use of 0.45–1.5 ms pulsed dye lasers. Patients may return to their work or social activities within a relatively short period of time. The development of the 10 mm spot size with the Gemini laser has greatly improved the treatment of rosacea associated telangiectasia and erythema. The individual telangiectasia are traced with contiguous laser pulses using a 3 –4 mm spot, pulse durations of 20– 40 ms and fluences of 10– 15 J/cm2. The background erythema can then be treated using the 10 mm spot with pulse durations of 20 – 30 ms and fluences of 6 – 8 J/cm2. Patients can expect transient erythema for several hours without purpura, and the possibility of urticarial papules for up to one day. Excellent clearing of the erythema and telangiectasia is achieved in 2– 3 treatments (Fig. 9.7).

4.2.

Leg Telangiectasias

The use of lasers to treat lower extremity telangiectasias is a topic that has evoked a large amount of controversy (1). While sclerotherapy has been the treatment of choice, this treatment is not without problems. The versapulse, Aura and Gemini lasers effectively treat superficial leg telangiectasia up to 110 mm in diameter (28 –31) (Fig. 9.8). Patients

Figure 9.7 A patient with rosacea associated telangiectasia and erythema (a) before and (b) after one treatment with the Gemini laser. (Courtesy of Vic Ross, M.D. and Laserscope.)


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Figure 9.8 Leg veins before (a) and after (b). Versapulsew laser treatment 2 Rx.

with Fitzpatrick skin types I –III are excellent candidates for this treatment. It is best to avoid treating patients with tanned skin and use caution in treating darker skin types because of competition with epidermal melanin. Lower extremity blood vessels are treated using similar techniques as for facial blood vessels but, longer pulse durations at 40 – 50 ms are generally used with a 4 mm spot and energies between 20 and 24 J. Single slightly overlapping pulses are delivered along the course of the vein with observed clinical endpoints of vessel disappearance of small vessels or persistent intervascular coagulation of larger vessels. Graying or immediate blistering of skin are important signs indicating that it is necessary to reevaluate the adequacy of cutaneous cooling or energy fluence. Unlike the face, however, delayed blisters with these fluences are not uncommon when treating leg veins. Larger diameter and deeper vessels are now better treated with near infrared Nd:YAG, alexandrite and diode lasers. 4.3.

Port-Wine Stains

Port-wine stains remain a therapeutic challenge for clinicians. The flashlamp pumped pulse dye laser (450 ms) has long been recognized as the gold standard for the treatment of this condition (9,10). Studies by Van Gemert et al. (27) and Dierickx et al. (32) suggested that longer pulse durations in the range of 1–10 ms may be more ideal for the treatment of this condition. In a bilateral study comparing the Versapulse laser at 532 nm with a pulse dye laser at 585 nm, equivalent responses were noted in lightening of port-wine stains (38). Port-wine stains treated with the Versapulse laser require similar techniques to those used in the treatment of facial telangiectasias and leg veins (Fig. 9.9). Single, slightly overlapping pulses and after multiple passes and often multiple passes are delivered to the

Figure 9.9 Port-wine stain before (a) and after (b). Versapulsew laser treatment 2 Rx.

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affected areas. Treatment energy fluences range between 12 and 20 J/cm2 using 10–50 ms pulse durations. Once again, proper contact of the chill tip with the skin is essential to reduce postoperative blistering and crusting at treatment sites and to enhance patient comfort. The Versapulse and Aura/Gemini laser have been found useful in treating children and adults with port-wine stains, which no longer respond to pulse dye laser treatment. KTP laser retreatment may cause additional lightening in approximately 50% of lesions. A number of 532 nm lasers are capable of accepting scanners. Unfortunately, small spot sizes used with scanners decreases tissue transmission and makes treating deeper blood vessels difficult and lack of an effective fluence in the deeper dermis due to the scattering of light.

4.4.

Poikiloderma of Civatte

This clinical entity is a challenging problem for clinicians and treatment of this condition should be approached with cauation. The pulsed KTP laser has been found useful in the treatment of this condition, however, physicians must be careful to use lower fluences since neck skin may exhibit delayed wound healing, persistent hypopigmentation and scarring from overzealous laser treatment. Patients with this condition can be treated with the Versapulse laser using a 5 or 6 mm spot at 8.5 –12 J/cm2 with 10 –30 ms pulse durations. Typically one to two treatments will result in significant improvement. Careful choice of fluence and use of contact cooling should reduce the incidence of complications seen in the treatment of this condition. Urticarial swelling of the lower neck can occur with this condition for 1 –2 days after treatment. Poikiloderma of Civatte can now be treated with a better risk-benefit ratio using the 10 mm spot size available with the Gemini laser, contact cooling and lower fluences. These parameters provide a decreased incidence of reticulation and hypopigmentation. Small test areas should be performed to determine the optimal laser parameters for each patient.

4.5.

Hemangioma, Venous Lakes, Cherry Angioma, and Spider Telangiectasia

All of these conditions may be treated by means of 532 nm lasers. Depending on the laser, treatment parameters will vary. Versapulsew laser treatment of hemangiomas can successfully improve these lesions. Spot sizes of 5 –6 mm and fluences between 14 and 20 J may be used to flatten these lesions. Venous lakes, cherry angiomas, and spider telangiectasia respond to one or two pulses matching spot size to the size of these lesions. In some cases, most often involving hemangiomas, multiple treatment sessions are necessary and complete response may not be seen. Venous lakes, cherry angiomas and spider telangiectasia respond favorably in one or two treatment sessions.

4.6

Lentigines, Freckles, Macular Seborrheic Keratoses

The pulsed KTP laser can also be used effectively to treat pigmented lesions including lentigines, freckles and macular seborrheic keratoses. A 2 – 4 mm spot size is used with pulse durations of 10 –15 ms and fluences of 15– 20 J/cm2. An immediate endpoint of tissue graying, but not whitening, should be observed. Sometimes a second pulse is required to achieve this effect. A fine crusts develops and may be present for 5 – 10 days, depending on the lesion location. Patients are instructed to apply an antibiotic ointment such as bacitracin or poilysporin daily until the treated areas have healed.


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Treatment of pigmented lesions must not be performed in individuals with Fitzparick skintypes IV or higher, or in fair skinned patients who have a suntan present.

5.

SUMMARY

There is no doubt that 532 nm green light radiation is effective in the treatment of wide variety of vascular lesions including facial telangiectasia, port-wine stains, hemangiomas, leg veins, poikiloderma of civatte, cherry angioma, and venous ectasia. Systems with large spot sizes, high fluences, and cutaneous cooling appear safer and more effective in the treatment of these conditions. Physicians who use any of these lasers should learn the performance characteristics of each individual system and adhere to published guidelines in order to provide safe and effective laser treatment.

REFERENCES 1. 2. 3. 4. 5.

6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18.

Dover JS, Sadick NS, Goldman MP. The role of lasers and light sources in the treatement of leg veins. Dermatol Surg 1999; 25:328 – 336. Apfelbert DB, Masr MR, Lash H. Extended clinical use of the argon laser for cutaneous lesions. Arch Dermatol 1979; 115:719. Noe JM et al. Port wine stains and the response to argon laser therapy. Successful treatment and the predictive role of color, age and biopsy. Plast Reconstr Surg 1980; 65:130. Dolsky RL. Argon laser skin surgery. Surg Clin North Am 1984; 64:861. Broska P, Mattinho F, Goodman MM. Comparison of the argon tunable dye laser with the flashlamp pulsed dye laser in treatment of facial telangiectasia. J Dermatol Surg Oncol 1994; 20:749 – 753. Apfelberg DB. Argon-pumped tunable dye laser. Ann Plast Surg 1994; 32:394 – 400. Goldberg DJ, Meine JG. A comparison of four frequency doubled Nd:YAG (532 nm), Laser systems for treatment of facial telangiectasia. J Dermatol Surg 1999; 25:463 – 467. Smith T et al. 532 Nanometer green laser beam treatment of superficial varicosities of the lower extremities. Laser Surg Med 1988; 8:130. Tan OT, Shelwood DK et al. Treatment of children with port wine stains using the flashlamp pulsed tunable dye laser. N Engl J Med 1989; 320:416. Sherwood KA, Tan OT. Tretment of a capillary hemangioma with the flashlamp pumped dye laser. J Am Acad Dermatol 1990; 22:136. Goldman MP, Fitzpatrick RE. Pulsed-dye laser treatment of leg telangiectasias with and without simultaneous sclerotherapy. J Dermatol Surg Oncol 1990; 16:338. Hsia J et al. Treatment of leg telangiectasia using a long pulse dye laser at 595 nm. Lasers Surg Med 1997; 20:1– 5. Thibauh PK. A patient’s questionnaire evaluation of krypton laser treatment of facial telangiectases. Dermatol Surg 1997; 23:37– 41. Dinehart SM, Waner M, Flock S. The copper vapor laser for treatment of cutaneous vascular and pigmented lesions. J Dermatol Surg Oncol 1993; 19:370– 375. Key JM, Waner M. Selective destruction of facial telangiectasia using a copper vapor laser. Arch Otolaryngol Head Neck Surg 1992; 118– 509. Dinehart SM, Waner M. Comparison of the copper vapor and flashlamp-pulsed dye laser in the treatment of facial telangiectasia. J Am Acad Dermatol 1991; 24:116. McCoy D, Hanna M, Anderson P, McLennan G, Repacholi M. An evaluation of the copper bromide laser for treating telangiectasia. Dermatol Surg 1996; 22:551 – 557. McDaniel DH, Ash K, Lord J, Newman J, Adrian RM, Zukowski M. Laser therapy of spider leg veins: Clinical evaluation of a new long pulsed Alexandrite laser. J Dermatol Surg 1999; 25:52 – 58.

256 19.

20. 21. 22.

23. 24. 25. 26.

27.

28. 29. 30.

31. 32.

33.

34. 35. 36. 37. 38.

Adrian, Tanghetti, and Kauvar Adrian RM, Griffin L. Long pulse alexandrite (755 nm) and diode (800 nm) lasers in the treatment of lower extrement telangiectasia. A comparative clinical study. Laser Surg Med 1999; 11:20. Weiss RA, Weiss MA. Early clinical results with a mutiple synchronized pulse 1064 nm laser for leg telangiectasias and reticular veins. J Dermatol Surg 1999; 25:399 – 402. Landthaler M, Haina D, Brunner R, Waidelich W, Braun-Falco O. Neodymium:YAG laser therapy for vascular lesions. J Am Acad Dermatol 1986; 14:107– 117. Landhaler M, Hohenleutner U, El Raheem TA. Therapy of vascular lesions in the head and neck area by means of argon, ND:YAG, CO2 and flashlamp-pumped pulsed dye lasers. Adv Otorhinolaryngol 1995; 49:81 – 86. Lanigan SW, Cotterill JA. The treatment of port-wine stains with the carbon dioxide laser. Br J Dermatol 1990; 229. Backer JW, Ratz JL, Richfield DF. Histology of port-wine stains treated with carbon dioxide laser. J Am Acad Dermatol 1984; 10:1014. Kaplan I, Peled I. The carbon dioxide laser in the treatment of superficial telangiectases. Br J Plast Surg 1975; 28:214. Bailin PL. Treatment of port-wine stains with the CO2 laser: early results. In: Arndt KA, Noe JM, Rosen S, eds. Cutaneous Laser Therapy; Principles and Methods. Chichester: John Wiley & Sons, 1983. Van Gemert MJC, Pickering JW, Welch AJ. Modeling laser treatment of port-wine stains. In: Tan OT, ed. Management and Treatment of Benign Cutaneous Vascular Lesions. Philidelphia: Lea & Febiger, 1992. Adrian RM, Tanghetti ET. Long pulse 532 nm laser treatment of lower extremity telangiectasias: a clinical and histologic study. Dermatol Surg 1997; 24– 28. Adrian RM, Tanghetti ET. Long pulse 532 nm laser treatment of facial telangiectasia. Dermatol Surg 1997; 24:71– 74. Bernstein EF, Kornbluth S, Brown DB, Black J. Treatment of spider veins using a 10 millesecond pulse duration frequency doubled neodymium YAG laser. Dermatol Surg 1999; 25:316 – 320. Massey RA, Katz BE. Successful treatment of spider leg veins with a high energy long pulse frequency double neodymium: YAG laser (Help G). Dermatol Surg 1999; 25:677 – 680. Dierickix CC, Casparian JM, Venugopalan V et al. Thermal relaxation of port-wine stain vessels probed in vivo: the need for 1 –10 millisecond laser pulse treatment. J Invest Dermatol 1995; 105:709. Welsh AJ, Moramedi M et al. Evaluation of cooling techniques for the protection of the epidermis during Nd:YAG laser radiation of the skin. In: Joeffe SN, ed. Neodymium-YAG Lasers in Medicine and Surgery. New York: Elsevier Science, 1983. Zenzie HH, Altshuler GB, Smirnov MZ, Anderson RR. Evaluation of cooling methods for laser dermatology. Lasers Surg Med 2000; 26:130 – 144. Goldman MP, Bennett RG. Treatment of telangiectasia: a review. J Am Acad Dermatol 1987; 17:167 – 182. Goldman MP, Weiss RA, Brody HJ. Treatment of facial telangiectasia with sclerotherapy, laser surgery and electrodessication: a review. J Dermatol Surg Oncol 1993; 19:899 – 906. Kauvar AN, Frew KE, Friedman PM, Ohmeimus RG. Cooling gel improves pulsed KTP laser treatment of faceal telangiectasia. Lasers Surg Med 2002; 30:149 – 153. Tanghetti ET, Adrian RM. Long-pulsed 532 nm laser treatment of port wine stains. Laser Surg Med 1998; 10:36.


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VASCULAR LASER TREATMENT CONSENT The procedure planned is treatment with the VersaPulse Laser, Pulsed Dye Laser, LPIRAlexandrite, Diode or Long Pulse Nd:YAG laser. The purpose of this procedure is to lighten, fade, or remove abnormal blood vessels or birthmarks. Alternative treatment methods include electrosurgery, sclerotherapy or no treatment. I understand the risks of this procedure include possible pain, bleeding, infection, blistering, hypopigmentation, hyperpigmentation, scarring, and unforeseen complications. The risks of scarring appear to be very small compared with the risks of the older Argon and CO2 laser treatments but are still possible with the newer vascular laser treatments. I understand that there is a possibility that this procedure will fail, need to be repeated, or require additional treatment of complications. I understand my responsibility for properly fulfilling the appropriate aftercare instructions as explained by the doctor and/or his staff. I further agree that any pictures taken of me may be used for either teaching or publication as the doctor considers appropriate unless I notify him in writing that he is not to use these photographs. Although part of all of the costs for this procedure may be reimbursed by insurance companies, some policies or companies mat not cover the procedure because they consider it cosmetic or for other reasons. I understand that I am responsible for all costs of the procedure. I have been asked at this time whether I have any further questions about this procedure, and I do not. I understand the procedure, accept the risks, and request that Dr. Robert Adrian or his nurse perform this procedure on me. Patient Name (Please Print)

Date of Surgery

Patient Signature

Date of Signature

Witness Signature

10 Q-Switched Ruby Laser Vic A. Narurkar San Francisco and University of California at Davis, Davis, California, USA

1. Introduction 2. Background 3. Laser Physics 4. Laser – Tissue Interaction 5. Laser Treatment Principles 6. Lesions Amenable to Treatment with the QSRL 7. Complications 8. Conclusions References

1.

259 259 260 260 260 261 262 262 263

INTRODUCTION

The development of Q-switched solid state lasers has revolutionized the treatment of a variety of cutaneous lesions. The challenge in selective destruction of targets has been to spare competing structures in the epidermis and the dermis. Selective photothermolysis, the use of narrow bands of light and pulse widths, and photoacoustic effects allow Q-switched laser delivery systems to preferentially target pigment-containing structures such as lentigines, ephelides and tattoos. Q-switched ruby lasers (QSRLs) utilize a wavelength of 694 nm and pulse durations of 20 –30 ns to effectively treat a variety of benign pigmented lesions.

2.

BACKGROUND

The ruby laser was first introduced for dermatologic applications in the 1960s for the treatment of benign pigmented lesions and tattoos (1,2). Technical limitations of the early ruby laser systems prevented them from gaining wide acceptance. Reid et al. reported the modification of the free running ruby laser to a Q-switched system, thereby permitting 259

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ultraselective destruction of amateur tattoos (3,4). Since that time, the QSRL has been used effectively for the treatment of benign epidermal pigmented lesions, dermal pigmented lesions, professional and amateur tattoos, and compassionate treatment of congenital nevi (5 –8).

3.

LASER PHYSICS

The Q-switched ruby laser typically employs pulse widths of 20 –40 ns, with this ultrashort pulse duration being shorter than thermal relaxation time of melanosomes, the target for destruction in epidermal and dermal pigmented lesions. The wavelength of 694 nm shows a high affinity for melanin, the target chromophore for pigmented lesions. Spot sizes of 2 – 4 mm are employed with fluences up to 10 J/cm2 to allow for optimal fluence to match spot size and ensure adequate destruction of the targets. Photoacoustic effects produced by the Q-switched mechanism produces a photomechanical effect which facilitates the destruction of melanosomes to be shattered into smaller particles which are later eliminated by the lymphatic system.

4.

LASER – TISSUE INTERACTION

Selective destruction of pigmented lesions and tattoos requires a careful interplay of wavelength, pulse duration, and fluence. Melanin, the endogenous chromophore has a broad absorption spectrum which has excellent absorption at 694 nm, the wavelength of the QSRL. Pulse durations are designed to reflect the thermal relaxation time of the target to be treated, which in the case of tattoos and pigmented lesions is the melanosome. Melanosomes have thermal relaxation times in the 50 – 100 ns range (9), sufficient energy fluence is also necessary to disrupt the desired targets. The QSRL employs an ultrashort pulse duration of 20 –40 ns and energy fluences to 10 J/cm2 (10), allowing for selective destruction of benign pigmented lesions and tattoos. Besides selective photothermolysis, photoacoustic effects produced by Q-switching (the use of an optomechanical shutter) are responsible for pigment destruction (11). The QSRL uses high energy, nanosecond pulse durations which produce expansion of ink particles followed by shattering. These laser irradiated fragments are then eliminated transepidermally and transdermally through the lymphatic system. Ultrastructural analysis has demonstrated reduction in dermal particles and fading of ink following QSRL treatment (12).

5.

LASER TREATMENT PRINCIPLES

QSRL treatment is a simple and well-tolerated office-based procedure. Patients are advised to avoid direct sun exposure and the use of tanning beds to avoid greater risks of unwanted melanocytic injury and pigmentation anomalies in treated areas. Anesthesia in the form of topical agents such as eutetic mixture of lidocaine (EMLA, Elamax) with or without the administration of field block anesthesia may be needed for treating tattoos. Pigmented lesions are usually treated with topical anesthesia or without any anesthesia. The treatment technique consists of delivering energy fluences which will produce a uniform whitening of the skin surface. For pigmented lesions, fluences of 2 –4 J are usually adequate, while for dermal tattoos and deeper dermal lesions fluences of 6 J and

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higher are necessary. The goal is to select the initial energy fluence at the lowest possible setting which will produce a uniform whitening of the skin surface. On subsequent treatments fluences may be increased and as the lesions start to fade, pinpoint bleeding may be noticed as the initial clinical response. Small test sites are advisable immediately prior to proceeding with definitive treatment to establish the optimal energy fluence (13). The “snowflake” color appearance immediately following treatment is replaced by a transient urticarial and mildly purpuric response in about 20 min. Immediately postoperatively, a topical antibiotic or lubricant such as aquaphor is applied to the treated sites. Vesiculation and scabbing may occur and the patient is advised to continue treating these areas with emollients. Healing is usually complete by 10 –14 days. Fading of the tattoo pigment is evident at 4– 6 weeks and treatment intervals of at least 6 – 8 weeks are recommended. Transient hyperpigmentation or hypopigmentation that may develop can persist up to 6 months or longer. Benign pigmented lesions usually clear in one or two treatments. Deeper dermal lesions require multiple treatments. Amateur tattoos usually clear in three to four treatments while professional tattoos may require a significantly greater number of treatments and complete fading is not always possible (14,15).

6.

LESIONS AMENABLE TO TREATMENT WITH THE QSRL

Table 10.1 summarizes the variety of benign pigmented lesions and dermal lesions which can be effectively treated with the QSRL. Successful treatment of benign epidermal lesions includes the selective treatment of lentigines, ephelides, labial lentigines, and Peutz – Jehngers pigmented lesions (16,17). Typically, one to two treatments effectively clear epidermal pigmented lesions since the pigment is more superficial and the size of melanosomes is smaller. Examples of dermal pigmented lesions amenable to QSRL treatment include amateur tattoos, traumatic tattoos, professional tattoos, nevus of Ota/Ito and Beckers nevus. Since these lesions tend to be deeper, have higher pigment density and exhibit larger melanosome size, greater number of treatments are necessary (18). The QSRL can effectively fade black, blue, and green color tattoos. Shades of red and yellow are unresponsive. Other colors respond variably. Other lesions which show a variable response to QSRL treatment include cafe-au-lait macules, congenital nevi and infraorbital hyperpigmentation (19). Attempts to treat melasma and postinflammatory Table 10.1 Lesions Amenable to Treatment with the QSRL Tattoos Amateur Traumatic Professional (black, blue, green) Cosmetic Nevus of Ota/Ito Becker’s nevus Ephelides Lentigos Peutz – Jehngers hyperpigmentation Infraorbital hyperpigmentation Melanocytic nevi (mostly junctional)

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hyperpigmentation have been generally disappointing with all pigmented lesion laser delivery systems. The treatment of melanocytic nevi with lasers remains controversial. Temporary fading is possible but recurrences are frequent as only the superficial portion of the nevus is destroyed. The deeper nevus cells may repopulate the superficial dermis and epidermis with resulting repigmentation. The danger is that a “nevus” treated with the laser is actually a “melanoma.” Laser treatment of a melanoma will make the diagnosis more difficult to make by altering the histologic features and delaying a definitive diagnosis. There are reports of treating congenital nevi with the QSRL, but recurrence is almost uniformly seen. If nevi are treated with the QSRL, close follow-up is important. Long-term studies are underway to establish the safety and efficacy of the QSRL, other Q-switched and long pulsed solid state lasers for the treatment of melanocytic nevi. Potential advantages of long pulsed solid state systems include longer thermal relaxation times which may facilitate better clearance. The longer pulse durations may also pose a disadvantage by producing higher risks of unwanted epidermal damage and scarring.

7.

COMPLICATIONS

The QSRL, if utilized properly and in the right patient group, carries a high safety margin. Complications are infrequent and can include hypopigmentation, hyperpigmentation, and textural change. Pigmentary changes are greatest in darker skin types because of increased interference of melanin absorption in darker skin types and excellent absorption of melanin at the 694 nm wavelength. Hyperpigmentation usually fades and can be prevented and/or corrected with the use of topical bleaching agents. Hypopigmentation is more persistent and not amenable to correction. Textural changes can occur if excessive energy fluence is utilized and is more prevalent in areas of the body susceptible to hypertrophic scarring. The risk of complications increase as the number of treatments of a given area increases. Spacing treatments further apart may reduce complication rates by allowing the tissue to recover more fully. An important complication for the QSRL and all Q-switched lasers is the concept of paradoxical darkening of tattoo ink. This can occur in cosmetic tattoos (e.g., lip-liner, eyeliner, areolar micropigmentation), skin-colored tattoos, and tattoos containing white ink. If these inks are exposed to the QSRL, these tattoo pigments promote reduction of titanium and ferric oxide components of the ink, thereby producing immediate black discoloration upon delivery of the laser energy. Single pulse test sites are recommended prior to proceeding with QSRL treatment. This black colored ink is variably responsive to additional QSRL treatment.

8.

CONCLUSIONS

The QSRL can successfully treat a variety of benign epidermal and dermal pigmented lesions and tattoos. The mechanism of selective photothermolysis and photoacoustic effects allow for selective destruction of these targets. A careful interplay of the 694 nm wavelength with a high affinity for melanin, an ultrashort pulse duration of 20 –40 ns and energy fluences of 10 J/cm2 permit the QSRL to allow for selective and effective destruction of these lesions. Complications are infrequent with a report of ,2% incidence of transient pigmentary changes, textural changes, and paradoxical darkening.

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REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13.

14. 15.

16.

17.

18. 19.

Goldman L, Rockwell RJ, Meyer R et al. Laser treatment of tattoos: a preliminary survey of three years clinical experience. J Am Med Assoc 1967; 201:163 – 166. Yules RB, Laub DR, Honey R et al. The effect of Q-switched ruby laser radiation on dermal tattoo pigment in man. Arch Surg 1967; 95:179– 180. Reid WH, McLeod PJ, Ritchie A et al. Q-switched ruby laser treatment of black tattoos. Br J Plast Surg 1983; 36:455 – 459. Vance CA, McLeod PJ, Reid WH et al. Q-switched ruby laser treatment of tattoos: a further study. Lasers Surg Med 1985; 5:179. Goldberg DJ. Benign pigmented lesions of the skin: treatment with the Q-switched ruby laser. J Dermatol Surg Oncol 1993; 19:376– 379. Ashinoff R, Geronemus RG. Q-switched ruby laser treatment of benign pigmented lesions. Lasers Surg Med 1992; 4S:73. Taylor CR, Gange RW, Dover JS et al. Treatment of tattoos by the Q-switched ruby laser: a dose response study. Arch Dermatol 1990; 126:893 –899. Lowe NJ, Luftman D, Sawcer D. Q-switched ruby laser—further observations on treatment of professional tattoos. J Dermatol Surg Oncol 1994; 20:307– 311. Polla LL, Margolis RJ, Dover JS et al. Melanosomes are the primary target of Q-switched ruby laser irradiation in guinea pig skin. J Invest Dermatol 1986; 89:281 – 286. Scheibner A, Kenny G, White W et al. A superior model of tattoo removal using the Q-switched ruby laser. J Dermatol Surg Oncol 1990; 16:1091 – 1098. Anderson R, Parrish J. The optics of human skin. J Invest Dermatol 1981; 77:13 – 19. Taylor C, Anderson R, Gange R et al. Light and electron microscopic analysis of tattoos treated by Q-switched ruby laser. J Invest Dermatol 1991; 97:131 – 136. Kilmer SL, Anderson RR. Clinical use of the Q-switched ruby and the Q-switched Nd:YAG (1064 and 532 nm) lasers for the treatment of tattoos. J Dermatol Surg Oncol 1993; 19:330 – 338. DeCoste SD, Anderson RR. Comparison of Q-switched ruby and Q-switched Nd:YAG laser treatment of tattoos. Lasers Surg Med 1991; (suppl 3):64. Kilmer SL, Lee MS, Anderson RR. Treatment of multicolored tattoos with the frequency doubled Q-switched Nd:YAG laser: a dose response study with comparison to the Q-switched ruby laser. Lasers Surg Med 1993; (suppl 5):54. Oshihiro T, Maruyama Y, Makajima H et al. Treatment of pigmentation of the lips and oral mucosa in Peutz-Jehgers syndrome using ruby and argon lasers. Br J Plast Surg 1980; 33:346 – 349. McMeekin TO, Goodwin D. Comparison of Q-switched ruby, pigmented lesion dye and copper vapor laser treatment of benign pigmented lesions of the skin. Lasers Surg Med 1992; 4S(suppl):74. Goldberg DJ, Nychay SG. Q-switched ruby laser treatment of the nevus of Ota. J Dermatol Surg Oncol 1992; 18:817 – 821. Oshiro T, Maruyama Y. The ruby and argon lasers in the treatment of naevi. Ann Acad Med Singapore 1983; 12:388 – 395.

11 The Q-Switched Nd:YAG (1064 1 532 nm) Laser Suzanne L. Kilmer Laser & Skin Surgery Center of Northern California, Sacramento, California, USA

Macrene R. Alexiades-Armenakas Private Practice, New York, New York, USA

Vicki J. Levine New York University School of Medicine, New York, New York, USA

Robin Ashinoff Mohs and Laser Surgery, Hackensack University, Hackensack, New Jersey, USA

1. Background 1.1. Laser Instrumentation and Properties 1.2. Laser – Tissue Interactions 1.2.1. Theory of Selective Photothermolysis 1.2.2. Target Chromophore Specificity 1.2.3. Mechanisms of Target Destruction 1.3. Histology 1.3.1. Depth of Penetration 1.3.2. Tattoo Removal 1.3.3. Removal of Melanocytic Lesions 1.3.4. Hair Removal 2. Treatment Indications 2.1. Tattoo Removal 2.1.1. Background 2.1.2. Mechanisms of Laser-Induced Tattoo Lightening 2.1.3. Comparative Studies 2.1.4. Q-Switched Ruby Laser-Resistant Tattoos 2.1.5. Treatment of Tattoos in Darkly Pigmented Patients 2.1.6. Medicinal and Traumatic Tattoos 2.1.7. Cosmetic Tattoos 2.1.8. Disadvantages in Tattoo Removal 2.2. Removal of Pigmented Lesions 2.2.1. Pigmented Lesions in General 2.2.2. Acquired Melanocytic Nevi 2.2.3. Congenital Nevi

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2.3. Hair Removal 2.4. Rhytids 3. Laser Technique and Parameters 3.1. Tattoo Removal 3.1.1. General Parameters and Protective Equipment 3.1.2. Professional and Amateur Tattoo Removal 3.1.3. Cosmetic Tattoo Removal 3.1.4. Medicinal and Traumatic Tattoo Removal 3.1.5. Tattoo Treatment of Darker Skin Types 3.2. Removal of Melanocytic Lesions 3.2.1. Epidermal Lesions 3.2.2. Dermal Melanocytic Nevi 3.2.3. Common Acquired Nevi 3.3. Hair Removal 3.4. Rhytids 4. Pre- and Postprocedure Management 4.1. Preprocedure Considerations 4.2. Postprocedure Considerations 4.2.1. Wound Care 4.2.2. Complications 5. Summary References

1. 1.1.

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BACKGROUND Laser Instrumentation and Properties

The neodymium:yttrium – aluminum –garnet (Nd:YAG) laser was developed by Geusic and colleagues in 1964 (1). Neodymium ions were introduced to the host crystal YAG and powered by a xenon arc lamp, a flashlamp pump consisting of a quartz tube containing xenon gas and fitted with two electrodes. A continuous high-density electrical discharge passes through the xenon gas and the emitted light is coupled via optical resonators into the gain medium (atoms predominantly in an excited rather than a resting state). This results in stimulated emission and the net release of energy as additional photons (2). The Nd:YAG laser has two major emission wavelengths in the near-infrared range, one at 1064 nm, and another at 1300 nm with selectivity determined by different optical resonators. Passing the 1064 nm beam through potassium titanyl phosphate (KTP) crystal in the laser cavity halves the wavelength (i.e., doubles the frequency) to 532 nm, which is in the green visible light range. The quality (Q)-switched (can abbreviate to QS) mechanism was first proposed in 1961 by Hellwarth (3). It employs rotating mirrors and other methods to store excessive energy within the laser cavity, then release it in very short bursts of high peak power (1000 W or 50 times the laser’s average power), with very short pulse durations of 4–10 ns. 1.2.

Laser – Tissue Interactions

1.2.1. Theory of Selective Photothermolysis The introduction of the theory of selective photothermolysis in 1982 by Anderson and Parrish (4) has enabled physician-scientists to design lasers that are highly specific for target structures in tissue and therefore less apt to cause scarring or pigmentary alteration.

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Based upon this theory, laser parameters may be adjusted to maximize absorption by and destruction of a specific target structure and to minimize energy transfer to the surrounding tissue. First, the light pulse should be of a wavelength that is highly absorbed by the target structure and preferably less well absorbed by surrounding nontargeted chromophores. Second, the pulse should be of sufficiently high energy density that it heats the target tissue to a temperature that exceeds the vaporization (or destruction) threshold of the target (Beer’s law), such that the target is successfully destroyed while thermal energy is carried away as steam and plume. In laser–skin interactions, this destruction of the target is mediated by thermal denaturation, mechanical damage by rapid thermal expansion or phase changes, and changes in primary chemical structure (5,6). Third, it should do so in a sufficiently short pulse duration such that heat is dissipated by destruction of the target, as described above, before diffusion of heat to surrounding tissues has time to occur. In other words, the pulse duration must be shorter than the target structure’s thermal relaxation time (TRT), the time necessary for half of its thermal energy to be lost by diffusion to surrounding tissues, in order for maximal thermal confinement to occur. Thus, the wavelength, peak energy, and pulse duration specifically target a given structure (selective photo-); the light energy is subsequently converted into thermal energy in the target structure (-thermo-), and destroys the target by the aforementioned mechanisms (-lysis) before it can dissipate heat to surrounding tissues. The pulsed and Q-switched laser systems adhere most closely to this theory by delivering high-energy bursts of light, of an appropriate wavelength, in very short pulse durations resulting in very specific thermal, mechanical and/or chemical destruction with the lowest risk of adjacent tissue damage. 1.2.2. Target Chromophore Specificity As mentioned earlier, the specificity of a laser for a target structure in tissue is dependent upon several variables, including wavelength, depth of penetration, peak energy, and pulse duration. Wavelength. First, a wavelength selectively absorbed by the specific target is chosen. The relative concentration of the targeted chromophore in skin structures, interference by absorption by other surrounding chromophores, and depth of penetration of the chosen wavelength are all important. Both endogenous (melanin, hemoglobin) and exogenous (tattoo ink, traumatically implanted material) chromophores in skin absorb the 532 and 1064 nm wavelengths emitted by the Nd:YAG laser. The 1064 nm wavelength is well absorbed by melanin, black tattoo ink particles and, to a lesser extent, hemoglobin (Fig. 11.1) (7). The 532 nm wavelength is absorbed well by hemoglobin, melanin, and red tattoo ink. Depth of penetration. Second, the laser beam’s depth of penetration determines the accessibility to a given target and is dependent upon the wavelength, the radiant exposure (fluence), and the spot size. In general, a gradual increase in the depth of penetration into skin occurs at longer wavelengths over the 650– 1200 nm part of the spectrum due to decreased scattering (4), although the far-UV and mid-far-IR regions penetrate least well due to protein absorption and water absorption, respectively. Experiments performed in vitro and in vivo suggest a mean depth of penetration of approximately 3.2 mm or a 50% penetration depth of 1.6 mm for the 1064 nm Q-switched Nd:YAG laser in normal fair Caucasian skin (5,8,9). Spot size also affects depth of penetration, as a result of optical scattering that occurs as the beam penetrates the dermis (10). Spot sizes for the currently available QS Nd:YAG lasers range from 0.8 to 8.0 mm and should be used at a spot size of at least 3 mm for optimal penetration.

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Figure 11.1

Hemoglobin and melanin absorption curve.

Pulse duration. Finally, the pulse duration should be maximized to enhance energy delivery yet not exceed the TRT of a given structure. The TRT is dependent upon the diameter, volume and surface area of the target. For most targets, an estimation of the TRT in seconds is proportional to the diameter of the structure in millimeter squared (5). The estimated TRTs for a melanosome measuring 0.5 mm (5 1024 cm) in diameter is 25 1028 s (250 ns) and for a 0.1 mm diameter capillary is 1022 s or 10 ms. Black tattoo particles estimated as 0.1 to 5 microns in diameter (see section on pathology), possess TRTs of roughly 10 – 5000 ns. The Q-switched Nd:YAG laser operates in the nanosecond domain, therefore providing high specificity for melanosomes and black tattoo inks that possess very short TRTs. 1.2.3.

Mechanisms of Target Destruction

As noted earlier, target chromophore and tissue destruction may occur through several mechanisms. The primary mechanism is photothermal, where heating and subsequent vaporization or thermal denaturation of the target occurs. Another is photochemical, such that light energy causes chemical alterations in the molecular structure of the target. Finally, a photoacoustic effect is possible when ultrashort pulse durations generate


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local pressure or shock waves. This may produce much of the damage associated with these QS lasers (11), as well as explain the remarkable purpura from shattered vessels seen when using the 532 nm wavelength. 1.3.

Histology

1.3.1. Depth of Penetration Anderson and coworkers (8) reported the first microscopic analysis of the effects of QS Nd:YAG laser irradiation. Exposures of animal skin to the 1064 nm wavelength at 1.0 J/cm2 altered melanosomes to a depth of 0.2 mm and at 3.0 J/cm2 to a depth of .1 mm (8). Investigators have since observed the QS Nd:YAG (1064 nm) laser penetrating up to 3– 6 mm in human subjects (12). The mean depth of penetration for the QS Nd:YAG (1064 nm) laser is 3.2 mm with a 50% penetration depth of 1.6 mm in normal fair Caucasian skin (5,8). The shorter 532 nm wavelength suffers more loss due to scattering and is better absorbed by melanin or hemoglobin, both limiting its depth of penetration. 1.3.2. Tattoo Removal Light and electron microscopic analysis was performed after QS Nd:YAG (1064 nm, 10 ns pulse duration, 6 –12 J/cm2 fluences, 2.5 mm spot size) laser irradiation of 25 tattoos (13). Following four treatments at 3 – 4-week intervals, skin biopsies demonstrated fragmentation of black ink particles that were present within cells in the dermis. Laserirradiated tattoo particles were smaller in size than preirradiation particles, and those located .1.5 mm depth in the dermis were larger and darker than those in the upper dermis (Fig. 11.2). The 532 nm green light effectively targeted red ink whereas green tattoo inks were unaltered. No fibrosis of the surrounding dermis was observed (13). Tattooed hairless guinea pigs irradiated with the QS ruby (694 nm, 20 –40 ns, 4.5 J/cm2, 6.5 mm), QS Nd:YAG (1064 and 532 nm, 7 and 4 J/cm2, respectively, 10 – 12 ns, 2 mm), and QS alexandrite (755 nm, 100 ns, 4 J/cm2, 3 mm) lasers were analyzed (14). At 6 weeks, the Nd:YAG laser at 1064 nm more effectively lightened the reddish-brown, dark brown, orange, and black tattoo inks, whereas red inks responded best to 532 nm. The alexandrite laser was more effective in lightening blue and green inks and the ruby laser was most effective for purple and violet inks. Scarring was not evident clinically, but epidermal and dermal damage were noted histologically to be most pronounced in the QS Nd:YAG laser-treated specimens, although this was prior to use of a larger spot size which diminishes side effects (10). Electron microscopic evaluation prior to irradiation showed polygonal pigment particles within intracellular organelles of fibroblasts, macrophages, and occasionally mast cells, in the superficial dermis. Immediately postirradiation, ablation and vacuolization of the pigment-laden cells was observed and 6 weeks later, the particles appeared more granular (14). Similar findings were noted in 35 tattoos biopsied before and following QS Nd:YAG (1064 þ 532 nm) laser treatment (15). Immediately postirradiation, ruptured blood vessels and corresponding areas of epidermal perforation were observed. Black pigment-containing cells formed vacuoles and ruptured after 1064 nm irradiation, red particles were altered and less numerous after 532 nm irradiation, and green, yellow, orange, and blue tattoo particles were unaltered by either wavelength. After three treatments, light amateur tattoos were histologically clear of residual pigment; professional or dense tattoos were clear in the papillary dermis, though the mid-dermis contained residual altered pigment, and the deep dermis contained unaltered pigment. After 6 months,

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Figure 11.2 Professional tattoo treated with the QS Nd:YAG laser (1064 nm). Histologic exam shows lighter laser irradiated tattoo particles more superficially and denser, poorly eradiated particles in lower dermis.

tattoos that were unresponsive to numerous treatments showed unaltered tattoo particles in the deep dermis at depths .1.5 mm. 1.3.3.

Removal of Melanocytic Lesions

In 1989, Anderson et al. compared the effects of the QS Nd:YAG laser pulses at 1064, 532, and 355 nm in guinea pigs. Although expected with the 532 nm wavelength, exposure to 1064 nm also showed melanosomal rupture in keratinocytes and melanocytes (8). The histologic effects of QS alexandrite (100 ns) and QS Nd:YAG (10 ns) lasers were compared at the same fluence (6.0 J/cm2) and spot size (3 mm) for treatment of benign acquired melanocytic nevi (16). Following three treatments at 6-week intervals, an equivalent reduction in epidermal melanin and melanocytes, and numbers of junctional and dermal melanocytic nests was noted for both lasers. Increased dermal melanophages and mild dermal fibrosis were also seen (16). Thus, the QS Nd:YAG (1064 nm) laser can rupture epidermal and dermal melanosomes. 1.3.4. Hair Removal Kilmer documented follicular pigment disruption with ring cell formation using a highpowered 1064 nm QS Nd:YAG (17) (Fig. 11.3) without use of an adjuvant topical carbon solution. Minimal thermal damage to the surrounding follicular apparatus or adjacent tissue was noted with these Q-switched pulses. In a separate study, 15 patients treated with the QS Nd:YAG resulted in a rapid switch from anagen to telogen and greater hair loss in sites with high anagen:telogen ratios (18). Thus, the mechanisms of laser-induced hair removal are beginning to be elucidated, but likely involve both destructive mechanisms


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Figure 11.3 Hair follicle treated with the QS Nd:YAG laser (1064 nm). Note ring cell formation (arrow) with melanin particles at periphery of ring cells.

and disruption of the hair follicle cycle. More importantly, the shorter pulse width does not supply sufficient thermal damage to permanently destroy hair follicles.

2.

TREATMENT INDICATIONS

2.1. 2.1.1.

Tattoo Removal Background

Tattoos are caused by the intradermal placement and subsequent phagocytosis of ink particles by histiocytes, fibroblasts, and mast cells. The ink particles measure nanometers in size and are contained in phagolysosomes (5). Those used in amateur tattoos are carbonbased, such as India ink, graphite, or ash. Professional tattoos typically consist of insoluble metal salts, oxides, or organic complexes. Past methods of tattoo removal have included surgical excision, dermabrasion, salabrasion, and CO2 laser vaporization. Goldman and colleagues (19) were the first to note the effectiveness of normal-mode pulsed ruby laser treatment in tattoo removal. The QS ruby laser has since been reported to successfully treat tattoos in the 1960s and 1980s (19 –21). Since then, multiple studies have demonstrated the effectiveness of the Q-switched ruby laser in treating black, blue-black, and green tattoos. The QS Nd:YAG (1064 nm) laser offered the theoretical benefit of increased depth of penetration and decreased epidermal melanin absorption, and thus was the next laser evaluated for tattoo removal. When used with the frequency-doubling crystal in place, the 532 nm wavelength (green light) can target red inks but is also well absorbed by melanin. 2.1.2. Mechanisms of Laser-Induced Tattoo Lightening The mechanisms by laser-induced tattoo lightening are beginning to be elucidated. Electron microscopic studies of QS ruby laser irradiation have shown that ink particles are

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fractured into 10 –100 smaller fragments and that the phagocytic cells that contain them are ruptured (22). As discussed earlier, light and electron microscopic analyses after QS Nd:YAG (1064 nm) laser irradiation have demonstrated black ink fragmentation, vacuolization and rupture of pigment-containing cells, followed by rephagocytosis of fragmented particles by macrophage and fibroblasts, and probable lymphatic clearance (see section on Histology). In addition, laser-induced photochemical alterations of tattoo inks may play a role in both their treatment and in the untoward effect of tattoo irreversible immediate darkening (see following text) (23). 2.1.3. Comparative Studies The earliest use of the QS Nd:YAG (1064 nm) laser was to treat tattoos (12). A side-byside comparison of the QS ruby (694 nm, 40 ns) and QS Nd:YAG (1064 nm, 30 ns) lasers at equal fluences (2 –6 J/cm2) and equal exposure spot diameters (5 mm) found them to be equally effective in black ink removal. The QS Nd:YAG laser was less effective at green ink removal; however, it was less apt to produce postinflammatory hypopigmentation, blistering, or textural changes. Use of the 532 nm wavelength treats red ink effectively. Since then, several studies have directly compared the efficacy of the QS ruby and the QS Nd:YAG laser in the treatment of tattoos. One study (24) compared the QS ruby and QS Nd:YAG lasers and found the former to be more effective at black and green ink removal, whereas red ink was minimally lightened by 1064 and 694 nm, a color very responsive to 532 nm. On the other hand, the QS ruby laser caused hypopigmentation more commonly than the QS Nd:YAG (1064 nm) laser, which produced greater textural change in this study. These findings are consistent with other comparison studies (12,25). Of note, new QS Nd:YAG lasers have larger spot sizes and better beam profiles with better efficacy noted. 2.1.4. Q-Switched Ruby Laser-Resistant Tattoos Tattoos refractory to the QS ruby laser were treated with the QS Nd:YAG laser (1064 nm, 5 – 10 ns, up to 12 J/cm2, 2.5 mm) (26) and .50% lightening was observed after the first treatment, most notably with higher fluences. In a subsequent study (13) ruby laserresistant and untreated tattoos were treated with fluences of 6, 8, 10, and 12 J/cm2 over four sessions at 3– 4-week intervals. Lightening of tattoos to .75% and 95% was observed in 77% and 28% of black tattoos, respectively. The highest fluence of 12 J/cm2 was more effective at removing black ink as compared to 6– 8 J/cm2 and amateur tattoos cleared more easily than professional tattoos. Green, yellow, white, purple, red, and orange inks responded minimally with 1064 nm, whereas 694 nm cleared green ink more readily (27). Mild hyperpigmentation and slight textural changes cleared with time except in two cases of the latter. Thus, the QS Nd:YAG (1064 nm) laser appears to be highly effective in lightening QS ruby laser-resistant blue-black tattoos, likely due to its greater depth of penetration and shorter pulse width. 2.1.5. Treatment of Tattoos in Darkly Pigmented Patients The greatest advantage of the QS Nd:YAG (1064 nm) laser is its use in treating tattoos in darkly pigmented patients. In contrast, the 532 nm wavelength should be avoided in these patients. Grevelink et al. (28) compared the 1064 nm QS Nd:YAG and ruby lasers in treating five tattoos in skin types V and VI with effective tattoo removal of 50 –60% for the 60 – 95% respectively, supporting earlier findings. Importantly, however, the QS Nd:YAG caused transient hypopigmentation in one patient; whereas, the QS ruby laser led to hypopigmentation that ranged from transient to permanent, in all patients treated


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(28). Skin type VI patients with amateur black tattoos were treated using the QS Nd:YAG (1064 nm, 6 ns, 3.2 – 8.3 J/cm2, and 3 mm spot size) and noted even better efficacy with no residual pigmentary or textural changes (29). Thus, because of its superior safety profile, the QS Nd:YAG at 1064 nm is preferable to the QS ruby laser for darkly pigmented patients. 2.1.6. Medicinal and Traumatic Tattoos Medicinal tattoos are often placed to identify the tumor or to mark radiation ports. Since these tattoos are usually small and consist of blue or black India ink, they can be easily removed with any of the QS lasers. Traumatic tattoos may occur secondary to trauma from motor vehicle accidents or other encounters with asphalt, explosives, or pencil puncture wounds. They are often carbon based in nature and located in the superficial dermis, which facilitates their removal. Several studies have shown that traumatic tattoos may be effectively treated with the QS Nd:YAG (1064 nm) laser, including one in which 50/51 traumatic tattoos completely cleared without textural or pigmentary changes (30). Other studies with QS Nd:YAG (1064 nm) laser treated traumatic tattoos reported similar results (31,32). Although comparative studies are lacking, the QS Nd:YAG (1064 nm) laser appears to be highly effective for traumatic tattoo removal, resulting in complete clearance in the majority of cases. In fact, in most cases, the associated scars improve as the traumatically implanted material is removed, decreasing the inflammatory and granulomatous changes triggered by the foreign material (Fig. 11.4). 2.1.7. Cosmetic Tattoos Cosmetic tattooing has become increasingly popular especially for eyebrow, lip, and eyeliner tattoos as well as, covering periorbital pigmentation, providing rosy cheeks,

Figure 11.4 Before and after QS Nd:YAG laser (1064 nm) treatment of remaining black panther tattoo. Note darkening of completely faded red claws on panther tattoo that occurred during treatment of the residual black ink.

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and disguising scars. The most frequently used inks include white, reddish-brown, red, flesh-tone, or dull orange. The tattoo industry is not regulated by a government agency, such as the Federal Drug Administration, so it is impossible to predict which pigments are present in each tattoo. Also, different tattoo artists may mix or even overlay the inks making it more difficult to identify which pigments were used. Development of immediate pigment darkening after pulsed laser treatment of tattoos is possible. This unfortunate occurrence is most often seen in the red, white, and fleshtoned ink colors frequently used in cosmetic tattoos. Blackened tattoo pigment cannot always be removed with successive laser treatments, therefore, a test site is recommended for any ink suspicious for potential darkening (see following text) (23,33).

2.1.8.

Disadvantages in Tattoo Removal

Tattoo ink restriction. The main disadvantage of the QS Nd:YAG laser (1064 nm) for tattoos is its restricted target color range to black and blue-black inks (34). The frequency-doubling feature of the laser to 532 nm may be employed to effectively treat red ink, and, to a lesser degree, orange and purple inks. Yellow, green and blue inks respond poorly to both frequencies (35). The risk of increased bleeding and tissue splatter during treatment has been noted but can be decreased by utilizing larger spot sizes with lower fluences (which gives equivalent efficacy). Tattoo ink darkening. As noted previously, darkening of flesh-colored tattoo pigments has been reported following treatment with several QS lasers, including the QS Nd:YAG (1064 nm) laser. Anderson et al. (23) first reported five cases of tattoo ink darkening, all with QS lasers. During QS Nd:YAG (1064 nm) treatment of a residual professional black ink tattoo immediate darkening occurred in adjacent normal skin in the site of an old completely faded red tattoo (Fig. 11.5). Two subsequent treatments of the darkened area with the same 1064 nm laser resulted in substantial, but incomplete clearing (23). The proposed mechanism for laser-induced tattoo ink darkening involves the reduction of ferric oxide, which has a reddish-brown color, to ferrous oxide, which is black (14). A retrospective study assessed 323 QS Nd:YAG laser-treated tattoos of which 180 were red, brown, yellow, orange, or white/flesh (36). Immediate darkening occurred in 33/180 tattoos during or after laser irradiation. White/flesh, crimson, brown, red, and yellow, in decreasing order of frequency, darkened either transiently or permanently. Red and brown tattoos darkened more frequently after 532 nm irradiation, as compared to 1064 nm; yellow tattoos darkened with equal frequency at the two wavelengths; and white/flesh-colored tattoos darkened after 1064 nm irradiation. An average of three additional laser treatments improved 20/33 of the darkened tattoos. Thus, roughly 20% of flesh-colored tattoos in this retrospective study darkened after QS Nd:YAG laser irradiation, with additional treatments improving most darkened tattoos; test sites help to predict how an individual tattoo will respond. Pigmentary alteration. The increased melanin absorption by shorter wavelengths leads to greater risk for epidermal disruption, especially with darker skin types or tanned individuals. Because of this, blistering and hypopigmentation is more common with the QS ruby, alexandrite, and frequency-doubled Nd:YAG (532 nm) lasers. Comparative studies, confirm that the QS Nd:YAG (1064 nm) laser results in a lower incidence of pigmentary changes and scarring, as compared to the QS ruby laser (37). Hypopigmentation is usually transient, especially with the 532 nm wavelength as its shallower depth of penetration minimizes lethal injury to the follicular melanocytic reservoir.


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Figure 11.5 Before and after a single treatment of traumatic tattoo treated with QS Nd:YAG at 1064 nm. Note improvement of scarring as well.

Hyperpigmentation tends to be more skin type dependent, with melanocytes in darker skin types more likely to react to injury with increased production of melanin. This can be minimized with use of a broad-spectrum sunscreen, preferably zinc oxide, and usually clears with a topical preparation containing hydroquinone or time alone. Microexplosions of gunpowder traumatic tattoos. This interesting adverse effect first noted by Taylor (personal communication), was recently reported following QS Nd:YAG (1064 nm) laser irradiation of gunpowder traumatic tattoos (38). Three patients with traumatic tattoos caused by gunshot wounds at close range were treated with the QS Nd:YAG at fluences ranging from 4 to 6 J/cm2, a 10 ns pulse duration, and 3 mm spot size. Sparks, bleeding, and transepidermal pitting occurred immediately following each pulse, which resulted in scarring in each case. 2.2.

Removal of Pigmented Lesions

Pigmented lesions can be epidermal [lentigos, seborrheic keratoses, cafe´-au-lait macules (CALM), nevus spilus], dermal [nevus of Ota, postinflammatory hyperpigmentation (PIH), melasma] or both (melasma, Becker’s nevus, junctional, compound, and congenital melanocytic nevi).

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2.2.1. Pigmented Lesions in General The 532 nm wavelength for benign epidermal pigmented lesions was examined with a dose– response study (39). Increasing the fluence from 2 to 5 J/cm2 (in 1 J/cm2 increments) produced better clearing but also more purpura and post treatment erythema. Lentigos are purely epidermal lesions and clear easily with a single treatment (40) (Fig. 11.6) whereas CALM usually take a few treatments and may recur (39,41). Hyperpigmented scars may respond to QS 532 nm (42) with softening and decreased pigmentation. The efficacy and side effect profile of QS ruby and QS Nd:YAG (1064, 532 nm) lasers were compared in the treatment of cutaneous pigmented lesions, including lentigines, CALM, nevus of Ota, nevus spilus, Becker’s nevus, PIH, and melasma (43). Twenty patients with pigmented lesions were treated with the QS ruby and QS Nd:YAG laser at 532 nm (solar lentigos, melasma, PIH, Becker’s nevus, nevus spilus, and CALM) or 1064 nm (nevus of Ota). With the exception of melasma for which poor results (,25% clearing) were noted in all cases, the QS ruby laser produced good-to-excellent results (50–95% clearing), as opposed to fair-to-good (25–75% clearing) results for the QS Nd:YAG for all remaining conditions. Neither laser caused scarring or textural changes. Nevus of Ota. In a prospective trial, acquired bilateral nevus of Ota-like maculae were treated with the QS Nd:YAG laser (1064 nm, 8 – 10 J/cm2, 2– 4 mm spot sizes) (44) and found to have 100% clearance in 68/70 women after two to five treatments. Transient hyperpigmentation occurred in 50%, without scarring or textural changes, and no recurrence was noted at 3 –4 years follow-up. In a similar study (45), 50% (33/66) of patients who received more than two treatments showed good-to-excellent results. Additional studies evaluated the treatment and side effect profile of the QS Nd:YAG (1064 nm) laser for nevus of Ota, with excellent clearing observed (45 –47). In a retrospective analysis (46), 129 patients were interviewed that had been treated with the QS alexandrite, the QS 1064 nm Nd:YAG, or both lasers. Complete clearing versus .50% lightening occurred in 0%/25.9% of the QS alexandrite-treated, 1.9%/38.1% of the QS Nd:YAG-treated cases, and 8.3%/72.9% of cases treated with both, respectively. Hypoand hyperpigmentation, textural changes and scarring were more common in those treated with the QS alexandrite or both lasers. Of note, 13 (5.2%) patients with .90% clearance developed a recurrence 3 –4 years posttreatment. Thus, the aforementioned studies suggest that the QS ruby laser may be most efficacious for nevus of Ota but a larger comparative study needs to be done. The QS Nd:YAG (1064 nm) laser is more effective than the QS alexandrite laser however and offers the advantage of the lowest incidence of untoward effects, such as pigmentary or textural changes or scarring; as it causes less epidermal disruption and, for darker skinned patients, is the preferred wavelength.

Figure 11.6 Solar lentigos on the hands of a middle-aged man before and after a single treatment of frequency-doubled QS Nd:YAG laser (532 nm).


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2.2.2. Acquired Melanocytic Nevi A side-by-side comparison of QS alexandrite (755 nm, 100 ns, 3 mm, and 6.0 J/cm2) and the Nd:YAG (1064 nm, 10 ns, 3 mm, 6.0 J/cm2) lasers for treatment of benign acquired melanocytic nevi (16) was done in 18 patients with a fluence of 6.0 J/cm2 and a 3 mm spot size. Three treatments at 6-week intervals, were done to opposite halves of a large (.1.5 cm) or to two small (.7 mm) adjacent nevi. After one treatment, 10% lightening was noted for both lasers whereas after three treatments, more lightening was observed after alexandrite (60%) than after Nd:YAG (30%) laser treatment possibly explained by the more superficial location of the target melanosomes (i.e., at the dermal – epidermal junction) in common acquired melanocytic nevi, as compared to nevi of Ota, which respond better to the longer and deeper penetrating wavelength of the QS Nd:YAG (1064 nm) laser.

2.2.3.

Congenital Nevi

Treatment of congenital nevi is much more controversial as the potential risk for malignant transformation is unknown. Reduction of the melanocytic load may decrease the risk or, conversely, irritation of the melanocytes by laser irradiation may increase the risk. Although most feel that the risk for triggering melanoma formation is low, it is currently not recommended to treat patients with a family or personal history of melanoma, as these patients are already at higher risk.

2.3.

Hair Removal

QS 1064 nm pulses effectively treated the deep dermal melanocytes in nevus of Ota suggesting follicular melanin was a viable target. A prospective trial assessing the effectiveness of QS Nd:YAG laser-induced hair removal was performed by Nanni and Alster (48). Attempts were made with the use of wax epilation, carbon suspension, and laser alone. None of the protocols utilizing the QS Nd:YAG laser was effective in permanently removing hair. Goldberg and coworkers (49) also evaluated topical suspensionassisted QS Nd:YAG (1064 nm) laser-induced hair removal in 35 subjects. At 12 weeks posttreatment, hair reduction of 65% was seen with mild hyperpigmentation in one patient. A comparison study by Kilmer et al. showed that a higher-powered QS Nd:YAG without topical carbon gave 30% permanent hair reduction 6 months after three treatments but this was much less than the LP alexandrite and ruby lasers (70%).

2.4.

Rhytids

A pilot study by Goldberg and Whitworth (50) compared the QS Nd:YAG (1064 nm) and two char-free CO2 lasers (10,600 nm) in 11 patients with facial rhytids. Rhytids were improved with QS Nd:YAG laser treatment in 9/11 patients: in three of these, improvement was equivalent between the QS Nd:YAG and the CO2 lasers, and in six patients, the CO2 lasers were more effective than the QS Nd:YAG laser. Re-epithelialization occurred after 3 – 5 days on the QS Nd:YAG sides and after 6 – 11 days on the CO2 laser sides of the face. No pigmentary alterations were observed. At 1-month postprocedure, erythema was observed in 11/11 CO2-treated sides and in the 3/11 Nd:YAG-treated sides that were most improved. More recently this technique as well as with the QS Nd:YAG alone have been shown to improve fine lines (51,52).

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LASER TECHNIQUE AND PARAMETERS

3.1. 3.1.1.

Tattoo Removal General Parameters and Protective Equipment

The QS Nd:YAG emits both a 1064 nm and a 532 nm wavelength with a pulse duration of 10 ns, which is delivered by a mirrored, articulated arm. Current models have spot sizes of 0.8 – 8.0 mm and operate from 10 to 100 Hz. The 1064 nm wavelength is most effective for treating blue-black tattoos but ineffective for green or red inks. To maximize penetration, a spot size of 3 mm or greater should be employed. When using the 1064 nm wavelength and a spot size of 3– 4 mm, a starting fluence of 3.5– 4.0 J/cm2 should be employed. The desired clinical endpoint is whitening, which is thought to be secondary to water vapor generated beneath the epidermis. Whitening generally clears within 20 –30 min following treatment. Only occasional pinpoint bleeding should be observed; higher fluences that produce frank bleeding should be avoided since there may be higher risk of scarring and pigment alteration. If bleeding or skin breakage is observed, decrease the fluence by 0.5 – 1.0 J/cm2. If whitening is not achieved, the fluence should be increased by this amount. The test site should be evaluated after 4 –6 weeks, the time interval recommended between treatments. Pulses should be delivered with a 10% overlap. Due to the very short pulse duration, the QS Nd:YAG laser generates a significant amount of “tissue splatter,” the vaporization or aerosolization of cellular debris which is composed of viable cells (34). This poses a theoretic risk of infectious disease transmission, necessitating the use of a cone device or splatter shield supplied by the manufacturer to protect the operator. In addition, protective eyewear is mandatory in order to guard against ocular damage and airborne plume. Gloves and laser masks should be worn to protect from possible blood contamination aerosolized cellular debris (34). 3.1.2.

Professional and Amateur Tattoo Removal

Generally, professional tattoos require 8– 12 treatments while amateur tattoos usually clear in 4– 6 sessions. It is difficult to predict the number of treatment sessions needed. Response rates vary for poorly understood reasons, likely relating to types of tattoo inks, location in the dermis, and rates of cellular and lymphatic clearance (53). Optimal treatment intervals are currently recommended at 6 –8-week intervals. Treatment parameters should be titrated as discussed above after an initial test at 1064 nm, spot size of 3– 4 mm, and starting fluence of 3.5 – 4.0 J/cm2. 3.1.3.

Cosmetic Tattoo Removal

The patient must be warned of the potential darkening of the treatment site, which may be irreversible. A test site should always be performed with a single pulse using the appropriate wavelength, then wait long enough for any laser-induced whitening to dissipate to assess whether darkening has occurred. If the ink does not darken you can proceed with treatment. If it darkens, photograph and immediately treat again with the 1064 nm. Re-evaluate in 1 month and compare with the photograph to see if lightening has occurred. If there is doubt, take another photograph and retreat the test spot and wait an additional month. Once it appears that the darkened ink will respond to further treatment, the whole tattoo can be lased, assuming the entire tattoo was placed at one time and with the same ink as the test site. A case of QS Nd:YAG (1064 nm) laser removal of eyeliner tattoo was reported (54) using a 1.5 mm spot size at 6 J/cm2 delivered in two treatment sessions 6 weeks apart with


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almost complete clearing of the tattoo. A metal ocular shield was placed over the globe and hair was protected with petrolatum during the procedure. An eye patch was applied for 3 h posttreatment and healing was complete in 5 days. 3.1.4. Medicinal and Traumatic Tattoo Removal Medicinal and traumatic tattoos are usually blue or black, the type of pigment is often carbon-based, and their location in the dermis is superficial, thereby making them good candidates for QS Nd:YAG (1064 nm) laser treatment (Fig. 11.4). Given the recent report of microexplosions and scarring secondary to irradiation of gunpowder traumatic tattoos (see earlier), proceed carefully and utilize test spots when treating such tattoos with the QS Nd:YAG laser. Otherwise these tattoos can be treated similarly to decorative tattoos with the likelihood that they will clear with fewer treatments given the pigment type and superficial location. Of note, some gang and prison tattoos, may be placed more deeply in the dermis, limiting the laser’s accessibility of the target. 3.1.5. Tattoo Treatment of Darker Skin Types The QS Nd:YAG (1064 nm) laser has been particularly effective with minimal risk of pigmentary change in tattoo removal among darker skin types (see section titled “Treatment of Tattoos in Darkly Pigmented Patients”). Begin with a test using fluences of 3.5 – 4.0 J/cm2, and titrating to the desired clinical endpoints, as described. Use of the 532 nm wavelength will be poorly tolerated due to its strong melanin absorption. 3.2. 3.2.1.

Removal of Melanocytic Lesions Epidermal Lesions

Epidermal lesion should be treated with the 532 nm wavelength laser. Brisk bright whitening should occur. Choose the appropriate spot size for the target lesion size and use the lowest fluence that still gives the desired whitening. Higher fluences produce more purpura, post op erythema with little or no added efficacy noted (39). Epidermolysis and pinpoint bleeding are not desired. 3.2.2.

Dermal Melanocytic Nevi

For dermal nevi, such as nevus of Ota, use 1064 nm for a blue-black to dark brown lesions but if it is light to medium brown, the pigment is usually more superficial and responds better to 532 nm. Sometimes a test site with both wavelengths is warranted. Metal eyeshields are needed to protect the eye when dealing with nevi that approach the lash line, otherwise wet gauze can be used to cover the area. Commence with the largest spot size and close to maximum fluence, increasing as tolerated. Of note, with a deeper nevus of Ota, brisk whitening is often not seen and pinpoint bleeding may occur several minutes after treatment. The test site should be evaluated after 6–8 weeks. Longer treatment intervals should be used to allow complete removal of targeted melanocytes and melanophages before treating the same area again. The risk of recurrence needs to be addressed at the time of consent. 3.2.3.

Common Acquired Nevi

The QS Nd:YAG (532 þ 1064 nm) is effective in lightening the junctional component of nevus spilus and some common acquired nevi (16). Lightening of nevi may theoretically preclude monitoring such nevi for the changes typically evaluated when examining a

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patient for melanoma, therefore, laser removal of common acquired nevi is discouraged in patients with dysplastic nevi or a personal or family history of melanoma. 3.3.

Hair Removal

Although the reports described herein suggest that the QS Nd:YAG (1064 nm) laser promotes a growth delay of up to 3 months—in most cases, hair completely regrows. Theoretically, the ideal lasers should target the stem cells of the hair follicle, which have recently been shown to reside in the bulge that is located at a depth of 1.5 mm (55). Such lasers would operate at a wavelength that penetrates to this depth optimally, namely 700 – 1000 nm. The pulse duration needs to be long enough to more effectively deposit heat in the follicle and permanently destroy it. Nd:YAG lasers in the millisecond range are now utilized. The QS Nd:YAG lasers do offer the ability to treat pseudofolliculitis barbae (56) by inducing a prolonged growth delay (temporary hair reduction), which may be preferable for those who do not wish to permanently eliminate beard hairs. 3.4.

Rhytids

Treatment of rhytids has been simplified to utilizing the 4 mm spot size and passing the beam over the area to be treated. In some cases, a topical carbon suspension is used to increase the effect although the added benefit is not clear. Pinpoint bleeding may occur necessitating use of ointment or a bandage immediately postop, although in most cases there is minimal epidermal disruption.

4. 4.1.

PRE- AND POSTPROCEDURE MANAGEMENT Preprocedure Considerations

A careful patient history should make note of any history of keloidal scarring, herpes simplex viral infections, or treatment with isotretinoin within the past year. A history regarding skin phototype should be taken in order to assess risk of pigmentary alteration. Written information regarding the nature of the procedure should be given to the patient preoperatively. Representative before and after photographs are helpful to prepare and inform the patient of what to expect. Patients should be advised that a test site may be necessary with a 6 – 8-week of treatment interval period, that multiple treatment sessions will be required, in the range four or more depending upon the indication, that total removal of the lesion may not be achieved, and that there is a possibility of recurrence in the case of nevi. Patients should be advised against treatment if they would be dissatisfied with a partially removed lesion. Aspirin and nonsteroidal pain relievers should be discontinued 1 week prior to laser treatment, if the risk of bleeding after treatment is a concern. A subset of patients may require either a topical anesthetic, such as EMLA cream (Astra, Westborough, MA), Ela-Max (Ferndale, Ferndale, MI) or injection of a local anesthetic, such as 1% lidocaine prior to treatment. 4.2.

Postprocedure Considerations

4.2.1. Wound Care Immediately following the procedure, a broad-spectrum antibiotic ointment, such as polysporin or mucipirocin, may be applied to the wound and covered with a nonstick dressing


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for 24 h. Postoperative wound care consists of cleansing the wound, followed by the application of antibiotic ointment, twice daily until the wound has reepithelialized. Strict sun avoidance and regular application of a broad-spectrum sunblock is emphasized to minimize hyperpigmentation. 4.2.2.

Complications

Tattoo ink darkening. The tattoo ink darkening immediately after laser irradiation may occur in flesh-colored tattoos, such as white/flesh, crimson, brown, red, orange, flesh, and yellow (see earlier). All of the QS lasers may cause this untoward effect, which may be improved with further treatments or may be irreversible. The patient should be warned prior to applying a single test pulse, followed by observation. Tattoo ink darkening may subsequently be managed by further treatments with the QS Nd:YAG (1064 nm), as discussed earlier (23,36). Allergic reaction. The development of localized and generalized allergic reaction is another complication following tattoo removal with the QS Nd:YAG (1064 nm) and QS ruby lasers. Two women treated with these lasers developed pruritic eruptions days-toweeks following repeat laser treatments. A skin biopsy of one case demonstrated a superficial perivascular mononuclear infiltrate and a spongiotic dermatitis, consistent with an id reaction. The allergic reactions resolved with administration of antihistamines and topical or systemic corticosteroids (57). Various components of tattoo inks have been shown to cause sensitization. Laserinduced rupture of pigment-containing cells and extracellular release of pigment particles likely triggers the allergic response. QS lasers mobilize ink, in contrast to the older methods where ink was removed transepidermally. Cessation of QS laser therapy is recommended when urticarial reactions occur in order to avoid a systemic allergic reaction and/or anaphylaxis. Also of concern, compartment syndrome has been reported following QS Nd:YAG laser treatment of a forearm tattoo. The significant swelling that can occur, especially with circumfluential tattoos can lead to this potentially disastrous complication (58). Pigmentary alterations and scarring. A distinct advantage to the 1064 nm QS Nd:YAG laser is the low incidence of pigmentary alteration, as compared to the QS ruby and alexandrite lasers (24,37,39). The 532 nm wavelength does lead to temporary hypopigmentation but this tends to resolve quickly. Postinflammatory hyperpigmentation appears to be transient in most cases (44). It should be assessed at 4 –6 weeks postprocedure and is best managed by initiating treatment with a broad spectrum sunscreen (preferably zinc oxide), 4% hydroquinone, and possibly a topical steroid for more severe or recalcitrant cases. Textural changes have been noted but found to resolve with time as well. In some cases, permanent scarring has resulted. Photographs are helpful for documenting preexisting scars that can arise from placement of the tattoo itself, however, the ink may camouflage any scar formation. In addition, some tattoos are purposefully placed to cover up preexisting scars.

5.

SUMMARY

In summary, the QS Nd:YAG laser at 1064 nm is highly effective for removal of blue-black tattoos, especially for darkly pigmented patients and those with traumatic tattoos whereas the 532 nm wavelength is best for reddish tattoos. The incidence of

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postprocedural pigmentary changes, textural changes or scarring is lower for the QS Nd:YAG (1064 nm) as compared to other laser systems. The QS Nd:YAG (1064 nm) is also very effective in removal of dermal melanocytic lesions, and for enduring a prolonged telogen phase to help slow hair growth; this is especially helpful for psuedofolliculits barbae. Further research is needed to compare the QS Nd:YAG (1064 nm) to other lasers in the emerging field of nonablative facial rejuvenation.

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12 Q-Switched Alexandrite Lasers Christopher A. Nanni Private Practice, Glendore, California, USA

1. Q-Switched Alexandrite Lasers 2. Endogenous Cutaneous Pigments 3. Exogenous Cutaneous Pigments 4. Treatment Considerations 5. Treatment Pearls 6. Treatment Side-Effects and Complications 7. Summary References

1.

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Q-SWITCHED ALEXANDRITE LASERS

The Q-switched alexandrite laser has been used extensively in cutaneous surgery for the treatment of a variety of cutaneous pigmented lesions (1 –9). A stimulated or “excited” alexandrite crystal produces photons of 755 nm wavelength light which is classified as red or near-infrared electromagnetic radiation and utilizes pulse durations from 50 to 100 ns (5). Dermatologic and aesthetic surgeons often refer to this laser as a “pigmentspecific laser” due to its ability to treat both endogenous and exogenous skin pigments. Lentigos, common and congenital nevi, melasma, ephilides, Becker’s nevi, Nevus of Ota, nevus spilus, and infraorbital-hyperpigmentation all have been successfully treated with the alexandrite laser (1 – 8). Exogenous pigments such as blue, black, and green tattoos, as well as graphite, traumatic, and foreign-body tattoos also have been reported to respond well to the alexandrite’s 755 nm pigment-specific wavelength (1 – 9). The alexandrite crystal itself is produced via a thermal process whereby a primary rod is formed under extremely high temperatures. This primary rod is then used to harvest anywhere from 2 to 10 secondary, smaller-diameter rods which are cored out from its center (Fig. 12.1). Once the secondary rods are examined for any structural abnormalities, they may then be used as a lasing medium. Generally, alexandrite rods are photodynamically “stimulated” by flashlamps which excite the stable, “resting” electrons within the alexandrite crystal to higher energy states. Once these electrons are no longer 285

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Figure 12.1 A primary alexandrite rod from which smaller rods have been harvested (note cored-out portions).

stimulated by the flashlamp, they fall back to their previous resting state and simultaneously emit a discrete photon of light with a wavelength of 755 nm. The laser chamber with its essential elements can cause the excitation of multiple electrons and produce numerous photons of light in a process known as light amplification. The complete details of this process will not be covered here, but it is these complex events which allow us to produce intense, monochromatic, collimated, and coherent light from what is known as a laser. Alexandrite lasers produce pulses of light that range from nanoseconds to milliseconds in duration. The light energy from most alexandrite systems is delivered via a fiberoptic cable which is believed to produce a more homogenous beam profile with a more consistent distribution of energy (3,5). Those lasers which produce high-energy 755 nm wavelength light in the nanosecond range do so by a process called quality-switching or Q-switching (10). The laser chamber is able to store photons until they are released through a switching mechanism known as a quality switch (Q-switch). This process allows a great number of photons to be released in an intense, brief laser pulse. Lasers that do not utilize a Q-switch produce longer pulse durations of light and are known as “normal mode” or “long-pulsed” systems. According to the theory of selective photothermolysis, a laser will be most effective and least destructive if its wavelength is selectively absorbed by a target and if the laser energy is applied to the target for a duration less than its thermal relaxation time (TRT)—the time it takes a target to cool to 50% of its heated temperature (11). Larger targets have less surface area and therefore cool down more slowly than smaller structures; therefore, larger targets have longer thermal relaxation times. In other words, the brief nanosecond pulses from the Q-switched alexandrite laser is best suited for smaller cutaneous targets, as compared to larger targets which are more appropriate for the long-pulsed alexandrite systems. From a clinical perspective, the Q-switched lasers are designed to be absorbed by small particles of tattoo pigments free in the dermis and trapped within macrophages. They also effectively damage small particles of melanin contained within keratinocytes, melanocytes, and melanasomes. In this way, tattoos as well as unwanted endogenous pigmented lesions may be treated and eliminated with minimal risk to surrounding tissue. In contrast, long-pulsed lasers are best suited for larger structures such as unwanted body and facial hair where the cutaneous target is the pigmented hair shaft and follicle (12,13). Due to the short pulse durations generated by the Q-switched alexandrite laser, pigmented targets are exposed to laser light for only brief time intervals and therefore

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rapidly absorb laser energy. This absorbed light energy is then transformed into thermal energy within the target. The thermal energy is produced rapidly within a given target, often causing it to rupture explosively generating pressure or acoustic waves (4 –6,14). A target then, may not only sustain thermal damage but may also become injured from these acoustic waves. Therefore, Q-switched systems such as the alexandrite laser are said to have both thermal as well as photoacoustic effects on their targets.

2.

ENDOGENOUS CUTANEOUS PIGMENTS

Endogenous pigmented lesions may be characterized by their location in the skin (epidermal vs. dermal) as well as their biological origins (acquired vs. inherited). These classifications may assist the laser surgeon in choosing which laser is best equipped to treat which type of lesion. For example, lentigines are acquired and are superficially located in the epidermis. Therefore, a laser does not need to penetrate deeply into the skin in order to treat these pigmented lesions (15). However, a Nevus of Ota is characterized by deep dermal pigment and responds best to laser light that penetrates effectively into the dermis such as the red light of the ruby and alexandrite lasers (3,5,16). The fact that red laser light penetrates easily into the dermis allows the alexandrite laser to treat lesions such as congenital nevi and Nevus of Ota more effectively than laser systems with shorter wavelengths (5). It is of interest to note that the biological origins of a pigmented target does not always help a surgeon to predict which lesions will respond to laser treatment most effectively. For example, melasma which is thought to result from sun exposure and hormonal factors is acquired and can be very recalcitrant to any laser or medical treatments. By contrast, Nevus of Ota are inherited lesions which are quite effectively removed by red laser light. Therefore, whether a person is genetically programmed to develop a particular lesion or whether a pigmented lesion develops from environmental factors may not help to predict the level of difficulty in treating a specific lesion. Lentigines are clinically characterized as brown macules which develop on areas of sun-exposed skin such as the face, chest, upper back, and the extensor surfaces of the upper and lower extremities. These acquired lesions respond well to the alexandrite laser and are effectively removed after only one to two laser treatments. Lentigines generally do reoccur, but a treated area that is re-exposed to sunlight may develop new lesions quite easily. Other small, monochromatic macules that appear similar to lentigines are known as ephilides or “freckles” and characteristically darken dramatically upon sun exposure (16). These pigmented lesions are also sensitive to alexandrite laser treatment and may be effectively removed in a matter of only one to two laser sessions. Nevus of Ota appear as brown, black, or blue macules and patches that develop at the periorbital region at birth or during adolescence (3,16). An ethnic predisposition has been documented in the Japanese population where incidence rates reach 0.2 –0.6% (3,16). Alexandrite laser treatment may require 5– 10 laser sessions, at treatment intervals of 6 – 8 weeks to allow for any postinflammatory hyperpigmentation to fade. Success in treating this pigmented lesion is high and recurrences are rarely noted.

3.

EXOGENOUS CUTANEOUS PIGMENTS

Tattoos may be composed of a wide array of colors and may be quite detailed in terms of their artistic form and the manner in which the pigment itself is produced and placed within the dermis. Tattoos may be categorized as amateur or professional, and may be further subdivided into decorative, cosmetic, or traumatic categories (1 –9).

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The most important characteristic of a tattoo in terms of selecting an appropriate laser wavelength for treatment is pigment color (4,6,9). Almost all of the “tattoo lasers” including the Q-switched ruby, alexandrite, and neodymium:yttrium – aluminum-garnet (Nd:YAG) wavelengths are effective at treating blue and black colored tattoos and traumatic tattoos. However, green, red, orange, yellow, and more complex color mixtures may need a specific wavelength for effective treatment or may be resistant to all of the tattoo-laser wavelengths. The alexandrite laser effectively treats blue, black, and green colored tattoos (1 – 9). Green tattoos may also be treated with a ruby laser but the alexandrite wavelength is usually considered the laser of choice for the treatment of green pigment. Multiple treatments are the rule when treating a tattoo and the popular misconceptions regarding the ease of laser tattoo removal can make patient education an arduous task during the initial consultation. Amateur tattoos are usually composed of India ink and are placed superficially in the dermis compared to professional tattoos (4,6). They are also less densely pigmented and therefore require a fewer number of laser treatments in order to produce adequate clearance. Treatment of cosmetic tattoos (lip and eyeliner pigments, tattoos designed to camouflage scars, etc.) especially those containing white, flesh-tone, and pink pigments may result in an adverse response known as pigment darkening (17). Although not reported specifically with the alexandrite laser, immediate and irreversible pigment darkening of cosmetic tattoos may theoretically occur with any Q-switched laser system. This phenomenon is thought to be due to a chemical reaction whereby heat generated from the laser reduces an iron-containing tattoo pigment from ferric oxide to the ferrous oxide form. While continued laser treatment may eventually clear the darkened pigment, results are not predictable and additional procedures such as surgical excision or CO2 laser resurfacing may be needed in order to effectively eliminate it. Other factors that affect tattoo removal are the age of the tattoo, the amount of pigment contained within the tattoo, and the depth of pigment placed within the dermis (2,6). However, tattoo treatment outcomes may be quite variable despite a thorough understanding of the history and composition of a given tattoo. In general, older less densely pigmented, monochromatic tattoos respond best to laser treatment. However, accuracy in predicting the number of treatments necessary to eliminate a given tattoo is low, indicating that unknown factors or a complex interaction of events probably dictate how well a tattoo responds to laser treatment. Certainly, the immune system plays a role in tattoo removal as macrophages in the dermis attempt to engulf tattoo pigments which are too large to be digested and remain stationary in the dermis with the pigment internalized. Tattoo pigment may also be found in lymph nodes draining untreated tattoos, suggesting that the lymph system is attempting to clear away tattoo pigment as debris (6). The exact mechanisms of tattoo removal are unclear and are most likely a complex interplay of both mechanical and immunologic events.

4.

TREATMENT CONSIDERATIONS

The treatment of pigmented lesions is not a simple task and laser treatment is not necessarily the perfect solution to all things that are colored and contained within the skin. Several patient, lesion, and environmental factors must be considered prior to embarking on laser treatment of any cutaneous pigment. In general, the ideal laser patient is one who has a clearly defined pigmented lesion, a patient who has a full understanding of the potential complications of laser surgery, and of the number of treatments necessary to achieve


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adequate lesion clearance. The laser surgeon, therefore, must consider several factors when evaluating a potential laser candidate. First, the exact biological nature of the lesion to be treated must be clear from either clinical or histopathological findings. It is not appropriate to treat any pigmented lesion that is suspicious, irregular, unfamiliar, or in any way atypical. If the diagnosis of a cutaneous lesion is unclear, it is essential to first perform a biopsy of the lesion prior to commencing with laser treatment. Second, consider how effective a given laser treatment will be and explain to the patient how many treatments may be necessary before improvement is noted. Never guarantee complete removal of any lesion, as laser treatment is often unpredictable. It is better to set patient expectations low rather than disappoint someone who is counting on clearance in a specific time period. Tattoos often clear rapidly up to a certain point, then clearance may peak and flatten, requiring many more treatments to achieve removal beyond 80– 90% (1 – 9). Some lesions, such as a cafe´ au lait macule may respond well to laser treatment initially but then reoccur rapidly upon sun exposure. It is important to make it clear to the patient that some lesions have a tendency to be either resistant to laser treatment, or may recur after laser treatment, or may even worsen as a result of laser irradiation. Melasma for instance tends to be recalcitrant to many types of treatment and may even worsens after laser therapy (18). This adverse reaction should be communicated to the patient prior to treatment to assure that there are no misunderstandings. Finally, side effects and complications of laser treatment must be fully articulated. The alexandrite laser targets pigment and while the goal of laser treatment is to destroy excess or unwanted cutaneous pigment, normal epidermal melanin is often adversely affected as well. Patients with Fitzpatrick skin types IV – VI and those with tanned skin are at high risk for laser complications and should be treated with caution (19 –21). Hypopigmentation, hyperpigmentation, vesiculation, crusting, edema, and erythema may all occur. However, some of these reactions may even be considered a normal or expected response to laser therapy. When treating lentigines on the hands, for instance, erythema, edema, and pigment darkening occur, causing lentigines to become even more prominent than they were prior to laser therapy. This darkening then leads to a gradual fading of these pigmented macules; however, significant lesion clearance occurs only after several postoperative weeks. Therefore, the patient needs to be prepared for this darkening effect (Fig. 12.2) and should plan to have the appearance of their hands worsen before it improves after laser treatment.

5.

TREATMENT PEARLS

In general, the more densely pigmented a particular lesion the lower the fluence required for effective treatment. Test sites are often helpful, especially if there is a concern regarding pigment darkening in a cosmetic tattoo or skin dyspigmentation occurring in a person with a dark skin type (19,20). However, while they may be helpful, test areas are not infallible as only a small portion of a lesion in question is usually being tested. In a tattoo for instance, some areas may be deeply pigmented and some areas may be faded and contain minimal ink. Therefore, high fluences may be appropriate to treat those faded areas but not areas rich in pigment. Excessive fluences may result in tissue splatter, punctate bleeding, epidermolysis, and subsequent textural changes. It is best to treat initially with a low fluence (5 – 6 J/cm2) while subsequent treatments may be adjusted based upon the immediate tissue reaction and postlaser healing response. As a general rule, pigmented lesions should be thoroughly reevaluated prior

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Figure 12.2 Hyperpigmented and slightly crusted solar lentigines on the dorsal aspect of the hand, 1 week after Q-switched alexandrite laser treatment.

to each treatment. If significant color lightening has occurred and the patient has no major complaints regarding healing, an increase in laser fluence of 0.5 –1 J/cm2 may be considered (Table 12.1). As there becomes less target (pigment) the energy must be increased in order to destroy the small amount of color remaining. A desirable intraoperative reaction is one characterized by immediate tissue whitening, mild to moderate edema formation, the development of an erythematous flare, and minimal to no tissue bleeding (Fig. 12.3). Vesiculation, obvious bleeding, tissue splatter, a loud “snap” upon laser impact, and significant treatment pain are indications for decreasing energy fluences. Interestingly, the shorter the pulse duration of a Q-switched alexandrite laser, the more splatter and punctate bleeding; however, shorter pulse durations are also more effective in clearing tattoos. Treatment intervals should take into account the fact that adequate healing must occur prior to subsequent treatments to prevent side effects such as scarring. Tattoo pigment must be immunologically removed from the treatment site and this process can take from several weeks to months. Epidermal pigment usually darkens and then peels away during 2– 4 weeks postlaser treatment. In patients who experience postinflammatory hyperpigmentation, it is best to wait until the skin darkening has faded significantly prior to commencing with further treatments. Therefore, on average, pigmented lesions are treated at 4 –6-week intervals. Immediate postoperative care of pigmented lesions and tattoos includes a petroleum-based topical antibiotic ointment with a nonstick bandage to be used for the Table 12.1

Q-Switched Alexandrite Laser Treatment Guidelines

Lesion Amateur tattoo Professional tattoo Lentigo Common melanocytic nevus Nevus of Ota

Fluence (J/cm2)

Treatment schedule (weeks)

Average number of treatments required

6–9 5–9 6–8 6–9 5–9

6–8 6–8 6–8 6–8 8 – 12

4 –10 7 –20 1 –4 3 –10 7 –20


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Figure 12.3 A professional tattoo, before and immediately after treatment with a Q-switched ruby for the green pigment and Q-switched frequently-doubled Nd:YAG for the red pigment. Note the ash-white appearance. Courtesy of Arielle N. B. Kauvar, M.D.

first 1– 3 days. Sun protection and sun avoidance are key as the greater the amount of epidermal melanin present, the less effective treatment will be and the greater the potential for complications (18 –20). While it may be tempting for patients, they must be instructed not to pick, peel, or scrub the treatment area. Pigment should be allowed to fade or peel away on its own during the postoperative period to avoid subtle textural changes or scarring.

6.

TREATMENT SIDE-EFFECTS AND COMPLICATIONS

The alexandrite laser’s wavelength of 755 nm effectively penetrates the dermis and is only minimally absorbed by epidermal melanin (2– 9,18 –20). Through the principles of selective photothermolysis, the Q-switched alexandrite attempts to confine thermal damage to a specific pigmented target and therefore minimizes damage to surrounding tissue (11). However, the skin’s natural pigment composed of epidermal melanin also absorbs 755 nm light energy (9,20,21). Therefore, both hypopigmentation and hyperpigmentation have been reported following treatment with the alexandrite laser (2,4). As many as 50% of patients may experience hypopigmentation after QS alexandrite tattoo treatment. However, nearly all patients repigment normally within 3– 6 months (2,4,9,20 – 22). Skin lightening tends to occur more commonly in deeply pigmented skin and in recently sun exposed and tanned skin. Hypopigmentation is often related to the number of treatments a specific lesion receives with an average of seven treatments necessary to induce significant skin lightening (4). Hyperpigmentation, is a rare event, occurring in fewer than 1% of cases (20,21). Immediate treatment effects include mild pain and an ash white appearance of lasertreated skin (6,10). Textural changes and scarring occur only rarely with the alexandrite laser and are often a result of inappropriate wound care postoperatively (4). However, reversible textural changes have been reported with the alexandrite laser as they have been reported with the ruby and Nd:YAG laser systems (4). Punctate bleeding and tissue splatter may occur with the alexandrite laser especially at high fluences and with those alexandrite systems utilizing very brief pulse durations. However, these epidermal side effects do not occur as frequently as they do with the use of the ruby and Nd:YAG lasers (4,22). Although not specifically reported with Q-switched alexandrite laser

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treatment, immediate irreversible pigment darkening of cosmetic, white, flesh-tone, and pink tattoos may theoretically occur with the alexandrite laser as it has been reported with other Q-switched laser systems (17). Cutaneous allergic reactions to tattoos may occur shortly after their placement into the dermis or may be quiescent until the tattoo has been treated with laser radiation (23,24). Allergic reactions to red tattoo pigments are most commonly seen (23) (Fig. 12.4). Reports of allergic reactions to yellow and blue pigment dyes may also occur but are less likely (6). Tattoos that manifest an allergic dermatitis after undergoing laser treatment may be caused from the dispersion of intracellular pigment into the extracellular space where it becomes antigenic. In a case report from Ashinoff et al. (25) patients with no history of allergy to their tattoo pigment prior to laser treatment experienced both generalized and localized urticaria, pruritus, and eczematous reactions after receiving several laser treatments. 7.

SUMMARY

The Q-switched alexandrite laser produces 755 nm wavelength light using pulse durations within the nanosecond range (Table 12.2). This flashlamp-powered laser primarily targets both endogenous and exogenous pigments contained within the skin. Based upon the principles of selective photothermolysis, the alexandrite laser targets a specific cutaneous pigmented lesion by producing a wavelength that is absorbed by the target, and by delivering a discrete amount of laser energy at a time interval at or below the target’s thermal relaxation time. This pulsed laser technology decreases collateral thermal injury to healthy tissue by limiting heat diffusion from the target to surrounding healthy tissue. Endogenous pigments composed of melanin may appear clinically different in coloration dependent upon their depth within the skin and their density. Exogenous pigments such as tattoos are dyes which are placed within the dermis either intentionally or via a traumatic implantation. The alexandrite laser functions by producing 755 nm wavelength

Figure 12.4

Edema and crust due to an allergic dermatitis to red tattoo pigment.

Q-Switched Alexandrite Lasers Table 12.2

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Q-Switched Alexandrite Systems and Specifications

Manufacturer/trade name Candela (ALEXLAZR)

Coherent (VersaPulse) Cynosure (Accolade)

Maximum fluence (J/cm2)

Spot size (mm)

Pulse duration (ns)

12 (2.4 mm spot) 10 (3.0 mm spot) 5.5 (4.0 mm spot) 1.6 – 14 15 (2.4 mm spot) 10 (3.0 mm spot)

20 3.0 4.0 2.0 – 6.0 2.4 3.0

50

45 69

light that is directed onto a cutaneous target. The target absorbs this intense light energy which is then converted into heat resulting in thermal injury. As this heat is generated quite rapidly during a laser pulse, the target expands and disintegrates causing an acoustic shock wave which is in turn destructive. Therefore, the Q-switched alexandrite laser destroys pigmented lesions through both thermal damage and photoacoustic effects. Inherent in all cutaneous laser procedures is an element of uncertainty in regards to efficacy and permanence. The Q-switched alexandrite laser also presents a challenge to both surgeon and patient in terms of predicting exactly how many treatments are necessary to eliminate a given lesion. Multiple treatments are the rule when using any pigment specific laser system. Alexandrite laser treatment of superficial, sun-induced lentigos may require only one to two treatments, whereas a professional multicolored tattoo may need 15 –20 treatments for greater than 90% clearance. This unpredictability in laser outcome is important to communicate to every patient prior to embarking on a treatment plan and underscores the importance of never guaranteeing complete removal of a lesion based upon a set number of laser sessions. In terms of complications and side effects, the Q-switched alexandrite has an excellent safety profile with few reported cases of long-term complications. Hypopigmentation, hyperpigmentation, vesicle formation, and crusting are the most common side effects which generally resolve in 1 –8 weeks. Scarring and permanent dyspigmentation are possible, as they are with any laser system, but these are extremely rare adverse events, especially in the hands of an experienced laser surgeon.

REFERENCES 1. 2. 3. 4. 5. 6. 7.

Alster TS. Successful elimination of traumatic tattoos with the Q-switched alexandrite (755-nm) laser. Ann Plast Surg 1995; 34:542– 545. Alster TS. Q-switched alexandrite laser treatment (755 nm) of professional and amateur tattoos. J Am Acad Dermatol 1995; 33:69 – 73. Alster TS, Williams CM. Treatment of nevus of Ota by the Q-switched alexandrite laser. Dermatol Surg 1995; 21:592 –596. Fitzpatrick RE, Goldman MP. Tattoo removal using the alexandrite laser. Arch Dermatol 1994; 130:1508 – 1514. Goldberg D. Laser treatment of pigmented lesions. In: Alster TS, Apfelberg DB, eds. Cosmetic Laser Surgery. New York: John Wiley & Sons Inc., 1998. Kilmer SL. Laser treatment of tattoos In: Alster TS, Apfelberg DB, eds. Cosmetic Laser Surgery. New York: John Wiley & Sons Inc., 1998. Kovac S, Alster TS. Comparison of the Q-switched alexandrite (755 nm) and Q-switched Nd:YAG (1064 nm) lasers in the treatment of infraorbital dark circles. Dermatol Surg 1998.

294 8.

9. 10. 11. 12. 13.

14.

15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25.

Nanni Rosenbach A, Williams CM, Alster TS. Comparison of the Q-switched alexandrite (755 nm) and Q-switched Nd:YAG (1064 nm) lasers in the treatment of benign melanocytic nevi. Dermatol Surg 1997; 23:239 –243. Spicer MS, Goldberg DJ. Lasers in dermatology. J Am Acad Dermatol 1996; 34:1– 25. Goldman MP, Fitzpatrick RE. Cutaneous Laser Surgery: The Art and Science of Selective Photothermolysis. St. Louis: Mosby, 1994. Anderson RR, Parrish JA. Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science 1983; 220:524 – 527. Kurban AK, Morrison PR, Trainor SW, Tan OT. Pulse duration effects on cutaneous pigment. Lasers Surg Med 1992; 12:282. Nanni CA, Alster TS. A practical review of laser-assisted hair removal using the Q-switched Nd:YAG, long-pulsed ruby, and long-pulsed alexandrite lasers. Dermatol Surg 1998; 24:1399 – 1405. Ara G, Anderson RR, Mandel KG et al. Irradiation of pigmented melanoma cells with high intensity pulsed radiation generates acoustic waves and kills cells. Lasers Surg Med 1990; 10:52. Kilmer S, Wheeland R, Goldberg D et al. Treatment of epidermal pigmented lesions with the frequency-doubled Q-switched Nd:YAG laser. Arch Dermatol 1994; 130:1515 – 1519. Lever WF. Histopathology of the Skin. Philadelphia: J.B. Lippincott Co., 1990. Anderson RR, Geronemus R, Kilmer SL et al. Cosmetic tattoo ink darkening: a complication of Q-switched and pulsed-laser treatment. Arch Dermatol 1993; 129:1010 – 1014. Taylor CR, Anderson RR. Ineffective treatment of refractory melasma and postinflammatory hyperpigmentation by QQ-switched ruby laser. J Dermatol Surg Oncol 1994; 20:592– 597. Ho C, Nguyen Q, Lowe NJ et al. Laser resurfacing in pigmented skin. Dermatol Surg 1995; 21:1035 – 1037. Nanni CA. Complications of laser surgery. Dermatol Clin North Am 1997; 15: 521 – 534. Nanni CA, Alster TS. Complications of cutaneous laser surgery: a review. Dermatol Surg 1998; 24:209 – 219. Stafford TJ, Lizek R, Tan OT. Role of the alexandrite laser for removal of tattoos. Lasers Surg Med 1995; 17:32– 38. Lowenthal LA. Reactions in green tattoos. Arch Dermatol 1973; 107:101 – 103. Novy FG. A generalized mercurial (cinnabar) reaction following tattooing. Arch Dermatol 1944; 49:172. Ashinoff R, Levine VJ, Soter NA. Allergic reactions to tattoo pigment after laser treatment. Dermatol Surg 1995; 21:291 –294.


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CONSENT FORM LASER TREATMENT OF PIGMENTED LESIONS I, , understand that I have a pigmented lesion known as a Dr. has explained to me that although laser surgery is effective in most cases, no guarantees can be made that I will benefit from treatment. I understand that several treatment sessions are usually needed in order to obtain a significant level of improvement. However, there are times when a tattoo or pigmented lesion will not completely clear. When this occurs, the treated lesion generally will become lighter and less densely colored; only rarely does a tattoo or pigmented lesion darken as a result of laser treatment. 1.

2.

3.

4.

5.

6.

7.

8.

9.

PAIN. Each laser pulse may feel similar to the snap of a rubber band. This discomfort is mild to moderate in severity and if needed, a numbing cream or injection can be given prior to treatment. WHITENING. Immediately after laser treatment, the surface of the treated area may appear white in color for 1 – 2 hours. There may also be redness around the treated site which fades within 1 –2 days. SWELLING. The treated area may become red and swollen. This swelling is an expected outcome to treatment and decreases in 1– 2 days. Ice packs and cold compresses may speed recovery. BLISTERS OR SCABS. If a blister or scab develops, notify your doctor. The area should be cleansed with peroxide and an ointment should be applied to the area twice daily. Do not pick at these areas. SKIN DARKENING (HYPERPIGMENTATION). This is usually a transient side-effect which normally resolves within 2– 3 months. This reaction is more common in patients who are sun-tanned, and those with naturally dark skin tone. Only rarely is this skin darkening permanent. SKIN LIGHTENING (HYPOPIGMENTATION). This may occur at the treatment site and is more common in areas which have received multiple treatments. These areas of light-colored skin usually repigment and only rarely are permanent. SCARRING. This is rare, but may occur if the treated area blisters, is traumatized, or scratched. It is important to follow the care your doctor prescribes after laser treatment to help avoid this complication. NO IMPROVEMENT OR WORSENING. Some pigmented lesions and tattoos may not respond to laser treatment or may reoccur. Some treatment sites may even darken after laser treatment, although this rarely occurs. ALLERGIC REACTION. An allergic reaction to the release of tattoo fragments in the skin can occur after laser treatment. Antibiotic ointments used after treatment may also cause a skin allergy.

13

Long-Pulsed Alexandrite Laser Cathy A. Slater Laser Skin & Vein Center of Virginia, Virginia Beach, Virginia and Boice-Willis Clinic, Rock Mount, North Carolina, USA

John B. Newman Laser Skin & Vein Center of Virginia, Virginia Beach, Virginia and Naval Medical Center Portsmouth, Portsmouth, Virginia, USA

David H. McDaniel Laser Skin & Vein Center of Virginia, Virginia Beach, Virginia and Eastern Virginia Medical School, Norfolk, Viriginia, USA

1. 2. 3. 4.

Historical Background Scientific Background Clinical Studies Using a LPA Laser for Hair Removal Practical Applications of the LPA Laser for Hair Removal 4.1. Patient Expectation 4.2. Medical History 4.3. Physical Examination 4.4. Protocol for Using the LPA for Hair Removal 4.5. Eye Safety 4.6. Suggested Treatment Parameters 5. Leg Telangiectasia Treatment 6. Pseudofolliculitis Barbae 7. New Horizons References

1.

297 298 300 303 303 303 304 304 305 305 305 308 310 310

HISTORICAL BACKGROUND

Alexandrite lasers are solid-state lasers that emit a 755 nm wavelength. Long-pulsed alexandrite lasers have become popular for hair removal and leg vein treatment.

The opinions or assertions expressed herein are those of the authors and are not to be construed as official or as reflecting the views of the Department of the Navy, the Department of Defense, or Naval Medical Center Portsmouth. 297

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Slater, Newman, and McDaniel

Alexandrite lasers first became well known in the late 1980s and early 1990s for use in laser lithostripsy to treat ureteral stones. Both Q-switched alexandrite and pulsed alexandrite lasers have been used (1 –3). Researchers have used alexandrite lasers as a light source in photodynamic therapy for cancer treatment and for inducing fluorescence imaging of tumors for detection and mapping (4 – 6). In dentistry, pulsed alexandrite lasers have been studied for dye-enhanced ablation of enamel (7). Early research into cutaneous medical uses of alexandrite lasers also involved “tissue welding” for skin closure, though this did not become a practical application (8). Significant breakthrough in using alexandrite lasers for cutaneous laser surgery came from the field of tattoo removal, when the Q-switched alexandrite laser showed promise as a treatment modality for tattoo removal without scarring (9). Soon the Q-switched alexandrite laser became established as one of several lasers effective in treating black, blue and gray tattoos (10 – 14). Along with other lasers targeting pigmented lesions, reports emerged using the Q-switched alexandrite laser for treatment of nevus of Ota (15), benign melanocytic nevi (16), and solar lentigos (17). In 1997, Alexandrite lasers emerged as a valuable tool for laser-assisted hair removal. Previous studies had already shown that ruby lasers were capable of hair removal. Spurred by public interest and cosmetic demand, the quest was on to develop the safest and most effective hair removal laser. Finkel et al. (18) published their favorable results using a pulsed alexandrite laser for hair removal. Further studies have confirmed efficacy of the alexandrite laser for hair removal. Leg vein treatment became the next focus of interest for alexandrite lasers. In 1999, McDaniel et al. (19) described results using the 755 nm long-pulsed alexandrite (LPA) laser for leg vein treatment. At present there are a number of LPA lasers available (Table 13.1). In addition to hair removal and leg vein treatment, LPA lasers show promise for treating pseudofolliculitis barbae.

2.

SCIENTIFIC BACKGROUND

The LPA laser operates on the principle of selective photothermolysis (20). This concept has been well described elsewhere in this book and in laser review articles (21 – 23). Table 13.1

Available Long-Pulsed Alexandrite Lasers (755 nm Wavelength) Gentle Lase

Apogee 6200

Apogee 9300

EpiTouch Plus

Manufacturer Price (US$) Pulse durations (ms) Spot sizes (mm)

Candela 69,000 3

Cynosure 64,500 5, 10, 20, 40

Cynosure 79,500 5, 10, 20, 40

ESC/Sharplan 79,000 2 – 40

8, 10, 12, 15 1 Up to 100 None

Cooling system

Yes, dynamic cooling

12.5, 15 (10 mm option) Up to 4 Up to 50 Option (70 70 mm) $11,000 Option $10,000

1 – 10 mm

Speed (Hz) Fluence (J/cm2) Scanner

12.5, 15 mm (10 mm option) Up to 3 Up to 50 Option (50 50 mm) $11,000 Option $10,000

Up to 5 Up to 50 Yes (50 50 mm) None, may be in future

Long-Pulsed Alexandrite Laser

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Selective photothermolysis allows selective injury to a desired target while sparing the surrounding structures or tissues. Laser wavelength, pulse duration, and fluence are combined to achieve selective injury. Selective photothermolysis entails choosing a laser wavelength that will match a portion of the absorption spectrum of the intended target. Preferably the surrounding tissues will not absorb this wavelength or the absorption by the target will be greater than the interfering, nontarget chromophores. The alexandrite wavelength frequency of 755 nm has light absorption by both melanin and hemoglobin. Melanin selectively absorbs wavelengths between about 650 and 1000 nm. Oxyhemoglobin and water, which are competing chromophores, absorb less energy at these wavelengths. Compared to the alexandrite wavelength of 755 nm, ruby lasers emit at a wavelength of 694 nm, diode lasers around 800 nm, and Nd:YAG lasers at 1064 nm. In addition, a pulse duration should be chosen that is less than or equal to the thermal relaxation time of the target. Thermal relaxation time is the time required for the target object to cool to half of its peak temperature. The thermal relaxation time for a hair follicle with a 250 mm diameter is 70 ms. The thermal relaxation time for overlying epidermis is 3 – 10 ms. According to some theories, the pulse width for hair removal lasers should fall between these thermal relaxation times (24). Finally, the fluence of the laser light should be above the threshold fluence that would lead to irreversible damage of the intended target. Since hair shaft diameters vary, the optimal pulse duration may also vary. Melanin within the hair follicle is the target chromophore for laser hair removal. When the laser beam detects its color-specific target, light is absorbed in the hair shaft melanin. Heat is generated which damages the hair follicle and possibly some adjacent supporting structures such as vessels. The exact melanocytic target within the hair follicle that is responsible for hair reproduction remains uncertain. The targets probably include the groups of cells near the base of the shaft in the papilla and the germinative cells of follicle in the area one-third of the way down the shaft known as the bulge (24). Melanin allows selective targeting of hair in the skin, since melanin in the hair shaft or follicle provides a chromophore that is not present in the surrounding dermis. Melanin pigment is naturally present in abundance in darker hairs; however, in blonde and graying hair, melanin pigment is less abundant and of somewhat different composition. Melanin pigment is also present in the epidermis surrounding the follicles and must be protected from damage absorption by melanin. The darker the skin type, the more at risk the epidermis is during laser treatment. Some protection of the epidermis is usually accomplished by cooling the skin surface. Nonetheless, epidermal damage, especially in dark skin types presents a safety issue for all melanin-targeting laser systems. Individuals with dark hair and light skin tone currently experience the best treatment results. The ruby laser’s 694 nm wavelength is ideal for melanin absorption, and hence hair removal, but places darker skinned patients at risk for epidermal damage. On the other end of the spectrum, the Q-switched Nd:YAG laser’s 1064 nm wavelength is safer for hair removal treatment of darker skin but is less effective for long-term hair removal. However, the Nd:YAG appears more effective for hair removal when using the longpulse mode at high fluence rather than the Q-switch mode. The alexandrite’s 755 nm wavelength and the diode’s 800 nm wavelength balance the desire for effective hair removal but with more protection for the epidermis. The longer wavelengths of the alexandrite and diode lasers compared to the ruby allow a slightly greater depth of penetration, along with a potential lower risk of epidermal damage since there is slightly less melanin absorption at these wavelengths (25). A corollary of selective photothermolysis is the concept of thermokinetic selectivity (TKS). This theory proposes that for the same chromophore, longer pulse durations allow

300


intrapulse cooling of smaller targets more rapidly than larger targets (24). In other words, the larger chomophore targets of the melanin in the hair follicle can be selectively injured more than the smaller chromophore targets of the melanin in the epidermis. Theoretically, if the pulse width is long enough, heat should build up within the hair follicle (the larger structure), and destroy both the hair follicle and structures immediately adjacent to it such as the bulge. The smaller melanin content in the epidermis (the smaller structure) is relatively spared because it is able to dissipate the heat more rapidly. Treatment safety may be improved if the pulse width selected is longer than the thermal relaxation time of the melanin in the epidermis but is shorter than the relaxation time of the melanin in the hair follicle. Theoretically, the epidermis can cool more efficiently and have reduced damage during the laser pulse. Some researchers (authors included) believe that much longer pulses (200 –800 ms) may also be effective and potentially safer for darker skin types. Anderson has recently introduced the concept of thermal destruction time (TDT) to illustrate this concept. Cooling devices such as dynamic cooling spray, contact cooling, or a chilled topical refractive index matching agent for the epidermis, can enhance cooling and protection. The concept of thermokinetic selectivity under girds the basis for using a long pulse duration in the LPA laser. Some LPA systems use trains of short pulses rather than a single continuous long pulse.

3.

CLINICAL STUDIES USING A LPA LASER FOR HAIR REMOVAL

Cosmetic concern over unwanted hair fuels the constant search for better removal techniques. Long pulsed alexandrite lasers join the ruby, diode, and the Nd:YAG lasers in the research and development of laser-assisted hair removal. Though the ruby has the highest wavelength selectivity for deep melanin absorption, the alexandrite has the advantages of a longer pulse width and a longer wavelength. The 755 nm wavelength, while slightly less selective for melanin, provides greater depth of penetration than the 694 nm one. Theoretically, the 755 nm wavelength of the alexandrite may be safer than the ruby for darker skin when no epidermal cooling is utilized, since the 755 nm wavelength is less well absorbed by melanin than the 694 nm wavelength. Finkel’s early study used a 2 ms free-running short-pulsed alexandrite laser at energy fluences of 25 –40 J/cm2 and showed significant hair growth delay. In this study, 126 patients who received up to five treatments at 4 –12-week intervals demonstrated 90% hair loss 3 months following the final treatment. Hair reduction was around 35% after one treatment (18). Connolly and paolini (26) also reported success using the alexandrite laser. They treated 20 patients with skin types I– V. Treatment parameters consisted of the LPA using a 10 ms spot, a 20-ms pulse width, and a fluence ranging from 14 to 25.6 J/cm2, depending on skin type. They found an 86% hair reduction at the 3-month follow-up period. Patient satisfaction was high and side effects minimal (26). Boss et al. (27) reported a comparison between the long- and short-pulsed alexandrite laser systems. They found no difference using the same fluence on paired anatomic sites between a 2-ms alexandrite laser and a 20-ms alexandrite laser in terms of return of hair growth and complications. Patients reported a 60 –80% reduction in hair growth at 6 months (27). Nanni and Alster (28,29) showed comparable clinical efficacy and side effects between alexandrite and long pulsed ruby lasers when used for hair removal. In addition, Nanni et al. have studied different pulse durations using the LPA laser. Thirty-six subjects were treated with an average fluence of 18 J/cm2, with a 10 mm spot size, on different quadrants at 5, 10, or 20 ms pulse duration. Hair counts were reduced by 66% at


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1 month, 27% at 3 months, and 4% at 6 months. No significant differences in clinical efficacy or side effect profiles were observed between treatment quadrants, yet a trend towards less posttreatment erythema and hyperpigmentation was noted with the 20 ms pulse duration (30). McDaniel et al. (21) have also studied the safety and long-term efficacy of the LPA laser (Figs. 13.1 and 13.2). Thirty-one sites on 22 patients, skin types I–III, were treated at 755 nm, single pulse, 10 mm spot size, 10% overlap, pulse durations of 5, 10, and 20 ms, and a fluence of 20 J/cm2. Hair reduction at 6 months varied both with the pulse duration and anatomic location. Maximum reductions observed were 40%, 56%, 50%, and 15% for the lip, leg, back, and bikini areas, respectively. The 10 ms pulse duration at 20 J/cm2 produced the greatest hair reduction. No permanent adverse effects occurred (21). In contrast, Goldberg and Ahkami (31) compared a 2-ms and a 10-ms alexandrite laser for hair removal. Paired anatomic sites were evaluated 6 months after three treatments. Hair reduction was 33.1% for the 2-ms pulse duration and 33.9% for the 10-ms alexandrite laser, indicating no significant difference in response. No long-term side effects were noted (31). A comparative study between the topical carbon suspension-assisted Q-switched Nd:YAG treatment (the Softlight TM process) and the LPA was done by Rogers et al. (32) Fifteen patients were treated with both lasers on bilateral axilla, though the right axilla only received one alexandrite treatment, while the left axilla received two Nd:YAG treatments. Two months posttreatment, hair reduction was 55% for the alexandrite laser and 73% for the Nd:YAG; after 3 months, the alexandrite laser-treated patients showed a reduction of 19% and the Nd:YAG laser-treated patients showed a 27% reduction. Pain was evaluated on a scale of 0– 10, with 0 being the absence of pain and 10 being the worst. Patients reported average pain values of 8 and 4 for the LPA and Nd:YAG laser sites, respectively (32). In a comparison study between alexandrite laser and electrolysis for hair removal, the average clearance rate of the hairs was 74% by laser and 35% by electrolysis 6 months after the initial treatment. Laser hair removal was noted to be more expensive but 60 times faster and less painful

Figure 13.1 Digital videomicroscopic photos of the identical site of the right upper lip at 30 magnification. (a) Pretreatment and (b) 6 months posttreatment after two long-pulsed alexandrite laser treatments (4 months after second treatment). Note the decreased hair shaft diameter and pigmentation changes of the same hairs [from Ref. (21)].

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Figure 13.2 (a) Pretreatment of the right and left upper lip of a 34-year-old woman with Fitzpatrick Type II skin. (b) Two months posttreatment, right and left upper lip, using longpulsed alexandrite laser with 10 mm spot diameter at 20 J/cm2, single pulse technique, 10% overlap, pulse duration 10 ms, with chilled K-Y jelly. (c) Three months post initial treatment and 1 month post second treatment of the right upper lip only using the same parameters as in B. (d) 6 months after second treatment to left upper lip, 6 months post initial treatment, and 4 months after second treatment to the right upper lip only using the same parameters as in (b) [from Ref. (21)].

than electrolysis, in addition to being more effective (33). Raulin and Greve (34) reported their experience with the alexandrite laser in a retrospective study on 30 female patients using an LPA (20 ms, 755 nm, up to 30 J/cm2, with a 10 or 12.5 mm beam diameter) over an 18-month treatment period. After an average of eight treatments, an average clearance rate of 75% was achieved (34). Several studies have examined the safety of the LPA. Nanni and Alster (35) compared the side effects of the LPA with the Q-switched Nd:YAG and the long-pulsed ruby. A retrospective chart review of the side effects resulting from 900 laser treatments over a 24-month period showed varying degrees of pain, erythema, edema, hypopigmentation and hyperpigmentation, blistering, crusting, erosions, purpura, and folliculitis. The majority of undesirable tissue effects occurred on tanned skin or in skin types III or higher. The effects of seasonal variations, anatomic treatment location, and sun exposure were considered striking within the ruby and alexandrite laser groups. No infections, scarring, or long-term complications occurred (35). Of interest, pili bigeminy has been noted in pubic hairs treated with low fluences with both the alexandrite and ruby laser (36). Though caution should be used in treating dark skin patients with the alexandrite laser, Garcia et al.’s study (37) is encouraging. They treated 150 patients with Fitzpatrick skin types IV– VI exclusively for a total of 550 treatment sites. Complications occurred in only 2% of cases. Of note, they did not find prelaser skin testing helpful in predicting


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the incidence of complications (37). Note: the authors of this chapter suggest caution about treating darker skin types with LPA without prior test areas. In conclusion, multiple studies have demonstrated the efficacy and safety of the pulsed alexandrite laser for hair removal. The longer pulse may have advantages over the shorter pulse alexandrite laser in term of side effects and efficacy, though there are conflicting reports. The optimal combination of wavelength, pulse duration, fluence, epidermal protective measures, and laser sources for hair removal are still in evolution. Further research and development is needed to define the best laser parameters for cutaneous therapies. New approaches and mathematical models to study lasers for hair removal are promising (38).

4. 4.1.

PRACTICAL APPLICATIONS OF THE LPA LASER FOR HAIR REMOVAL Patient Expectation

Patient expectations need to be discussed carefully. No laser produces permanent results all the time. The LPA usually produces a complete hair loss that is temporary, followed by a partial but long-term hair reduction. Patients need to understand the distinction between permanent hair reduction and permanent hair removal. Patients should expect sequential treatments. Realistic expectations should be clearly established. Patients need to know that results vary depending on skin type, hair color, anatomic site and the nature of the human hair growth cycle. In general, skin types V and VI do not respond as well. Also sometimes after two to three treatments, dark hair may turn light and be less responsive, though for most patients this lightening is an improvement compared to the previous dark color hair. Alternative treatments should be discussed, including shaving, waxing, depilatories, and electrolysis. Advantages of the LPA laser for hair removal include being a quick, effective, and safe treatment, with minimal discomfort, no recovery period. There is usually excellent temporary removal, and probable cumulative permanent reduction similar to diode lasers at equivalent parameters, though this has not been published at this writing. 4.2.

Medical History

Patient’s history should include patient’s general medical condition, local skin infections, history of scarring, medications, and skin or endocrine diseases. Patients with a history of herpes simplex may be placed on oral antiviral medications beginning the day before treatment when treating the upper lip or bikini line, though this is usually not necessary. Some authorities believe patients ideally should be off Accutane at least 6 months before hair removal. Shorter intervals off Accutane may be permissible as the presence of increased risk for laser hair removal has not been established. Patients should discontinue tretinoin 2 weeks prior to laser hair removal. Medications such as prednisone and cyclosporine may interfere with the final outcome and should be noted on the medical record. Laser hair removal should be avoided in patients on photosensitizing medications. Patients should be asked if cosmetic tattoos or permanent make up (including lip and eyebrow liner) exist in the areas to be treated. Laser treatment may possibly remove or lighten tattoos or nevi. Tattoos containing iron or titanium oxide pigment may darken; often flesh-toned, white, or burnt amber tattoos darken or change to an unacceptable color. Such areas should be avoided (or patients should be warned of these risks prior to treatment and test areas performed).

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The sun-tanned patient should be counseled extensively on the risk of posttreatment pigment changes. Individuals who have had recent sun exposure but yet have no visible tan are at higher risk for post treatment pigmentary changes also. Sun avoidance is strongly encouraged as the patient progresses through the treatment protocols.

4.3.

Physical Examination

Ascertain skin type such as Fitzpatrick classification of skin types. Type I Type II Type III Type IV Type V Type VI

Always burns, never tans Always burns, sometimes tans Sometimes burns, always tans Rarely burns, always tans Moderately pigmented Black skin

(The Lancer Ethnicity scale is also a useful adjunct to the Fitzpatrick skin types.) Skin types I–IV can be treated, but types V and VI are less good candidates. Recent improvements in epidermal cooling options are changing these guidelines. If any significant tan is present, it is best to postpone treatment until the tan is faded (6 weeks). Patients may use bleaching agents to lighten hyperpigmented areas to be treated. Patients should also avoid tanning parlors. The patient’s hair color should be noted. Dark hair usually shows better long-term reduction whereas blonde or white hair may show little or no reduction. Patients with red and gray can be advised that they may or may not achieve permanent hair reduction. The presence of tattoos or nevi in the treatment area should be noted. There should be no electrolysis, plucking, or waxing for 3 weeks prior to laser treatment. Hair is shaved prior to treatment; depilatory creams can be used if the patient objects to shaving. Patients will experience heat or feel pain similar to a rubber band snapping against skin. Chilling devices reduce this pain. Topical anesthesia is generally only used if patients are pain sensitive or if sensitive areas are treated such as the upper lip and the bikini line. Topical lidocaine or EMLA may be applied 60 –90 min prior to treatment. Application over large areas is not recommended because of the risk of systemic lidocaine toxicity.

4.4.

Protocol for Using the LPA for Hair Removal

The laser operator should wear gloves. All persons in the treatment room should wear appropriate protective eyewear. Remove any topical anesthetic. The hair is usually clipped to ,1 mm in length or shaved by patient prior to treatment. If no chilling device is available, laser pulses may be delivered through a thin (0.5 mm) layer of K-Y Jelly chilled in an ice water bath. Laser pulses are set at the desired fluence and spot size. Pulses are delivered with the handpiece pressed firmly perpendicular against the skin. Ideally, skin is stretched prior to delivery to ensure maximum skin contact. Mild pressure is applied in order to maximize skin contact and hence follicle penetration. The handpiece is then lifted and placed firmly on an adjacent site until entire area is treated. Pulses should be delivered with minimal to no overlap, but placed in a way to avoid checkerboard or corn row-putting patterns. The goal is to use a fluence in which the hair is carbonized, followed by very selective follicular swelling and redness. The endpoint is defined by a red halo around each hair but without vesiculation. A polarized light source with magnifying loupe aides in


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visualization of the hair follicles. Often after a few days after treatment, hair casts may be shed from the hair follicle. The highest fluence tolerated is used to reach this optimal endpoint. Fluence levels that may lead to blister formation should be avoided, as this signifies epidermal damage and potential pigmentary changes. To decrease the risk of hypo- or hyperpigmentation, lower fluences than those suggested below should be used. If epidermal damage is present (blistering, graying) the fluence should be lowered. Multiple pulsing increases the risk of pigment changes. Wipe away damaged surface hair. After a few minutes, diffuse erythema and edema may appear. This sunburned feeling usually last 1 –3 h. Applying ice or cold compress immediately posttreatment will provide relief and reduce the swelling duration. If moderate erythema occurs, a mild topical steroid preparation may be applied. Sometimes redness lasts for a few days, but can be covered by make up. If there are blisters, then the patient should use an antibiotic ointment and call the physician. Patients should avoid sun exposure for at least a few days after treatment. All body sites except the eye can be treated. Second treatments should be given when the hair begins to regrow. This may be at different times for different body areas. Generally speaking, for the face, axilla, and bikini, treatment may be scheduled after 1 – 2 months; for the back and legs, 2 –3 months. 4.5.

Eye Safety

Lasers are capable of causing severe retinal injury when applied near the surface of a patient’s eye. This laser should not be used on or near the surface of patient’s eye. Use of this laser anywhere inside the bony orbit may potentially cause direct eye injury. Patient and operating personnel must wear proper eye protection to prevent inadvertent exposure to the eyes. Infrared light such as 755 nm can be especially dangerous because of our inability to see the laser light. 4.6.

Suggested Treatment Parameters

In general, select the largest available spot size which will deliver the desired fluence. Adjustments for photoaging and darker skin types are advisable and test spots should be utilized whenever there is uncertainty. Due to the variations in pulse durations and cooling options from the various manufacturers, the authors elected not to specify “cookbook” parameters for the LPA laser, but rather refer the reader to the clinical endpoint descriptions as well as the most current guidelines from the manufacturer of the specific model of laser in use (Sample Form 1 and Sample Form 2).

5.

LEG TELANGIECTASIA TREATMENT

The principle of selective thermolysis also applies to laser treatment of vascular lesions, where the target chromophore is hemoglobin. The heat generated after absorption by hemoglobin is transferred from blood to the vessel wall. The goal is to achieve the optimal combination of laser wavelength, pulse duration, and fluence to inflict irreversible damage to a given vascular structure. Telangiectasias are dilated venules, capillaries, or arterioles visible to the human eye and measuring 0.1 –1.0 mm in diameter. Telangiectasia may further be classified into four categories based on clinical appearance: linear, arborizing, spider, and papular (39).

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Unwanted spider telangiectasias on legs occur in 29 – 41% of women and in 6 – 15% of men. Leg telangiectasias develop in the second to third decade due to a number of factors including heredity, obesity, pregnancy, and trauma. Sclerotherapy remains the best overall treatment option for leg telangiectasias. However, side effects with sclerotherapy include pigment changes, cutaneous necrosis, pain, scarring, telangiectatic matting, and recurrence of telangiectasias (19). The LPA laser is one among a variety of lasers that has been used for treating leg telangiectasias. Other lasers which have been used for leg telangiectasias include the 585 nm pulsed dye laser; the longer pulsed dye lasers of 585, 595, and 600 nm wavelengths; the long-pulse frequency-doubled 532 nm Nd:YAG laser; the 810 nm diode laser; and an intense pulse light device with a spectrum of 515– 1200 nm (40 – 46). The response of spider veins on the legs to these devices has been met with varying degrees of success. Sclerotherapy remains the gold standard. In addition, laser adverse effects are often comparable and sometimes greater than traditional sclerotherapy. Also treatment with these devices is usually more costly than sclerotherapy. Leg telangiectasias have been more difficult to treat than facial telangiectasias. Leg telangiectasias often have a deeper location and a larger diameter. Nonetheless, lasers are improving in the treatment of leg spider veins. Lasers can be especially useful in the treatment of telangiectatic matting, in cases recalcitrant to sclerotherapy, and for patients who cannot tolerate needles. The target chromophore for leg telangiectasias is oxyhemoglobin, though deoxyhemoglobin may also be a secondary target with this wavelength. Oxyhemoglobin has several distinct peaks. The LPA laser has been attractive as a potential leg vein treatment because of its wavelength of 755 nm. Compared to the other lasers with wavelengths from 532 to 600 nm, the LPA 755 nm was intended to take advantage of targeting the absorption peak of hemoglobin where there is decreased interference by melanin. Another factor to consider is pulse duration. Based on the concept of selective photothermolysis, the pulse duration of laser light should be equal to or less than the thermal relaxation time of the vessel treated. The optimal pulse duration varies according to the vessel size Goldman and Fitzpatrick found that small leg telangiectasias ,0.2 mm in diameter responded well to flash lamp pulsed dye treatments. Larger telangiectatic vessels need to be treated with longer wavelength lasers in order to achieve deeper penetration. The longer wavelength of the LPA is another motivation is its use. McDaniel and colleagues examined the effectiveness of the 755 nm LPA laser for the treatment of leg telangiectasias (19) (Figs. 13.3 and 13.4). Twenty-eight patients with variable sized telangiectasias were evaluated using five treatment parameters (15 J/cm2 1 pulse, 20 J/cm2 1 pulse, 20 J/cm2 2 pulses, 20 J/cm2 3 pulses, or 30 J/cm2 1 pulse). The optimal treatment parameters for LPA therapy as a solo treatment (without combination sclerotherapy) appeared to be 20 J/cm2, double pulsed at a repetition rate of 1 Hz. After three treatments at 4-week intervals, subjective grading indicated a 63% reduction in leg telangiectasias. Vessels were grouped into small (,0.4 mm), intermediate (0.4 – 1.0 mm), and large (1.0 –3.0 mm). Medium-diameter vessels responded best with small vessel diameters responding poorly. In the aforementioned LPA leg vein study, 23.4% hypertonic saline sclerotherapy was performed 3– 7 days after laser therapy (20 J/cm2, single pulsed, 5 ms) which resulted in an 87% reduction in leg telangiectasias. The study also examined biopsies after LPA treatment. The biopsies revealed that vessel wall endothelial cell necrosis occurs 3–7 days post-LPA treatment, with fibrosis occurring at 3 weeks (Figs. 13.5 and 13.6). The optimal clinical window for sclerotherapy


307

Figure 13.3 (a) Leg veins pretreatment. (b) Two weeks after single treatment with long-pulsed alexandrite laser, 20 J/cm2, 10 ms pulse duration, single pass with 10 mm spot size [from Ref. (19)].

was felt to coincide with the period of endothelial cell necrosis. Overall, the authors conclude that LPA therapy is most effective for leg telangiectasias 0.4–3.0 mm in diameter and is ineffective for veins ,0.4 mm. The combination of LPA with sclerotherapy showed the best results. Sclerotherapy is advised 3–21 days post-LPA treatment. Compression stockings of 10–20 mm may be useful (7 days during waking hours is recommended). Caution must be exercised in using LPA therapy in patients who are tanned, possess darker ethnic skin types, or have severely photoaged skin. Pigmentary changes (primarily hypopigmentation) may result; usually such changes are transient but may be long lasting. LPA laser treatment is better tolerated with the addition of a cooling device. Kauvar and Lou (47) demonstrated excellent clinical results using dynamic cooling to treat of leg veins with fluences up to 80 J/cm2. Twenty patients with 54 treatment sites consisting of vessels 0.3 –2.0 mm in diameter were treated once using a 755 nm, 3 ms alexandrite laser (Candela) with an 8 m spot. At the 12-week follow up, 65% of 51 treatment sites showed .75% clearance, and there was .50% clearance in an additional 22% of sites. Hyperpigmentation occurred in approximately one-third of patients, but resolved within 3 months. The dramatic response observed by Kauvar and Lou can be attributed to the safe use of higher laser energies afforded by the cryogen cooling (Sample Form 3 and Sample Form 4).

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Figure 13.4 (a) Leg veins pretreatment. (b) Three months after long-pulsed alexandrite laser and sclerotherapy showing postinflammatory hyperpigmentation which resolved by 5 months [from Ref. (19)].

6.

PSEUDOFOLLICULITIS BARBAE

Pseudofolliculitis barbae is a disorder in which short hairs curl over and reenter the skin leading to a foreign body inflammatory reaction. This condition can occur in all skin types, but is found most frequently among African Americans. Shaving is a predisposing factor. In early stages, the clinical presentation is follculitis-like with erythematous papules and pustules. In some chronic cases, keloid scarring, hyperpigmentation, and hypopigmentation may occur. Pseudofolliculitis barbae can be recalcitrant to traditional treatments of topical tretinoin, topical steroids, and topical and oral antibiotics. Permanent hair removal is the only definitive cure. Laser hair removal is currently being studied as an approach to this condition, and hopefully it will offer the advantages of better efficacy, safety, and efficiency over traditional forms of hair removal, such as surgical depilation and electrolysis. Nanni et al. (48) have published an abstract on successful treatment of pseudofollculitis barbae with a long pulsed alexandrite laser. Ten patients with pseudofolliculitis barbae and skin types IV or greater were treated with a 755 nm wavelength, 20 ms pulse duration, 12.5 mm nonoverlapping spot size, and fluences from 5 to 8 J/cm2.


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Figure 13.5 Histology with H&E stain, 45 magnification, showing telangiectasia 5 days after long-pulsed alexandrite laser treatment: 20 J/cm2, 10 ms pulse duration, single pass with 10 mm spot size [from Ref. (19)].

Patients were treated at 4-week intervals for a total of six treatments. All subjects achieved at least a 50% reduction in lesion count and subjective symptoms. One-fourth had a 75% or greater reduction in the signs and symptoms of pseudofolliculitis. No long-term side effects occurred. Hair regrowth was delayed for 4 months but was permanently removed (48).

Figure 13.6 Histology with H&E stain, 10 magnification, showing telangiectasia 21 days after long-pulsed alexandrite laser treatment: 20 J/cm2, 10 ms pulse duration, single pass with 10 mm spot size [from Ref. (19)].

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7.


NEW HORIZONS

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312 45. 46.

47. 48.

Slater, Newman, and McDaniel Weiss RA, Weiss MA, Goldman MP. Photothermal sclerosis of resistant telangiectatic leg and facial veins using the Photoderma VL. Lasers Surg Med 1996; 8:40– 41. Goldman MP, Martin DE, Fitzpatrick RE, Ruiz-Esparza J. Pulsed dye laser treatment of telangiectasias with and without subtherapeutic sclerotherapy. J Am Acad Dermatol 1990; 23:23 – 30. Kauvar AN, Lou WW. Pulsed alexandrite laser for the treatment of leg telangiectasia and reticular veins. Arch Dermatol 2000; 136:1371 – 1375. Nanni C, Brancacciio R, Cooperman M. Successful treatment of pseudo-folliculitis barbae with long-pulsed alexandrite laser irradiation (abstr). Lasers Surg Med 1999; (suppl 11):61.

Sample Form 1 LPA Laser for Hair Removal Consent Form The procedure planned is laser-assisted hair removal using a long-pulsed alexandrite laser. The purpose of this procedure is to diminish or remove hairs. This procedure may require one or more treatments and may not produce permanent hair removal. Alternative methods are electrolysis, other laser-assisted hair removals and various topical therapies, shaving, etc. I understand that the risks of this procedure include possible pain, infection, scarring, drug reactions or interactions or unforeseen complications. There is also a risk of mismatch in the color or the texture of the skin, temporary redness, hive-like reaction or bruising, brownish skin discoloration, activation of fever blisters (herpes), temporary increased susceptibility to sunburn or persistent pinkness for months. I understand that there is a possibility that this procedure will fail, be unsuccessful, need to be repeated, or may require additional treatment of complications. If tattooed “permanent” makeup or a “decorative” tattoo is in the area to be treated with laser hair removal, lightening of decorative tattoos, or blackening of makeup tattooing can occur. I understand my responsibility for properly fulfilling the appropriate aftercare instructions as explained by Dr. ______________________ , his nurse and/or any written or videotape instructions provided. Although part or all of the cost for this procedure may, in rare situations, be reimbursed by insurance companies, many policies/companies consider this procedure cosmetic or not covered for various other reasons. I understand that I am responsible for all costs whether or not covered by my insurance. I have been asked at this time whether I have any questions about this procedure, and I do not. I understand the procedure and accept the risks, and request that this procedure be performed on me by Dr. ______________________ , Physician’s Assistant, or one of his laser nurses, laser technicians, or other laser doctors.

Patient Name

Date of Surgery

Time of Surgery

Signature of Patient

Witness

Today’s Date


313

Sample Form 2 LPA Laser for Hair Removal Aftercare Instructions After Treatment: Hair should gradually fall out within seven to ten days; occasionally it takes up to two weeks. If desired, remaining hairs may be removed after 4 –5 days by GENTLY using a Loofa pad or a gentle exfoliating wash IF the skin is not irritated. Shaving or tweezing is permitted after one week. Things to Avoid: 1.

Do not apply harsh skin products for one week (astringents, alcohol, witch hazel, Retin-A, Renova, glycolic Acid (AHA) or similar products).

2.

Do not allow skin to become sunburned or go to tanning beds for two weeks before and after treatment.

3.

Do not bleach hair. Do not wax or tweeze 4 weeks before next treatment.

4.

Do not go in hot tubs, Jacuzzi, pool or ocean for one week to reduce chance of irritation or infection.

5.

If possible, do not apply makeup for 24 hours.

Things to Do: 1.

Use intermittent cold compresses or ice packs.

2.

Take Tylenol or Advil if uncomfortable.

3.

Aloe gel may also be applied to soothe skin.

If Blistering, Crusting, or Oozing Occurs: Apply hydrogen peroxide, then Polysporin or Bacitracin ointment and promptly call our office and speak to the doctor or nurse.

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Sample Form 3 LPA Laser (and Sclerotherapy) for Leg Vein Treatment Consent Form I acknowledge that I have had an in-depth discussion on vein sclerotherapy and/or laser treatment in layperson’s terms with my physician. I understand the techniques, the indication for and limitations of the procedure. I understand that complications which could occur include, but are not limited to, pain with injection or laser treatment, brown or white discoloration of skin, temporary muscle cramps, local or generalized allergic reaction, temporary ankle swelling, development of new fine veins around treated site, hair loss, lumpy feeling along the vein and even an open sore, infection or scar. Most of these problems are minor and will clear with proper treatment. If laser treatment is selected, there is also risk of accidental eye injury from the laser beam if I remove my protective eyewear. The infrequent occurrence of permanent skin discoloration, failure to improve, or unforeseen complications have been discussed. I understand that treatment may be performed with different solutions or various lasers. Dr. has discussed the advantages and disadvantages of each and the reason for selection of the method he believes is best suited for my individual circumstances. I understand that for 24 –48 hours the post-procedural course should not include: strenuous exercise (e.g., stairmaster, leg work) exercise classes (e.g., aerobics), heavy work, i.e. lifting or hauling, jogging, running and/or other types of leg movement over and above routine walking or working unless specifically approved or suggested by Dr. . If my profession is one that requires heavy work/exercise/activity, I understand it is strongly recommended that therapy be performed before a 1– 2 day period of off time, such as a weekend. I understand to obtain maximum benefits from treatment, the above regimen should be adhered to, and that very heavy exercise/work normally performed by me will be gradually re-introduced over a period of 2– 5 days. I also realize dressing or pressure stockings (which may be applied after the procedure in selected patients) may be infrequently recommended in very specific cases and should be considered part of the post-procedural course, because they aid in achieving the best results. Although part of all of the costs for this procedure is still occasionally reimbursed by insurance companies, most policies/companies may consider the procedure cosmetic or not covered for various reasons. I understand that I am responsible for all costs not covered by my insurance. Since multiple treatments are usually required, this consent continues for subsequent treatments by Dr. regardless of the time between treatments. I have been asked at this time whether I have questions about this procedure, and I do not. I understand the procedure and accept the risks, and request that this procedure be performed on me by Dr. .

Patient Name

Date of Surgery

Time of Surgery

Signature of Patient

Witness

Today’s Date


315

Sample Form 4 LPA Laser/Sclerotherapy for Leg Veins Aftercare Instructions 1.

Most patients may return to work immediately or the next day; however, it is recommended to avoid strenuous activities for 24 hours if possible (e.g., Aerobics, running, biking, etc.)

2.

Some redness, burning or very mild ankle swelling is normal in first 24 hours. Report any increasing redness, warmth or tenderness after 24 hours to our office immediately.

3.

Avoid aspirin products one week before and 3 –4 days after treatment (Tylenol two hours prior to treatment will help alleviate discomfort).

4.

Avoid sun exposure for 24 hours; avoid tanning beds for at least one week before and after treatment.

5.

Continue usual skin care except avoid sunburn. Do not use tanning beds for at least one week before and after treatment.

6.

Do not wax, use depilatories or have electrolysis performed without our prior approval.

7.

Call us for special instructions if any blisters form.

8.

Use of compression stockings for up to 7 days after treatment may be useful in some cases (your doctor will advise you if these are suggested).

Even very limited use of tanning beds now appears hazardous to your health. We advise to NEVER use tanning beds. The discussion of tanning beds is only because we acknowledge their frequent usage.

14 Diode Lasers Murad Alam and David A. Wrone Northwestern University, Chicago, Illinois, USA

Beatrice Berkes Loma Linda University, Loma Linda, California, USA

1. Introduction 2. Background and Scientific Basis 3. Indications: Efficacy, Technique, and Potential Complications 3.1. Pulsed Diode Lasers (800 nm) 3.1.1. Hair Removal 3.1.2. Pseudofollicultis Barbae 3.1.3. Leg Veins 3.1.4. Other Vascular Lesions 3.1.5. Pigmented Lesions 3.2. Bare Fiber Diode Lasers (800 nm) 3.2.1. Saphenous Vein Closure 3.3. Diode Laser (1450 nm) 3.3.1. Nonablative Rejuvenation 3.3.2. Acne 3.4. Research Applications of Diode Lasers 3.4.1. Photodynamic Therapy 3.4.2. Laser Tissue Soldering 3.4.3. Wound Healing 3.4.4. Squamous Cell Carcinoma (SCC) 3.4.5. Imaging 4. Conclusions References

1.

317 318 319 319 319 325 325 326 326 326 326 327 327 328 329 329 329 330 330 330 330 331

INTRODUCTION

Diode lasers are small semiconductors (1,2). They have no moving parts, and since they are extremely energy efficient, minimal cooling needs. Such devices are durable, and can function for very long periods. 317

318

Alam, Wrone, and Berkes

There is some variability in the wavelength, frequency, and pulse parameters of diode lasers. Commonly used emission wavelengths include 800, 940, and 1450 nm. Most devices in dermatologic use emit at approximately 800 nm, which is a physiologically useful output. This wavelength is less well absorbed by melanin than are shorter wavelengths, and coincides with a small peak of hemoglobin absorption that permits the treatment of vascular lesions. Available since 1962, diode lasers have only recently been adapted for medical use. At present, 800 nm diode lasers are used most commonly for hair removal. Diode-pumped, frequency-doubled Nd:YAG lasers (532 nm) are used for the treatment of fine facial telangiectasia. Leg veins may be treated with variable efficacy with diode lasers in the 800 – 950 nm range. Longer wavelength diode lasers, specifically the 1450 nm lasers, are used for nonablative reduction of fine periorificial wrinkles, as well as for treatment of active acne. Investigational research applications of diode lasers include photodynamic therapy of cutaneous malignancies, laser welding, and facilitation of wound healing. These and other indications are detailed below.

2.

BACKGROUND AND SCIENTIFIC BASIS

Along with gas lasers and solid-state lasers, diode lasers are one of major classes of lasers available today (Table 14.1) (3). Like most other lasers, diode lasers include an optical gain medium in a resonant optical cavity. Diode lasers are different from these other types primarily in their capacity to be directly pumped by an electric current. This process tends to culminate in more efficient operation. Power conversion efficiencies approaching or exceeding 50% are not unusual for a diode laser, while efficiencies approximating 1–10% are closer to the norm for gas and solid-state lasers, which are typically pumped by plasma excitation or incoherent optical flashlamp source, respectively. Given their longer cavities and more narrow gain bandwidth, gas and solid-state lasers do, however, usually have more coherent outputs than simple semiconductor lasers. More advanced single-frequency diode lasers can have linewidths in the low megahertz range, as do the other classes of lasers. The crucial components of diode lasers are much smaller than those of other types of laser devices. Gas and solid-state lasers are typically many tens of centimeters in length, but diode laser chips are about the size of a grain of salt. Packaging and containment results in an overall size increase to approximately 1 cm3. Another characteristic of diode lasers that has led to their ubiquitous use is their high level of reliability. The useful lifetime of gas or solid-state lasers may be thousands of hours, but finely constructed and mounted diode lasers have useful lifetimes measured in centuries. Table 14.1

Listing of Available Lasers

Laser Lightsheer Palomar SLP1000 Opus Medical F1 MedArt R 435 MedDioStar HC/C Dornier Medilas D Candela Smoothbeam

Wavelength (nm)

Fluence (J/cm2)

Spot sizes (mm)

Pulsewidth (ms)

Pulse rate (Hz)

Cooling

800 810 810 810 810 940 1450

10–60 Max 574 Max 21 –40 90 W (power) Max 64 Max 100 Max 8– 25

9, 12 (square) 4, 8, 12 (round) 5, 7 1–8, scanner 10, 12, 14 0.5–6 4, 6

5–100 50–1000 15–40; XLP 50–1000 Variable 200–2000 250

up to 2 up to 3 up to 4 Variable up to 4 up to 5 1

Contact Contact Contact Contact Contact Contact DCD

Diode Lasers

319

Crystal structure within diode lasers consists of gallium arsenide, which may be doped with an additional element, such as aluminum or silicon. Passage of electric current through a single diode results in emission of light from its edge or surface. Multiple-diode lasers arrayed in lines or two-dimensional formats can replace flashlamps in the pumping of solid-state lasers. Indeed, the use of diode laser to pump solidstate lasers, as in the case of the diode-pumped Nd:YAG (see chapter on pulsed KTP lasers), is one of the most successful recent applications of diode lasers. Such pumped lasers provide the best advantages of both technologies.

3.

INDICATIONS: EFFICACY, TECHNIQUE, AND POTENTIAL COMPLICATIONS

3.1. 3.1.1.

Pulsed Diode Lasers (800 nm) Hair Removal

The most common dermatologic application of the long-pulse diode laser is hair removal. In general, the treatment technique resembles that for other lasers, including the ruby laser (694 nm), the alexandrite laser (755 nm), the intense pulsed light source (590 –1200 nm), and the neodymium:yttrium –aluminum-garnet (Nd:YAG) laser (1064 nm), used for the same purpose. The 800– 810 nm diode laser also operates on the principle of selective photothermolysis of the melanin in the hair follicles. Multiple treatments at approximately 1 month intervals are required [Figs. 14.1(a)– (c)] and dark hair on light skin is treated most safely and effectively (Figs. 14.2 – 14.5).

Figure 14.1 (a) Picture of hairs (close up) before removal (dark hairs, light skin). (b) Picture of hairs (close up) after three treatments (30– 40% reduction). (c) Picture of hairs (close up) after six treatments (60 – 70% reduction, and residual hairs slightly lighter and thinner).

320

Figure 14.2


Picture of optimal candidate: very fair skin, dark black hair.

Mechanism. The mechanism for diode laser hair removal has been described in some detail. The target chromophore is melanin, which is found mostly in the epidermis, hair bulb, hair shaft, and bulge region and absorbs radiation at 300– 1200 nm (4 –10). For effective hair removal, the optimal laser beam for hair removal should penetrate 2 – 7 mm into the skin to encompass the entire follicle, specifically destroying the dermal papilla and the bulge region (11,12). Anagen hairs are believed to be most susceptible to laser injury, given that in the anagen phase stem cells migrate from the bulge to the dermal papilla,

Figure 14.3

Picture of suboptimal candidate: type II– III skin, brown hair.

Diode Lasers

Figure 14.4

321

Picture of suboptimal candidate: type IV – V skin, black hair.

where new hair is synthesized (13). The average depth of the anagen dermal papilla varies based on anatomic region, and may be 1 –4.7 mm deep, or commonly 2.5 –4 mm deep on the legs (13). For hair removal to be selective, thermal damage must be restricted to the follicle to prevent nonspecific tissue injury (15,16). Provided the pulse width is longer than the thermal relaxation time (TRT) (17) of adjacent structures but shorter than the TRT of hair follicles (40 –100 ms, for terminal hair follicles 200– 300 mm in diameter), the

Figure 14.5

Picture of suboptimal candidate: type I– II skin, blonde hair.

322


follicles can be heated beyond their thermal damage threshold while the surrounding epidermis and other tissues are relatively spared (18). A pulse duration in excess of the TRT of epidermis (3 – 10 ms) permits heat extraction from the skin surface during the laser firing (19). Q-switched lasers with exceedingly brief nanosecond pulse durations typically have been unable to produce permanent hair loss due their inability to induce terminal disruption of the follicle. Very long pulse durations permit greater heat diffusion into the hair shaft and bulb, thus inducing more even heat distribution, but if pulses are much longer than the TRT, the effective volume that is heated will exceed the bounds of the hair unit targeted (11). Epidermal cooling during laser use not only decreases discomfort but also protects the epidermis from thermal damage, allowing higher fluences to be used (11). The most common cooling modalities with the long-pulse diode laser are the actively cooled sapphire window or the pulsed cryogen spray. Dermal compression achieved with the cooled window may decrease the distance to the hair bulb and partially exclude blood during treatment. For hair removal, larger spot sizes have been recommended to make it easier to avoid undesirable overlapping and because larger surface areas, such as backs, may be covered faster (16). The ideal exposure spot for hair removal has been postulated to be 10 mm or greater in diameter (11). Radiation from the 800 nm diode laser is 30% less absorbed by melanin than the 694 nm ruby laser, but optical penetration into the dermis is superior with the former device as light penetration increases with wavelength to a maximum of approximately 1000 nm (20,21). In addition to being associated with less epidermal absorption than the ruby, the diode is associated with less water absorption than the Nd:YAG laser (13). Overall, the 800 nm wavelength is poorly absorbed by water. For darker skinned patients, longer wavelength lasers, such as the Nd:YAG may be preferable to the diode since longer wavelengths are less absorbed by melanin and less likely to cause epidermal damage (22). Efficacy. There have been several small- to medium-sized studies to investigate the efficacy of the diode laser for hair removal. Most of these have been performed with 800 –810 nm devices (4,13,16,17,20,22 –28). One to four treatments have been typically delivered usually to patients with Fitzpatrick skin types I–IV, and fluences and follow-up periods have varied. Table 14.2 lists the parameter selection based on skin Table 14.2 Treatment Parameters (Hair Removal/Lightsheer): Parameter Selection as a Function of Skin Type (9 9 Spot) Initial fluence (J/cm2)

Fluence range (J/cm2)

I

40

15 – 60

II

35

15 – 60

III

30

10 – 45

IV

20–25

10 – 40

15–20 10–15 One level darker than patient type

10 – 35 10 – 30 —

Fitzpatrick type

V VI Tanned skin (all types)

Pulse duration Auto 30 ms if high density Auto 30 ms if high density Auto—finer hair 30 ms—coarser, denser 30 ms—finer hair 100 ms—coarse, dense 100 ms 100 ms 100 ms

Diode Lasers

323

type. Outcome parameters have ranged from physical to photographic comparison, often by blinded observers, as well as serial hair counts. While methodologies and results have varied, some general conclusions can be offered (11,29,30). Growth delay or degree of permanent reduction of hair appears associated with the peak fluence of individual treatments as well as the number of treatments. As the time from the last treatment increases, so does regrowth, with a corresponding reduction in the degree of hair reduction. Histologically, even when severe hair unit damage is observed, hairs are seen in some cases to regenerate, presumably because part of the bulge apparatus was inadvertently preserved. Another factor limiting the hair removal benefit of individual treatments is that only hairs in anagen phase are generally considered vulnerable to permanent laser hair removal. This has led to the recommendation that tweezing or waxing be eschewed for several weeks prior to laser treatments, but some new data suggests that this may not be necessary to ensure efficacy (Fig. 14.6) (31). Thinner, lighter hairs are less effectively treated since the small diameter and low endogenous melanin results in quick cooling and insufficient injury. Conversely, coarser dark hairs that are not completely destroyed may become finer and lighter after treatment. See Table 14.3 for parameter selection as a function of hair type. Hair removal using the diode laser has been compared to similar laser procedures with other devices. In two studies of the long-pulse diode vs. the long-pulse alexandrite laser, three to four treatments with each device resulted in approximately equivalent immediate and long-term hair reduction, as well as similar histologic findings, in patients with skin types I– IV (16,25). An additional study found that the alexandrite laser for this laser was less painful than the diode, but the pain from each treatment was reduced by preapplication of topical 5% lidocaine cream to the relevant skin area (28). Different results may be the norm in darker-skinned patients. Diode lasers (810 nm) with super long pulse (SLP) durations (200 –1000 ms) may be particularly effective in treating African-American patients (23) and types II – IV patients with suntans (32). There is some evidence to indicate that even the less long pulse durations (e.g., 100 ms

Figure 14.6 Starting several weeks before treatment and continuing until the end of the laser hair removal treatments, patients typically refrain from plucking and waxing hairs, although new evidence suggests this may not be necessary. Clipping and shaving hairs during the laser treatment course has always been deemed acceptable.

324


Table 14.3 Treatment Parameters (Hair Removal/Lightsheer): Parameter Selection as a Function of Hair Type (9 9 Spot) Hair Light to medium brown Fine to medium diameter Light to medium brown Fine to medium diameter Dark brown to black Fine to medium diameter Dark brown to black Fine to medium diameter Dark brown to black Dark brown to black Light to dark brown Medium to large diameter Light to dark brown Medium to large diameter

Skin I –III

Hair density

Pulse duration

I –III

Lower density: axilla trunk, pubic, leg Higher density: cheeks upper lip, beard, chin Low and high density

Auto or 30 ms

I –III

Low and high density

Auto or 30 ms

IV IV V, VI

Low and high density Low and high density Low and high density

30 ms 30 or 100 ms 100 ms

Tanned

Low and high density

100 ms

I –III

Auto Auto or 30 ms

in a laser with 30– 100 ms range) may be safely used to treat patients with skin types V and VI, but postoperative complications may result (33). Far Eastern and Indian patients may likewise benefit from long-pulse lasers, although at least one study showed equivalent efficacy in hair reduction with normal pulse diode 800 nm diode laser and Nd:YAG laser for Chinese patients (22). Potential Complications. Unavoidable effects during treatment include mild pain or discomfort, followed by transient erythema and perifollicular edema that may last up to 24 h (Fig. 14.7). Other side effects (4,17,20,23,25,26,28,34) are more common at high fluences or in patients with relatively dark skin types. Vesiculation, blistering, erosions,

Figure 14.7 Perifollicular edema (goosebumps) and erythema right after laser (no hairs visible because they were shaved before laser treatment).

Diode Lasers

325

ulcerations, and crusting can occur in the short term, and these may culminate in longerlasting textural changes. Scarring is uncommon. More frequently, significant epidermal injury may lead to hyperpigmentation or hypopigmentation, which will almost always resolve within 6 months. Urticaria has been reported, and there is at least one report of urticarial vasculitis, possibly associated with the laser wavelength or the type of cooling used (34). Of course, a potential undesirable result is inadequate hair removal, or hair regrowth months to years after the last treatment. This problem may be remedied by more treatments, use of higher fluences or change of other parameters, and by substitution of the diode with another laser. For hair removal, the diode laser appears to be less painful than the Nd:YAG one (22,35). 3.1.2.

Pseudofollicultis Barbae

Pseudofolliculitis barbae, so-called “razor bumps,” have been treated with the 800 – 810 nm diode laser (17,36,37). The mechanism here appears to be hair removal, after which ingrown hairs and the resulting inflammatory, hyperpigmented, painful nodules are less likely. Multiple treatments at 4– 6-week intervals may reduce the incidence of pseudofolliculitis-associated papulopustules by 75%. There is variation among the recommended treatment settings, which range from 30– 38 J/cm2 and 20 ms pulse duration, to 10 J/cm2 at 30 ms (36,37). Black patients with pseudofolliculitis barbae may require up to 7 –10 treatments each, and pre- and posttreatment with 4% hydroquinone may be necessary to mitigate hyperpigmentation caused by the laser. During the treatment process, clear aloe vera gel (green-tinted gel is recognized as pigment and may burn the skin) can facilitate gliding of the handpiece over the skin, reduce friction trauma, and clear carbonated hair fragments from the lens. 3.1.3. Leg Veins While the diode laser is not commonly considered the most effective laser for the treatment of leg veins, it has been used for this purpose. At present, intense-pulsed light devices, pulsed-dye lasers, and most promisingly, Nd:YAG lasers, are more frequently employed in the treatment of small telangiectasia and medium-sized reticular veins of the legs. Efficacy. There are some data to confirm the efficacy of the long-pulsed diode for the treatment of leg veins. The 810 nm diode with super long pulse and sapphire-window cooling has been used to address smaller veins on the upper thighs and lower legs as well as larger reticular veins in the lower thigh and upper calves (38). Two treatments 4 – 6 weeks apart resulted in inconsistent but occasionally impressive outcomes, with 29% of the diode laser sites showing greater than 75% improvement, compared with 33% and 88% of the alexandrite laser and Nd:YAG laser sites, respectively, manifesting a commensurate degree of benefit. The 940 nm diode laser has also been reported to be successful for the treatment of leg veins (39). One report noted a greater than 50% clearance of vessels in 75% of subjects with a fluence of 300 – 350 J/cm2 using a single pass of a 1 mm spot at pulse width of 40 – 70 ms; at 815 J/cm2 and 50 ms using a 0.5 mm spot, greater than 75% improvement was noted in all subjects. Potential Complications. Short-term side effects after diode laser vein treatment include mild to moderate pain, urtication, and blurring of the treated vessels, all of which usually resolve within 24 h (38 –41). Hemosiderin deposition, especially in larger vessels, can culminate in hyperpigmentation along vessels (38). This can develop slowly and persist for weeks or months before gradually resolving. Hypopigmentation along the treated vessels, slight superficial textural changes, telangiectatic matting, and

326


significant inflammation have also been reported. Telangiectatic matting may be less of a problem with the diode than with the alexandrite or Nd:YAG lasers (38). However, compared to radiofrequency (RF) endovenous treatment, diode fiber treatment appears more likely to induce vessel wall perforations that permit fluid extravasation after treatment; additionally, the peak temperatures attained during laser fiber treatment can approach 10008C while RF peaks remain below 1008C (41). 3.1.4.


Mechanism. The vascular effect of the diode laser derives from the relatively deep penetration of long wavelength visible and near infrared light into the skin. Moreover, there is a small peak of hemoglobin absorption at 800– 900 nm (42,43). Efficacy. Spider veins to moderately deep larger reticular veins may be susceptible to 800, 810, 930, and 940 nm diode laser energy. Indeed, relatively larger vessels may respond better (42,43). The diode-pumped frequency-doubled 532 nm Nd:YAG laser is commonly used for the treatment of fine facial telangiectasia (44). This is a safe and effective device that can trace away fine vessels without the induction of purpura. Larger vessels on the nose or cheeks will often not resolve, and other vascular lasers, such as the pulsed-dye, or the intense-pulsed light device may be indicated if the further improvement is desired. 3.1.5.

Pigmented Lesions

The long-pulse diode laser is not the gold-standard for the treatment of pigmented lesions. In general, the most conservative authorities recommend that nevi and other structures potentially capable of malignant transformation not be deliberately treated with laser light, as this may theoretically induce atypia. Lentigines and tattoos, on the other hand, are most frequently treated with nanosecond domain Q-switched lasers. Efficacy. In one study assessing alternative treatments for solar lentigines, the diode-pumped 532 nm laser was compared to liquid nitrogen, the frequency-doubled Q-switched Nd:YAG 532 nm laser, and the krypton laser (521 and 530 nm) (45). While all the lasers were found to be superior to liquid nitrogen, the Q-switched device was associated with the least pain, erythema, and time to complete healing. The diodepumped laser was judged the second most effective modality. Potential Complications. Inadvertent treatment of nevi is possible during hair removal with the diode laser. Investigators noted new-onset clinical atypia without inflammation in preexisting nevi 1 month after patients underwent two laser hair treatments with the 810 nm device (46). Upon biopsy, the atypical nevi were found to be histologically similar, displaying subepidermal blisters and elongation and disruption of nevus cells. Only small foci of nevus cells could be identified in some specimens, all of which had homogenization of papillary dermal collagen. 3.2. 3.2.1.

Bare Fiber Diode Lasers (800 nm) Saphenous Vein Closure

Bare diode fibers have also been threaded into leg veins in interventional procedures designed to collapse these veins. In one study, an 810 nm sterile bare-tipped laser fiber was placed into vessels via percutaneous or stab wound incisions (40). Energy was delivered endovenously 1– 2 cm below the saphenofemoral junction and along the course of the greater saphenous vein while the fully advanced catheter was withdrawn in 3– 5 mm tugs.

Diode Lasers

327

Ten to 14 W were delivered in 1– 2 s bursts, treatment was followed by the wearing of class II (30 – 40 mmHg) support stockings, and sclerotherapy was used to treat the remaining branch varicosities after closure of the greater saphenous vein. The authors reported 100% short-term efficacy of the laser technique. In comparison with endovenous occlusion using RF energy aimed at sapheno-femoral reflux, laser occlusion of varicose veins appears relatively less efficacious. When an 810 nm bare-tipped diode fiber and a RF device were used on three goat jugular veins, the diameter of the lasered vessels was reduced by 26%, vs. 77% shrinkage with RF application (41). The technique of endoveneous laser therapy (EVLT) is obviously more complex than use of a standard out-of-the-box 800 – 810 nm diode laser (41). The bare-tipped optical fiber used is typically 600 mm in diameter, the target vein is compressed with tumescent anesthesia prior to entry to exclude intravenous blood as a chromophore, placement may be facilitated with duplex ultrasound guidance, and brief pulses are delivered as the fiber is pulled out at a steady rate.

3.3.

Diode Laser (1450 nm)

The 1450 nm diode laser is a 14 W device (Smoothbeam, Candela Corp, Wayland, MA) that also emits in the mid-infrared range. In investigational protocols, pulse widths of 160 – 260 ms have been used with a repetition rate of 0.5 –1.0 Hz. Cooling is via a dynamic cooling device (DCD), and laser energy is delivered through a 4 or 6 mm spot size (47).

3.3.1. Nonablative Rejuvenation Nonablative laser resurfacing is a process in which the epidermis is left grossly intact and the dermis is selectively heated by laser light so as to yield increase in collagen deposition and subjective improvement in the appearance of photodamaged skin. Efficacy. Very little published research is available regarding the nonablative efficacy of the 1450 nm diode laser, which is marketed as a nonablative device. An early report (48) indicated that the 980 nm diode laser emitting at 25 W, at a pulse duration of 400 ms, and 1 Hz, successfully treated in vitro breast and facial skin in a nonablative manner. Tissue shrinkage was immediately apparent after treatment, and new collagen formation was demonstrated by histology after 21 days. The epidermis was not visibly ablated. More recently, nonablative resurfacing of facial rhytides has been achieved with the 1450 nm diode laser, which is now the diode laser of choice for this indication (47). Goldberg et al. (47) in a recent study involving 19 women and 1 man, who collectively spanned Fitzpatrick skin types I– IV, and ranged in age from 42 to 70 years, treated Glogau class I and class II rhytides. In 12 subjects, the treated rhytides were perioribital, and in the remainder, they were perioral. Two to four treatment sessions, at 1-month intervals, were performed for each patient. Unfortunately, Goldberg et al., do not provide any treatment parameters such as fluence, pulse width, repetition rate, or number of passes. Outcome measures were pre- and postoperative photography, pre- and postoperative optical profilometry, and clinical assessment. Seven of 20 patients showed no obvious improvement after treatment, 10 experienced mild improvement, and 3 had moderate improvement at the sites of their laser-treated rhytides. Clinical improvement was correlated with optical profilometry findings but not with the number of treatments. Perioral sites were least improved.

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Additional studies are apparently in preparation. Tanzi and Alster (49 –51) describe studies in which they have found randomized patients to receiving treatment to either the left or the right sides of their faces, with the contralateral side serving as a control. A study of 20 patients has examined treatment of transverse neck lines, and outcome measures have included blinded rater assessment as well as in vivo microtopography (PRIMOS Imaging System; GFM, Germany). In this investigation, mean fluences of 11.6 J/cm2 were used with a 6 mm spot and cooling settings of 10 ms of precool, 20 ms of intracool, and 20 ms of postcool. According to Tanzi and Alster, the treated sides experienced clinical and histologic improvement of rhytides, with periorbital rhytides improving more than perioral rhytides. Three-dimensional in vivo microtopography confirmed this clinical finding. For the treatment of atrophic facial scars, 1450 nm diode laser has been compared to 1320 nm Nd:YAG laser, according to a pending study of 20 patients in which the diode treated side received fluences of 9– 14 J/cm2 via nonoverlapping 6 mm spots during a single pass. Possibly, the 1450 nm laser may be superior to the 1320 nm Nd:YAG device for nonablative treatment of atrophic facial scars. Potential Complications. Immediate erythema almost always occurs after nonablative use of the 1450 nm laser for treatment of facial rhytides. This can vary from mild to severe and may be concomitant with the emergence of small edematous papules, lasting 1– 7 days, which were first noted by Goldberg et al. (47). Postinflammatory hyperpigmentation is rare, and hypopigmentation, persistent erythema, and scarring are not reported. Overall, nonablative resurfacing is considered a “lunchtime” procedure, with rapidly resolving erythema and edema that is camouflaged by cosmetic cover-up. 3.3.2. Acne The 1450 nm laser has also been used for treatment of active acne. Acne treatment can be considered an extension of the nonablative applications of this laser since the mechanism, directed dermal injury, appears to be the same. Specifically, acne appeared improved following the laser-induced necrosis of sebaceous glands. Efficacy. Acne treatment with the 1450 nm device has been reported in studies that have targeted back acne. After recruiting 27 male subjects with back acne, Paithankar and colleagues (53) randomized a 36 cm2 area on one side of each back to be the treatment site, with an equivalent-sized area on the other side serving as a control treated with cryogen alone. Four treatments spaced 3 weeks apart were administered to the entire treatment sites, rather than to just where acneiform papules had been marked. The average treatment fluence was 18 J/cm2. Apart from clinical assessments, outcome measures included lesion counts and skin biopsies immediately after treatment, and at 6, 12, and 24-week follow-up visits. Paithankar et al. (53) found a statistically and clinically significant reduction in acne lesion counts after treatment, and the mean reduction was five or more lesions. Fourteen of the 15 patients completing their 24-week follow-up had no residual acne lesions on their treated areas. Histologic findings were epidermal preservation but rupture of the pilosebaceous unit and thermal coagulation of the sebaceous lobule and follicle. Given the low density of sebaceous glands on the back, these changes were not observed in many biopsy samples. The authors report that long-term follow-up biopsies of similarly treated back and face skin showed no difference from baseline in adnexal structures, including sebaceous glands and follicles. Significantly, research with shorter pulse (810 nm) diode lasers used in combination with indocyanine green (ICG) dye has indicated similar transient necrosis of sebaceous glands followed by long-term improvement

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of acne (54). The underlying mechanism of epidermal sparing and dermal injury is consistent with the nonablative paradigm and different from aminolevulinic acid (ALA)-photodynamic therapy (PDT) and other laser/light based acne treatments that achieve their effect by depopulating P. acnes. Further studies of the treatment of facial acne are under way. Potential Complications. After the use of this laser for nonablative treatment of acne, side effects are similar as for the nonablative rejuvenation indication (15). The hallmarks are erythema and edema, with mild to severe hyperpigmentation in about 10% of subjects. Purpura and scarring are not seen.

3.4. 3.4.1.

Research Applications of Diode Lasers Photodynamic Therapy

One use of the diode laser is as the light source in the PDT of nonmelanoma skin cancers and other cutaneous malignancies (55) (see chapter on PDT). Diode lasers with wavelengths ranging from 600 to over 800 nm have been employed for this purpose, and some unusual treatment protocols have been attempted. For instance, pretreatment with the 1064 nm Q-switched Nd:YAG laser may enhance the susceptibility of melanoma to conventional photodynamic therapy with the 774 nm diode laser and injected Si(IV)-naphthalocyanine (56). At a fluence of 100 J/cm2, the 805 nm diode has also been demonstrated to be effective in the photodynamic therapy of AIDS-associated Kaposi’s sarcoma using ICG dye as the photosensitizer (57). Cutaneous Kaposi’s patients can expect blistering and crusting to heal within 2 weeks, after which they may have residual hyperpigmentation and an atrophic scar. Remissions have been noted to last at least 2 years (58). Other diodes used in photodynamic therapy include the 652 nm laser (59,60). 3.4.2.

Laser Tissue Soldering

Mechanism. Laser-assisted tissue soldering entails concurrent use of diode laser light and a solder mixture, including human albumin, hyaluronic acid, and ICG dye, that was developed at Columbia University (61,62). ICG is a tricarbocyanine dye with peak absorption between 780 and 805 nm (63,64). Efficacy. Some investigators have found that laser tissue soldering is effective for the closure of skin wounds. In one experiment, suturing was found to be faster than soldering, but tensile strength of the soldered wounds was immediately equivalent to that of sutured wounds at 7– 10 days (61). At 14 days, the laser soldered wounds continued to be stronger than the sutured sites, and no thermal injury or foreign body reactions marred the soldered areas. Another study observed little benefit to increasing ICG concentration during the soldering process, with wound tensile strength being more a function of laser power density (65). While higher fluences were associated with more secure closure, very high fluences also increased thermal damage, possibly compromising day 10 tensile strength. Indeed, high fluences may permit the laser solder process to function as an ablative modality comparable to CO2 laser for the removal of superficial cutaneous lesions (63). Laser-assisted closure may be useful even if solder is not used. When, after wounds were closed with deep sutures, superficial closure was attempted by either laser-assisted skin closure using an 815 nm diode laser or by the insertion of superficial sutures, the lasered wounds were treated more quickly, healed faster, developed better scars, and

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demonstrated greater tensile strength (66). The dearth of studies in this area suggests the need for more research to verify these results. 3.4.3.

Wound Healing

There have been reports that recurrent application of low-power diode laser energy can facilitate local wound healing. Six treatments from postoperative day 8 to day 26 with a 830 nm diode laser having a 0.03 cm2 spot size and fluence range of 0.5– 2.0 J/cm2 were reported to improve survival of skin grafts threatened by hematomas (67). Similarly, laser irradiation for 6 min per day for five consecutive days apparently increased survival of skin flaps in experimental subjects compared to controls (68). The mechanism is not understood but possibly laser stimulation of vessel proliferation may occur. Another low power (1.5 W) 815 nm diode laser system was found to induce expression of heat shock protein in rat skin, with this potentially contributing to tissue regrowth and rapid wound healing (69). A schedule of 12 daily and alternate day treatments with a 904 nm diode laser have been noted to result in diminished musculoskeletal discomfort associated with injuries and degenerative processes (70). Similar beneficial results have been seen with the joint application of diode laser and hyperbaric oxygen therapy in ischemic and diabetic wounds in rats, as well as in acute and chronic wounds in humans, including children, crew members on a submarine, and Navy SEAL team personnel (71). When surgical incisions are made with the diode laser, at 7, 14, and 21 days postinjury, the tensile strength of these healing wounds is less than that of similar incisions made with a scalpel (72). Laser incisions have more inflammation, a lag in fibroblast invasion, and delayed collagen production. 3.4.4.

Squamous Cell Carcinoma (SCC)

PDT for skin cancers has been performed with diode lasers, and is discussed extensively elsewhere in this book. Additionally, there is a single report (73) of diode laser used in direct treatment of cutaneous SCC. Specifically, multiple passes of carbon dioxide laser were used to debulk a 5 mm margin around visible SCC, and then a final pass with the 810 nm diode laser at 60 J/cm2, 30 ms pulse duration, and with a 9 9 mm spot size was used to remove hair follicles at the periphery. Follicular necrosis at the wound edges was confirmed by skin biopsy. The authors suggested that concurrent use of the diode laser may optimize the cure rate of SCC in nonglabrous skin. 3.4.5.

Imaging

Diode lasers can be used for skin imaging. A sensor mounted on a movable table can analyze healing wounds in a three-dimensional format which permits calculation of the lesion volume (74). Estimation of burn depth in burn wounds can also be performed with a diode laser (75). After the injection of ICG dye into the affected site, illumination with a 785 nm diode laser has been found to demonstrate a burn depth that correlates well with histology. 4.

CONCLUSIONS

While the diode laser is most commonly used for hair removal, it has been successfully applied to the treatment of vascular lesions, including leg veins. Data on the efficacy and safety profiles of less common indications is limited. Given current trends, nonablative resurfacing is likely to become a major application in the future.

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Laser Hair Removal/Diode Laser Consent Form Lasers and other powerful light sources have been shown to reduce hair growth in many individuals. These technologies have been in use for several years. They operate by destroying the region that makes new hairs while sparing the rest of the skin from damage. However, there are risks, described below, that you should be aware of:

The treatment itself is associated with mild stinging discomfort that lasts while the laser is being used. Creams can be applied an hour before treatment to numb the skin to reduce this discomfort.

Blisters, scabs, crusts, and eroded areas can occasionally develop after treatment. These can last 1– 2 weeks, and usually are not associated with permanent effects. Redness can sometimes last for several weeks after treatment.

Darkening (hyperpigmentation) or lightening (hypopigmentation) of the treated skin area can occur. This is more common in dark-skinned or tanned individuals, and usually goes away completely with time. Skin darkening may be treated with bleaching agents and other medicines.

Bruising can occur after treatment and last up to two weeks. This bruising may change from a light purple to a dark purple/black, and then gradually fade as a brown discoloration of the skin. The brown color may not completely go away for several months.

Swelling after treatment can last up to a week. Some people experience more swelling, which is most common on the cheeks and upper lip. Redness associated with this swelling can be concealed by make-up, and ice-packs may help reduce the swelling.

Infection can occur. This is uncommon, but may require treatment with antibiotic ointments or oral antibiotics.

Changes in the texture of the skin and scarring can occur. These are uncommon side effects.

In most people, many treatments will be needed to provide enough hair removal for them to be satisfied. Hair removal may not be permanent, and some or all of the removed hair may regrow. Often the regrown hair will be lighter and thinner than before the treatment.

In some people, laser light can increase the growth of hair. This is uncommon, and when it is seen, tends to occur among darker skinned patients ethnically from southern Europe and the Mediterranean region. There are several steps you can take to help you get the good results from this treatment and have a low risk of side effects:

You will be given protective eyewear during the procedure to protect you from the laser light. We recommend that you wear this as directed, and additionally, we also recommend that you keep your eyes closed while the laser is on.

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After the treatment, you can apply ice-packs or a cool dressing to soothe the area. We also recommend that you use a moisturizing ointment once or twice a day at home for the first week after treatment. During this time, clean the treated area gently.

Sunlight can cause skin aging and increase the risk of skin cancer. The risks of sunlight are even greater after a laser procedure, so we recommend that you reduce sun exposure as much as possible for 4– 6 weeks after the treatment. You should also wear sunscreen and a hat when you go out.

Please take this opportunity to make sure that you have shared your complete medical, surgical, and drug history with your physician. Knowing this information will help us treat you safely and appropriately.

If you have any problems with this procedure, please let us know as soon as possible so that we may take appropriate steps to protect your health. Before we can begin, please review the following statements: I certify that my physician has discussed this procedure with me and I have had an opportunity to ask questions about my condition, treatment procedure, risks and hazards involved. I believe I understand this procedure well enough to give permission to receive it. I further understand that rare or uncommon side effects that have not been discussed may occur, and there is no guarantee that this treatment will result in satisfactory hair removal. I request performance of the procedure described above. I also will follow the instructions. I have been given and notify the physician of any problems after the treatment. I agree to have before and after photographs taken. These photographs will be maintained in a confidential database, and may be used for educational purposes, including publication.

Patient/Guardian Name Patient/Guardian Signature Date I have explained the purpose, technique, benefits, and side effects of the laser hair removal procedure and alternative procedures. I have answered all questions and believe that the patient/guardian understands the procedure and its limitations.

Clinical Staff Signature

Date

Physician Signature

Date

15 Long-Pulsed Nd:YAG (1064 nm) Lasers Neil Sadick Weil Medical College of Cornell University, New York, USA


1. Introduction 2. Laser Physics 2.1. Wavelength 2.2. Pulse Duration 2.3. Spot Size 2.4. Skin Cooling and Epidermal Protection 3. Laser Tissue Interaction 3.1. Vascular Lesions 3.2. Hair Removal 3.3. Skin Rejuvenation 4. Clinical Studies 4.1. Vascular Lesions 4.2. Hair Removal and Pseudofolliculitis Barbae 4.3. Skin Rejuvenation 5. Presently Available Long-Pulsed Nd:YAG Lasers 6. Treatment Guidelines 6.1. Vascular Lesions 6.2. Hair Removal and Pseudofolliculitis Barbae 6.3. Skin Rejuvenation 7. Complications and Their Management 8. Conclusions References

1.

337 338 338 339 340 340 340 340 341 342 342 342 344 345 347 348 348 349 351 352 352 353

INTRODUCTION

The long-pulsed Nd:YAG laser has gained increasing popularity over recent years for treatment of both vascular and pigmented lesions as well as skin rejuvenation. 337

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Sadick and Kauvar

The advantages of the 1064 nm wavelength are its deeply penetrating wavelength coupled with its hemoglobin absorption and to a lesser extent, water, and melanin absorption. Vascular lesions presently treated with the long-pulsed Nd:YAG laser include facial and leg telangiectasia, venulectasia and veins, spider and acquired angiomas, venous lakes, and larger vessel vascular malformations. Hair removal is another application of long pulsed Nd:YAG lasers which exhibit high safety profiles in the treatment of Fitzpatrick phototypes IV – VI as well as suntanned skin. The 1064 nm lasers are also being employed for rejuvenation of photodamaged skin based on their ability to heat dermal water and stimulate collagen production.

2.

LASER PHYSICS

2.1.

Wavelength

At 1064 nm, there is weak melanin, hemoglobin, and water absorption. The absorption by these discrete chromophores is low compared to vascular-specific and pigment-specific lasers, and the water absortion is much lower at 1064 nm compared to the mid-infrared wavelengths of 1.3– 1.5 mm (Fig. 15.1). Nd:YAG laser irradiation produces deeply penetrating photons into the dermis due to decreased scattering of light at this wavelength (1). The lack of very strong absorbing chromophores coupled with good dermal penetration results in deep tissue heating. Skin irradiation at 1064 nm produces volumetric heating of a cylinder of tissue below the laser pulse, extending millimeters into the dermis (Fig. 15.2). A 5 and 10 mm spot produce depth of penetrations of 5 and 10 mm, respectively, in skin.

20,000 10,000 Hb Absorbance (cm–1)

1000 Water 100 Melanin 10 HbO2 1

0.1 200

1000

5000

Wavelength (nm)

Figure 15.1 Absorption spectra of major skin pigments at concentrations for which they typically occur. Values shown are absorption coefficients (ma) for pure water, human hemoglobins at 11 g/dL, and dihydroxyphenylalanine (DOPA)-melanin, which has an absorption spectrum similar to pigmented epidermis at 15-mg/dL concentration to water. DOPA-melanin concentration shown is approximately equivalent to heavily pigmented human epidermis. Absorption coefficient of single melanosomes is unknown. Hb, Hemoglobin; HbO2, oxyhemoglobin. [Taken from Anderson RR (22).]

Long-Pulsed Nd:YAG (1064 nm) Lasers

Figure 15.2

2.2.

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The depth of penetration increases with larger spot sizes. (Courtesy of Laserscope).

Pulse Duration

The theory of selective photothermolysis developed by Anderson and Parrish (2) describes the necessary requirements for selective destruction of site-specific targets in tissue using electromagnetic radiation. Selective targeting of tissue targets requires (a) the use of a wavelength preferentially absorbed by the chromophore, (b) a pulse duration less than or equal than the thermal relaxation time (TRT), or cooling time, of the targeted structure, and (c) sufficient fluence to produce irreversible damage. In 2001, Drs. Altshules, Anderson, and colleagues proposed the extended theory of selective photothermolysis (3), which describes the pulse duration requirements for nonuniformly pigmented structures in tissue, such as blood vessels and hair follicles. When treating a tattoo or pigmented lesion, heating of the structure will destroy the lesion, and the heat does not flow out of the target until it is fully damaged. When targeting a nonuniform structure, such as a blood vessel or a hair follicle, there are portions of the structure that exhibit much greater absorption than others. The weakly absorbing portions of the structure are then damaged by heat diffusion from the highly absorbing areas of the structure. In the case of a leg vein, the blood is the “absorber,” but closure of the vein requires coagulation of the vein wall which must be heated by diffusion from the blood. Similarly, the hair shaft and matrix cells are the “absorbers” for hair follicles, but the other follicular tissues including the stem cells do not contain chromophores absorbing in the near-infrared. Consequently, the treatment pulse duration for nonuniformly pigmented targets is significantly longer than the thermal relaxation time, and has been termed the thermal damage time (TDT).

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Spot Size

Large spot sizes (Fig 15.2) will enhance photon penetration and will heat a deeper zone of tissue due to a reduction in the scattering of the photons. Light scattering occurs at the periphery of the beam and becomes less of a factor with larger spot sizes where the ratio of the surface area to the circumference of the beam is increased. A spot size of 1, 5, and 10 mm can be expected to produce approximate depths of penetration of 1, 5, and 10 mm in tissue. 2.4.

Skin Cooling and Epidermal Protection

Skin cooling for epidermal protection is essential with millisecond-domain Nd:YAG lasers. Heat must be extracted from the skin’s surface to prevent epidermal damage resulting from heat diffusion following volumetric heating of the dermis. Proper skin cooling techniques are essential to avoid epidermal damage and full thickness skin burns, particularly when very high fluencies are used for the treatment of vascular lesions. Inadvertent pulse overlapping and pulse stacking can lead to blisters, epidermal necrosis, and full thickness burns. Skin cooling techniques used with Nd:YAG lasers include cryogen spray cooling, contact cooling, and air cooling (Figs. 15.3 and 15.4).

3. 3.1.

LASER TISSUE INTERACTION Vascular Lesions

The 1064 nm wavelength exhibits oxyhemoglobin absorption as well as deep penetration into the dermis. There is a broad oxyhemoglobin absorption peak beyond 900 nm (Fig. 15.1) which enables selective photocoagulation of blood vessels when sufficiently high fluences are used. Compared to pulsed potassium – titanyl – phosphate (KTP) lasers (532 nm) and pulsed dye lasers (585 –600 nm) which penetrate skin to a depth of 1– 1.5 mm, the 1064 nm wavelength can penetrate skin to a depth of 5 – 10 mm (3) because of its lower scattering coefficient. The development of the pulsed Nd:YAG

Figure 15.3 Contact cooling with a water-cooled sapphire tip on the Laserscope Lyra handpiece.


Figure 15.4

341

Cryogen spray cooling on the Candela GentleYAG.

laser greatly improved our ability to photocoagulate leg telangiectasia and reticular veins. Leg veins, compared to facial telangiectasia, have larger diameters, thicker vessel walls, a deeper location in skin and elevated hydrostatic pressures (4). The use of shorter, visible light wavelengths for vessels of larger diameter and deeper location produces partial vessel damage by photocoagulating a superficial layer of blood in the vessel (5). Full thickness coagulation and endothelial wall heating is required for vessel closure and irreversible damage. When sufficiently high fluences are used, and pulse durations are chosen to match the thermal damage times of the vessels, Nd:YAG lasers will safely and effectively photocoagulate telangiectasia and veins up to 4 mm in diameter. Heat diffusing from the blood will irreversibly damage the vessel wall. Pulsed Nd:YAG lasers may be used for the treatment of a wide range of vascular lesions including facial and leg telangiectasia, venulectasia and veins, venous lakes, spider and acquired angiomas, and venular vascular malformations. Pulse durations used for the treatment of telangictasia, venulectasia, and veins range from 20 to 100 ms, and full thickness coagulation of the vessels appears to be relativley independent of the chosen pulse duration within this range, assuming sufficient fluence is utilized. 3.2.

Hair Removal

The deep penetration depth of the Nd:YAG laser is also an advantage in laser hair removal because the hair follicles reside several millimeters below the skin surface. Melanin in the

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hair shaft and follicle provides the major chromophore for laser targeting of hair. The hair shaft and the bulb are the most melanin-rich portions of the anagen hair follicle, but the two potentially important targets for permanent inactivation of hair growth are the bulb, comprising the neurovascular papilla at the base of anagen hair follicles that supplies the matrix to produce the hair shaft, and the stem cells residing in the bulge, an area located near the insertion of the arrector pili muscle and residing 1.5 mm below the skin surface. Permanent hair removal is accomplished by thermally damaging the entire hair follicle tissues via heating of the pigmented portions of the follicle. Thermal damage times for hair follicles are in the 30 –100 ms range (6). Laser hair removal requires lasers that will target melanin in the hair follicles while avoiding damage in the pigmented epidermis. The shorter wavelengths used for hair removal including 694, 755, and 810 nm have higher melanin absorption coefficients, and the epidermis is protected by means of various cooling techniques used to prevent laser heating of the epidermal pigment. Melanin absorption at 1064 nm is lower, decreasing the risk of side effects related to damage of the melanin-containing epidermis, but sufficient to provide selective photothermolysis of the pigmented hair follicle. Of the hair removal systems that are available today, the 1064 nm laser provides the highest margin of safety for laser hair removal in phototypes V and VI skin. In individuals with phototypes V and VI, the pigmented hair follicle is usually darker than the pigmented epidermis. Although melanin absorption at 1064 nm is relatively weak, we can take advantage of the differences between the melanin concentration in the epidermis and the hair bulb and shaft. The relative absorption of 1064 nm laser light for black coarse hair is 1.5 times that of a deeply pigmented epidermis (7). With the application of deep cooling, the relative light absorption by the follicles allows selective heating of hairs without epidermal damage. 3.3.

Skin Rejuvenation

Water absorption at 1064 nm is weak compared to the mid-infrared wavelengths used for rejuvenation. The deep scattering at this wavelength and relatively weak absorption by the skin’s major chromphores results in volumetric heating of the dermis. When epidermal cooling methods are properly employed, the dermis is heated without the creation of an epidermal wound. This results in fibroblast activation and new collagen production. Electron microscopic analysis of skin following irradiation with a 1064 nm laser, pulse duration of 300 ms, spot size of 5 mm, and fluence of 13 J/cm2, showed a decrease in the collagen fiber diameter in the papillary dermis 1 and 3 months after treatment (8). This finding is consistent with the deposition of new collagen. Histological studies by Lee (9) demonstrated a zone of new collagen measuring 150 –200 mm following six treatments with a combination of a KTP and Nd:YAG laser. Six treatments with the Nd:YAG laser alone produced, in skin biopsies taken from treated skin of the inner arm, a new band of collagen measuring 50– 80 mm. Several clinical studies have demonstrated that skin textural improvement and tightening can be achieved using 1064 nm lasers (9 –11).

4. 4.1.

CLINICAL STUDIES Vascular Lesions

The first report of successful leg vein treatment with an Nd:YAG laser was using the Vasculight (Lumenis) (12) A 6 mm spot was used with pulse durations of 10 to 30 ms and fluences of 80– 120 J/cm2 with 75% clearance achieved at 3 months follow up. Similar results were reported by Kauvar et al. (13,14) using the Cool Glide (Atlus/Cutera) with


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a 10 mm spot, 50 mm pulse duration and a fluence of 100 J/m2 (9), and the Lyra (Laserscope), using a 3 mm spot, a 50 mm pulse duration, and a fluence of 150 J/cm2 (13). A comparative pilot study (15) evaluating leg vein treatment with a long-pulsed Nd:YAG laser and sclerotherapy demonstrated equivalent efficacy and side effect profiles. Sadick (16) found 64% of 24 patients showed .75% improvement at 1 year follow-up following a maximum of three treatments for vessels 0.204 mm in diameter. Matched bilateral patches of leg veins were treated in 20 patients, where one side was randomized to Nd:YAG laser treatment and the other to sotradechol sclerotherapy. One to Two treatments were performed at 8-week intervals. Clearing of laser treated areas was 2.5/4 compared to 2.3/4 for the sclerotherapy treated sites. There was no statistical difference between these side effects profiles observed on the sclerotherapy treated side and the laser treated side. This study demonstrated that equivalent results could be achieved with a long-pulsed Nd:YAG laser to sclerotherapy treatment. Facial telangictasia and veins have also been successfully treated with the long pulsed Nd:YAG laser (17). Thirty two sites were treated in 17 patients with skin types I– IV using an Nd:YAG laser equipped with cryogen cooling. Vessels up to 1 mm were treated with a 6 mm spot, 25 ms pulse width and a fluence of 125– 150 J/cm2. Reticular veins were treated with a 6 mm spot, 50– 100 ms pulse width and fluence of 150 J/cm2. Excellent resolution of the reticular veins was observed in the reticular veins, and good clearance in the telangictasia. In the authors’, experience excellent clearance of facial vessels .0.2 mm in diameter can be achieved with the appropriate pulse width and fluence combinations (Figs. 15.5– 15.7).

Figure 15.5 Before (a), immediately after 9 (b), and 3 weeks following treatment (c) with the GentleYAG 1064 nm laser using a 3 mm spot, 280 J/cm2, 40 ms pulse duration and a cryogen spray of 40 ms. (Courtesy of Candela.)

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Figure 15.6

4.2.

Before and 6 weeks after treatment with a 1064 nm laser. (Courtesy of Laserscope.)

Hair Removal and Pseudofolliculitis Barbae

A histological study of the long-pulsed Nd:YAG laser was preformed 24 – 72 h following laser irradiation of black hair using a 50 ms laser. Fluence dependent selective thermal injury to hair follicles was demonstrated with an average depth of injury being 1.06, 0.85, and 1.1 mm for fluences of 30, 50, and 100 J/m2, respectively (18). A prospective clinical study (19) of lower extremity hair removal was preformed in 29 subjects. Five test areas were treated 1– 5 times at monthly intervals. Up to five treatments produced hair loss of 71.5%, and a 40% reduction in hair was maintained at 1 year follow-up. Tanzi and Alster (20) studied 36 subjects with phototype I –VI skin and dark terminal hair with a 1064 nm using a 10 mm spot size at 30– 60 J/m2. Pulse durations were 10, 20, and 30 ms, respectively, for skin types I/II, III/VI, and V/IV. At 6 months following three consecutive laser treatments, there was a mean hair reduction of 41 – 40% on the face


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Figure 15.7 Treatment of nasal vessels with the GentleYAG using a 3 mm spot, 130 J/cm2, 20 ms pulse and cryogen spray of 40 ms. (Courtesy of Dr. Eubanks and Candela.)

and 48– 53% on the body. Ross et al. (21) demonstrated that a long-pulsed Nd:YAG laser equipped with contact cooling provided excellent cleaning of pseudofolliculitis barbae in skin types IV – VI. All test sites received treatment with a pulse duration of 50 ms. Five millimeter pulses were generated with a laser scanner without spot overlap. Hair and pulse counts were performed 90 days after treatment. There was 33%, 43%, and 40% hair reduction for fluences of 50, 80, and 100 J/cm2, respectively. Mean papules counts were 1.0 for the treated sites and 6 –95 for the control sites. This study demonstrated that the Nd:YAG laser is an excellent modality for the treatment of pseudofolliculitis barber in darker phototypes (Fig. 15.8).

4.3.

Skin Rejuvenation

The long-pulsed Nd:YAG laser, when used with epidermal cooling methods, can produce deep dermal tissue heating. These lasers have therefore been investigated for their ability

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Figure 15.8 Laserscope.)

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Treatment of pseudofolliculitis barbae in type VI skin. (Courtesy of Dr. Vic Ross and

to stimulate neocollagenesis and collagen remodeling in an effort to achieve improvement in skin texture and laxity. Goldberg and Samady performed a split-face study comparing 3 to 5 treatments with an intensed pulsed light (IPL) (Lumenis/ESC), using 590 and 755 nm cutoff filters, with Nd:YAG laser treatment. The Nd:YAG laser (Lumenis/ESC) was with a 3–8 ms pulse, a 6 mm spot, and fluences of 100–130 J/cm2. There were similar improvements in wrinkles and skin texturein all treated sites, but the 1064 nm Nd:YAG laser was better tolerated in terms of treatment discomfort and had fewer side effects. Lee (10) treated 50 subjects with an Nd:YAG laser (lyra and Laserscope) with a 10 mm spot equipped with a sapphire chilled window at 58C, 30– 65 ms pulses and fluences of 24 – 30 J/cm2. Each subject received 3 –6 treatments and there was up to 18 months follow-up. There was a 10 – 20% reduction in redness, a 10– 30% improvement in skin tightness, but no observed improvement in skin pigmentation. Dayan et al. (9) used the same device with a 10 mm spot, 50 ms pulse duration, a fluence of 22 J/cm2 with contact cooling set at 1.58C, in 51 subjects who receive up to seven treatments


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with follow-up as long as 6 months. Objective grading of standardized photographs showed a 12% decrease in coarse wrinkles, a 17% decrease in skin laxity, and a global improvement of 20%. In a recent study, the long-pulsed Nd:YAG laser produced facial skin tightening comparable to radiofrequency treatment in a spilt-face comparison trail. Taylor performed a split-face and neck study in nine patients, comparing a radiofrequency device (Thermacool and Thermage) and a ling pulsed Nd:YAG laser (GentleYAG and Candela). The radiofrequency treatment consisted of three passes using standard treatment parameters, and the Nd:YAG laser was used to perform three passes with a 10 mm spot, 50 ms pulse, a 40 ms cryogen spurt with a 20 ms delay, and a fluence of 50 J/cm2. At 6 months follow-up, a blinded comparison of standardized photographs revealed the same or greater skin tightening on the Nd:YAG laser treated side. There was less pain and fewer side effects with laser treatment when compared with radiofrequency treatment (Fig. 15.9).

5.

PRESENTLY AVAILABLE LONG-PULSED Nd:YAG LASERS

There are multiple Nd:YAG lasers currently being manufactured (Table 15.1). Most of the systems come equipped with a range of spot sizes, millisecond-range pulse durations and skin cooling. The Candela and Cool Touch systems use cryogen cooling; the Cutera, Laserscope, Lumenis, Sciton, and Wavelight devices use contact cooling; and the Cynosure system uses air cooling. The 10 mm headpiece on the Gemini Laser employs photon recycling to improve utilization of the energy generated by the laser. At 1064 nm, 60% of the indent photons are back-scattered out of the tissue. Photons recycling uses a reflector to redirect the back-scattered photons to the target tissue, thereby increasing the effective fluence by 50% (Figs. 15.10 and 15.11).

Figure 15.9 Before and 6 months after treatment with a long-pulsed Nd:YAG laser equipped with cryogen cooling. (Courtesy of Dr. Mark Taylor and Candela.)

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Table 15.1

1 Long-Pulsed Nd:YAG Lasers.

Manufacturer Laser Name Candela Gentle YAG Cool Touch Varia Cutera/Atlus Cool Glide Cynosure Cynergy Fontana Dualis Laserscope Lyra Gemini Lumenis Quantum VasuLight Sciton Profile Wavelight Mydon

6. 6.1.

Max. Energy (J)

Pulse Duration (ms)

Spot Size (mm)

600

0.25 – 300

1.5– 10

Cryogen

500

0.3 –500

3 – 10

Cryogen

300

0.1 –300

3 – 10

Contact

300

0.4 –300

3 – 10

Air

400

5 – 200

2 – 10

900 900

20– 100 10– 100

1 – 5, 10 1 – 5, 10

90– 150 90– 150

5 – 38 2 – 48

6 6

Contact

400

0.1 –200

3, 6

Contact

450

0.5 –90

1.5– 10

Contact or air

Cooling

TREATMENT GUIDELINES Vascular Lesions

Long-pulsed Nd:YAG lasers are used for treatment of a wide range of vessel sizes, from 0.3 to 6 mm in diameter. Deep penetration at this wavelength permits photocoagulation of deeper lying vessels. In general, the spot size is adjusted until it is 25 –50% wider than the vessel. This decreases the volume of tissue being heated below and reduces treatment discomfort. For telangictasia and venulectasia, pulse duration in the range of 20– 50 ms are used, and pulse durations .50 – 100 ms are used for veins .2 mm. Owing to the deep penetration of tissue and even heating of larger vessels, the Nd:YAG laser is also an excellent modality for venous lakes and the superficial component of venous malformations. Lower fluences are used with larger spot sizes due to the enhanced photon penetration and higher effective fluence reaching deeper targets. With 5–6 mm spots, fluences in the range of 80–120 J/cm2 are used; 3–4 mm spots require fluence in the 150–200 J/cm2, and 1–2 mm spots may require fluences as high as 350–500 J/cm2, depending on the laser system being used. The treating physician should consult the manufacturer’s guidelines for treatment parameters used with their system. Treatment is performed with the application of contiguous laser pulses. Spot overlap and pulse stacking has the potential to cause epidermal damage and full thickness necrosis due to overheating of the tissue and must be avoided. Proper skin cooling techniques aid in preventing the epidermis and extracting heat from the dermis. The desired treatment endpoint is vessel spasm or blanching. The skin should be observed for 1 – 2 min on test areas. The fluence can be increased by increments of 10% from the base setting until an appropriate clinical endpoint is reached. A second pass, but not pulse stacking, may be performed on vessels that remain patent following laser


Figure 15.10

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Candela GentleYAG.

irradiation. Follow-up and possible re-treatment is performed at 6– 8 weeks intervals (Figs. 15.12 and 15.13). 6.2.

Hair Removal and Pseudofolliculitis Barbae

Most patients require 5 – 6 treatments sessions, regardless of treatment site, to achieve a desirable clinical outcome. Treatment intervals vary depending on the hair growth cycle for a given site, and, generally are 4 weeks for facial hair, 6 weeks for axillary and inguinal hair, and 8 weeks for hair on the trunk and extremities. The long-pulsed Nd:YAG works best on thick terminal hairs because of the lower absorption coefficient for melanin at this wavelength compared to the 755 nm alexandrite and 800 nm diode lasers. They are safest for the treatment of phototype V/VI skin. Adjustments are made in pulse duration and fluence to compensate for different phototypes, hair color, and thickness. When treating light completed patients, the fluence is increased and pulse duration is decreased to deliver higher peak powers to the hair follicle in a short time-frame. Treatment of darker phototypes requires the use of longer pulse durations and lower fluences to protect the pigmented epidermis. The treatment fluence is decreased by 10% over bony areas and in regions of high hair density such as the beard. The

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Figure 15.11

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Laserscope Lyra.

Figure 15.12 VascuLight technique, Direct application of VascuLight (Lumenis) handpiece to lower-extremity vessel immersed in cooling gel.


Figure 15.13

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Sciton profile laser treatment through water-cooled sapphire plate.

epidermis is cooled with contact cooling, air cooling, or cryogen cooling. Treatment parameters will vary with each laser system, and the manufacture should provide guidelines for appropriate parameters. The same parameters are utilized for hair removal and pseudofolliculitis barbae treatment. Before treatment, the area is cleansed and shaved. If contact cooling is used a clear water-based gel is applied to the skin. The gel improves the efficiency of cooling and laser light transmission. Test spots on darker skin types are observed for 10– 15 min for excessive edema or graying, which may indicate epidermal damage. Once the appropriate parameters are chosen, contiguous laser pulses are applied to the treatment area. The skin should be cooled briefly after treatment with hydrogel dressings or ice packs. Perifollicular erythema and edema can be expected following treatment and may last for up to 1 –2 days in areas of dense, thick, coarse hairs. Laser hair removal may lighten tattoos or pigmented lesions. Care should be taken to avoid treatment in these locations unless the patient finds lightening of these lesions acceptable. Laser irradiation of suspicious pigmented lesions should be avoided. The longpulsed Nd:YAG lasers are deeply penetrating and should not be used to treat skin within the orbital rim. Therefore, eyebrow shaping should be avoided with these lasers. 6.3.

Skin Rejuvenation

Long-pulsed Nd:YAG lasers can be used to achieve mild skin tightening and skin textural improvement with a series of 5 – 6 biweekly or monthly treatments. For this indication,

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a large spot size is used, usually 10 mm. Typical treatment parameters are 50– 60 ms pulse durations and fluences of 20 – 50 J/cm2, depending on the system being utilized. Two to three laser passes are performed by painting in the area with contiguous laser pulses. The lower range of fluences are used for phototype IV – VI skin. Visble improvement should not be expected for 6 – 8 weeks following treatment. 7.

COMPLICATIONS AND THEIR MANAGEMENT

Compliations observed with the long pulsed Nd:YAG lasers include protracted erythema, pigmentary abnormalities, vesiculation, ucleration and scarring. All of these observed side effects relate to the use of overly aggressive treatment parameters for the given indication or the patient’s skin pigmentation. The 1064 nm lasers produce deep tissue heating. If good apposition between the laser tip and skin are not made for contact-cooled handpieces, or misfiring of the cryogen occurs, vesiculation and ulceration can result. Tissue necrosis can also be induced by using too high a fluence, too short a pulse duration, especially in darker skin, or by inadvertent pulse stacking. When tissue graying or vesiculation occurs, the skin should be cooled immediately with ice to prevent further damage. The wounds are treated with application of a topical antibiotic ointment at least twice daily until complete reepithelialization occurs. These skin areas should be protected from the sun for a period of 6–8 weeks (Figs. 15.14 and 15.15). Erythema may occur after treating leg telangiectasia with Nd:YAG lasers and usually resolves in 30 –60 days. Partial stenosis or photocoagulation of larger veins may result in the development of thrombi, which require needle aspiration, followed by hemosiderin deposition. Post-inflammatory hyperpigmenation and matting, however, is a rare occurrence following Nd:YAG laser treatment of leg telangiectasia, compared to other laser wavelengths and sclerotherapy treatment. If hyperpigmenation does develop following laser treatment, the use of hydroquinones, kojic acid, and a high SPF sunscreen will speed resolution of the pigment. 8.

CONCLUSIONS

The long-pulse Nd:YAG lasers are extremely versatile devices due to their deep tissue penetration and absorption by melanin, water, and hemoglobin. Indications for their use

Figure 15.14

Hyperpigmentation after long-pulse 1064 nm Nd:YAG laser treatment at 2 months.


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Figure 15.15 Epidermal ulceration 3 weeks after long-pulse 1064 nm Nd:YAG laser treatment of lower-extremity vessels. This sequelae is most commonly related to overtreatment. Wound healing measures such as topical antibiotics and bio-occlusive dressings are utilized to minimize scarring potential.

are diverse and include the treatment of vascular lesions, hair removal, and skin rejuvenation. Of the lasers used for these purposes, this wavelength possesses one of the highest safety profiles for the treatment of darker skin types.

REFERENCES 1. 2. 3. 4. 5. 6. 7.

8.

9. 10. 11.

Goldman M, Fitzpatrick R, eds. Cutaneous laser surgery: the art and science of selective photothermolysis. St. Louis: Mosby, 1994. Anderson R, Parrish J. Selctive photothermolysis: precise minorsurgery by selective absorption of pulsed radiation. Science 1983; 220:524. Altshuler GB, Anderson RR, Manstein D et al. Extended theory of selective photothermolysis. Laser Surg Med 2001; 29:416 – 432. Kauvar ANB. The role of lasers in the treatment of leg veins. Seminars in cutaneous medicine and surgery. Seminars Cutan Med Surg 2000; 19(4):245 –252. Ross EV, Domakevitz Y. Laser treatment of leg veins: physical mechanisms and theoretical considerations. Laser Surg Med 2005; 36:105 –116. Dierickx C. Hair removal by lasers and intensive pulse light sources. Dermatologic Clinics 2002; 20(1):135– 146. Jacques SL, McAuliffe OJ. The melanosome: threshold temperature for explosive vaporization and internal absorption coefficient during pulse laser irradiation. Photochem Photobiol 1991; 53:769 – 775. Schmults CD, Phelps R, Goldberg DJ. Non-ablative facial remodeling: erythema reduction and histologic evidence of new collage formation using a new 300 microsecond, 1064-nm Nd:YAG laser. Arch Dermatol 2004; 140:1373 –1376. Dayan SH, Vartanian AJ, Menaker G et al. Nonablative laser resurfacing using the long pulse (1064 nm) Nd:YAG laser. Arch Facial Plast Surg 2003; 5(4):310 – 315. Lee MW. Combination 532 nm and 1064 nm lasers for noninvasive skin rejuvenation and toning. Arch Dermatol 2003; 139:1265 – 1276. Taylor MB. Split face/neck comparison of a single treatment of radiofrequency vs. a single treatment of long pulse Nd:YAG for skin laxity of the face and neck. Lasers Surg Med 2005; 17(suppl):76.

354 12. 13. 14. 15. 16. 17. 18. 19.

20. 21.

22.

Sadick and Kauvar Weiss RA, Weiss MA. Early clinical results with a multiple synchronized pulse 1064 nm laser for leg telangictasia and reticular veins. Dermatol Surg 1999; 25:399 – 402. Kauvar ANB. Optimizing treatment of small (0.1– 1.0 mm) and large (1.0 –2.0 mm) leg telangiectasia with a long pulsed Nd:YAG laser. Laser Surg Med 2001; (suppl 13):24. Omura NE, Dover JS, Arndt KA, Kauvar AN. Treatment of reticular veins with a 1064 nm long pulsed Nd:YAG laser. J Am Acad Dermatol 2003; 48:76 – 81. Coles M, Werner RS, Zelickson BD. Comparative pilot study evaluating the treatment of leg veins with a long pulsed Nd:YAG laser and sclerotherapy. Laser Surg Med 2002; 30:154. Sadick NS. Long term results with a multiple synchronized pulse 1064 nm Nd:YAG laser for the treatment of leg venulectasias and ventricular veins, Dermatol Surg 2001; 27:365 – 369. Eremia S, Li CY. Treatment of face veins with a cryogen spray variable pulse width 1064 nm Nd:YAG laser: a prospective study of 17 patients. Dermatol Surg 2002; 28:244 – 247. Goldberg DJ, Silapunt S. Histologic evaluation of a millisecond Nd:YAG laser for hair removal. Laser Surg Med 2001; 28:159– 161. Lorenz S, Brunnberg S, Laudthaler M, Hoben Leutner U. Hair removal with the Long pulsed Nd:YAG laser: a prospective study with one year follow up. Laser Surg Med 2002; 30:127 – 134. Tanzi E, Alster TS. Long pulsed 1064 nm Nd:YAG laser assisted hair removal in all skin types. Dermatol Surg 2004; 30:13– 17. Ross EV, Cooke LM, Timko AL, Overstreet KA, Graham BS, Barnette DJ. Treatment of pseudofolliculitis barbae in skin types IV, V, and VI with a long-pulsed neodymium:yttrium aluminum garnet laser. J Am Acad Dermatol 2002; 47:263– 270. Anderson RR. Optics of the skin. In: Lim HW, Soter MA, eds. Clinical photomedicine, New York: Marcel Dekker, 1993.

16 Noncoherent Light Source Robert A. Weiss and Margaret A. Weiss Johns Hopkins University, School of Medicine, Baltimore, Maryland, USA

1. The Intense Pulsed Light Device 1.1. Introduction 1.2. Wavelength 1.3. Spot Size 1.4. Cooling 1.5. Pulse Durations 1.6. Concepts of Multiple Pulsing 2. Specific Indications for IPL 2.1. Leg Telangiectasias 2.2. Facial Telangiectasias 2.3. Poikiloderma 2.4. Photorejuvenation 2.5. Hair Removal 3. Treatment Techniques 3.1. Vascular Lesions 3.2. Hair Removal Technique 4. Adverse Reactions 5. Summary References

1. 1.1.

355 355 356 358 359 360 361 363 363 364 364 366 367 368 368 369 370 371 372

THE INTENSE PULSED LIGHT DEVICE Introduction

One of the most controversial light-based technologies, first introduced for clinical studies in 1994, and cleared by the US Food and Drug Administration (FDA) in late 1995 as the PhotodermTM (ESC/Sharplan, Norwood, MA), is the noncoherent filtered flashlamp intense pulsed light (IPL) source. It was initially launched and promoted as a radical improvement over existing methods for elimination of leg telangiectasias and as a specific modality to minimize the possibility of purpura common to pulsed dye lasers (PDLs). In reality, the device turned out to be of greater utility for other indications 355

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than leg telangiectasias, and the road to usability, reproducibility and good results was a long one. The initial claims of less purpura than a PDL laser have remained valid and have been confirmed by numerous investigators (1–10). Present-day indications have expanded far beyond the initial ones, however, to include hair removal, facial telangiectasias, pigmentation, poikiloderma of Civatte, scars, and most recently, the new domain of nonablative facial rejuvenation or photorejuvenation (1 – 3,11,12). The IPL device consists of a flashlamp housed in an optical treatment head, in which reflecting mirrors are designed to deliver the light through an optical waveguide. The flashlamps are normally water cooled in order to maximize the lifetime of the lamp and enable the system to deliver high output energy. Some technologies use interchangeable, “snap in” quartz waveguides to transmit the light to the skin. In most designs, these quartz waveguides are coated with a dielectric (multilayer, reflective) coating. Although a dielectric, also known as dichroic, coating is very efficient in reflecting certain wavelengths of light, they are also very angle dependent. This limits the selectivity of the output from the flashlamp. Newer technologies now incorporate a dual filtration method (patent pending— Palomar Medical Technologies) which employs both a dielectric (dichroic) reflective coating and an absorption coating surrounding the lamp. With this innovation, IPL technology begins to mimic the selectivity of laser systems. Since the evolution of the IPL from 1995, the technology has developed from low energy, nonselective units, to high energy, very selective and clinically effective devices. There are approximately 20 types of competitive units in this market place, however, most are low energy units. 1.2.

Wavelength

When unfiltered, the IPL device is capable of emitting a broad bandwith output from 400 – 1400 nm. The broad wavelength output is filtered, as stated above, by a few methods. Similar to laser systems, the choice of output wavelength should be determined by the target chromophore. The three primary chromophores are blood (oxy- and deoxyhemoglobin), melanin in epidermal pigmented lesions and melanin in the hair shaft. Many systems have multiple, snap in filters which start at short wavelengths (Lumenis 515, 560, and 645 nm, etc.) and other systems use individual, specifically tuned hand pieces, with dual filtration and produce more selective outputs (Palomar Medical Technologies, Inc. StarLux—Lux V, 400 –700 nm and 870 – 1200 nm; Lux G, 500 – 650 nm and 870– 1200 nm). These dual wavelength range hand pieces enable the user to more selectively target the desired chromophore. The choice of wavelength from an IPL device is a function of output of the xenon flashlamp (Fig. 16.1) and the

Table 16.1

Intense Pulsed Light Devices

Manufacturer

Brand NameTM

Cutera Cynosure Derma Med Lumenis

CooGlide XEO Cynergy PL Quadra Q4 VascuLight Elite/ Lumenis One EsleLux/MediLux StarLux Profile

Palomar Sciton

Output (nm) 600 – 850 400 – 1200 480 – 1200 515 – 1200 470 – 1400 500 – 670, 870 – 1400 400 – 1400

Noncoherent Light Source

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choice of wavelength filtration techniques relative to targeting the desired chromophore. Although many companies produce numerous “cut-off” filters, the real choice for improved selectivity for IPL technology is match the wavelength selectivity of the “cutoff” filters to maximize the absorption of the target chromophore. Specific hand pieces with the dual filtration process of improved selectivity can be applied to selective target such as vascular lesions. The 500 –650 nm and 870– 1200 nm dual wavelength range (Palomar EstiLux/MediLux/StarLux Lux G hand piece) matched the primary absorption peaks of oxyhemoglobin (538 and 577 nm) with most of its output and then the remaining output matched the secondary absorption peaks near 900 nm. In addition, the long wavelength emission range begins to cover the absorption of water in the dermis. The choice of wavelength range for targeting epidermal melanin is empirically easier because the absorption curve of melanin is relatively linear. Melanin absorption is significantly higher in the shorter wavelength range (400 nm) than in the longer wavelength range (1200 nm). In fact, the absorption coefficient is almost 15 times higher in the blue region (400 nm) region of the spectrum than in the infrared (1200 nm) region of the spectrum. Therefore, when choosing a specific hand piece wavelength range or cut-off filter for targeting epidermal melanin, the shorter wavelengths are certainly more effective. The trade-off of wavelength choices is dependent on the amount of melanin present in the target relative to the amount of melanin present in the background skin. In other words, the ratio of melanin concentration of the primary target relative to the Fitzpatrick skin type of the individual will determine the choice of wavelength range to use as well as the treatment fluence. As with vascular lesions, if the skin type of the patient will tolerate shorter wavelengths well, the use of shorter wavelength, “blue” light will provide significantly higher selectivity for treating unwanted, epidermal pigmentation. Although lasers can provide excellent selectivity for treating epidermal pigmented lesions, the user is limited in choices by the very limited availability of short wavelength “blue” light systems. Therefore, for lasers, “green” wavelengths are most commonly used for treating pigmented lesions. As stared above, these “green” wavelengths (532 nm) are quite effective for treating vascular lesions and darker pigmented lesions, but are somewhat limited in treating lighter colored pigmented lesions. In this application area, IPL technology has a distinct advantage because the output wavelengths of the standard xenon lamps begin at 400 nm. Consequently, the IPL technology may actually provide more selectivity for treating pigmented lesions than laser technology.

Figure 16.1 Emission spectrum of an intense pulsed light head with the 515 nm filter at 10 ms pulse duration. Peak output is at 600 nm. (Courtesy of Holger Lubatschowski, PhD, Laser Zentrum, Hannover, Germany.)

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Figure 16.2 Absorption curve of hemoglobin in different states of oxygenation. Since collagen absorbs very little on its own, the primary components absorbing light are hemoglobin and melanin (melanin not shown). There is a zone from 600 to 750 nm in which deoxyhemoglobin has preferential absorption. (Courtesy ESC/Sharplan.)

1.3.

Spot Size

When treating blood vessels of the legs, spot size plays a very important role, because spot size, along with wavelength, affects penetration depth. A small spot size leads to rapid scatter with a rapid decay of fluence by depth (14). Penetration is therefore more efficient with a large spot size. A depth of 4 mm should be attainable with the 8 mm 35 mm rectangular spot size of the IPL device considering an average wavelength of 800 nm (Table 16.2). Larger spot sizes are always more effective in delivering light deeper into the skin. The dimension of the spot size is also a factor because the actual shape of the output spot of the IPL is also very important. For example, if a 6.0 cm2 spot hand piece were designed, one could choose numerous designs for the hand piece. However, if the hand piece were built with a 20 mm 30 mm surface, the depth of penetration into the skin would be significantly deeper than if the hand piece was designed with a 10 mm 60 mm output surface (Effects of Fluence and Pulse duration for Flashlamp Exposure on Hair Follicles Manatein, Pourshagh Anderson et al.). Even though both surface areas are equal, the unit with the larger width in relationship to its length will product a better scattering result in the skin. Therefore, although larger surface area output waveguides are very important for good scattering and depth of penetration, not all designs are equal. The larger spot sizes Table 16.2

Spot Size vs. Wavelength

Spot size (mm)

Light penetration depth at 595 nm (mm)

Light penetration depth at 800 nm (mm)

0.8 1.1 1.25

1.5 2.0 2.5

1 2 3

Note: For 800 nm the penetration appears to be half the diameter of the spot size. Therefore an 8 mm wide crystal should permit penetration down to 4 mm. (Data provided by ESC/Sharplan, Norwood, MA.)


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play in increasing important role especially for the use of IPL technology in photoepilation. When the target is the hair follicle, deep penetration is essential in order to provide adequate heating of the hair follicle. Again the physical dimensions of the output waveguide surface area are very important in determining the effective fluence at the depth of the target. However, IPL technology does present a different problem when considering the treatment of smaller, more superficial targets. Ectatic blood vessels (i.e., telangectasia, angiomas, etc.) are located in the upper legions of the dermis. Therefore, deep scattering into the reticular dermis is not necessarily a desirable output from a hand piece. Large area spot size hand pieces actually are a disadvantage for treating linear or distinct vascular lesions and many pigmented lesions. The control or focusing of incoherent light is very different than that of laser light. As stated above, xenon flashlamps produce multiple wavelengths of light and because different wavelengths of light have different focal points, it is very difficult to focus accurately incoherent light. In other words, if one were to focus a laser beam, one would choose a lens that produced the appropriate spot size based on the wavelength of the laser and based on the fact that all of the laser light was coherent, directional, in-phase and monochromatic so a very small, tight spot could be produced. This is clearly how small spot size laser beams are produced for treating vascular lesions or for microspot treatments of small biological structures. However, this feature is impossible to duplicate with incoherent light. Being multiwavelength, mulit-directional and incoherent, IPL light is difficult to focus. With the use of complex optical schemes, small spot size hand pieces have been designed (Palomar Medical Technologies, Inc. Lux G and B hand pieces) for selectively treating vascular lesions. Spot sizes as small as 12 mm 12 mm and 10 mm 15 mm can then produce fluences over 50 J/cm2. At these fluences, even large vascular lesions can be effectively treated in one or two sessions. Therefore, spot size issues are multifaceted, depending largely on the choice of depth of the target. Larger spot sizes are most effective for delivering light to deep targets and small spot sizes are more effective for delivering high fluences to more superficial targets.

1.4.

Cooling

Whether using lasers or IPL technology, cooling of the epidermis during a procedure is important. Cooling can be divided into three areas, precooling, parallel cooling, and

Figure 16.3 (a) Proper spacing of the crystal from the skin with a 2 mm layer of gel or floating the crystal in gel. If the crystal rests directly on the skin, the likelihood of epidermal injury is far greater. (b) With a Peltier cooling device incorporated into the crystal, the layer of gel required is much smaller.

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postcooling. Precooling and parallel cooling are generally the more important of the cooling processes. As previously explained, cooling can be passive or active (contact or dynamic spray cryogen) in design and each has some advantages or disadvantages. The distinction between passive and active is very significant. Passive cooling has been employed in the past using ice-packs, CoolRoll frozen metal rollers or chilled water based gels. Gels commonly are messy and very variable in their cooling capabilities. Techniques such as “floating” the hand pieces in the gel were designed to attempt to prevent burning of the epidermis if the hand piece came in contact with the epidermis, but this technique also introduced significant variability into the effectiveness of the treatment procedure. While the rollers work well, their ability to produce long term cooling is very limited. With the advent of active, pre- and parallel cooling on IPL systems, higher fluences and be employed and a larger variety of skin types can be treated. Active contact cooling falls into numerous smaller categories, but the differences in systems can be easily divided into two broader categories. First, the choice of waveguide materials is very important. Many technologies use quartz as the choice for the waveguide to carry the light pulse to the tissue. Quartz is an insulator and therefore a very poor thermal conductor. On the contrary, sapphire is the only crystalline material that has the same thermal conductivity properties of a metal. In other words, sapphire conducts heat from the surface of the skin in the same fashion as a piece of cold, opaque piece of metal. Secondly, the design of heat extraction from the waveguide is very important as well. The heat extraction rate from the is not a function of the set cooling temperature, but instead, it is a function of the surface area in contact with the skin, the thickness of the sapphire of the waveguide and the heat transfer rate of the hand piece design. Because each flash of the IPL delivers significant thermal energy to the skin, the heat load of the skin and the rise in temperature of the waveguide all affect the temperature rise of the skin. If the hand piece is designed to minimize the temperature rise because if the hand pieces ability to remove a proportional amount of heat from the skin as the input heat load, then the system will effectively handle high fluence IPL treatments. Human skin is actually a very good reflecting medium and because of this feature, a considerable amount of the input light from an IPL flash or laser pulse may be reflected or scattered from the skin. The ability to recapture this light and redirect it into the skin is a patented process termed “photon recycling” (Anderson, et al./Palomar Medical Technologies Inc.) and involves specific optical designs. Direct contact with the skin, the use of refractive index matching gels or lotions and the proper waveguide design all contribute to the success of minimizing photon leakage or scattering from the skin. It is not only reflection from the stratum corneum that matters, but also scattering from other structures throughout the epidermis and dermis that contribute to the total amount of input light normally lost with each light pulse. Photon recycling (especially on skin types I– III) may increase the effective fluence 2 –3 times. 1.5.

Pulse Durations

Allowing proper thermal relaxation time between pulses theoretically prevents elevation of epidermal temperatures above 708C and is an inherent advantage of “multiple sequential pulsing” of the IPL device. Thermal relaxation time is the amount of time it takes for the temperature of a tissue to decrease by a factor of 1 ¼ 2.72 as a result of heat conductivity. For a typical epidermis thickness of 100 mm, thermal relaxation time is approximately 10 ms. For a typical vessel 100 mm (0.1 mm), thermal relaxation time is approximately 4 ms, for a vessel of 300 mm (0.3 mm), thermal relaxation time is approximately 10 ms. Therefore, vessels .0.3 mm cool more slowly than the epidermis with a


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single pulse. For larger vessels, however, multiple pulses may be advantageous with delay times of 10 ms or more between pulses for epidermal cooling. This delay time must be increased with larger vessels as thermal diffusion across a larger vessel elongates the thermal relaxation time. Multiple sequential pulsing with delay times permits successive heating of targeted vessel(s) with adequate cooling time for epidermis and surrounding structures. These theoretical considerations imply: (1) vessels ,0.3 mm should theoretically only require a single pulse, although a double pulse should have no adverse effect on treatment; (2) double or triple pulses should be spaced 10 ms or longer to accommodate normal epidermal thermal relaxation times, and that even safer might be a 15 ms thermal relaxation time; (3) bright red lesions (oxyhemoglobulin) are better treated with 515 – 590 nm filters; (4) violaceous lesions (deoxyhemoglobulin) should be treated with 590 nm or higher filters; and (5) darker skin (melanin) should always be treated with the highest filter available accompanied by increasing delay times between pulses to allow for increased skin thermal relaxation times. The treatment of darker skin individuals becomes of increasing concern when performing photoepilation. In these cases, the 755 nm filter is used primarily with delay times between pulses from 50 to 100 ms to allow plenty of time for the skin to cool down avoiding thermal damage. 1.6.

Concepts of Multiple Pulsing

The newest concepts for IPL and what has most contributed to the success of the technique, is the ability to elongate pulse duration for larger vessels, shorten pulses for smaller vessels and to use these in a variety of combinations of synchronized short and long pulse widths. For many laser devices reported to treat leg veins, a longer pulse duration (up to 50 ms) has led to better clinical results (15). For a small vessel (0.3 mm), heat distribution is assumed to be instantaneously Gaussian. For a larger vessel this cannot be assumed, since more time is required to have heat pass from just inside the wall all the way to the core. Additional cooling time is required to release the accumulated heat from the core to the vessel surface. These principles were demonstrated using double pulse experiments with the 585 nm yellow dye laser in which larger vessels of PWS (.0.1 mm) absorbed greater energy fluences before reaching purpura after double pulses spaced 3– 10 ms apart (16). In another study using pulsed laser irradiation at 585 nm, pulse durations were chosen between short pulse (0.45 ms) and long pulse (10 ms) (17). Results demonstrated that long-duration pulses caused coagulation of the larger diameter vessels while small-caliber vessels and capillaries showed resistance to photothermolysis at these parameters. This concept has been termed photokinetic selectivity. Applying this to IPL, we have found that increasing pulse duration for IPL up to 12 ms causes larger vessels (0.5 mm or greater) to undergo more effective clinical photothermal coagulation while sparing the epidermis (6). Obeying the principles of “thermokinetic selectivity” using IPL, we understand that the smaller overlying vessels in the papillary dermis do not absorb efficiently at longer pulse durations, causing less epidermal heating. Longer thermal diffusion times for larger vessels are best served with longer pulse durations for IPL. Most commonly employed pulse durations and pulse combinations in our practice are an initial pulse of 2.4 ms followed by a second pulse delivered after a delay or rest interval 10 –20 ms. The second coupled or synchronized pulse is set for 2.4– 8 ms depending on the diameter of the vascular target with smaller diameter (0.1 –0.2 mm) bright red vessels treated with the shorter second pulse duration of 2.4 – 4.0 ms and larger vessels

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Figure 16.4 Immediate clinical endpoint for treatment of fine red vessels on the nasal ala. (a) Before treatment. (b) Immediately after showing redness but no visible signs of the telangiectasias.

(0.3 –0.5 mm) treated with the second pulse duration of 5 –8 ms. These are adjusted based on the immediately observed clinical response depending on the clinical response. For small vessels we wish to see immediate clearing with slight background erythema as our clinical endpoint (Fig. 16.4). The concept for double pulsing of larger telangiectasias is to allow preheating of vessels with absorption by smaller vessels with the first pulse, then allow surrounding structures to cool. The second coupled longer pulse then heats up the larger vessels in the area under the crystal. This results in an immediate darkening of the vessels with an urticarial flare as seen in Fig. 16.5. Newer IPL technologies have “smoothed” out the multiple, spiked pulse technologies that have been employed in the past. The concept of a single, smooth or square or flat-top pulse profile has developed since 2001 as a method to deliver increased fluence with less risk for epidermal damage. Patented technology (Palomar Medical Technologies, Inc.) in this area has now enabled pulse durations from as short a 1 ms to as long a 500 ms to be delivered in a single pulse, without interruption or without spikes. Therefore, the technique for treating vessels is now easier to define. Short, single, smooth pulses are used to treat small vessel disease and longer, smooth pulses are used to treat larger, ecstatic vessels. Incorporating this newer pulsing technology with active, contact cooling has enabled users to treat at significantly higher fluences and treat significantly larger vessels in a safer manner than before. Similar principles can also be applied to pigmented lesions and photoepilation.

Figure 16.5 Endpoints of photothermal coagulation of larger telangiectasias (0.5 mm). Vessel is dark with surrounding urticarial edema.


2. 2.1.

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SPECIFIC INDICATIONS FOR IPL Leg Telangiectasias

The initial report on treating leg telangiectasias with IPL was very optimistic with clearance of 75– 100% achieved in 79% of treated lesions and better than 50% clearance was achieved in 94% of cases (18). However, these data were obtained from dozens of centers with widely different techniques of treatment and data recording and therefore could not be reproduced on a regular basis by some users (19). For at least 6 years we have treated several thousand patients with multiple parameters with multiple combinations of short and long pulses in an attempt to obtain the most consistent results. Typically, our patients have been screened for the absence of major reverse flow or reflux using a digital-PPG, Doppler and/or Duplex ultrasound. If major reflux from the saphenous or lateral venous systems is present, endovenous obliteration techniques, ambulatory phlebectomy, or sclerotherapy must first eliminate this. Many telangiectatic webs are often seen in association with reticular veins on the lateral leg. These reticular veins show reverse flow in the direction of these telangiectatic veins. An unpredictable response will occur when telangiectasias are treated by any method while associated reticular veins remain patent. Most of our patients treated with IPL for leg veins have been those resistant to sclerotherapy or in which reticular veins have simultaneously been treated with sclerotherapy or the long pulse Nd:YAG laser. We have found IPL useful for the telangiectatic matting that occurs on the inner thighs following sclerotherapy (Fig. 16.6). Based on theoretical considerations discussed above, new parameters for more effective treatment of leg telangiectasias have been employed. A progressive series of parameters has been developed. These include initial parameters of both a short and long

Figure 16.6 Residual telangiectatic matting remains on the inner thigh above the knee. (a) After sclerotherapy. (b) Immediately after treatment. Parameters are 2.4 ms, 10 ms delay, 7 ms pulse, 570 nm filter, 38 J/cm2. (c) After two treatments spaced 1 month apart.

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pulse of 2.4 ms and 6 ms at 40 J/cm2 with 570 nm cutoff filter, separated by a 10 ms delay (thermal relaxation interval). Visual endpoints include complete darkening of the targeted vessel(s) with a 2 mm or greater urticarial flare within 10 min (Fig. 16.5). When this endpoint is not seen, pulse durations to adjacent sites are increased to a maximum of 10 ms for two consecutive pulses separated by a 20 –30 ms thermal relaxation time (570 nm cutoff filter) with total fluences of up to 65 J/cm2. By combining a shorter pulse (2.4 – 3 ms) with a longer pulse (7 – 10 ms), it is theoretically possible to ablate smaller and larger vessels overlying one another in the dermis. Smaller more superficial vessels theoretically absorb the shorter pulses more selectively, while the larger diameter vessels absorb the longer pulses. A response rate of 74% in two treatments with an 8% incidence of temporary hypo- or hyperpigmentation has been reported (6). The choice of a cutoff filter was based on skin color with light skinned patients using a 550 nm filter and darker skinned patients using a 570 or 590 nm filter. These sets of leg vein parameters are listed in Table 16.3. 2.2.

Facial Telangiectasias

The treatment of facial telangiectasia is most rewarding with IPL, similar to other light based devices. As facial telangiectasias are generally more uniform in size and depth with a thinner overlying epidermis than leg telangiectasias they are much more susceptible to penetration by photons. Response is more predictable with our clinical results approaching an 85% resolution rate of facial telangiectasias after one to three treatments (data on file, Maryland Laser Skin and Vein Institute, Baltimore, MD). The parameters for IPL of facial telangiectasia include a single or double pulse of approximately 2.4 –3 ms duration with a 550 nm filter typical, using delay times of 10 ms between pulses. Fluences required are much less than leg veins typically in the 20– 32 J/cm2. The advantage to IPL is that with the large spot size an entire cheek of telangiectatic matting can be treated with less than a dozen pulses in ,10 min (Fig. 16.7). For larger more purple telangiectasias typically seen on the nasal alae, or for venous lakes or adult port wine stains, the same settings may be employed as for small vessels of leg, that is, a short pulse followed by a long pulse. Resistant darker vessels may need treatment with long-pulse Nd:YAG. Parameters for various types of facial vascular lesions are listed in Table 16.4. 2.3.

Poikiloderma

Patients with poikiloderma of Civatte usually seek treatment for cosmetic reasons, to improve the erythematous, pigmented and finely wrinkled appearance that occurs in Table 16.3 Vein size (mm) ,0.2 0.2 – 0.5 0.6 – 1 1 – 1.5 1.5 – 2.0 Unresponsive to .2

Suggested IPL Parameters for Leg Veins Filters (nm)

First pulse (ms)

Delay time (ms)

Second pulse (ms)

Fluence (J/cm2)

550 550– 570 570– 590 570– 590 590 590

2.4 2.4 2.4 2.4 8 12 (long pulse mode)

10 15 15 15 – 25 20 – 50 30 – 40

2.4 5–6 6 7 – 12 8 – 12 12 (long pulse mode)

25 – 35 25 – 40 30 – 40 35 – 45 40 – 60 60 – 70


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Figure 16.7 (a) Patient with rosacea and the entire cheek is treated with 15 pulses. (b) Results after three treatments spaced 1 month apart.

visible areas, mostly on the neck and the upper chest. For areas of poikiloderma on the neck and lower cheeks consisting of pigmentation and capillary matting, the IPL device is ideal with use of a 515 nm filter which allows absorption both by melanin and hemoglobin (Fig. 16.8). For patients with more dyspigmentation, one begins with a 550 nm filter to prevent too much epidermal damage which would result in crusting and swelling lasting for several days. Treatment of poikiloderma has turned out to be one of the most effective uses of the IPL techology (Fig. 16.9). In a recent study, 135 patients randomly selected with typical changes of poikiloderma of Civatte on the neck and/or upper chest were treated with one to five treatments using IPL. Parameters included the 515 and 550 nm filters with pulse durations of 2 –4 ms either single or double with a 10 ms delay. Fluences reported were between 20 and 40 J/cm2. Clearance over 75% was reported in the telangiectasias and hyperpigmentation with achieved color matching of the uninvolved skin in the shadow area of the chin. The total incidence of side effects was 5% including pigment changes. In many cases, vastly improved skin texture was noted both by physician and patient as a consequence of treatment. Possibly due to the near-infrared component of IPL there appears to be a collagen remodeling effect with improved skin texture reversing the cutaneous atrophy component of poikiloderma of Civatte. Table 16.4 Suggested IPL Parameters for Common Facial Vascular Lesions and Photorejuvenation Filters (nm)

First pulse (ms)

Delay time (ms)

Second pulse (ms)

Fluence (J/cm2)

550

2.4

10 –15

2.4 – 4.0

22 – 30

Nasal alae telangiectasia Hemangioma Poikiloderma

570 570 515, 550

2.4 2.4 2.4

10 –15 10 –20 10 –20

5.0 – 7.0 6.0 – 8.0 2.4 – 4.0

32 – 44 32 – 42 22 – 36

Photodamage—mild Photodamage—moderate (first treatment) Photodamage—severe

550– 570 570– 590

2.4 2.4

10 –20 10 –20

2.4 – 4.0 4.0 – 6.0

25 – 38 22 – 34

Single or double Double Double Single or double Double Double

590 or higher

2.4– 4.0

20 –40

4.0 – 6.0

22 – 40

Double

Vascular Lesion Telangiectatic matting

Number of sequential pulses

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Figure 16.8 Treatment of poikiloderma of neck. Initial treatment of single 3 ms pulse, 25 J/cm2, 515 nm filter shows clearance in area of two test pulses.

2.4.

Photorejuvenation

The overall appearance of aging skin is primarily related to the quantitative effects of sun exposure with resultant UV damage of structural components such as collagen and elastic fibers. Appearance, however, is also affected by genetic factors, intrinsic factors, disease processes such as rosacea, and the overall loss of cutaneous elasticity associated with age. With vast sun exposure during recreational acitivities and depletion of the ozone layer, visible signs of aging, damage, and disease have become more evident in younger and younger individuals. Photorejuvenation has been described as a dynamic nonablative process involving the use of noncoherent IPL in a low fluence nonablative manner to reduce mottled pigmentation, telangiectasias, and smooth the textural surface of the skin (2). The treatment is generally administered in a series of five to six procedures in 3-week intervals. The entire face is treated, rather than a limited affected area, and the patient may return to all activities immediately. This has also been termed with various service trademarks such as Photofacial, Fotofacial, Facialite, and others.

Figure 16.9

Poikiloderma of the neck: (a) before; (b) after two treatments.


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In a recent study, 49 subjects with varying degrees of photodamage were treated with a series of four or more full-face treatments at 3-week intervals using IPL (VasculightTM IPL, ESC/Sharplan, Norwood, MA). Fluences varied from 30 to 50 J/cm2 with typical settings of double or triple pulse trains of 2.4–4.7 ms with pulse delays of 10–60 ms. Cutoff filters of 550 or 570 nm were used for all treatments (2). Photodamage including wrinkling, skin coarseness, irregular pigmentation, pore size, and telangiectasias was improved in .90% of the patients. Treatments involved IPL of the entire facial skin except in males who elected to avoid treatment of the beard area because of potential hair loss. In this study, 72% of subjects reported a 50% or greater improvement in skin smoothness; 44% reported a 75% or greater improvement. Minimal side effects were reported with temporary discoloration consisting of a darkening of lentigines which resolved completely within 7 days. Two subjects reported a “downtime” of 1 and 3 days due to moderate to severe swelling. An example of photorejuvenation is seen in Fig. 16.10. The authors and others have also used the newer, single, smooth pulse technology (Palomar StarLux) with active cooling to reduce the number of treatments required with the older technology and more effectively treat large vessel disease. Patient satisfaction has increased as well with a higher percentage of patients acknowledging improvements more rapidly. 2.5.

Hair Removal

It has been shown that IPL photoepilation may produce long-term, “permanent,” cosmetically significant hair removal (11). The major proposed mechanism of action is “selective photothermolysis”, with follicular melanin as the major target chromophore. Wavelengths in the red and infrared range (600–1100 nm) of the electromagnetic spectrum are generally agreed to be optimal for this purpose as this allows deeper penetration of photons with a uniform beam, targeting deeper follicles while achieving “epidermal by-pass” to minimize surface absorption. IPL used for hair removal (EpilightTM ESC/Sharplan, Norwood, MA) is

Figure 16.10 Photorejuvenation. Improvement is seen even after one treatment in this female patient who is 45 years old. She returns for yearly treatments to maintain the improved skin texture and more even pigmentation. Parameters utilized in this patient were 570 nm filter, 2.4 ms pulse, 20 ms delay, 6 ms pulse, and fluence of 36 J/cm2.

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slightly different than that used for vascular lesions in that the software allows modulation of a pulse into a series of two to five minipulses, the duration and delay of which are customizable within the millisecond range. A larger footprint spot size of 10 45 mm is also available for faster coverage of larger skin surfaces. In addition, the flashlamp has a water cooling blanket with circulating water to reduce the recycle time to 3 s. The first published report of successful IPL long-term hair removal was for terminal beard hairs in two transsexual patients (male to female) (20). Histology demonstrated atrophy of entire follicles with no scarring at the skin surface. At 6 months following an unusually high number of treatments (13 and 41), no pigmented or textural skin changes were observed, while direct visual observation revealed that hair was virtually absent. In an initial study in 1996, we treated 23 patients with an IPL source with a double treatment protocol (cutoff filter 615– 645 nm based on Fitzpatrick skin type, pulse duration 2.8 – 3.2 ms, triple pulse, fluence 40– 42 J/cm2), and showed hair reduction of 42% at 8 weeks and 33% at 6 months. In another study in 37 subjects, after a single treatment at 12 weeks, 60% hair reduction by hair counts was noted (21). Typical parameters for hair removal are shown in Table 16.5. The most recent study demonstrated a mean hair reduction efficiency of 75.5% after a mean of 3.7 treatment sessions, in patients followed up for an average of 21.1 months (11). Data from this study documented the long-term clinical efficacy of IPL-induced hair removal in light and dark skin and hair phenotypes. The documentation of maintenance of diminished hair counts for up to 30 months after last treatment supports the long-term value of IPL technology in the treatment of hirsutism. “Permanent” hair reduction was achieved by a reduction in the number of hairs over an interval longer than the normal hair cycle (usually 1–3 months depending on the particular given anatomic region) (Fig. 16.11). Hair reduction was not significantly related to skin type, hair color, anatomic site, or number of treatments. Side effects were mild and reversible and occurred in a minority of patients (hyperpigmentation in 9.3% and superficial crusting in 5.6%). As stated earlier, larger spot sizes are more effective for photoepilation. With the newer technologies that employ active cooling with higher fluences, investigators have been able to use over 50 J/cm2 and spot sizes as large as 7.35 cm2 (16 46 mm Palomar Medical Technologies, Inc. Lux Rs, Lux R or Lux Y hand pieces respectively) to demonstrate equal or superior results to the most commonly accepted photoepilation laser systems. With the use of “smooth” pulses and active cooling, IPL technology can now be safely used on all skin types without damaging the epidermis.

3. 3.1.

TREATMENT TECHNIQUES Vascular Lesions

A thick layer of gel must be placed onto the crystal and absolutely no pressure applied as the crystal is placed over the target area, floating the crystal in gel. Compressing this Table 16.5 Fitzpatrick skin type II III IV V

Suggested Parameters for IPL Photoepilation Filter (nm)

Fluence (J/cm2)

Pulse durations (ms); number of pulses

Delay between pulses (ms)

615 645 695 695, 755

39–42 34–36 34–40 38 –40

3.3 – 5; 2 3.0; 3 3.0; 3 5 – 7; 2

30 30 40 50 –60


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Figure 16.11 Long-term hair reduction. (a) Before treatment. (b) One year after the last treatment, total of three treatments.

2 – 3 mm layer of gel against the skin will result in crystal placement too close to the skin thus greatly increasing the risks of epidermal injury. Plastic spacers are available to increase the uniformity of distance of crystal and thickness of gel, although most users simply float the crystal holding the weight of the IPL head in their hands. Newer head designs have taken this into account and have become much more lightweight and have incorporated integral Peltier cooling devices to keep the crystals at 18C (Quantum SRTM , Quantum HRTM , ESC/Sharplan, Norwood, MA). For light-colored legs with very fine telangiectasia, excellent results can usually be obtained; when large areas are involved, the large spot size of the IPL allows rapid treatment. If a gray appearance of the skin is noted immediately after a pulse and this is accompanied by the epidermis feeling loose and sliding with touch, the fluence is too high or the crystal too close to the skin. Epidermal desquamation will occur in a few hours, so subsequent treatments must be performed with reduced fluence, longer pulse durations and/or increased delay times between pulses. In order to minimize rectangular foot printing, a 10% overlap of pulse placement is used or alternatively, a second pass may be performed with the direction 908 from the original direction. Attaching a cooling device which surrounds the crystal has been shown to produce better results with fewer side effects (12). Cooling is maintained by circulating water at 18C through the metal collar around the crystal. When this contact-cooling device is utilized, only a small layer of water-based gel is placed on the cooling collar of the treatment crystal. This remains in contact for at least 10 s to chill down to the temperature of the circulating water set at 1 – 48C. With absolutely minimal pressure the cooling device with the crystal is placed directly onto the skin overlying the targeted area. No pressure is applied as the target vessels may shut with compression. No EMLA cream is used before treatment as there is a high incidence of vasoconstriction produced by the prilocaine component of EMLA. ELA-max 4% lidocaine (Ferndale Labs, Ferndale, MI) is a better choice but is usually not necessary with cooling.

3.2.

Hair Removal Technique

Hairs should be 1 – 3 mm just above the skin surface as hair shaft melanin is the target chromophore and a protruding hair shaft may theoretically act as a “wick” to conduct photons down the hair shaft. The crystal is floated in a thick 3 – 4 mm layer of gel which is kept on ice prior to use to be at a temperature of 18C. The cool gel minimizes the discomfort of treatment and protects the epidermis. Typically, hairs may be clipped

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with an electric clipper just prior to treatment. Personal experience has shown that hairs shaved totally smooth with the skin surface do not allow for proper immediate visual feedback and thus may adversely affect treatment outcome. We rely primarily on a visual endpoint (Fig. 16.12) of depigmentation of the treated hairs, as well as shortening, curling or vaporization to the skin surface of the hair stubble. The smell of denatured hair protein is another helpful source of feedback. These must be also accompanied by very little erythema at the skin surface indicating no damage to the epidermis or dermis immediately below. If erythema is seen, then the fluence is reduced. Within minutes, an urticarial response surrounding the treated follicles is expected. Our experience has taught us that when these features are seen, the likelihood of long-term (.12 months) reduction in hair count is very likely. 4.

ADVERSE REACTIONS

During our initial clinical trials with IPL, two tanned legs developed immediate desquamation of the epidermis resulting in hypopigmentation (2.5%) lasting for 4– 6 months with no permanent pigment change. This occurred at 40 J/cm2 with a single pulse of 3 ms. No reaction like this has been observed on the face. No long-term sequelae were noted. In our subsequent experience with thousands of treatment sessions, there has been about a 2% incidence of scattered areas of crusting in areas of increased pigmentation. This typically heals within 7 days by peeling off. We accelerate this process by having the patients apply a moisturizer twice a day. Crusting occurs primarily on curved body areas such as the neck over the sternocleidomastoid muscle curvature. Purpura occurs in scattered, isolated pulses in about 4% of treatments. Purpura is more likely when the 515 nm filter is used or when the pulse durations are too short such as coupling a 2.4 ms pulse duration with another 2.4 ms pulse duration. The purpura from IPL is different than typical short pulse PDL purpura in that resolution occurs within 2 –5 days. Other adverse effects of IPL include a stinging pain described as a brief grease splatter, electric shock, or rubber band snapping on the skin during treatment typically easily tolerated for up to 60 pulses per session or which can be minimized by pretreatment with ELA-Max (lidocaine 4%) (Ferndale Labs, Ferndale, MI). Occasionally, a thin nontreated stripe between reticular footprints can be seen (Fig. 16.13). This is easily corrected with subsequent treatment applying the crystal over the nontreated sites or proceeding with treatment using the crystal rotated 908 from the original direction. In the past 6 years, we have observed a total of

Figure 16.12 Endpoint for IPL hair removal; depigmentation of hairs with shortening, curling or vaporization to the skin surface.


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Figure 16.13 (a) Rectangular footprints with too little overlap of pulses. A 10% overlap during treatment is recommended. (b) Crusting a side effect which clears within several days to a week. This only occurs when an erythematous rectangular footprint is observed immediately post-treatment.

two patients in whom small rectangular spots of hypopigmentation at the lateral neck margins have persisted at the end of 2 years. This was preceded by epidermal desquamation. With the newest progressive set of parameters, the incidence of acute side effects has been markedly reduced. The importance of not treating tanned areas of skin cannot be over-emphasized. Side effects include a mild burning sensation lasting ,10 min noted in 45%, and erythema which typically lasts several hours to 3 days. Mild cheek swelling or edema occurs 25% of the time with full face treatments primarily after the initial treatment and lasts from 24 to 72 h. Short-term hyper- or hypopigmentation (,2 months) has been noted in approximately 8– 15% of sites treated.

5.

SUMMARY

IPL is a system in which a flashlamp is pulsed under computer control with the use of filters to remove the wavelengths emitted by the flashlamp. The peak emission is

Figure 16.14 Combined treatment of IPL and sclerotherapy. The smaller telangiectasias are treated by IPL initially. This is followed by injection of 0.5 mL of sclerosing solution into the associated reticular vein. The authors prefer to sequence the IPL first in order to minimize the possibility of blood from the needle puncture contaminating the IPL crystals.

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yellow but the entire spectrum is 400 –1200 nm of this noncoherent light source. IPL has turned out to be more valuable than initially thought for facial telangiectasias, irregular pigmentation, textural skin smoothing, reduction of poikilodermatous changes, and hair removal. Treatment of leg telangiectasia must be accompanied by a method such as sclerotherapy or long pulse Nd:YAG laser to reduce venous pressure from associated reticular varicosities (Fig. 16.14). Excellent clinical results for small red telangiectasias are achieved by use of synchronized pulses with an initial short pulse of 2.4 – 3 ms coupled with a second longer pulse duration of 5 –8 ms with a progressive increase of duration and fluence based on increasing vessel size. Safety is greatly enhanced by floating the crystal in gel. When using non-actively cooled, non-smooth pulse technologies, safety is greatly enhanced by floating the crystal in a gel. However, actively cooled models permit increased fluences and greater efficacy with a greater safety margin. Adverse effects include epidermal crusting but proper technique and adherence to published parameters minimize this possibility. Hair removal has been shown to be long-term using total pulse durations of 10 –20 ms but the same treatment principles of proper distance of crystal from the skin with sufficient thermal relaxation time between pulses is necessary to achieve good results.

REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9.

10. 11. 12.

13. 14. 15.

Weiss RA, Goldman MP, Weiss MA. Treatment of poikiloderma of Civatte with an intense pulsed light source. Dermatol Surg 2000; 26(9):823 – 827. Bitter PH. Noninvasive rejuvenation of photodamaged skin using serial, full-face intense pulsed light treatments. Dermatol Surg 2000; 26(9):835 – 842. Goldberg DJ, Cutler KB. Nonablative treatment of rhytids with intense pulsed light. Lasers Surg Med 2000; 26(2):196– 200. Raulin C, Schroeter CA, Weiss RA, Keiner M, Werner S. Treatment of port-wine stains with a noncoherent pulsed light source: a retrospective study. Arch Dermatol 1999; 135(6):679– 683. Jay H, Borek C. Treatment of a venous-lake angioma with intense pulsed light. Lancet 1998; 351(9096):112. Weiss RA, Weiss MA, Marwaha S, Harrington AC. Hair removal with a non-coherent filtered flashlamp intense pulsed light source. Lasers Surg Med 1999; 24(2):128 – 132 (letter). Raulin C, Schroeter C, Maushagen-Schnaas E. Treatment possibilities with a high-energy pulsed light source (PhotoDerm VL). Hautarzt 1997; 48(12):886– 893. Raulin C, Weiss RA, Schonermark MP. Treatment of essential telangiectasias with an intense pulsed light source (PhotoDerm VL). Dermatol Surg 1997; 23(10):941– 945. Raulin C, Goldman MP, Weiss MA, Weiss RA. Treatment of adult port-wine stains using intense pulsed light therapy (PhotoDerm VL): brief initial clinical report. Dermatol Surg 1997; 23(7):594– 597 (letter). Schroeter C, Wilder D, Reineke T et al. Clinical significance of an intense, pulsed light source on leg telangiectasias of up to 1 mm diameter. Eur J Dermatol 1997; 7:38– 42. Sadick NS, Weiss RA, Shea CR, Nagel H, Nicholson J, Prieto VG. Long-term photoepilation using a broad-spectrum intense pulsed light source. Arch Dermatol 2000; 136(11):1336– 1340. Weiss RA, Sadick NS. Epidermal cooling crystal collar device for improved results and reduced side effects on leg telangiectasias using intense pulsed light. Dermatol Surg 2000; 26(11):1015– 1018. Sommer A, Van MP, Neumann HA, Kessels AG. Red and blue telangiectasias. Differences in oxygenation? Dermatol Surg 1997; 23(1):55– 59. Keijzer M, Jacques SL, Prahl SA, Welch AJ. Light distributions in artery tissue: Monte Carlo simulations for finite-diameter laser beams. Lasers Surg Med 1989; 9(2):148 – 154. Adrian RM. Treatment of leg telangiectasias using a long-pulse frequency-doubled neodymium:YAG laser at 532 nm. Dermatol Surg 1998; 24(1):19 – 23.

Noncoherent Light Source 16.

17. 18. 19. 20. 21. 22.

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Dierickx CC, Casparian JM, Venugopalan V, Farinelli WA, Anderson RR. Thermal relaxation of port-wine stain vessels probed in vivo: the need for 1– 10 millisecond laser pulse treatment. J Invest Dermatol 1995; 105:709 – 714. Kimel S, Svaasand LO, Hammer-Wilson M, Schell MJ, Milner TE, Nelson JS et al. Differential vascular response to laser photothermolysis. J Invest Dermatol 1994; 103(5):693– 700. Goldman MP, Eckhouse S. Photothermal sclerosis of leg veins. ESC Medical Systems, Ltd Photoderm VL Cooperative Study Group. Dermatol Surg 1996; 22(4):323 – 330. Green D. Photothermal sclerosis of leg veins. Dermatol Surg 1997; 23(4):303 – 305 (letter; comment). Raulin C, Werner S, Hartschuh W, Schonermark MP. Effective treatment of hypertrichosis with pulsed light: a report of two cases. Ann Plast Surg 1997; 39(2):169 – 173. Gold MH, Bell MW, Foster TD, Street S. Long-term epilation using the EpiLight broad band, intense pulsed light hair removal system. Dermatol Surg 1997; 23(10):909– 913. Weiss RA, Weiss MA. Early clinical results with a multiple synchronized pulse 1064 nm laser for leg telangiectasias and reticular veins. Dermatol Surg 1999; 25(5):399 – 402.

17 Excimer Lasers James M. Spencer Mount Sinai School of Medicine, New York, New York, USA

1. 2. 3. 4.

Technology Laser – Tissue Interactions Tissue Ablation Laser Phototherapy 4.1. Psoriasis 4.2. Hypopigmented Scars 4.3. Vitiligo 5. Safety Considerations 6. UVB Lasers and Light Sources 7. Treatment Guidelines 7.1. Psoriasis 7.2. Vitiligo and Hypopigmented Scars 8. Conclusion References

1.

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TECHNOLOGY

Excimer lasers are a class of lasers with multiple medical uses in fields such as ophthalmology, cardiology, orthopedics, and most recently, dermatology. Excimer is short for excited dimer, and refers to a series of lasers operating in essentially the same fashion in the ultraviolet range. Examples include the 193 nm argon-fluoride, 248 nm kryptonfluoride, 351 nm xenon-fluoride, and of particular interest to dermatology, the 308 nm xenon-chloride laser. These lasers were initially used in medicine for their ability to produce “cold ablation” of tissue, and more recently as a method of nonablative phototherapy. All of the excimer lasers utilize a mixture of a rare gas and a halogen as a lasing material. Normally, the gaseous components of the laser exist as separate and stable compounds. High power electrical energy is delivered to the gas mixture, which ionizes the gases and produces dimer formation. An example would be the xenon-chloride laser in which Xeþ and Cl2 ions are produced, which in turn bond to form a dimer. At least 375

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two states of the dimer are produced: an excited dimer (from which the name excimer is derived) and a nonexcited dimer. The excited dimer is metastable and quickly decays to the nonexcited state. Light is emitted as the excited dimer decays, and through the process of stimulated emission, laser light is created. The nonexcited dimer quickly decays to the monoatomic state (to Cl2 and Xe in the case of the xenon-chloride laser) without the emission of light. The gas mixtures are usually held at increased pressure with inert buffering gases. With repeated use, the gas tends to wear out as repeated electrochemical processes create side compounds, such as HCl in the case of the xenon-chloride laser buffered with H2 . Furthermore, the halogen can react with components that make up the lasers’ electrodes and cavity. For these reasons, repeated use required relatively frequent changing of the gas when these lasers were first developed. Recent technical advances in the gas preparation and storage have made these lasers much more stable, with less frequent gas exchanges necessary. The laser light from excimer lasers can be delivered via a fiberoptic cable, which facilitates their use in medicine. They can function in a liquid medium, which has allowed their use in cardiology and orthopedics. Initially, the delivery fibers were thick and brittle and therefore a bit difficult to use. Advances in delivery systems have made these fibers more convenient and reliable as well.

2.

LASER – TISSUE INTERACTIONS

The interaction of the excimer lasers with a variety of tissues has been extensively studied but is still not well understood. Most lasers of medical interest work by a thermal mechanism, that is, the target of the laser is heated and thus destroyed. The theory of selective photothermolysis has allowed the spatial confinement of the heat to spare surrounding structures (1), but the basic mechanism is to boil or “cook” the target. This leads to at least some spread of heat by thermal conduction. It was initially observed that the ultraviolet light excimer lasers could etch precise patterns in organic polymer films with no apparent thermal effect (2). Surface material measuring fractions of micrometers thick could be predictably removed leaving etch marks with clean, sharp borders with no evidence of a thermal effect (3,4). It has been theorized this process is photochemical rather than thermal. The photons of excimer laser light are of very high energy delivered in short pulses usually in the range of 20 –60 ns. For some organic molecules, the energy of the photons can exceed the energy of the chemical bonds holding the material together. Therefore, the target may decompose into fragments that are carried away from the surface by the gaseous or liquid environment surrounding the surface of the target. It is thought that most of the energy of the laser goes into producing these fragments, and in turn any residual energy from the laser pulse is carried away from the surface by these fragments. This phenomenon has been termed ablative photodecomposition (4). A variety of tissues were tested for this effect, including cornea, cartilage, vessels, and skin (5 –7). It was found that the surface of these tissues could be ablated quite precisely with almost no effect measurable beneath the ablated surface. In fact, for most material, no disruptions beyond 5 –10 mm beneath the surface could be detected (8). It is thought that as long as the pulse energy exceeds the level necessary to break molecular-bonds, very little thermal effect is generated. As laser energy is lowered below this threshold, thermal effects are observed. It has also been observed that higher repetition rates (the rate at which the laser delivers pulses) favor the creation of thermal effects (9).

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TISSUE ABLATION

The ability to ablate tissue with essentially no damage to surrounding tissue has allowed the excimer laser a variety of uses in medicine. First, the 193 nm laser has been extensively used in ophthalmology to reshape the cornea. The 308 nm excimer laser has been extensively studied in cardiology for its ability to remove clot and plaque from coronary blood vessels as an alternative to balloon angioplasty. In addition to removing clot following an acute myocardial infarction, the laser can also remove underlying atherosclerotic plaque. Furthermore, the laser light seems to have the effect of reducing the ability of platelets to aggregate, thus helping dissolve clots (10). The 308 nm laser has also been investigated as a therapy for congestive heart failure. The “cold ablation” produced by the laser is utilized to make holes in the left ventricle with no damage to the walls of the new channel. This appears to stimulate vascularization of the myocardium and improve perfusion. The 308 nm excimer laser has also been used in orthopedics to ablate cartilage and soft tissue in knee and spine surgery. The laser is delivered by a fiberoptic cable and works well in a liquid medium, so has been particularly effective for arthroscopic surgery (11). Initial evaluations of the excimer lasers in dermatology focused on skin ablation (7,9,12). It was found that the 193, 248, and 308 nm could all produce precise skin ablation with almost no thermal damage to surrounding tissues. Despite initial enthusiasm, alternative laser resurfacing systems were developed, including the pulsed CO2 and erbium:YAG lasers. Research on resurfacing with the excimer lasers was largely abandoned. Possible hindrances to the development of ultraviolet light resurfacing systems include the necessity for very large power sources to achieve ablative thresholds, technical problems with laser reliability, and the possibility of carcinogenesis with ultraviolet light. The current generation of excimer lasers have solved many of the technical problems of laser reliability. The issue of the carcinogenic potential is unlikely to be a concern as the UV irradiated cells are ablated. It is possible this is an area of dermatologic therapy that may be revisited in the future. Of interest in the initial research into the ablative properties of the excimer lasers were studies using the 351 nm xenon-fluoride laser. This laser is so strongly and selectively absorbed by melanin that selective thermal ablation of melanosomes with relative sparing of other cellular components is observed (13). Despite this observation, little additional research has been done with this laser in dermatology.

4.

LASER PHOTOTHERAPY

Dermatologic research in the use of excimer lasers paused while the ablative properties were investigated in other medical fields. In 1997, Bonis et al. (14) published a pilot study with a novel application of excimer technology: the use of low energy, subablative laser light as a source of UVB phototherapy. Ultraviolet light phototherapy has a long and extensive therapeutic history in dermatology, and is utilized to treat a variety of cutaneous diseases. Phototherapy with UVC, UVB, and UVA have all been extensively utilized over the last century. Currently, phototherapy has been confined to the UVB (290 –320 nm) and UVA (320 – 400 nm) ranges. 4.1.

Psoriasis

Psoriasis is one disease that responds well to UV phototherapy. Attempts to measure the action spectrum for psoriasis suggested that the optimal wavelength for treatment is

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around 313 nm (15). The xenon-chloride excimer laser emits at 308 nm, which is quite close to the optimal wavelength of 313 nm. In the pilot study, 10 patients with discreet, stable plaques of psoriasis were treated with escalating doses of subablative excimer laser light. The laser utilized emitted 15 ns pulses at a repetition rate of 20 pulses per second. From the tissue’s point of view, this laser functions as a continuous wave laser. The fluence of the laser was fixed at 5.5 mJ/cm2. The patients were treated three times a week, as this is a common outpatient schedule for conventional UVB phototherapy. Exposure time was increased each visit, which is analogous to increasing exposure time with conventional phototherapy. With conventional phototherapy units, the intensity of the light bulbs is fixed: the only variable is how long the patient stays in the light box. The 308 nm excimer laser for phototherapy functions the same way. Complete clearing was seen in 7 – 11 treatments (mean 8.6), with hyperpigmentation as the only side effect. Narrow band UVB phototherapy, with peak emission at 311 nm from conventional filtered light bulbs, offers excellent therapeutic efficacy for the treatment of psoriasis and is thought to be superior to conventional UVB phototherapy. Previous experience with this mode of therapy indicates around 30 treatments are necessary for clearing. The 308 nm excimer laser was directly compared to narrow band UVB phototherapy in six patients. These patients had bilateral, symmetric areas of psoriasis, such as both knees or both elbows. One side was treated with the laser, the other side with narrow band UVB phototherapy. As expected, the laser side cleared in 8 –10 treatments (mean 8.3), whereas the narrow band side required 29– 33 (mean 30.1). This study suggested a number of exciting possibilities of the excimer laser. First, the patient’s psoriasis improved significantly faster than with conventional phototherapy. Second, only diseased skin was irradiated with ultraviolet light, and thus normal uninvolved skin was spared the potentially harmful effects of UV light. Finally, the mean cumulative dose required to produce clearance with the laser was 4.81 J/cm2 vs. 31.1 J/cm2 for narrow band phototherapy, again lowering the patient’s exposure to potentially harmful UV exposure. Follow-up at 2 years revealed 8 of the 10 original patients remained in remission (16). This pilot study was followed by a larger dose –response trial in which 13 patients were treated with multiple doses and treatment schedules to determine optimal treatment parameters (17). In this study, 13 patients were enrolled who each had four separate stable plaques of psoriasis. The minimal erythema dose (MED) was determined on normal skin for each patient, then separate test sites within each plaque received doses of 0.5, 1, 2, 3, 4, 6, 8, and 16 times the MED. This pattern was repeated within each of the four plaques, and each plaque received 1, 2, 4, and 20 treatments, respectively. There was significantly better response in test sites receiving high multiples of the MED (8 – 16 times the MED) with complete clearing seen in as little as one treatment. However, this dose produced significant blistering and discomfort, and was only given to 4 patients out of the original 13. Lower multiples of the MED (3 –4 times the MED) also produced clearing in some test sites, but required more than one treatment. Sites treated at high multiples of the MED (8–16 times the MED) remained clear 4 months after treatment, while all sites treated with lower fluences recurred. This suggested that utilizing high fluences was the most significant variable for therapeutic effect, however, the very high fluences used were poorly tolerated and are not realistic for clinical practice. However, more modest multiples of the MED were well tolerated, and produce a therapeutic effect in considerably less time than that required of conventional phototherapy. Of note was that moderate multiples of the MED (3 – 4 times the MED) are very well tolerated within the psoriatic plaques but would produce unacceptable burns on surrounding uninvolved skin. Use of the laser allows only the psoriatic plaque to be treated.

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Trehan and Taylor treated a larger number of patients at high fluences (18). Sixteen patients each with two plaques of psoriasis completed the study. Each plaque was divided into two halves: one to receive excimer laser phototherapy, the other to serve as a control. Each patient’s MED was determined, then the plaques were treated. One plaque served as 8 times the MED test site, and the other plaque received 16 times the MED, each for one dose only. Eleven of the sixteen patients showed significant improvement (.75% better) 1 month after only one treatment. Sixteen times the MED produced a slightly longer remission than eight times, otherwise there was not a significant difference between the doses. The treatment itself was quick and painless, however, moderately painful bullae developed at the treatment sites in 6 –12 h, which crusted and healed without scarring in about 1 week. Although very high multiples of the MED appears to be quickly effective in the treatment of psoriasis, it may not be well tolerated in clinical practice. Therefore, multiple treatments with medium doses as opposed to a single treatment with a high dose were tested (19). Twenty patients each with seven stable plaques of psoriasis were enrolled. Six plaques were treated, and one served as a control. Following determination of the MED, medium doses of excimer laser were given three times a week. As in conventional phototherapy, a flexible, slowly escalating dosing schedule was used based on patient response. Following this schedule, it was found that it was possible to achieve .95% clearance in a mean of 10.6 treatments. The mean remission time was 3.5 months. Clearance in 2 –3 weeks represents a significant improvement over conventional phototherapy, which typically requires a mean of at least 30 treatments. Using moderate dosing regimes, it was possible to avoid the unpleasant side effects seen with high dose therapy and still achieve clearing more quickly than is possible with conventional phototherapy. These findings were confirmed in the largest trial to date, in which 80 patients received 308 nm excimer laser at low multiples of their MED twice a week for a total of 10 treatments or clearing, whichever came first (20). The MED of uninvolved skin was determined, then the psoriatic plaques were treated at a low multiple of this MED. Exposure time was increased based on response to treatment. It was found that 72% of the patients achieved 75% or greater clearance at an average of 6.2 treatments. In sum, nonblistering doses of excimer laser can produce clearing in the majority of patients in about 2 –3 weeks, a significantly faster response time than that of conventional phototherapy (Fig. 17.1). This results in a lower cumulative dose of UV radiation, and spares the normal surrounding skin any exposure at all.

Figure 17.1 Treatment of chronic inverse psoriasis: (left) after 3 weeks and (right) after 6 months.

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Difficult to treat areas of psoriasis include the scalp and the groin (inverse psoriasis). Excimer laser may offer distinct advantages in treating difficult areas. In a single case report, Muffing et al. (21) reported a single patient with chronic inverse psoriasis cleared completely following 3 weeks of laser treatment, and remained clear at followup of 6 months. 4.2.

Hypopigmented Scars

In addition to psoriasis, a variety of skin disease respond to ultraviolet light, opening up multiple other possibilities for the use of the excimer lasers in dermatology. One such use is the repigmentation of hypopigmented lesions. Friedman and Geronemus (22) reported two cases of hypopigmentation following laser resurfacing in which the 308 nm excimer laser led to partial repigmentation. The first patient had 75% repigmentation in 8 treatments, whereas the second had 50 – 75% repigmentation in 10 treatments. 4.3.

Vitiligo

Therapy for vitiligo is another hypopigmented lesion that excimer laser holds great therapeutic promise. In a pilot study, Spencer et al. (23) treated 23 patches of vitiligo in 12 patients three times per week for a minimum of 2 weeks (six treatments). Treatments were begun at the lowest exposure time of the laser, then slowly increased every other treatment as the patient tolerated. Predetermination of the MED on normal skin was not done, as the response of normal skin is not relevant to the response of the vitiliginous areas. At least some repigmentation was seen in 57% of the treated areas in only 2 weeks. The repigmentation was perifollicular, suggesting that new melanocytes were recruited from hair follicles. The repigmentation was far from complete, with only 9% showing complete repigmentation, but that observation that the majority of patients were beginning to respond after only 2 weeks of treatment was encouraging. In the same study, 11 patches of vitiligo in six patients received treatment three times a week for 4 weeks (12 treatments total). In this group, 82% showed at least some repigmentation, and the degree of repigmentation was greater than at 2 weeks. In this group, 18% showed complete repigmentation (Fig. 17.2) This pilot study suggested that excimer laser may offer a superior therapeutic option for vitiligo than conventional phototherapy. Both PUVA and narrow band UVB are utilized for this condition, but require months to

Figure 17.2 (Left) A patient with vitiligo before treatment and (right) after treatment with 308 nm excimer later.

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years of treatment for response rates of 50% or less. At our center, we have now treated over 60 patches of vitiligo twice a week for a minimum of 30 treatments, or repigmentation, whichever comes first. Patients will be dissatisfied with only partial repigmentation, so success is defined as 75% or greater repigmentation. We have found that different locations respond with dramatically different results. On the face, 72% of patients repigment, elsewhere on the head and neck 60% repigment, in the genital region 50% repigment, on the limbs 47% repigment, on the torso 40% repigment, and the hands and feet none of the patients completely repigment. We have also observed that darker skinned patients respond better than fair skinned individuals, and that newer lesions respond better than older lesions. To date, the repigmentation has been persistent, even in patients with active vitiligo who develop new patches in untreated areas. Ongoing studies are continuing to evaluate what appears to be a very effective therapy for many vitiligo patients. Other conditions responsive to UV phototherapy, such as atopic dermatitis and cutaneous T cell lymphoma, are similarly being evaluated.

5.

SAFETY CONSIDERATIONS

Ultraviolet light is believed to be the causative agent of the vast majority of skin cancers, so UV phototherapy raises the possibility of iatrogenically generated tumors. For nonmelanoma skin cancer, the shorter wavelengths are thought to be more carcinogenic (UVC . UVB . UVA), while the action spectrum for melanoma remains unclear. There is a long history of conventional phototherapy, and while it has never been positively demonstrated that UVB phototherapy increases patient’s risk of skin cancer, PUVA has been associated with an increased risk of both melanoma and squamous cell carcinoma (24,25). Although there has been repeated concern of tumor induction from the 308 nm excimer laser, no long-term human use data is available. Laboratory studies have provided some reassurance. Hendrich and Siebert (26) used an in vitro tissue culture transformation assay with BALB/3T3 cells exposed to varying subablative doses of 308 nm excimer laser irradiation. There was no significant difference between the excimer exposed cells and negative control cells. Multiple exposure also did not produce a transformation rate different than negative controls. In contrast, a positive control using X-ray irradiation produced a significant transformation rate. On theoretic grounds, the excimer laser may actually be safer than conventional phototherapy. First, only the effected area of skin is exposed, as opposed to the whole body exposure typically given with conventional phototherapy. Second, studies of psoriasis and vitiligo have shown a significantly lower number of treatments, and thus a lower cumulative dose is needed to produce a therapeutic effect. Long-term follow-up from clinical practice will be needed to truly assess the true risks of 308 nm excimer laser phototherapy.

6.

UVB LASERS AND LIGHT SOURCES

The ability of the 308 nm excimer laser to deliver high dose phototherapy to diseased skin only is an obvious benefit, and in response targeted conventional phototherapy units have been developed. Recently, FDA has approved for clinical use, two very similar targeted UVB phototherapy devices: the Bclear and ReLume systems, both manufactured by the Lumenis Corporation. Both of these systems are compact conventional mercury vapor arc lamps in which the UV light is filtered to give UVB light (290 –320 nm) delivered through a fiberoptic cable. The mercury vapor arc lamp is an old UV producing lamp,

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and provides incoherent light, not laser light. In the past, UV producing bulbs were arrayed in a cabinet in which the patient stands or lays down in. The novel feature of these new systems is that the light is delivered through a fiber optic hand piece with a spot size of 16 mm. This allows targeted application of the UVB light to affected skin only and spares normal surrounding skin. The light can be delivered continuously, as an conventional phototherapy. The UVB light can also be pulsed, the effectiveness of which is unclear. There is certainly no question that conventional UVB phototherapy is effective for a variety of skin diseases, therefore it stands to reason these devices should be clinically effective. There are currently no published studies evaluating these devices, but studies are currently being performed. The Bclear is marketed for psoriasis, whereas the ReLume system is marketed for hypopigmented lesions, such as leukoderma following laser resurfacing or chemical peels, or hypopigmented stretch marks (striae alba). As previously mentioned, these two systems are both filtered mercury vapor arc lamps delivered via a fiberoptic cable to a 16 mm spot size. Both operate in continuous or pulsed mode. The Bclear will deliver higher fluences, which is essentially the only difference between the two units.

7.

TREATMENT GUIDELINES

Phototherapy with the 308 nm excimer laser is still in its infancy, and detailed studies to delineate optimal dosing and treatment schedules are still being conducted. The greatest experience with this laser has been in the treatment of psoriasis. An early observation in the use of this laser is that psoriatic plaques can receive significantly more UVB light than normal skin and not develop a noticeable sunburn reaction. Targeted phototherapy with the 308 nm laser therefore allows one to safely deliver therapeutic doses of UV light to psoriatic plaques that would otherwise produce an unacceptable sunburn reaction on surrounding normal skin. The energy output and duration of each pulse of the laser is fixed, and thus the actual energy output of each laser pulse cannot be changed. However, the laser is rapidly pulsed, and thus from the tissue’s perspective, the laser functions as a continuous wave device. The variables that can be adjusted are the repetition rate of the pulses (pulses per second) and the total time the laser is on. The laser is constructed to operate in one of two modes in which one can adjust exposure time (tile mode) or repetition rate during a fixed exposure time (paint mode). It is not possible to adjust both repetition rate and exposure time at the same time. Rather, one must choose which parameter one wishes to control. In each mode, there are a number of dosing increments the operator can set. Each mode is set such that the total dose delivered is increased by 50 mJ/cm2 at each increment. The operator chooses one of 20 possible dosing levels by adjusting two settings labeled MED and multiplier. There is redundancy in the possible settings, so although 35 combinations of the MED and multiplier settings are possible, actually only 20 dosing levels exist. Although there are two settings to be made, they do the same thing: adjust the repetition rate or the total exposure time. The laser could have been constructed with only one setting to be made: dosing level 1 –20. A simple chart showing all possible combinations of the two settings (MED and multiplier) reveals that dose delivered can vary from a minimum of 100 mJ/cm2 to a maximum of 2100 mJ/cm2 in increments of 50 mJ/cm2 (Fig. 17.3). 7.1.

Psoriasis

For psoriasis therapy, the MED is first determined on normal skin. It has been found that for the majority of people, this can be by exposing normal skin to six doses, conveniently

Excimer Lasers

Figure 17.3 settings.

383

Treatment doses obtained by for all possible combinations of MED and multiplier

labeled MED I –VI, all with a multiplier setting of 1. Therapy is begun at or slightly above (2 –3 times) the MED on normal skin. In general, psoriatic plaques will tolerate 2 – 3 times the MED without a noticeable sunburn reaction. The dose is increased 50 mJ each treatment session as tolerated. If a sunburn develops, treatment is withheld until it resolves. Treatment frequency has not been studied. Therefore, it is not clear how many treatments per week is advisable. A sunburn reaction from UVB takes about 12 h to develop, so certainly treatment more than once a day is dangerous. Most studies have looked at treatment two or three times per week because this is a realistic outpatient schedule for patients. It has been our experience that twice a week is easier for most patients than three times per week, however, there is a suggestion from studies using narrow band UVB that more frequent dosing works more quickly. As excimer laser most closely resembles narrow band UVB, it is reasonable to consider the narrow band data. In a study comparing narrow band phototherapy for psoriasis five times per week vs. three times per week, Dawe et al. (27) found the median time to significant improvement to be 35 vs. 40 days, respectively. However, the five times per week received a significantly greater cumulative dose of UVB for a modest gain in time to clearance. In a similar study comparing twice a week with three times per week (28), the same group found that it took 1.5 times as long for the twice a week group to significantly improve as the three times per week group. It will be necessary to conduct similar studies with the laser to determine the optimal dosing schedule. The laser light is delivered as a square spot of 18 18 mm, and overlapping is not recommended. However, there appears to be an area of greater intensity in the center of the beam profile. An iris covering the delivery head is now available. This enables the user to create a circular spot of smaller diameter for smaller areas. This is particularly important when one wishes to avoid tanning the surrounding skin. 7.2.

Vitiligo and Hypopigmented Scars

Treatment of vitiligo and other hypopigmented lesions requires special consideration. Determining the MED on normal skin is irrelevant to the hypopigmented areas, as they will burn much more easily than normal skin. It has been our experience to begin treatment at the lowest or close to the lowest dosing level, then carefully increase the dose by 50 mJ

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every other treatment. It is easy to sunburn the involved areas, so caution is wise as one gains experience. It has been our observation that as opposed to psoriasis, there is no benefit for repigmentation in burning the hypopigmented area. In fact, a sunburn delays repigmentation as one must hold treatment until the burn resolves. The optimal frequency of exposure is unknown, but again most patients will find it very difficult to come to the office for therapy more than two or three times a week. The use of adjuvant topical medications, both for psoriasis and vitiligo, may be found to enhance treatment. However, no studies have been published addressing this area, and it remains a topic of of active research. Sunburn is really the only complication one is likely to encounter. As previously mentioned, burning an area of psoriasis seems to speed clearing. There is no advantage to burning a hypopigmented lesion. For mild burns, mild topical emollients and the use of nonsteroidal antiinflammatories is helpful. If blistering occurs, use of a topical antibiotic to prevent infection is wise. Tanning of the surrounding normal skin may also be seen, but as with any tan this will fade with time.

8.

CONCLUSION

Phototherapy has a long, proven record of success in dermatology. Phototherapy with the excimer 308 nm laser appears to be a significant improvement, with more rapid, complete responses for those diseases so far studied. Furthermore, it may offer therapy for skin lesions previously untreatable with conventional phototherapy, such as hypopigmented scars and stretch marks. As more is learned about optimal dosing and treatment parameters, we can only expect this therapeutic option to improve. REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13.

Anderson RR, Parrish JA. Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science 1983; 220:524 – 527. Parrish JA. Ultraviolet-laser ablation. Arch Dermatol 1985; 121:599– 600. Srinivasan R, Mayne-Banton V. Self-developing photoetching of poly(ethylene terephthalate) films by far-ultraviolet laser radiation. Appl Physics Lett 1982; 41:576 – 578. Srinivasan R, Leigh WJ. Ablative photodecomposition: action of far-ultraviolet (193 nm) laser radiation on poly(ethylene terephthalate) films. J Am Chem Soc 1982; 104:6784 – 6785. Trokel SL, Srinivasan R, Braren B. Excimer laser surgery of the cornea. Am J Ophthalmol 1983; 96:710 – 715. Linsker R, Srinivasan R, Wynne JJ et al. Fat-ultraviolet laser ablation of atherosclerotic lesions. Lasers Surg Med 1984; 4:201– 206. Lane RJ, Listker R, Wynne JJ et al. Ultraviolet-laser ablation of skin. Arch Dermatol 1985; 121:609 – 617. Buchelt M, Papaioannou T, Fishbein M et al. Excimer laser ablation of fibrocartlidge: an in vitro and in vivo study. Lasers Surg Med 1991; 11:271 –275. Kaufmann R, Hibst R. Pulsed Er:YAG and 308 nm UV-Excimer laser: An in vitro and in vivo study of skin-ablative effects. Lasers Surg Med 1989; 9:132– 140. Topa On, Minisi AJ, Bernardo NL et al. Alterations of platelet aggregation kinetics with ultraviolet laser emission: the stunned platelet phenomenon. Thromb Haemost 2001; 86:1087–1093. Gossop ND, Jackson RW, Koort HJ et al. The excimer laser in orthopedics. Clin Ortho Relat Res 1995; 310:72 –81. Lane RJ, Linsker R, Wynne JJ. UV-laser ablation of the skin. Arch Dermatol 1985; 121:609–617. Murphy GF, Shepard RS, Paul BS et al. Organelle-specific injury to melanin-containing cells in human skin by pulsed laser irradiation. Lab Invest 1983; 49:680 – 685.

Excimer Lasers 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25.

26. 27.

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Bonis B, Kemeny L, Dobozy A et al. 308 nm UVB excimer laser for psoriasis (Letter). Lancet 1997; 350:1522. Parrish JA, Jaenicke KF. Action spectrum for phototherapy of psoriasis. J Invest Dermatol 1981; 76:359 – 362. Kemeny L, Bonis B, Dobozy A et al. 308 nm excimer laser therapy for psoriasis. Arch Dermatol 2001; 137:95 – 96. Asawanonda P, Anderson R, Chang Y et al. 308-nm excimer laser for the treatment of psoriasis. Arch Dermatol 2000; 136:619 – 624. Trehan M, Taylor CR. High-dose 308-nm excimer laser for the treatment of psoriasis. J Am Acad Dermatol 2002; 46(5):732– 737. Trehan M, Taylor CR. Medium-dose 308 nm excimer laser for the treatment of psoriasis. J Am Acad Dermatol 2002; 47(5):701– 708. Feldman SR, Mellen BG, Housman TS et al. Efficacy of the 308-nm excimer laser for treatment of psoriasis: results of a multicenter trial. J Am Acad Dermatol 2002; 46(6):900–906. Muffing EA, Friedman PM, Kauvar AN et al. Treatment of inverse psoriasis with the 308 nm excimer laser. Dermatol Surg 2002; 28(6):530– 532. Friedman PM, Geronemus RG. Use of the 308-nm excimer laser for post resurfacing leukoderma (Letter). Arch Dermatol 2001; 137(6):824– 825. Spencer JM, Nossa R, Ajmeri J. Treatment of vitiligo with the 308-nm excimer laser: a pilot study. J Am Acad Dermatol 2002; 46(5):727– 731. Stern RS, Lange R. Non-melanoma skin cancer occurring in patients treated with PUVA five to ten years after first treatment. J Invest Dermatol 1988; 91:120 –124. Stern RS, Nichols KT, Vakeva LH. Malignant melanoma in patients treated for psoriasis with methoxsalen (psoralen) and ultraviolet A radiation (PUVA). The PUVA follow-up study. N Engl J Med 1997; 336:1041 – 1045. Hendrich C, Siebert WE. Mutagenic effects of the excimer laser using a fibroblast transformation assay. Arthroscopy 1997; 13(2):151– 155. Dawe RS, Wainwright NJ, Cameron H et al. Narrow-band (TL-01) ultraviolet B phototherapy for chronic plaque psoriasis: three times or five times weekly treatment? Br J Dermatol 1998; 138(5):833– 839. Cameron H, Dawe RS, Yule S et al. A randomized, observer-blinded trial of twice vs. three times weekly narrowband ultraviolet B phototherapy for chronic plaque psoriasis. Br J Dermatol 2002; 147(5):973 –978.

18 Photodynamic Therapy Shirley Jean-Baptiste, David A. Wrone, and Murad Alam Northwestern University, Chicago, Illinois, USA

1. Introduction 2. Photosensitizers 3. Light Delivery 3.1. Polychromatic Light Sources 3.2. Lasers 3.3. Light Dosimetry 4. Photoinduced Destruction 5. Applications in Dermatology 5.1. Actinic Keratoses 5.2. Basal Cell Carcinoma 5.3. Bowen’s Disease 5.4. Squamous Cell Carcinoma 5.5. Melanoma 5.6. Skin Conditions Other than Nonmelanoma Skin Cancer 5.7. Recalcitrant Warts 5.8. Acne 5.9. Psoriasis 5.10. Cutaneous T-cell Lymphoma 5.11. Skin Rejuvenation 5.12. Prevention and Management of Complications 6. Conclusions References

1.

387 388 389 389 389 390 390 391 391 394 395 396 396 396 396 396 397 397 397 398 398 399

INTRODUCTION

Photodynamic therapy (PDT) is a treatment modality that utilizes three elements, a photosensitizing drug, light, and oxygen, to induce targeted cell death of neoplastic or abnormal tissue (1). Specifically, sensitization of the target tissue is selective and occurs via the topically or systemically administered photosensitizing agent. After administration, the photosensitizer is activated by light and reacts with oxygen and other metabolites to 387

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produce highly reactive oxygen intermediates and free radicals that result in destruction of targeted tissue (2). The concept of PDT has existed for nearly a century, but it has developed into a feasible clinical modality only in the last 25 years (3). In 1978, Dougherty et al. (4) reported successful treatment of a variety of cutaneous and solid-organ tumors with intravenous PDT using hematoporphyrin derivative (HPD) as a sensitizer that was irradiated with a red light source. The disadvantage of this and other systemic PDT is that patients may be rendered photosensitive for up to 8 weeks, during which period they must avoid natural or strong interior light (5). Dougherty’s pioneering work was succeeded by Kennedy et al.’s (6) introduction of topical PDT for cutaneous neoplasms in 1990. The introduction of a new photosensitizer prodrug, 5-aminolevulinic acid (5-ALA), represented a novel approach for induction of photosensitization as this substance penetrates the stratum corneum to reach the deep stroma of skin tumors, where it is transformed into the highly photoactive endogenous protoporphyrin IX (PpIX) (7).

2.

PHOTOSENSITIZERS

The major classes of photosensitizers include the porphyrin derivatives, porphines, phthalocyanines, chlorin derivatives, and texaphyrins (1,8). Only the HPDs and 5-ALA, both members of the porphyrin group, have been evaluated in skin disease. Indeed, most studies in dermatology have examined the application of 5-ALA. 5-ALA is a precursor in the heme biosynthetic pathway. Once absorbed preferentially by abnormal keratin, it is transformed within tumor cells into highly photoactive endogenous PpIX. Topical administration of 5-ALA allows the first rate-limiting step (the synthesis of ALA from glycine and succinyl-CoA) of porphyrin metabolism to be bypassed, thereby promoting accumulation of this precursor in abnormal keratinocytes. Downstream in the heme biosynthetic pathway, ALA is converted to PpIX. PpIX in normal physiologic conditions is ultimately converted to heme by the enzyme ferrochetalase. In many epithelial tumors, however, ferrochetalase activity (catalyzes the second rate-limiting step of the pathway—the incorporation of iron into PpIX to form heme) is reduced, further promoting the accumulation of the photosensitizing agent PpIX (3,8 – 11). The route of topical application associated with ALA is convenient and permits localization specifically on neoplastic tissue (5). Interestingly, 5-ALA is a hydrophilic molecule and poor penetrant of intact or normal keratinocytes; possibly, its tumor selectivity reflects the abnormal permeability of diseased epithelium (1). While there is limited uptake of 5-ALA by normal cells, the chemical is retained longer in tumors and proliferating tissue (1). A major advantage of ALA-PDT is the avoidance of generalized and prolonged photosensitivity due to its short half-life and rapid clearance from normal tissue. Generally ALA-derived PpIX fluorescence cannot be detected in the skin 24 h after completion of topical ALA application (9). Time-dependent changes in surface skin fluorescence is commonly used to measure ALA pharmacokinetics such as peak accumulation and mean clearance half-life after topical admininistration. Another characteristic of an optimal photosensitizer is a short duration between administration of drug and maximal accumulation in the tumor. PDT with 20% ALA has been shown to maximally accumulate at 11 h in lesional skin as measured by surface skin fluorescence peak intensity. The time to peak concentration determines when it is appropriate to apply light, and hence the practicality of the therapy in the clinical setting. Additionally, the photosensitizer must be activated at wavelengths that penetrate deeply, yielding copious generation of singlet oxygen (8,12,13). PpIX, the ultimate

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product in ALA-PDT, has a maximum absorption peak around the Soret band (360 – 400 nm) with four smaller absorption peaks at 505, 540, 580, and 630 nm. Hence this substrate may not be ideal for deeper processes, since the wavelength necessary for deep penetration (630 nm) corresponds to a weaker peak of the absorption spectrum. The “ideal” photosensitizer is yet to be discovered. A significant number of experimental photosensitizing agents are currently being evaluated primarily in the management of parenchymal and solid-organ tumors.

3.

LIGHT DELIVERY

PpIX absorbs light maximally around the Soret band but also shows decreasing absorption at four additional bands between 500 and 650 nm (1). The light applied in ALA-PDT therefore is part of the visible part of the spectrum (400 –700 nm). Penetration of light through tissues is not uniform at all wavelengths. Red light sources (630 –650 nm) penetrate deepest, down 6 mm from the surface of the skin. Blue light sources (400 nm) coincide with the maximum absorption peak (the Soret band), but only reach a maximum depth of 2 mm (1,11). Most light sources used in PDT utilize the red (630 nm) absorption peak of PpIX to maximize tissue penetration. Furthermore, light delivery range between 600 and 800 nm is considered the “therapeutic window” for clinical treatment because of significant absorption of light by hemoglobin at wavelengths ,600 nm, and by water at wavelengths .1200 nm (9,10). Green light sources (500 – 550 nm) penetrate up to 3 mm, deeper than blue light. Both blue and green light are reported to be effective in the treatment of actinic keratoses (AK), which are associated with pathologic changes restricted to the epidermis (14). 3.1.

Polychromatic Light Sources

Both laser and nonlaser light sources have been used for ALA-PDT. The nonlaser or incoherent light sources include xenon arc/discharge lamps and incandescent filament lamps. Nonlaser light sources appear to be as effective as laser light sources (1,15). Incoherent lights sources such as halogen (600 – 800 nm), xenon (600 – 660 nm), and fluorescent lamps (412 –422 nm), are the most widely used light sources because of their low cost, wide availability, and simple operation. Furthermore, the broad band emissions of lamps in the 400– 750 nm range may activate photoproducts in addition to PpIX, thereby augmenting the photodynamic effect (1,9). For instance, the light of the common slide projector (400 –650 nm) equipped with red pass filters was employed in early studies with good clinical results (16). Among the light sources specifically designed for PDT are the Waldmann PDT1200 (Germany), a metal halide lamp that emits from 600 to 750 nm at 10– 200 mW/cm2; the Photocure Curelight (Norway) a tungsten/halogen lamp that emits at 570– 670 nm at ,150 mW/cm2; the Paterson PTL (UK), a xenon arc lamp that emits at 630 + 15 nm at 10– 130 mW/cm2; and the DUSA BLU-U (USA), a fluorescent lamp that emits at 417 + 5 nm at 10 mW/cm2 (14). Intense pulsed light (IPL) sources are effective in activating ALA and are being used in dermatologic applications. 3.2.

Lasers

The purpose of lasers in PDT is to serve as the light source for driving the photodynamic effect. This is in contrast to other laser applications in dermatology, where photothermal

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and photomechanical effects are employed for indications such as skin resurfacing or removal of vascular and pigmented lesions (17). The advantage to using lasers in PDT is that their monochromatic output can be precisely selected to correspond with a photosensitizer’s peak absorption wavelength so as to maximize drug activation efficiency. Additionally, it may be possible to produce laser light at specified wavelengths at irradiances sufficient to keep exposure times within practical limits when treating patients (17). Tunable pumped dye lasers such as the argon-dye laser and the neodymium:YAGdye laser have been widely used laser devices for PDT because of their range of selectable wavelengths. The argon-dye laser system emits light continuously and can be tuned to suit the selection properties of various photosensitizing compounds (8). Pulsed lasers such as the gold vapor (628 nm) and copper vapor (578 nm) have also been used in PDT, but their use is limited to treatment of superficial lesions because of their shortwavelength output. Furthermore, their use have become less common due to their expensive price and exploitation, and fixed wavelength, which may fit only one sensitizer. Though randomized data are limited for laser sources, one comparative study suggests that continuous wave (argon-PDL) and pulsed laser systems (gold vapor laser) have equivalent tumoricidal effects (17,18). Lasers are optional, expensive light sources for PDT since coherent light is not a requirement. Because of the low average power output of dye lasers, longer exposure times are required to treat large areas or areas with multiple lesions. Semiconductor diode lasers are small, low-power, portable light sources with a fixed bandwidth. These less expensive and more compact alternatives are presently in development for PDT (8). Long pulsed dye lasers at 585 and 595 nm (19) have been shown to be effective in activating ALA.

3.3.

Light Dosimetry

Optimal light dose (J/cm2) and dose rate (mW/cm2) have not been defined in ALA-PDT. Comparison of dosimetry across studies is further limited by the ubiquity of different light sources and disease indications. Peng (9) reports fluences within a wide range of 20 – 250 J/cm2 for laser sources and 30 – 540 J/cm2 for nonlaser light sources, with the possibility that light exposure may have been overdosed in many clinical trials. Oxygen is essential for completing the photodynamic effect of PDT, and oxygen depletion is a concern at fluence rates .50 mW/cm2. Also to avoid hyperthermia, a fluence rate lower than 150 mW/cm2 is recommended (14), although this upper limit has been approached to reduce treatment times (1). Due to the many potential indications for topical ALAPDT, clinical protocols for particular uses should include specific parameters, including the administered ALA dose and vehicle, the drug-illumination interval, the wavelength/ band, the fluence rate or irradiance (mW/cm2), and fluence or dose (J/cm2) (14).

4.

PHOTOINDUCED DESTRUCTION

Absorption of a light photon by PpIX in ALA-PDT leads to a highly unstable excited triplet state. This unstable triplet sensitizer interacts with surrounding molecules to produce free radicals and singlet oxygen species. Interaction of singlet oxygen species with different biomolecules results in membrane lipid peroxidation, protein cross-linking, increased membrane permeability, and ultimately cell death (8). The potential for carcinogenesis in PDT is low as the photosensitizing agents do not localize to the nucleus (8).


5.

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APPLICATIONS IN DERMATOLOGY

Most clinical experience with topical ALA-PDT concerns the treatment of AK, basal cell carcinoma (BCC), Bowen’s disease, and squamous cell carcinoma (SCC). ALA has also been used for photodynamic diagnosis (PDD), a method of tumor delineation designed to guide tumor therapy. The term PDD is considered a misnomer since generation of reactive oxygen species does not occur with this method. Rather, irradiation with Wood’s light (370 –405 nm) is used to detect porphyrin fluorescence of an ALA-treated site in order to clinically define tumor margins (2). 5.1.

Actinic Keratoses

AK represent one of the most successful indications for ALA-PDT in dermatology (Figs. 18.1 –18.4). A number of studies report response rates of 71 –100% for facial AK after a single treatment (20 – 24). For the treatment of AK, a variety of noncoherent and coherent light sources have been used with wavelengths ranging from 417 to 630 nm and light doses and dose rates ranging from 10 to 540 J/cm2 and 10 –300 mW/cm2, respectively. Most studies of ALA-PDT for AKs are limited by lack of histologic confirmation, and have short follow-up periods ranging from 3 to 20 months. In one study of 50 AKs with an initial complete response rate of 100%, Calzavar-Pinton (21) observed tumor remnants in 3 of 17 histologically examined lesions. The remaining 33 lesions were followed for 24 –36 months (median 29 months), with clinical recurrence of five lesions. The rate of complete response remained high (final response rate 86%) although it was revised downward slightly after taking into consideration the results of serial histologic examination and long-term follow-up (21). Nonfacial hyperkeratotic lesions respond poorly to ALA-based PDT and have weighted clearance rates of 44%, compared with 91% for facial lesions (14,24–27). Response rates of ALA-PDT appear to be comparable to those of topical 5-fluorouracil

Figure 18.1

Levulan Kerastick (ALA) application. (Courtesy of George J. Hruza, MD.)

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Figure 18.2 Irradiation for 16 min 14– 18 h after application of ALA. (a) Light source; (b) side view of patient being irradiated; (c) rear view of patient being irradiated. (Courtesy of George J. Hruza, MD.)

(5-FU) and cryotherapy. In a randomized paired comparison of 17 patients with extensive AK affecting both hands, Kurwa et al. (28) compared a single treatment of ALA-PDT using a metal halogen lamp emitting red light at 580 nm (150 J/cm2, 86 mW/cm2) to a 3-week course of topical 5-FU applied twice daily. They found that topical ALA-PDT is tolerated as well as topical 5-FU, and does not demonstrate any therapeutic advantage over 5-FU. The reduction in lesional area with PDT (73%) was not statistically significant from that of 5-FU application (70%) (28). There are no reports comparing the efficacy of 5-ALA to cryotherapy. One randomized multicenter study compared ALA-PDT with cryotherapy using methyl 5-ALA, an ester derivative of ALA that has increased lipophilicity and thus better penetration than 5-ALA. Szeimes (24) reported overall response rates 3 months after a single treatment (69%) to be comparable to those with cryotherapy (75%). The majority of studies on AK utilized red light sources. This is not technically imperative, since while light delivery in the 600 –800 nm range may be optimally therapeutic for photoactivation of deeper neoplastic processes, AKs are superficial pathologic changes. Indeed, PpIX is more efficiently photoactivated by blue light than red light. Jeffes et al. (29) reported the efficacy of blue light (DUSA BLU-417 light source) for the


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Figure 18.3 ALA-PDT for actinic keratoses. (a) Male dorsal arm before treatment; (b) arm 3 weeks after treatment. (Courtesy of George J. Hruza, MD.)

treatment of AK in a multicenter randomized vehicle study. The clinical response (CR) was dependent on the dose of light administered with a maximum response reported at 10 J/cm2 (88% CR), rather than 5 and 2 J/cm2. There was a statistically significant increase in the clearance response from 8 (66%) to 16 (85%) weeks, demonstrating the benefit of repeated treatment cycles. DUSA BLU-U has also been tested as a light source for ALA-PDT treatment of AK. This process led to Food and Drug Administration (FDA) approval, with delivery of 10 J/cm2 at 10 mW/cm2 now licensed for the treatment of nonhyperkeratotic AKs of the face and scalp with the topical 5-ALA formulation Levulan Kerastick. ALA-PDT for darker-skinned Asian patients is hampered by melanin absorption of light, but Itoh et al. (26) report comparable results to Caucasian patients although up to six treatment sessions were required to achieve a clearance rate of 82%. In summary, ALA-PDT is efficacious for nonhyperkeratoic AKs of the face and scalp, and its efficacy appears to be comparable to that of cryotherapy and 5-FU.

Figure 18.4 ALA-PDT for facial actinic keratoses. (a) Left face before treatment; (b) immediately after treatment; (c) 2 months after treatment. (Courtesy of George J. Hruza, MD.)

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The US FDA approved topical ALA-based PDT in December 1999 for the treatment of nonhyperkeratotic AKs on the face and scalp. Phase III trials (n ¼ 243) in which patients were randomized to receive the topical 5-ALA formulation Levulan Kerastick or vehicle plus BLU-U blue light (417 nm) resulted in complete clearing of AKs in 72% of patients at 12 weeks. Of the partially cleared patients, 88% had more than 75% clearance of their AKs (Package insert for Levulan Kerastick). FDA approval is for the delivery of 10 J/cm2 at 10 mW/cm2 with Levulan Kerastick. Levulan Kerastick is a 20% wt/vol ALA solution in a plastic application tube with premeasured ALA-HCl and solution vehicle contained in separated ampules within each kerastick. The BLU-U illuminator is a 417 nm blue light source fixed at 10 J/cm2, 10 mW/cm2. Sites are irradiated with 16 min of the BLU-U illuminator 14– 18 h after application of topical solution without occlusion. One application and one dose of illumination per treatment site are recommended per treatment session. There is often significant erythema, edema, and occasional crusting that gradually resolves over 1 –2 weeks. Unresolved lesions may be treated a second time after 8 weeks. Patients are to avoid excessive sun exposure in the interim and before and after treatment. Unfortunately, the treatment is often quite painful for the patient in spite of fans, topical anesthetics and oral analgesics. Recently, a much less painful way to do the treatment has been developed with the ALA-painted skin irradiated 45 min to 1 h after application with pulsed dye laser at 595 nm, 6– 10 ms pulse duration, 7.5 J/cm2 10 mm spot size, and one to two passes. Pain, erythema, and edema are dramatically reduced without compromising efficacy. Other light sources such as intense pulsed light have been used as well to activate the ALA.

5.2.

Basal Cell Carcinoma

For the treatment of BCCs, several noncoherent and coherent light sources with wavelengths ranging from 570 to 630 nm and light doses and dose rates ranging from 30 to 540 J/cm2 and 19 –300 mW/cm2, respectively, have been used with ALA-PDT (9). The effect of ALA-PDT treatment of BCCs is contingent largely on the BCC histological type. Published complete response rates for ALA-PDT of superficial basal cell carcinomas range from 79% to 100% with up to 18 months follow-up (9,21,30– 32). However, longterm clearance rates and verification of histologic clearance are based on a small number of studies, and appear to hover near 50% for superficial BCCs (33 –36). Haller (37) suggested routine double treatments of superficial BCCs 1 week apart (using a xenon arc light source, 630 nm, 120 –134 J/cm2, 50 –100 mW/cm2 4 h after 20% ALA application) reduce the relapse rate. The initial complete response of 100% was only reduced slightly to 96% at follow up at 27 months follow-up (range 15 – 45 months). Nodular and noduloulcerative BCCs show low complete response rates in the range of 10 – 50% (9,32). Tumor thickness determines therapeutic response to PDT, with lesions ,2 mm thick on diagnostic biopsy achieving complete clearance histologically after treatment (38). Nonhomogenous uptake of ALA and/or insufficient conversion to PpIX in tumor cells may account for lack of efficacy for thicker tumors (14,32). Using laser light from a pulsed frequency doubled Nd:YAG laser pumping a dye laser with light emission at 630 nm (60 J/cm2, 110 mW/cm2 after 6 h of 20% ALA application), Svanberg et al. (30) showed clinical clearance for nodular BCCs improved from 64% to 100% after one additional treatment at 3 weeks follow-up. Thissen et al. (39) showed a 92% clinical and histologic clearance rate 3 months after treatment with ALA-PDT in association with pretreatment tumor debulking.


395

The addition of ethylenediamine tetraacetic acid (EDTA) to the ALA vehicle, or pretreatment of tumor with dimethyl sulfoxide (DMSO), resulted in complete clearance in 55– 91% of lesions, compared to 34 –67% without EDTA/DMSO (3). The addition of desferrioxamine (DFO) an iron chelator, to the ALA vehicle also appears to enhance PpIX accumulation as ferrochelatase mediates an iron-dependent process (17). Soler et al. (40) reported an initial clinical clearance rate (at 3– 6 months) of 92% for 119 nodular BCC .2 mm thick when ALA-PDT treatment was preceded by debulking and curettage in combination with topical DMSO. Only 6 of 119 (5%) cases recurred at clinical examination 12 –26 months (mean 17 months) later. Using methyl 5-ALA, the more lipophilic ester derivative of 5-ALA, combined with prior curettage, resulted in a total recurrence rate of 11% at 2– 4 years (mean 35 months) of follow-up. Morton et al. (41) suggest that ALA-PDT may be potentially advantageous for the treatment of large or multiple BCCs. They report an initial clearance rate of 88% and 90%, respectively, with a small decrease in overall response to 78% and 86%, respectively, after 34 month’s follow-up (range 12 – 60 months). Pigmented BCCs are generally not responsive to ALA-PDT since melanin absorption of light decreases the effective fluence delivered to the tumor. Morpheaform BCCs are also nonresponsive as topical ALA-PDT fails to induce detectable PpIX within such lesions (8). One randomized study compared ALA-PDT to cryotherapy for both superficial and nodular BCCs and found the two modalities to be approximately equally efficacious, though repeated treatments were more often required with PDT. Shorter healing time, less scarring, and better cosmetic outcome were associated with treatment with ALA-PDT (42). In summary, repeated cycles of ALA-PDT may eliminate superficial BCCs with good cosmetic results. PDT may also be beneficial in managing patients with multiple recurring BCCs that are mostly superficial. Adjunctive therapies for thicker lesions may improve the efficacy of ALA-PDT. Nevertheless, for BCCs with a deep component, conventional procedures such as surgical excision, electrodessication and curettage, radiotherapy, cryotherapy, and Mohs surgery provide lower long-term recurrence rates (10.1%, 7.7%, 8.7%, 7.5%, and 1%, respectively) (8) than PDT. 5.3.

Bowen’s Disease

The reported cure rates for Bowen’s disease using PDT are 50 – 100% with noncoherent and coherent light sources emitting from 570 to 630 nm at fluences between 60 and 300 J/cm2 (9). The lower observed efficacies may be due to impaired ALA penetration into the thickened epidermis (2). Use of more deeply penetrating light sources for treatment of Bowen’s disease is supported by a randomized study that demonstrated a significantly higher clearance rate with a red light source compared to green light (14). Like BCCs, tumor size reduction by PDT using penetration enhancers such as EDTA and DMSO may improve complete clearance or facilitate subsequent surgical excision (7). As in the case of BCC treatment by PDT, the therapeutic challenge of treating large (.20 mm) or multiple lesions of Bowen’s disease has been addressed. Morton et al. (40) report initial clearance rates for such lesions of 88% and 98%, respectively, with a decrease in overall response to 78% and 89%, respectively, after 34 months follow-up (range 12– 60 months). Also observed were improvements in initial clearance with repeated PDT sessions (up to 3) for both Bowen’s and BCC, with a corresponding reduction in recurrence rate to ,10% for both large and multiple lesions. Morton et al. (43) also compared PDT with cryotherapy in the treatment of small plaques of Bowen’s disease and reported no ulceration, infection, or recurrence with

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cryotherapy but not with PDT. Salim et al. (44) compared ALA-PDT (xenon lamp 630 nm, 100 J/cm2, 48 mW/cm2, 4 h after 20% ALA) to topical 5-FU BID for 21 days and showed that PDT is as effective, with fewer side effects. In summary, ALA-PDT may be particularly useful when conventional therapy is difficult to employ. For instance, extensive lesions not amenable to other modalities or potentially slow-healing sites in patients with multiple morbidities may be suited to such treatment. 5.4.

Squamous Cell Carcinoma

Only a few studies have evaluated the use of ALA-PDT for SCCs. The complete response rate has been reported to be 67– 92% for early invasive SCCs and 0 –67% for nodular SCCs, with recurrence rates being unacceptably high (7). In light of the associated risk of recurrence and metastasis, SCCs should only be treated with topical PDT only when conventional methods are not feasible (8). 5.5.

Melanoma

PDT has in general not proven effective for the treatment of primary cutaneous melanoma. This is mostly a consequence of the fact that light absorption by superficial melanin is sufficient to inhibit light penetration into deeper areas. Management of cutaneous metastases with topical ALA-PDT also has not been successful (8). Systemic PDT of melanoma lesions using intravenous agents such as porfirmer sodium or HPD has been associated with a significant but relatively short-lasting response (8). 5.6.

Skin Conditions Other than Nonmelanoma Skin Cancer

Topical ALA-PDT has been successfully used to treat skin diseases other than nonmelanoma skin cancer. Small case series with encouraging reports are available to describe topical PDT for unwanted hair, actinic cheilitis (45), keratoacanthoma (46), scleroderma (47), extramammary Paget’s disease (48), hirsuitism (49), and condyloma accuminata (50). Single case reports describe successful treatment of erythroplasia of Queyrat (51), nevus sebaceous (52), epidermodysplasia verruciformis (53), lichen planus (54), and sarcoidosis (55) hidradenctis supparativa (56) and sebaceavs hyperplasia (57,58). The nononcologic dermatologic diseases most often treated with PDT have been verruca vulgaris, acne vulgaris, and psoriasis. PDT has also been tried for cutaneous T-cell lymphoma (CTCL). 5.7.

Recalcitrant Warts

Recalcitrant warts have reported clearance rates of 56 –100%, with superior efficacy of repeated cycles of ALA-PDT compared to cryotherapy (14,59 – 62). Moderate to severe pain immediately and 24 h following irradiation is reported, and could potentially limit the use of ALA-PDT for warts, especially in children. 5.8.

Acne

Endogenous prophyrins in Propionibacterium acnes, and the selectivity of ALA-induced porphyrin fluorescence for pilosebaceous units make PDT a possible treatment for acne (63). The efficacy of visible light phototherapy in the absence of exogenous porphyrin


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precursors for the treatment of acne has previously been established, with combined red and blue light showing superior efficacy (64). In an open randomized controlled study in 22 subjects with moderate truncal acne, a series of up to four treatments using 20% ALA cream and broadband irradiation at 150 J/cm2 resulted in significant reduction in sebum production, sebaceous gland size, and P. acnes fluorescence. Clinical improvement was maintained for up to 20 weeks (65). This prolonged remission was further observed in subsequent reports using low-dose single treatment ALA-PDT with a pulsed excimer dye laser (635 nm, 5 J/cm2) or a broadband halogen source (600 – 700 nm, 13 J/cm2) (63). Despite the reported efficacy of ALA-PDT in the treatment of facial and truncal acne, this modality is limited by adverse effects such as folliculitis, discomfort, dyspigmentation, and crust formation (14). 5.9.

Psoriasis

Small case series using systemic PDT of psoriatic plaques with HPD have been evaluated previously. Evaluation of topical PDT has been of recent interest since photosensitizer accumulation and photobleaching (photo- and oxygen-induced reaction of the porphyrin sensitizer) of psoriatic lesions have been established (14,65). Efficacy comparable to that with dithranol has been demonstrated in one small study (66). Interestingly, differences have been observed in the intensity of PpIX fluorescence among treated psoriasis sites on the same individual as well as across patients (67). Given the significant variation in treatment response and procedure-related discomfort, PDT remains an experimental treatment modality for psoriasis. 5.10. Cutaneous T-cell Lymphoma Clinical studies of the use of topical ALA-PDT in the treatment of patch, plaque, and tumor stage mycosis fungoides are limited, with small case series predominating (68 – 72). The mechanism of selectivity in these cases is based on photosensitization of T cells shown to inhibit lymphocyte proliferation in a manner similar to a combination of psoralen and long-wave ultraviolet radiation (8). Selective uptake of photosensitizers into lymphocytes after topical PDT, with inhibition of T cells and photobleaching, has also been demonstrated in CTCL (14). Series of multiple treatments followed by recurrences are prominently noted in isolated reports. 5.11. Skin Rejuvenation Three recent studies have opened new possibilities for more rapid and broader use of ALA-PDT in both medical and cosmetic dermatology. Touma et al. (73) studied 1, 2, and 3 h drug incubation with topical 5-ALA and blue light at 10 mw/cm2 and found no difference in efficacy for clearing facial actinic keratoses (.85% lesion clearance rates) vs. published (74) overnight drug incubation (12 – 18 h). Touma’s study also showed reduced side effects and significantly improved patient tolerability with the shorter topical ALA-PDT drug incubation times. Alexiades-Armenakas et al. (75) used both shorter topical ALA-PDT drug incubation (3 h) and overnight topical ALA-PDT drug incubation (14 –18 h) activated by long pulsed dye laser (595 nm) for treating actinic keratoses (AK) of the face and found similar AK clearance rates (.90% lesion clearance). The treatments with long pulsed dye laser and topical ALA were not time consuming (full face can be treated in less than 10 min) and were very well-tolerated by patients. Goldman et al. (76) used an intense pulse light to activate topical ALA for the treatment of actinic keratoses and photodamage and overnight drug incubation (14 – 18 h) and again

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found this approach to be well-tolerated and efficacious. The ability to use much shorter drug incubation times along with activating the ALA with commonly used light sources as intense pulse lights and long pulse dye lasers will most likely increase the adoption of topical ALA-PDT in medical as well as cosmetic dermatology applications. 5.12.

Prevention and Management of Complications

Regardless of indication, a stinging or burning sensation is commonly experienced during topical ALA-PDT. This discomfort peaks within minutes, then levels off during the remainder of therapy. Overall duration of the pain may be a few hours, or rarely a few days. Pain occurs in coincidence with the erythema and edema that immediately follows illumination of the target lesion. Subsequent crust formation and healing occur over 2 –6 weeks. These various signs and symptoms may be treated with topical mild corticosteroid agents. Strategies for pain reduction include topical or injected local anesthetic, cooling with liquid nitrogen or a fan, premedication with benzodiazepines, and spraying water on lesions during therapy (14). Since systemic absorption of ALA after topical application is negligible, adverse side effects are generally limited to the cutaneous area treated. Following topical application of ALA, the treated site becomes photosensitive. Patients should be advised to wear a wide-brimmed hat or other protective apparel to shade the treated areas from sunlight or bright indoor light such as examination lamps, operating room lamps, tanning beds, and lights at close proximity. Incidental exposure to intense light sources is to be avoided for .40 h. Sunscreen will not effectively protect against photosensitivity reactions caused by visible light. Exposure to such sources may result in significant pain, erythema, and edema (Package insert for Levulan Kerastick). Lasers that deliver high-intensity light with radiation in the blue, ultraviolet, or infrared wavelengths may pose a greater potential hazard to the skin and eyes. The retina is at risk from the photochemical hazard of blue light (400 –450 nm) which could irreversibly damage the photosensitive neurotransmitters of the macula. Staff and patients are advised to wear protective goggles to limit the transmission of high intensity light (14). The cosmetic results of PDT are very good and widely reported, and superior cosmesis is generally considered one of the significant advantages of this modality. Scar formation is a minimal risk, and pigmentary changes appear to resolve within a few months (8). Contraindications to PDT include cutaneous photosensitivity, history of photoinduced dermatoses, such as porphyria, or known allergies (Package insert for Levulan Kerastick). Patients with concomitant disorders provoked or exacerbated by ultraviolet light should be cautiously evaluated for ALA-PDT (8).

6.

CONCLUSIONS

Although the numerous studies using topical ALA-based PDT vary in their methodology and thus are difficult to compare, clinical results have supported the efficacy of this modality for the treatment of a variety of nonmelanoma skin cancers. The potential benefits of PDT include good cosmetic outcome, minimal trauma, repeatability, and patient acceptance (7) ALA-PDT is now an accepted modality for the treatment of actinic kerntoses, and is a useful modality for the treatment of photodamaged skin. Based on existing data, PDT is not superior to any current treatment modality for


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nonmelanoma skin cancers; however, it serves as an effective and feasible alternative when conventional therapy is infeasible. Recent studies indicate that ALA-PDT shows promise in the treatment of moderate to severe acne. REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9.

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19 Skin Cooling in Laser Dermatology Kristen M. Kelly and J. Stuart Nelson University of California, Irvine, Irvine, California, USA

1. Introduction 2. Methods of Cooling 2.1. Contact Cooling 2.2. Evaporative Cooling 2.3. Convective Cooling 3. Lasers Utilizing Cooling 4. The Future of Cooling References

1.

403 405 405 406 407 408 411 412

INTRODUCTION

During the last decade, cooling has emerged as an important concept in laser dermatology. The addition of cooling during laser therapy allows the use of higher incident light doses, increases the threshold for epidermal damage, permits safer treatment of darker skin types, and reduces pain. Conductive, evaporative, and convective cooling methods are currently utilized with laser treatment. In this chapter we will discuss the advantages and disadvantages of each of these cooling methods and describe their use in the clinical management of patients. Early attempts to use lasers for the treatment of skin disease resulted in an unacceptable incidence of scarring and skin dyspigmentation (1). In 1983, selective photothermolysis was introduced as a means of achieving targeted chromophore destruction by careful selection of laser wavelength and pulse duration (2). Selective photothermolysis significantly improved clinical results; however, patients and physicians were still confronted with incomplete lesion removal despite multiple treatments, and a lower, but still clinically significant, incidence of adverse effects. In many cases, problems arose because of nonspecific epidermal absorption of laser energy. Epidermal melanin represents an “optical barrier” through which light must pass to reach the targeted dermal chromophore. Except during treatment of epidermal melanoses, melanin absorption is deleterious, reducing the light dose reaching the target, 403

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thereby decreasing the amount of heat produced and leading to suboptimal removal of the lesion. Moreover, melanin absorption causes localized heating of the epidermis, which may, if not controlled, produce permanent complications such as scarring or dyspigmentation. Unfortunately, for many lesions the threshold incident light dose for epidermal injury is close to or below the threshold for permanent target removal, precluding the use of potentially more effective higher light doses. Patients with darker skin types have a higher concentration of epidermal melanin and an increased risk of epidermal damage and thus, laser treatment with visible and near-infrared wavelengths is especially problematic in this group. Lower energies must be used and there is a higher risk of adverse effects as a result of epidermal injury. Other factors also contribute to elevated skin surface temperatures, limiting the maximum incident light dose that may be delivered during treatment and contributing to adverse effects. Diffuse backscattered light and Fresnel (total internal) reflection can increase the epidermal fluence several times above the incident light dose. Higher epidermal temperatures result, increasing the risk of skin damage. In addition, as air is an excellent thermal insulator, heat generated in the irradiated target diffuses to the skin surface and is trapped at the air –skin interface. The heat builds up near the skin surface and may persist for several seconds after laser exposure until it is ultimately dissipated by surface convection, radiation, or evaporation or diffuses into the dermis with subsequent cooling by blood perfusion. Epidermal damage as a result of temperature elevation can be avoided by staying below the threshold for tissue denaturation (60 – 658C). If the epidermis is adequately cooled, the epidermal temperature elevation will not exceed the threshold for damage, allowing the use of higher incident light doses and longer pulse durations to deliver more energy to the targeted dermal structure. Cooling must be confined to the superficial layers of the skin. If the target is also cooled, any increase in the threshold for epidermal damage achieved by cooling is offset by the additional energy required to heat the dermal target to a temperature sufficient for permanent destruction (Fig. 19.1). During treatment of superficial targets such as port-wine stain (PWS) blood vessels or collagen during nonablative laser skin rejuvenation, a large temperature gradient is required at the skin surface

Figure 19.1

The importance of selective epidermal cooling.

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in order to prevent target cooling. This requires good thermal contact and a very cold cooling medium requiring only short cooling times to lower the epidermal temperature to adequate levels. Cooling precision is less essential during treatment aimed at deeper structures such as hair follicles.

2.

METHODS OF COOLING

Research on epidermal cooling has focused on three methods of heat transfer: conductive, evaporative, and convective.

2.1.

Contact Cooling

Conductive, or as it is more commonly known, contact cooling, is heat transfer through a solid material and relies on heat exchange at the molecular level. Contact cooling was the first method explored in conjunction with laser therapy. In the early 1980s, Gilchrest et al. (3) utilized ice cubes to chill PWS skin prior to argon laser treatment. Even this relatively simple approach to cooling diminished the incidence of scarring but the majority of patients did not achieve improved PWS blanching. Since then, other approaches to contact cooling have been investigated including cooled gels and sapphire plates. Cooled gels, such as those used for ultrasound, are the simplest contact cooling media currently in use. Gels increase hydration of the stratum corneum, improving thermal conductivity at the skin surface (4). Gels are inexpensive but heat transfer is limited because the gel –skin surface temperature gradient is low and rapidly eliminated as there is no means of heat extraction. Much better results are achieved when a recirculating coolant is encased in a glass or sapphire plate, as the thermal conductivity of these devices is much higher than that of cooled gels. As an example, Palomar Medical Corporation (Lexington, MA) developed an advanced contact cooling device for use with their E2000 hair removal systemw (Fig. 19.2) (5). The temperature of the 10 mm diameter cooled sapphire block can be set

Figure 19.2

Contact cooling handpiece of Palomar Medical Corporation’s E2000 laser.

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by software to either 08C or 2108C and maintained by extracting heat using recirculating water. The desired cooling of the basement membrane can be achieved by control of the precooling time and thermal contact. The handpiece contains thermal sensors that monitor the sapphire temperature near the epidermis– sapphire interface. By recording the sapphire block temperature as a function of time after contact and measuring the slope of the time –temperature curve, the thermal contact quality can be evaluated and the basement membrane temperature predicted. Placement of cooling plates onto the skin requires local pressure. This may be advantageous during procedures such as laser hair removal because the distance between the skin surface and the targeted deep follicular structures is decreased (4). However, pressure can reduce the concentration of hemoglobin in vascular lesions leading to suboptimal light absorption. During treatment of superficial vascular lesions, the clinician must be careful that the applied pressure does not decrease or eliminate blood flow in the targeted vessels. The cooling plate must remain in close contact with the skin surface to prevent loss of heat transfer at the air –skin interface. The rate of heat extraction during contact cooling is dependent on the thermal conductivity of the cooling medium and the skin surface temperature (4). Air acts as an insulator because it has a thermal conductivity 1/25 that of water, which is 1/50 that of a sapphire plate. If close contact is lost between the cooling plate and the skin surface, epidermal protection may be compromised and adverse effects may result. Some plates are incorporated into handpieces, which can be maneuvered rapidly across the skin surface after application of a gel, which also helps to maintain close contact between the skin and cooling plate. The contact surface accumulates heat during light exposure. If this heat is not subsequently removed, cooling efficiency is diminished. A recirculating coolant system (often water) can be used to extract heat and maintain the cooling plate at a constant temperature. Water condensation may accumulate on the plate surface and periodic wiping may be required to prevent light beam attenuation (4). As noted above, it is important that cooling remains confined to superficial layers of the skin, especially during treatment of targets in the superficial dermis. Mathematical models of heat transfer indicate that contact periods longer than 1 s are likely to result in temperature reductions deep in the dermis (6). Experimental data indicate that the in vivo basal layer cooling rate using a sapphire plate cooled to 248C is significantly slower than that of the commercial cryogen spray cooling (CSC) device (Candela, Wayland, MA) (7). Longer cooling times result in reduced spatial selectivity and lower temperatures in deeper skin layers. 2.2.

Evaporative Cooling

The second method of cooling, evaporative, relies on heat transfer from a solid surface to an adjacent fluid and is dependent on fluid motion between regions of unequal temperature density. In 1994, Nelson et al. (8 – 10) developed CSC or dynamic cooling as a form of evaporative cooling adapted for use with laser therapy. CSC is an efficient and effective method of achieving spatially selective epidermal cooling. A millisecond cryogen spurt (Fig. 19.3) is applied to the skin surface immediately before laser exposure. As the liquid cryogen rapidly evaporates, the skin temperature is reduced as a result of supplying the latent heat of vaporization. Tetrafluoroethane (C2H2F4), an environmentally compatible, nontoxic, nonflammable freon substitute (11), has been demonstrated in multiple studies to be a safe and effective cooling agent (11) and is the only cryogenic compound currently approved by the Food and Drug Administration for use in dermatology.


Figure 19.3

407

Cryogen spray contacting the skin immediately before laser exposure.

The phase change induced by evaporative cooling results in a high heat transfer coefficient and large temperature gradient at the skin surface. Relatively large temperature reductions are achieved within milliseconds and this rapid heat transfer allows selective epidermal cooling without affecting the temperature of the deeper dermal targets, leaving the latter susceptible to laser induced thermal injury. Recent studies indicate that the cryogen droplets may actually cool to a temperature of 2508C by the time they impinge on the skin surface (12). Further, the cryogen spurt duration and the delay between the spurt termination and laser pulse can be electronically controlled allowing cooling to the desired depth and minimizing the risk of thermal injury by the laser pulse or frostbite as a result of cooling. CSC does rely on cryogen atomization, which may result in unequal droplet size and, consequently, nonuniform coverage over the treatment site. CSC nozzles in current use have been carefully designed to minimize this problem. Condensation of atmospheric water on the skin surface may result in formation of an ice film, which can significantly affect the incident light dose delivered to the target due to optical scattering (13). However, observable frost appears to form on the skin surface only after the liquid cryogen layer has retracted (100 ms after a 40 ms cryogen spurt), long after the therapeutic laser pulse (14). If desired, frost formation could by minimized by blowing a dry gas such as nitrogen over the skin surface. 2.3.

Convective Cooling

The third method of skin cooling, a cold air current, utilizes convective rather than contact or evaporative heat transfer. A continuous flow of air, chilled from 248C to 2328C, is delivered to the treatment site before, during, and after laser exposure (Fig. 19.4). The operating cost of air cooling is low and no substrate is applied to the skin surface; therefore, optical scattering of the incident laser light is not an issue. However, the heat transfer coefficient for forced convection is lower than that for evaporative or contact cooling requiring the use of longer cooling times (several seconds). “Bulk” cooling of the entire skin results, with minimal spatial selectivity. At present, it is unclear whether this method will be as efficacious as contact or evaporative cooling; but recent evidence indicates that this approach might have potential.

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Figure 19.4

Cynosure’s Photogenicaw laser with SmartCoolw air cooling.

Biesman et al. (15) compared cooling with the Zimmer Cold air blowerw (at 2208C) to that of a thermoelectric chip cooled sapphire window (58C) during diode laser treatment on colored piglets. The maximum tolerated fluence (MTF) without epidermal injury in light colored piglets was 250 J/cm2 with no cooling, 325 –350 J/cm2 with the cooled sapphire window, and 400 J/cm2 with cold air. In dark-colored piglets, the MTF was 50 J/cm2 with no cooling, 75 J/cm2 with the cooled sapphire window, and 150 J/cm2 with cold air. Cold air cooling has increased in use recently and has now been incorporated into several laser devices. Several air chillers can be purchased separately for use in conjunction with lasers that do not have their own cooling device. Hammes and coworkers (16,17) treated 166 patients with vascular lesions, tattoos, or hypertrichosis using lasers in conjunction with Cynosure’s (Chelmsford, MA) SmartCoolw device and reported decreased treatment pain. Three percent of patients disliked the cold air device because of respiratory or ocular problems during facial treatment, pain from the cold air current, or noise. However, sufficient epidermal protection was provided to increase the treatment light dose by 15 –30% while simultaneously reducing crusting. Greve et al. (18) used air cooling during pulsed dye laser (PDL) treatment of PWS and reported similar reductions in pain as compared to laser treatment without cooling.

3.

LASERS UTILIZING COOLING

It is now widely accepted that cooling improves laser treatment outcome and manufacturers have capitalized on this opportunity. Many laser systems have successfully incorporated cooling methods (Tables 19.1 – 19.3). Several manufacturers (Table 19.1) offer a 532 nm laser in conjunction with a contact cooling device. For example, Lumenis (Santa Clara, CA) has the VersaPulsew laser containing a handpiece with an attachable chilled sapphire plate cooled by recirculating water. The chilled plate must be kept in close contact with the skin surface

Skin Cooling in Laser Dermatology Table 19.1

409

Some Lasers with Cooling Available for Treatment of Vascular Lesions

Laser/manufacturer Medlite Cw, Cutera Versa Pulsew, Lumenis Aura (Starpulse)w, Laserscope Photogenica VLSw, Pulsed Dye Laser, Cynosure ScleroPLUSw, Candela Corporation Vbeamw, Candela Corporation GentleLasew, Candela Corporation LightSheerw, Lumenis Epistarw, Nidek Palomar SLP 1000w, Palomar Medical Cool Glidew, Cutera Imagew, Sciton Lyraw, Laserscope Variaw, CoolTouch Vasculightw, Lumenis

Wavelengths (nm) 532 532 532 585– 600 585– 600 595 755 800 810 810 1064 1064 1064 1064 515– 1200; 1064

Cooling device Contact cooling Contact cooling Contact cooling Air cooling Cyogen spray cooling Cryogen spray cooling Cryogen spray cooling Contact cooling Contact cooling Contact cooling Contact cooling Contact or air cooling Contact cooling Cryogen spray cooling; contact cooling option Contact cooling

during laser irradiation to maintain adequate cooling and prevent adverse effects such as pitted scars. This laser has been used for treatment of facial vascular lesions with good results and minimal side effects (19,20). Adrian and Tanghetti (21) treated 40 patients with facial telangiectasias and achieved .75% clearance of vessels 1.5 mm in diameter in all patients after one treatment. Most patients who underwent a second treatment achieved 90– 100% clearance. Because use of the VersaPulsew laser is not associated with posttreatment purpura, many patients prefer this device to the PDL for treatment of facial telangiectasias.

Table 19.2 Lasers with Cooling Available for Hair Removal Laser/manufacturer

Wavelengths (nm)

Ruby Starw, Asclepion Laser Technologies E2000w, Palomar Medical GentleLasew, Candela Corporation Apogee Series, Cynosure LightSheerw, Lumenis Epistarw, Nidek SLP 1000w, Palomar MeDioStar HCw, Asclepion-Meditec F1 Diode Laserw, Opusmed CoolGlidew, Cutera GentleYAGw, Candela Corporation Imagew, Sciton Variaw, CoolTouch

694 694 755 755 800 810 810 810 810 1064 1064 1064 1064

Lyraw, Laserscope Vasculightw, Lumenis

1064 515 – 1200

Cooling system Contact cooling Contact cooling Cryogen spray cooling Air cooling Contact cooling Contact cooling Contact cooling Contact cooling Air cooling Contact cooling Cryogen spray cooling Contact and air cooling Cryogen spray cooling; contact cooling option Contact cooling Contact cooling

410 Table 19.3

Kelly and Nelson Lasers with Cooling Available for Nonablative Skin Rejuvenation

Laser/manufacturer

Wavelengths (nm)

Cooling system

Aura/Lyraw, Laserscope VBeamw, Candela Corporation PhotoGenicaw series, Cynosure VascuLightw series, Lumenis CoolTouchw, CoolTouch SmoothBEAMw, Candela Corporation

532/1064 595 585– 600 515– 1200; 1064 1320 1450

Contact cooling Cryogen spray cooling Air cooling Contact cooling Cryogen spray cooling Cryogen spray cooling

CSC has been incorporated into Candela’s (Wayland, MA) SPTL1b, ScleroPLUSw, and V-Beamw PDLs for treatment of vascular lesions. A recent retrospective study demonstrated that this combination permits the use of higher incident laser light doses, which expedites PWS clearing (22) without adverse effects. Ninety-eight patients received laser therapy without CSC utilizing standard treatment fluences of 5 –7 J/cm2. An additional 98 patients received laser therapy with CSC utilizing fluences of 8 – 10 J/cm2. Cryogen parameters were a spurt duration of 50 ms and a delay time between cryogen delivery and laser irradiation of 10 ms. Pre- and posttreatment photographs were evaluated by three physicians not involved in the study and graded for lesion clearance using a scoring system where 1 indicated poor blanching (,25%) and 4 indicated excellent blanching (76 –100%). After an average of three to four treatments, the mean blanching scores for patients who received laser therapy with and without CSC were 2.92 and 2.32, respectively, a clinically and statistically significant difference ( p , 0.001). Further, while scarring was noted in 3.1% of the patients without CSC, no permanent scarring was observed in the CSC and laser treated group. A subsequent study demonstrated the safe use of even higher light doses (6 – 15 J/cm2) in conjunction with CSC for treatment of PWS (23). CSC during PWS treatment has also been demonstrated to decrease the pain associated with laser therapy, especially in patients with darker skin types (8,24,25). Excellent clearance without adverse effects has been reported with laser therapy in conjunction with CSC for hemangiomas, telangiectasia, and other vascular lesions (26). Conductive, evaporative, and convective cooling devices have been incorporated into laser systems used for treatment of leg telangiectasia. Cooling is important for this indication, as higher laser light doses are required to achieve permanent removal of leg telangiectasia, which are generally much larger than vessels targeted on the face or in PWS. Increased hydrostatic pressure in these vessels also makes treatment difficult. While a variety of studies have demonstrated improvement in leg veins after laser irradiation (27 – 31), treatment results even with cooling are highly variable and a clinically significant incidence of hyper- and hypopigmentation is generally reported. Most experts agree that sclerotherapy remains the treatment of choice for lower-leg telangiectasia but laser treatment may be useful in patients with small veins (,0.5 mm diameter), those refusing sclerotherapy secondary to needle phobia, and those with telangiectatic matting. Cooling has also been incorporated into laser systems designed for hair removal (32) (Table 19.2). Current systems target the entire follicle because the follicular structure responsible for hair regeneration has not been conclusively identified (33). Laser treatment requires the use of high fluences capable of heating a large volume of tissue and long pulse widths, on the order of milliseconds (33). The target chromophore for laser hair removal is


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melanin, and skin dyspigmentation as a result of epidermal melanin absorption is the most common adverse effect. Patients with darker skin types, who have a higher concentration of epidermal melanin, are at greatest risk of dyspigmentation. Use of longer wavelengths and pulse widths is beneficial for diminishing epidermal melanin damage, but the best results have been achieved with laser systems developed in association with a cooling gel, sapphire tip contact cooling, CSC, or air cooling. Cooling has also been utilized in the development of novel approaches to nonablative laser skin rejuvenation (Table 19.3) (34 – 36). While ablative CO2 and Er:YAG lasers can achieve good treatment results for rhytides, removal of the epidermis results in an open wound, puts the patient at risk of complications including infection, prolonged erythema, and postinflammatory dyspigmentation, and requires meticulous postoperative wound care. In an effort to decrease or eliminate the incidence of these adverse effects, nonablative laser skin rejuvenation has been developed. CoolTouch (Roseville, CA) has a 1320 nm Nd:YAG laser in conjunction with CSC that is capable of stimulating tissue fibroblasts without epidermal injury. A multicenter study evaluated periorbital rhytid improvement in 35 adults after three nonablative laser treatments performed sequentially at intervals of 2 weeks (34). Treatment fluences of 28– 36 J/cm2 were utilized with a 20 – 40 ms cryogen spurt duration and a delay time between cryogen spray and laser irradiation of 10 ms. Small, but statistically significant, clinical improvements were noted in mild, moderate, and severe rhytid groups 12 weeks after the final treatment. Twenty-four weeks after the last treatment, only the severe rhytid group showed statistically significant clinical improvement. Transient hyperpigmentation (5.6%) and a low incidence (2.8%) of barely perceptible pinpoint pitted scars were the only adverse effects. This study demonstrated that CSC is a safe and promising method of protecting the epidermis during nonablative laser skin rejuvenation of facial rhytides while avoiding much of the morbidity associated with ablative skin resurfacing. Treatment results with this device have subsequently been improved by addition of a surface temperature sensor, which allows the clinician to individualize treatment fluences and more accurately target the maximum safe temperature range of 40 – 458C. Several laser and noncoherent light source systems have now been developed or modified for nonablative skin rejuvenation (Table 19.3). While an extensive discussion of these devices is beyond the scope of this chapter, it is important to note that cooling is essential for epidermal protection, allowing the delivery of high light doses to the dermis, resulting in dermal heating and subsequent collagen remodeling.

4.

THE FUTURE OF COOLING

Cooling has been incorporated into several dermatologic laser systems and such use has benefited patients by improving clinical outcome and diminishing treatment pain and adverse effects. However, many questions remain to be answered. The advantages and disadvantages of the available cooling methods are debated. Many scientists and clinicians are biased in favor of one technique or the other. We believe CSC to be an ideal method of epidermal cooling because evaporative cooling is inherently efficient, allowing rapid and highly selective epidermal cooling. Further, the spurt duration can be easily controlled to obtain the desired depth and duration of cooling. However, there are clinical indications such as laser hair removal where the target is large and relatively deep in the skin, for which cooling precision is less important and the various cooling modalities may be equally efficacious.

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Currently, research is under way to optimize all methods. For conductive cooling, issues regarding the timed application and heat removal of the devices must be addressed and optimized. Several fundamental questions regarding the thermodynamics of CSC on the skin surface also need to be answered. Variables including cryogen selection, droplet size and velocity, delivery distance between the nozzle and skin surface, and orientation of the spray relative to the skin surface require further investigation. Improved heat removal may be achieved by utilizing sequential cryogen spurts during and after laser irradiation (37). Investigation of convective cooling is relatively new and optimization of this technique and comparison to evaporative cooling are yet to be accomplished. Other researchers are exploring methods to image and determine the depth and size of targeted structures on an individual patient basis. Such information combined with measurement of the patient’s epidermal melanin concentration could be used to individualize cooling parameters with the expectation of improving therapeutic outcome (38 –46). Selective epidermal cooling has become a guiding principle for the field of dermatologic laser therapeutics. Skin cooling has been incorporated into many aspects of laser therapeutics and has significantly improved results, enhancing treatment effect while decreasing discomfort and adverse effects. Further research will optimize cooling technology and augment its benefits.

REFERENCES 1. 2. 3. 4. 5. 6.

7.

8. 9.

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11. 12.

Dixon JA, Huether S, Rotering R. Hypertrophic scarring in argon laser treatment of port-wine stains. Plast Reconstr Surg 1984; 73:771– 779. Anderson RR, Parrish JA. Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science 1983; 220:524 – 529. Gilchrest BA, Rosen S, Noe JM. Chilling port wine stains improves the response to argon laser therapy. Plast Reconstr Surg 1982; 69:278 – 283. Ross EV, Ladin Z, Kriendel M, Dierickx C. Theoretical considerations in laser hair removal. Dermatol Clin 1999; 17:333 – 355. Zenzie HH, Altshuler GB, Smirnov MZ, Anderson RR. Evaluation of cooling methods for laser dermatology. Lasers Surg Med 2000; 26:130 – 144. Anvari B, Milner TE, Tanenbaum BS, Nelson JS. A comparative study of human skin thermal response to sapphire contact and cryogen spray cooling. IEEE Trans Biol Eng 1998; 45:934 – 941. Pope K, Lask G. Epidermal temperature evaluation during dynamic spray cooling, contact cooling, and ice. Presented at the 20th Annual Meeting of the American Society for Laser Medicine and Surgery, Reno, NV, Apr 5 – 9, 2000. Nelson JS, Milner TE, Anvari B, Tanenbaum BS, Kimel S, Svaasand LO. Dynamic cooling of the epidermis during laser port wine stain therapy. Lasers Surg Med 1994; 6S:48. Nelson JS, Milner TE, Anvari B, Tanenbaum BS, Kimel S, Svaasand LO. Dynamic epidermal cooling during pulsed laser treatment of port-wine stain. A new methodology with preliminary clinical evaluation. Arch Dermatol 1995; 131:695 – 700. Nelson JS, Milner TE, Anvari B, Tanenbaum BS, Svaasand LO, Kimel S. Dynamic epidermal cooling in conjunction with laser-induced photothermolysis of port wine stain blood vessels. Lasers Surg Med 1996; 19:224 – 229. Nelson JS, Kimel S. Safety of cryogen spray cooling during pulsed laser treatment of selected dermatoses. Lasers Surg Med 2000; 26:2 – 3. Torres JH, Nelson JS, Tanenbaum BS, Milner TE, Goodman DM, Anvari B. Estimation of internal skin temperatures in response to cryogen spray cooling: implications for laser therapy of port wine stains. IEEE 1999; 5:1058– 1065.

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Anvari B, Milner TE, Tanenbaum BS, Kimel S, Svaasand LO, Nelson JS. Selective cooling of biological tissues for thermally mediated therapeutic procedures. Phys Med Biol 1995; 40:241 – 252. Majaron B, Kimel S, Verkruysse W, Aguilar G, Pope K, Svaasand LO, Lavernia EJ, Nelson JS. Cryogen spray cooling in laser dermatology: effects of ambient humidity and frost formation. Lasers Surg Med 2001; 28:469 – 476. Biesman B, Chang D, Richards S, Reinisch L. A comparison of cold air vs. a thermoelectrically cooled sapphire window for epidermal protection. Lasers Surg Med 2002; S14:36. Hammes S, Fuchs M, Raulin C. Cold air in laser therapy. first experiences with a new cooling system. Dermatology 1999; 5:338 – 342. Raulin C, Greve B, Hammes S. Cold air in laser therapy. First experiences with a new cooling system. Lasers Surg Med 2000; 27:404 –410. Greve B, Hammes S, Raulin C. The effect of cold air cooling on 585 nm pulsed dye laser treatment of port-wine stain. Dermatol Surg 2001; 27:633– 636. West TB, Alster TS. Comparison of the long-pulse dye (590 – 595 nm) and KTP (532 nm) lasers in the treatment of facial and leg telangiectasias. Dermatol Surg 1998; 24:221 – 226. Dummer R, Graf P, Greif C, Burg G. Treatment of vascular lesions using the VersaPulsew variable pulse width frequency doubled neodymium:YAG laser. Dermatology 1998; 197:158 – 161. Adrian RM, Tanghetti EA. Long pulse 532-nm laser treatment of facial telangiectasia. Dermatol Surg 1998; 24:71– 74. Chang CJ, Nelson JS. Cryogen spray cooling and higher fluence pulsed dye laser treatment improve port wine stain clearance while minimizing epidermal damage. Dermatol Surg 1999; 25:767 – 772. Kelly KM, Nanda VS, Nelson JS. Treatment of port wine stain birthmarks using the 1.5 ms pulsed dye laser at high fluences in combination with cryogen spray cooling. Dermatol Surg 2002; 28:309 – 313. Waldorf HA, Alster TS, McMillan K, Kauvar ANB, Geronemus RG, Nelson JS. Effect of dynamic cooling on 585-nm pulsed dye laser treatment of port-wine stain birthmarks. Dermatol Surg 1997; 23:657 –662. Fiskerstrand EJ, Ruggem K, Norvang LT, Svaasand LO. Clinical effects of dynamic cooling during pulsed laser treatment of port wine stains. Skin laser Today 1998; 7:25 – 37. Chang CJ, Kelly KM, Nelson JS. Cryogen spray cooling and pulsed dye laser treatment of cutaneous hemangiomas. Ann Plast Surg 2001; 46:577 – 583. Bernstein EF, Lee J, Brown DB, Geronemus RG, Lask GP, Hsia J. Treatment of spider veins with the 595 nm pulsed-dye laser. J Am Acad Dermatol 1998; 39:746 – 750. Reichert D. Evaluation of the long-pulse dye laser for the treatment of leg telangiectasias. Dermatol Surg 1998; 24:737 –740. Adrian RM. Treatment of leg telangiectasias using a long-pulse frequency-doubled neodymium:YAG laser at 532 nm. Dermatol Surg 1998; 24:19– 23. Weiss RA, Dover JS. Laser surgery of leg veins. Dermatol Clin 2002; 20:19– 36. Buscher BA, McMeekin TO, Goodwin D. Treatment of leg telangiectasia by using a longpulse dye laser at 595 nm with and without dynamic cooling device. Lasers Surg Med 2000; 27:171 – 175. Nelson JS, Majaron B, Kelly KM. Active skin cooling in conjunction with laser dermatologic surgery. Semin Cutan Med Surg 2000; 19:253– 266. Ort RJ, Anderson RR. Optical hair removal. Semin Cutan Med Surg 1999; 18:149– 158. Kelly KM, Nelson JS, Lask GP, Geronemus RG, Bernstein LJ. Cryogen spray cooling in combination with nonablative laser treatment of facial rhytides. Arch Dermatol 1999; 135:691 – 694. Goldberg DJ, Rogachefsky AS, Silapunt S. Non-ablative laser treatment of facial rhytides: a comparison of 1450-nm diode laser treatment with dynamic cooling as opposed to treatment with dynamic cooling alone. Lasers Surg Med 2002; 30:79 – 81.

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Kelly and Nelson Kelly KM, Majaron B, Nelson JS. Nonablative laser and light rejuvenation. Arch Facial Plast Surg 2001; 3:230– 235. Majaron B, Aguilar G, Basinger B, Randeberg LL, Svaasand LO, Lavernia EJ, Nelson JS. Sequential cryogen spraying for heat flux control at the skin surface. SPIE 2001; 4244:74 – 81. Nelson JS, Jaques SL, Wright WH. Determination of thermal and physical properties of port wine stain lesions using pulsed photothermal radiometry. SPIE 1992; 1643:287 – 298. Milner TE, Norvang LT, Svaasand LO, Tran N, Tanenbaum BS, Nelson JS. Photothermal tomography of subcutaneous chromophores. SPIE 1993; 2077:228 – 236. Milner TE, Goodman DM, Tanenbaum BS, Nelson JS. Depth profiling of laser heated chromophores in biological tissues using pulsed photothermal radiometry. J Opt Soc Am 1995; 12:1479 – 1488. Nelson JS, Milner TE, Tanenbaum BS, Goodman DM, van Gemert MJC. Infrared tomography of port wine stain blood vessels in human skin. Lasers Med Sci 1996; 11:199 – 204. Milner TE, Goodman DM, Tanenbaum BS, Anvari B, Svaasand LO, Nelson JS. Imaging laser heated subsurface chromophores in biological materials: determination of lateral physical dimensions. Phys Med Biol 1996; 41:31– 44. Milner TE, Smithies D, Goodman DM, Lau A, Nelson JS. Depth determination of chromophores in human skin by pulsed photothermal radiometry. Appl Opt 1996; 35:3379 – 3385. Nelson JS, Kelly KM, Zhao Y, Chen Z. Imaging blood flow in human port wine stain in-situ and in real-time using optical Doppler tomography. Arch Dermatol 2001; 137:741– 744. Majaron B, Verkruysse W, Tanenbaum BS, Milner TE, Telenkov SA, Goodman DM, Nelson JS. Combining two excitation wavelengths for pulsed photothermal profiling of vascular lesions in human skin. Phys Med Biol 2000; 45:1913 – 1922. Majaron B, Verkruysse W, Tanenbaum BS, Milner TE, Nelson JS. Pulsed photothermal profiling of hypervascular lesions: some recent advances. SPIE 2000; 3907:114– 125.

20 Reflectance Confocal Microscopy for Basic and Clinical Dermatology Salvador Gonza´lez Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts and Dermatology Service, Memorial Sloan-Kettering Cancer Center, New York, New York, USA

Robert H. Webb and R. Rox Anderson Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA

Milind Rajadhyaksha Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts and Lucid, Inc., Henrietta, New York, USA

1. Introduction 2. Confocal Microscopy 2.1. Principles of Reflectance Confocal Microscopy 2.2. Confocal Image Formation and Contrast 2.3. Optimal Design and Imaging Parameters 3. Confocal Imaging of Normal Skin 3.1. Interpretation of Images 3.2. In Vivo Morphometric Analysis of Normal Skin 4. Clinical Applications: Confocal Characterization of Skin Lesions 4.1. Benign Proliferative and Inflammatory Skin Diseases 4.1.1. Psoriasis 4.1.2. Acute Contact Dermatitis 4.1.3. Other Non-neoplastic Skin Lesions 4.2. Tumors of the Skin 4.2.1. Nonmelanocytic Tumors of the Skin 4.2.2. Melanocytic Tumors of the Skin 5. Applications in Skin Surgery 5.1. Adjunct to Dermatologic Surgery and Mohs Micrographic Surgery 5.2. Evaluation of Laser Treatment 6. Advances in Confocal Microscopy: Technology, Basic Research, Clinical Applications 7. Summary Acknowledgments References

416 416 416 417 418 419 419 421 422 422 422 422 425 426 426 429 432 432 432 433 435 435 435 415

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1.

INTRODUCTION

To date, biopsies for routine histology and light microscopic analysis prevail in dermatology as the gold standard for diagnosing skin tumors and other diseases. The procedure involves excision of a typically 2 –8 mm skin sample, processing of the excised tissue by either chemical fixation or freezing, slicing the specimen in 3 – 5 mm thin sections, and appropriate staining for microscopic visualization. The slides are subsequently examined by an expert pathologist who issues a comprehensive report of the histologic findings from his or her knowledge-based interpretation. This technique allows highly resolved visualization of tissues; the resolution is typically on the order of 1 mm lateral in 3 – 5 mm thin sections. However, the interpretation is limited to the excised sample tissue from the study area, is time consuming, and more importantly, does not provide realtime information. Histopathology is therefore less helpful for time-course and follow-up analysis. In addition, biopsies pose a risk of infection and unwanted scars. Fast, noninvasive microscopy of the skin in vivo could potentially solve many of these problems. During the last decade, advances in imaging technologies included optical coherence tomography (OCT) (1), computed tomography (2), high-frequency ultrasound (3), magnetic resonance imaging (MRI) (4), and reflectance confocal microscopy (CM) (5 –8). The resolution has been a limitation to adequately visualize cellular and nuclear detail. In general, optical techniques such as OCT and CM have provided higher resolution (1 –10 mm) than that of ultrasound and MRI (10 –100 mm). To our knowledge, reflectance CM is the only technique at present that provides high resolution (lateral 1 mm, axial or section thickness 3 mm) comparable to the gold standard routine histology and light microscopy. CM is an optical tool for noninvasively imaging tissue (9 –12). This technique allows one to image thin “sections” within a thick specimen with high resolution and contrast, using light that is backscattered from the tissue (8,13 – 15). During the last decade, this technique has been applied to humans for in vivo imaging of skin and oral mucosa (5 –8,16,17). In 1995, the design and development of a video-rate laser scanning confocal microscope with the ability to image nuclear- and cellular-level detail in human skin in vivo was reported (8). For both tandem scanning confocal and laser scanning confocal microscopy, visible (400 –700 nm) wavelengths allow imaging of tissue up to the dermoepidermal junction. Near-infrared wavelengths (800 – 1064 nm) allow imaging tissue well into the papillary dermis. Imaging is at video-rate (30 Hz) producing the equivalent of a microscopic movie. Dynamic processes such as blood cells flowing through a vessel are easily seen. Living human skin can thus be visualized in vivo, in real-time on a computer and/or video monitor. Efficient methods have been developed to keep the skin stable while imaging. However, reflectance CM has limitations, such as limited depth of imaging, and lack of stains which label specific tissue components.

2. 2.1.

CONFOCAL MICROSCOPY Principles of Reflectance Confocal Microscopy

The confocal microscope was invented over four decades ago (18). A confocal microscope consists of a point light source, either laser or nonlaser, which illuminates a single point (small volume) within the turbid object under study, and this illuminated area is then imaged through a point aperture onto a detector. The light source, illuminated spot and detector aperture are arranged to be in optically conjugate focal planes. The point aperture (usually a small pinhole) that is in front of the detector rejects all backscattered light from

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planes that are out of focus and from points in the focal plane that are not conjugate to both illumination and detection points, and allows only backscattered photons from the plane that is in focus (i.e., the plane of interest) to reach the detector. High-resolution optical sectioning is achieved because the detector selectively collects backscattered photons from the in-focus plane in the object. Imaging is performed by sequentially illuminating many single points. Therefore, to visualize the whole plane (or field of view) within the sample under study, the illumination spot has to be scanned in two dimensions on the in-focus plane. Scanning may be undertaken by either moving the object relative to a static light beam (specimen scanning) or by moving the illumination beam relative to a stationary specimen (beam scanning). Fast in vivo imaging is facilitated by scanning the light beam rather than the tissue. The arrangement illustrated in Fig. 20.1 shows the scheme of a confocal microscope operating in reflection.

2.2.

Confocal Image Formation and Contrast

In reflectance CM, image contrast results from light backscatter due to local variations of refraction index (8,19 – 22). In skin, the nuclei are seen as dark central areas surrounded by a bright cytoplasm. The brightness in the cytoplasm is due to hydration differences, filamentous proteins such as keratin, presence of mitochondria, ribosomes, and other cytoplasmic organelles. Although the nuclei appear dark, we occasionally see bright nuclear structures which are probably chromatin. From Mie theory, backscattering is known to increase when the scattering structure has a high refractive index and is of size similar to the illumination wavelength (23). Melanin absorbs visible and near-infrared light; however, melanosomes also strongly backscatter photons and act as an endogenous contrast agent for confocal microscopy (8). This happens due to at least two phenomena: high refractive index (n ¼ 1.7) (24) relative to that of epidermis (n ¼ 1.34) (1) and size of melanosomes (0.6 – 1.2 mm), which is similar to the illumination wavelength (0.4 – 0.7 mm visible, 0.8 –1.0 mm near-infrared). This explains the brightness of basal keratinocytes and melanocytes at the dermoepidermal level, mainly in dark skin phototypes, sun-exposed skin sites (8,25), and pigmented lesions (26).

Figure 20.1 Scheme of a reflectance mode confocal microscope illustrating noninvasive imaging of a thin (focused) plane of skin. Backscattered light is detected from the skin rather than transmitted light. The small aperture (pinhole) in front of the detector collects only the light in focus, while rejecting light that is out of focus.

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2.3.

Optimal Design and Imaging Parameters

As previously indicated, either white light or laser illumination may be used for in vivo confocal imaging. Compared to the white light tandem scanning design, laser scanning has the advantages of efficient light throughput, brighter illumination power, and the possibility of selectively choosing wavelengths. For imaging healthy and diseased human skin, optimum illumination power, wavelength, objective lens numerical aperture, and detector aperture size will thus depend on the application. Confocal resolution, both lateral and axial (section thickness) varies directly with wavelength (l) and inversely with objective lens numerical aperture (NA). The theoretical lateral resolution is 0.46l/NA and axial resolution is 1.4nl/NA2 (11). In practice, the resolution also depends on detector aperture size; as size increases the resolution decreases (i.e., section thickness increases). Shorter wavelengths provide higher lateral resolution and thinner sectioning than longer wavelengths. However, longer wavelengths and larger detector apertures can image deeper because scattering decreases with wavelength and larger detector apertures collect more backscattered light. For superficial imaging, such as analysis of stratum corneum topography, the optimum parameters might be: short visible wavelength (e.g., argon 488 nm), very high numerical aperture (e.g., 1.2), and small detector aperture (e.g., diameter 1 – 2 resels). For a deeper imaging application, for example, imaging dysplastic cells, cell nests and tissue architecture in deeper epidermis or dermis, the optimum parameters might be long near-infrared wavelength (e.g., diode laser 830 nm or Nd:YAG 1064 nm), moderately high numerical aperture (e.g., 0.8 –0.9), and somewhat larger detector aperture (e.g., diameter 1– 5 resels). The maximum potential for deep imaging with confocal microscopy has not been tested. Table 20.1 illustrates appropriate parameters for various applications. Water-immersion objective lenses are better than the previously common oilimmersion objective lenses (27). Water has a refractive index of 1.33, which is very close to that of soft tissues (e.g., epidermis refractive index is 1.34) (1), and thus tissueinduced spherical aberrations are minimized (17,22,28 – 32). Image resolution and contrast degrades when we image deeper in the tissue, due to tissue-induced spherical aberrations and mutiple-scattered background light (27). When imaging tissue in vivo at high-resolution, tissue motion can cause significant wobble and distortion in the images. To reduce tissue motion during imaging, we use an objective lens-to-skin surface contact device that limits lateral motion to ,+25 mm (22). The contact device allows precise location and imaging of 0.2 –5.0 mm areas on the skin.

Table 20.1 Optimum Range Parameters for Reflectance Confocal Imaging of Human Skin for Basic and Clinical Applications Wavelengths Objective lens Detector aperture diameter Refraction index medium Imaging rate Illumination power Tissue stability a

400– 700 nm (visible) 800– 1064 nm (near-infrared) 30 – 100, 0.7– 1.2 NA 1 – 5 lateral reselsa 1.33 (water) 10– 30 frames per second Up to 40 mW at the tissue surface Microsocpe – tissue clamping fixtureb

Resolution element. Minimize lateral motion to ,25 mm. Note: These parameters allows an experimentally measured lateral resolution of 0.5 –1 mm and an axial (virtual skin section) resolution of 2–5 mm. b


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CONFOCAL IMAGING OF NORMAL SKIN Interpretation of Images

Confocal images of skin appear different from routine histology. Confocal images are horizontal (en face) virtual sections parallel to the skin surface, whereas conventional histology is seen in vertical sections perpendicular to the skin surface (Fig. 20.2). Confocal images are gray-scale (since the illumination is of a single color or wavelength); in routine histology, the intranuclear structure (acidic) appears purple because of hematoxylin (basic) staining and the cytoplasm (basic) is stained pink with eosin (acidic) staining. Under coherent laser illumination, the cytoplasm shows a “grainy” appearance which in some extent is due to the effect of speckle produced by multiply backscattered light from the optically rough tissue microstructure (organelles and melanosomes have sizes similar to that of the illumination wavelength) (8,21,22). Under incoherent white light illumination, the grainy structure of the cytoplasm is less prominent and the speckle artifact is absent. When imaging skin, the first few optical sections on the top surface correspond to transverse sections of the stratum corneum, which is regularly seen as an intensely bright, refractive layer. The refractive index of stratum corneum is approximately 1.5, while that of water and deeper epidermis is 1.33– 1.4. Confocal imaging of stratum corneum thus requires well-controlled and optimal imaging parameters in order to avoid light saturation that can hide structural details. These parameters include power illumination, pinhole size, dry vs. water- and oil-immersion objective lenses. When these parametes are taken into account, individual as well as large “islands” of corneocytes between skin folds may be easily elucidated [Fig. 20.2(A)]. Just below the stratum corneum, the granular layer keratinocytes (25 – 35 mm diameter) are seen [Fig. 20.2(B)], typically two to four layers of nucleated cells. Each granular cell has a dark central area, the nucleus, surrounded by a bright grainy structure, the cytoplasm. Deeper in the epidermis, the cells decrease in diameter and have clearly demarcated cell borders. These cells are the spinous keratinocytes (15 mm in diameter). They have a polygonal shape resembling a honeycomb pattern [Fig. 20.2(C)]. Below the spinous cell layers, basal keratinocytes are mostly seen as bright, highly refractive cells, due to the presence of melanin above their nuclei (called “melanin hats” or “umbrellas”). Melanin as indicated previously provides a major source of contrast for reflectance confocal microscopy of epidermis. Therefore, en face sections at the level of the suprapapillary plates clearly show basal cells of greater brightness and contrast than the surrounding spinous keratinocytes [Fig. 20.2(D)]. At the dermoepidermal level, dermal papillae are always seen as bright/gray structures (collagen) surrounded by basal keratinocytes [Fig. 20.2(E)]. In the upper dermis, the network of bright collagen bundles is clearly seen, containing capillary loops with peripheral blood cells flowing through [Figs. 20.2(E) and (F)]. Additionally, hair follicles and sweat duct epithelium may be also found. Of note, realtime video images are much more informative than still, grabbed images. Live images are far superior because human perception “fills in” between video frames (33). Based on the research of several groups, we can interpret and understand the gross architecture of skin including cellular and nuclear morphology. However, there are issues still to be addressed, for example, in confocal images of oral mucosa, cells are seen as dark areas centered by a bright structure, the nucleus (Fig. 20.3) (17). The inversion of contrast may be due to inverted refractive index differences of nucleus-cytoplasm compared to epidermal cells.

Figure 20.2 Correlation between vertical and transverse sections (H&E and in vivo confocal) of normal skin. In confocal images, the corneocytes appear as bright polygonal shapes (A2, arrows), and are of size 10– 30 mm. Granular cells (B2, arrows) are regularly seen at depths of 10 – 15 mm. The dark oval areas correspond to nuclei within the bright cytoplasm. Spinous keratinocytes (C2, arrows) are seen at 20– 100 mm below the stratum corneum. Note basal keratinocytes (D2, arrows), located around of a dermal papillae (p, D), are brighter than keratinocytes of spinosum (ss, C2) and granulosum layers (sg, B2). Blood vessels (arrows, E) and collagen bundles (arrows, F ) are also seen (A1, A2, B1, C1, D1, 40/0.65 NA dry objective lens; B2, C2, D2, E, F, 30/0.9 NA water-immersion objective lens; scale bar, 25 mm). Source: Ref. (22). Reprinted by permission of Blackwell Science, Inc.


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Figure 20.3 Confocal image of superficial epithelial cell layer of lip mucosa in vivo. The diskshaped central structures are the nuclei (arrows), and the surrounding dark areas are the cytoplasm (30, 0.9 NA water-immersion objective lens; scale bar 25 mm).

3.2.

In Vivo Morphometric Analysis of Normal Skin

Morphometric measurements in vivo can be made with confocal microscopy. For example, the thicknesses of stratum corneum, epidermis, and the elongation of the dermal papillae or rete ridges can be measured. Meaningful measurements can be obtained if the experimenter is able to precisely locate starting and end planes for the different layers. For example, to measure stratum corneum thickness, one can use the very top surface as the starting plane and the first granular cell as the end plane. Viable epidermal thickness can be measured from the first granular cell layer as the first cluster of basal cells that are seen on the top of a dermal papilla. Elongation of the rete ridges can be measured from this cluster of basal cells to the image where the neighboring clusters have joined each other which suggests that the bottom of the rete ridge has been reached. The density of dermal papillae is easily determined by counting their number per field in images through the dermoepidermal junction. Such measurements have been published for normal skin, but not for a variety of lesions (7,8,25,34). In our studies, 10– 30 measurements were made at different sites showing the normal biological variability in the skin. There is uncertainty in the data because the axial resolution was 3 mm, and also because of axial tissue motion and because each layer of cells that we use as a reference plane has finite thickness. For example, basal cells have thickness of 10 mm, so when we see a cluster of basal cells, the question is: where within those 10 mm can we precisely and repeatedly determine a reference plane? But within these constraints, there is reasonably good correlation between confocal data and histology. We have also measured nuclear and cellular dimensions, cell density, and nuclear/ cytoplasm ratios (8,25). Again, there is inherent biological variability in size, and uncertainty because of cell shape, and section placement. The thickness of the epidermis varies depending on the topographic location. We recently have analyzed topographical area variations based on several stereological parameters. They included thickness of stratum corneum, thickness of the epidermis at both suprapapillary plates and rete peges, diameter of capillary loops at specific depth below the top surface of the imaged skin site, numerical density of keratinocytes within en face sections obtained within different compartments. Our results outline statistically significant differences among topographical areas (25). These differences are even more evident when skin sites categorized as sun-exposed (e.g., outer forearm, cheek and

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forehead skin) are compared to those regularly protected against sunlight (e.g., inner forearm, back, and leg skin). As an example, the latter showed a greater epidermal thickness at the rete ridges compared with the sun-protected skin sites while the suprapillary epidermal plates thicknesses were similar. As expected, the stratum corneum is found more fissured and bright in those areas chronically exposed to sunlight compared to those sites located on the back, legs, and inner forearm (25).

4.

CLINICAL APPLICATIONS: CONFOCAL CHARACTERIZATION OF SKIN LESIONS

CM at present allows real-time in vivo visualization of skin architecture to a maximum depth of 350 mm in normal, healthy skin. In diseased skin, the maximum depth of imaging varies between 100 and 350 mm in normal, depending on the skin condition. Initial research has concentrated on the most clinically relevant lesions. We have recently imaged and characterized psoriasis, acute contact dermatitis, and other skin conditions. Confocal images were qualitatively and quantitatively correlated to corresponding horizontal (en face) histology sections. The goal was to define and understand skin morphology as seen with a confocal microscope. These preliminary studies will help us develop our ability to understand and interpret confocal images of skin disorders. These lesions can be classified as benign proliferative and inflammatory skin conditions (psoriasis and acute contact dermatitis), nonmelanocytic skin neoplasms (basal and squamous cell carcinomas) and melanocytic tumors (benign and dysplastic nevi, and melanoma). Below, we present images of these lesions, discuss their interpretation and correlation to histopathology in order to describe their confocal features, as seen in vivo with reflectance CM. 4.1.

Benign Proliferative and Inflammatory Skin Diseases

4.1.1. Psoriasis Psoriasis, a benign proliferative skin disease, has been recently investigated (34). The histological features of lesional and non-lesional skin in five psoriatic patients were both descriptively and quantitatively evaluated and correlated with routine histology. Morphometric analysis showed significant increase in epidermal height (acanthosis) and length of dermal papillae (papillomatosis). As illustrated in Fig. 20.4, CM allowed us to quantify numerical differences not only between lesional psoriatic skin and normal skin but also between normal appearing skin of psoriatic subjects and the skin of healthy controls. The major histologic features of lesional psoriatic epidermis may also be elucidated. They include retention of nuclei within the stratum corneum revealing a parakeratotic stratum corneum [Fig. 20.4(A)], collection of leukocytes, the so-called Munro microabsceses seen as collections of highly refractile round or oval structures [Fig. 20.4(B)], and papillomatosis as noted by an increased number of dermal papillae per surface unit [Fig. 20.4(C)]. Thinning or disappearance of stratum granulosum, and inflamed dermis outlined by inflammatory infiltrate and tortuous and dilated dermal microvasculature were also observed in vivo. In a previous report, we showed that CM can microscopically demarcate the lateral margins of a psoriatic lesion in vivo (Fig. 20.5) (35). 4.1.2. Acute Contact Dermatitis Contact dermatitis (CD) is the most common occupational disease in dermatology. The two mechanisms of CD, irritant and allergic, have many shared characteristics upon


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Figure 20.4 Confocal images showing the major histological features of psoriasis in vivo. (i) Focal parakeratosis in a psoriatic lesion: (A) Vertical H&E-stained section showing corneocytes retaining flatted nuclei (arrows) (100, scale bar, 25 mm). (B) Confocal image shows nuclei (arrows) within corneocytes (30, 0.9 NA water-immersion objective lens; scale bar, 50 mm). (ii) Microabscess of Munro: (C) Accumulation of piknotic neutrophils (arrows) within stratum corneum. (D) Collection of live infiltrating leukocytes is seen close to skin fold (white arrows) (100, 1.2 NA; scale bar, 15 mm). (iii) En face papillomatosis: En face H&E stained skin section (E; 40; scale bar, 25 mm) shows good correlation with confocal images of live psoriatic skin (F; 30, 0.9 NA water-immersion objective lens; scale bar 50 mm). Source: Ref. (34). Reprinted by permission of PJD Publications.

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Figure 20.5 Sequence of frames (confocal images grabbed from videotape) showing an increase in dermal papillae across the margin of a psoriatic lesion. Arrow points to a specific papilla in the sequence (30, 0.9 NA water-immersion objective lens; scale bar 50 mm). Source: Ref. (35). Reprinted by permission of Blackwell Science, Inc.

clinical examination, making differentiation between the two difficult. In fact, conventional histology has frequently been used without success in assessing differences between irritant and allergic CD. This lack of success is possibly due to their morphological similarities, and other limitations such as lack of early time data, destruction of the target, and exogenous artifacts from fixation, processing, and staining. CM allows histologic visualization of the dynamic changes taking place during skin reactions in vivo, and therefore may overcome some of the limitations of routine histology while providing new criteria to differentiate both irritant and allergic CD. The development of acute CD was studied in our laboratories (36). Confocal features were evaluated on skin reactions developed on inner forearm skin of five subject volunteers with known clinical history of skin allergy. During the first day after elicitation of allergic CD, an intact stratum corneum, parakeratotic in some of the cases, was observed along with spongiosis and microvesicle formation [Fig. 20.6(A)]. Round and dendritic-shaped infiltrating cells were seen in the spongiotic spinous epidermal compartment. Dendritic cells were only seen in contact to epidermal keratinocytes while round cells could also be seen immersed in the microvesicle content [Fig. 20.6(B)]. Dermal microvasculature was not visualized with CM during the early phases of acute allergic contact dermatitis, perhaps due to a transient spongiosis and epidermal thickening [Fig. 20.6(C)]. All confocal features correlated very well with the histological findings observed in routine histology. At 3 or 4 days after challenging, a disrupted, necrotic stratum corneum was seen together with dilated dermal microvasculature. By contrast, in skin reactions induced by standard irritants (e.g., nonanoic acid, sodium lauryl sulfate), an early necrosis of the stratum corneum and upper epidermal layers together with prominent dermal vasodilation were observed (Fig. 20.7). Dendritic-shaped cells were not seen. Differences in the kinetic of these changes during the recovery phase in both nonanoic acid and sodium lauryl sulphate were also detected (37). These data warrant additional studies to confirm the use of confocal microscopy to differentiate irritant from allergic contact dermatitis.


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Figure 20.6 Vertical H&E-stained section of allergic skin reaction 24 h after removal of Finn chamber (scale bar 25 mm). (A) Confocal image of stratum corneum obtained at 24 h after removal of Finn chamber shows the presence of nuclei (arrows) (100, 1.2 NA water-immersion objective lens; scale bar 25 mm). (B) and (C) Confocal images obtained immediately after removal of Finn chamber. Round cells (B, arrows) and dendritic-shaped cells (C, arrow) are clearly seen between keratinocytes or within microvesicles (v). Note dendritic cell in contact with surrounding spinous keratinocytes (B, 100, 1.2 NA water-immersion objective lens; scale bar 25 mm; C, 60, 0.85 NA water-immersion objective lens; scale bar 50 mm). Source: Ref. (36). Reprinted by permission of Mosby, Inc.

4.1.3.

Other Non-neoplastic Skin Lesions

CM has been applied to other non-neoplastic skin conditions. Features characterizing some of these are described next: Rosacea: Enlarged pilosebaceous duct; dilated and tortuous dermal capillarities; presence of perivascular and perifollicular inflammatory infiltrate as well as pustules with collections of leukocytes (38). Darier-White’s disease: Grains and corps ronds were easily identifiable within the upper epidermis and stratum corneum (Fig. 20.8) (39). While grains were seen similar to parakeratotic corneocytes, corps ronds were viewed as round-shaped structures with a central round or oval nucleus, surrounded bya highly backscattering halo and peripheral dark rim of diskeratotic material. En face suprabasal clefts were also visualized and easily distinguished from dermal papillae, mainly by the presence of peripheral bright acantholytic keratinocytes and lack of blood vessels. Bacteria and fungi: Presence of hyphae was easily distinguished from the keratotic background in tinnae pedis (40) and from the nail plate in case of onychomycosis (41,42). CM was able to distinguish fungi in the nail plate and in the horny layer as well as other adjunct microscopic findings at the clinical examination

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Figure 20.7 Irritant contact dermatitis. Confocal images obtained immediately after removal show necrotic stratum corneum (sc, A, B) and dilation of dermal vessels (arrows, C) within the papillary dermis (dp, C). Infiltrating leukocytes (arrowheads, A) and acantholytic keratinocytes (B) are also seen. (30, 0.9 NA water-immersion objective lens; scale bar 25 mm).

without any specific preparation. Superficial folliculitis showed the presence of vesicle-pustules located in the upper epidermis containing numerous polymorphonuclear neutrophils (PMNs) (43) (Fig. 20.9). Macerated epidermis revealed a fibrillar appearance. Dilated vessels were seen within the papillary dermis. 4.2. 4.2.1.

Tumors of the Skin Nonmelanocytic Tumors of the Skin

Epidermal Neoplasms. High-resolution imaging of epidermal neoplasms in vivo continues to be a major program in our laboratories.

Figure 20.8 Vertical section of Darier-White’s papule. The lines mark the approximate level of en face optical sectioning of various epidermal layers as viewed by confocal microscopy. (A) and (B) Confocal images showing upper malphigian compartment containing corps ronds (arrowheads, A) and grains (arrows, B). (C), (D), and (E). Confocal images of suprabasal cleft (L, C) at different depths from top to bottom. Detachement of dyskeratotic keratinocytes is characterized at the cleft’s edges (arrows, D and E) (60, 0.85 NA water-immersion objective lens; scale bar 25 mm). Source: Ref. (39). Reprinted by permission of Munksgaard, International Publishers Ltd.


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Figure 20.9 Confocal images of a superficial folliculitis. (A) Inflammatory cells (arrows) are seen within the spinous compartment (SS). (B) Hair follicle (hf ) surrounded by a significant number of inflammatory cells (arrow) is seen. (C) and (D). Note an eccrine duct (sd) close to a dense collection of inflammatory cells (30, 0.9 NA water-immersion objective lens; scale bar 25 mm).

Actinic keratosis. High-resolution imaging of actinic keratosis in vivo is potentially important since histologically and clinically there is a continuum and progression between it and squamous cell carcinoma. To date there is no definite way to distinguish both of them without performing an invasive biopsy. CM imaging of actinic keratosis in vivo revealed the pathologic features of hyperkeratosis, nuclear enlargement with altered polarity and pleomorphism in lower epidermis, and architectural keratinocytic disarray (Fig. 20.10) (44). These features compared very well with the histological findings obtained in the skin biopsies performed after imaging. As in psoriatic lesions, insufficient depth of imaging penetration is a major drawback for imaging hypertrophic forms of actinic keratoses where the view of dermoepidermal junction is fundamental. Though granular nuclear enlargement and pleomorphism support the diagnosis of invasive squamous cell carcinoma (SCC), the distinction between invasive SCC and SCC in situ or bowenoid actinic keratoses is impossible without visualizing the dermopidermal junction. Despite these limitations, CM may become an alternative to biopsy in the diagnosis of actinic keratoses. Basal and squamous cell carcinomas. Nonmelanoma skin cancers are the most common malignancies among the caucasian population in the USA. The most frequent of these cutaneous neoplasms are basal cell carcinomas (BCCs) and SCCs. Except for certain SCCs, they are not metastazing tumors, but their prevalence and morbidity pose a significant public health problem. In our experience, both BCCs and SCCs show relevant cellular and architectural confocal miscroscopic features. CM imaging of BCC shows indistinct borders with variably sized elongated, atypical nuclei [Fig. 20.11(A)] (45).

Figure 20.10 Vertical H&E section of actinic keratosis. Lines represent depths in the epidermis corresponding to horizontal sections. Left column corresponds to en face conventional histopathology while right column corresponds to confocal images. (A) Stratum corneum showing irregular hyperkeratosis ( ). (B) Stratum granulosum demonstrates uniform, evenly spaced, broad keratinocytes. (C) Stratum spinosum shows enlarged, pleomorphic nuclei with haphazard orientation. (D) Stratum basale shows enlarged, pleomorphic nuclei with haphazard orientation. Dermal papillae appear as well-demarcated, dark holes in epidermis (arrow), containing blood vessels (30, 0.9 NA waterimmersion objective lens; scale bar 25 mm). Source: Ref. (44). Reprinted by permission of Mosby, Inc.


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Figure 20.11 Confocal images of dysplasia within BCC and SCC. (A) Atypical nuclei (arrows) with non-anaplastic pattern that is characteristic of BCC. (B) Individual keratinization figures (arrows) within en face anaplastic pattern of a SCC (A, 60, 0.85 NA water-immersion objective lens, and B, 30, 0.9 NA water-immersion objective lens; scale bar, 20 mm). Source: Ref. (45). Reprinted by permission of SPIE—The International Society for Optical Engineering.

A nonanaplastic en face pattern composed of a uniform population of dysplastic cells along with increased microvasculature flow and prominent inflammatory infiltrate is also seen in most of cases of superficial BCC. Reflectance CM imaging of SCCs on the other hand shows keratinocyte disarray and cell enlargement within spinous and granular compartments. Anaplastic tumoral pattern containing distinctive dysplastic figures is frequently found [Fig. 20.11(B)] (45). These architectural findings observed at low magnification allow confocal imaging to detect lateral margins of these skin neoplasms. Benign Cutaneous Appendage Tumors Sebaceous gland hyperplasia. In sebaceous gland hyperplasia, in vivo CM revealed hyperplastic sebaceous ducts surrounded by a prominent crown of blood vessels [Fig. 20.12(A)] (46,47). Therefore, a dilated duct opening to the surface containing a plug of bright material was seen as common feature [Fig. 20.12(B)]. Sebaceous acini with nearby blood vessels were also visualized in some lesions due to superficial location perhaps due to hypertrophy of the gland [Fig. 20.12(C)]. Individual sebocytes were seen as large sized cells containing highly refractile lipid droplets surrounding the nucleus. Eccrine poroma. Eccrine poroma showed very distinctive features of benign behaviour. Presence of a dense population of uniform cells, each with a central, round dark nucleus and well-demarcated spaces surrounding the tumor nests was characteristic. Round dark spaces within the tumor nests considered to be cuticulas were also elucidated (48). 4.2.2. Melanocytic Tumors of the Skin Malignant melanoma is the most common fatal neoplasm in the skin. Its rising incidence has led to greater interest and awareness in physicians and patients resulting in large number of programs aimed to their detection in early phases. Early detection represents the best opportunity to improve patient survival and quality of life. Therefore, feasible demonstration of microscopic features of malignancy in vivo in melanocytic lesions is the definitive goal for any noninvasive imaging technique applied to dermatology. CM has the unique advantage of being able to reveal nuclear, cellular, and architectural detail in the epidermal layers during the early phase of lesion formation. An additional advantage is the increased amount of melanin which is the best endogenous contrast agent for imaging skin, and thus adds some specificity for lesion detection and

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Figure 20.12 Sebaceous gland hyperplasia histopathology. Depth of confocal images are drawn onto the vertical histopathologic section. Confocal images show hyperplastic sebaceous ducts (arrows, A) surrounded by capilary loops (arrows, B), where delineation of individual peripheral blood cells is possible (arrowheads, B). Intracellular detail is seen in in vivo sebocytes (arrows, C) (A, 60, 0.85 NA water-immersion objective lens; scale bar 40 mm; B and C, 100, 1.2 NA water-immersion objective lens; scale bar 25 mm). Source: Ref. (46). Reprinted by permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.

identification. Currently, there are not enough data to demonstrate CM accuracy in terms of sensitivity and specificity for diagnosis of melanocytic lesions and clinical trials are ongoing. Benign Melanocytic Tumors Common acquired melanocytic nevi. Reflectance CM imaging of pigmented melanocytic lesions shows high refractility and contrast due to increased amount of melanin. Backscattered light in these pigmented lesions is stronger than that in normal skin. Confocal images of benign melanocytic junctional nevus show prominent changes in basal lamina level featured by nested highly refractile cells with ocassional dendritic branches


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(Fig. 20.13). Confocal images of benign compound and dermal nevi show further dermal nests of bright oval, monomorphous cells that frequently are surrounded by capillary loops of larger diameter than those seen in normal skin. Individual bright cells is a common finding in dermal level confocal images.

Figure 20.13 Confocal images of melanocytic lesions. (A) and (B) correspond to en face sections of a junctional nevus showing an uniform pattern of bright monomorphic cells, nevomelanocytes (arrowheads) and pigmented basal keratinocytes (arrows). (C) and (D) correspond to en face sections of dysplastic compound nevus. Branching dendritic structures at epidermal level (arrows) and highly refractile individual nevomelanocytes (arrowhead) at the dermal level are also seen. (E) and (F ) correspond to en face section of a compound nevus. Arrows point dermal nest of nevomelanocytes. (30/0.9 NA water-immersion objective lens; scale bar 30 mm).

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Dysplastic nevi. In dysplastic nevi, the presence of individual bright nevomelanocytes and dendrites may be also seen. Irregularly shaped, non-necessarily centered, nucleus as well as highly refractive dendritic branches have been also clearly delineated. Malignant Melanoma. Confocal images of malignant melanoma revealed the presence of intensely bright, pleomorphic and irregularly shaped cells in disarray at the epidermis and dermis levels, occasionally with stellate morphology (49). Atypical nuclei of eccentric location may be also elucidated in dysplastic cells. Architectural changes in the spinous compartment along with the presence of refractive dust-like particles either clumped or as individual microobjects were seen within the malphygian compartment and stratum corneum.

5. 5.1.

APPLICATIONS IN SKIN SURGERY Adjunct to Dermatologic Surgery and Mohs Micrographic Surgery

A major goal in our investigation of nonmelanoma skin cancers was to test the usefulness of this noninvasive technique to guide dermatologic surgery. Confocal imaging can potentially demarcate the microscopic margins in vivo prior to surgery. We have demonstrated that CM is capable of microscopically demarcating lateral margins of the tumor versus surrounding non-neoplastic skin; however an important limitation has been to demarcate the deep margins of the tumor in vivo since, as in other skin lesions, the maximum depth of imaging is not sufficient. An alternative is to examine freshly excised tissue to investigate clear margins during dermatologic surgery; we recently developed a simple technique for rapid detection of nonmelanoma skin cancers in freshly excised tissue during Mohs micrographic surgery (49 –51). Rapid detection is possible because the brightness of the tumors relative to the surrounding normal tissue (i.e., contrast) can be significantly improved by washing the tissue with 5% acetic acid or 10% citric acid which makes the neoplastic nuclei bright, and illumination/detection in cross-polarized mode which makes the surrounding dermis dark. Low-resolution confocal mosaics can be made to rapidly survey large excised slices, followed by high-resolution imaging of the morphology of individual nuclei. The cross-polarized confocal low-resolution screening followed by high-resolution inspection of nuclear morphology is similar to the procedure for examining histopathology (Fig. 20.14). Currently, an ongoing multicenter clinical trial to evaluate the sensitivity of the adjunct use of confocal microscopy to Mohs micrographic surgery is being conducted. Confocal microscopy may be also used to image freshly excised tissue without processing and/or staining as it is performed with routine histology. 5.2.

Evaluation of Laser Treatment

To date, research on the changes that dynamically take place after laser treatment of skin lesions have been performed by invasive methods (i.e., biopsies and histological analysis). Confocal microscopy allows the study of these changes in vivo and, therefore, may provide a better understanding of the action mechanisms of laser – tissue interactions. In this regard, we have investigated the mechanisms of two different lasers on a common vascular lesion, cherry angioma, by analyzing the microscopic changes that these lesions underwent over 3 weeks after laser targeting. Interestingly, while the lesion treated with a 585 nm pulsed dye laser (pulse of 5 J/cm2 and 5 mm spot size) underwent an immediate replacement of the blood vessels by amorphous refractile cords conforming to the original vessel shape, the lesion treated with a 568 nm continuous wave krypton laser (fluence of


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Figure 20.14 H&E-stained section (A) and confocal cross-polarized image of an acetic acid washed skin sample from a Mohs micrographic procedure containing BCC nests. Nests are easily distinguished from the surrounding dermis because of their increased nuclear density (BCC) (30, 0.9 NA water-immersion objective lens; scale bar 500 mm). Courtesy of Dr. Gregg Menaker and Peter Dwyer, Dermatology Surgery Unit, Massachusetts General Hospital.

0.75 W and 1 mm spot size) resulted in dark nonrefractile spaces that widen and develop later ragged edges (Fig. 20.15) (52). Confocal images similar to the former were observed in the vascular compartment of sebaceous hyperplasia lesions (46,47). At 3 weeks after laser targeting, complete wound healing with normal features at both epidermal and upper dermal levels was recorded; biopsies were not required to view at high-resolution dynamic changes over time.

6.

ADVANCES IN CONFOCAL MICROSCOPY: TECHNOLOGY, BASIC RESEARCH, CLINICAL APPLICATIONS

Currently, visible and near-infrared CM has the capability of visualizing healthy and diseased skin at the highest resolution in vivo. Thus, it is an excellent research tool and has tremendous potential of becoming a valuable diagnostic tool for clinical dermatology and dermatologic surgery. Currently, one of the most important limitations for interpretation and understanding of the confocal images is that real-time imaging only provides en face sections (parallel to skin surface) while routine histopathology is based upon interpretation of vertical sections (perpendicular to skin surface). Vertical views have been possible by performing three-dimensional software reconstruction of a stack of horizontal sections that were grabbed at video-rate. In these vertical views, the nuclear and cellular morphology is poorly despicted. This is because axial resolution (section thickness) is generally three to five times worse than the lateral resolution (27). Although vertically displayed confocal sections do not compare well to the histology sections, the current views may nevertheless be of use to analyze stereological location of structures, such as nests of melanocytes in case of pigmented lesions or bullae in case of bullous diseases as well as for parameters morphometrically analyzed from still grabbed images, such as epithelium thicknesses including elongation of the rete ridges taking place in psoriasis. However, loss of resolution and contrast reduce the potential for analyzing subcellular detail that is of paramount interest for investigating neoplastic lesions. A tremendous impact in health care can be the potential for real-time telepathologic consultation. This is an important application of in vivo confocal microscopy for

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Figure 20.15 Cherry angioma. (A1) Conventional histopathology, line indicates the depth of the confocal section. (A2) Confocal image showing dilated blood vessels (arrows) between collagen bundles in papillary dermis. (B) Confocal images illustrating the microscopic changes immediately, 4 h and 1 day after pulsed dye laser exposure. Amorphous cords of refractile material conform to shape of original vessels are seen. (C) Confocal images illustrating the microscopic changes immediately, 4 h and 1 day after krypton laser exposure. Dark nonrefractile spaces are seen where blood vessels had been (30, 0.9 NA water-immersion objective lens; scale bar 25 mm). Source: Ref. (52). Reprinted by permission of Mosby, Inc.

diagnosing skin lesions since it allows noninvasive microscopic information and expert interpretation of confocal features while the patient is in the clinical setting. Guidance of invasive biopsies and/or screening for skin tumors is then possible. A good example of this endeavor is the potential of screening previous to and after treatment of neoplastic lesions (53). The potential use of this novel tool for pharmaceutical and cosmeceutical purposes has not been discussed in this chapter; however, investigations on drug delivery and distribution are ongoing. Finally, the devices can be of small size (hand-held CM). In fact, every compact disc player contains a high-quality near-infrared confocal reflectance microscope. In these devices, a small semiconductor diode laser is focused to a point on an embossed


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surface inside the spinning disc, and bits of digital information are read nearly confocally by an integrated detection system. Based on this example it is reasonable to assume that small confocal imaging systems will be developed and optimized for a variety of imaging applications.

7.

SUMMARY

The use of CM for imaging human skin in vivo has been going on for the last 10 years. Confocal reflectance microscopes resolve microstructures within living skin to a controlled depth of 200 – 350 mm below the stratum corneum with lateral and axial (section thinkness) resolutions that compare very well with routine histology. Visualization of cells and nuclei in the epidermal layers, and the underlying dermis, including collagen bundles, capillaries, and circulating peripheral blood cells is possible. The earliest work characterizes the morphology of normal human skin, while recent papers have elucidated the major histological features of several inflammatory and proliferative skin conditions in vivo including skin cancers and evaluating laser treatment in benign skin lesions. These studies demonstrate the potential of in vivo CM for basic and clinical research. As a diagnostic tool, clinical studies testing the sensitivity and specificity are currently warranted. Ultimately, CM may be used in specific clinical settings for screening or diagnosis lesions, leading to avoidance of biopsies and real-time guidance during surgery.

ACKNOWLEDGMENTS The construction of the prototype confocal scanning laser microscope for imaging human skin in vivo was funded by DOE grant DE-FG02-91ER61229 and by a grant from the Whitaker Foundation to MR. Initial development of the commercial real time, reflectance mode confocal microscope was funded by SBIR 2 R44CA58054-03 from the National Cancer Institute to Lucid, Inc. The authors also want to thank Dr. Ernesto Gonza´lez and Dr. Zeina Tannous for critical reading of the manuscript, and Dr. James Zavislan for his input during the development of the project. We gratefully acknowledge David Aghassi, Sri Atluri, Vanessa Campo-Ruiz, Christine Choi, Anastasia Drohan, Misbah Huzaira, Ramsey Markus, Gennady Rubinstein, Rieko Tachihara, and Matt White. These fellows have been working on in vivo confocal microscopy imaging in clinical dermatology under the supervision of SG during their stay at Wellman Laboratories of Photomedicine. REFERENCES 1.

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Tearney GT, Brezinski ME, Southern JF, Bouma BE, Hee MR, Fujimoto JG. Determination of the refractive index of highly scattering human tissue by optical coherence tomography. Opt Lett 1995; 20:2258 – 2260. Allemond R. Basic technical aspects and optimization prblems in X-ray computed tomography. In: Guzzardi R, ed. Physics and Engineering of Medical Imaging. Boston: Martinus Nijhoff Publishers, 1987:207 –217. Mansotti L. Basic principles and advanced technical aspects of ultrasound imaging. In: Guzzardi R, ed. Physics and Engineering of Medical Imaging. Boston: Martinus Nijhoff Publishers, 1987:263 – 317.

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Sheppard CJR, Gu M. Aberration compensation in confocal microscopy. Appl Opt 1991; 30:3563 – 3568. Carlsson K. The influence of specimen refractive index, detector signal integration, and non-uniform scan speed on the imaging properties in confocal microscopy. J Microsc 1991; 163:167–178. Hell S, Reiner G, Cremer C, Stelzer EHK. Aberrations in confocal fluorescence microscopy induced by mismatches in refractive index. J Microsc 1993; 169:391– 405. Gibson SF, Lanni F. Experimental test of an analytical model of aberration in an oilimmersion objective lens used in three-dimensional light microscopy. J Opt Soc Am A 1992; 9:154 – 166. Watson AB. Temporal sensitivity. In: Boff KR, Kaufman L, Thomas JP, ed. Handbook of Perception and Human Performance. Vol. 1, ch. 6. Sensory Processes and Perception. New York: John Wiley and Sons, 1986:6.34– 6.35. Gonza´lez S, Rajadhyaksha M, Rubinstein G, Anderson RR. Characterization of psoriasis in vivo by reflectance confocal microscopy. J Med (J Med Clin Exp Mol) 2000; 30(5 – 6):337– 356. Gonza´lez S, Rajadhyaksha M, Anderson RR. Non-invasive (real-time) imaging of histologic margin of a proliferative skin lesion in vivo. J Invest Dermatol 1998; 111:538 – 539. Gonza´lez S, Gonza´lez E, White WM, Rajadhyaksha M, Anderson RR. Allergic contact dermatitis: correlation of in vivo confocal imaging to routine histology. J Am Acad Dermatol 1999; 40:708 – 713. Drohan A, Atluri S, Rajadhyaksha M, Anderson RR, Gonza´lez S. Confocal imaging of irritant skin reactions in vivo (abstract). Am J Contact Dermatol 1999; 10(2):104. Tachihara R, Choi C, Anderson RR, Gonza´lez S. Real-time confocal microscopy imaging of Rosacea in vivo (abstract). 13th International Congress of Photobiology, San Francisco, CA, 2000. Gonza´lez S, Rubinstein G, Mordovtseva V, Rajadhyaksha M, Anderson RR. In vivo abnormal keratinization of Darier-White’s disease as viewed by real-time confocal imaging. J Cutan Pathol 1999; 26:504 –508. Markus R, Huzaira M, Anderson RR, Gonza´lez S. A better KOH prep? In vivo diagnosis of tinea with confocal microscopy. Arch Dermatol 2001; 137:1076 – 1078. Pierard GE, Arrese JE, Pierre S, Bertrand C, Corcuff P, Leveque JL, Pierard-Franchimont C. Microscopic diagnosis of onychomycosis. Ann Dermatol Venereol 1994; 121(1):25 – 29. Hongcharu W, Dwyer P, Gonza´lez S, Anderson RR. Confirmation of onychomychosis by confocal microscopy. J Am Acad Dermatol 2000; 42:214 – 216. Gonza´lez S, Rajadhyaksha M, Gonza´lez-Serva A, White WM, Anderson RR. Confocal reflectance imaging of folliculitis in vivo. Correlation of confocal imaging to routine histology. J Cutan Pathol 1999; 26:201– 205. Agashi D, Anderson RR, Gonza´lez S. Confocal laser microscopic imaging of actinic keratoses in vivo: a preliminary report. J Am Acad Dermatol 2000; 43:42 –48. Gonza´lez S, Rajadhyaksha M, Anderson RR. Confocal Imaging of benign and malignant proliferative skin lesions in vivo. Proc SPIE 1999; 3590:59 – 65. Gonza´lez S, White WM, Rajadhyaksha M, Anderson RR, Gonza´lez E. Confocal imaging of sebaceous gland hyperplasia in vivo to assess efficacy and mechanism of pulsed dye laser treatment. Lasers Surg Med 1999; 25:8 –12. Agashi D, Gonza´lez E, Anderson RR, Rajadhyaksha M, Gonza´lez S. Elucidating the pulsed dye laser treatment of sebaceous hyperplasia in vivo using real-time confocal scanning laser microscopy. J Am Acad Dermatol 2000; 43:49– 53. Tachihara R, Choi C, Anderson RR, Langley RL, Gonza´lez S. In vivo confocal imaging of pigmented eccrine poroma. J Dermatol 2002; 204(3):185– 189. Rajadhyaksha M, Menaker G, Gonza´lez S. Confocal microscopy of excised human skin using acetic acid and crossed polarization: rapid detection of non-melanoma skin cancers. Proc SPIE 2000; 3907:84 – 88. Rohrer T, Meyers S. The use of confocal laser scanning microscopy in Mohs micrographic surgery (abstract). Lasers Surg Med 2000; 12(suppl):3– 4.

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Section III: Lasers Treatment of Cutaneous Disorders

21 Laser Treatment of Port Wine Stains Arielle N. B. Kauvar New York Laser and Skin Care, New York; New York University School of Medicine, New York; and Suny Downstate Medical Center, New York, New York, USA

1. 2. 3. 4.

Differentiating PWS from Other Vascular Anomalies Related Syndromes Pathogenesis of PWS Principles of Laser Tissue Interaction 4.1. Selective Photothermolysis 4.2. Wavelength 4.3. Pulse Duration and Thermal Relaxation Time 4.4. Spot Size 5. Treatment of PWS with Continuous Wave Lasers 6. Flashlamp-Pumped Pulsed Dye Laser 6.1. Prognostic Indicators 6.2. Early vs. Later Treatment 6.3. PWS Recurrence 7. Advances in Pulsed Dye Laser Treatment 7.1. Wavelength 7.2. Spot Size and Overlap 7.3. Pulse Duration 7.4. Skin Cooling 8. Treatment of PWS with Other Lasers and Light Sources 8.1. Pulsed KTP Lasers 8.2. Near Infrared Lasers 9. Treatment Technique 10. Complications and their Management 10.1. Reticulation 10.2. Immediate Skin Graying or Whitening 10.3. Hyperpigmentation 10.4. Hypopigmentation 10.5. Atrophic and Hypertrophic Scars 10.6. Dermatitis 11. Conclusions References

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Lasers and light-based therapies are currently the only acceptable modalities for the treatment of port wine stains (PWS). Prior to the development of laser technology, PWS were treated with radiation, surgical excision and grafting, cryosurgery, and camouflage with cosmetics or tattoos. All of these techniques produced unsatisfactory results and poor aesthetic outcomes. The development of the pulsed dye laser in the 1980s permitted selective photocoagulation and destruction of the lesional blood vessels without damaging the surrounding skin. Laser treatment produces dramatic clearing of PWS with minimal scarring or epidermal damage, minimizes lesional hypertrophy, decreases the risk of bleeding from hypertrophy or pyogenic granulomas formation, and reduces the associated psychosocial morbidity.

1.

DIFFERENTIATING PWS FROM OTHER VASCULAR ANOMALIES

PWS are capillary vascular malformations that occur in 0.3% neonates (1). PWS begin as cutaneous patches predominately located on the head or neck, and change in color with age from pink to purple. These lesions are usually present at birth and grow proportionally with the child. Up to 40% of newborns have similar-appearing macular stains on the face and neck, often referred to as “salmon patch,” “angel kiss,” or “nevus flammeus neonatorum,” but these lesions fade during infancy (2). In contrast, PWS never regress; they thicken with age, become darker in color, increasingly nodular, and cause psychological distress (Fig. 21.1). Many patients report low self-esteem and difficulties in their personal and professional relationships attributed to their capillary vascular malformations (3). By the fifth decade of life, up to 65% of patients develop hypertrophy or nodularity of the lesion, and these changes are associated with a risk of spontaneous bleeding or hemorrhage with injury to the site (4). Hypertrophy of lesions in the periorbital and nose region may obstruct vision, and in the perioral and nose region may interfere with eating and breathing (5). Soft tissue and skeletal hypertrophy occur in some facial PWS and may require surgical correction or orthodontic treatment. Diagnosis of PWS must be differentiated from hemangiomas (6). Hemangiomas are common benign vascular lesions of childhood, and are defined as tumors rather than malformations. They are present at birth in 2– 3% of newborns (7), up to 12% of

Figure 21.1 Progression of PWS without laser treatment (a, b). Results following 25 pulsed dye laser treatments (c). (Courtesy of Gerald Goldberg, M.D.)

Laser Treatment of PWS

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infants by 1 year of age, and up to 22% of preterm infants weighing ,1000 gm (8). Hemangiomas have a female to male preponderance of 3:1 (9) and 60 –70% are localized to the head and neck. Clinically, the rapid proliferation of hemangiomas differentiates them from vascular malformations such as PWS, venous, arterio-venous, and lymphatic malformations (6). Hemangiomas are characterized histologically by endothelial hyperplasia. They initially appear as white or pink macules or telangiectasia with surrounding vasoconstriction, and then undergo a period of rapid proliferation out of proportion to the growth of the infant during the first year of life. Lesions may grow rapidly both in height and lateral spread, and sometimes reach gigantic proportions. At age 1 year, most hemangiomas begin a slow period of involution that requires 5– 12 years. Involution may not be complete, and 50% of patients are left with residual telangiectasias, redundant fibro-fatty tissue, and epidermal atrophy (10,11). Lasers and light sources also play a role in the treatment of hemangiomas (see Chapter 22). Differentiation of PWS, hemangiomas, and other vascular malformations is important in determining the long-term prognosis, identifying potentially dangerous complications, and implementing appropriate therapy. Sophisticated laboratory or radiology tests are usually not necessary, and the diagnosis can generally be made through history and physical examination.

2.

RELATED SYNDROMES

PWS are usually isolated lesions, but some are associated with serious syndromes that must be recognized in a timely fashion. These include Sturge –Weber syndrome (12), Klippel – Trenaunay syndrome (13), and other less common constellations of findings. Sturge – Weber syndrome comprises of a large facial PWS (Fig. 21.2) with ipsilateral leptomeninigal vascular malformations, ipsilateral choroidal vascular malformations, and glaucoma. The distribution of facial PWS along the ophthalmic (V1) distribution of

Figure 21.2

Infant with facial PWS and Sturge– Weber syndrome.

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the trigeminal nerve is determinant of central nervous system or ocular anomalies (14). Patients with V1 distribution PWS are further divided into “high risk” and “low risk” groups. Patients at high risk for Sturge – Weber show involvement of the entire V1 area with or without V2 and V3. Low risk patients have incomplete involvement of V1 with or without V2 and V3 involvement. There is no risk of neuro-ocular anomalies in patients with V2 or V3 distributed PWS in the absence of V1 involvement, and these individuals require no further medical workup. There is a significantly higher incidence of glaucoma and/or central nervous system abnormalities associated with eyelid PWS, bilateral trigeminal PWS, and unilateral PWS involving distribution of all three trigeminal branches (14,15). Children with PWS in these distributions should undergo appropriate testing for central nervous system and ocular abnormalities. Ophthalmic examination is recommended twice annually until the age of two and yearly thereafter, as glaucoma may have a later onset (16,17). Klippel –Trenaunay syndrome constitutes a capillary-venous vascular malformation accompanied by hypertrophy of the affected limb of body part. Clinically, the findings may range from barely noticeable limb discrepancy to debilitating limb asymmetry requiring wheel chair confinement. The cutaneous capillary malformations may be patchy on the involved leg, and can be associated with hemolymphatic vesicles. There may be associated anomalous superficial veins, deep vein hypoplasia, and lymphatic malformations (16). Leg involvement is the most common presentation of the syndrome. One study (18) showed greater predominance of right sided lesions. Complications of Klippel – Trenaunay syndrome include thrombosis, coagulopathy, pulmonary embolism, heart failure, or bleeding from abnormal vessels in the genitalia, gut, or kidney. Patients generally undergo annual noninvasive vascular imaging adding limb girth measurements if there is clinical evidence of asymmetry. Lesions that extend to the pelvis or trunk can cause hematuria or hematochezia and warrant evaluation with noninvasive imaging and endoscopy. Shoe lifts are commonly used for leg discrepancies .1.5 cm, and compression garments are useful for limbs with venous insufficiency or bleeding from superficial vesicles. Severely hypertrophic limbs may require surgical debulking or limb length adjustment (16,18). PWS may also be present in a number of other rare syndromes. PWS in the sacral area may indicate occult spinal dysraphism, lipomenigocele, or a tethered cord (19). These lesions require further workup. Other associated syndromes include ParkesWeber syndrome (16,20), Cobb syndrome (20 – 22), Proteus syndrome (23 – 25), and phakomatosis pigmentovascularis (26,27).

3.

PATHOGENESIS OF PWS

The pathogenesis of PWS is poorly understood but is thought to relate to abnormal angiogenesis owing to altered neural regulation of the dermal vasculature (28). Histologically, these lesions have an increased number of ectatic capillary channels in the papillary dermis. Immunohistochemical analysis of the major structural components of the vessel walls, such as fibronectin and type IV collagen, shows normal morphology (29). There are normal staining patterns of endothelial-specific antigens such as factor VIII, PAL-E, ELAM-1, and ICAM-1 (30). The density of cutaneous nerves within these lesions is significantly reduced on the basis of studies using antibodies against neuronal cytoplasmic protein (PTP 9.5), neuron-specific enolase (NSE) (31,32), and S 100 protein. Others suggest that the decreased density of cutaneous nerves may be secondary to chronic ischemia in the lesion (33).


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Most capillary vascular malformations are sporadic, but there is evidence to suggest a genetic predisposition. There are reports of families in which these lesions segregate in a dominant manner with incomplete penetrance (34 –37). Up to 7– 22% of PWS patients have relatives with a cutaneous stain (36,38,39). PWS occur in 1.8% of first-degree relatives of patients with Klippel –Trenaunay syndrome, a prevalence rate significantly higher than in the general population (40). Genome-wide linkage analysis was performed on six families with inherited PWS by Eerola et al. (41). PWS co-segregated with a large locus (CMC1) on chromosome 5q. Chromosome 5q has also been implicated in the genesis of other vascular anomalies such as Klippel – Trenaunay syndrome (42) and hemangiomas (43 –45).

4. 4.1.

PRINCIPLES OF LASER TISSUE INTERACTION Selective Photothermolysis

The concept of selective photothermolysis was developed by Anderson and Parrish in 1983 (46), and with its formulation, inaugurated a new era in the application of lasers to cutaneous disease. The term “selective photothermolysis” describes the production of site-specific, thermally mediated injury of microscopic, chromophoric tissue targets by selectively absorbed pulses of radiation. Selective photothermolysis is achieved with lasers and light sources when the following basic elements are met: (1) the wavelength of light is preferentially absorbed by the desired target structures and can penetrate the tissue sufficiently to reach that structure; (2) the pulse duration or exposure time is less than or equal to the time necessary for cooling of the target structures; (3) sufficient fluence, or energy density, is used to reach an irreversibly damaging temperature within the target structure. 4.2.

Wavelength

The wavelength of light chosen must be preferentially absorbed by the target structure (47). Blood is the major chromophore in vascular lesions. Blood absorption is dominated by oxyhemoglobin and reduced hemoglobin absorption and exhibits strong bands in the UV, blue, green, and yellow wavelengths (48). Oxyhemoglobin has major absorption peaks at 418, 542, and 577 nm and is present at high concentrations within PWS vessels. The strongest peek is at 418 nm (blue), but strong absorption by melanin and its limited penetration depth preclude the use of this wavelength. The 577 nm (yellow) absorption band of oxyhemoglobin was initially chosen for targeting superficial small vessels using the flashlamp-pumped pulsed dye laser (49). There is also a broad oxyhemoglobin band beyond 900 nm that provides preferential absorption by hemoglobincontaining targets and much greater depth of penetration. Other lasers emitting in the green and near infrared region, as well as the intense pulse light source (IPL) emitting a broad spectrum of light from green to near-infrared, have been applied more recently to the treatment of vascular anomalies. 4.3.

Pulse Duration and Thermal Relaxation Time

Thermal relaxation time refers to the time needed for significant cooling of the small target structure. Maximal thermal confinement occurs when the laser exposure or pulse duration is less than the thermal relaxation time (50 –54). The thermal relaxation time (tr) for heat conduction is proportional to the square of the object size. To achieve selective

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photothermolysis, the exposure time or pulse duration must be chosen to match the diameter of the blood vessels being treated. For most tissue targets, the tr can be approximated in seconds as the square of the target dimension in millimeters. A 0.1 mm PWS vessel should therefore cool in approximately 1022 s or 10 ms. 4.4.

Spot Size

The laser beam diameter or spot size affects the effective fluence at a given depth in tissue (55,56). Small spot sizes produce a greater fraction of photon scatter outside the beam and are clinically ineffective. Larger spot sizes produce increased scattering in the superficial dermis and provide greater heating or dermal targets. The ratio of dermal to epidermal heating increases as the spot size increases. Lower fluences can therefore produce the same effect with larger spot sizes compared to smaller spot sizes with higher fluences.

5.

TREATMENT OF PWS WITH CONTINUOUS WAVE LASERS

The introduction of the argon laser in the early 1970 represented the first major advance in PWS therapy (57 – 60). The blue –green light (488 and 514 nm) is preferentially absorbed by oxyhemoglobin in the ectatic dermal vessels. Light energy absorbed within the vessels is converted to heat and produces thermal damage and thrombosis. Despite the ability to concentrate thermal energy and heating within the PWS vessels, the long exposure times of the argon laser permitted diffusion of heat from the injured vessels to surrounding structures. Nonspecific damage was also caused by absorption of the light energy by epidermal and dermal melanin. In histologic studies, the argon laser produced nonspecific coagulation throughout the epidermis, papillary dermis, and upper reticular dermis to a depth of 0.45 mm. Specific damage to chromophore-containing organelles extended to the depth of 0.75 mm in a subjacent zone. Clinically, this laser produced a high incidence of scarring, atrophy, and hypopigmentation, particularly on the lip and perialar regions of infants and young children. Similar results were observed with other continuous and quasicontinuous lasers, including the argon-pumped tunable dye, copper vapor, Nd:YAG, and carbon dioxide lasers.

6.

FLASHLAMP-PUMPED PULSED DYE LASER

First introduced in the 1980s, the flashlamp-pumped pulsed dye laser was the first instrument to implore the concepts of selective photothermolysis (61). A wavelength of 577 nm was initially chosen to provide strong absorption by oxyhemoglobin present within the blood vessels and reduced absorption by melanin in the surrounding tissue. The laser wavelength was subsequently increased from 577 to 585 nm to provide increased depth of penetration in tissue and improve clearance of PWS (62). Early pulsed dye laser systems used for studying PWS treatment used pulse durations ranging from 300 to 500 ms. Since the late 1980s the commercially available pulsed dye lasers have been manufactured with a wavelength of 585 nm and a pulse duration of 450 ms. In histological studies, pulsed dye laser treatment produces intravascular thrombosis formation without epidermal or dermal damage (63). Approximately 1 month after treatment, normal appearing vessels replace the ectatic lesional vessels. The vast majority of pediatric patients show a beneficial response to pulsed dye laser therapy. The range of improvement reported following pulsed dye laser treatment in


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children has been from 50% lightening in 87% of patients to nearly 100% clearance (64 –68). Direct comparison of these studies is difficult because of the varying number of treatments and dose ranges. In adult PWS lesions, 36 – 44% of patients demonstrate 75% lightening, and 75% of patients show at least 50% lightening after four laser treatments (69,70). Even with relatively refractory lesions, continued lightening is achieved with additional laser treatments. Kauvar and Geronemus (71) found that additional lesional treatment was achieved in patients who underwent 10– 25 repetitive treatments after not achieving .75% lightening in nine treatment sessions. Patients who do not achieve substatial lightening after pulsed dye laser therapy represent ,10% of those treated and may be candidates for treatment with other lasers or light sources that are capable of photocoagulating larger diameter and deeper vessels. Damage to vascular tissue is so selective with a pulsed dye laser that there is inconsequential absorption by melanin in fair-skinned individuals. The laser can be safely used in skin types I– III and photo type IV when there is no suntan present. Epidermal damage is rarely seen. In a study of 500 patients (72), atrophic scarring was reported in ,0.1% of patients, spongiotic dermatitis in 0.04%, hyperpigmentation in 1%, and hypopigmentation in 2.6% of patients. Pulsed dye laser cannot be used to treat skin types V and VI because the higher density of melanin results in decreased vascular absorption and the possibility for epidermal damage (73). Newer studies of cryogen-cooling techniques (74) throughout the pulse sequence suggest that safe treatments of darker skin phototypes may be possible in the near future.

6.1.

Prognostic Indicators

The response of PWS to pulsed dye laser treatment depends, in part, on the lesional size, anatomic location, and size of vessels in the lesion. Among PWS located on the head and neck, lesions present on the forehead and lateral cheeks show a faster response to laser therapy (75). PWS present in the central facial area or in a V2 dermatomal distribution respond more slowly. PWS located on the extremities respond more slowly than lesions on the trunk, and lesions on the distal extremities respond the slowest (76). Distal lower extremities are the most difficult to treat, presumably owing to the thickerwalled vessels. Lesions with smaller surface area respond more quickly to laser therapy than larger diameter lesions. In a study of 91 consecutive patients (77), Nguyen et al., found that the mean decrease in lesion size was 67% for lesions ,20 cm2 compared with the 23% decrease for lesions .40 cm2, after the same average number of treatment sessions. Vessel morphology correlates with PWS color and response to therapy (78,79). Pink lesions have the smallest diameter vessels and purple lesions have the largest ones. Red-colored PWS comprise more superficially located vessels than pink or purple ones. Red color is predictive of a good response, whereas pink color is predictive of a poor response to laser therapy. In a histological study, Fikerstrand et al. (78) showed that lesions with a poor response to a 585 nm, 400 ms dye laser had small vessels. Moderate responses were observed for PWS with deeper and larger vessels. The best response was seen in superficially located larger diameter vessels. A study of PWS with videomicroscopy demonstrated two types of vascular ectasia within PWS (80). One type showed ectasia localized to the capillary loops, and the other was composed of ring-like, dilated, ectatic vessels in the superficial horizontal plexus. The capillary loop ectasia correlated with a poor response to laser treatment, and the superficial horizontal plexus vessels correlated with a good response.

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6.2.

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Early vs. Later Treatment

Several studies of pulsed dye laser treatment for PWS during infancy indicate that more rapid clearing is possible. In a study of 35 children, 3 months to 14 years of age, Tan et al. (65) found that children less than 7 years old required fewer laser treatment sessions than older children for PWS clearing. Another study of 73 children between the ages of 3 months and 6 years showed increased clearing of their lesions after one laser treatment compared to children between 7 and 14 years of age (63). Pulsed dye laser treatment of PWS in 83 children produced complete clearing in 32% of those who began treatment before 1 year of age compared to 18% of those treated after 1 year of age (81). A study of 133 children and adults found the highest percentage of good and excellent clearing in those patients who were 0 – 10 years during treatment (82). Alster and Wilson reported 87% lesional clearance in patients less than 2 years and 73% in patients 16 years and older (83). In contrast, a study by Van der Horst et al. (84) found no difference in treatment results between age groups. The validity of this study is questionable because only partial treatment of PWS lesions was performed during each treatment session, and treatment intervals were excessively long (84). The greater success of pulsed dye laser treatment in infants and young children can be attributed to decreased skin thickness, permitting better laser penetration, smaller vessel diameter, and smaller lesional surface area (Figs. 21.3 and 21.4). Successful treatment is possible in adults with hypertrophic lesions (Fig. 21.5), but they may require a higher number of treatment sessions.

6.3.

PWS Recurrence

Recurrence of PWS after successful laser treatment was reported by several investigators. Ortin et al. (85) reported that 2 of 64 patients showed darkening of their PWS 1 year after completing therapy. At 1 –2 years, 5 of 24 patients (20.8%) and at 2– 3 years, 4 of 10 patients (40%) showed lesional darkening. Two of 4 patients developed recurrence 3 years after completing laser treatment. Mork et al. (86) observed a PWS recurrence rate of 11%. Darker PWS with larger, deeper vessels recurred more frequently, and lesions that achieved nearly complete resolution recurred less frequently. These observations suggest that early treatment, when lesional vessels are smaller and fewer, enable greater elimination of ectatic PWS vessels when a 585 nm, 0.45 ms pulsed dye laser is used. This laser has limited efficacy on vessels .1.0 mm in depth or .150 mm in diameter. In a retrospective study of 147 patients who completed laser therapy, Michel et al. (87) found a 16.3% incidence of PWS recurrence, with no occurrence of lesional darkening

Figure 21.3

Infant with facial PWS before (a) and after (b) two pulsed dye laser treatments.


Figure 21.4

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Child with lower extremity PWS before (a) and after (b) five laser treatments.

in children who completed therapy under 10 years of age. These results also suggest that early treatment may reduce the risk of PWS recurrence. The majority of PWS do not recur following pulsed dye laser treatment. The lesions with the highest risk for darkening following treatment are those with larger, deeper vessels. It is likely that this subset of patients will benefit from treatment using longer, deeper-penetrating wavelengths, such as alexandrite and Nd:YAG lasers. Individuals who do experience some darkening of their lesions following treatment will usually only require one or two treatments to clear the new vessels. 7. 7.1.

ADVANCES IN PULSED DYE LASER TREATMENT Wavelength

Longer wavelength pulsed dye lasers have been explored for the treatment of PWS with the goal of targeting deeper-lying blood vessels. Kauvar (88) found increased clearance of PWS in patients treated with a 595 nm, 1.5 ms pulsed dye laser as compared to a 585 nm, 0.45 m laser. Scherer et al. (89) compared treatment with a 585 nm, 0.45 ms pulsed dye laser, using wavelengths of 585–600 nm, in 62 untreated PWS. Optimal fading was in achieved in 30 patients when wavelengths .585 nm were used. Twelve patients had improved clearance with the 585 nm, 0.45 ms laser and no difference was found in 20 patients. 7.2.

Spot Size and Overlap

The introduction of larger spot sizes improved PWS therapy. Kauvar and associates demonstrated improved clearance of PWS by increasing the laser spot size from 5 to

Figure 21.5 Hypertrophic PWS on the hand of an adult before (a) and after (b) eight laser treatments.

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Kauvar

7 mm (97), and then to 10 mm in diameter (98). When the diameter of the spot size is increased, light scattering at the periphery of the beam decreases relative to the surface area and enables greater depth of penetration of the laser light and more effective treatment at low fluences. Larger spot sizes allow more photons to remain within the diameter of the incident beam of light. Fluences can therefore be decreased with larger spot sizes compared with smaller spot sizes. A 10 mm spot size requires only one-half to two-thirds the fluence of a 5 mm spot size with the 585 nm pulsed dye laser. Multiple lower-fluence pulses can be delivered to single skin sites to produce selective photocoagulation. Troccoli (99) studied a 585 nm, 160 ms pulsed dye laser on 50 mm diameter hamster cheek pouch venules. One-half of the vessels were photocoagulated at the threshold fluence for hemorrhage of 6 J/cm2. When lower fluences of 2 –4 J/cm2 were delivered in a series of 10 –100 pulses at 0.5 Hz, vessel closure was consistently achieved without hemorrhage. Direct overlapping or stacking of laser pulses cannot be performed when fluences at the damage threshold are used, because of the risk of tissue injury. Hemorrhage caused by the first laser pulse provides a diffuse interstitial target of hemoglobin no longer confined to the intravascular space, which may result in widespread spread injury with subsequent laser energy absorption. Multiple lower-fluence pulses that do not produce hemorrhage and allow thermal injury to gently accumulate over time achieve selective photothermolysis of the lesional vessels without an increased risk of tissue injury. Dierickx et al. (100) showed that repetitive low-fluence pulsed dye laser treatment of PWS produce cumulative thermal injury without epidermal damage and better clearing than single, higher fluence pulses. 7.3.

Pulse Duration

The theoretical formulation of selective photothermolysis predicted that the ideal laser parameters required for clearing pediatric PWS were a wavelength of 577 nm, pulse duration of 1 ms, and fluence .2 J/cm2 (90). Studies of a 577 nm, 1 ms pulsed dye laser (i.e., a pulse duration 1/1000 of the predicted thermal relaxation time of PWS vessels) produced extensive hemorrhage from dermal blood vessels. Pulse durations much shorter than the thermal relaxation time of the vessels led to explosive mechanical vessel rupture from rapid vaporization of blood (93). Lengthening of the pulse duration to the 300 – 500 ms range reduced dermal hemorrhage and increased the required fluence for photocoagulation, as predicted by the theory of selective photothermolysis (94). Despite the remarkable success achieved with the 0.3 –0.5 ms pulsed dye lasers, the pulse duration was still shorter than ideally predicted. Newer pulsed dye lasers were developed in the 1990s with pulse widths .1 ms in an effort to improve treatment efficiency and lesional lightening. In a landmark in vivo study of PWS thermal relaxation times, Dierickx et al. (95) showed that the thermal relaxation time for 60 mm diameter vessels was 1– 10 ms as originally theorized. Longer pulse durations reduce mechanical rupture of the vessels and purpura production. When a 532 nm laser with pulse durations of 1– 30 ms was used to irradiate rabbit ear vessels, blood was expelled from the vessel without rupture (96). Laser treatment resulted in the formation of empty photocoagulated vessels, and there was no purpura production. 7.4.

Skin Cooling

The goal of laser therapy is to maximize thermal damage to target chromophores while minimizing injury to the overlying skin (101 – 109). For many lesions, the threshold light dosage for epidermal injury owing to melanin absorption can be very close to that


451

for irreversible damage of the target chromophores. This problem can be overcome by selectively cooling the superficial layers of the skin during laser therapy and preventing thermal injury despite some melanin absorption. Active skin cooling used to selectively cool the epidermis has several advantages. First, epidermal damage is decreased by preventing it from reaching a temperature that is above its threshold for denaturation (608C). Secondly, epidermal cooling permits the use of higher light dosages for treatment of resistant lesions. Thirdly, active skin cooling may enable treatment of patients with darker skin (types V and VI) (108). Fourthly, skin cooling reduces pain and post-treatment swelling (109). Various methods have been developed for cooling human skin in conjunction with laser therapy. These include contact cooling, cryogen spray cooling, and air cooling. With all of these techniques, a precooled medium comes in contact with the skin’s surface. Heated targets in the dermis transfer their heat, by diffusion, toward the cooled surface of the skin and subsequently to the cooling medium. The rate of heat transfer across the interface between the skin and cooling medium depends primarily on the temperature difference between the two materials as well as other parameters. The cooling efficiency of any method is characterized by the proportionality constant [transfer coefficient (k)]. Contact cooling of skin is achieved by heat conduction into an adjacent precooled solid body that is kept at a constant temperature, usually 2108C to 48C, by a cooling system. Contact-cooling plate materials include sapphire, copper, and quartz. Laser pulses are delivered through or adjacent to the plate that is firmly pressed against the patient’s skin. Dynamic cooling is the name applied to the process of using a cryogen spray to achieve active skin cooling (103) (Fig. 21.6). This process was developed by Dr. J. Stuart Nelson of the Beckman Laser Institute. The cryogen used for this purposes is tetrafluoroethane (TFE), which is currently FDA approved for use of dermatologic laser surgery. With cryogen cooling, heat is extracted from the dermis by means of

Figure 21.6

Candela’s Dynamic Cooling Device (DCD).

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Figure 21.7 Infant with facial PWS before (a) and after (b) treatment with high fluence 595 nm, 1.5 msec laser (Candela) with cryogen cooling. (Reprinted with permission, Arch Derm 2000; 136:942.)

rapid evaporation of the cryogen on the skin surface. Liquid cryogen is sprayed onto the skin surface as atomized droplets with temperatures between 2408C and 2608C. Cryogen spray cooling provides a rapid, spatially selective reduction in the epidermal temperature. Epidermal cooling can also be achieved by using precooled air that is blown onto the surface of the skin at temperatures as low as 2308C (107). Compared with the other skin-cooling methods, air cooling has the lowest heat transfer coefficient, and long cooling times (in the order of several seconds) are necessary to provide significant reductions in epidermal temperature. As a result, air cooling produces bulk cooling of the entire skin, with less spatial selectivity than with other methods. The addition of active skin cooling during pulsed dye laser treatment of PWS improves therapeutic outcomes. Kauvar et al. (110) examined the use of cryogen spray in conjunction with a 595 nm, 1.5 ms pulsed dye laser and found an overall decrease in healing time from 9.5 to 5 days with reduced edema, erythema, and crusting. This study also demonstrated that a laser fluence of 10 J/cm2 could be safely administered in infants, children, and adults because of the epidermal protection afforded by the skin cooling. Kelly et al. (111) also demonstrated that cryogen spray cooling enabled the safe use of higher fluences for PWS therapy. On the basis of the results, studies were undertaken to evaluate higher fluences (up to 15 J/cm2) in the treatment of pediatric and adult PWS. Faster clearing was achieved in fewer treatments with the safe use of higher laser fluences afforded by the cryogen spray cooling used to protect the epidermis (112,113) (Fig. 21.7).

8.

TREATMENT OF PWS WITH OTHER LASERS AND LIGHT SOURCES

The pulsed dye laser remains the treatment of choice for most PWS. Other lasers and light sources have shown some benefit in refractory lesions. IPL systems are high intensity flashlamps that emit a broad spectrum of polychromatic light from 515 to 1200 nm. Cutoff filters are used to match the spectrum of delivered light to the required depth of optical penetration and to maximize absorption by the targeted chromphores. By filtering out shorter visible wavelengths, deeper of larger diameter blood vessels are more effectively targeted. The pulses are delivered as single or multiple synchronized pulses with exposure times of 1–50 ms. The pulse duration is matched to the thermal relaxation time of vessels being treated. The interpulse delays allow cooling of the epidermis and smaller vessels while heat is retained in the larger vessels. Raulin et al. (114) reported good results


453

using the IPL for purple, hypertrophic PWS, and treatment-resistant lesion in 37 patients. Dark purple and red lesions cleared after an average of 15 treatments, and pink lesions after an average of 4 treatments. Other authors (115–120) have reported similar results. 8.1.

Pulsed KTP Lasers

A study of a pulsed KTP laser (532 nm) in 30 patients with pulsed dye laser-resistant lesions showed increased lesional lightening, but a much higher rate of adverse effects including scarring and pigmentary alterations (121). Fifty-three percent of patients showed .50% clearing and 17% showed greater than 25% clearing. The best results were found with fluences from 18 to 24 J/cm2 and pulse durations of 9 to 14 ms. 8.2.

Near Infrared Lasers

Millisecond-domain alexandrite (122), diode, and Nd:YAG (123) lasers permit vascular selectivity coupled with deeper skin penetration. These lasers are now being explored for the treatment of nodular and hypertrophic PWS.

9.

TREATMENT TECHNIQUE

Since the development of active skin-cooling techniques, regional or general anesthesia is rarely used in adults. Most adults tolerate the treatment well with either no anesthetic or the use of topical anesthetic creams such as EMLA or LMX. The topical anesthetic creams should be carefully washed off several minutes prior to laser treatment to prevent interference with laser light transmission. There are maximal limits of these products based on the patient’s weight, which are provided in the manufacturer’s drug information. Pediatric patients, particularly those with extensive lesions, often require general anesthesia. When general anesthesia is used, leakage of flammable anesthetic in the treatment field must be avoided. There have been reports (124,125) of igniting fires in this setting during pulsed dye laser treatment of PWS. Endotracheal tubes and laryngeal masks provide better seals than face masks for this purpose. The airway tube and mouth region should be covered with wet drapes. Hair-bearing skin should be moistened with surgilube (see Chapter 3). Laser fluences will vary depending on the wavelength and pulse duration of the system being used. Higher fluences may be used when skin-cooling techniques are employed. Test sites are performed during the initial evaluation to determine the appropriate laser parameters (Fig. 21.8). A test endpoint of graying indicates the use of too high a fluence and resultant epidermal damage. If graying does occur, the skin is immediately cooled with ice. When skin-cooling techniques are used, the patient is observed for several minutes after treatment to visualize the final tissue reaction, which may be delayed. Treatment should be performed with the lowest possible fluence that produces purpura without tissue graying. Purpura is produced with the 0.45 and 1.5 ms pulsed dye lasers and lasts 7– 10 days (Fig. 21.9). A topical antibiotic ointment such as polysporin or bacitracin is applied twice daily if crusting develops. The development of crusting indicates overly aggressive treatment parameters, and appropriate changes should be instituted with subsequent treatments. Following the resolution of purpura, lesional lightening ensues over 4 – 8 weeks. Repeat treatment should be delayed until all traces of reactive erythema have subsided.

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Figure 21.8

10. 10.1.

One month following test treatment with a pulsed dye laser.

COMPLICATIONS AND THEIR MANAGEMENT Reticulation

Reticulated erythema may be observed after pulsed dye laser treatment of PWS. This was a relatively common occurrence when smaller spot sizes (3 – 5 mm) were used at higher fluences, producing “footprinting” of the laser spots. After a second or third laser session, the reticulation would resolve, with more homogeneous clearing of the lesion. This problem has been obviated by the development and use of larger (10 mm) spot sizes. Reticulation is avoided by using larger spots and applying the pulses with 10 – 15% overlap.

10.2.

Immediate Skin Graying or Whitening

The development of immediate skin graying following laser pulse application is a consequence of epidermal heating. Test sites should always be performed on untreated lesion and observed for several minutes. Similarly, the first few pulses applied during any treatment session should be observed for the tissue reaction. Tissue whitening is indicative of epidermal damage and indicates the use of overly aggressive laser parameters or poor skincooling techniques. To avoid epidermal necrosis, the area should be immediately cooled with ice. A topical antibiotic ointment is used to prevent crusting.

Figure 21.9 Purpura before (a) and immediately following (b) treatment of a PWS with a 595 nm, 1.5 msec laser with a 10 mm spot.


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10.3. Hyperpigmentation Hyperpigmentation may be observed following pulsed dye laser treatment of PWS, but is transient. It is more common when treating lesions on the extremities, or individuals with phototype III or IV skin. Judicious use of sunscreen can decrease the incidence and duration of hyperpigmentation. The use of active skin-cooling techniques, which protect the epidermis, has decreased the incidence of this side effect. 10.4. Hypopigmentation Hypopigmentation is an adverse event that may appear following the development of crusting or scabbing. The presence of hypopigmentation usually indicates the use of overly aggressive laser fluences, improper skin-cooling techniques, or the treatment of suntanned skin. Hypopigmentation is almost always transient, but can last up to 3 months. 10.5. Atrophic and Hypertrophic Scars Scarring rarely occurs following pulsed dye laser treatment of PWS. The incidence was ,0.1% in early studies before the development of active skin-cooling methods. The incidence of scarring has decreased even further with epidermal-cooling techniques. 10.6. Dermatitis Pulsed dye laser treatment of PWS in the pediatric population may produce dermatitis in the treatment areas in atopic individuals. The dermatitis responds well to treatment with a mild corticosteroid cream in combination with a topical antibiotic ointment. Parents of pediatric patients should be counseled about this possibility. 11.

CONCLUSIONS

Pulsed dye laser therapy remains the treatment of choice for pediatric and adult PWS. The preponderance of evidence indicates that treatment should be initiated as early as possible during infancy in order to achieve the fastest resolution of the lesion and decrease the likelihood of lesional recurrence. Nevertheless, mature and hypertrophic lesions do respond well to laser treatment, and therapy can be initiated at any time. Laser treatment should be considered a medical necessity in these patients. Without treatment, hypertrophy of PWS over time can lead to complications including obstruction of vital organs, facial or limb asymmetry, disfigurement, bleeding, and psychosocial problems. Laser treatment of PWS has indeed been shown to obviate the development of psychological problems or improve existing ones in these individuals. Advances in laser technology continue to improve therapeutic outcomes and decrease the required number of treatment sessions. The application of newer infrared lasers to PWS with larger diameter and deeper vessels should improve clinical outcomes. REFERENCES 1. Jacobs A, Walton RG. The incidence of birthmarks in the neonate. Pediatrics 1976; 58:218 – 222. 2. Pratt AG. Birthmarks in infants. AMA Arch Derm Syph 1967; 67:302. 3. Lanigan SW, Cotterill JA. Psychological disabilities amongst patients with port wine stains. Br J Dermatol 1989; 121:209 – 215

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Dierickx CC, Casparian JM, Venugopalan V, Farinelli WA, Anderson RR. Thermal relaxation of port wine stain vessels probed in vivo: the need for 1 – 10 msec laser pulse treatment. J Invest Dermatol 1995; 105:709. Keijzer M, Pickering JW, van Germert MJ. Laser beam diameter for portwine stain treatment. Lasers Surg Med 1991; 11:601. Ross E, Farinelli W, Skrobal M, Anderson R. Spotsize effects on purpura threshold with the pulsed dye laser. Laser Surg Med 1995; 7(suppl):54 (abstract). Dixon JA, Huether SE, Rotering SH. Hypertrophic scarring in argon laser treatment of portwine stains. Plast Reconstr Surg 1984; 73:771 – 779. Hobby LW. Argon laser treatment of superficial vascular lesions in children. Lasers Surg Med 1986; 6:16. Brauner GJ, Schliftman A. Laser surgery for children. J Dermatol Surg Oncol 1987; 13:178. Brauner G, Schliftman A, Cosman B. Evaluation of Argon laser surgery in children under 13 years of age. Plast Reconstr Surg 1991; 87:37. Tan OT, Stafford TJ. Treatment of port-wine stains at 577 nm: clinical results. Med Instr 1987; 21:218 – 221. Tan OT, Morrison P, Kurban AK. 585 nm for the treatment of port-wine stains. Plast Reconstr Surg 1990; 86:1112 – 1117. Reyes BA, Geronemus R. Treatment of port-wine stains during childhood with the flashlamppumped pulsed dye laser. J Am Acad Dermatol 1990; 23:1142 – 1148. Tan OT, Sherwood K, Gilchrest BA. Treatment of children with PWS using the flashlamppulsed tunable dye laser. New Engl J Med 1989; 320:416. Geronemus RG. Pulsed dye laser treatment of vascular lesions in children. J Dermatol Surg Oncol 1993; 19:303 –310. Crosland JG, Roberts LJ. Pulsed dye laser therapy for port wine stains in children. J Pediatr 1994; 124:161 – 162. Alster TS, Wilson F. Treatment of port-wine stains with the flashlamp-pumped pulsed dye laser: extended clinical experience in children and adults. Ann Plast Surg 1994; 32:478 – 484. Ashinoff R, Geronemus RG. Flashlamp-pumped pulsed dye laser for port wine stains in infancy: earlier versus later treatment. J Am Acad Dermatol 1991; 24:467 – 472. Garden JM, Polla LL, Tan OT. The treatment of PWS by the pulsed dye laser. Arch Dermatol 1988; 124:889 – 896. Glassberg E, Lask GP, Tan EML et al. The flashlamp-pumped 577 nm pulsed tunable dye laser. Clinical efficacy and in vitro studies. J Dermatol Oncol 1988; 14:1200 –1208. Kauvar ANB, Geronemus RG. Repetitive pulsed dye laser treatments improve persistent port wine stains. Dermatol Surg 1995; 21:515 – 521. Levine VJ, Geronemus RG. Adverse effects associated with the 577- and 585-nanometer pulsed dye laser in the treatment of cutaneous vascular lesions: a study of 500 patients. J Am Acad Dermatol 1995; 32:613 – 617. Ashinoff R, Geronemus RG. Treatment of a port-wine stain in a black patient with the pulsed dye laser. J Dermatol Surg Oncol 1992; 18:147. Kao B, Kelly KM, Aguilar G, Hosaka Y, Barr RJ, Nelson JS. Evaluation of cryogen spray cooling exposure on in virto model human skin. Lasers Surg Med 2004; 34(2):146 – 54. Renfro L, Geronemus RG. Anatomical differences of port-wine stains in response to treatment with the pulsed dye laser. Arch Dermatol 1993; 129:182 – 188. Kauvar ANB, Renfro LR, Geronemus RG. Anatomical differences of PWS located in the trunk and extremities in response to treatment with the pulsed dye laser. Laser Surg Med 1994; 14:47. Nguyen CM, Yohn JJ, Huff C et al. Facial port wine stains in childhood: prediction of the rate of improvement as it functions of the age of the patient, size and location of the port wine stain and the number of treatments with the pulsed dye (585 nm) laser. Br J Dermatol 1998; 138:821 – 825.

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Nelson JS, Majaron B, Kelly KM. Active skin cooling in conjunction with laser dermatologic surgery. Semin Cutan Med Surg 2000; 19:253– 266. Grossman MC, Dierickx C, Farinelli W. Damage to hair follicles by normal-mode ruby laser pulses. J Am Acad Dermatol 1996; 35:889. Nelson JS, Milner TE, Anvari B et al. Dynamic epidermal cooling in conjunction with laser induced photothermolysis of port wine stain blood vessels. Lasers Surg Med 1996; 19:224. Anvari B, Milner TE, Tanenbaum BS et al. Selective cooling of biological tissues: application for thermally medicated therapeutic procedures. Phys Med Biol 1995; 40:241. Chess C, Chess Q. Cool laser optics treatment of large telangiectasia of the lower extremities. J Dermatol Surg Oncol 1993; 19:74. Greve B, Hammeres S, Raulin C. The effect of cold air cooling on 585 nm pulsed dye laser treatment of port wine stains. Dermatol Surg 2001; 27:633– 636. Greve B, Hammes S, Raulin C. The effect of cold air cooling on 585 nm pulsed dye laser treatment of port wine stains. Dermatol Surg 2001; 27:633– 636. Aguilar G, Diaz SH, Lavernia EJ, Nelson JS. Cryogen spray cooling efficiency: improvement of port wine stain laser therapy through multiple-intermittent cryogen spurts and laser pulses. Lasers Surg Med 2002; 31:27 – 35. Waldorf HA, Alster TS, McMillan K, Kauvar ANB, Geronemus RG, Nelson JS. Effect of dynamic cooling on 585-nm pulsed dye laser treatment of port-wine stain birthmarks. Dermatol Surg 1997; 23:657 –662. Kauvar ANB, Grossman MC, Bernstein LJ, Kovacs SO, Quintana AT, Geronemus RG. The Effects of cryogen spray cooling on pulsed dye laser treatment of vascular lesions. Lasers Surg Med 1998; 10(suppl):211. Kelly KM, Nanda VS, Nelson JS. Treatment of port wine stains birthmarks using the 1.5 msec pulsed dye laser at high fluences in conjunction with cryogen spray cooling. Dermatol Surg 2002; 28:309. Geronemus R, Quintana A, Lou W, Kauvar ANB. High fluence modified pulsed dye laser photocoagulation with dynamic cooling of PWS in infancy. Arch Dermatol 2000; 6:942 – 943. Kauvar ANB, Lou WW, Zelickson B. Effect of Cryogen Spray cooling on 595 nm, 1.5 msec pulsed dye laser treatment of port wine stains. Laser Surg Med 2000; 12(suppl):2. Raulin C, Schroeter CA, Weiss RA, Keiner M, Werner S. Treatment of port-wine stains with a noncoherent pulsed light source. A retrospective study. Arch Dermatol 1999; 135:679 – 683. Goldman MP. Treatment of benign vascular lesions with the PhotoDerm VL high-intensity pulsed light source. Adv Dermatol 1998; 13:503 –521. Bjerring P, Christiansen K, Troliusa. Intense pulsed light source for treatment of dye laser resistant port wine stains. J Cutan Laser Therapy 2003; 5:7 – 13. Angermeier MC. Treatment of facial vascular lesions with intense pulsed light. J Cutan Laser Ther 1999; 1:95– 100. Schroeter CA, Neumann M. An intense light source. The PhotoDerm VL-flashlamp as a new treatment possibility for vascular skin lesions. Dermatol Surg 1998; 24:743 – 748. Cliff S, Misch K. Treatment of mature port wine stains with the PhotoDerm VL. J Cutan Laser Ther 1999; 1:101– 104. Raulin C. Goldman MP, Weiss MA, Weiss RA. Treatment of adult port wine stains using intense pulsed light therapy (PhotoDerm VL): brief initial clinical report. Dermatol Surg 1997; 23:594 – 601. Chaudhary MMU, Harris S, Lanigan SW. Potassium titanyl phosphate laser treatment of resistant port wine stains. Br J Dermatol 2001; 144:814 – 817. Ghotzen VA, McClaren M, Kilmer SL. Treatment of bulky congenital vascular malformations with long pulsed lasers. Lasers Surg Med 2002; 14(suppl):231. Groot D, Rao J, Johnston P et al. Algorithm for using a long pulsed Nd:YAG laser in the treatment of deep cutaneous vascular lesions. Dermatol Surg 2003; 29:35– 42. Fretzin S, Beeson WH, Hanke CW. Ignition potential of the 585-nm pulsed dye laser. Review of the literature and safety recommendations. Dermatol Surg 1996; 22(8):699 – 702 (review). Waldorf HA, Kauvar NB, Geronemus RG, Leffel DJ. Remote fire with the pulsed dye laser: risk and prevention. Am Acad Dermatol 1996; 34(3):503 –506.

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22 Lasers and the Treatment of Hemangiomas Milton Waner St. Lukes—Roosevelt Hospital, New York, New York, USA

Jay Kincannon University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA

1. Laser Treatment of the Vascular Component 1.1. Proliferating Hemangiomas 1.1.1. Ulcerated Lesions 1.1.2. Compound or Deep Lesions 1.2. Involuting Hemangiomas 2. Laser Treatment of Atrophic Scarring 3. Surgical Correction References

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Hemangiomas are common benign vascular lesion of childhood that enlarge rapidly by cellular proliferation and then involute. Rapid proliferation is a hallmark of hemangiomas and helps to differentiate these birthmarks from other vascular malformations such as portwine stains, venous malformations, arterio-venous malformations, and lymphatic malformations (1). After about 1 year, hemangiomas undergo a slow regression that takes between 2 and 10 years. Involution is not always complete and 50% of patients may be left with residual telangiectasias, epidermal atrophy, and redundant fibrofatty tissue (2,3). Hemangiomas are further classified by their depth with respect to skin and the extent of their involvement (4,5). Superficial hemangiomas comprise a cutaneous component that presents as a bright-red vascular papule or plaque when fully developed (Fig. 22.1). Deep hemangiomas have only a subcutaneous component without the superficial red plaque. They appear as a bluish-colored nodule within the skin (Fig. 22.2). Compound hemangiomas have both a superficial and a deep component (Fig. 22.3). Hemangiomas may also be focal or diffuse (5). Focal lesions present as solitary masses and appear to occur along lines of embryological fusion (Fig. 22.4). Eighty-five percent of lesions are focal. On the other hand, diffuse lesions are segmental in distribution. They present as superficial or compound plaque-like lesions and exhibit a high incidence of ulceration (Fig. 22.5). Generally, involution begins after the first year of life. Clinical signs of involution include a gradual change in color from red to dull purple or mottled gray. The lesion 461

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Figure 22.1

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An infant with a superficial segmental hemangioma.

becomes softer with fine wrinkling of the overlying skin. The rate and completeness of resolution of a hemangioma are unrelated to sex, race, size, or clinical appearance. The only known determinant appears to be the speed of involution (2). There is evidence to suggest that lesions that involute slowly are more likely to leave a residuum, whereas lesions that involute rapidly are more likely to completely involute (2,3). As all hemangiomas spontaneously regress, conservative management has been advocated for the majority of these lesions. Under these circumstances, indications for treatment included interference of any vital function including vision, respiration, feeding, urination, and defecation. Ulceration and bleeding are common complications that also require intervention. More recently, these indications have been expanded, although at this point, there is still some controversy (6,7). Several modalities are effective in treating hemangiomas. These include pharmacological agents such as corticosteroids interferon and vincristine, lasers, and surgery (8). Each of these modalities has a specific role. In general, lasers can be used to treat the vascular ectasia of hemangiomas, to treat the atrophic scarring, and to reduce the mass of the lesion.

Figure 22.2

An infant with a deep focal hemangioma.

Lasers and the Treatment of Hemangiomas

Figure 22.3

1.

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An infant with a compound nasal tip hemangioma.

LASER TREATMENT OF THE VASCULAR COMPONENT

In 1981, Apfelberg et al. (9) successfully treated three patients with complicated hemangiomas with an argon laser. Subsequent studies also showed promise for argon lasers, but the risk of scarring outweighed the potential benefits (10,11). This, coupled with the fact that hemangiomas eventually involute, led to poor acceptance of laser treatment. With the development of the 585 nm pulsed-dye laser for the treatment of portwine stains in the late 1980s, physicians now had a specific tool for selective photothermolysis of cutaneous vascular tissue. The first reported use of pulsed-dye lasers for the treatment of hemangiomas appeared in 1989 and since then pulsed-dye lasers have become widely used for treatment of the superficial component of hemangiomas (12 –14).

Figure 22.4

An infant with a focal compound hemangioma.

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Figure 22.5

1.1.

An infant with a segmental V1 hemangioma.

Proliferating Hemangiomas

The premise for treating proliferating hemangiomas is to resolve or at least prevent further proliferation and to treat ulceration. Glassberg et al. (12), and a year later, Sherwood and Tan (15) reported complete resolution of a superficial hemangioma after several treatments. Ashinoff and Geronemus (16) reported mixed results in a series of 10 children with both superficial and deeper hemangiomas. Thick proliferating lesions did not respond, as well as involuting lesions. Given the limited depth of penetration of yellow light at 585 nm (1 –2 mm), these results were not unpredictable. Garden and later Waner treated a series of proliferating hemangiomas with a pulsed-dye laser (13,14). Garden et al. showed that papular lesions raised ,1 mm off the surface of the skin responded best to treatment (14). Garden et al. also showed that the thicker the lesion, the less the response. The paper was published in 1992 and a conventional pulsed-dye laser (585 nm), with a 5 mm spot size was used without cooling. Waner et al. treated a series of superficial proliferating hemangiomas and found that it was able to resolve all of the lesions with up to six treatments long before normal involution would have taken place (13). All of these lesions were superficial, and all were in their proliferative phase. Scheepers and Quaba (17) also showed that superficial lesions responded best. They felt that there was no effect on the deeper subcutaneous component. Barlow et al. (18), on the other hand, did show some reduction in mass of compound proliferating hemangiomas. The pulsed-dye laser can, therefore, be used effectively to treat superficial hemangiomas during their proliferative phase of growth. The laser can be used to minimize or even halt the superficial growth of the hemangioma (Fig. 22.6 –22.13). Treatment should be administered at 3– 4 week intervals in an effort to minimize re-growth between visits, and should continue until the superficial component has been ablated. The precise incidence of complications from pulsed dye laser treatment has not been adequately computed, but there is no reason to believe that it is any different from that seen with the treatment of portwine stains. With the first generated pulsed dye lasers, transient hypopigmentation and hyperpigmentation was rarely observed and the incidence of atrophic or hypertrophic scarring was less than 1%. The addition of skin cooling has


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Figure 22.6 An infant before and after treatment with a pulsed-dye laser. A total of six treatments were administered at four weekly intervals.

likely further reduced these side effects. It is common to observe atrophy, textural change, and depigmentation resulting from the natural involution of hemangiomas, and laser treatment will not prevent this from occurring. All of the earlier mentioned data was generated with first generation pulsed-dye lasers. The parameters used included a 450 ms pulsewidth, a 5 mm spot size, and a wavelength of 585 nm. Recent improvements in pulsed-dye laser technology will doubtless impact the treatment of hemangiomas. We now have lasers with longer pulsewidths (up to 40 ms), larger spot sizes (up to 10 mm), and longer wavelengths (up to 600 nm). We are also able to cool the surface of the lesion during treatment which in turn enables us to safely treat at much higher fluences. These improvements will no doubt enable us to penetrate much deeper. The best results are presently achieved using a pulsed-dye laser at 595 nm, 9 – 10 mm spot size, 1.5 pulse duration, and fluence of 6.0– 6.5 J/cm2 when cryogen cooling is used. The fluence should be lowered if skin cooling methods are not employed.

Figure 22.7 A proliferating hemangioma at 3 weeks of age. Courtesy of Arielle N. B. Kauvar, M.D.

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Figure 22.8 The same patient after eight pulsed-dye laser treatments at 3 week intervals. Courtesy of Arielle N. B. Kauvar, M.D.

To minimize epidermal damage, surface cooling is essential either with the dynamic cooling device 30 ms on with a 20 ms delay before the laser pulse or using the SmartCool cold air blower. Higher fluences seem to enhance lesion fading. For efficacy, purpura should be seen immediately after pulsed-dye laser irradiation. 1.1.1.

Ulcerated Lesions

About 12% of focal lesions ulcerate, whereas 65% of diffuse or segmental lesions ulcerate (5). Ulceration is painful, especially in areas that are frequently irritated or soiled such as the perianal region. The cause of ulceration is unclear, but the outcome is almost always a scar (3) (Fig. 22.14). Ulceration usually appears in the first few weeks of life

Figure 22.9 A proliferating mixed type hemangioma of the nasal tip, before and after five pulsed-dye laser treatments at 3 – 4 week intervals. Courtesy of Arielle N. B. Kauvar, M.D.


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Figure 22.10 A proliferating mixed type hemangioma involving the ear and lateral cheek at 6 weeks of age. Courtesy of Arielle N. B. Kauvar, M.D.

Figure 22.11 The same patient after four pulsed-dye laser treatments at 4 week intervals. Courtesy of Arielle N. B. Kauvar, M.D.

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Figure 22.12 A proliferating hemangioma of the lower lip, before and after treatment with a combination of pulsed-dye laser and intralesional corticosteroid treatment. Courtesy of Arielle N. B. Kauvar, M.D.

or during periods of rapid growth. An ulcer may therefore heal, only to re-appear at some later date. The management of ulcers includes local wound care and the use of systemic corticosteroids. More recently, laser treatment with a pulsed-dye laser has been advocated (19). Ulcers respond well if the ulcerative component is limited and the rate of proliferation is moderate (Fig. 22.15 – 22.17). The laser treatments are usually administered at 2 week intervals, and resolution of the ulceration can be expected after 3– 4 weeks. Parameters recommended are similar to those used to treat the superficial component of a hemangioma with a 15– 20% decrease in energy fluence. Although there is no doubt that laser treatment with a pulsed-dye laser is beneficial, on occasion, the extreme opposite has been seen. Pulsed-dye laser treatment during the very early proliferative stage of a segmental hemangioma may in fact lead to ulceration (20). This adverse response has only

Figure 22.13 A child with an extensive segmental hemangioma before and after treatment with steroids, pulsed-dye laser treatment, and surgical resection.


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Figure 22.14 A 5 year-old after involution of a large parotid hemangioma that had ulcerated. The child is left with residual telangiectasia, fibro-fatty tissue, and atrophic, as well as hypertrophic scarring.

been experienced with very early lesions, and the precise circumstances under which this is likely to occur are not known at this point. For this reason, we recommend the use of systemic corticosteroids for early proliferating segmental hemangiomas that have ulcerated. A dose of between 4 and 5 mg/kg is recommended, followed with an appropriate taper. Lasers can be used at a later date, once the degree of proliferation has slowed.

Figure 22.15 A child with a large lip hemangioma that had ulcerated. The child is seen after surgical correction and pulsed-dye laser treatment.

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Figure 22.16 An ulcerated hemangioma of the buttock that required hospitalization for a systemic infection. One treatment with the pulsed-dye laser resulted in rapid reepithelialization. Courtesy of Arielle N. B. Kauvar, M.D.

We therefore prefer not to administer laser treatment before 5 –6 months of age for segmental lesions. Focal lesions, on the other hand, appear to react differently. This adverse effect of early laser treatment has not been seen with focal lesions and thus, pulsed-dye laser treatment of early proliferating, ulcerated focal lesions appears to be safe, and indeed, beneficial. 1.1.2. Compound or Deep Lesions Given the limited depth of penetration of light at 585 nm, anything deeper than the papillary dermis will not be affected by treatment of the surface of the lesion. For this reason, alternative methods have been sought. Interstitial laser therapy (ILT) was originally developed to treat malignant tumors, but has since been adapted for vascular lesions. An optical

Figure 22.17 An ulcerated mixed type hemangioma of the scrotum, before and after four pulseddye laser treatments. Courtesy of Arielle N. B. Kauvar, M.D.


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quartz fiber coupled to a near infrared laser (Nd:YAG laser or a diode laser) is introduced percutaneously or transmucosally into the substance of a hemangioma, with or without ultrasound guidance. A low intensity of light (1 –2 W ) is then delivered to the interstitium of the tumor for a prolonged period (500 – 1000 s). The light is scattered in an isotropic fashion around the emission surface of the fiber until it is absorbed by hemoglobin within the substance of the hemangioma. A photothermal reaction will then coagulate the lesion (21,22). One can expect a diameter of coagulation of up to 15 mm from the point of emission of a 600 mm quartz fiber (21). The effect can be monitored in real time with ultrasound, and the epidermis and papillary dermis can be protected from thermal damage by careful placement of the quartz fibers. Alternatively, one can cool the surface with ice (23). ILT has been used successfully in several centers and is a useful technique for shrinking a large hemangioma (23,24). Its role in the management of hemangiomas must, however, be considered in light of improved surgical techniques. It is possible to completely and safely remove a hemangioma surgically with minimal blood loss. Furthermore, careful placement of a surgical incision will minimize the visibility of a surgical scar. If complete removal is preferred, then surgery should be considered. On the other hand, if shrinkage is the desired endpoint, then ILT should be considered. In some cases, ILT may result in as good a result as surgery. It would therefore not be unreasonable to attempt ILT prior to surgery if the risks of surgery are considerable. Newer vascular lesion lasers with longer wavelengths such as the 755 nm alexandrite and 1064 nm Nd:YAG lasers may prove useful for the deep component of hemangiomas.

1.2.

Involuting Hemangiomas

During involution, one is frequently left with residual telangiectasia. This often coexists with hypopigmentation, atrophic scarring, and residual fibrofatty tissue. All of these sequelae of a hemangioma are correctible. Residual telangiectasia can be treated with any of the lasers or devices specific for blood vessels (Fig. 22.18). These include pulsed-dye lasers, KTP lasers, copper bromide lasers, and intense pulsed light sources. The choice of device or laser will depend on the expertise of the physician and the availability of equipment. Excellent results can be obtained with all of the earlier mentioned devices and published data has confirmed this (Fig. 22.6). The technique will depend on the device being used. Although any one of the earlier mentioned devices will suffice, we have tended to use a pulsed-dye laser for residual telangiectatic matting, a KTP laser for ectatic solitary, and/or groups of vessels and intense

Figure 22.18 An 8 year old male with residual telangiectasia left after involution of a hemangioma, before and after one pulsed-dye laser treatment. Courtesy of Arielle N. B. Kauvar, M.D.

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pulsed light sources for deeper more ectatic vessels that have not responded to a KTP laser. The shorter exposure time and the larger spot size of a pulsed-dye laser are ideal for the treatment of vascular matting. The constituent vessels are superficial capillaries with small diameters. Individual telangiectasias have a larger diameter and are suitable for the vessel tracing technique and the smaller spot size of the KTP family of lasers. The longer wavelength and the longer exposure time of the intense pulsed light sources are useful for more ectatic, deeper vessels. If telangiectasia co-exists with atrophic scarring or excessive fibro-fatty tissue, it is usually treated first, especially in circumstances where a surgical flap is to be developed using skin involved with telangiectasia. Pre-treatment will lighten the burden of raising a very vascular flap and also obviate the need for excessive skin resection. If skin resurfacing is contemplated (cf. the treatment of atrophic scarring), the telangiectasia should once again be treated first, as skin resurfacing will exacerbate the telangiectasia.

2.

LASER TREATMENT OF ATROPHIC SCARRING

Destruction of the papillary dermis by a proliferating hemangioma will lead to atrophy. Skin resurfacing can restore the atrophic papillary dermis and by doing so, it improves the appearance (25) (Fig. 22.19). Early experience with a CO2 and more recently with a long-pulse/short-pulse Er:YAG laser has been extremely encouraging. Significant intraoperative collagen shrinkage is seen with both of the lasers, although it is more dramatic with the earlier mentioned CO2 laser. This is followed by a prolonged period of remodeling and tissue tightening which lasts up to 18 months (26 – 28). The net effect is smoothing of the scarred and atrophic areas. Early experience with a CO2 laser led to a dramatic improvement in many of the patients. Complications were not dissimilar from those seen with the treatment of rhytides and included prolonged erythema, hyper and hypopigmentation, and hypertrophic scarring. The time to re-epithelialize was 10 –12 days. Our initial experience with shortpulsed Er:YAG lasers was unfavorable. The reduced zone of thermal damage resulted in more intraoperative bleeding, which in turn prevented us from attaining the desired depth. Due to the vascular nature of hemangiomas, intraoperative bleeding was considerably more than normal and was quite excessive at times. The net effect was a less dramatic outcome with less tissue remodeling. This may well have been related purely to the inadequate depth of thermal damage. The more recent, “third generation” Er:YAG laser seems to have overcome this. By adding a long pulse to the configuration, subablative thermal heating of collagen will take place. This in turn will result in collagen shrinkage,

Figure 22.19 A child with a large nasal hemangioma before and after pulsed-dye laser treatment, surgical excision, and skin resurfacing.


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which prevents the excessive bleeding seen with short pulse Er:YAG lasers. Tissue remodeling similar to that seen with a CO2 laser will ensue as well as tissue remodeling. The timing of skin resurfacing is important. We usually recommend resurfacing to be done only once; all of the residual telangiectasia has been adequately treated with a pulsed-dye laser. Resurfacing prior to this can exacerbate the telangiectasia and should therefore be avoided. We also recommend resurfacing to follow any surgical correction, as resurfacing may well improve the surgical scar.

3.

SURGICAL CORRECTION

Most complex cases require both laser treatment and surgical correction. In most cases, with the exception of skin resurfacing, laser treatment should be completed prior to any surgical correction. There are several advantages of completing laser treatment prior to surgical correction. These relate to the ease of raising a skin flap that has previously been treated and is less vascular and the ability to resect less skin during the procedure (Figs. 22.11– 22.18).

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10. 11. 12.

13.

Mulliken JB, Glowacki J. Hemangiomas and vascular malformations in infants and children: a classification based on endothelial characteristics. Plast Reconstr Surg 1982; 69:412 – 420. Finn M, Glowacki J, Mulliken JB. Congenital vascular lesions: clinical approach of a new classification. J Pediatr Surg 1983; 18:894. Waner M, Suen JY. The natural history of hemangiomas. In: Waner M, Suen JY, eds. Hemangiomas and Vascular Malformations of the Head and Neck. New York, NY: John Wiley & Sons, 1999. Waner M, Suen JY. A classification of congenital vascular lesions. In: Waner M, Suen JY, eds. Hemangiomas and Vascular Malformations of the Head and Neck. New York, NY: John Wiley & Sons, 1999. Waner M, North PE, Scherer KA, Frieden IJ, Waner A, Mihm MC Jr. The nonrandom distribution of facial hemangiomas. Arch Dermatol 2003. 139(2):869– 875. Frieden IJ. Management of hemangiomas. Special symposium. Pediatr Dermatol 1997; 14(1):57– 83. Waner M, Suen JY. The treatment of hemangiomas. In: Waner M, Suen JY, eds. Hemangiomas and Vascular Malformations of the Head and Neck. New York, NY: John Wiley & Sons, 1999. Waner M, Suen JY. Treatment options for the management of hemangiomas. In: Waner M, Suen JY, eds. Hemangiomas and Vascular Malformations of the Head and Neck. New York, NY: John Wiley & Sons, 1999. Apfelberg DB, Greene RA, Maser MR, Lash H, Rivers JL, Laub DR. Results of argon laser exposure of capillary hemangiomas of infancy: preliminary report. Plast Reconstr Surg 1981; 67:188 – 193. Hobby LW. Further evaluation of the potential of the argon laser in the treatment of strawberry hemangiomas. Plast Reconstr Surg 1983; 71:481 – 485. Landthaler M, Haina D, Waidelich W et al. A three years experience with the argon laser in dermatotherapy. J Dermatol Surg Oncol 1984; 10:456 – 461. Glassberg E, Lask G, Rabinowitz LG, Tunnessen WW. Capillary hemangiomas: case study of a novel laser treatment and a review of therapeutic options. J Dermatol Surg Oncol 1989; 15(11):1214– 1223. Waner M, Dinehart S, Mallory SB, Suen JY. Laser photocoagulation of superficial proliferating hemangiomas. J Dermatol Surg Oncol 1994; 20:1 –4.

474 14. 15. 16. 17.

18. 19. 20. 21.

22. 23.

24. 25. 26. 27. 28.

Waner and Kincannon Garden JM, Bakus AD, Paller AS. Treatment of cutaneous hemangiomas by the flashlamppumped pulsed dye laser: prospective analysis. J Pediatr 1992; 120(4):555– 560. Sherwood KA, Tan OT. Treatment of a capillary hemangioma with the flashlamp pumped-dye laser. J Am Acad Dermatol 1990; 22:136 –137. Ashinoff R, Geronemus RG. Capillary hemangiomas and treatment with the flashlamp-pumped pulsed dye laser. Arch Dermatol 1991; 127:202 – 205. Scheepers JH, Quaba AA. Does the pulsed tunable dye laser have a role in the management of infantile hemangiomas? Observations based on 3 years’ experience. Plast Reconstr Surg 1995; 95:305 – 312. Barlow RJ, Walker NPJ, Markey AC. Treatment of proliferative hemangiomas with the 585 nm pulsed dye laser. Br J Dermatol 1996; 134:700 – 704. Morelli JG, Tan OT, Weston WL. Treatment of ulcerated hemangiomas with the pulsed tunable dye laser. AJDC 1991; 145:1062 –1064. Metry DW. Potential complications of segmental hemangiomas of infancy. Sem Cutan Med Surg 2004; 23(2):107– 115. Mathewson K, Coleridge-Smith P, O’Sullivan J, Northfield T, Brown S. Biological effects of intrahepatic neodymium: yttrium-aluminum-garnet laser photocoagulation in rats. Gastroenterology 1987; 93:550– 557. Mathewson K, Barr H, Traulau C, Brown S. Laser photocoagulation: studies in a transplantable fibrosarcoma. Br J Surg 1989; 76:378. Berlien HP, Muller G, Waldschmidt J. Lasers in pediatric surgery. In: Angerpointner TA, Gauderer MWL, Hecker WCH et al., eds. Progress in Pediatric Surgery. New York, NY: Springer-Verlag NY Inc, 1990; 25:6– 22. Apfelberg D. Intralesional laser photocoagulation-steroids as an adjunct to surgery for massive hemangiomas and vascular malformations. Ann Plast Surg 1995; 35:144. Waner M. Laser resurfacing and the treatment of involuting hemangiomas (abstract). Lasers Surg Med 1996 (suppl 8):40. Alster TS. Cutaneous resurfacing with CO2 and erbium:YAG lasers: preoperative, intraoperative, and postoperative considerations. Plast Reconstr Surg 1999; 103:619 – 632. Stuzin JM, Baker TJ, Baker TM, Kligman AM. Histologic effects of the high energy pulsed CO2 laser on photoaged facial skin. Plast Reconstr Surg 1997; 99:2036 –2050. Walia S, Alster TS. Prolonged clinical and histologic effects from CO2 laser resurfacing of atrophic acne scars. De:rmatol Surg 1999; 25:926– 930.

23 Laser Treatment of Acquired Vascular Lesions Tina B. West 5530 Wisconsin Avenue Suite 1440, Chevy Chase, Maryland, USA

1. Introduction 1.1. Continuous Wave Lasers 1.1.1. Argon Laser 1.1.2. Argon-Pumped Tunable Dye Laser 1.1.3. Copper Vapor Laser 1.1.4. Copper Bromide Laser 1.1.5. Krypton Laser 1.2. Long-Pulsed Lasers 1.2.1. Nd:YAG Laser 1.2.2. KTP and Frequency-Doubled Nd:YAG Laser 1.3. Pulsed Dye Lasers 2. Intense Pulsed Light Source 3. Summary References

1.

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INTRODUCTION

The term telangiectasia refers to a dilated venule, capillary, or arteriole visible to the human eye and measuring 0.1 – 1.0 mm in diameter (1). Telangiectasias develop on the face secondary to genetic predisposition, chronic actinic damage, collagen vascular disorders, topical corticosteroid application, and disorders of vascular regulation such as acne rosacea. Linear and “spider” telangiectasias develop on the legs, especially in women, beginning in the second to third decade due to multiple factors including genetic predisposition, gravity, pregnancy, and trauma. Papular telangiectasias are frequently seen as part of genetic syndromes, such as Osler – Weber –Rendu syndrome, and are also seen in collagen vascular disorders (2). Spider telangiectasias typically 475

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occur in school-age children, with most persisting into adulthood. They present a cosmetic concern as well as the propensity to bleed with minor trauma (1). The predominant presenting symptom of patients with facial telangiectasia is cosmetic disfigurement. Therefore, effective treatment should be as free of adverse sequelae as possible. Traditional treatment modalities for superficial telangiectasias have included sclerotherapy, electrodesiccation, and more recently, laser therapy. Sclerotherapy remains the gold standard of treatment for telangiectasias of the lower extremities and involves the injection of a chemical sclerosing agent into a vessel, which damages the vessel wall with subsequent fibrosis. Adverse sequelae include ulceration, scarring, hyperpigmentation, and telangiectatic matting. Facial telangiectasias are less responsive to sclerotherapy than those located on the leg and are additionally more prone to complications (1). Electrodesiccation is generally used in the treatment of small-caliber facial vessels but has the potential to produce scarring due to its nonspecific thermal effect (3). In addition, electrodesiccation often results in incomplete lesional response or recurrence when used to treat larger caliber vessels. Theoretically, lasers and intense pulsed light sources should provide certain advantages over traditional treatment methods including the ability to eradicate most types of facial vascular lesions with virtually no risk of scarring due to vascular specificity (4). 1.1.


A variety of continuous wave (CW) and quasi-continuous wave (quasi-CW) lasers with wavelengths ranging from 532 to 578 nm have been used to treat facial telangiectasias. Longer wavelengths are more vascular selective, whereas shorter wavelengths are more suitable for the treatment of melanocytic lesions. The quasi-CW lasers are pulsed using a shuttering mechanism, which can produce individual 30 ms pulses [e.g., argon-pumped tunable dye laser (APTDL)] or trains of 30 – 50-ns pulses at the rates of 6000 – 15,000 repetitions/s (e.g., copper vapor laser). The rapid delivery of nanosecond pulses in the copper vapor laser system effectively acts like a CW laser, whereas the 30 ms “pulse” of the APTDL is 100-fold longer in duration than the traditional pulsed dye systems (5). On the basis of the theory of selective photothermolysis, it follows that a quasi-CW laser system may be used to treat large-caliber vessels with longer thermal relaxation times, whereas shorter pulse durations which limit heat conduction to surrounding structures are preferable in the treatment of small telangiectasias in order to prevent scarring. Chopped light from a CW laser, however, exhibits characteristics that are distinctly different from those of pulsed light because a shuttered CW pulse rarely has sufficient energy fluence to achieve effective blood vessel coagulation without causing collateral damage. 1.1.1. Argon Laser The argon laser emits a visible blue – green CW beam, such that 80% of the light emitted falls within the 488 –514 nm range of the electromagnetic spectrum with a penetration depth of 1 – 2 mm (6). The argon laser was initially chosen for the treatment of cutaneous vascular lesions because its 488 nm (blue) and 514 nm (green) wavelengths are absorbed by oxyhemoglobin (7). When the argon laser beam is absorbed, its light energy is transformed into heat that results in thermal damage and thrombosis of blood vessels (8). Parameters used have included powers ranging from 0.8 to 2.9 W, exposure times of 50 ms, 0.2 s, and 0.3 s, and spot sizes of 0.1 and 1 mm. Despite the success of this laser in treating vascular lesions (9), adverse sequelae of treatment have included scarring,

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hypopigmentation, and inadequate response of some lesions such as port-wine stains. It has been shown that the exposure intervals used with the CW argon laser exceed the thermal relaxation time of the target tissue, thereby increasing the risk of scarring and dyspigmentation (10). In addition, excessive heat is created by the high fluences required to penetrate the melanin-rich epidermis (11). Argon laser light is also significantly scattered by the skin, further decreasing its specificity. The end result may be nonspecific, diffuse thermal destruction of the epidermis and papillary dermis with extension to adjacent tissue (12). Histologic examination following argon laser treatment of telangiectasias shows diffuse coagulative necrosis of the epidermis and papillary dermis (11). In order to limit nonspecific tissue injury, an automated scanning laser handpiece (hexascan) may be attached to produce numerous 1 mm spots which result in a larger hexagonalshaped treatment area. For small diffuse telangiectasias, the hexascan is used with average fluences of 18– 20 J/cm2 and pulse widths of 30 – 100 ms (5). However, even with the use of the robotized device, pulse duration and tissue dwell time are too prolonged to achieve selective photothermolysis (13). With the advent of newer, more vascular-specific systems [pulsed dye lasers (PDL)], the argon laser has fallen out of favor as the laser of choice for the treatment of vascular lesions (14 – 16). However, because the yellow PDL was designed to treat small-caliber superficial vascular malformations, it often proves less effective in treating hypertrophic vascular lesions compared with the argon, krypton, KTP, or copper vapor lasers, which produce more diffuse tissue coagulation. On the basis of their longer thermal relaxation times, current indications for use of the argon laser include vascular mucosal lesions and large-caliber vessels on the face. Newer pulsed lasers, exhibiting greater vascular specificity, are now preferred for the treatment of most telangiectatic lesions due to their shorter pulse durations which prevent excessive heat conduction to normal surrounding collagen. 1.1.2.

Argon-Pumped Tunable Dye Laser

The APTDL is a quasi-CW laser that demonstrates greater vascular selectivity than the argon laser, because the dye laser can be precisely tuned to emit photons at wavelengths that match specific absorption peaks of tissue chromophores (from 488 to 638 nm) and shuttered to produce pulses as short as 20 ms (1,2). However, the shortest practical exposure duration that delivers therapeutically useful energy fluence of most APTDL lasers is 100 ms, which is at least five times longer than the thermal relaxation time of the average telangiectasia (17). At 577 –585 nm, the laser produces a yellow light that is efficiently absorbed by hemoglobin. Beam sizes may be varied from 50 mm to 6.0 mm. Linear telangiectasias are generally traced with a spot size of 100 mm, a low power of 0.1 – 0.4 W, and pulse duration of 0.05 – 0.1 s (5). The APTDL was one of the first lasers to be used successfully in the treatment of cutaneous vascular lesions without scarring (7,18). However, because of its quasi-CW nature, this laser is associated with a higher risk of scarring than the PDL. Adverse sequelae following treatment include mild redness (80%) and swelling (60%) (20). Other side effects encountered with the use of the APTDL include hypopigmentation, hyperpigmentation, and depressed scars (2,19,20). 1.1.3.

Copper Vapor Laser

The copper vapor laser is used at its 578 nm (yellow) wavelength for the treatment of telangiectasias. The laser delivers a quasi-CW light in 20 ns pulses at a frequency of 15,000 pulses/s. This train of pulses interacts with tissue in the same manner as does a

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continuous beam because of the accumulation of heat when a large number of pulses are delivered per unit time (2). This laser is thus best suited for the treatment of large caliber blood vessels with their longer thermal relaxation times, deeper dermal location, and greater heat tolerance (21,22). In a study comparing the copper vapor and flashlamp-pumped PDL in the treatment of facial telangiectasias, results achieved with the two systems were comparable at 2 and 6 weeks (17). The authors noted, however, that the copper vapor laser was much more operator dependent, requiring skill in the use of magnifying loupes as well as the ability to keep the laser beam in focus while moving it along the course of the vessel. On the basis of greater postoperative swelling, healing time, and incidence of postinflammatory hyperpigmentation with the use of the flashlamp-pumped PDL in comparison to the copper vapor laser, the authors preferred the copper vapor laser for the treatment of simple and arborizing facial telangiectasias. For treatment of facial telangiectasias with the copper vapor laser, a 150 mm handpiece is used with an average power of 350 – 550 mW. The light is chopped by an electronic shutter at 0.2 s exposure intervals. Visual magnification of 3.5 to 6 is recommended (17,21). Side effects of treatment with the copper vapor laser include fine linear scabbing or blistering which resolve within 7 – 14 days (17,23) as well as hypopigmentation secondary to epidermal melanin absorption of laser energy and nonspecific thermal injury. In addition, edema in the treated and adjacent areas, such as the periorbital region, frequently occur within the first 3 days following copper vapor laser treatment when extensive regions are lased. 1.1.4.

Copper Bromide Laser

Like the copper vapor laser, the copper bromide laser emits light in the yellow portion of the visible spectrum at 578 nm in trains of 30 ns pulses at 16 kHz. The beam is interrupted by a mechanical shutter resulting in exposure times from 7 ms to 6 s. The shutter speed generally employed results in 2.5–3 pulses/s (tissue exposure durations of 300–400 ms) with energy densities ranging from 13 to 36.4 J/cm2 (24). In a study performed by McCoy et al. (24), 23 subjects obtained good to excellent results following treatment of benign vascular lesions on the head, neck, and anterior chest with the copper bromide laser. Results were most impressive in patients with medium and large telangiectasias. The authors concluded that the copper bromide laser produced results similar to those achieved with the PDL for most facial telangiectasias without purpura or hyperpigmentation (24–26). 1.1.5.

Krypton Laser

The krypton laser, which produces green light at wavelengths of 520 and 530 nm and yellow light at 568 nm, is a CW laser that can be shuttered to produce pulse durations as brief as 50 ms. Vascular lesions may be treated with yellow light or with a combination of yellow and green lights. The 530 nm wavelength of the krypton laser provides two significant advantages over the 514 nm wavelength utilized by the argon laser in the treatment of vascular lesions (36). Because the 530 nm wavelength penetrates the dermis to a greater degree than does 514 nm, the krypton laser is able to photocoagulate superficial dermal vessels using lower fluences (2). In addition, the 530 nm wavelength is closer to an absorption peak of hemoglobin (542 nm), thereby exhibiting a greater affinity for hemoglobin than for melanin when compared with the argon laser (23). In the treatment of telangiectasias, a 100 mm collimated handpiece or a 1 mm handpiece is used with a 0.2 s pulsed or CW to trace individual vessels, with vessel disappearance as the treatment endpoint (27). In a study comparing the copper vapor and krypton lasers, powers utilized with the krypton laser ranged from 0.4 to 0.6 W using a 100 mm handpiece and from 0.7 to


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0.9 W using a 1 mm handpiece. Patients reported significantly less pain associated with krypton laser compared with copper vapor laser treatment, however, there was no significant difference in patient satisfaction with treatment results (23). Side effects reported following the use of the krypton laser include immediate erythema, which usually resolves within 48 h, periorbital edema following treatment of extensive areas of the cheeks, and occasionally mild blistering or crusting (23). 1.2. 1.2.1.

Long-Pulsed Lasers Nd:YAG Laser

On the basis of broad band of absorption of hemoglobin from 800 to 1100 nm, the use of a long-pulsed 1064 nm wavelength in the treatment of vessels produces injury of larger, deeper deoxygenated ectatic veins while sparing the epidermis due to the minimal interaction of this wavelength with melanin. The Nd:YAG laser (1064 nm) has been used to treat leg telangiectasia for more than a decade (28). Its average depth of penetration in human skin is 0.75 mm and reduction to 10% of the incident power occurs at a depth of 3.7 mm (29). Initial studies found the 1064 nm wavelength to be effective with energy fluences of 60– 120 J/cm2 and pulse durations of 10– 30 ms (30). Epidermal cooling is provided either through cold gel, cryogen spray or a skin chilling device at 1 –48C. Vessels up to 3 mm can be treated when using the 1064 nm wavelength at pulse durations of 10– 30 ns (31). More recently, Sarradet et al. (32) evaluated the millisecond pulse duration 1064 nm Nd:YAG laser in the treatment of one facial half of 15 subjects with a 3 mm spot size, 120 – 170 J/cm2, and 5 – 40 ms pulse durations with contact cooling. The authors noted that generally higher fluences and shorter pulse durations were required to blanch smaller and redder vessels, the clinical endpoint. Each study subject received two treatments to same side of the face at day 0 and day 30. Moderate to significant improvement was seen in 73% of patients at day 30 and in 80% of patients at 3 months. Improvement was noted in both larger red/blue as well as smaller red facial telangiectasias. Two subjects experienced mild blistering but there was no evidence of infection, scarring, or postinflammatory hyperpigmentation. It is important to note that the use of pre and posttreatment contact cooling compensated for the increased risk of blistering and scarring at the parameters used. 1.2.2. KTP and Frequency-Doubled Nd:YAG Laser The KTP laser utilizes a Nd:YAG crystal (1064 nm) to produce light which is then passed through a potassium titanyl phosphate crystal in order to yield a frequency-doubled wavelength of 532 nm. The laser light is shuttered to produce a quasi-continuous beam and may be used with a robotized scanner at a variety of spot sizes and power settings. On the basis of absorption spectrum of oxyhemoglobin with its three peaks at 418, 542, and 577 nm, the 532 nm light delivered by the KTP laser is closest to the 542 nm absorption peak of oxyhemoglobin. Although this wavelength penetrates only 0.75 mm into the dermis, vascular damage is relatively specific compared to the argon laser due to the more appropriate pulse duration (1 – 50 ms). Several investigators have achieved good results with the use of the KTP laser for the treatment of facial telangiectasias ranging from fine matted vessels to those of larger caliber (33 – 36). The laser handpiece is traced along the course of the vessel in a noncontact mode with a clinical endpoint of vessel disappearance. Variable parameters in the use of the KTP laser include fluence, pulse duration, pulse rate, and handpiece diameter. Elimination of a vessel may require one laser pass for small-caliber telangiectasias or two or more passes for larger caliber vessels. In one study, 38.2% of treated facial

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vessels achieved at least a 70% improvement following one laser treatment, whereas 31.9% required a second treatment to achieve similar results (33). Cases in which involvement was more severe or extensive were more likely to require multiple treatments. The most common side effect was linear crusting along the course of the treated area, which generally resolved within 1 week following treatment. There were no instances of purpura, scarring, or pigmentary change. Two recent studies have compared the KTP and PDL in the treatment of facial telangiectasias (34,35). In both studies, patients preferred the KTP laser on the basis of its reduced incidence of posttreatment purpura, pain, and swelling. Hevia (34) found no significant difference in clinical results obtained from the two laser systems following one laser treatment (65% clearance for the KTP laser and 64% clearance for the 585 nm pulse dye laser). Although West and Alster (35) also found the KTP laser preferable to patients on the basis of its low side effect profile, clinical results were superior with the PDL (590 nm) following one or two laser treatments for facial telangiectasias. For the treatment of telangiectasias, the KTP laser was calibrated to 10– 15 J/cm2 with a 10 ms pulse duration using a 1 or 2 mm handpiece at a rate of 2 –3 pulses/s. In a study comparing four different frequency-doubled Q-switched Nd:YAG lasers at 532 nm, all of the laser systems employed for the treatment of facial telangiectasias produced good results with no significant difference noted between the lasers (36). All treated blood vessels measured ,1 mm in diameter. All study subjects described treatment discomfort as mild to moderate, except for four individuals treated with the VersaPulse VPW laser, who noted no discomfort. Other side effects included crusting and swelling. An additional study evaluating the use of a variable pulse width frequency-doubled Nd:YAG laser at 532 nm (VersaPulse VPW) on 40 patients showed 75– 100% clinical clearance after a single treatment without significant side effects (37). Most recently, a longer pulse duration of 20– 50 ms and a larger 5 mm spot size used at the highest fluence of 20 J/cm2 has increased the efficacy of this laser system with a reduction in nonspecific pigmentary change. It should be noted that scarring may result from treatment with excessive energy fluences using the frequency-double Nd:YAG laser, especially around the nasal alae where it may be more difficult to ensure contact cooling (Fig. 23.1).

1.3.

Pulsed Dye Lasers

In the early 1980s, Anderson and Parrish (38,39) predicted with their theory of selective photothermolysis that the destruction of blood vessels without injury to surrounding

Figure 23.1 Atrophic scar following treatment of linear telangiectasias along the nasal alae with the VersaPulse long-pulsed frequency-doubled Nd:YAG laser.


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dermal structures could be accomplished by using a wavelength of 577 nm, correlating with the third and largest peak in the absorption spectrum of oxyhemoglobin. The first pulsed laser system, the flashlamp-pumped PDL, was developed specifically for the treatment of vascular lesions, particularly port-wine stains (40 –42). Preclinical work with the PDL indicated a relationship between the pulse duration of laser light and the thermal relaxation time of the target (38,39). The thermal relaxation time is defined as the time during which 63% of the absorbed heat is radiated out of the vessels to adjacent tissues. Theoretically, the pulse duration of laser light should be equal to or less than the thermal relaxation time of the vessel being treated (38). This time varies according to the vessel size. For treatment of telangiectatic vessels between 100 and 200 mm in diameter, the optimal duration of exposure is 5 – 20 ms. The excellent results obtained with the PDL in the treatment of vascular lesions when compared with the argon laser are due to the proper application of the theory of selective photothermolysis. The wavelength of 577 nm is preferable to 514 nm (argon) because of its superior absorption by oxyhemoglobin, its deeper penetration into the dermis and its weaker absorption by melanin. The pulse width of 450 ms is superior to the CW mode of the argon because heat is confined inside the vessel. CW lasers nonselectively destroy vessels along with the superficial dermis and epidermis (43), whereas the PDL selectively destroys ectatic vessels up to 1 mm into the dermis. The selective effect on vascular structures minimizes damage to the surrounding normal dermis, which explains the absence of scarring or textural change observed even after several consecutive PDL treatments to the same area (7,44). As its development, the wavelength of the PDL has been adjusted from 577 to 585 – 600 nm, providing greater depth of penetration into the dermis without loss of vascular specificity. The pulse duration has been expanded to a range from 450 ms to 40 ms, well within the thermal relaxation time range of small to medium-size blood vessels. In original studies on port-wine stains, histologic evidence confirms the theoretical benefits of the PDL over CW lasers. Laser-treated papillary and upper reticular dermal vessels reveal agglutination of erythrocytes and vessel wall degeneration to a depth of 1.2 mm (43,44). Fine granulation tissue replaces the damaged vessels after 1 week. Histology at 1 month shows a normal-appearing dermis and epidermis with fine capillaries and normal adnexal structures without fibrosis. Clinically, these changes correlate with a 7– 14 day period of posttreatment purpura with partial or complete vessel clearance without scarring at 1 month. These findings are the basis for the minimum 4 week interval between PDL treatment sessions (27). Laser – tissue interaction with the PDL depends on spot size and energy density in addition to wavelength and pulse duration. Variation in the size of the beam changes the absorption of laser light. The PDL is available with handpieces producing 5, 7, 10, and 3 mm 10 mm diameter beams of laser light. Energy fluence (the total energy per unit area) ranges therapeutically from 3 to 20 J/cm2. Because smaller spot sizes result in a decreased amount of energy delivered to the tissue due to scattering within the dermis, a higher fluence is required when a smaller beam is applied to produce comparable clinical results to those achieved with larger spot sizes. In addition, on the basis of melanin’s interference with absorption of PDL light energy, the darker the skin tone being treated, the less energy is effectively delivered to underlying blood vessels (45). Desirable laser settings should result in purpura without excessive edema, crusting, blistering, or other epidermal changes (27). The PDL is useful for a range of telangiectatic lesions. The location and morphology of the lesion being treated determine the initial laser parameters (27). More than 70% of spider telangiectasias of the face in children and 93% in adults clear after one FPDL treatment using fluences of 6.0– 7.5 J/cm2 with a 5 mm handpiece (46,47). Fluence may be

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increased in older children, adults, or for subsequent treatment of resistant vessels. If the entire lesion is confined within the diameter of the laser beam, one pulse to the central punctum of a spider telangiectasia should result in lesional clearance. If radiating vessels are not covered with the central pulse, then they should be individually treated using the same energy density. Purpura of the treated lesions should be immediately apparent and the lesion should no longer blanch with pressure. Linear telangiectasias, which frequently occur around the nasal alae, are often of larger caliber than those located elsewhere on the face and may require more than one treatment session. These larger vessels may appear blue and respond less well than smaller red vessels to traditional PDL treatment based on their longer thermal relaxation times and higher ratio of deoxygenated to oxygenated hemoglobin (42). The use of a long-PDL with a 3 mm 10 mm elliptical handpiece and 1.5 ms pulse duration at energy densities ranging from 12.0 to 15.0 J/cm2 provides excellent clinical results in the treatment of larger caliber linear facial telangiectasias and has been shown to produce significantly better clinical results than the 532 nm KTP laser following both one and two laser treatments (35). The FPDL produces excellent results when used to treat diffuse arborizing facial telangiectasias such as those associated with acne rosacea, actinic damage, and chronic corticosteroid use. In addition, treatment with the PDL has been shown to reduce the incidence of inflammatory lesions in patients with acne rosacea treated for facial telangiectasias (46). Other conditions characterized by widespread telangiectasias, including Rothmund– Thomson (47) and Goltz (48) syndromes as well as scleroderma (49), have responded well to treatment with the PDL. The treatment of large areas of diffuse telangiectasias is best accomplished with the use of the 10 mm handpiece at fluences ranging from 6.0 to 7.5 J/cm2 with dynamic cooling. Because significant overlapping of laser pulses is contraindicated, patients should be informed at the initial consultation that several treatment sessions may be required in order to achieve maximum vessel clearance. In 1993, Ross et al. (20) compared the 585 nm APTDL with a robotized handpiece to the 585 nm PDL in the treatment of facial telangiectasias. The APTDL was used to trace out individual vessels while the PDL was applied using the overlapping field method (20). The PDL was judged to be superior in both ease of use and clinical results, but was preferred by ,50% of patients secondary to its resultant purpura and transient postinflammatory hyperpigmentation. These results corroborated previous findings by Broska et al. (19) revealing significantly greater improvement in facial telangiectasias receiving one treatment with the PDL compared with the APTDL. In their study, the PDL required only one-third the treatment time of the APTDL and resulted in excellent results in 78% of patients compared with 28 – 35% with the APTDL; however, 54% of subjects preferred APTDL treatment, probably because of the greater incidence of swelling and purpura following PDL treatment (19). In addition, 2 weeks after treatment, 85% of PDL-treated patients showed mild to moderate postinflammatory hyperpigmentation, whereas there were no pigmentary changes observed in 92% of the APTDL-treated sites. At 6 weeks, all of the PDL-treated sites had only mild or no hyperpigmentation, with one patient showing very mild hyperpigmentation which persisted for 3 months. Neither laser resulted in cutaneous scarring nor atrophy. In general, the subjects who preferred the PDL had more extensive facial telangiectasias and observed the greatest improvement (excellent rating after treatment) (19). Other findings reported in this study include an increased sensitivity to both lasers in the periorbital region and decreased laser efficacy on nasal blood vessels when compared with telangiectasias located on the cheeks. On the basis of an increased risk of adverse effects on the neck and anterior chest, use of the PDL in these regions necessitates caution in the selection of energy settings.


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In addition, great care should be taken to avoid overlapping of laser pulses. Poikiloderma of Civatte has been cleared effectively following an average of four treatment sessions using the 7 mm handpiece with fluences of 6.5– 7.0 J/cm2 (50). However, hypertrophic scarring on the anterior chest has been reported in a test area treated with the PDL using a 5 mm spot size at an energy density of 6.5 J/cm2 (51). In addition, keloid formation has been reported following treatment with the PDL on the anterior chest (6.0 J/cm2, 5 mm spot size) in a patient concomitantly taking oral isotretinoin, whereas no such scarring had been observed following treatment at the same fluence prior to medication use (52). In general, the treatment of telangiectasias with the PDL is safe and effective when proper energy densities, spot sizes, and nonoverlapping laser techniques are used. Topical anesthesia is almost always adequate for pain control during laser treatment. The use of a dynamic cooling device can also dramatically diminish pain during treatment of port-wine stains with the PDL without reducing treatment efficacy (53). In addition, precooling the skin with the dynamic cooling device permits the use of higher laser fluences, which may expedite lesional clearance without inducing epidermal change. The most objectionable aspect of PDL treatment is the development of posttreatment purpura that lasts from 7 to 14 days. Patients should be instructed to apply an antibiotic ointment for the first 3 – 4 days following treatment and should avoid applying makeup until the fourth day after treatment. In their review of a series of 500 patients undergoing PDL treatment for port-wine stains, telangiectasias, and hemangiomas, Levine and Geronemus (54) reported no hypertrophic scarring, ,0.1% incidence of atrophic scarring, spongiotic dermatitis in 0.04% of patients following multiple port-wine stain treatments, transient hyperpigmentation in 1%, and transient hypopigmentation in 2.6%. The V-beam long-PDL (Candela Corp., Wayland, MA) is representative of the most current PDL systems available. The wavelength of the laser is fixed at 595 nm, and the pulse duration may be adjusted from 1.5 to 40 ms, depending on the size and depth of the target vessel. Excellent clinical results may be achieved in the treatment of telangiectasias (Fig. 23.2), spider angiomata (Fig. 23.3), cherry angiomata, poikiloderma

Figure 23.2 Facial telangiectasias before (a), immediately after (b), and 8 weeks following treatment (c) with the V-beam long-PDL (3 ms, 12 J/cm2, 7 mm).

484

West

Figure 23.3 Spider angioma before (a) and 6 weeks after (b) treatment with the V-beam longPDL (3 ms, 6.5 J/cm2, 10 mm).

(Fig. 23.4), venous lakes, and pyogenic granulomas. The PDL has also been utilized for nonablative photorejuvenation, based on its ability to selectively heat the dermis, stimulate collagen remodeling, and reduce wrinkles (55). The clinical endpoint of treatment with the long-pulsed system is transient purpura which is visualized immediately following laser impact and then dissipates over several seconds.

2.

INTENSE PULSED LIGHT SOURCE

A noncoherent intense pulsed light source has recently been developed in an attempt to treat a wide variety of benign vascular lesions including the larger and deeper blood vessels of the legs (56 – 58). The device received US Food and Drug Administration marketing clearance in 1995. The intense light system emits a wide band of noncoherent intense pulse light with a broad spectrum of wavelengths ranging from 400 to 1200 nm. Selectivity is achieved by choosing either different filters that cut-off the spectrum of light emitted by the flashlamp below that particular wavelength. With some technologies, that will mean inserting a

Figure 23.4 Poikiloderma before (a), immediately after (b), and 3 months following 1 treatment session (c) with the V-beam long-PDL (3 ms, 6.5 J/cm2, 10 mm).


485

particular cut-off filter, while in other technologies, it may include an entirely different hand piece with more unique spectral filtering. For example, in the Lumenis technology, a 565 nm cut-off filter may be chosen to treat vascular lesions, while with the Palomar system, the user will choose a Lux G hand piece with the dual filtration system (500 –650 nm and 870 –1200 nm) to more selectively overlap the blood absorption curves. IPL technology permits the user to better target larger portion of the absorption spectra of a target chromophore than the narrow wavelength availability of a laser. Therefore, advantages may exist in treating certain types of lesions. Pulse durations also may vary between technologies. Multiple short pulses with a delay time may be used in some models while other systems use the single, smooth pulse technology employed to better protect the skin. As with other IPL applications, both large surface areas and small spot sizes offer distinct advantages for different areas. The size and depth of the target blood vessel, along with the patient’s skin type, determine the parameters required to achieve vessel destruction. The variable parameters which set intense pulsed light apart from the aforementioned laser systems include cutoff filters, pulsed mode, pulse width, and delay time. Small-caliber (,0.4 mm diameter) superficial blood vessels absorb light and heat evenly throughout their circumferences using the lower cutoff filters of 515 and 550 nm. These shorter filters allow adequate penetration of light to cause full-thickness heating of these smaller vessels. Larger, deeper vessels require the longer cutoff filters, which allow longer wavelengths of light to penetrate the skin. Attempts to use shorter cutoff filters to treat larger and deeper vessels results in inadequate heating of the entire circumference of the vessel. Thus, only the more superficial aspect of the vessel becomes heated while most of the vessel remains at its ambient temperature. In addition, use of short cutoff filters allows more absorption by melanin, resulting in increased thermal damage to the epidermis. Short cutoff filters can be safely used with skin types I and II; however, skin types III and IV require longer cutoff filters in order to minimize nonspecific melanin absorption, even if the target lesion is small in size and superficial. Use of the 515 nm cutoff filter in the treatment of lower extremity vessels is rarely suggested because the relatively high absorption of emitted light by melanin minimizes penetration into the deeper tissue.

3.

SUMMARY

In general, both CW and pulsed lasers provide excellent results in the treatment of facial telangiectasias with minimal complications. While some patients may prefer repeated treatments with a CW or quasi-CW system (e.g., KTP, copper vapor, APTDL) based on fewer immediate posttreatment side effects, the PDL has been shown to be more effective when the same number of treatments are performed. Recent technological advances resulting in lasers with longer wavelengths and pulse durations have improved treatment outcomes with PDL, particularly with regard to large-caliber facial vessels. An intense pulsed light system is also an effective tool for the treatment of facial telangiectasias. More than 75% improvement is commonly seen after two to three treatment sessions using any of these lasers or light systems. REFERENCES 1.

Goldman MP, Weiss RA, Brody HJ et al. Treatment of facial telangiectasia with sclerotherapy, laser surgery, and/or electrodesiccation: a review. J Dermatol Surg Oncol 1993; 19:889 – 906.

486 2.

3. 4. 5. 6. 7. 8. 9. 10. 11.

12.

13. 14. 15. 16. 17.

18. 19.

20.

21. 22. 23. 24. 25. 26.

West Goldman MP, Fitzpatrick RE. Treatment of cutaneous vascular lesions. In: Goldman MP, Fitzpatrick RE, eds. Cutaneous Laser Surgery: The Art and Science of Selective Photothermolysis. St. Louis: Mosby-Year Book, 1994:19 – 105. Bollinger A, Holzer J. The problem of electrocoagulation of the smallest telangiectasias. Zentralbl Phlebol 1966; 5:85– 188. Goldman MP, Eckhouse S et al. Photothermal sclerosis of leg veins. Dermatol Surg 1996; 22:323 – 330. Alster TS. Laser treatment of vascular lesions. In: Alster TS, ed. Manual of Cutaneous Laser Techniques. Philadelphia: Lippincott-Raven, 1997:24 – 44. McBurney E. Clinical usefulness of the argon laser for the 1990’s. J Dermatol Surg Oncol 1993; 19:358 – 362. Polla LL, Tan OT, Garden JM, Parrish JA. Tunable pulsed dye laser for the treatment of benign cutaneous vascular ectasia. Dermatologica 1987; 174:11– 17. Wheeland RG, Bailin PL. Dermatologic applications of the argon and carbon dioxide laser. Curr Concepts Skin Disorders 1984; 5:1– 25. Arndt KA. Argon laser therapy of small cutaneous vascular lesions. Arch Dermatol 1982; 118:200 – 224. Dixon J, Huether S, Rotering RH. Hypertrophic scarring in argon laser treatment of portwine stains. Plast Reconstr Surg 1984; 73:771– 780. Neumann RA, Knobler RM, Leonhartsberger H et al. Comparative histochemistry of port-wine stains after copper vapor laser (578) nm and argon laser treatment. J Invest Dermatol 1992; 99:160 – 167. Noe JM, Barsky SH, Geer DE et al. Port wine stains and the response to argon laser therapy: successful treatment and the predictive role of color, age and biopsy. Plast Reconstr Surg 1990; 65:130 – 139. McDaniel DH. Clinical usefulness of the hexascan. J Dermatol Surg Oncol 1993; 19:312 – 319. Tan OT, Stafford TJ. Treatment of port wine stains at 577 nm. Med Instrument 1987; 21:218 – 221. Garden JM, Polla LL, Tan OT. The treatment of port wine stains by the pulsed dye laser: analysis of pulse duration and long-term therapy. Arch Dermatol 1998; 124:889 –896. Morelli J, Tan OT, Garden J et al. Tunable dye laser (577 nm) treatment of portwine stains. Lasers Surg Med 1986; 6:694 – 699. Waner M, Dinehart SM, Wilson MB, Flock ST. A comparison of copper vapor and the flashlamp-pumped pulsed dye lasers in treatment of facial telangiectasia. J Dermatol Surg Oncol 1993; 19:992 – 998. Orenstein A, Nelson JS. Treatment of facial vascular lesions with a 100 mu spot 577 nm pulsed continuous wave dye laser. Ann Plast Surg 1989; 23:310 – 316. Broska P, Martinho E, Goodman M. Comparisons of the argon tunable dye laser with the flashlamp pulsed dye laser in the treatment of facial telangiectasia. J Dermatol Surg Oncol 1994; 20:749 – 754. Ross M. Watcher MA, Goodman MM. Comparison of the flashlamp pulsed dye laser with the argon tunable dye laser with the robotized handpiece for facial telangiectasia. Lasers Surg Med 1993; 13:374 – 378. Dinehart SM, Waner M, Flock S. The copper vapor laser for treatment of cutaneous vascular and pigmented lesions. J Dermatol Surg Oncol 1993; 19:370– 375. Pickering JW, Walker EP, Butler PH et al. Copper vapour laser treatment of port-wine stains and other vascular malformations. Br J Plast Surg 1990; 43:273 – 282. Thibault PK. Copper vapor laser and microsclerotherapy of facial telangiectasias. J Dermatol Surg Oncol 1994; 20:48 – 54. McCoy S, Hanna M, Anderson P et al. An evaluation of the copper-bromide laser for treating telangiectasia. Dermatol Surg 1996; 22:551 – 557. Tan OT, Gilchrest BA. Laser therapy for selected cutaneous vascular lesions in the paediatric population: a review. Pediatrician 1988; 82:652 – 662. Ruiz-Esparza J, Goldman MP, Fitzpatrick RE et al. Flashlamp-pumped dye laser for treatment of telangiectasia. J Dermatol Surg Oncol 1993; 19:1000 – 1003.

Acquired Vascular Lesions 27. 28. 29. 30. 31. 32. 33. 34. 35. 36. 37. 38. 39. 40.

41. 42. 43. 44. 45. 46. 47. 48. 49.

50. 51. 52. 53.

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Waldorf HA, Lask GP, Geronemus RG. Laser treatment of telangiectasias. In: Alster TS, Apfelberg DB, eds. Cosmetic Laser Surgery. New York: Wiley-Liss, 1996:93 – 109. Apfelberg DB, Smith T, Maser MR, Lash H, White DN. Study of three laser systems for treatment of superficial varicosities of the lower extremity. Lasers Surg Med 1987; 7:219– 223. Glassberg E, Lask GP, Tan EM, Uitto J. The flashlamp-pumped 577-nm pulsed tunable dye laser: clinical efficacy and in vitro studies. J Dermatol Surg Oncol 1988; 14:1200– 1208. Weiss RA, Weiss MA. Early clinical results with a multiple synchronized pulse 1064 nm laser for leg telangiectasias and reticular veins. Dermatol Surg 1999; 25:399 – 402. Goldman MP, Weiss RA. Treatment of leg telangiectasia with laser and high-intensity pulsed light. Dermatol Ther 2000; 13:38 – 49. Sarradet DM, Hussain M, Goldberg DJ. Millisecond 1064-nm Neodymium:YAG laser treatment of facial telangiectases. Dermatol Surg 2003; 29:56– 58. Silver BE, Livshots YL. Preliminary experience with the KTP/532 nm laser in the treatment of facial telangiectasia. Cosmet Dermatol 1996; 9:61– 64. Hevia O. New laser treatment for facial telangiectasias: a randomized study. Cosmet Dermatol 1997; 10:53 – 56. West TB, Alster TS. Comparison of the 590 nm long-pulsed (1.5 ms) and KTP (532 nm) lasers in the treatment of facial and leg telangiectasias. Dermatol Surg 1998; 24:221– 226. Gold berg DJ, Meine JG. A comparison of four frequency-doubled Nd:YAG (532 nm) laser systems for treatment of facial telangiectasias. Dermatol Surg 1999; 25:463– 467. Adrian RM, Tanghetti EA. Long pulse 532-nm laser treatment of facial telangiectasia. Dermatol Surg 1998; 24:71– 74. Anderson RR, Parrish JA. Microvasculature can be selectively damaged using dye lasers: a basic theory and experimental evidence in human skin. Lasers Surg Med 1981; 1:263– 276. Anderson RR, Parrish JA. Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science 1983; 22:524 – 527. Alster TS, Wilson F. Treatment of port-wine stains with the flashlamp-pumped pulsed dye laser: extended clinical experience in children and adults. Ann Plast Surg 1994; 32:478 – 484. Goldman MP, Fitzpatrick RE, Ruiz-Esparza J. Treatment of port-wine stains (capillary malformation) with the flashlamp-pumped pulsed dye laser. J Pediatr 1993; 122:71 – 77. Tan OT, Sherwood K, Gilchrest BA. Treatment of children with port-wine stains using the flashlamp-pulsed tunable dye laser. N Engl J Med 1989; 320:416 – 421. Greenwald J, Rosen S, Geer DE et al. Comparative histological studies of the tunable dye (at 577 nm) laser and argon laser. J Invest Dermatol 1981; 77:305– 310. Gonzalez E, Gange RW, Momtaz KT. Treatment of telangiectases and other benign vascular lesions with the 577 nm pulsed dye laser. J Am Acad Dermatol 1992; 27:220 – 226. Dover JS, Arndt KA, Geronemus RG et al. Understanding lasers. Illustrated Cutaneous Laser Surgery: a Practitioner’s Guide. Norwalk, CT: Appleton and Lange, 1990:1– 19. Geronemus R. Treatment of spider telangiectasias in children using the flashlamp-pumped pulsed dye laser. Pediatr Dermatol 1991; 8:61– 63. Goldman MP, Fitzpatrick RE, Ruiz-Esparza J. Treatment of spider telangiectasias in children. Contemp Pediatr 1993; 10:16 – 19. Lowe NJ, Behr KL, Fitzpatrick R et al. Flashlamp-pumped dye laser for rosacea-associated telangiectasia and erythema. J Dermatol Surg Oncol 1991; 17:522 – 525. Potozkin JR, Geronemus RG. Treatment of poikilodermatous component of the Rothmund – Thomson syndrome with the flashlamp-pumped pulsed dye laser: a case report. Pediatr Dermatol 1991; 8:162 – 165. Geronemus R. Poikiloderma of Civatte [letter]. Arch Dermatol 1990; 26:547 – 548. Swinehart JM. Hypertrophic scarring resulting from flashlamp pulsed dye laser surgery. J Am Acad Dermatol 1991; 25:845 – 855. Bernstein LJ, Geronemus RG. Keloid formation with the 585 nm pulsed dye laser during isotretinoin treatment [letter]. Arch Dermatol 1997; 133:111 – 112. Waldorf HA, Alster TS, McMillan K et al. Effect of dynamic cooling on 585 nm pulsed dye laser treatment of port-wine stain birthmarks. Dermatol Surg 1996; 23:657– 662.

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West Levine VJ, Geronemus RG. Adverse effects associated with the 577 and 585 nanometer pulsed dye laser in the treatment of cutaneous vascular lesions: a study of 500 patients. J Am Acad Dermatol 1995; 32:613 – 617. Zelickson BD, Kilmer SL, Bernstein E et al. Pulsed dye laser therapy for sun damaged skin. Lasers Surg Med 1999; 25:229 – 236. Raulin C, Goldman MP, Weiss MA et al. Treatment of adult port-wine stains using intense pulsed light therapy (Photoderm VL): brief initial clinical report. Dermatol Surg 1997; 23:594 – 601. Raulin C, Weiss RA, Schonermark MP. Treatment of essential telangiectasias with an intense pulsed light source (Photoderm VL). Dermatol Surg 1997; 23:941 – 946. Green D. Photothermal removal of telangiectases of the lower extremities with the Photoderm VL. J Am Acad Dermatol 1998; 38:61 –68.

24

Lasers in the Treatment of Pigmented Lesions Jeffrey S. Dover SkinCare Physicians of Chestnut Hill, Chestnut Hill, Massachusetts and Yale University School of Medicine, Connecticut, USA

Kenneth A. Arndt SkinCare Physicians of Chestnut Hill, Chestnut Hill and Harvard Medical School, Massachusetts; Yale University School of Medicine, Connecticut, USA

Richard J. Ort SkinCare Physicians of Chestnut Hill, Chestnut Hill and Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA

1. 2. 3. 4.

Background Laser – Tissue Interactions in Pigmented Skin Q-switched and Pulsed Lasers and Light Sources Clinical Treatment 4.1. Epidermal Pigmented Lesions 4.1.1. Lentigines 4.1.2. Cafe-au-lait Macules 4.1.3. Other Epidermal Pigmented Lesions 4.2. Dermal Pigmented Lesions and Tattoos 4.2.1. Nevus of Ota 4.2.2. Melanocytic Nevi 4.2.3. Other Dermal Pigmented Lesions 4.2.4. Tattoos 4.2.5. Side Effects and Complications References 1.

489 490 491 493 493 493 494 495 496 496 497 498 500 500 500

BACKGROUND

In 1963, Goldman and colleagues first demonstrated that ruby laser radiation with a 0.5 ms pulse duration was selectively absorbed by pigmented skin (1). These same investigators demonstrated that the threshold radiant exposure for epidermal damage was 10– 100 times lower for a Q-switched ruby laser (QSRL) with pulse width of 50 ns (2). Despite these initial reports, the ability of QSRL to selectively target pigment was not appreciated

Modified from Kaminer MS, Arndt KA, Dover JS eds. Atlas of Cosmetic Surgery. Philadelphia: Harcourt Saunders, 2002. 489

490

Dover, Arndt, and Ort

and pigmented lesions for many years were treated with nonselective continuous wave sources such as the argon (3) and CO2 lasers (4). Since the late 1980s, based on a large amount of basic and clinical investigation performed with pulsed lasers, Q-switched lasers have become the treatment of choice for both epidermal and dermal pigmented lesions, including tattoos.

2.

LASER – TISSUE INTERACTIONS IN PIGMENTED SKIN

In 1983, Anderson and Parrish described the principle of selective photothermolysis (5), which predicted that selective thermal damage to an absorbing target could be achieved using suitable laser parameters. This concept requires the use of a wavelength well absorbed by the target, a pulse duration shorter than the thermal relaxation time of the target (defined as the time required for a heated target to cool by 50%), and sufficiently high energy density to achieve the desired tissue effect. This principle was first applied to the treatment of port wine stains with oxyhemoglobin as the target chromophore. Thereafter, it was applied to the treatment of pigmented lesions where either endogenous melanin or an exogenous chromophore such as carbon particles served as the target. Melanin has a broad absorption spectrum within the ultraviolet, visible, and nearinfrared range, but absorption decreases steadily with longer wavelengths (6) (see Fig. 24.1). It is the primary absorber between 600 and 1100 nm, the “optical window” where light penetrates deeply into the dermis (6). Microscopically, melanin consists of melanosome granules that evolve through four stages of increasing melanization before being transferred from melanocytes to keratinocytes. With a diameter of 1 mm, melanosomes are predicted to have a thermal relaxation time of 50 – 500 ns (5,7). Depending on coloration, individual tattoo pigments can be characterized by their own absorption spectra (8). For example, black pigment absorbs broadly from 600 nm to near-infrared while red pigment has maximum absorption from 505 to 560 nm (8). With a diameter of 40 nm, the most common type of tattoo pigment particle has a predicted thermal relaxation time ,10 ns (9,10). The principle of selective photothermolysis predicts that thermal confinement to the melanosome or tattoo particle will occur over a range of wavelengths if the laser

Figure 24.1

Absorption spectrum of melanin.

Lasers in Treatment of Pigmented Lesions

491

pulsewidth is ,1 ms. The delivery of an extremely high energy laser pulse within this time span results in rapid heating of the target particle (estimated at 10 million degrees/s), causing it to explode (11). Selective damage to melanosomes in human skin was first demonstrated with a 351 nm XeF excimer laser delivering 20 ns pulses (12). Although light at 351 nm is well absorbed by melanin, it penetrates ,100 mm into the skin because of pronounced dermal scattering at shorter wavelengths (6). Longer wavelengths penetrate progressively deeper into the skin, such that wavelengths 694 nm penetrate at least 1 mm (6). It was subsequently demonstrated that selective damage to melanosomes could be produced by the pulsed tunable dye laser (13,14) (wavelength 435– 750 nm, pulsewidth 300– 750 ns), QSRL (7) (wavelength 694 nm, pulsewidth 40 ns), and the Q-switched neodymium:YAG (Nd:YAG) laser (15) (wavelength 355, 532, and 1064 nm, pulsewidth 10 – 12 ns). Electron microscopy confirmed highly selective, dose-dependent disruption of melanosomes within melanocytes and melanized keratinocytes. Destruction of pigment-containing cells is likely due to mechanical damage from acoustic waves that emanate from the absorbing melanosome or tattoo particle (9,16). Damage to these cells results in vacuolization, condensation of pigment, and nuclear material at the cellular periphery, and subepidermal vesiculation at the level of the lamina lucida. In both guinea pig (17) and human skin (18) treated with the QSRL, necrotic pigmented cells slough in a fine scale/crust over several weeks, followed by transient hypopigmentation and gradual repigmentation without textural change. Repigmentation results from migration of residual melanocytes within adnexal structures or within unirradiated adjacent skin. Q-switched lasers produce an immediate ash-white color at the site of impact. Although the exact cause of this tissue response is unknown, it is most likely due to scattering of visible light by steam cavities formed within melanosomes (17). The threshold exposure dose for melanosome damage correlates well with the clinical threshold for immediate skin whitening. Darker skin has a lower threshold whitening dose due to higher epidermal melanin content (18). The required threshold dose increases progressively with longer wavelength, grossly consistent with the melanin absorption spectrum (14,15). Longer wavelengths up to 1064 nm penetrate more deeply into the dermis, causing melanosome alterations within follicles at a depth .1 mm (15). Subthreshold fluences appear to actually stimulate melanogenesis due to activation of epidermal melanocytes after nonlethal injury (18).

3.

Q-SWITCHED AND PULSED LASERS AND LIGHT SOURCES

A variety of lasers can be used to treat pigmented lesions of the skin. These can be categorized into lasers that are pigment nonselective, those that are somewhat pigment selective, and those that are highly selective for pigment removal. Pigment nonselective lasers such as the carbon dioxide (4,19), (10,600 nm) and erbium:YAG (2940 nm) lasers can be used to eliminate epidermal pigment because of their ability to target water and remove the entire epidermis, including melanocytes and melanized keratinocytes, in atraumatic fashion. Pigment is removed as a secondary event. Continuous wave (CW) and quasiCW visible light lasers, for example, argon laser (488, 514 nm), copper vapor laser (511 nm), and krypton laser (521, 530 nm), can be used to selectively remove epidermal pigmented lesions, although reproducible spatial thermal injury confinement is not possible. The risk – benefit ratio is higher with these devices than with pulsed lasers. To date, only pulsed lasers have been shown to treat both epidermal and dermal pigmented lesions effectively in a safe, reproducible manner (see Table 24.1).

492 Table 24.1

Dover, Arndt, and Ort Treatment of Pigmented Lesions

Laser Q-switched ruby (694 nm) Q-switched Nd:YAG (1064 nm) Q-switched Nd:YAG (532 nm) Q-switched Nd:YAG (585 nm) Q-switched Nd:YAG (650 nm) Q-switched Alexandrite (755 nm) Pulsed dye (510 nm)

Epidermal lesions

Dermal lesions

Mixed lesions

þþþþ þþ þþþþ þþþ þþþ þþþ þþþþ

þþþþ þþþþ þ to þþ þ to þþ þ to þþ þþþ þþ

þ þ þ þ þ þ þ

Note: þ, poor; þþ, fair; þþþ, good; þþþþ, excellent.

There are four principle, short-pulsed, pigment-selective lasers, three of which are widely used today: QSRL, the Q-switched alexandrite laser, and the Q-switched Nd:YAG laser. The pigmented lesion pulsed dye laser is no longer produced. These lasers specifically target melanosomes or tattoo particles by delivering high intensity, shortpulsed radiation at appropriate wavelengths. The term Q-switched is short for “qualityswitched,” which refers to the ability to store large amounts of energy in the laser cavity through the use of an optical shutter. When the laser fires, the shutter releases an extremely high-powered pulse (109 W) with an ultrashort pulse duration (nanosecond range). The QSRL emits red light at a wavelength of 694 nm and pulse duration of 28 – 40 ns. Light is delivered through a mirrored articulated arm. The Q-switched Nd:YAG laser emits infrared light at 1064 nm. By placing a frequency-doubling KTP (potassium –titanyl – phosphate) crystal in the laser beam’s path, the wavelength may be halved to 532 nm (green light). Dye impregnated handpieces can convert the 532 nm wavelength to either 585 nm (yellow) or 650 nm (red) light. Pulses of 5 –10 ns duration are delivered through an articulated arm at a repetition rate of up to 10 Hz. The Q-switched alexandrite laser has a wavelength of 755 nm (infrared), pulse duration of 50 –100 ns, spot size of 2– 4 mm, and repetition rate of up to 10 Hz. Light is delivered through an articulated arm or through a semiflexible fiberoptic cable. The pigmented lesion pulsed dye laser (non-Q-switched) used a xenon flashlamp to pump a coumarin-containing dye which emitted pulses of laser energy at 510 nm (green light). It has a somewhat longer pulse duration of 400 ns, spot size of 3– 5 mm, firing rate of 1 Hz, and a fiberoptic delivery system. Long-pulsed (millisecond domain) 532 nm (KTP) Nd:YAG lasers, which are commonly used to treat vascular lesions, can be used to treat superficial pigmented lesions. However, the long pulsewidth of these lasers approximates the thermal relaxation time of the entire epidermis (10 ms) (20) and does not allow for selective damage to subcellular organelles such as melanosomes. Owing to the limited penetration depth of the 532 nm wavelength, these lasers are not effective for treatment of dermal pigmented lesions. Long-pulsed ruby, alexandrite, and Nd:YAG lasers, widely used for laser hair removal, share the same wavelengths as their Q-switched counterparts but operate in a normal (non-Q-switched) mode and deliver high energy pulses in the millisecond rather than the nanosecond domain. Because of their higher fluences and longer pulse duration, these lasers can target large pigmented structures such as hair follicles or nests of cells rather than individual melanosomes or pigmented cells. The role of these long-pulsed lasers in the treatment of congenital and acquired nevi is currently being investigated (21,22). Pigment removal can also be accomplished with a noncoherent light source that emits polychromatic light ranging from 515 to 1200 nm (visible to infrared). Filters are used to cut off the light below a predetermined wavelength. Light is emitted as a sequence


493

of single, double, or triple pulses (millisecond domain) that are separated by variable time intervals. This laser-like device has been primarily used for treatment of vascular lesions and hair removal, and aside from anecdotal reports, there are no studies addressing its efficacy in the treatment of pigmented lesions of the skin (23).

4.

CLINICAL TREATMENT

4.1.

Epidermal Pigmented Lesions

Numerous clinical studies have confirmed the efficacy and safety of Q-switched lasers (24 –26) and the 510 nm pulsed dye laser (27) in the treatment of various epidermal pigmented lesions, including ephelides, lentigines (Fig. 24.2), cafe-au-lait macules (CALMs), seborrheic keratoses, nevi spilus, and Becker’s nevi (Table 24.2). Pigment in epidermal lesions is located superficially, so shorter wavelength devices can be used effectively despite their limited penetration depth. For example, the 510 nm wavelength of the pulsed dye laser penetrates only 250 mm into the skin but is highly absorbed by melanin (6). The Q-switched ruby and alexandrite lasers effectively treat both epidermal and dermal lesions since their wavelengths are well absorbed by melanin and penetrate deeply into the dermis. The 1064 nm wavelength of the Nd:YAG laser penetrates deeply but is poorly absorbed by melanin, making the 532 nm wavelength a better choice when treating epidermal lesions. At the 510 and 532 nm (green) wavelengths, hemoglobin competes with melanin for absorption of light. Ultrashort (nanosecond range) pulses at these wavelengths cause rupture of superficial blood vessels, which is evident clinically as purpura (14). 4.1.1.

Lentigines

Lentigines are extremely common hyperpigmented macules that most often result from chronic sun exposure. Histologically, melanocytes in the basal layer are increased in

Figure 24.2 (a) A woman in her early 40s with significant photoaging and numerous lentigines prior to treatment. (b) Six weeks after one single treatment with a QSRL. There is 70% improvement of the lesion. No further treatments were requested by the patient.

494


Table 24.2

Standard Treatment Parameters for Pigmented Lesions Laser

Spot size (mm)

Fluence (J/cm2)

Retreatment interval

QS ruby QS Nd:YAG (532 nm) QS Alexandrite Pulsed dye (510 nm) QS ruby QS Nd:YAG (532 nm) QS Alexandrite Pulsed dye (510 nm) QS ruby QS Nd:YAG (532 nm) QS Nd:YAG (1064 nm) QS Alexandrite QS ruby QS Nd:YAG (532 nm) QS Nd:YAG (1064 nm) QS Alexandrite QS ruby QS Nd:YAG (1064 nm) QS Alexandrite

6.5 3 3 3 6.5 3 3 5 6.5 3 3 3 6.5 3 3 3 6.5 3 3

2.0– 4.0 0.7– 1.0 4.0– 6.0 2.5 3.0– 4.5 1.0– 1.5 2.5– 3.5 2.0– 3.5 3.0– 4.5 1.5– 1.8 4.0– 5.0 5.0– 6.0 3.0– 4.5 1.5– 2.0 4.0– 4.4 4.0– 6.0 5.0– 6.0 4.0– 5.0 5.5– 6.5

4 – 8 weeks

Lesion Lentigines

Cafe-an-lait macules

Becker’s nevus

Nevus spilus

Nevus of Ota

4 – 8 weeks

4 – 8 weeks

4 – 8 weeks

6 – 12 weeks

Note: QS, Q-switched.

number without nesting and rete ridges are elongated. Lentigines can be classified into several categories, including those due to chronic sun exposure (solar lentigines), those associated with a syndrome (e.g., Peutz-Jegher), and the labial melanotic macule. All three Q-switched lasers and the 510 nm pulsed dye laser are highly effective in the treatment of lentigines. After one treatment, at least 50% clearing is expected, although additional treatments may be required to remove residual pigment. Labial melanotic macules respond equally well to laser treatment (28,29) (Fig. 24.2). One study determined that treatment of facial lentigines with the 532 nm Q-switched Nd:YAG laser was more effective than application of 35% trichloroacetic acid (30). In another study, blinded observers found that the 532 nm Q-switched Nd:YAG laser was superior to cryotherapy with liquid nitrogen in efficacy, healing time, and patient preference (31). 4.1.2.

Cafe-au-lait Macules

CALMs are well-circumscribed, light brown macules that may occur as isolated lesions in the general population or as multiple lesions in association with a syndrome (e.g., neurofibromatosis and Albright’s syndrome). Histologically, one sees an increase in the number of melanocytes, hypermelanosis of melanocytes and keratinocytes, and giant melanin granules. The efficacy of lasers in the removal of CALMs is variable, and results are often unpredictable (Fig. 24.3) (32). Short-term lightening or clearing is frequently achieved after multiple treatments. However, recurrences are common, seen in up to 50% of treated lesions, even when complete clearing has occurred initially. Transient postinflammatory hyperpigmentation is frequent following laser treatment of CALMs, especially in patients with skin phototypes types III and higher. Alster (33) reported complete elimination of most CALMs after an average of 8.4 treatment sessions with the


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Figure 24.3 (a) CALM of the thigh. (b) CALM after four treatments with a QSRL showing near complete clearing of the lesion. There is one small focal scar which is the result of a skin biopsy.

510 nm pulsed dye laser, indicating that multiple treatments may be necessary to achieve optimal results. Complete clearing of a dark facial CALM previously resistant to QSRL and Nd:YAG laser treatment has been reported after erbium:YAG laser resurfacing (34).

4.1.3.

Other Epidermal Pigmented Lesions

Ephelides (freckles) are small hyperpigmented macules located on sun-exposed skin. Histologically, there is hyperpigmentation of the basal layer but no increase in the concentration of melanocytes. These lesions uniformly respond well to Q-switched and 510 nm pulsed dye laser treatment (Fig. 24.4). Flat seborrheic keratoses also respond well to laser treatment (27), but thicker lesions are resistant and should be treated with cryosurgery. Nevi spilus and Becker’s nevi, which may have combined epidermal and dermal components, respond variably to laser treatment. Results are unpredictable, and incomplete clearing or recurrences are not uncommon. Successful clearing of the darker nevocellular component of nevus spilus has been reported with the QSRL, but the background cafe-au-lait component tends to recur (24). Becker’s nevus is a large, hyperpigmented, slightly verrucous plaque that occurs most commonly on the shoulder area of males. These lesions are reported to be similar to CALMs in their response to laser

Figure 24.4 (a) Japanese male with extensive numbers of freckles prior to treatment. (b) After treatment with a QSRL, the freckles are entirely clear.

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treatment, with a high incidence of posttreatment hyperpigmentation and recurrence within 6 –12 months (35). 4.2.

Dermal Pigmented Lesions and Tattoos

Q-switched lasers have revolutionized the treatment of dermal pigmented lesions including melanocytoses, some melanocytic nevi, and tattoos. Prior to the use of Q-switched lasers, treatment of these lesions was limited to nonspecific destructive methods such as excision (36,37), dermabrasion (38), salabrasion (39), liquid nitrogen (40), solid CO2 ice (41), or continuous wave laser ablation (42). Treatment was relatively ineffective and almost always resulted in scarring or pigmentary changes. By selectively targeting the dermal pigment, Q-switched lasers provide highly effective treatment of these lesions while dramatically reducing the risk of textural or permanent pigmentary change. The QSRL, alexandrite, and 1064 nm Nd:YAG lasers are most commonly used. The wavelength range of these lasers falls within the optical window that transmits light deeply into the dermis. Shorter wavelengths such as 510 or 532 nm are highly scattered by dermal collagen and penetrate poorly into the dermis (300 mm) (6), making them inappropriate sources for the treatment of dermal pigment. Because they are so well absorbed by the color red, however, they are effective for treating red tattoo pigment. 4.2.1.

Nevus of Ota

Nevus of Ota is a mottled, bluish or gray-brown patch that is usually located unilaterally within the distribution of the first and second branches of the trigeminal nerve. It is classified into four types, depending on extent and distribution of pigmentation (I—small, II—moderate, III—extensive, IV—bilateral). Nevus of Ota may affect mucosal surfaces such as cornea, sclera, nasal and buccal mucosa, and tympanic membrane. The lesion is present at birth in 50% of cases, while the remainder usually appear by the second decade of life. Asians are most commonly affected, with an incidence of 1 in 500 reported in Japan (Fig. 24.5) (43). The incidence in Caucasians is

Figure 24.5 (a) A young girl with a nevus of Ota extending over a significant portion of the face prior to treatment. (b) After a series of treatments with a QSRL there is impressive lightening of the lesion with no textural change.


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significantly lower. Women are five times more likely to be affected than men. The occurrence of melanoma within nevus of Ota has been reported (44) but is rare. Histologically, dendritic melanocytes are scattered within the papillary and reticular dermis. Q-switched lasers provide an extremely effective means of treating this condition. The degree of lightening is usually directly proportional to the number of treatments performed. Lightening of 70% has been reported in the vast majority of patients treated four or five times with the QSRL (45). Although pigmentary change such as hyperpigmentation or hypopigmentation occurs occasionally, textural change has not been reported. Posttreatment biopsies have revealed degeneration of melanocytes up to a depth of 1.5 mm from the skin surface (45). Although the QSRL has been most widely used (45 – 49), the Q-switched alexandrite (50) and Nd:YAG (25) lasers appear as effective. 4.2.2.

Melanocytic Nevi

Laser treatment of nevomelanocytic lesions is controversial, as it is unclear whether nonlethal laser irradiation has any potential to induce malignant change in nevomelanocytic cells. In vitro studies of melanoma cells treated with Q-switched lasers have found changes in cell surface integrin expression, with subsequent alteration of such cellular behavior as migration (51). In addition, benign lesions that recur following treatment may show clinical and histologic atypia, a condition termed pseudomelanoma (52). However, true malignant transformation of a benign pigmented lesion following laser treatment has never been reported (53). Theoretically, laser treatment of melanocytic lesions might decrease the risk of malignant transformation by reducing the population of available premalignant cells (54). Additional study is required to assess the effects of Q-switched laser irradiation on nevomelanocytic cells. For the time being, it is recommended that Q-switched laser treatment be reserved for benign nevomelanocytic lesions exhibiting little to no atypia. If any doubt exists about the clinical diagnosis, a biopsy should be performed prior to laser treatment. Studies indicate that the QSRL, alexandrite, and 1064 nm Nd:YAG lasers all have some degree of effectiveness in the removal of flat or slightly raised, junctional or compound, acquired nevi (55 – 57). Lighter nevi often respond best to shorter wavelengths which maximize melanin absorption, while darker nevi typically respond to any wavelength. Multiple treatments are usually necessary for maximal lightening. It is often not possible to achieve complete clearing of nevi (57), and recurrence after laser treatment is not uncommon. There may be persistence of nevomelanocytes containing little or no pigment or located within deeper layers that are shielded from laser radiation by pigmented superficial cells (55). Q-switched laser radiation does not penetrate sufficiently to effectively treat thicker lesions such as papillated or dome-shaped dermal nevi. The QSRL has been reported to successfully eliminate flat blue nevi (58). Although Q-switched lasers may effectively lighten congenital nevi, there is a high rate of repigmentation due to persistence of nevomelanocytes within the deeper reticular dermis and within adnexae (53,54). In theory, millisecond-domain pulses are more appropriate than Q-switched pulses for treating thick lesions such as congenital nevi because they produce less selective thermal damage, destroying entire nests of cells rather than individual pigmented cells. Japanese investigators have reported impressive long-term clearing of congenital nevi treated with the millisecond-domain normal-mode ruby laser (Fig. 24.6) (21,22). Clinical lightening is associated with the development of a subtle microscopic scar up to 1 mm thick, which obscures residual nevus cells. Long-pulse ruby lasers also offer the potential to reduce the amount of hair within congenital nevi. Because congenital nevi have the potential to transform into malignant melanoma, and

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Figure 24.6 (a) A congenital nevus of the upper and lower eyelid prior to treatment. (b) After a series of treatments with a long-pulsed ruby laser, there is significant lightening but incomplete clearing of the nevus.

residual nevus cells persist in the dermis after laser treatment, cautious long-term followup of nevi treated with lasers is required. In Japanese studies, no histological or clinical evidence of malignancy has been demonstrated up to 8 years after normal-mode ruby laser treatment (21,22). Both continuous wave lasers (59,60) and the QSRL (61) have been used to treat lentigo maligna. However, there are several reports of lentigo maligna recurring following laser treatment, most likely due to persistence of melanocytes within deeper adnexal structures (62,63). Laser treatment of lentigo maligna should be considered only in situations where surgical excision is not feasible due to large lesion size, advanced patient age, or underlying medical condition. Close follow-up to detect any early recurrence is essential. 4.2.3. Other Dermal Pigmented Lesions Melasma is a common acquired facial hypermelanosis, occurring most commonly on the cheeks, forehead, upper lip, nose, and chin and varying in color from brown to blue-gray. It is particularly common in women of childbearing age and in individuals with skin phototypes III or higher. It is associated with sun exposure, pregnancy, and use of oral contraceptives, although its presence often cannot be ascribed to any known cause. Postinflammatory hyperpigmentation is another type of acquired hypermelanosis which may develop following nearly any cutaneous injury or inflammatory process. Histologically, three types of pigmentation occur in these two conditions: (1) the epidermal type in which there is increased melanin in the epidermis; (2) the dermal type in which melanophages are found in the superficial and mid-dermis; and (3) a combination of epidermal and dermal types. Traditional treatment of these disorders includes cessation of offending medication such as oral contraceptives, sun protection, and use of topical steroids, hydroquinone, retinoids, azeleic acid, and superficial chemical peels. While the epidermal component often responds to this regimen, dermal pigmentation is generally resistant. Studies have shown that Q-switched lasers are, for the most part ineffective in the treatment of melasma and postinflammatory hyperpigmentation (25,64), Q-switched laser treatment may actually cause an increase in dermal melanophages and worsening of hyperpigmentation. Carbon dioxide (65) or erbium: YAG (66) laser resurfacing provides an alternative treatment modality for melasma, but postinflammatory hyperpigmentation is an almost universal occurrence in the postoperative period. Aggressive topical therapy should be initiated promptly following laser resurfacing. The use of these lasers should be reserved only for refractory melasma not responsive to conventional therapy.


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Infraorbital hyperpigmentation (dark circles) may result from a variety of causes, including dermal melanin deposition, postinflammatory hyperpigmentation from atopic or allergic contact dermatitis, prominent superficial blood vessels, and shadowing from skin laxity and infraorbital swelling (67). The QSRL has been reported to effectively treat infraorbital hyperpigmentation when due to deposition of dermal melanin (67). Improvement of this condition has also been reported following carbon dioxide laser resurfacing (68). Blepharoplasty may be indicated when infraorbital darkening is due to excessive skin laxity. Minocycline therapy may cause localized or diffuse mucocutaneous pigmentation. Minocycline-induced pigmentation occurs in 5% of acne vulgaris patients treated with the drug after prolonged use (69). Two patterns of pigmentation have been reported. In type I, focal blue-gray pigmentation occurs in inflamed or scarred skin, or in previously normal skin. Histological studies show pigment within dermal macrophages which stains positively for melanin and iron (70). Type II consists of generalized blue to brown discoloration which is more prominent on sun-exposed areas. Histologically, epidermal and superficial dermal pigment is present which stains only for melanin (70). Although pigmentation typically fades after discontinuation of the drug, it may persist for years following cessation of therapy. The QSRL is highly effective in treating minocycline-induced pigmentation, with clearing occurring after 1– 4 treatment sessions without untoward sequelae (71 – 73). Successful treatment has also been reported with the Q-switched 532 and 1064 nm Nd:YAG laser (74,75), although the latter wavelength has not proved effective in several reports (73,74). Similar results have been reported with amiodaroneinduced hyperpigmentation treated with the QSRL (76). In order to prevent recurrences, laser treatment of these conditions should be deferred until the offending medication has been discontinued and sufficient time has elapsed to allow most of the pigmentation to resolve spontaneously.

Figure 24.7 (a) An amateur tattoo of the back of the young man prior to treatment. (b) The tattoo 6 weeks after the third treatment.

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Figure 24.8 (a) Multicolored tattoo of the arm prior to treatment. (b) Tattoo after six treatments shows dramatic lightening of all colors of the tattoo but some residual tattoo ink. Incomplete clearing of tattoos is not uncommon with Q-switched laser treatment.

Q-switched laser treatment may cause paradoxical hyperpigmentation in patients receiving certain medications. In one report, localized chrysiasis developed in a patient on parenteral gold therapy who underwent treatment with a QSRL for postinflammatory hyperpigmentation (77). This phenomenon is due to a laser-induced alteration in the physiochemical properties of dermal gold deposits and resembles the pigment darkening that may occur following Q-switched laser treatment of tattoos containing iron oxide or titanium dioxide (discussed subsequently). 4.2.4.

Tattoos

Tattoos are discussed in detail in Chapter 25 (Figs. 24.7 and 24.8). 4.2.5.

Side Effects and Complications

Although Q-switched lasers are far safer than traditional treatment modalities, treatment is not without some risk. In general, because treatment of dermal lesions and tattoos is more aggressive, it is associated with a higher risk of side effects than treatment of epidermal lesions. The most common side effect is the occurrence of pigmentary change. Hyperpigmentation is commonly seen in patients with darker skin phototypes but almost always resolves with time. Use of topical hydroquinone creams may help speed resolution. Patients at risk for hyperpigmentation should avoid sun exposure and use a UVA/UVB sunblock of SPF30 or higher for at least several months after treatment. Transient hypopigmentation is also common but true depigmentation is extremely rare. The risk of hypopigmentation is wavelength dependent, with shorter wavelength devices such as the QSRL posing higher risk due to greater injury to epidermal melanocytes. The risk of scarring with pigment-specific lasers is extremely low. When appropriate parameters are used, the risk of scarring from treatment of epidermal lesions is negligible. Preoperative photographs provide essential documentation. REFERENCES 1. 2.

Goldman L, Blaney DJ, Kindel DJ, Franke EK. Effect of the laser beam on the skin:preliminary report. J Invest Dermatol 1963; 40:121 – 122. Goldman L, Wilson RG, Hornby P, Meyer RG. Radiation from a Q-switched ruby laser: effect of repeated impacts of power output of 10 megawatts on a tattoo of man. J Invest Dermatol 1965; 44:69 – 71.

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Ohshiro T, Maruyama. The ruby and argon lasers in the treatment of naevi. Ann Acad Med 1983; 12:388 – 395. Dover JS, Smoller BR, Stein RS, Rosen S, Arndt KA. Low-fluence carbon dioxide laser irradiation of lentigines. Arch Dermatol 1988; 124:1219– 1224. Anderson RR, Parrish JA. Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science 1983; 220:524 – 527. Anderson RR, Parrish JA. The optics of human skin. J Invest Dermatol 1981; 77:13– 19. Polla LL, Margolis RJ, Dover JS, Whitaker D, Murphy GF, Jacques SL, Anderson RR. Melanosomes are a primary target of Q-switched ruby laser irradiation in guinea pig skin. J Invest Dermatol 1987; 89:281 – 286. Hodersdal M, Bech-Thomsen N, Wulf HC. Skin reflectance-guided laser selections for treatment of decorative tattoos. Arch Dermatol 1996; 132:403– 407. Taylor CR, Anderson RR, Gange RW, Michaud NA, Flotte TJ. Light and electron microscopic analysis of tattoos treated by Q-switched ruby laser. J Invest Dermatol 1991; 97:131– 136. Ross EV, Naseef G, Lin C, Kelly M, Michaud N, Flotte TJ, Raythen J, Anderson RR. Comparison of responses of tattoos to picosecond and nanosecond Q-switched Neodynium:YAG lasers. Arch Dermatol 1998; 134:167 – 171. Levins PC, Anderson RR. Q-switched ruby laser for the treatment of pigmented lesions and tattoos. Clinic Dermatol 1995; 13:75– 79. Murphy GF, Shepard RS, Paul BS, Menkes A, Anderson RR, Parrish JA. Organelle-specific injury to melanin-containing cells in human skin by pulsed laser irradiation. Lab Invest 1983; 49:680 – 685. Sherwood KA, Murray S, Kurban AK, Tan OT. Effect of wavelength on cutaneous pigment using pulsed irradiation. J Invest Dermatol 1989; 92:717 – 720. Margolis RJ, Dover JS, Polla LL, Watanabe S, Shea CR, Hruza GJ, Parrish JA, Anderson RR. Visible action spectrum for melanin-specific selective photothermolysis. Laser Surg Med 1989; 9:389 – 397. Anderson RR, Margolis RJ, Watenabe S, Flotte T, Hruza GJ, Dover JS. Selective photothermolysis of cutaneous pigmentation by Q-switched Nd:YAG laser pulses at 1064, 532, and 355 nm. J Invest Dermatol 1989; 93:28– 32. Ara G, Anderson RR, Mandel KG, Ottesen M, Oseroff AR. Irradiation of pigmented melanoma cells with high intensity pulsed radiation generates acoustic waves and kills cells. Laser Surg Med 1990; 10:52– 59. Dover JS, Margolis RJ, Polla LL, Watanabe S, Hruza GJ, Parrish JA, Anderson RR. Pigmented guinea pig skin irradiated with Q-switched ruby laser pulses. Arch Dermatol 1989; 125:43– 49. Hruza GJ, Dover JS, Flotte TJ, Goetschkes M, Watanabe S, Anderson RR. Q-switched ruby laser irradiation of normal human skin. Arch Dermatol 1991; 127:1799– 1805. Nakamura Y, Hossain M, Hirayama K, Matsumoto K. A clinical study on the removal of gingival melanin pigmentation with the CO2 laser. Laser Surg Med 1999; 25:140 – 147. Ross EV, Ladin Z, Kreindel M, Dierickx C. Theoretical considerations in laser hair removal. Dermatol Clinic 1999; 17:333– 355. Ueda S, Imayama S. Normal-mode ruby laser for treating congenital nevi. Arch Dermatol 1997; 133:355 – 359. Imayama S, Ueda S. Long- and short-term histological observations of congenital nevi treated with the normal-mode ruby laser. Arch Dermatol 1999; 135:1211 – 1218. Gold MH, Foster TD, Bell MW. Nevus spilus successfully treated with an intense pulsed light source. Dermatol Surg 1999; 25:254 – 255. Taylor CR, Anderson RR. Treatment of benign pigmented epidermal lesions by Q-switched ruby laser. Int J Dermatol 1993; 32:908– 912. Tse Y, Levine VJ, McClain SA, Ashinoff R. The removal of cutaneous pigmented lesions with the Q-switched ruby laser and the Q-switched neodynium:yttrium – aluminum – garnet laser. J Dermatol Surg Oncol 1994; 20:795– 800. Kilmer SL, Wheeland RG, Goldberg DJ, Anderson RR. Treatment of epidermal pigmented lesions with the frequency-doubled Q-switched Nd:YAG laser. Arch Dermatol 1994; 130:1515–1519.

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Grevelink JM, van Leeuwen RL, Anderson RR, Byers R. Clinical and histological responses of congenital melanocytic nevi after single treatment with Q-switched lasers. Arch Dermatol 1997; 133:349 – 353. Waldorf HA, Kauvar ANB, Geronemus RG. Treatment of small and medium congenital nevi with the Q-switched ruby laser. Arch Dermatol 1996; 132:301 – 304. Vibhagool C, Byers R, Grevelink JM. Treatment of small nevomelanocytic nevi with a Q-switched ruby laser. J Am Acad Dermatol 1997; 36:738 – 741. Rosenbach A, Williams CM, Alster TS. Comparison of the Q-switched alexandrite (755 nm) and Q-switched Nd:YAG (1064 nm) lasers in the treatment of benign melanocytic nevi. Dermatol Surg 1997; 23:239 –245. Duke D, Byers R, Sober AJ, Anderson RR, Grevelink JM. Treatment of benign and atypical nevi with the normal-mode ruby laser and the Q-switched ruby laser: clinical improvement but failure to completely eliminate nevomelanocytes. Arch Dermatol 1999; 135:290 – 296. Milgraum SS, Cohen ME, Auletta MJ. Treatment of blue nevi with the Q-switched ruby laser. J Am Acad Dermatol 1995; 32:307 – 310. Arndt KA. Argon laser treatment of lentigo maligna. J Am Acad Dermatol 1984; 10:953 – 957. Kopera D. Treatment of lentigo maligna with the carbon dioxide laser. Arch Dermatol 1995; 131:735 – 736. Thissen M, Westerhof W. Lentigo maligna treated with ruby laser. Acta Derm Venereol 1997; 77:163. Arndt KA. New pigmented macule appearing 4 years after argon laser treatment of lentigo maligna. J Am Acad Dermatol 1986; 14:1092. Lee PK, Rosenberg CN, Tsao H, Sober AJ. Failure of Q-switched ruby laser to eradicate atypical-appearing solar lentigo: report of two cases. J Am Acad Dermatol 1998; 38:314 – 317. Taylor CR, Anderson RR. Ineffective treatment of refractory melasma and postinflammatory hyperpigmentation by Q-switched ruby laser. J Dermatol Surg Oncol 1994; 20:592 – 597. Nouri K, Bowes L, Chartier T, Romagosa R, Spencer J. Combination treatment of melasma with pulsed CO2 laser followed by Q-switched alexandrite laser: a pilot study. Dermatol Surg 1999; 25:494 –497. Manaloto RMP, Alster T. Erbium:YAG laser resurfacing for refractory melasma. Dermatol Surg 1999; 25:121 –123. Lowe NJ, Wieder JM, Shorr N, Boxrud C, Saucer D, Chalet M. Infraorbital pigmented skin: preliminary observations of laser therapy. Dermatol Surg 1995; 21:767 – 770. West TB, Alster TS. Improvement of infraorbital hyperpigmentation following carbon dioxide laser resurfacing. Dermatol Surg 1998; 24:615 – 616. Dwyer CM, Cuddihy AM, Kerr REI, Chapman RS, Allam BF. Skin pigmentation due to minocycline treatment of facial dermatoses. Br J Dermatol 1993; 129:158 – 162. Argenyi ZB, Finelli L, Bergfeld WF et al. Minocycline-related cutaneous hyperpigmentation as demonstrated by light microscopy, electron microscopy and X-ray energy spectroscopy. J Cutan Pathol 1987; 14:176– 180. Collins P, Cotterill JA. Minocycline-induced pigmentation resolves after treatment with the Q-switched ruby laser. Br J Derm 1996; 135:317– 319. Knoell KA, Milgraum SS, Kutenplon M. Q-switched ruby laser treatment of minocyclineinduced cutaneous hyperpigmentation. Arch Dermatol 1996; 132:1251– 1253. Tsao H, Dover JS. Treatment of minocycline-induced hyperpigmentation with the Q-switched ruby laser. Arch Dermatol 1996; 132:1250 – 1251. Wilde JL, English JC, Finley EM. Minocycline-induced hyperpigmentation: treatment with the neodynium:YAG laser. Arch Dermatol 1997; 133:1344 – 1346. Greve B, Schonermark MP, Raulin C. Minocycline-induced hyperpigmentation: treatment with the Q-switched Nd:YAG laser. Laser Surg Med 1998; 22:223– 227. Karrer S, Hohenleutner U, Szeimies RM, Landthaler M. Amiodarone-induced pigmentation resolves after treatment with the Q-switched ruby laser. Arch Dermatol 1999; 135:251 – 253. Trotter MJ, Tron VA, Hollingdale J, Rivers JK. Localized chrysiasis induced by laser therapy. Arch Dermatol 1995; 131:1411 – 1414.

25 Laser Treatment of Tattoos Suzanne L. Kilmer Laser and Skin Surgery Center of Northern California, Sacramento, California, USA

1. Introduction 2. Laser Treatment 2.1. Thermal Tissue Destruction with Lasers 3. Pulsed Laser Treatment of Tattoos 4. Q-Switched Lasers 4.1. Q-Switched Ruby Laser (694 nm) 4.2. Q-Switched Nd:YAG Laser (1064 nm) 4.3. Q-Switched Nd:YAG Laser (532 nm) 4.4. Q-Switched Alexandrite Laser 4.5. Candela PDPL (510 nm, 300 ns) 5. Q-Switched Laser Treatment in General 5.1. Recommended Treatment Parameters 5.2. Number of Treatments 5.3. Treatment Intervals 6. Side Effects 6.1. Pigmenting and Textural Changes 6.2. Allergic Reactions 6.3. Ink Darkening 6.4. Epidermal Debris 7. Comparative Studies of Q-Switched Lasers References

1.

505 506 506 507 508 508 509 510 510 511 511 511 512 512 512 513 513 513 514 514 515

INTRODUCTION

Decorative tattoos appear to fulfill an inherent need as evidenced by their popularity throughout time and across many cultures and continents (1). Removal of these personal markings as well as traumatic tattoos [e.g., asphalt (Fig. 25.1), pencil lead, gun powder] and tattoos placed for identification purposes [e.g., radiation port sites, gang members (Fig. 25.2), prisoners of war] is often desired. Unfortunately, in the past, tattoo was usually replaced by an equally undesirable scar. Many different methods for tattoo removal have been explored. Older techniques involve destruction or removal of the outer skin layers by mechanical (dermabrasion, 505

506

Kilmer

Figure 25.1 Traumatic tattoo from motor vehicle accident and impact with pavement before (a) and after (b) 2 Q-switched Nd:YAG laser treatments (1064 nm, 6 mm, 4 – 5 J/cm2).

salabrasion, excision), chemical, or thermal (direct heat, cautery, infrared coagulator) means, accompanied by inflammation. Transepidermal elimination of pigment occurs through denuded skin (2 –5) with the exudative phase allowing tattoo pigment to migrate to the wound surface to be absorbed onto the dressing. The accompanying inflammatory response may also promote macrophage activity with increased phagocytosis facilitating additional pigment loss during the healing phase. Newer techniques centered on the use of lasers, sometimes with other adjuvant treatments. Most recently, Q-switched lasers have been shown to effectively lighten, if not permanently remove, most tattoos with minimal or no change to the surrounding skin. 2. 2.1.

LASER TREATMENT Thermal Tissue Destruction with Lasers

The early work with lasers was attempted in the hope that they would offer a precise means of inducing predictable thermal necrosis to tattoo-containing tissue in a manner that would

Figure 25.2 Gang related tattoos before (a) and after (b) 2 Q-switched Nd:YAG treatments (1064 nm, 6 mm spot size, 4– 5 J/cm2). Note that the tattoos are lighter, but residual ink remains.

Laser Treatment of Tattoos

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minimize or eliminate scarring. Tattoo removal with the ruby and argon laser was first proposed by Goldman in 1963 (6), and a relatively enthusiastic report of the normal mode ruby laser (7) was soon followed by ones using Q-switched ruby lasers (QSRLs) (8 –12). These early reports were largely ignored for 15 years as attention focused on the newly emerging field of argon and CO2 laser surgery. The initial use of the argon laser for treatment of tattoos was based on selective absorption of energy with vaporization from its 488 and 514 nm wavelengths by complementary tattoo pigment colors (13 – 15). Unfortunately, the clinical usefulness of this factor is severely limited by melanin and hemoglobin absorption of laser energy, resulting in unwanted thermal damage to tissue and a high incidence of hypertrophic scarring (Fig. 25.3) (15,16). With the CO2 laser, tattoo pigment is removed by direct vaporization, as well as by thermal necrosis of adjacent tissue with transepidermal loss during the exudative healing phase. Dermal tissue is replaced by fibrosis and scar tissue. Recently applied tattoos responded more readily to treatment with the CO2 and argon lasers presumably because pigment is more uniformly superficial in the papillary dermis, lying free rather than within dermal fibroblasts (particularly during the first month after application). Because of the increased risk of scarring, the CO2 and argon lasers are now rarely used, although new high-powered CO2 and erbium lasers can play a role in removing tattoo ink that is inciting an allergic reaction (see what follows).

3.

PULSED LASER TREATMENT OF TATTOOS

The principle of selective photothermolysis revolutionized the treatment of tattoos. Anderson and Parrish (17) proposed that if a wavelength was well absorbed by the target and the pulse width was equal to or shorter than the target’s thermal relaxation time, the heat generated would be confined to the target. To specifically target tattoos, both the laser wavelength and pulse duration must be appropriately chosen. One of the earliest studies of pulsed laser treatment of tattoos (16) examined the effects of a tunable dye laser at three wavelengths (505, 577, and 680 nm) using a 1 ms pulse to remove black, blue, red, and white tattoo pigments. They found that the threshold dose to induce the same histologic changes was much less than that required for the argon laser, and that each wavelength reacted only with complementary colors of tattoo pigment.

Figure 25.3 Hypertrophic scar from CO2 laser treatment (right edge of tattoo) immediately adjacent to an area where impacts from a QSRL can be seen. Note there is no textural change and excellent clearing with the single QSRL treatment.

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Despite the short 1 ms pulse width, widespread tissue necrosis was observed and tattoo lightening occurred only as a result of significant dermal necrosis and resultant fibrosis, suggesting that even shorter nanosecond pulses would interact best with the micronsized pigment granule’s approximate thermal relaxation time. The optimal wavelength achieves selective absorption for that ink color while minimizing absorption by the primary endogenous chromophores, hemoglobin and melanin. Reflectance spectra data for tattoo ink colors may aid in choosing the best available wavelength. Black pigment is absorptive at all wavelengths (having minimal reflectance), and competition from melanin absorption in the epidermis decreases gradually as wavelength increases. Absorption for blue and green is greatest for wavelengths of 600 – 800 nm, whereas red absorbs best below 575 nm, tan below 560 nm, flesh-colored pigment below 535 nm, and yellow below 520 nm (18). The best pulse duration to match the micron-sized particles is in the nanosecond (or shorter) domain.

4. 4.1.

Q-SWITCHED LASERS Q-Switched Ruby Laser (694 nm)

In the early 1960s (7,8) Goldman studied the reaction of a dark blue tattoo to a microsecond pulsed ruby laser and a nanosecond QSRL. Nonspecific thermal necrosis was noted with microsecond impacts, whereas nanosecond impacts only produced transient edema accompanied by a peculiar whitening of the impact area, lasting about 30 min. Although originally interpreted as a failure, continued monitoring showed gradual fading of the treated area. Three years later others confirmed and expanded these results (11,12) using a QSRL to successfully remove blue and black tattoo pigments without tissue damage. Biopsies performed after 3 months showed absence of tattoo pigment and no evidence of thermal damage. Reid et al. reported good results on removal of black pigment in professional and amateur tattoos, but noted several disadvantages: the need for multiple treatments (often 6), the potential for scarring (emphasizing the need to use relatively low powers but above the threshold to produce immediate tissue whitening), and a treatment interval of at least 3 weeks to allow for tissue healing and pigment removal by macrophages (19). Studies of the QSRL preferentially damaging melanized cells in animal skin (20,21) and the tattoo studies previously cited, stimulated Taylor et al. to complete a detailed dose –response study (22) using a 40– 80 ns pulsed QSRL, 1.5 – 4 J/cm2. Overall results were excellent in 78% of amateur tattoos, but only 23% of professional tattoos. Despite these discouraging statistics, the authors were optimistic that the QSRL would develop into a preferred treatment for tattoos, because of the rare scarring. Competitive absorption by melanosomes led to hypopigmentation in 39% (low fluences) to 46% (higher fluences) which slowly resolved in most cases. Later studies (23,24) reported increased efficacy with higher fluences. Newer ruby lasers with shorter pulse durations (25 ns), higher fluences (8–10 J/cm2), and/or a better beam quality more rapidly clear tattoos (25 –28). Kilmer and Anderson (29) initiated treatment at a fluence of 6 – 8 J/cm2 with a 40 – 80 ns pulse width and reported black and green ink to be most responsive, with other colors requiring significantly more treatments. Amateur tattoos typically required fewer (usually 4– 6) treatments than professional tattoos (usually 6 –10), but in some instances up to 20 treatments were needed. Brisk, bright whitening of the treated area immediately following the laser pulse seems to signify sufficient fluence for effective lightening of the ink. Acceptable clearing


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varies from patient to patient, with some individuals more accepting of vague residual pigment. In summary, the QSRL is remarkably effective in removing tattoos with minimal scarring, although multiple treatment sessions are necessary. Hypopigmentation is common and, although usually transient, (2– 6 months), may be permanent (29). Transient hyperpigmentation is also common and seems to be more related to skin type than laser treatment. Scarring and textural changes occur more rarely. The risk of adverse tissue response and speed of clearing both appear to be fluence and pulse width related, with higher fluences and shorter pulses being more effective but causing more nonspecific tissue damage as well. The ruby laser is very effective for removing black, blue –black, and green ink, although green ink can be difficult, even though reflectance spectra predict that it should respond well at 694 nm. Other colors are poorly responsive to the ruby laser. The laser has a repetition rate of 1 pulse every 1– 2 s. Bleeding and tissue splatter can be cumbersome, but use of a larger spot size with a lower fluence is equally efficacious with less tissue splatter and the use of a cone device protects the operator from exposure.

4.2.

Q-Switched Nd:YAG Laser (1064 nm)

Addition of a Q-switching device to the solid state Nd:YAG laser was then explored in anticipation that its longer wavelength (1064 nm) would increase dermal penetration and decrease melanin absorption, improving the response of ruby laser-resistant tattoos and avoiding pigmentary changes. An initial report showed the Nd:YAG laser to be equal to the ruby laser in removal of blue –black tattoos at 6 J/cm2 with lower incidence of hypopigmentation and skin texture changes. Green and red pigments were not removed with the 1064 nm Nd:YAG laser, whereas some green pigment was removed with the ruby laser (30). The ability of the Q-switched Nd:YAG laser (1064 nm, 10 ns) to remove pigment in ruby-resistant tattoos was assessed in the treatment of 28 tattoos using fluences of 6 – 12 J/cm2 (31). Kilmer et al. investigated both ruby-resistant and previously untreated tattoos in a prospective, blinded, dose – response study using the Q-switched Nd:YAG laser (1064 nm, 10 ns, 2.5 mm spot size) (32). Twenty-five professional and 14 amateur tattoos were treated in quadrants using 6, 8, 10, and 12 J/cm2. Four treatment sessions were performed at 1 month intervals. In most cases, .50% lightening of residual tattoo ink was noted with the first treatment with the greatest improvement seen with higher fluences. After 4 treatments, .75% ink removal was seen in 77% and .95% ink removal was seen in 28% of black tattoos (11/39) treated at 10 –12 J/cm2. There was no significant difference in the response of previously untreated tattoos and ruby-resistant tattoos. Treatment at the highest fluence (12 J/cm2) proved to be significantly more effective at removing black tattoo ink than the lower two doses. Green, yellow, white, red, purple, and orange inks responded minimally. Although textural changes were noted during the course of treatment, these cleared with time and only 2/39 tattoos were graded as having trace present textural changes. No hypopigmentation and a single case of hyperpigmentation were noted. These results were similar to those reported by Ferguson and August (33). The lack of scarring both clinically and histologically, despite the increased bleeding and tissue splatter seen, is most likely due to the lack of thermal injury to collagen. The dermis and epidermis sustain mechanical injury from the photoacoustic wave, but this trauma is apparently highly reparable. Textural changes generally resolve within 4 –6 weeks, suggesting an optimal treatment interval of 6 weeks or longer.

510

Kilmer

The Q-switched Nd:YAG laser is very advantageous for treating darker skinned patients. Both Jones et al. (34) and Grevelink et al. (35) demonstrated effective tattoo removal with minimal hypo- or hyperpigmentation. This provides a significant benefit over the QSRL for darker skinned patients where melanin absorption is a hindrance. 4.3.

Q-Switched Nd:YAG Laser (532 nm)

A frequency-doubling crystal converts 1064 –532 nm green light, which is absorbed well by red ink, as well as melanin and hemoglobin. Greater than 75% removal of red ink has been reported with four treatment sessions. Orange and some purples respond almost as well; however, yellow ink responds poorly, presumably because of the dramatic drop in absorbance between 510 and 520 nm (18). Because of its absorbance by the competing endogenous chromophores, melanin, and hemoglobin, blistering and purpura frequently occur with 532 nm use. In summary, the Q-switched Nd:YAG laser has proven to be somewhat more effective in removal of black ink with rare textural changes and almost no hypopigmentation [Fig. 25.4(a) and (b)]. The improved efficacy is attributed to the longer wavelength, higher fluence, and shorter pulse width. The same factors cause more bleeding and tissue splatter during treatment, making the treatment itself more cumbersome. The faster repetition rate (1 –10 Hz) shortens the treatment session. Larger spot sizes up to 6 mm are now available with new, higher-powered Nd:YAG laser systems, enabling deeper penetration and more effective treatment of deeper, denser tattoos (36). Better beam profiles have minimized epidermal damage, decreased bleeding, tissue splatter, and transient textural changes. Often little wound care is needed. The frequency-doubling crystal emits green light thereby targeting red ink and increasing the utility of this laser. 4.4.

Q-Switched Alexandrite Laser

The Q-switched alexandrite laser has a wavelength of 755 nm, a pulse width of 50– 100 ns, and a repetition rate of 1 Hz (37 –40). The 3 mm diameter beam is delivered via a fiberoptic system or an articulated arm. Reflectance studies at 755 nm suggest excellent absorption by black pigment, good absorption by blue and green, and poor absorption by red pigments. One treatment session in a tattooed Yucatan pig provided excellent

Figure 25.4

Blue– black tattoo before (a) and after (b) 8 QS Nd:YAG (1064 nm) treatments.


511

results in removal of black ink, good results with blue and green, and poor results with red ink with efficacy being fluence related (41). Fitzpatrick et al. then studied the Q-switched alexandrite laser (41) on tattoos using fluences of 4.5 –8 J/cm2. Approximately 25% clearing of tattooed pigment required 1.7 treatments, 50% clearance required 2.8 treatments, 75% clearance required 5 treatments, 90% clearance required 6.4 treatments, and total clearance required 10.4 treatments (range 4 – 16). Professional tattoos cleared as well as amateur tattoos although the latter were more rapidly responsive, requiring approximately three fewer treatments to reach complete clearance although some professional tattoos responded rapidly as well. About half of the patients develop transient hypopigmentation, but it is often not apparent until after 5– 7 treatment sessions and typically resolves .1– 12 months. As with the other Q-switched lasers, hyperpigmentation is more dependent on skin type and clears with hydroquinone and sunscreen. Although transient surface textural changes have been noted in 10% of patients, all resolved within 3 –9 months, except one patient who developed a small scar secondary to excoriating a treated area. On laser impact, there is an immediate flash of white light from the tattoo followed by epidermal whitening and slight edema as seen with both the Q-switched ruby and the Q-switched Nd:YAG lasers. When higher fluences are used, purpura is noticed, and pinpoint bleeding may occur. Tissue splatter and erosions were not seen at any of the fluences utilized with the 100 ns pulse width, but the shorter 50 ns pulse width, which reportedly increases tattoo clearance, is associated with more epidermal debris. In summary, the Q-switched alexandrite laser is effective and safe for removing blue, black, and green tattoo pigments. Four to ten treatments performed at 1–2 month intervals usually clear the tattoo without scarring; however, half of the patients develop transient hypopigmentation. 4.5.

Candela PDPL (510 nm, 300 ns)

The flashlamp pulsed laser (510 nm, pulse width of 300 + 100 ns), initially developed as a companion to the Q-switched alexandrite laser for the treatment of epidermal melanocytic lesions, is no longer commercially available. This wavelength is also well absorbed by red pigment and the pulse width is short enough to fragment ink granules. Successful ink clearing without scarring usually occurred in 3 –7 treatments performed at 1 month intervals using 3 – 3.75 J/cm2 (42). Purple, orange, and yellow pigments required an average of 5 treatments for complete ink removal. No hypopigmentation, textural change, or scarring was noted. Histologically, fragmentation of red pigment particles is observed followed by macrophage engulfment. In addition, because of the epidermal absorption of this laser, some transepidermal ink loss occurs.

5. 5.1.

Q-SWITCHED LASER TREATMENT IN GENERAL Recommended Treatment Parameters

The main parameters to be chosen include pulse duration, wavelength, fluence, and spot size. All Q-switched lasers are in the nanosecond domain and the pulse width is predetermined by the laser used. The wavelength is chosen on the basis of the best available wavelength for the tattoo ink color to be treated. In other words, red ink is best treated by a green wavelength (510 or 532 nm) and green ink is best treated by a red wavelength (694 or 755 nm). When melanin is present, the 1064 nm wavelength is the best choice to avoid disrupting the epidermis.

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Fluence should be sufficient to produce immediate whitening, but immediate bleeding or blistering should be avoided. Larger spot sizes allow more forward scattering for deeper penetration and should be utilized as long as sufficient fluence can be obtained. This will maximize distribution of laser light to the dermal pigment and minimize epidermal injury (36). 5.2.

Number of Treatments

It is difficult to predict the number of treatment sessions necessary for tattoo removal. Initial treatment sessions frequently produce a more dramatic response than subsequent sessions. Very definite sites of clearing, corresponding to laser impacts, are often visible. Other tattoos are strongly unresponsive during early treatment phases, even though biopsies reveal fragmentation of tattoo granules. The explanation of these differences in response from one patient to another is likely to involve the efficiency of mobile macrophages in removal of fragmented tattoo pigment debris, as well as the density, amount, and molecular basis of the tattoo pigment present. The speed of the macrophage response, as well as the maximum amount of pigment removed per session, likely varies from patient to patient and to some extent from treatment to treatment. The more superficial the tattoo pigment and the lesser the total volume of tattoo pigment, the fewer the number of treatments likely to be needed to remove the pigment. Traumatic tattoos typically respond well to Q-switched lasers (43) [Fig. 25.1(a) and (b)] likely because of their predominant superficial location and carbon-based pigment. Textural changes and any accompanying hypertrophic or granulomatous scars associated with the inciting trauma are often improved as well. 5.3.

Treatment Intervals

The recommended treatment interval has lengthened over the past decade from 3– 4 weeks to 8 weeks, although the optimal treatment interval is poorly understood. In a study with the Q-switched alexandrite laser, three treatment intervals were compared: a condensed treatment protocol (37) comprising 3 treatments 7– 10 days apart followed by a 3 month wait, 3 treatments at 1 month intervals (15,16), and 3 treatments 2 –3 months apart. All resulted in 50% clearing after the three treatment sessions. There was essentially no difference in the rate of tattoo clearing noted. However, as the number of treatments increases, the potential for tissue reaction increases as well; therefore, occasional rest periods or longer treatment intervals of 2 –3 months are recommended to allow recovery of melanin as well as normalization of any transient textural changes to avoid adverse responses. Higher fluences and shorter pulse widths appear to remove tattoo pigment more rapidly but have the potential of inducing excessive shock wave tissue reaction, and therefore must be balanced with the desire to remove pigment without scarring or hypopigmentation. Therefore, the current recommendation is to treat at 2 month intervals unless a longer period is needed for tissue recovery. These longer intervals also likely to maximize the amount of tattoo ink particles removed by the macrophages.

6.

SIDE EFFECTS

In contrast to previous modalities, the Q-switched lasers are much more effective with very few side effects which are discussed in what follows.


6.1.

513

Pigmenting and Textural Changes

The increased melanin absorption seen with shorter wavelengths increases the risk for hypopigmentation. With the 510 and 532 nm wavelengths, the hypopigmentation typically resolves; however, with the QSRL, long term hypopigmentation is possible. Hyperpigmentation, however, is more related to the patient’s skin type with darker skin more prone to this no matter which wavelength is used. Treatment with hydroquinones and broad spectrum sunscreens will usually resolve the hyperpigmentation within a few months, although in some cases it can be more prolonged. Transient textural changes are often noted but resolve ,1– 2 months, whereas permanent textural changes or scarring are, luckily, very rare. If a patient is more prone to pigmentary or textural changes, longer treatment intervals are recommended. 6.2.

Allergic Reactions

Local allergic responses to many tattoo pigments have been reported (44 – 46), and allergic reactions to tattoo pigment after Q-switched laser treatment are also possible (47). Unlike the destructive modalities previously described, Q-switched lasers mobilize the ink and may generate a systemic allergic response (48). If an allergic reaction to the ink has been noted, Q-switched laser treatment is not advised. The erbium and high-energy, pulsed CO2 lasers can be used to de-epithelialize the tattoo, promoting transepidermal elimination of the ink (49). Multiple treatments are required and the risk for dyspigmentation and scarring is increased. Use of oral antihistamines and anti-inflamatory steroids such as prednisone have also been used (47). 6.3.

Ink Darkening

Paradoxical darkening of flesh-tone, red, and white tattoo inks with Q-switched ruby, Q-switched Nd:YAG, and Q-switched alexandrite laser treatment has been reported (50) [Fig. 25.5(a) and (b)]. In vitro tests with various tattoo pigments in agar have found that a surprising number of pigments (most containing iron oxide or titanium dioxide) will change color when irradiated with Q-switched laser energy (50,51). Iron oxide is known to change color from brown to black when raised to a temperature .14008C as ferric oxide is ignited. In clinical practice, tattoo pigments of multiple colors, including flesh tones, red, white, and brown (iron oxide, titanium dioxide) and even several green and blue tattoo pigments have changed to black when irradiated

Figure 25.5 Red lipliner tattoo immediately after a single test site (QS Nd:YAG 1064 nm) which demonstrates ink darkening (a). One month later the darkened ink at the test site had cleared and the entire tattoo was then treated which resulted in 90% clearing after single treatment (b).

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with Q-switched laser pulses, likely via this oxidation-reduction reaction or ignition of ferric oxide above 14008C. These reactions require the extreme temperatures known to be generated during the very short pulse of Q-switched lasers; several hundreds to thousands of degrees are estimated. Laser treatment of cosmetic tattoos, especially red or flesh-tone ones must be approached with caution. The resultant gray –black tattoo may be difficult to remove and is certainly more visible than a flesh-tone; therefore, test sites are recommended with good patient consent. If pigment darkening occurs, one can immediately re-treat the area then wait several weeks to assess the darkened tattoos response. If it has lightened significantly, treatment can proceed. Q-switched lasers appear to be ideal for removal of large areas of black facial tattoos (tarsal fanning of pigment, eyebrow tattoo). However, the beam size (2 – 6.5 mm) may make removal of small dots of precisely confined tattoo pigment, as found in eyeliner tattoo, technically difficult without temporary or permanent hair loss from heat damage to the terminal hair. The use of high fluences and very short pulses with the Q-switched lasers may increase the risk of tissue reaction and should be approached with caution. The potential irreversible pigment darkening induced by laser interaction with iron oxide or titanium dioxide pigments warrants a test site as noted previously. Selected cases, especially eyeliner tattoos, may be treated with highpowered CO2 and erbium lasers because of the precision available and/or the need to bypass the ink darkening phenomenon.

6.4.

Epidermal Debris

These high-energy short pulses cause a pressure shock wave that ruptures blood vessels and aerosolizes tissue with potentially infectious particles, requiring the use of a protective barrier or cone device to protect the operator from tissue and blood contact. The use of lower fluences eliminates this problem to a large degree but results in the need for more treatment sessions. The occurrence of scarring or tissue textural changes has also been attributed to hot spots within the beam and pulse-to-pulse variability (52). Maintaining a high-energy output but with a larger spot size, which decreases the fluence, is equally effective with less hazard to the operator and fewer side effects (less epidermal disruption) for the patient (36).

7.

COMPARATIVE STUDIES OF Q-SWITCHED LASERS

Direct comparison studies of the various available wavelengths are difficult as treatment parameters including pulse width, spot size, and fluence are hard to standardize and results are, therefore, often inconclusive. Several comparative studies have been done using different lasers on the same tattoos. A comparison of the ruby and Nd:YAG lasers (32) found them to be equally effective in removal of black ink, but the ruby laser was more effective for green ink. A second comparison of the ruby and Nd:YAG lasers was limited to one treatment session (53), and a similar response was noted. After 1 month, the Nd:YAG was judged to cause more textural change and hyperpigmentation than the ruby laser (possibly related to the smaller spot size used) and the ruby laser caused more hypopigmentation. Comparisons between the Q-switched ruby and alexandrite lasers revealed the ruby laser to remove more pigments as well as cause more textural changes, hypopigmentation, and hair loss (54). A comparison at two to three treatment sessions may not be optimal as only 50– 60% of the tattoo has been


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removed and speed and efficacy of tattoo removal as well as the avoidance of textural changes, scarring, hair loss, and pigment alterations must be examined. In summary, Q-switched lasers provide a dramatic improvement over previous modalities for tattoo removal. Appropriate wavelength choice will facilitate clearing of multicolored tattoos. Cosmetic tattoos should be approached with caution. In addition, exploration into the use of picosecond lasers is underway and may further enhance our ability to treat tattoos (55,56).

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19. 20. 21. 22. 23.

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Kaufmann R, Hibst R. Pulsed erbium. YAG laser ablation in cutaneous surgery. Lasers Surg Med 1996; 19(3):324– 330. Anderson RR, Geronemus R, Kilmer SC et al. Cosmetic tattoo ink darkening: a complication of Q-switched and pulsed-laser treatment. Arch Dermatol 1993; 8:1010. The transition elements. In: Cotton FA, Wilkinson G, eds. Advanced Inorganic Chemistry. New York: Interscience Publishers, 1972. Kilmer SL, Casparian JM, Wimberly JM, Anderson RR. Hazards of Q-switched lasers. Lasers in Surg Med 1993; (suppl 5):56. Levine V, Geronemus R. Tattoo removal with the Q-switched ruby laser and the Q-switched Nd:YAG laser: a comparative study. Cutis 1995; 55(5):291 –296. McMeekin TO, Goodwin DP. A comparison of the alexandrite laser (755 nm) with the Q-switched ruby laser (694 nm) in the treatment of tattoos. Lasers Surg Med 1993; (suppl 5):43. Kilmer SL, Fitzpatrick RE, Da Silva LB, Marshall R, Ghiselli R. Picosecond and femtosecond laser treatment of tattoo ink. Lasers Surg Med 1996; (suppl 18):36. Ross V, Naseef G, Lin G, Kelly M, Michaud N, Flotte TJ, Raythen J, Anderson RR. Comparison of responses of tattoos to picosecond and nanosecond Q-switched neodymium:YAG lasers. Arch Dermatol 1998; 134(2):167– 171.

26 Carbon Dioxide Laser Treatment of Epidermal and Dermal Lesions in Principles and Practices in Cutaneous Laser Surgery Leslie C. Lucchina Aesthetic Dermatology, Department of Dermatology, Brigham and Women’s Hospital, Instructor in Dermatology, Harvard Medical School, Boston, Massachusetts, USA

Suzanne M. Olbricht Department of Dermatology, Lahey Clinic, Burlington and Department of Dermatology, Harvard Medical School, Boston, Massachusetts, USA

1. Background 2. Clinical Indications 2.1. Epidermal and Mucosal Lesions 2.1.1. Human Papillomavirus Disease 2.2. Dermal Lesions 2.3. Advantages and Limitations 2.4. Carbon Dioxide Laser Safety 3. Technique 4. Complications 5. Conclusion References

1.

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BACKGROUND

The use of the carbon dioxide laser in dermatology has greatly altered the path by which we treat many skin diseases and understand wound healing processes. The carbon dioxide laser emits far-infrared light at a wavelength of 10,600 nm and is absorbed by water. Directing carbon dioxide laser light energy on skin results in a heating and vaporization of intracellular water resulting in tissue vaporization. This tissue interaction can be harnessed by mechanical and/or manual manipulations of the beam, allowing for predictable vaporization. Carbon dioxide laser systems have been shown to be quite 519

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useful in the successful treatment of many epidermal and dermal skin lesions where there is no specific target chromophore other than water. The earliest carbon dioxide lasers, used clinically since 1960s, delivered the energy as a continuous wave beam. At that time, it was appreciated that if the energy of the carbon dioxide laser is emitted as a tightly focused beam with very high power densities, highly localized thermal destruction is produced which can be precisely directed using a terminal attachment to produce cutting. If the beam is unfocused and of a lower power density, it can be directed with precision to ablate cutaneous lesions. Ablation produced by the carbon dioxide laser occurs through vaporization and coagulative necrosis and is modified by wound healing. Further studies defined the nature of thermal damage created by carbon dioxide laser energy. Although the energy of continuous wave carbon dioxide lasers is absorbed in the upper 20 mm of a layer of water, skin absorption and evidence of thermal damage is affected by several factors: scatter of the laser energy in the tissue, spot size of the laser beam at the tissue surface, duration of exposure, and the amount of water within the tissue. Early instrumentation allowed for mechanical control of power output; however, spot size was controlled manually. As a prism in the hand piece focused the beam, holding the hand piece closer or farther from the skin could create effective spot sizes from 0.1 to 6 mm in diameter with varying power densities at the tissue surface. In addition, power density was affected by duration of exposure which was controlled by a mechanical shutter, foot pedal, or manual movement of the energy across the tissue surface. Despite these variables, for most clinical uses, it is assumed that continuous wave or shuttered pulsed carbon dioxide laser energy penetrates tissue .1 mm. In a guinea pig model, a laser beam with a power density of 10 kW/cm2, easily obtained with a 30 W commercially available carbon dioxide laser, takes 12.5 ms to penetrate 1 mm of skin in vivo. A laser beam with a power density of 1 kW/cm2 takes 125 ms to do so (1). The duration of energy delivery affects both vaporization and adjacent thermal damage. The volume of tissue vaporized varies directly with the power density at the tissue level. The width of the zone of thermal damage of the adjacent tissue (coagulation) is directly proportional to the duration of exposure. If exposure times are shorter than the time it takes the heated tissue to cool (termed thermal relaxation time), adjacent thermal damage is minimized, because there is no excessive heat energy available for diffusion (2). Therefore, a short laser exposure time with a high power density vaporizes the same volume of tissue as a longer exposure at a lower power density, but with much less adjacent thermal damage. Tissue damaging temperature elevations have been recorded as far as 2 mm from the wound edge (3). The area of adjacent thermal damage largely determines the extent of the wound and subsequent healing processes. During 1990s, carbon dioxide lasers with very short pulses (,1 ms) and high peak powers sometimes attached to rapid scanners were developed using the earlier principles (4). Pulsed and rapid beam scanner carbon dioxide lasers allow the rapid and precise ablation of tissue (20 mm of skin) with minimal residual thermal damage (50 – 150 mm) because the thermal relaxation time of the target tissue is 1 ms, a time, that is, slightly longer than the pulse duration of the laser (5). The development of mechanical means to control duration of exposure to laser energy opened up new applications for the use of carbon dioxide lasers such as resurfacing (Chapter 29). However, many of the techniques used in the 1980s remain useful in the treatment of some skin lesions.

2.

CLINICAL INDICATIONS

Table 26.1 identifies cutaneous disorders that may be successfully treated with the carbon dioxide laser. Laser treatment is the first choice for some of the disorders because of the

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Table 26.1 Epidermal Skin Lesions that may Be Treated by Ablation with the Carbon Dioxide Laser Actinic keratosis Condyloma acuminatum Epidermal nevus Inflammatory linear verrucous epidermal nevus Familial benign pemphigus (Hailey – Hailey disease) Keratosis follicularis (Darier– White disease) Lichen sclerosis Porokeratosis Verruca plantaris Verruca vulgaris

ease of the procedure, effectiveness, and minimal amount of surrounding tissue damage. The carbon dioxide laser may also be used as an alternative method of treatment for other cutaneous disorders in which the laser treatment achieves clinical results similar to results obtained by more conventional means, but facilitates the procedure, making it easier for the patient and the surgeon. The carbon dioxide laser may offer an additional therapeutic option for some patients with lesions that have not responded to conventional medical or surgical therapies. In the past 30 years, there have been many reports of skin disease treated with the carbon dioxide laser (6). Over this time period, many new lasers have been developed that have been shown to yield better results in the treatment of many skin lesions such as vascular lesions, lentigines, and tattoos. Frequent use of the laser for some procedures has also redefined its utility. For example, there have been reports of using the carbon dioxide laser in the cutting mode for the removal of simple lesions such as a pilar cyst or keloid. It is now appreciated that the ease of treatment and results are not different than the use of cold steel scalpel excision. Although superpulse and ultrapulse capabilities have broadened the utility of the carbon dioxide laser, some procedures are still more effective when done with a continuous wave beam or shuttered continuous wave beam. Ablating a wart successfully requires vaporizing and coagulating a large volume of tissue, which is more quickly produced by a continuous wave laser. If a carbon dioxide laser is being used for its hemostatic properties for cutting or ablation, a continuous wave or long pulse carbon dioxide laser should be used. 2.1.

Epidermal and Mucosal Lesions

Epidermal and mucosal lesions are easily accessible to treatment by the carbon dioxide laser. Carbon dioxide laser ablation is the treatment of choice for actinic cheilitis. Secondary to excessive sun exposure, actinic cheilitis is characterized histopathologically as atypical epidermal cells that are confined to the squamatizing mucosa of the lower lip. The carbon dioxide laser is used to ablate rapidly and precisely a thin layer of mucosal lower lip. The coagulated tissue and thermal debris separate in 3– 7 days. Re-epithelialization occurs within 4 weeks. Morbidity is minimal and results are excellent (7 –11). Cytologic atypia is absent at 6 months (12). Scarring is usually not seen. The incidence of charring is minimized by the selection of laser parameters that result in vaporization and not charring (13). With experience and dexterity, the surgeon can use the continuous wave beam for this procedure. The use of the superpulse laser has also been described and may allow for faster healing (14). It is useful to note that a very superficial wound will heal quickly but may not be sufficient for cure.

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Other epidermal processes for which the carbon dioxide laser is an effective treatment include squamous cell carcinoma in situ of the penis (erythroplasia of Queyrat) and vulva (15 – 17). Also reported is the use of the continuous wave carbon dioxide laser in the treatment of squamous cell in situ of the fingers (18). At these anatomically difficult surgical sites where there is a lack of hair follicles allowing extension of atypical cells more deeply in the tissue, superficial ablation of the lesion with surrounding wide margins is produced quickly and heals well. Balanitis xerotica obliterans (19,20), Zoon’s balanitis (21), oral florid papillomatosis (22), oral leukoplakia (23), and sublingual keratoses (24) may be treated in a similar fashion. The carbon dioxide laser has also been used to treat epidermal diseases that have failed medical therapy or are not amenable to conventional surgical excision, although the mechanism by which improvement occurs is not clear. These diseases usually have a superficial dermal component, and successful ablation probably extends to at least some coagulative changes at that tissue level. Disorders in this category include epidermal nevus (25), inflammatory linear verrucous epidermal nevus (ILVEN) (26), porokeratosis of Mibelli (27), lesions of familial benign pemphigus (Hailey – Hailey disease) (28), keratosis follicularis (Darier –White disease) (29), and lichen sclerosus et atrophicus (30). Paget’s disease of the skin often located in the genitalia can be treated this way though the patients need to be followed closely as extension occurs along adnexal structures and may give rise to reoccurrence if the coagulative changes do not extend to that level (31). 2.1.1. Human Papillomavirus Disease The carbon dioxide laser has been used extensively in the treatment of the manifestations of human papillomavirus (HPV) infection (32), verruca vulgaris, verruca plantaris, condyloma acuminatum (33), and Bowenoid papulosis. HPV is a family of at least 70 known subtypes that cause epithelial or mucosal hyperplasia and may cause squamous cell atypia as is best described for Bowenoid papulosis. For some subtypes, evidence has mounted for the progression to frank carcinoma in cervical and anogenital lesions (34,35), in immunosuppressed patients (36 –38), and even in otherwise healthy patients (39). Given that the pathologic process resides on the surface, it appeared that treatment using the carbon dioxide laser would be effective; however, cure rates vary from 32% to 70% (40 –46) with the lower figures in studies of recurrent warts. The significant recurrence rate of warts after treatment with the carbon dioxide laser is not entirely clear. However, it may be related to the persistence of the virus in clinically adjacent uninvolved skin. In a study of women with vulvar warts, the HPV was found a centimeter from lesional skin (44). There is considerable morbidity associated with the carbon laser treatment of warts located on glabrous skin. The wound healing time is 2 –3 weeks for wounds on the hands and 3 –6 weeks for wounds on the feet. Complications include significant post-operative pain, temporary loss of function, atrophic scarring, and rarely infection and hypertrophic scarring. For patients with mucosal or anogenital lesions, the morbidity may be less than for other means to treat the lesions and scarring is usually not seen. Given these considerations, carbon dioxide laser treatment of warts may be best reserved for those warts recalcitrant to other means of treatment, warts that are particularly large and bulky, or warts that are anatomically located where the use of the carbon dioxide laser may facilitate treatment. In particular, extensive areas of involvement in the anogenital skin can be treated easily. For large, exophytic and bulky warts, the carbon dioxide laser may be used to first cut excessive tissue followed by vaporization.

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As the rate of recurrence is high, the patient should be aware that the HPV would probably not be eradicated and long-term observation must be done in treated patients where there is potential for malignant degeneration. 2.2.

Dermal Lesions

Dermal lesions that are extensive and at least partially extrude above the surrounding normal epidermal surface are particularly well suited for treatment with carbon dioxide vaporization. In comparison to standard surgical excision and closure or electrosurgery, the use of the carbon dioxide laser allows for faster removal of a greater number of lesions. Even atrophic scarring after treatment of multiple or confluent tumors may be a marked cosmetic improvement (47,48). Good results are reported for the treatment of adenoma sebaceum and angiofibromas (49,50) in tuberous sclerosis, apocrine hidrocystomas (51), cylindromas (52), leiomyomas (53), neurofibromas (54), syringomas (55,56), trichilemmomas of Cowden’s disease (57), pearly penile papules (58,59) and trichoepitheliomas (60,61). Other dermal lesions that have been treated successfully with the carbon dioxide laser include chondrodermatitis nodularis helicis (62), granuloma faciale (63), hidradenitis suppurativa (64), myxoid cyst (65), nodular amyloidosis (66), pyogenic granuloma (67), xanthomas (68), and xanthelasma (69) (Table 26.2). The carbon dioxide laser may add another therapeutic choice in difficult to treat diseases such as lichen sclerosis (70). While lymphangioma circumscriptum has been treated with relative success (71,72), the process is usually fed by deep vascular abnormalities and may recur at some point. The first laser treatment of tattoos was with the carbon dioxide laser used to vaporize overlying epidermis, then the pigment was removed in part by vaporization and in the slough of tissue that was coagulated (73). At best, a thin atrophic scar resulted when healing was complete. Most tattoos are treated now with Q-switched wavelengths that are specific for the pigment and do little damage to the epidermis, although the complete Table 26.2 Dermal Lesions that may Be Treated by Ablation with the Carbon Dioxide Laser Adenoma sebaceum Angiofibromas Angiokeratoma Apocrine hidrocystoma Chondrodermatitis nodularis helicis Granuloma faciale Hidradenitis suppurativa Lymphangioma circumscriptum Myxoid cyst Neurofibroma Pearly penile papules Pyogenic granuloma Sebaceous hyperplasia Syringoma Trichoepithelioma Tricholemmoma Xanthelasma Xanthoma

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or nearly complete removal of pigment commonly requires six to eight treatments. There remain, however, some indications for the use of the carbon dioxide laser, for example, Q-switched laser resistant tattoos or tattoo pigment that darkens when treated with a Q-switched laser, and tattoos complicated by reactions to the pigment. In addition, the carbon dioxide laser generally removes the tattoo in one treatment though wound care is required for several weeks. It is, therefore, a satisfactory treatment for patients who prefer minimal number of treatments and do not mind the formation of a scar. Rhinophyma is hypertrophy of the sebaceous glands of the nose commonly associated with rosacea in middle aged to elderly men. It is easily treated with the carbon dioxide laser (74). The excess tissue is first removed by cutting with the carbon dioxide laser and the nose is then reshaped by ablation of the surface. Re-epithelialization occurs rapidly, within 3– 4 weeks, thought to be from epidermal cells at the base of the hair follicles. The surface is often somewhat shiny and atrophic; however, when the entire cosmetic unit of the nose is treated, it blends in well. Care must be taken when treating the ala because over-treatment causes contraction and distortion of both the ala and the nostril opening which is often somewhat spatulous even before treatment. Treatment of dermal lesions requires careful attention to the intended volume of tissue destruction, taking into account vaporized tissue as well as coagulative necrosis that sloughs post-treatment. Enough tissue has to be vaporized or coagulated for the lesion to be ablated. Generally this means that a scar is produced, although in some areas where the skin heals very well, such as the eyelid, the scar may not be apparent. Scarring may be minimized when a pulsed or rapidly scanned carbon dioxide laser system is used; however, an experienced operator will be able to produce the same result more quickly using a continuous wave beam manipulated manually. 2.3.

Advantages and Limitations

In the appropriate clinical setting, the use of the carbon dioxide laser has many advantages. Tissue can be vaporized rapidly and precisely with effective hemostasis. A sterile wound bed is created. Hyperkeratotic debris and nail may be ablated more easily than with other destructive modalities. Bone can also be ablated, although significant charring is produced. The laser does not interfere with pacemakers or monitoring devices. There are limitations to using the carbon dioxide laser for treatment of epidermal and dermal lesions. Reproducibility of technique and results is limited because of variables such as nonuniform size and shape of lesions as well as the changing thickness of tissue compartments depending on anatomic site. For ablative procedures, it is not possible to precisely calculate power densities and duration of exposure for each treatment. Of particular note, when the carbon dioxide laser is used for ablation, no tissue specimen is available for evaluation by the dermatopathologist. Hence, any lesion of questionable diagnosis should be biopsied and sent for histopathologic evaluation prior to treatment with the carbon dioxide laser. When the laser is used for cutting, the specimen obtained may be sent to pathology and it is generally possible to evaluate all but the last 0.5 – 1 mm of the margins for residual tumor. 2.4.

Carbon Dioxide Laser Safety

All personnel within the laser workspace must be trained in the safety procedures and policies regarding the use of the carbon dioxide laser (75). Each office or institution should have training and credentialling processes prior to personnel assisting in surgery utilizing a laser.

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The room in which the carbon dioxide laser is used must have several safety features that vary from a usual procedure room. The door must be posted with warning signs. There should be as few reflective surfaces as possible and any reflective surfaces present including windows must be covered. Fire extinguishers must be readily available. Surgical tools should be nonreflective or have a black coating to prevent deflection of the laser beam. During a laser procedure, the door must be closed and posted for active laser use. Some safety officers recommend that the room be locked from within. All personnel in the laser treatment room must wear laser surgical masks which filter particles as small as 0.1 mm. For the treatment of lesions of infectious etiology, such as verruca vulgaris, the patient must also wear a mask. When a carbon dioxide laser is used, all personnel and the patient must wear clear plastic or glass safety goggles to avoid corneal damage. Carbon dioxide laser treatment around the eyes requires nonreflective metal eye shields to be placed over the patient’s sclerae. The patient or personnel should not wear jewelry. No flammable materials, such as alcohol, should be used or located within the workspace. There should be no dry sponges in the treatment field. Normal saline or sterile water soaked sponges and drapes should be placed around the treatment area. Water must be readily available. A high efficiency smoke evacuator that filters particles as small as 0.1 mm should always be used with the suction hose within 1 cm of the treatment area. Unfortunately, reports of unintentional burns to the personnel or the patient, fire, and laryngitis secondary to a failed smoke evacuator system have all been reported (76).

3.

TECHNIQUE

The surgeon relies on visual inspection of the treatment site after each pass of the laser and wiping the site with wet then dry sponges in order to determine the extent of the lesion and surrounding tissue damage. The surgeon may need to alter the laser parameters as the treatment progresses depending on the clinical results. The power density may be varied by changing the power output, beam configuration, spot size, movement speed of hand piece, or shuttering the laser beam. These changes may be done either by hand or with the use of a mechanical scanning device. Clinically, during the first pass with a carbon dioxide laser, vaporization of skin results in a white and slightly scaly surface. Once the treated area is gently wiped with a wet sponge, the epidermis may still be visible if the treated lesion is particularly thick or the power density was very low and the speed of movement was very fast. If the epidermis is thin and a greater power density is delivered, the superficial dermis is seen with normal dermatoglyphic markings. When the dermis is heated or vaporized, visible collagen contraction is noted. If coarse and woven collagen bundles are seen, the tissue has been ablated into the deep dermis. If ablation is continued further, subcutaneous fat will be obvious. If charring is seen, there has been slow tissue burning at very high temperatures resulting in heat diffusion to surrounding tissues rather than tissue ablation. Charring is therefore not desired. Optimal use of the carbon dioxide as an ablative instrument includes many steps. First, the laser surgeon must determine the desired clinical end point which varies depending on the lesion treated. Actinic cheilitis is successfully treated when the end point of coagulation or white discoloration of the entire external lower mucosal (Table 26.3) lip is seen. The clinical end point for the treatment of an epidermal nevus is evidence of some coagulation in the dermis under the ablated area. The clinical end point for the treatment of a plantar wart is the presence of normal dermis under the visible wart as well as 5–10 mm surrounding it.

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Table 26.3 Mucosal Lesions that may Be Treated by Ablation with the Carbon Dioxide Laser Actinic cheilitis Balanitis xerotica obliterans Bowenoid papulosis Squamous cell carcinoma of the penis (erythroplasia of Queryat) Oral florid papillomatosis Oral leukoplakia Sublingual keratosis Zoon’s balanitis

The clinical end point for the treatment of small appendageal tumors of the face includes vaporization of epidermis and dermis to a depth just beneath the surrounding uninvolved skin. With a surgical marking pen, the lesion(s) is outlined with appropriate margins. Anesthesia is administered and may include local infiltration, regional blocks, or sedation. After reviewing a list of laser safety procedures and testing the beam on an inaminate object such as a tongue blade, the laser surgeon focuses the laser beam at the treatment site and the procedure is begun. Air brush-like movements with the defocused laser beam of the continuous wave carbon dioxide laser or discrete pulses of the pulsed or rapidly scanned carbon dioxide laser create visible vaporization and/or coagulation. At the completion of the first pass with the laser beam, the treatment site is gently wiped with a normal saline or sterile water soaked sponge to remove tissue fragments, char, or coagulum after which the area is blotted dry with a sterile sponge. A judgement is then made by the laser surgeon to continue with the same laser parameters or to modify them. Each individual site and lesion to be treated will vary, even within the same site or lesion, in many characteristics affecting the laser injury including thickness of normal skin, thickness of lesion, amount of tissue fluid, and amount of tumescence from anesthesia. Skilled laser technique means being aware of and utilizing these differences, and constantly modifying the energy parameters for an optimal result. Vaporization and debridement are then repeated until the desired clinical end point has been achieved. The quantity of tissue ablated depends on the power output, exposure duration and spot size diameter at the skin surface, and movement speed of the hand piece. When using the carbon dioxide laser in the continuous wave mode, a defocused beam is maintained by keeping the hand piece further away from the skin than the focal length of the lens. In doing so, the spot size is increased thereby delivering the same amount of power to a greater surface area. This results in less tissue damage. The use of the carbon dioxide laser in the continuous wave mode with a defocused beam is demonstrated in the treatment of a plantar wart. An epidermal lesion, the plantar wart requires extensive ablation to prevent recurrence (Table 26.4, Fig. 26.1). This is in comparison to the treatment of the syringomata. A dermal lesion, the syringoma is small, well circumscribed, and typically located on the face where the skin is consistently thin. Treatment of the syringomata includes using a pulsed or rapidly scanned carbon dioxide laser system that uses very short pulses of energy to precisely ablate the lesion (Table 26.5). When treating a superficial mucosal lesion such as actinic cheilitis, continuous wave with a defocused beam, pulsed or rapidly scanned carbon dioxide lasers may be used. Treatment includes ablating a very superficial layer of mucosa (Table 26.6). The carbon dioxide laser is also used in the cutting mode followed by vaporization to treat extensive epidermal and dermal lesions. This treatment is commonly used in the

CO2 Laser Treatment Table 26.4

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Technique for the Treatment of Plantar Warts

Surgical plan—end point is the ablation of the plantar wart and 5 –10 mm of surrounding uninvolved epidermis. Demarcation—treatment margins are outlined with a surgical marking pen. Anesthesia—local infiltration of 1% lidocaine with epinephrine into the treatment area. Regional block may also be useful. Preparation—place normal saline or sterile water soaked sponges and drapes around treatment area. Set laser parameters—power output 15– 25 W, waveform (continuous wave, pulsed or scanned), spot size (defocused beam with spot size of 3 – 5 mm at skin surface). Vaporization—move hand piece with air brush-like movements over wart and surrounding epidermis to margins. Debridement—curettage large pieces of desiccated wart from surface. Wipe treated area with a normal saline or sterile water soaked sponge then blot with dry sponge. Repeat vaporization and debridement as necessary until normal dermis is identified. Dressing—bacitracin ointment, sterile nonadherent dressing, and tape. Post-operative instructions—wash area with soap and water, apply bacitracin and dressing twice daily. Elevation of foot, post-operative shoe, and crutches may be necessary to avoid weight bearing.

treatment of rhinophyma, where the focused carbon dioxide laser beam is used to excise the nodular portion of the nose followed by the defocused carbon dioxide laser beam to reshape the nose (Table 26.7, Fig. 26.2). It is of utmost importance that the laser surgeon be conservative in the amount of tissue removed from the site in order to minimize the risk of hypertrophic scarring and unilateral alar lift (77). Large and bulky veruccae may be treated in a similar fashion. However, as described in the treatment of warts (Table 26.4), it is important to ablate an area of clinically normal appearing skin around the wart lesions (Table 26.6). Wounds created by vaporization with a carbon dioxide laser heal by secondary intention with a time frame dependent on the anatomic location and the depth of the treatment. A surgical dressing is selected, that is, appropriate for the size and anatomic location of the wound. Written wound care instructions are always reviewed and given to the patient.

Figure 26.1 (a) Periungal wart, preoperative view, (b) periungal wart, immediately after ablation, with coagulation of surface and some char visible, (c) periungal wart, immediately post-procedure, and (d) periungal wart, 8 week followup.

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Table 26.5

Technique for the Treatment of Syringomas

Surgical plan—end point is the ablation of syringoma to a depth just beneath the surrounding uninvolved skin surface. Demarcation—syringoma is outlined with a surgical marking pen. Anesthesia—local infiltration into the superficial dermis (just enough to raise a bleb) with 1% lidocaine with epinephrine. Preparation—place normal saline or sterile water soaked sponges and drapes around the treatment area. Set laser parameters—power 15 W, waveform (shuttered continuous wave, pulsed or scanned beam at 0.1– 0.2 s), spot size (defocused beam with spot size of 2 – 3 mm at skin surface). The spot size may be adjusted manually with the diameter of the lesion. Vaporization—direct the shuttered beam to the lesion with one or two pulses. Debridement—wipe treated area with a normal saline or sterile water soaked sponge then blot with dry sponge. Repeat vaporization and debridement, as necessary to reach desired end point. The remaining eyelid epidermis may be superficially vaporized in order to blend any pigment changes caused by the treatment. Dressing—bacitracin ointment. Post-operative instructions—wash area with soap and water then apply bacitracin twice daily.

4.

COMPLICATIONS

The most frequently noted complication of carbon dioxide laser treatment is the development of a scar that may be either atrophic or hypertrophic. In addition, intraoperative or post-operative hemorrhage, excessive pain, prolonged healing, and infection can occur. Events reported rarely include reactive tissue processes post-operatively such as excess granulation tissue, pyogenic granuloma, and lip mucocele (76).

Table 26.6

Technique for Treatment of Actinic Cheilitis

Surgical plan—end point is the coagulation or white discoloration of the entire external lower mucosal lip. Demarcation—vermilion border is outlined with a surgical marking pen. Anesthesia—mental block with 2% lidocaine, local infiltration into the superficial submucosa, particularly at lateral commissures with 1% lidocaine with epinephrine. Preparation—place a normal saline or sterile water soaked sponge over teeth and cutaneous lower lip. Set laser parameters—power 15 W, waveform (continuous wave, pulsed or scanned beam), spot size (defocused beam with spot size of 4 – 5 mm at skin surface). Vaporization—quickly, move the hand piece with air brush-like quality along the lower lip, starting within the mouth and proceeding to the vermilion border. The epidermis will “bubble.” One or two slightly overlapping passes are typically sufficient. The hand piece is being moved too slowly if char is noted. Debridement—wipe treated area with a normal saline or sterile water soaked sponge then blot with a dry sponge. Repeat vaporization and debridement if thick or scaly areas persist. Dressing—bacitracin ointment. Post-operative instructions—wash area twice daily with soap and water, apply bacitracin several times daily while awake.

CO2 Laser Treatment Table 26.7

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Technique for Treatment of Rhinophyma

Surgical plan—the endpoint is a sculpted nose, with ablation deep or superficial of the entire nasal unit. Nodules may be aggressively obliterated, treatment of ala and tip should be a less aggressive as contraction will occur with healing. Demarcation—nodular areas are outlined with a surgical marking pen. Anesthesia—paranasal sensory nerve block with 2% lidocaine, local infiltration into the nose with 1% lidocaine with epinephrine as needed. Preparation—place normal saline or sterile water soaked sponges and drapes around treatment area. Set laser parameters for the initial excision of nodular areas with the focused carbon dioxide laser beam—power 20–25 W, waveform (continuous wave, pulsed or scanned beam), spot size at focal point. Excision—direct the beam parallel to the surface of the nose to excise the nodular and pedunculated areas on the nose. Grabbing the nodules with forceps or towel clamps may facilitate cutting. Debridement—wipe treated area with a normal saline or sterile water soaked sponge then blot with a dry sponge. Set laser parameters for the vaporization of the nose with the defocused carbon dioxide laser beam—power 20– 25 W, waveform (continuous wave, pulsed or scanned beam), spot size 3– 5 mm. Vaporization—quickly, move the hand piece with air brush-like quality over the nose. Debridement—wipe treated area with a normal saline or sterile water soaked sponge then blot with a dry sponge. Repeat vaporization until the contour is appropriate and the surface is smooth, taking into account the postlaser coagulum slough. Sebaceous glands or their oily products may be visible in the wound bed. Dressing—bacitracin ointment, sterile nonadherent dressing, and tape. Post-operative instructions—wash area twice daily with soap and water and reapply bandage.

To hasten wound healing and minimize scarring, the laser surgeon must select the appropriate carbon dioxide laser waveform and laser parameters, pay attention to surgical technique and apply appropriate wound care. Although carbon dioxide laser wounds heal by secondary intention, excellent wound care is essential. The wounds are cleansed twice daily with soap and water, rinsed well, and patted dry. An antibacterial ointment is applied followed by a sterile nonadherent dressing and sponge that are taped in place. A bioocclusive dressing such as Vigilon (CR Bard, Murray Hill, NJ) or Duoderm (Convatec, Princeton, NJ) may be used as an alternative for wounds not on the face and may speed re-epithelialization. Topical care is continued until complete re-epithelialization occurs which may be as long as 6 weeks depending on the anatomic location and the size and depth of the wound. Wound care should be continued beyond re-epithelialization to minimize scar tissue formation. This includes moisturizing and massaging the wound area. Constant pressure items such as compression earrings, tailor-made pressure garments as well as splints may deter hypertrophic scarring.

5.

CONCLUSION

The carbon dioxide laser is useful for the treatment of many epidermal and dermal lesions where there is no specific target chromophore other than water. The relevant issues in the treatment of epidermal and dermal lesions with the carbon dioxide laser include

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Figure 26.2 (a) Rhinophyma, preoperative view, (b) rhinophyma, preoperative view, (c) rhinophyma, immediately post-procedure, and (d) rhinophyma, 6 months followup.

maintenance of safety procedures, knowledge of the clinical end point of treatment, selection of appropriate laser waveform and laser parameters, and optimal wound care.

REFERENCES 1.

2. 3. 4. 5.

Schomacker KT, Walsh JT, Flotte TJ, Deutsch TF. Thermal damage produced by highirradiance continuous wave carbon dioxide laser cutting of tissue. Lasers Surg Med 1990; 10:74 – 84. Anderson RR, Parrish JA. Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science 1983; 220:524 – 527. Walsh JT, Flotte TJ, Anderson RR, Deutsch TF. Pulsed carbon dioxide laser tissue ablation: effect of tissue type and pulse duration on thermal damage. Lasers Surg Med 1988; 8:108– 118. Fulton JE, Shitabata PK. Carbon dioxide laser physics and tissue interaction in skin. Lasers Surg Med 1999; 24:113 – 121. Alora, Anderson RR. Recent developments in cutaneous lasers. Lasers Surg Med 2000; 26:108 – 118.

CO2 Laser Treatment 6. 7. 8. 9. 10. 11.

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Hruza GJ. Laser treatment of warts and other epidermal and dermal lesions. Dermatol Clin 1997; 15:487 – 506. Stanley TH, Roenigk RK. The carbon dioxide laser treatment of actinic cheilitis. Mayo Clin Proc 1988; 63:230– 235. Zelickson BD, Roenigk RK. Actinic cheilitis. Treatment with the carbon dioxide laser. Cancer 1990; 65:1307 – 1311. Dufresne RG, Garett AB, Bailin PL et al. Carbon dioxide laser treatment of chronic actinic cheilitis. J Am Acad Dermatol 1988; 19:876 – 878. David LM. Laser vermilion ablation for actinic cheilitis. J Dermatol Surg Oncol 1985; 11:605 – 609. Johnson TM, Sebastien TS, Lowe L et al. Carbon dioxide laser treatment of actinic cheilitis: clinicohistopathologic correlation to determine the optimal depth of destruction. J Am Acad Dermatol 1992; 27:737 – 745. Whitaker DC. Microscopically proven cure of actinic cheilitis by carbon dioxide laser. Lasers Surg Med 1987; 7:520 – 523. Fitzpatrick RE, Goldman MP. Carbon dioxide laser surgery. In: Goldman MP, Fitzpatrick RE, eds. Cutaneous Laser Surgery: The Art and Science of Selective Photothermolysis. St. Louis: Mosby, 1994:198 – 258. Sanders PL, Reinisch L. Wound healing and collagen thermal damage in 7.5-microsec pulsed carbon dioxide laser skin incisions. Lasers Surg Med 2000; 26:22 – 32. Greenbaum SS, Glogau R, Stegman SJ et al. Carbon dioxide laser treatment of erythroplasia of Queyrat. J Dermatol Surg Oncol 1989; 15:747 – 750. Malek RS. Laser treatment of squamous cell lesions of the penis. Lasers Surg Med 1992; 12:246 – 249. Eliezri YD. The toluidine blue test: an aid to the diagnosis and treatment of early squamous cell carcinoma of mucous membranes. J Am Acad Dermatol 1988; 18:1339 – 1349 Tanitikun N. Treatment of Bowen’s disease of the digit with carbon dioxide laser. J Am Acad Dermatol 2000; 43:1080 – 1083. Ratz JL. Carbon dioxide laser treatment of balanitis xerotica obliterans. J Am Acad Dermatol 1984; 10:925 – 928. Hrebinko RL. Circumferential laser vaporization for severe metal stenosis secondary to balanitis xerotica obliterans. J Urol 1996; 156:1735– 1736. Baldwin HE, Geronemus RG. The treatment of Zoon’s balanitis with the carbon dioxide laser. J Dermatol Surg Oncol 1989; 15:491– 494. Persley MS. Carbon dioxide laser treatment of oral florid papillomatosis. J Dermatol Surg Oncol 1984; 10:64– 66. Roodenburg JL, Panders AK, Vermey A. Carbon dioxide laser surgery of oral leukoplakia. Oral Surg Oral Med Oral Pathol 1991; 71:670 – 674. Frame JW. Treatment of sublingual keratosis with the carbon dioxide laser. Br Dent J 1984; 156:243 – 246. Boyce S, Alster TS. CO2 laser treatment of epidermal nevi: long-term success. Dermatol Surg 2002; 28:611 – 614. Molin L, Sarhammar G. Perivulvar inflammatory linear verrucous epidermal nevus treated with CO2 laser. J Cutan Laser Ther 1999; 1:53– 56. Rabbin PE, Baldwin HE. Treatment of porokeratosis of Mibelli with carbon dioxide laser vaporization versus surgical excision with split-thickness skin graft. A comparison. J Dermatol Surg Oncol 1993; 19:199 – 202. Christian MM, Moy RL. Treatment of Hailey–Hailey disease (or benign familial pemphigus) using short pulsed and short dwell time carbon dioxide lasers. Dermatol Surg 1999; 25:661–663. McElroy JA, Mehregan DA, Roenigk RK. Carbon dioxide laser vaporization of recalcitrant symptomatic plaques of Hailey –Hailey disease and Darier’s disease. J Am Acad Dermatol 1990; 23:893 – 897. Windahl T, Hellstens. Carbon dioxide laser treatment of lichen sclerosis et atrophicus. J Urol 1993; 150:868 – 870.

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Lucchina and Olbricht Ewing TL. Paget’s disease of the vulva treated by combined surgery and laser. Gynecol Oncol 1991; 43:137 – 140. Sood S, Hurza GJ. Treatment of verruca vulgaris and condyloma acuminatum with lasers. Dermatol Therapy 2000; 13:90 – 101. Johnson PJ, Mirzai TH, Bentz ML. Carbon dioxide laser ablation of anogenital condyloma acuminata in pediatric patients. Ann Plast Surg 1997; 39:578 – 582. Schiffman M, Kjaer SK. Natural history of anogenital human papillomavirus infection and neoplasia. J Natl Cancer Inst Monograph 2003; 3 – 13. Hernandez-Hernandez DM, Omlas-Barnal D, Guido-Jimenez M et al. Association between high-risk human papillomavirus DNA load and precursor lesions of cervical cancer in Mexican women. Gynecol Oncol 2003; 90:310 –317. Adamson R, Obispo E, Dychter S, Dembitsky W, Daily PO et al. High incidence and clinical course of aggressive skin cancer in heart transplant patients: a single-center study. Transplant Proc 1998; 30:1124– 1126. Jensen P, Hansen S, Moller B et al. Skin cancer in kidney and heart transplant recipients and different long-term immunosuppressive therapy regimens. J Am Acad Dermatol 1999; 40:177 – 186. Del Mistro A, Chieco Bianchi L. HPV-related neoplasias in HIV-infected individuals. Eur J Cancer 2001; 37:1227 – 1235. Bragg JW, Ratner D. HPV type 2 in a squamous cell carcinoma of the finger. Dermatol Surg 2003; 29:766 – 768. Logan RA, Zachary CB. Outcome of carbon dioxide laser therapy for persistent cutaneous viral warts. Br J Dermatol 1989; 121:99– 105. Apfelberg DB, Druber D, Maser MR et al. Benefits of the carbon dioxide laser for verruca resistant to other modalities of treatment. J Dermatol Surg Oncol 1989; 15:371– 375. Street ML, Roenigk RK. Recalcitrant periungual verrucae: the role of carbon dioxide laser vaporization. J Am Acad Dermatol 1990; 23:115 – 120. Calkins JW, Masterson BJ, Magrina JE et al. Management of condyloma acuminata with the carbon dioxide laser. Obstet Gynecol 1982; 59:105– 108. Baggish MS. Carbon dioxide laser surgery for condyloma acuminata venereal infection. Obstet Gynecol 1980; 55:711– 715. Bellina JH. The use of the carbon dioxide laser in management of condyloma acuminata with eight year follow-up. Am J Obstet Gynecol 1983; 147:375 – 378. Bar-Am A, Shilon M, Peyser MR et al. Treatment of male genital condylomatous lesions by carbon dioxide laser after failure of previous non-laser methods. J Am Acad Dermatol 1991; 24:87 – 89. Sajben FP, Ross EV. The use of the 1.0 mm handpiece in the high energy, pulsed carbon dioxide laser destruction of facial adnexal tumors. Dermatol Surg 1999; 25:41 – 44. Dover JS, Arndt KA, Geronemus RG et al. Illustrated cutaneous laser surgery. A Practitioner’s Guide. Appleton & Lange: East Norwalk, CT, 1990:98 – 104. Song MG, Park KB, Lee ES. Resurfacing of facial angiofibromas in tuberous sclerosis patients using carbon dioxide laser with flashscanner. Dermatol Surg 1999; 25:970 – 973. Janniger CK, Goldberg DJ. Angiofibromas in tuberous sclerosis comparison of treatment by carbon dioxide and argon laser. J Dermatol Surg Oncol 1990; 16:37– 320. Bickley LK, Goldberg DL, Imaeda S et al. Treatment of multiple apocrine hidrocystomas with the carbon dioxide laser. J Dermatol Surg Oncol 1989; 15:599– 602. Stoner MF, Hobbs ER. Treatment of multiple dermal cylindromas with the carbon dioxide laser. J Dermatol Surg Oncol 1988; 14:1263– 1267. Christenson LJ, Smith K, Arpey CJ. Treatment of multiple cutaneous leiomyomas with carbon dioxide laser ablation. Dermatol Surg 2000; 26:319– 322. Becker DW. Use of the carbon dioxide laser in treating multiple cutaneous neurofibromas. Ann Plast Surg 1991; 26:582 – 586. Kang WH, Kim NS, Kim YB, Shim WC. A new treatment for syringoma. Combination of carbon dioxide laser and trichloracetic acid. Dermatol Surg 1998; 24:1370– 1374.

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Wang JI, Roenigk HH Jr. Treatment of multiple facial syringomas with the carbon dioxide laser. Dermatol Surg 1999; 25:136– 139. Wheeland RG, McGillis ST. Cowden’s disease—treatment of cutaneous lesions using carbon dioxide laser vaporization. J Dermatol Surg Oncol 1989; 15:1055 – 1059. Magid M, Garden JM. Pearly penile papules: treatment with the carbon dioxide laser. J Dermatol Surg Oncol 1989; 15:552 – 554. McKinlay JR, Graham BS, Ross EV. The clinical superiority of continuous exposure versus short-pulsed carbon dioxide laser exposures for the treatment of pearly penile papules. Dermatol Surg 1999; 25:124 – 126. Sawchuk WS, Heald PW. Carbon dioxide laser treatment of trichoepithelioma with focused and defocused beam. J Dermatol Surg Oncol 1984; 10:905 – 907. Rosenbach A, Alster TS. Multiple trichoepitheliomas successfully treated with a high energy, pulsed carbon dioxide laser. Dermatol Surg 1997; 23:708 – 710. Taylor MB. Chondrodermatitis nodularis chronica helicis. Successful treatment with the carbon dioxide laser. J Dermatol Surg Oncol 1991; 17:862 – 864. Wheeland RG, Ashley JR, Snick DA et al. Carbon dioxide laser treatment of granuloma faciale. J Dermatol Surg Oncol 1984; 10:730– 733. Finley EM, Ratz JL. Treatment of hidradenitis suppurativa with carbon dioxide laser excision and second intention healing. J Am Acad Dermatol 1996; 34:465 – 469. Leshin B, Whitaker DC. Carbon dioxide laser matrixectomy. J Dermatol Surg Oncol 1988; 14:608 – 611. Hamzavi I, Lui H. Excess tissue friability during carbon dioxide laser vaporization of nodular amyloidosis. Dermatol Surg 1999; 25:726– 728. Dover JS, Arndt KA, Geronemus RG et al. Illustrated cutaneous laser surgery. A Practitioner’s Guide. Appleton & Lange: East Norwalk, CT, 1990:21 – 73. Carpo BG, Grevelink SV, Brady S et al. Treatment of cutaneous lesions of xanthoma disseminatum with a carbon dioxide laser. Dermatol Surg 1999; 25:751 –754. Raulin C, Schoenermark MP, Werner S, Greve B. Xanthelasma palpebrarum: treatment with the ultrapulsed carbon dioxide laser. Lasers Surg Med 1999; 24:122– 127. Kartamaa M, Reitamo S. Treatment of lichen sclerosis with carbon dioxide laser vaporization. Br J Dermatol 1997; 13:356 – 359. Haas AF, Narurkar VA. Recalcitrant breast lymphangioma circumscriptum treated by ultrapulse carbon dioxide laser. Dermatol Surg 1998; 24:893 –895. Huilgol SC, Neill S, Barlow RJ. CO2 laser of vulvar lymphangioma circumscriptum. Dermatol Surg 2002; 28:575 –577. Dufresne RG Jr, Garrett B, Bailin PL et al. Carbon dioxide laser treatment of traumatic tattoos. J Am Acad Dermatol 1989; 20:137 – 138. Karim AM, Streitmann MJ. Excision of rhinophyma with the carbon dioxide laser: a ten-year experience. Ann Otol Rhinol Laryngol 1997; 106:952 – 955. Fader DJ, Ratner D. Principles of carbon dioxide and erbium laser safety. Dermatol Surg 2000; 26:235 – 239. Olbricht SM, Tang SV, Stern RS et al. Complications of cutaneous laser surgery: a survey. Arch Dermatol 1987; 123:345 – 349. Nanni CA, Alster TS. Complications of cutaneous laser surgery. A review. Dermatol Surg 1998; 24:209 – 219.

27 Skin Resurfacing with CO2 Lasers Richard E. Fitzpatrick and Elizabeth Rostan Dermatology Associates of San Diego County, Inc., Encinitas, California, USA

1. Introduction 2. Principles of CO2 Laser Resurfacing 2.1. Single Pulse Vaporization 2.2. Collagen Shrinkage 2.3. Collagen Remodeling and Regeneration 3. Technique 4. Results 5. Complications 5.1. Postoperative Swelling 5.2. Erythema 5.3. Itching 5.4. Infection 5.5. Acne and Milia 5.6. Hyperpigmentation 5.7. Hypopigmentation 5.8. Petechiae 5.9. Scarring 5.10. Ectropion 5.11. Synechiae 6. Sequential CO2/Erbium Laser Resurfacing 7. Superficial Resurfacing References

1.

535 537 537 538 539 539 542 544 544 544 545 545 546 546 547 547 547 548 549 549 549 550

INTRODUCTION

In the last decade, laser resurfacing with short-pulsed CO2 lasers has been used to treat facial photodamage and acne scars. Vaporization of the outer 200 mm of skin results in rejuvenation of the epidermis with collagen contraction and remodeling of the dermis, thus improving the visible signs of photodamage. In this chapter, we will review the 535

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role of CO2 resurfacing in the treatment of photodamaged skin, outline our technique for resurfacing, and discuss the prevention and management of complications. Clinically, photoaged skin consists of both fine and deep wrinkles, coarse texture, mottled pigmentation and lentigines, and skin laxity. Histologically, these features of photoaging are demonstrated by the epidermal flattening and atrophy with areas of dysplasia. In the dermis, there is a loss of the normal collagen structure and the atrophic epidermis rests on a thin layer of collagen referred to as the “Grenz layer”. Below this, is a layer of altered collagen and elastic tissue of variable thickness known as solar elastosis. In severe photodamage, the layer of solar elastosis appears as a thick amorphous mass that stains blue with hematoxylin and eosin and lacks any normal elastic fibers (1 – 4). With both intrinsic or chronologic aging and photoaging, decreased numbers of eccrine glands and fibroblasts are observed and the sebaceous glands become hyperplastic (5,6). With age, fibroblasts become more proteolytic and over-express collagenase while under-expressing pro-collagen and collagenase inhibitors. Ultraviolet radiation also stimulates enhanced collagenase activity (5). Medical therapy of photoaged skin involves products directed to prevent further sun damage and products to improve the clinical signs of photodamage. The first step in treating photodamaged skin is a full spectrum sunscreen that blocks both UVA and UVB, such as Parsol 1789 or micronized titanium dioxide or transparent zinc oxide. Of agents designed to reverse the signs of sun damage, tretinoin cream or Retin-ATM has been studied the most extensively and has proven benefits in reversing photoaging. In addition, tretinoin may have an additional benefit of preventing further sun damage (5,7 – 12). Kligman and Graham have demonstrated that tretinoin results in replacement of the flat, atrophic epidermis with hyperplasia, a reduction in keratinocyte dysplasia, and a more uniform distribution of melanin granules. In the dermis, new collagen deposition and angiogenesis were observed (8). Fisher et al. defined a possible role of tretinoin in the prevention of sun damage by demonstrating that tretinoin, by binding to the retinoic acid receptor, inhibited the UVR-induced production of collagenase without affecting levels of collagenase inhibitor (5,11). Antioxidants such as vitamins C and E may be valuable in both protecting dermal structures from the free-radical damage and in aiding in the repair of damage (13 – 17). Alpha-hydroxy acids may have a role in the treatment of photodamage by reducing stratum corneum cohesiveness, increasing epidermal thickness, and increasing glycosaminoglycans in the dermis, but these potential effects are less well studied and the mechanism of action remains unknown (18,19). Topical regimens as outlined earlier are valuable in the treatment of photoaging, but need to be adhered to long term in order to achieve a significant effect. We routinely use preoperative regimens of Retin-A, vitamins C and E, and a broad-spectrum sunscreen prior to resurfacing. Preoperative retinoic acid has been shown to enhance wound healing after dermabrasion and chemical peels and, in a porcine study, following laser resurfacing. Similarly, vitamin C is thought to enhance wound healing but no published reports have objectively confirmed this observation. In addition to enhancement of wound healing and initiation of the biochemical process that helps reverse photoaging, use of these agents preoperatively establishes a long-term regimen to treat and prevent further sun damage following resurfacing. Topical treatments for photoaging often do not achieve the specific clinical results desired by the patient; so surgical options must be explored. Surgical treatments for photoaging include resurfacing procedures such as dermabrasion, chemical peels, and laser resurfacing, which remove the damaged layer of skin, and facelift procedures, which do not alter the damaged skin layer but effectively remove excess, lax skin. The major disadvantage of any lifting procedure is that the primary problem,

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photodamage, is not addressed and continues unaltered. Furthermore, the central face areas—glabella, mid-forehead, perioral and periorbital areas—are often areas of primary concern and are not effectively treated with facelift procedures. Chemical peels and dermabrasion effectively remove photodamage, but present problems relating to difficulty in controlling the depth of the procedure. There is variable and uncontrolled depth of penetration with chemical peels, and loss of pigment is frequently associated with deep peels such as the phenol peels. Subsequently, a cautious approach to chemical peel leads to a tendency to treat too superficially, thus resulting in persistence of deeper lines. Dermabrasion, in addition to presenting difficulties in evaluating depth, is technically difficult and carries an increased risk of exposure to blood-borne pathogens. Thus, laser vaporization using the principles of selective photothermolysis has become widely accepted as the treatment of choice in treating photodamage of the face (20 –26). The advantages of the laser for resurfacing relate to the ability to remove fine layers of tissue (50 – 100 mm/pass) in a controllable and predictable manner. Areas that are not well corrected with a facelift procedure show significant improvement following laser resurfacing. Additionally, deeper lines may be targeted specifically and treated more aggressively. The resurfacing lasers now in use include pulsed and flashscanned CO2 lasers in the microsecond domain, pulsed CO2 lasers in the 2 –6 ms domain, and erbium:YAG lasers. All of these lasers may be useful in resurfacing; however, when utilizing a CO2 laser, a high energy microsecond-pulsed system is preferred as the pulse width is less than the thermal relaxation time of tissue. The CO2 laser offers the following unique clinical advantages over the erbium laser and other resurfacing modalities: 1.

2.

3.

4.

2.

Efficient single-pass removal of the epidermis: A subepidermal bulla develops secondary to thermal damage and results in lifting of the epidermis. Thus, the epidermis is easily and completely removed with a single pass with minimal residual thermal damage (27 – 30). Heat-induced collagen shrinkage: This results in significant clinical improvement, especially in the periorbital area, nasolabial folds and cheeks, and in atrophic scars. Collagen contraction is always a significant component of the improvement seen with CO2 laser resurfacing. Limited ablation depth with single pulse vaporization: With CO2 resurfacing, an ablation plateau is reached thus limiting depth of the wound and risk of undesirable side effects. Hemostasis: Hemostasis during the procedure allows visualization of surface irregularities and permits fine control of tissue sculpting.

PRINCIPLES OF CO2 LASER RESURFACING

An understanding of the basic mechanisms of CO2 laser resurfacing is essential in order to achieve maximal results. These mechanisms include (1) single pulse vaporization, which allows efficient removal of skin layers without significant heat transfer to surrounding tissue, (2) collagen shrinkage with subsequent skin tightening, (3) new collagen formation and remodeling, and (4) multiple pulse vaporization, which produces additive thermal effects and may be used cautiously to achieve deeper ablation. 2.1.

Single Pulse Vaporization

Single pulse vaporization utilizes the principles of selective photothermolysis to minimize heat transfer to adjacent tissue. Thus, a pulse width of ,1 ms, which is less than the

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thermal relaxation time of skin, is necessary to confine heat to the ablated tissue (31,32). Longer pulse widths may lead to heat accumulation and subsequent diffusion to surrounding tissue. Additionally, the pulse energy must be adequately high in order to achieve vaporization with a single pulse (33). For a 2.5 mm beam, a pulse energy .250 mJ is required. Observations of multiple passes using the coherent ultrapulse laser in conjunction with the computerized pattern generator (CPG) revealed no apparent clinical effect on tissue ablation or tightening beyond the first three or four passes. Additional residual thermal damage was not clinically apparent; however, in the absence of ablation, heat diffusion was a concern. We therefore performed a study to evaluate vaporization depth and residual thermal damage following single pulse vaporization with multiple passes (up to 10) vs. multipulse vaporizations (two and three pulse stacking). With single pulse vaporization, we found that a plateau of tissue ablation occurs after three to four passes, and vaporization deeper than 200 –250 mm into tissue was not possible. Residual thermal damage did not exceed 100 mm, even when 10 passes were performed. Thus, with single pulse vaporization, once the ablation plateau is reached, heat delivered by the CO2 laser is inadequate for vaporization but does not accumulate in tissue because single pulses are delivered with a pulse width below 1 ms. The same vaporization plateau was observed with double and triple pulse stacking, but increasing thermal necrosis occurred with each pass and was accelerated with triple vs. double pulsing. We concluded that pulse stacking results in progressive loss of control of residual thermal damage without a significant effect on the depth of ablation, and that with single pulse vaporization, minimal thermal necrosis can be maintained. The depth of vaporization of the dermis becomes progressively less with each pass and plateaus after three to four passes (34). 2.2.

Collagen Shrinkage

Collagen molecules are composed of three polypeptide chains assembled in a helical conformation. Tensile strength is provided through intermolecular crosslinks. Heat-induced shrinkage occurs through a molecular structure transition involving these crosslinks in which the interpeptide bonds are broken but the assembled collagen polypeptide helix remains intact. Heat-induced collagen shrinkage was first noted 100 years ago in corneal reshaping studies that demonstrated that collagen fibrils can shrink up to onethird of their original length (35). Contraction of collagen occurs at temperatures that allow tissue survival and maintenance of the intact collagen fibrils. Studies with human corneal collagen have shown that collagen contracts sharply at temperatures of 55 – 608C, relaxes at temperatures of 65 – 708C, and necroses at temperatures .708C (36). Rate of temperature change further affects collagen response. Instantaneous higher temperatures result in faster, more complete collagen shrinkage than slower heating. In human skin, a peak temperature of 638C produces the greatest and most immediate collagen contraction (37 – 40). Both slower heating and lower peak temperatures result in less collagen contraction. Mature collagen contains less soluble interpeptide bonds, so a higher temperature is needed to produce shrinkage than with new collagen which contracts at a lower temperature. Our knowledge of collagen tightening comes from biochemical studies, thermokinetic studies, in vitro tissue studies, and clinical studies of keratoplasty, orthopedics, and tissue welding. There have been over 150 publications regarding collagen tightening. It is a real phenomenon and a distinct process from wound contraction. We studied the effects of heat-induced collagen contraction vs. tissue contraction of wound healing in


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upper eyelid skin. Nine patients had four tattoo dots placed on the upper eyelids. One eyelid was then treated with three passes of a pulsed CO2 laser and the other with a short-pulsed erbium laser to the point of pinpoint bleeding. Measurements of the vertical and horizontal distances between tattoo dots were made after each laser pass and monthly for 6 months. The skin was then excised in a blepharoplasty procedure. The pulsed CO2 laser induced an average of 43% immediate, intraoperative contraction in the vertical plane, which gradually diminished to an average of 34% by 6 months, whereas wound contracture induced by erbium resurfacing was not observed until 1 month postoperatively when an average of 42% tightening was noted, gradually diminishing to 36% at 6 months. In the horizontal plane, the CO2 laser produced 31% intraoperative tissue contraction, which decreased to 19% at 6 months; the erbium-induced wound contraction at 1 month was 12%, which remained unchanged at 6 months. This study demonstrated heat-induced collagen shrinkage and tissue tightening secondary to wound healing to be unique and separate processes, both of which are limited by adjacent tissue resistance (as seen with limited contraction in the horizontal plane) (41). Collagen tightening is a significant component of the improvement seen after laser resurfacing, especially on the thin eyelid skin and cheeks. Redundant tissue folds of the cheek tighten, making nasolabial lines less pronounced and producing tightening of skin along the jawline. Heat-induced collagen shrinkage is also a major factor in the improvement seen with resurfacing of atrophic acne scars, thus giving the CO2 laser an advantage over other techniques such as chemical peeling, dermabrasion or short-pulse erbium resurfacing. The degree of improvement that can be expected may be judged by slightly stretching the skin to see how well they flatten with tension. Acne scars that flatten well with stretching generally respond well to CO2 laser resurfacing. 2.3.

Collagen Remodeling and Regeneration

In addition to tightening by collagen contraction, rhytides and acne scars are improved by CO2 laser resurfacing through collagen remodeling and formation of new collagen. Histologic studies comparing preoperative and postresurfacing specimens obtained at 90 day intervals have demonstrated significant new collagen formation in the papillary dermis with up to a 600% increase in thickness observed within this Grenz zone region. Clinically, this is observed as gradual improvement in lines or acne scars up to 12 months following a resurfacing procedure. This collagen formation and remodeling play an important role in the improvement seen after resurfacing, especially in acne scars and deep perioral wrinkles.

3.

TECHNIQUE

Prior to treatment with the CO2 laser, moist drapes are placed around the field and the patient’s eyes are protected with proper eyeshields (Fig. 27.1). Protective eyewear must be worn by all operative staff. Regardless of which laser is used for resurfacing, the basic protocol remains the same—use of single pulse vaporization with minimal overlap of the pulses. The goal of the first pass is to completely remove the epidermis. A pattern of single pulse impacts is selected and delivered to the skin without overlap, each pattern being placed adjacent to the other in a manner similar to which tile is laid on a floor (Fig. 27.2). The entire face is treated to just below the jawline and under the chin. The desiccated tissue debris is then removed with moist gauze, thus completely removing the epidermis [Fig. 27.3(a) and (b)]. When only a single pass is intended, it

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Figure 27.1


Prior to resurfacing, moist towels are draped around the surgical field.

has been found preferable to leave the desiccated debris in place rather than wiping it away; the debris then acts as a biologic dressing and less pain and inflammation occur. If more than one pass will be performed, this debris should be removed in order to enhance laser – tissue interaction. If the neck is to be resurfaced, all facial epidermal debris is wiped clean; however, if no resurfacing of the neck is planned, then the epidermal debris just below the jawline is not wiped away and is left intact [Fig. 27.3(b)]. No further passes with the CO2 laser are made in this area below the jawline. This method allows improved blending at the border of treated facial skin and untreated neck skin. A second pass is applied with a 908 orientation to the first pass (Fig. 27.4). The primary tissue reaction of the second pass is visible tissue tightening, but there is also an additional 50 –70 mm of tissue ablated with this pass. In almost every patient, two complete passes are done over the entire face. A third pass is then performed in areas with more severe photodamage or rhytides that remain visible after the first two laser passes. This last pass with the CO2 laser is generally done in the glabella and central forehead, nose, perioral area, and lateral cheeks (Fig. 27.5). The first pass is performed with CPG settings of pattern 3 or 5, density 6, and size 9. The density is decreased to 5 for the second pass but the other settings are unchanged. For the third pass, the density may be varied from 4 to 6, depending on the level of tightening desired. Around the eyes, a smaller pattern and

Figure 27.2 Appearance after one pass of UPCO2 prior to removal of debris with salinesoaked gauze.


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Figure 27.3 (a) Firm pressure with a saline-soaked gauze is used to completely remove epidermal debris after one pass of UPCO2 . (b) Appearance after removal of desiccated debris on face, following one pass of UPCO2 . Epidermal debris is left intact along lower jawline to improve blending of resurfaced facial skin and untreated neck skin.

density are utilized—pattern 5, density 5, and size 9. For the second pass to the periorbital area, density is further decreased to 4. Not more than two passes with the CPG are done on the eyelids. The pulse energy may be decreased to 200 mJ, if less tissue heating and collagen contraction are needed, and faster healing will be seen. After all passes with the CPG have been performed, the 3 mm spot is then utilized with a pulse energy of 500 mJ and a repetition rate of 6– 10 Hz, depending on the physician’s comfort level with speed of movement of the beam. The 3 mm spot is used to remove any persistent seborrheic keratoses or actinic keratoses. By means of holding the beam in place and stacking pulses, complete lesion flattening and desiccation can be achieved. The 3 mm spot is also employed to remove any remaining areas of epithelium that were missed or unreachable with the CPG (such as areas near the hairline and around eyebrows). Next, the 3 mm spot is applied to the shoulders of persistent, deep lines and around deeper acne scars in order to achieve deeper ablation and greater tightening (Fig. 27.6). This is typically needed in the deep glabellar and upper lip lines and the lateral aspect of the nasolabial folds. Around the eyes, the 3 mm spot is applied in multiple single spots on the upper and lower lid skin in order to achieve greater tightening; it is also used to carefully remove a small strip of epithelium below the lower lash line, which is

Figure 27.4 A second pass is applied utilizing the CPG with the pattern oriented 908 to the direction used in the first pass.

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Figure 27.5 A third pass with the CPG is performed in areas of most severe photodamage and usually includes the central forehead, glabella, nose, perioral area, and lateral cheeks.

often missed with the CPG. Lastly, a more concentrated deposition of 3 mm spots is applied to the cutaneous surface of the vermilion border of both the upper and lower lips in order to enhance the lip line. This pass around the vermilion border is usually applied with double pulse impacts. A final pass with an erbium:YAG laser is performed to remove the nonspecific thermal damage left behind by the CO2 laser passes (Fig. 27.7).

4.

RESULTS

A number of groups investigating the use of various pulsed CO2 laser systems report improvement in the appearance of photodamaged skin in the range of 50 – 70% at 90 days postoperatively (21 –26,36). Our group found that when photodamage is graded on a scale of 1 –9, the preoperative score is typically decreased by 50% (22). In addition to tightening and improvement of rhytides, the skin has a healthier, more vibrant appearance and improved texture (Fig. 27.8). At the present time, if reversal of photodamage is desired, resurfacing is the best option to address all aspects of photodamage, and CO2 resurfacing has consistently produced the most significant and predictable results.

Figure 27.6 The 3 mm spot is applied to the elevated borders of acne scars to achieve further ablation and tightening.


Figure 27.7

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As a final step, thermal damage is ablated with one pass of erbium:YAG laser.

Long-term follow-up has shown that there is excellent preservation of results achieved by a CO2 resurfacing procedure. In our practice, patients who were 1 –4 years postresurfacing were evaluated and found to have maintained 80% of their improvement that was observed at 90 days postoperatively. Other studies by different investigators have found similar preservation of results (28,42,43). In addition, greatly diminished rates of premalignant lesions are observed, and many patients have complete remission of actinic keratoses for a number of years after resurfacing (44 – 47). Treatment of the neck with CO2 laser has not been found to be predictable enough to be clinically useful in our experience. The risk for scarring and permanent hypopigmentation is great, especially for the lower one-third of the neck, even with a single pass of the CO2 laser at the same fluences as used on facial skin. Lower pulse energies that cause only intraepidermal injury may be more successful. This would compensate for the thinner epidermis of the neck and limit the potential thermal injury to the dermis.

Figure 27.8 Patient appearances (a) before and, (b) 3 months following full-face UPCO2 resurfacing.

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5.


COMPLICATIONS

The incidence of complications after CO2 resurfacing is significantly associated with depth of resurfacing and the patient’s skin type. Pre- and postoperative regimens may also affect the occurrence of complications and adverse sequelae. Complications of resurfacing include infection, pigment alterations, acne and milia, scarring, and ectropion. Edema, erythema, pruritus, and petechiae are considered normal sequelae following CO2 resurfacing but may vary among patients in intensity and duration (48 – 50). 5.1.

Postoperative Swelling

Postoperative edema is generally mild to moderate and peaks at days 2 – 3 with resolution occurring by days 5 – 7. Patients are encouraged to apply ice packs or bags of frozen peas for the first 48– 72 h postoperatively and to rest with their heads elevated in order to minimize swelling. Steroids are not recommended for routine use; however, in the case of extreme edema, IM Celestone (6–9 mg) or oral prednisone (40 –60 mg daily for 3 – 5 days) may be helpful (48). 5.2.

Erythema

The increased blood flow and angiogenesis associated with normal wound healing is manifested by erythema that occurs to some degree in all patients after resurfacing (Fig. 27.9). There are unknown individual variables that affect the degree and duration of erythema in a given patient; however, controllable variables such as the depth of injury and the extent of thermal damage as well as preoperative and postoperative regimens also affect the severity of erythema. In order for wound healing to occur after resurfacing, residual thermal necrosis must be removed by inflammatory cells; this inflammatory reaction may be a factor in prolonging erythema (40). Removal of this layer of thermal necrosis with the erbium:YAG laser has been shown to diminish erythema and enhance healing (51). Avoidance of secondary injury of the healing skin by bacterial overgrowth or by

Figure 27.9

Erythema present at 3 weeks post UPCO2 resurfacing.


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allergic or irritant contact dermatitis is very important, as this may be a primary cause of prolonged erythema. 5.3.

Itching

Itching is a common postoperative complaint, particularly during the second postoperative week. Itching most commonly reflects the normal wound healing process; however, it may signal infection, particularly candidiasis. If other signs such as patchy, beefy erythema, poor wound healing, and areas of exudate are noted, an infection must be considered and cultures taken. Contact dermatitis should also be considered, especially if topical products are being applied and if pruritus persists beyond 2– 3 weeks postoperatively. Generally, once infection and contact dermatitis have been excluded, pruritus responds well to an oral antihistamine such as diphenhydramine (Benadryl, 25 mg), cetirizine (Zyrtec 10 mg), or loratadine (Claritin, 10 mg). In addition, a topical corticosteroid such as Aclovate or hydrocortisone may be useful.

5.4.

Infection

Viral, bacterial, and fungal infections may occur after resurfacing and are most common in the first postoperative week. Prompt diagnosis and intervention will prevent further complications of delayed healing, prolonged erythema, and scarring. An infection should be suspected if (1) the patient reports intense or burning pain that is of new onset at day 2 or 3 or pain that is persistent, (2) yellow exudates or crusts, patchy intense erythema, erosions, pustules or papules are noted on examination, or (3) previously healed areas become eroded (Fig. 27.10). Herpes virus outbreaks occur in 2 – 7% of resurfacing patients and can be widespread; so, prophylaxis with antiviral medication is recommended (50,52). Bacterial

Figure 27.10 Staph aureus infection at 8 days post laser resurfacing evidenced as patches of yellow exudate and poor wound healing.

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infections should be treated according to culture and sensitivity results. The use of antibacterial prophylaxis remains controversial.

5.5.

Acne and Milia

Milia formation as well as acne exacerbation is commonly observed after laser resurfacing. Though petrolatum-based thick ointment may contribute to the development of acne and milia, the incidence of these conditions appears to be related to the degree of thermal injury to the skin. It has been proposed that thermal injury to the sebaceous glands causes a shock effect on the glands resulting in disruption and dedifferentiation of their structures and subsequent aberrant re-formation of the sebaceous canal with healing. Treatment consists of usual acne protocols. Gentle extraction on milia and comeodomes at 2– 4 week intervals is also beneficial.

5.6.

Hyperpigmentation

Hyperpigmentation is related predominately to skin type and occurs in 20 – 30% of those patients with Fitzpatrick type II skin and nearly 100% of patients with type IV skin (53,54) (Fig. 27.11). Hyperpigmentation usually appears at the end of the first postoperative month and generally takes 2 – 4 months to resolve with aggressive topical treatment. Occasionally the pigmentation may persist beyond 4 months and as long as 9 months postoperatively but in our experience always resolves if treated properly once it has developed (54). Topical therapies including tretinoin, hydroquinone, glycolic acid, vitamins C and E, and broad-spectrum sunscreen containing zinc oxide or Parsol 1789 are beneficial. Strict sun avoidance is crucial to resolution of the hyperpigmentation. Use of these agents preoperatively has not been shown to be beneficial in preventing this complication (54,55).

Figure 27.11 Patient with Fitzpatrick type IV skin with significant postinflammatory hyperpigmentation at 3 weeks post full-face laser resurfacing.


5.7.

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Hypopigmentation

Hypopigmentation following laser resurfacing occurs as a delayed phenomenon, usually not apparent for 6 – 12 months postoperatively. It is important to distinguish between “true hypopigmentation” and “pseudohypopigmentation,” which occurs as normal pigmentation in the resurfaced skin, but contrasts to the more darkly pigmented, sun-damaged skin that has not been resurfaced. True hypopigmentation reflects a loss of melanocytes and correlates both with the depth of resurfacing and the degree of thermal injury. Many of these patients have other sequelae associated with thermal injury including long-lasting erythema, milia, and/or acne, and may have areas of scarring. Patients with hypopigmentation often have been treated with free-hand techniques thus allowing pulse stacking to occur or with CPG patterns having .50% overlap (correlating to CPG density settings greater than 8). This risk for hypopigmentation is also increased when more than 3 laser passes are performed. Pseudohypopigmentation should be considered a normal consequence of resurfacing; however, patients should be advised of this outcome prior to the procedure. This can be minimized by either treating the face more lightly (i.e., a single pass) or treating the neck to blend color and avoid a line of demarcation.

5.8.

Petechiae

Petechiae are almost always of no long-term significance; however, can be distressful to the patient. They appear as nonblanchable, erythematous macules, occasionally in a linear arrangement, usually at 7– 10 days postoperatively and commonly on the lower cheeks. Petechiae are small subepithelial hemorrhages that are likely a result of an immature basement membrane and poorly formed rete ridges. The factors make newly resurfaced skin more fragile and easily injured with minor trauma, especially rubbing or scratching. Petechiae may continue for several weeks after resurfacing but usually resolve without treatment. Occasionally, the pulsed dye laser is utilized to remove any petchiae that persist beyond 6 –8 weeks postoperatively.

5.9.

Scarring

Erythematous and hypertrophic scars after laser resurfacing are often the result of excessive depth of tissue injury. This may occur because of high laser density or failure to keep the handpiece moving results in pulse stacking and excessive heat delivery to the tissue. Additionally, patients who are treated more aggressively with multiple passes of the laser will have a thicker layer of thermal necrosis that may predispose to infection. Scarring is also more common in patients who have developed a postoperative infection, as the infection alters the wound healing environment, creating a wound deeper than that created with the laser and impeding healing. Sometimes scarring occurs inexplainably even though the procedure has been done properly and superficially and there has been no secondary event such as infection or dermatitis. Such cases are rare and difficult to explain. One such patient in our practice was found to have an ANA of 1:1280 though there were no clinical signs of a collagen vascular disease. Whether this was related in a casual manner is unknown. Scarring is a much more common occurrence when resurfacing is performed on nonfacial areas such as the neck or chest. Factors that predispose to scarring in these areas include decreased adnexal structures, thinner dermis, and increased tissue tension and motion. In a study of 10 patients, the neck was resurfaced with one CO2 laser pass at

548


300 mJ and a CPG density of 6. Scarring of the lower third of the neck was seen in three patients and four patients developed patchy hypopigmentation. The key to prevention of scars is close observation for any signs of infection or delayed healing and early intervention. The first sign of a developing scar is typically erythema and pruritus, which may also signal infection. The affected area should be cultured to rule out infection, and a topical high-potency corticosteroid should be applied two to three times daily. If thickening of the affected area is noted, intralesional injection of triamcinolone (10 mg/mL) with 5-fluorouracil (50 mg/mL) in a 1:9 dilution (1 mg triamcinolone with 45 mg 5-fluorouracil) is initiated and repeated every 2–3 days until flattening occurs. Topical silicone dressings may be of additional benefit particularly in areas of trauma or friction (56). If further progression of the scar is noted, then we advise treatment with the 585 nm flashlamp pumped pulsed dye laser or other vascular laser every 4 weeks. With early intervention and utilization of these techniques, permanent scarring may be avoided. 5.10.

Ectropion

Ectropion most commonly occurs in a setting of previously scarred tissue such as a patient who has previously or concurrently undergone a lower lid blepharoplasty. Laser resurfacing of this tissue leads to excessive contraction and exposure of the conjunctiva (Fig. 27.12). Ectropion may also occur following laser resurfacing that is too aggressive without attention to laser –tissue interaction in the loose, thin skin of the lower eyelid. Preoperative evaluation of skin recoil or elasticity of the lower eyelid by means of the snap-test and evaluation of lid margin with applied tightening of loose skin, may help minimize the occurrence of ectropion. If the lid margin is easily moved with tension or the lid slow to recoil from a stretch, then particular caution and observation during laser resurfacing of the eyelid skin is necessary in order to prevent excessive tightening. In every patient, resurfacing of the eyelids should be performed after resurfacing of the cheeks in order to observe the degree of tightening in the lid area achieved with treatment of the

Figure 27.12

Ectropion of left lower eyelid at 2 months post full-face laser resurfacing.


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cheek. Also, laser density should not exceed 20 –30% (which corresponds to a CPG density of 4 or 5) in order to limit thermal damage and no more than two passes should be performed. In an evaluation of 1000 resurfacing procedures, scleral show was seen in 3% of patients at less than 4 months postoperatively, and 2% of patients greater than 4 months postoperatively. Ectropion was reported in 0.3% of patients in this series (57). 5.11. Synechiae Synechiae are adhesions that occur when two adjacent areas of de-epithelialized skin are in contact with each other in a fold and form a bridge of epithelium over the fold. These adhesions primarily occur on the lower eyelid and can be easily treated by cutting the epidermal bridge with fine scissors or a scalpel blade. To avoid a recurrence, the patient is instructed to frequently roll a moist cotton-tipped applicator over the area. Synechia almost always resolve with no residual.

6.

SEQUENTIAL CO2/ERBIUM LASER RESURFACING

The adverse events associated with CO2 laser resurfacing (infection, pigment alteration, prolonged erythema, delayed healing, and scarring) are primarily related to thermal injury and tissue necrosis. The presence of necrotic debris in a wound impedes normal wound healing and directly contributes to adverse sequelae. Removal of necrotic tissue after resurfacing should enhance wound healing. So we investigated the use of the erbium laser as a sequential step following CO2 resurfacing to remove the layer of thermally damaged tissue. Histologic studies revealed that the necrotic debris after CO2 resurfacing is effectively removed with one or two passes of the erbium laser (see chapter 29 “Combined Laser Resurfacing Techniques”). In clinical use, the erbium laser is used for two passes or to the point where pinpoint bleeding is observed. If erbium ablation is continued to the point of significant bleeding, the tissue contraction caused by the CO2 laser is immediately lost. Re-use of the CO2 laser at this point will re-establish collagen tightening. If only the necrotic tissue is ablated, tissue tightening from collagen contraction is maintained. Clinical studies and observations in our patients have shown faster healing, more rapid resolution of erythema, and decreased incidence of infection when this sequential CO2/erbium resurfacing technique is employed (51). In addition to removal of the layer of thermal necrosis, the erbium laser may be utilized to further ablate surface irregularities. This is accomplished by directing the laser at an acute angle to the skin in order to ablate the elevated borders of deep wrinkles thus further improving textural irregularities. This technique utilizes the unique features of CO2 laser (efficient epidermal removal, collagen tightening, hemostasis) and those of the erbium laser (thin ablation without tissue heating) for their combined advantages.

7.

SUPERFICIAL RESURFACING

Some patients may benefit from only superficial removal and can achieve correction of pigment irregularities, removal of superficial precancerous lesions, and some improvement in skin texture. Other patients with deeper photodamage most appropriately addressed with deep resurfacing, but do not have the time required for complete healing, may achieve some improvement with superficial procedure with decreased

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healing time. There are also patients with darker skin types who are at greater risk for pigment loss with a deeper resurfacing procedure. These patient groups have been asserted as ideal candidates for erbium resurfacing and the erbium laser has been promoted for treatment of these patients. In reality, the CO2 laser may be used very successfully and more efficiently and with a similar safety profile as the erbium laser. As previously discussed, the laser – tissue interaction of the CO2 laser is unique in the epidermis with heat dispersing laterally at the dermal/epidermal junction and resulting in complete, precise removal of the epidermis in a single pass. This occurs in a predictable, reproducible manner as a matter of physics, whereas the purely ablative mechanism of the erbium laser is a tedious, imprecise, and technically difficult process where the dermal/epidermal junction must be continuously searched and is not easily identified.

REFERENCES 1. 2. 3.

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Frances C, Robert L. Elastin and elastic fibers in normal and pathologic skin. Int J Dermatol 1984; 23:166. Smith JG, Davidson EA, Sams WM et al. Alterations in human dermal connective tissue with age and chronic sun damage. J Invest Dermatol 1962; 39:347. Bernstein EF, Chen YZ, Kopp JB et al. Long-term sun exposure alters the collagen of the papillary dermis: comparison of sun-protected and photoaged skin by Northern analysis, immunohistochemical staining, and confocal laser scanning microscopy. J Am Acad Dermatol 1996; 34:209 – 218. Taylor CR, Stern RS, Leyden JJ et al. Photoaging/photodamage and photoprotection. J Am Acad Dermatol 1990; 22:1 –15. Fisher GJ, Wang ZQ, Datta SC et al. Pathophysiology of premature skin aging induced by ultraviolet light. N Engl J Med 1997; 337:1419 – 1428. Gilchrest BA. Skin aging and photoaging. Dermatol Nurs 1990; 2:79. Goldfarb MT, Ellis CN, Weiss JS et al. Topical tretinoin therapy: its use in photoaged skin. J Am Acad Dermatol 1989; 21:645 – 650. Kligman AM, Graham CG. Histological changes in facial skin after daily application of tretinoin for 5 to 6 years. J Dermatol Tx 1993; 4:113– 117. Weiss JS, Ellis CN, Headington JT et al. Topical tretinoin improves photoaged skin: a doubleblind vehicle-controlled study. J Am Med Assoc 1988; 259:2527 – 2532. Griffiths CEM, Russman AN, Majmudar G, Singer RS et al. Restoration of collagen formulation in photodamaged human skin by tretinoin (retinoic acid). N Engl J Med 1993; 329:530–535. Fisher GJ, Datta SC, Talwar HS et al. Molecular basis of sun-induced premature skin aging and retinoid antagonism. Nature 1996; 379:335 – 339. Kang S, Duell EA, Fisher GJ et al. Application of retinol to human skin in vivo induced epidermal hyperplasia and cellular retinoid binding proteins characteristic of retinoic acid but without measurable retinoic acid levels or irritation. J Invest Dermatol 1995; 105:549 – 556. Rice-Evans CA, Burton RH, eds. Free Radical Damage and Its Controls. New York: Elsevier Press, 1994. McCay P. Vitamin E: interaction with free radicals and ascorbate. Ann Rev Nutr 1985; 5:323 – 340. Niki E. Action of ascorbic acid as a scavenger of active and stable oxygen radicals. Am J Clin Nutr 1991; 54:1119S– 1124S. Colvin RM, Pinnell SR. Topical vitamin C in aging. Clinics in Dermatol 1996; 14:227– 234. Darr D, Combs S, Dunston S, Manning T, Pinnell S. Topical vitamin C protects porcine skin from ultraviolet radiation-induced damage. Br J Dermatol 1992; 127:247– 253. Ditre CM, Griffin TD, Murphy GF et al. The effect of alpha hydroxyacids (AHAs) on photoaged skin: a pilot clinical, histological and ultrastructural study. J Am Acad Dermatol 1996; 34:187.

Skin Resurfacing with CO2 Lasers 19. 20.

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Lavker RM, Kaidbey K, Leyden JJ. Effects of topical ammonium lactate on cutaneous atrophy from a potent topical corticosteroid. J Am Acad Dermatol 1992; 26:535. Fitzpatrick RE, Tope WD, Goldman MP, Satur NM. Pulsed carbon dioxide laser, trichloroacetic acid, Baker– Gordon phenol, and dermabrasion: a comparative clinical and histological study of cutaneous resurfacing in a porcine model. Arch Dermatol 1996; 132:469 – 471. Weinstein C. Ultrapulse carbon dioxide laser removal of periocular wrinkles in association with laser blepharoplasty. J Clin Laser Med Surg 1994; 12(4):205 – 209. Fitzpatrick RE, Goldman MP, Satur NM, Tope WDP. Pulse carbon dioxide laser resurfacing of photoaged skin. Arch Dermatol 1996; 132:395– 402. Waldorf HA, Kauvar ANB, Geronemus RG. Skin resurfacing of fine to deep rhytids using char-free carbon dioxide laser in 47 patients. Dermatol Surg 1995; 21:940 –946. Lask G, Keller G, Lowe N, Gormley D. Laser skin resurfacing with the Silktouch flashscanner for facial rhytids. Dermatol Surg 1995; 21:1021 – 1024. Alster TS. Comparison of two high-energy pulsed carbon dioxide lasers in the treatment of periorbital rhytids. Dermatol Surg 1996; 22:541 – 545. Chernoff G, Shoenrock L, Cramer H et al. Cutaneous laser resurfacing. Int J Aesthe Rest Surg 1995; 3:57 – 68. Fulton JE, Shitabata PK. CO2 laser physics and tissue interactions in skin. Lasers Surg Med 1999; 24(2):113– 121. Weinstein C. Carbon dioxide laser resurfacing: long-term follow-up in 2123 patients. Clin Plast Surg 1998; 25:109 – 130. Kauver ANB, Waldorf HA, Geronemus RG. A histopathological comparison of “char-free” carbon dioxide lasers. Dermatol Surg 1996; 22:343. Cotton J, Hood AF, Gonin R et al. Histologic evaluation of preauricular and postauricular human skin after high-energy, short-pulse carbon dioxide laser. Arch Dermatol 1996; 132:425. Walsh JT, Flotte TJ, Anderson RR et al. Pulsed CO2 laser tissue ablation: effect of tissue type and pulse duration on thermal damage. Lasers Surg Med 1988; 8:108. Green HA, Domankevitz Y, Nishioka NS. Pulse carbon dioxide laser ablation of burned skin: in vitro and in vivo analysis. Lasers Surg Med 1990; 10:476. Reid R. Physical and surgical principles governing carbon dioxide laser surgery on the skin. Dermatol Clin 1991; 9:297. Fitzpatrick RE, Smith SR, Sriprachya-anunt S. Depth of vaporization and the effect of pulse stacking with a high-energy, pulsed carbon dioxide laser. J Am Acad Dermatol 1999; 40:615–622. Lans LJ. Experimentelle Untersuchungen u¨ber Entstehung von Astigmatismus durch nicht-perforirende Corneawunden. Graefes Asrch Ophthalmol 1898; 45:117. Stringer H, Parr J. Shrinkage temperature of eye collagen. Nature 1964; (December):1307. Stringer HCW, Highton TC. The shrinkage temperature of skin collagen. Austral J Dermatol 1960; 5:230 – 234. Vangsness CT Jr, Mitchel W III, Nimni M, Elrich M et al. Collagen shortening: an experimental approach with heat. Clin Orthop Relat Res 1997; 337:267 – 271. Ross EV, Naseef M, Skrobal JM, Grevelink RR et al. In vivo dermal collagen shrinkage and remodeling following CO2 laser resurfacing. Lasers Surg Med 1996; 19(S8):38. Goldman MP, Fitzpatrick RE. Cutaneous Laser Surgery. 2nd ed. St. Louis: Mosby, 1999. Fitzpatrick RE, Rostan EF, Marchell N. Collagen tightening induced by carbon dioxide laser versus erbium:YAG laser. Lasers Surg Med 2000; 27:395 – 403. Fitzpatrick RE, Manuskiatti W, Goldman MP. Long-term effectiveness and side effects of carbon dioxide laser resurfacing for photoaged facial skin. J Am Acad Dermatol 1999; 40:401–411. Ross EV, Grossman MC, Duke D, Grevelink JM. Long-term results after CO2 laser skin resurfacing: a comparison of scanned and pulsed systems. J Am Acad Dermatol 1997; 37:709 – 718. Fitzpatrick RE, Goldman MP. Resurfacing of photodamage of the neck using the Ultraspulse CO2 laser. Lasers Surg Med 1997; 9(suppl):33. Goldberg D. Treatment of photoaged neck skin with the pulsed erbium:YAG laser. Dermatol Surg 1998; 24:619 –621.

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Fitzpatrick and Rostan Gonzales-Uiloa M, Castillo A, Stevens E et al. Preliminary study of total restoration of facial skin. Plast Reconstr Surg 1954; 13:151– 161. Goldman MP, Fitzpatrick RE, Manuskiatti W. Laser resurfacing of the neck with the erbium:YAG laser. Dermatol Surg 1999; 25:162 – 168. Goldman MP, Fitzpatrick RE, Smith SR. Resurfacing complications and their management. In: Coleman WP, Lawrence N, eds. Laser Resurfacing. Baltimore: William & Wilkins, 1997. Lowe NJ, Lask G, Griffin ME et al. Laser skin resurfacing pre and post-treatment guidelines. Dermatol Surg 1995; 21:1017 –1019. Nanni CA, Alster TS. Complications of CO2 laser resurfacing: an evaluation of 500 patients. Lasers Surg Med 1997; 9(suppl):242. Goldman MP, Manuskiatti W. Combined laser resurfacing with the UPCO2 and Er:YAG lasers. Derm Surg 1999; 25:160– 163. Monheit GD. Facial resurfacing may trigger the herpes simplex virus. Cosmetic Dermatol 1995; 8:9. Ho C, Nguyen Q, Lowe NJ et al. Laser resurfacing in pigmented skin. Dermatol Surg 1995; 21:1035. Sriprachya-anunt S, Marchell N, Fitzpatrick RE, Goldman MP, Rostan EF. Facial resurfacing in patients with Fitzpatrick skin type IV. Lasers Surg Med 2002; 30:86 –92. West TB, Alster TS. Effect of pretreatment on the incidence of hyperpigmentation following cutaneous CO2 laser resurfacing. Dermatol Surg 1999; 25:15– 17. Fitzpatrick RE. Treatment of inflamed hypertrophic scars using intralesional 5-FU. Dermatol Surg 1999; 25:224 –232. Roberts TL, Lettieri JT, Ellis LB. CO2 laser resurfacing: recognizing and minimizing complications. Aesthet Surg Q 1996; 16:141.

28 Skin Resurfacing with Erbium:YAG Lasers Kucy Pon and Vivek Iyengar SkinCare Physicians of Chestnut Hill, Chestnut Hill, Massachusetts, USA

Thomas Rohrer SkinCare Physicians of Chestnut Hill, Chestnut Hill and Boston University School of Medicine, Massachusetts, USA

1. Carbon Dioxide Laser 2. Erbium:YAG Laser 3. Clinical Treatment with Er:YAG Laser 3.1. Patient Selection 3.2. Pretreatment Regimen 3.3. Immediate Preoperative Procedure 3.4. Anesthesia 3.5. Treatment Technique 3.6. Postoperative Care 4. Complications 5. Conclusion References

554 554 556 556 557 557 558 558 560 562 565 566

Facial skin rejuvenation has always been a topic of great interest. Ancient Egyptians used a variety of methods which included vegetable extracts, mud packs, and soured milk to refresh the skin. The recent era has brought about topical agents such as retinoic acid, retinol, antioxidants, alpha-hydroxy acids, trichloroaectic acid, phenol, and physical modalities such as dermabrasion, microdermabrasion, as well as carbon dioxide and erbium:yttrium-aluminium-garnet (Er:YAG) lasers. In order to achieve rapid and significant improvement of sun-damaged skin, the outer photodamaged layer must be removed, allowing subsequent healing and re-epithelialization. A combination of intrinsic and extrinsic processes leads to aging of the skin. Intrinsic factors include cellular damage from free radicals and programed cell death. Changes of intrinsic aging are seen in areas of nonsun-exposed skin. With advanced age, these areas demonstrate thinning of the epidermis, decreasing amounts of collagen and elastic tissue, loss of dermal blood vessels, and hypocellularity of the dermis. The net effect is fine wrinkling of the skin with sagging and loss of elasticity (1 – 4). Extrinsic damage is caused by various environmental exposures. By far, the most damaging is chronic UV radiation. Over 90% of skin changes found in sun-exposed areas may be related to 553

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sun-induced photodamage. These changes include fine to course wrinkling, textural abnormalities, skin sag and laxity, pigmentary alterations, sallow color, dryness, scaling and roughness, telangiectasias, and easy bruisability (5 –7).

1.

CARBON DIOXIDE LASER

The CO2 laser was developed in 1964, and by 1968 there were reports of its use for the treatment of actinic cheilitis (8). By the 1980s and early 1990s, high energy, shortpulsed CO2 lasers were being used to resurface actinically damaged skin (9 –15). The introduction of laser resurfacing was an enormous step forward in the field of facial skin rejuvenation, because it allowed precisely controlled removal of thin layers of skin and tightening of the underlying tissue without excessive collateral thermal damage. The 10,600 nm wavelength of the CO2 laser is preferentially absorbed by water to a depth of 30 mm in the skin (16,17). When enough energy is given to heat intracellular water to 1008C, vaporization occurs with ablation of the skin. Studies and calculations demonstrate that a pulse fluence of 5 J/cm2 is necessary for the CO2 laser to ablate skin (16 –18). The energy pulse must be delivered in ,1 ms (19), the estimated thermal relaxation time of 30 mm of skin (16,17), in order to confine the depth of damage and prevent heat diffusion. Histology shows that with one pass, the CO2 laser vaporizes 20– 30 mm of tissue and creates a zone of thermal damage measuring 40– 120 mm (20,21). With continuous heating, the target water is removed, tissue desiccation occurs, and heat accumulates creating a widespread zone of nonselective thermal necrosis. Thermal necrosis .100 mm thick interferes with wound healing and carries a significant risk of scarring (22). Besides tissue vaporization, the CO2 laser causes dermal changes, such as heatinduced collagen shrinkage, which contributes to skin tightening (12). When collagen in the skin is heated to 60 – 708C, it contracts to about one-third to one-quarter its original length (23 – 25). Collagen shrinkage is thought to occur within a zone of reversible thermal injury found below the zone of irreversible thermal damage. Actual tissue contraction is seen immediately following CO2 laser resurfacing, and is most noticeable on the first dermal pass. In addition, the zone of thermal necrosis stimulates new collagen formation and collagen remodeling with additional clinical improvement. Although the degree of tightening achieved depends on the number of passes delivered, skin thickness, and anatomic location, resurfacing with the CO2 laser achieved very reproducibly impressive clinical improvement of facial rhytides. Unfortunately, resurfacing with a CO2 laser also carried with it significant healing time and risk of postoperative complications. The majority of the postoperative recovery time and complications are related to the significant zone of thermal necrosis below the level of vaporization. With this in mind, research turned to wavelengths with more efficient absorption by water.

2.

ERBIUM:YAG LASER

The Er:YAG laser was looked into as an alternative to CO2 lasers for skin resurfacing. Its wavelength of 2940 nm closely corresponds to an absorption peak of water and is approximately 16 times better absorbed by water than the 10,640 nm CO2 laser (26). Given this efficient absorption by water, the Er:YAG is absorbed in the most superficial cells and penetrates to only approximately 1/20th the depth of the CO2 laser (27). This superficial absorption, however, allows for ablation of even finer layers of skin than with the CO2 laser with significantly less collateral thermal damage (Fig. 28.1). Measurements show

Skin Resurfacing with Er:YAG Lasers

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Figure 28.1 (a) Histology following a single pass with the erbium:YAG resurfacing laser at a fluence of 5 J/cm2. Note superficial ablation and no visible residual thermal damage. (b) Histology following a three consecutive passes with the erbium:YAG resurfacing laser at a fluence of 10 J/cm2. Note deep ablation with minimal residual thermal damage.

that fluences of 0.6 –5 J/cm2 will allow the Er:YAG laser to ablate skin, and 4 mm of tissue is vaporized per J/cm2 of energy (28). Therefore, a fluence of 5 J/cm2 will vaporize the entire epidermis in four passes, and 8 – 12 J/cm2 will vaporize the epidermis in two passes (29). A single pass with a Q-switched (90 ns pulse duration) Er:YAG will leave a zone of thermal damage of only 5 –10 mm, whereas a normal pulsed (200 ms pulse duration) laser creates 10 –40 mm of thermal damage (28 –32). Because the Er:YAG laser creates such a small zone of thermal injury compared with the CO2 laser, it has somewhat different effects than the CO2 laser. A small zone of thermal damage produces less tissue desiccation, and therefore each subsequent pass with the Er:YAG brings about very similar effects, unlike the CO2 laser which shows significantly diminished returns with each pass. Furthermore, given the thin zone of thermal damage, ablation with the Er:YAG laser is not hemostatic, and bleeding eventually often becomes an issue and may limit the depth of ablation achievable. The CO2 laser has the ability to coagulate blood vessels 0.5 mm or smaller in diameter, thus offering the benefit of relatively bloodless resurfacing surgery (33). The Er:YAG and CO2 lasers also have different effects on dermal collagen. The peak of collagen absorption is 3000 nm, very close to the wavelength of the Er:YAG laser. This results in significantly less nonselective heating of the dermis with the Er:YAG laser, and subsequently less collagen contraction and tightening. Depending on the depth of ablation and settings used, it is estimated that Er:YAG lasers may achieve between 0% and 14% tissue contraction (34) when compared with 20 –30% collagen contraction with the CO2 laser (35). Histologic changes seen with long-term follow-up demonstrate that CO2 laser treatment induces a significant amount of new collagen formation, whereas the Er:YAG laser used alone produces much less new collagen (36). Therefore, overall clinical improvement of rhytides and skin sag is typically more impressive following CO2 laser resurfacing. However, the minimal thermal damage to tissue following Er:YAG laser leads to an abbreviated healing time, erythema which is decreased in intensity and of shorter duration, and a lower incidence of scarring when compared with the CO2 laser. Many laser surgeons now resurface using a combination of CO2 and Er:YAG lasers in order to achieve benefits of both methods. Typically, the CO2 laser is performed first, followed by one to two passes with the Er:YAG in order to remove some of the thermal damage and necrotic tissue created by the CO2 . This sequence seems to decrease healing time, hasten re-epithelialization, diminish erythema, and crusting, while maximizing the therapeutic benefits obtained with the CO2 laser (37,38). The author employs a different “sandwich” technique, using the

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Er:YAG first to reach the dermis without causing the thermal damage of the CO2 , followed by the CO2 to provide nonselective heating of dermal collagen, and finishing with one to two passes of the Er:YAG to remove some of the CO2 induced thermal damage. In an attempt to deliver greater thermal effects to tissue, and attain collagen tightening and hemostasis, as seen with the CO2 laser, variable pulse Er:YAG lasers have also been developed. These systems offer the ability to change the pulse duration from a short, ablative pulse to a longer, more thermally damaging pulse. Clinical and histologic studies demonstrate that these variable pulse Er:YAG lasers can achieve results approaching those seen with CO2 lasers, but with less postoperative morbidity and decreased risk of complications (39 –41). The more precise wavelength of the Er:YAG in targeting dermal collagen, and the resulting decrease in nonselective thermal damage may help to explain this phenomenon. Due to the more superficial ablation and limited thermal damage, the Er:YAG laser has been used safely to resurface nonfacial skin such as the neck, hands, and forearms (42,43). This is a distinct advantage over CO2 laser resurfacing of nonfacial skin, which is often complicated with poor healing, and carries an unacceptably high risk of scarring. However, Er:YAG laser resurfacing of nonfacial skin is not commonly performed and should be done cautiously and only by experienced laser surgeons. Besides resurfacing photoinduced rhytides, the Er:YAG laser has been used to treat actinic keratoses (44), acne scarring (45,46), traumatic and surgical scarring (47), sebaceous hyperplasia (45), rhinophyma (48), xanthelasma (49,50), syringoma (45,50), eruptive vellus hair cysts (51), epidermal nevi (52), common wars (44) cafe´ au lait macules (53), and tattoos (52).

3. 3.1.

CLINICAL TREATMENT WITH Er:YAG LASER Patient Selection

Perioral and periorbital rhytides are difficult to treat with face-lifts, chemical peels, and dermabrasion, but often respond dramatically to laser resurfacing. Although it may be tempting to resurface an isolated cosmetic unit with a CO2 laser, treatment of the entire face usually produces a better result. Given the 10% risk of hypopigmentation with CO2 resurfacing, full-face resurfacing would result in more predictably even pigmentation, whereas treating a single area or an isolated wrinkle may result in a patchy unnatural appearance. Therefore, most patients undergoing CO2 laser resurfacing receive full-face treatment. Although it is still preferable to treat the entire face with the Er:YAG laser, it is not mandatory, and treating one or two cosmetic units may be performed with much less risk of pigmentary differences between adjacent units. Although the superficial ablation and minimal collateral thermal damage achieved with the Er:YAG laser allow physicians to treat patients with more confidence, careful patient selection is still essential. Absolute contraindications to laser resurfacing include active bacterial or viral infections, impaired immune system, use of Accutanew in the past year, and history of poor healing, especially hypertrophic scars or keloids in the treatment area. Skin that has received extensive radiation therapy or patients with scleroderma show decreased amounts of adnexal structures and should not be resurfaced because of risks of poor healing. Patients with unrealistic expectations should not be resurfaced. Pregnant patients are also not treated due to the unknown risk of anesthesia on the fetus. Relative contraindications include history of prior skin dyspigmentation, skin types V and VI, and koebnerizing diseases such as vitiligo or labile psoriasis. Patients who had a prior blepharoplasty or who have significant eyelid laxity should be approached


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cautiously, since the tightening achieved during laser resurfacing may result in ectropion formation. A discussion detailing the procedure itself, the postoperative course, potential complications, and expected benefits helps to minimize patient fears and anxiety. Before and after photographs can also show patients what to anticipate during the short- and long-term healing phase, as well as the end result.

3.2.

Pretreatment Regimen

There are many pretreatment regimens but few studies have examined their effects on laser skin resurfacing. Topical retinoids have been shown to speed-up healing and re-epithelialization after dermabrasion (54), and despite any controlled studies showing a benefit in laser resurfacing, and are frequently used daily for 1 –2 months prior to resurfacing (55). Alpha-hydroxy acid preparations and topical vitamin C are often substituted in patients that cannot tolerate topical retinoids. Postinflammatory hyperpigmentation is a fairly common occurrence following laser resurfacing, especially in darker skin types. To reduce the risk of hyperpigmentation, most laser surgeons prescribe topical hydroquinone, kojic acid, or azelaic acid to be used for 1 – 2 months preoperatively in patients with skin types IV –VI (55). Postoperative sun avoidance and use of sunscreen are essential in the prevention and treatment of postinflammatory hyperpigmentation. There are several well-documented cases of herpes simplex outbreaks occurring after resurfacing, and disseminating widely over the entire denuded skin. This leads to prolonged healing and resultant scarring. This complication has occurred both in patients with and without a history of herpes labialis. Therefore, all patients undergoing laser resurfacing of the face are typically prophylactically given either acyclovir 400 mg PO tid, valacyclovir 500 mg PO bid, or famcyclovir 250 mg PO bid. The antiviral is started 2 days prior to the procedure and continued for 10 days after the procedure. Following a laser resurfacing procedure, a layer of thermally necrotic tissue is produced, which provides an optimal environment for bacterial growth. Postoperative bacterial infections lead to delayed healing and may result in scarring. Prophylactic use of systemic antibiotics, such as dicloxacillin, cephalexin, or azithromycin in penicillin allergic patients, is therefore given 2 days prior and continuing until the skin has re-epithelialized, to diminish the incidence of postoperative infection. In situations with a high likelihood of gramnegative pseudomonas infection, such as prolonged use of an occlusive dressing, ciprofloxacin has been advocated. A moist, warm wound environment also promotes candidal infections. Occasionally, a single dose of fluconazole may be given on the day of surgery to patients, especially those with a significant history of recurrent vaginal yeast infections. Alternatively, a dose may be given at day 3, or if pruritus or unusual erythema is noted (56).

3.3.

Immediate Preoperative Procedure

The patient’s face should be gently cleansed with soap and water to remove any make-up and surface residue. The skin may be prepped with an antiseptic solution such as betadine. If an alcohol antiseptic is used, it should be completely dry before starting the procedure. Rhytides or acne scars are typically outlined with a sterile marking pen. Damp cloths may be draped on the patient’s chest, neck, and periphery of the face, to prevent injury to skin not intended for treatment or ignition of flammable materials by any unintentional laser

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impacts. Headbands are helpful in keeping hair-off the face and out of the way during treatment. The patient’s eyes are protected using opaque, metal, nonreflective eye shields.

3.4.

Anesthesia

Facial resurfacing with any laser is a painful procedure and requires anesthesia in order to keep the patient comfortable and provide optimal treatment conditions for the laser surgeon. The pain is caused by ablation of epidermal and dermal tissue, and the associated collateral thermal damage. Because Er:YAG lasers generate significantly less thermal damage, the pain associated with Er:YAG laser resurfacing per pass is less than that with CO2 laser resurfacing. Some physicians use only topical anesthetic creams, such as lidocaine –prilocaine (EMLAw) cream with occlusion, but in our experience this is often insufficient. Nerve blocks combined with local infiltration can provide more complete anesthesia for Er:YAG laser resurfacing. Supraorbital, supratrochlear, infraorbital, and mental nerve blocks can be easily performed, and are used for the majority of the central face. The jawline, lateral cheeks, temples, eyelids, and oral commissures are supplemented with local infiltration. Preoperative sedatives, such as lorazepam or diazepam, are also useful in making the nerve blocks, local infiltration, and the entire resurfacing procedure less uncomfortable. Intravenous sedation is, generally, not necessary for Er:YAG laser resurfacing.

3.5.

Treatment Technique

Many different operative techniques are employed by various laser surgeons, and achieve great success. Here, we describe our experience. Mild to moderate rhytides or acne scars are treated first with the Er:YAG laser using a small spot size at high fluences to even out the surface of the rhytid or the scar shoulder. When doing this, it is often better to follow and treat the entire wrinkle or scar to its endpoint rather than to limit treatment to a cosmetic unit. Once the contour is smooth, or an appropriate depth has been reached, a larger spot size or scanner is used to treat the entire cosmetic unit. The direction and pattern of passes are alternated in order to prevent a striped or patterned appearance to the treated area. Fewer passes are made at the periphery of the treated area to feather the effect out and blend into the untreated skin. It is our experience that it is better to treat the individual lines or scars first before treating the entire cosmetic unit, because edema from the impact of the first passes often distorts the contours and masks the rhytides. Then in the weeks following treatment, when the edema resolves, the residual rhytides appear. Er:YAG resurfacing can be performed either freehand or with a scanner. If the freehand method is used, it is important to ensure that overlapping of pulses is moderate, but not great. Significant overlapping and stacking of pulses will increase the depth of ablation and collateral thermal damage. The number of passes necessary to vaporize the epidermis depends on the fluence and spot size used. In general, a fluence of 5 – 7 J/cm2 will ablate the epidermis in two to four passes and a fluence of 8 –15 J/cm2 will do so in one or two passes (29). Subsequent passes will ablate between 5 and 40 mm of tissue depending on the energy fluence used. A quick wipe between passes with moistened gauze is recommended to remove the fine tissue debris, to rehydrate the skin, and to allow better visualization of the plane being treated. This process only takes a few seconds and does not require the time and effort associated with wiping between CO2 passes.


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The total number of passes done depends on the depth of the rhytides, scars, or other lesions being treated, bleeding encountered which precludes further treatment, or maximum number of laser passes considered safe. The visual endpoint for treatment with the Er:YAG laser differs from that of the CO2 laser. The chamois yellow color seen with CO2 resurfacing, which indicates that the deep papillary dermis or superficial reticular dermis is reached, is not seen with Er:YAG laser resurfacing. Therefore, the physician must be mindful of the estimated depth of ablation associated with each pass of the laser at the fluence being used, and compare that with the average depth of the epidermis and dermis of the area being treated. As the collateral thermal injury induced by the Er:YAG laser is insufficient to coagulate medium-sized vessels, a common visual clue indicating that ablation has reached the mid-dermis is pinpoint bleeding (Fig. 28.2). This bleeding will often inhibit further treatment beyond a certain level. If the rhytides, acne scars, or other lesions are adequately effaced before the bleeding and exudate limit further treatment, then one or two additional passes are done to compensate for the impact edema. If oozing is remarkable, gauze soaked with 1% lidocaine with epinephrine can be placed over the resurfaced area at the end of the procedure. For moderate to severe rhytides, a combination of CO2 and Er:YAG lasers is often used to obtain better clinical results, while minimizing postlaser side effects and complications. The procedure is started as mentioned earlier, with flattening of the rhytides or acne scar shoulders first, followed by a single pass over the rest of the cosmetic unit with the Er:YAG laser. The CO2 laser is then used over the entire treatment area to induce collagen tightening. Often a single pass with the CO2 is adequate, but on occasion, a second pass is needed. After the CO2 laser, the Er:YAG laser is repeated in order to remove some of the thermal damage produced by the CO2 laser. This sequence minimizes the zone of thermal necrosis, and therefore shortens healing time and decreases posttreatment erythema, while still inducing tissue contraction. Many laser surgeons recommend performing two passes with the CO2 laser first followed by several passes with the Er:YAG laser. However, by using the Er:YAG laser at the beginning, the epidermis may be ablated with minimal residual thermal necrosis. This serves to eliminate one of the passes performed with the CO2 laser, which will also decrease the zone of thermal necrosis. Results attained using this combined method approaches those attained with the CO2 laser alone, and have a significantly reduced healing time and a lower incidence of complications. An alternative to switching between two different lasers is to use an Er:YAG laser with a variable pulse width (Contour from Sciton and CO3 from Cynosure). When used with a longer pulse duration, “CO2-like” effects may be achieved. The increased pulse

Figure 28.2 Upper lip region exhibiting fine pinpoint bleeding associated with dermal depth ablation. The pinpoint bleeding serves as a visual cue as to depth of penetration.

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duration extends the zone of thermal damage, induces collagen contraction, and coagulates small dermal blood vessels. Shortening the pulse duration gives typical “Er:YAGlike” effects with minimal thermal injury and superficial ablation. Therefore, the short pulse mode can be used to initially smooth rhytides and scars, then the long pulse mode can tighten tissue, and finally the short pulse mode used again to remove the layer of necrotic tissue in order to hasten healing. Thus, one can achieve results with one dual mode Er:YAG laser approaching those only previously seen with the use of the CO2 laser. In addition, due to the wavelength selectivity of the Er:YAG, the longer pulse delivers the “CO2-like” benefit of thermal damage and subsequent collagen contraction, whereas decreasing risk of deleterious effects seen with the CO2 laser including hypopigmentation (57). An additional application of the contour is the ability to perform a mild one pass 10 mm resurfacing for the treatment of lentigines and mild photodamage without the need for anesthesia or significant downtime. Although not achieving significant improvement of rhytides, this treatment provides results comparable to a TCA peel but with more consistent and even depth of vaporization, as well as more versatility and control. Patients with lentigines and mild photodamage on the majority of the face but significant perioral or periorbital rhytides can receive the deeper dual mode treatment in those subunits requiring collagen contraction, and the milder treatment on the remainder of the face. Thus, one can tailor treatment to optimize the benefits, while minimizing postoperative healing and morbidity. Clinical results with both Er:YAG and combined CO2/Er:YAG treatments have been very impressive. Although quantifying the amount of improvement is often difficult, reports have stated an average of 25 – 75% improvement of facial rhytides with Er:YAG resurfacing. Those with mild to moderate rhytides are the ideal candidates for treatment with the Er:YAG laser or a combined CO2/Er:YAG approach (Fig. 28.3 –28.6). 3.6.

Postoperative Care

Following laser resurfacing, the skin is denuded and there is a significant amount of serous exudate and pinpoint bleeding. Erythema and swelling usually increase over the first few days before improving. Ice packs and sleeping in a more upright position may help to minimize some of the edema. Re-epithelialization occurs over 3 –10 days, and during this time, it is crucial that the skin be kept moist and not allowed to desiccate. There are advantages and disadvantages to each dressing used postoperatively, and no consensus exists as to which is the best for postresurfacing wound care. Closed dressings have been shown to accelerate wound healing by 30% or more, decrease pain, and reduce inflammation (58,59). In addition, a silicone occlusive dressing (Silon-TSR) was shown to

Figure 28.3 (a) Preoperative mild to moderate periorbital rhytides. (b) Same area 2 weeks following erbium:YAG periorbital resurfacing.


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Figure 28.4 (a) Preoperative mild to moderate perioral rhytides. (b) Same area 3 months following erbium:YAG perioral and mucosal lip resurfacing.

decrease the severity and duration of erythema, swelling, and crusting (60). Faster re-epithelialization associated with occlusive dressings is attributed to the moist wound environment, lack of crust formation which would impede cellular movement, and higher levels endogenous growth factors. However, this moist, warm environment, coupled with necrotic tissue debris, promotes the growth of bacteria and may increase the risk of infection, and subsequent scarring if left in place too long (61). Therefore, we recommend that occlusive dressings not be left on the skin for more than a few days at a time. Open-wound care involves thoroughly soaking the skin with 0.25% acetic acid, normal saline, or cool tap water every 1 – 2 h, and then thickly coating the skin with a petrolatum such as Aquaphor healing ointment between soakings. We recommend the application of a biosynthetic dressing, such as Vigilon, Silon, or Second Skin, for the first 24– 48 h after resurfacing. When occlusive dressings are left on for a short period of time, there does not seem to be a significant risk of infection, and re-epithelialization is hastened dramatically (60). Most patients also prefer this type of dressing during the initial recovery period, because it decreases the amount of discomfort and burning. During this period, ice packs, head elevation, and anti-inflammatory medications, such as acetaminophen, are encouraged to help minimize edema. Patients are seen at postoperative day 1 or 2 and evaluated. On postoperative day 3, patients are changed over to the open system with frequent soaks, followed by liberal use of Aquaphor healing ointment, giving a semi-occlusive dressing. Topical antibiotic ointments such as Neosporin, Bacitracin, or Polysporin during the healing phase have been associated with an increased incidence of allergic contact and irritant dermatitis (62), and are therefore not recommended.

Figure 28.5 (a) Full-face actinic damage, lentigenes, and mild rhytides. (b) Same area 3 months following full-face erbium:YAG resurfacing.

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Figure 28.6 (a) Full-face actinic damage, lentigenes, actinic bronzing, and mild rhytides. (b) Same patient 1 month following full-face resurfacing with a combined erbium:YAG/CO2 “sandwich” technique. This patient also had a 20% TCA peel of her neck to minimize any line of demarcation between treated and nontreated areas.

Prophylactic antibiotic and antiviral medications started preoperatively are continued for a full 10 days until epithelialization is completed. A prescription for analgesics is given for patients to use as needed for postoperative pain. There seems to be more pain associated with Er:YAG laser resurfacing than with CO2 laser resurfacing in day 1 or 2 following the procedure. This may be due to the limited thermal damage of the Er:YAG laser not cauterizing the nerve endings, as well as the CO2 laser. Most patients experience pruritus in the first few weeks after resurfacing. This is often self-limited and can be controlled with a combination of cool compresses, anti-histamines, and mild topical steroids. If itching is severe, and not responsive to conservative treatment, complications such as infections, particularly candidiasis or contact dermatitis should be considered. Erythema occurs to some degree in all patients and can last for a few weeks following laser resurfacing. Once the skin has re-epithelialized (1 week), this redness can usually be camouflaged with make-up. Sun avoidance and the use of sunscreens are important in the first month following the procedure to reduce the risk of postinflammatory hyperpigmentation. Perhaps, the most important component of postoperative care is close monitoring of the patient for any problems or complications. Not only are frequent follow-up visits reassuring for the patient, but also they allow the physician to intervene and treat any side effect or complication at the earliest possible moment. Early aggressive intervention is critical in preventing permanent complications.

4.

COMPLICATIONS

All surgical procedures carry a risk of complications, and Er:YAG laser resurfacing is no exception. Although the incidence of complications seen with Er:YAG lasers is very low compared with dermabrasion, deep chemical peels, and even CO2 laser resurfacing, significant problems can occur. Side effects and potential complications seen with Er:YAG resurfacing are identical to those seen with CO2 resurfacing; however, they usually occur less frequently and with less intensity. Burning discomfort, erythema, swelling, and itching are normal predictable sequelae, but may be more prominent and longer lasting in some patients. The burning sensation may be an exception to the less intense rule with Er:YAG resurfacing, and patients often feel intense discomfort in the first 24 – 48 h postresurfacing. This is likely due to the decreased thermal effect seen with


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the Er:YAG laser. With CO2 resurfacing, the larger zone of thermal necrosis, besides being beneficial from a hemostasis point of view, may actually cauterize nerve endings sufficiently to diminish the immediate postoperative pain. Potential complications with Er:YAG resurfacing include pigmentary alteration, infection, milia and acne, and scar formation. Postoperative erythema occurs in all patients following resurfacing as a result of inflammation, increased blood flow, and angiogenesis associated with the healing process. It usually lasts between 1 and 3 months with CO2 resurfacing (63 –65). With Er:YAG laser resurfacing, the duration of erythema is generally reduced to approximately 1 – 4 weeks (66,67). Although some patients may experience more persistent erythema, none of our patients have had erythema lasting longer than 12 weeks following Er:YAG resurfacing. Because postoperative erythema is transient, it is usually not treated. It may be masked with make-up containing a green base. Careful evaluation for an allergic or irritant reaction, infection, and trauma should be done on any patient with unusual erythema. If erythema persists longer than 6 weeks, we often treat the area with a pulsed-dye laser. Swelling is generally mild to moderate and typically resolves in 4–7 days. Soaks with cool water, ice packs, and head elevation all help to minimize edema. Rarely, a patient may develop marked swelling that warrants a short course of oral corticosteroids. Pruritus is common during the healing process and is treated with a combination of cool compresses, oral anti-histamines, and topical steroids. It is important to treat pruritus in order to improve the patient’s level of comfort and to prevent excoriations, which could lead to scarring. In addition, if the pruritus is severe or does not readily respond to treatment, the patient should be fully evaluated for potential infection and/or contact dermatitis. The most common adverse effect seen with CO2 resurfacing is transient postinflammatory hyperpigmentation, occurring in up to 37% of patients (68). Although it is significantly less common in patients treated with the Er:YAG laser, it still occurs in 5% of patients (Fig. 28.7). Postinflammatory hyperpigmentation, typically, is more common in darker skin types, but it may occur in patients with Fitzpatrick types I–III skin. The risk of hyperpigmentation may be reduced using sun avoidance and sunscreens, as well as hydroquinone, azelaic acid, and alpha-hydroxy acids in the postoperative period. Any evidence of hyperpigmentation developing should be treated early with bleaching agents. Permanent hypopigmentation is a late complication, usually occurring 6 – 12 months after resurfacing. It has been reported in up to 16% of patients treated with CO2

Figure 28.7 Hyperpigmentation of periorbital area 3 weeks following erbium:YAG resurfacing. Hyperpigmentation resolved by 3 months.

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resurfacing (68). Thus far, we have not seen it in any of our patients treated with the Er:YAG. However, one report relates a rate of 4% in a series of 50 patients treated with the dual mode Er:YAG alone (57). This presumed lower risk of hypopigmentation may allow treatment of single cosmetic units without the risk of a dramatic color mismatch between treated and untreated skin. Lack of a protective epidermal barrier, a moist wound environment, and necrotic tissue all increase the risk of bacterial, viral, and fungal infections in the postoperative period. All patients are started on antibiotics and antivirals preoperatively and these are continued for 7 –10 days following the procedure. New onset of pain or prolonged pain, intense itching, abnormal erythema, yellow exudate or crust, papules, pustules, vesicles, erosions, or delayed healing may be indicative of an infection, and appropriate smears and cultures should be taken. Early and aggressive treatment is critical to prevent permanent scarring. Increasing the dose of the antiviral, or switching to a different antiviral agent is recommended for a localized herpes simplex infection. Disseminated herpes simplex should be treated with intravenous antiviral therapy. Bacterial infections may require changing the antibiotic started prophylactically to ciprofloxacin, which covers against Pseudomonas. Candida infections respond well to systemic antifungal agents. Following any type of resurfacing procedure, there is a risk of milia and acne exacerbation (Fig. 28.8) (68). Use of occlusive ointments, in combination with follicular re-epithelialization, are probable exacerbating factors in milia formation. Reducing or stopping occlusive ointments once re-epithelialization has occurred may help to prevent the production of milia. Gentle extraction of individual milia may be performed using a #11 blade and a comedo extractor. Although acne flares are typically seen in patients with a past history of acne, it may occur in patients without a significant history of acne. Treatment of postresurfacing acne is similar to treatment of regular acne. Scarring following laser resurfacing is rare, but can occur even in the most experienced hands. Although reported much less frequently than with CO2 lasers, the Er:YAG laser is by no means free of the risk of scarring. Proper patient selection, conservative treatment parameters, paying close attention to the number of passes performed and treatment endpoints, good postoperative care, and most importantly, close follow-up with prompt intervention to any early warning signs will significantly decrease the incidence of scarring. Postresurfacing scarring may be treated with potent topical steroid, intralesional injection of steroids with or without 5-fluorouracil, pulsed-dye laser, silicone gel sheeting or other occlusive dressing, and/or firm massage directly to the scarred areas. Aggressive, early management with any or all of these measures may prevent permanent scar formation.

Figure 28.8

Outbreak of acne in perioral area following perioral erbium:YAG resurfacing.


5.

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CONCLUSION

Laser resurfacing has added considerably to the armamentarium of facial skin rejuvenation. Results of CO2 laser resurfacing have been very impressive, showing significant skin tightening and an average of 40 –75% improvement of facial rhytides (64,69). Er:YAG laser resurfacing has been reported to improve rhytides on average by 25– 75% (66,67). These numbers are likely even higher when using a dual mode Er:YAG lasers or a combined Er:YAG/CO2 approach. Combining the resurfacing treatment with botulinum injection may further improve results by immobilizing the treated area during the healing process. In clinical practice, patients with mild rhytides, usually, get near full correction with either the CO2 or the Er:YAG laser. The main advantages of the Er:YAG laser are the dramatically reduced healing time and the lower incidence of complications. During the healing phase, there is less erythema, oozing and crusting, and faster re-epithelialization. For moderate rhytides, either laser system can be used, but the degree of improvement is usually more impressive with the CO2 laser. These patients may also be treated with a combination of Er:YAG and CO2 lasers in order to obtain advantages of both. Patients with severe rhytides, generally, require CO2 or combined Er:YAG/CO2 resurfacing for noticeable improvement of severe wrinkles. With the advent of variable pulsed erbium:YAG systems, it is now possible to have one system capable of treating the very mild to very severe rhytides. With proper skin care and sun avoidance, results are long standing. Although there are few long-term studies, many of our patients resurfaced 5 years ago have maintained the majority of their clinical improvement with nothing more than proper skin care (Fig. 28.9). When combined with other cosmetic procedures such as botulinum toxin injection, light chemical peels, or microdermabrasion results may be sustained even longer.

Figure 28.9 (a) Preoperative mild to moderate periorbital rhytides. (b) Same area 1 month following erbium:YAG periorbital resurfacing. (c) Same area 5 years following erbium:YAG periorbital resurfacing.

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Although many “nonablative” laser and light sources now exist that are able to improve the texture of the skin to some degree, none improve it as much as the resurfacing lasers. The “nonablative” lasers and light sources have the advantage of a better safety profile and of being able to be performed without any subsequent healing or “downtime.” The results of “nonablative” systems, however, are much less consistent and not nearly as impressive as that seen with CO2 or Er:YAG resurfacing lasers. In addition, “nonablative” treatments are comprised of multiple sessions over many months, and the results of each treatment require months to be seen. The results seen with CO2 or Er:YAG resurfacing lasers are consistently impressive and visually apparent after the week of recovery. In our practice, patients able to tolerate the week of recovery time associated with resurfacing lasers have been uniformly extremely pleased with their improvement.

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Warren R, Garstein V, Kligman AM et al. Age, sunlight, and facial skin: a histologic and quantitative study. J Am Acad Dermatol 1991; 25:751 – 760. Frances C, Robert L. Elastin and elastic fibers in normal and pathologic skin. Int J Dermatol 1984; 23:166 – 179. Daly CH, Odland GF. Age related changes in the mechanical properties of human skin. J Invest Dermatol 1979; 73:84 – 87. Escoffier C, deRigal J, Rochefort A et al. Age related mechanical properties of human skin: an in vivo study. J Invest Dermatol 1989; 93:353 – 357. Gilcrest BA. Skin aging and photoaging. Dermatol Nurs 1990; 2:79. Nicol NJ, Fenske NA. Photodamage: cause, clinical manifestations and prevention. Dermatol Nurs 1993; 5:263 – 275. Taylor CR, Stern RS, Leyden JJ et al. Photoaging/photodamage and photoprotection. J Am Acad Dermatol 1990; 22:1 –15. Goldman L, Shumrick DA, Rockwell J. The laser in maxillofacial surgery: preliminary investigative surgery. Arch Surg 1968; 96:397 – 400. Fitzpatrick RE, Ruiz-Esparza J, Goldman MP. The clinical advantage of the superpulse carbon dioxide laser. Lasers Surg Med 1990; 2(suppl):52. Fitzpatrick RE, Ruiz-Esparza J, Goldman MP. The depth of thermal necrosis using the CO2 laser: a comparison of the superpulsed mode and conventional mode. J Dermatol Surg Oncol 1991; 17:340– 344. Fitzpatrick RE, Goldman MP, Ruiz-Esparza J. Clinical advantage of the CO2 laser superpulsed mode: treatment of verruca vulgaris, seborrheic keratoses, lentigines and actinic cheilitis. J Dermatol Surg Oncol 1994; 20:449– 456. Fitzpatrick RE, Goldman MP, Satur NM et al. Pulsed carbon dioxide laser resurfacing of photo-aged skin. Arch Dermatol 1996; 132:395 – 402. David LM, Lask GP, Glassberg E et al. Laser abrasion for cosmetic and medical treatment of facial actinic damage. Cutis 1989; 43:583 – 587. Weinstein C. Ultrapulse carbon dioxide laser removal of periocular wrinkles in association with laser blepharoplasty. J Clin Laser Med Surg 1994; 12:205– 209. Lowe NJ, Lask G, Griffin ME et al. Skin resurfacing with the UltraPulse carbon dioxide laser: observations on 100 patients. Dermatol Surg 1995; 21:1025 – 1029. Green HA, Domankebitz Y, Nishioka NS. Pulsed carbon dioxide laser ablation of burned skin: in vitro and in vivo analysis. Lasers Surg Med 1990; 10:476 –484. Walsh JJ, Deutsch TF. Pulsed CO2 laser tissue ablation: measurement of the ablation rate. Lasers Surg Med 1988; 8:264 – 275. Green HA, Burd E, Nishioka NS et al. Middermal wound healing: a comparison between dermatomal excision and pulsed carbon dioxide laser ablation. Arch Dermatol 1992; 128:639 – 645.

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Walsh JJ, Flotte TT, Anderson RR et al. Pulsed CO2 laser tissue ablation: effect of tissue type and pulse duration on thermal damage. Lasers Surg Med 1998; 8:108– 118. Fitzpatrick RE, Tope WE, Goldman MP et al. Pulsed carbon dioxide laser, trichloroacetic acid, Baker – Gordon phenol, and dermabrasion: a comparative clinical and histologic study of cutaneous resurfacing in a porcine model. Arch Dermatol 1996; 132:469 – 471. Yang CC, Chai CY. Animal study of skin resurfacing using the ultrapulse carbon dioxide laser. Ann Plast Surg 1995; 35:154– 158. Olbricht SM. Use of the carbon dioxide laser in dermatologic surgery: a clinical relevant update for 1993. J Dermatol Surg Oncol 1993; 93:364– 369. Shaw EL, Gasset AR. Thermokeratoplasty temperature profile. Invest Ophthalmol 1974; 13:181 – 186. Stringer H, Parr J. Shrinkage temperature of eye collagen. Nature 1964; 1307. Stringer HCW, Highton TC. The shrinkage temperature of skin collagen. Aust J Dermatol 1960; 5:230. Hale GM, Querry MR. Optical constants of water in the 200 nm to 200 m wavelength region. App Opt 1973; 12:555 – 563. Vogler K, Reindl M. Erbium laser parameters for new medical applications. Biophoton Int 1996; Nov/Dec:40 – 47. Kaufmann R, Hibst R. Pulsed erbium:YAG laser ablation in cutaneous surgery. Lasers Surg Med 1996; 19(3):324– 330. Ziering CL. Cutaneous laser resurfacing with the erbium:YAG laser and the char-free carbon dioxide laser: a clinical comparison of 100 patients. Int J Aesthetic Reconstr Surg 1997; 5:29–37. Hohenleutner U, Hohenleutner S. Baumier W et al. Effective skin ablation with an Er:YAG laser: determination of ablation rates and thermal damage zones. Lasers Surg Med 1997; 20:242 – 247. Walsh JT, Flotte TJ, Deutsch TF. Er:YAG laser ablation of tissue: effect of pulse duration and tissue type on thermal damage. Lasers Surg Med 1989; 9:314 – 326. Walsh JT, Deutsch TF. Er:YAG laser ablation of tissue: measurement of ablation rates. Lasers Surg Med 1989; 9:327 – 337. Slutzki S, Shafir R, Bornstein LA. Use of the carbon dioxide laser for large excisions with minimal blood loss. Plast Reconstr Surg 1977; 60:250– 255. Hughes PS. Skin contraction following Er:YAG laser resurfacing. Dermatol Surg 1998; 24:109 – 111. Weinstein C, Roberts TL. Aesthetic skin resurfacing with the high energy ultrapulsed CO laser. Clin Plast Surg 1997; 24:379 – 405. Greene D, Egbert BM, Utley DS et al. In vivo model of histologic changes after treatment with the superpulsed CO laser, erbium:YAG laser, and blended lasers: a 4– 6 month prospective histologic and clinical study. Lasers Surg Med 2000; 27:362 – 372. Goldman MP, Manuskiatti W. Combined laser resurfacing with the 950-microsec pulsed CO2 þ Er:YAG lasers. Dermatol Surg 1999; 25:160 – 163. McDaniel DH, Lord J, Ash K et al. Combined CO2/erbium:YAG laser resurfacing of peri-oral rhytides and side by side comparison with carbon dioxide laser alone. Dermatol Surg 1999; 25:285 – 293. Rostan EF, Fitzpatrick RE, Goldman MP. Laser resurfacing with a long pulse erbium:YAG laser compared to the 950 ms pulsed CO2 laser. Lasers Surg Med 2001; 29:136– 141. Pozner JM, Goldberg DJ. Histologic effect of a variable pulsed Er:YAG laser. Dermatol Surg 2000; 26:733 – 736. Newman JB, Lord JL, Ash K et al. Variable pulse erbium:YAG laser skin resurfacing of perioral rhytides and side by side comparison with carbon dioxide laser. Lasers Surg Med 2000; 26:208 – 214. Jimenez G, Spencer JM. Erbium:YAG laser resurfacing of the hands, arms, and neck. Dermatol Surg 1999; 25:831 –834. Goldberg DJ, Meine JG. Treatment of photoaged neck skin with the pulsed erbium:YAG laser. Dermatol Surg 1998; 24:619 –621.

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Pon, Iyengar, and Rohrer Wollina U, Konrad H, Karamfilov T. Treatment of common warts and actinic keratoses by erbium:YAG laser. J Cutan Laser Ther 2001; 3:63 – 66. Riedel F, Bergler W, Baker-Schreyer A et al. Controlled cosmetic dermal ablation in the facial region with the erbium:YAG laser. HNO 1999; 47:101– 106. Bradley DT, Park SS. Scar revision via resurfacing. Facial Plast Surg 2001; 17:253 – 262. Rohrer TE, Ugent SJ. Evaluating the efficacy of using a short-pulsed erbium:YAG laser for intraoperative resurfacing of surgical wounds. Lasers Surg Med 2002; 30(2):101 – 105. Orenstein A, Haik J, Tamir J et al. Treatment of rhinophyma with Er:YAG laser. Lasers Surg Med 2001; 29:230– 235. Borrelli C, Kaudewitz P. Xanthelasma palpebrarum: treatment with the erbium:YAG laser. Lasers Surg Med 2001; 29:260 – 264. Riedel F, Windberger J, Stein E et al. Treatment of peri-ocular skin lesions with the erbium:YAG laser. Ophthalmologe 1998; 95:771– 775. Kageyama N, Tope WD. Treatment of multiple eruptive hair cysts with erbium:YAG laser. Dermatol Surg 1999; 25:819 –822. Kaufmann R, Hibst R. Pulsed erbium:YAG laser ablation in cutaneous surgery. Lasers Surg Med 1996; 19:324– 330. Alora MB, Arndt KA. Treatment of cafe´-au-lait macule with the erbium:YAG laser. J Am Acad Dermatol 2001; 45:566 – 568. Alt TH. Technical aids for dermabrasion. J Dermatol Surg Oncol 1987; 13:638 – 648. Lowe NJ, Lask G, Griffin ME. Laser skin resurfacing: pre- and post-treatment guidelines. Dermatol Surg 1995; 21:1017 –1019. Conn H, Nanda VS. Prophylactic fluconazole promotes reepithelialization in full-face carbon dioxide laser skin resurfacing. Lasers Surg Med 2000; 26(2):201 – 207. Zachary CB. Modulating the Er:YAG laser. Lasers Surg Med 2000; 26:223 – 226. Hinman CC, Maibach H, Winter GD. Effect of air exposure and occlusion on experimental human skin wounds. Nature 1962; 193:293. Kannon GA, Garrett AB. Moist wound healing with occlusive dressings: a clinical review. Dermatol Surg 1995; 21:583 –590. Batra RS, Ort RJ, Jacob C et al. Evaluation of a silicone occlusive dressing after laser skin resurfacing. Arch Dermatol 2001; 137:1317– 1321. Sriprachya-Anunt S, Fitzpatrick RE, Goldman MP et al. Infections complicating pulsed carbon dioxide laser resurfacing for photoaged facial skin. Dermatol Surg 1997; 23(7):527 – 535. Fitzpatrick RE, Williams B, Goldman MP. Preoperative anesthesia and postoperative considerations in laser resurfacing. Semin Cutan Med Surg 1996; 15:170– 176. Weinstein C, Ramirez O, Pozner J. Postoperative care following carbon dioxide laser resurfacing. Dermatol Surg 1998; 24:51 – 56. Fitzpatrick RE, Goldman MP, Tope WD. Pulsed carbon dioxide laser resurfacing of photoaged facial skin. Arch Dermatol 1996; 132:395 – 402. Lask G, Keller G, Lowe N et al. Laser skin resurfacing with the Silktouch flashscanner for facial rhytides. Dermatol Surg 1995; 21:1021 – 1024. Perez MI, Bank DE, Silvers D. Skin resurfacing of the face with erbium:YAG laser. Dermatol Surg 1998; 24:653 –659. Weinstein C. Computerized scanning erbium:YAG laser for skin resurfacing. Dermatol Surg 1998; 24:83 – 89. Nanni CA, Alster TS. Complications of carbon dioxide laser resurfacing: an evaluation of 500 patients. Dermatol Surg 1998; 24:315– 320. Waldorf HA, Kauvar AN, Geronemus RG. Skin resurfacing of fine to deep rhytides using a char-free carbon dioxide laser in 47 patients. Dermatol Surg 1995; 21:940 –946.

29

Combined Laser Resurfacing Techniques Mitchel P. Goldman Dermatology/Cosmetic Laser Associates of La Jolla, Inc., La Jolla, California, USA

Elizabeth Roston Dermatology/Cosmetic Laser Associates of San Diego County, Inc., San Diego, California, USA

1. Introduction 2. Theoretical Considerations 3. Resurfacing with UPCO2 Followed by the Er:YAG Laser 4. Derma-K Laser Resurfacing 5. CO3 Laser Resurfacing 6. Sciton Contour Laser Resurfacing 7. Recommendations References

1.

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INTRODUCTION

Since the early 1990s, laser resurfacing with short-pulsed, high energy carbon dioxide (CO2) lasers has been utilized to treat photodamaged skin and acne scars. The introduction of short-duration erbium:YAG (Er:YAG) lasers in the mid-1990s offered another option for resurfacing either with the Er:YAG alone or in combination with a CO2 laser. The use of the various CO2 lasers and their adverse effects have been detailed in Chapter 33. Perhaps the most common and also the most easily avoidable of these is prolonged erythema and delayed wound healing. Avoidance of these two adverse effects requires intensive patient education as well as close postoperative surveillance and early intervention when signs first appear. We have previously demonstrated that these adverse effects are secondary to nonspecific thermal damage present after laser resurfacing (1).

Portions of this chapter were modified from Goldman MP, Manuskiatti W, Fitzpatrick RE. Combined laser resurfacing with the UPCO2 þ Er:YAG lasers. In: Goldman MP, Fitzpatrick RE, eds. Cosmetic Laser Surgery. St. Louis: Mosby, Inc., 2000. 569

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The extent of nonspecific thermal damage after laser resurfacing can be decreased with the use of the Er:YAG laser as detailed in Chapter 34. Histologic evaluation immediately after laser resurfacing with various microsecond-pulsed CO2 laser systems (10,600 nm wavelength) shows tissue ablation of 35 mm and 80 –140 mm of nonspecific thermal damage (2 –4). Er:YAG laser vaporization at the usual 350 ms pulse produces thinner ablation (20 mm) and far less thermal damage, only 5 –10 mm, because the 2940 nm wavelength has an affinity for water 10 times stronger than the 10,600 nm wavelength of the CO2 lasers (5,6). This shorter depth of ablation makes the Er:YAG more time-consuming and less efficacious than the CO2 laser in treating significant photodamage (wrinkling). In addition, the Er:YAG laser does not promote the same extent of collagen contraction and new collagen formation as the CO2 laser. Therefore, the use of Er:YAG laser in resurfacing assumes a specialized role. We first demonstrated that its sequential use following CO2 laser resurfacing decreased the extent of nonspecific damage resulting in decreased postoperative erythema and improved wound healing (7). The advantages of this combination approach have been demonstrated by others (8 – 10). This chapter will discuss our recommendations regarding combining these two lasers as well as minimizing the risks inherent in their combination. A step-by-step method will be presented about our technique. Finally, new laser systems will be discussed, including the Derma-KTM (ESC Medical Systems, Needham, MA), which combines the CO2 laser modality with the Er:YAG in a near-simultaneous exposure, and two systems combining normal Er:YAG laser parameters with a second nearsimultaneous nonablative long-pulsed Er:YAG pulse—ContourTM (Sciton, Palo Alto, CA) and CO3 (Cynosure, Chelmsford, MA).

2.

THEORETICAL CONSIDERATIONS

Before re-epithelialization of a wound can occur, inflammatory cells and macrophages are recruited to eliminate potential contaminants (bacteria/yeast) as well as nonviable tissue. Inflammatory mediators stimulate angiogenesis, attract additional inflammatory cells, and stimulate production and release of various growth factors. The localized presence of these factors in the wound stimulates epidermal migration and proliferation as well as dermal remodeling (11 –13). Wound healing occurs through a balance of inflammatory mediators and inflammatory cells. If excessive inflammation occurs, persistent and/or excessive angiogenesis may result, thus leading to prolonged clinical erythema and delayed wound healing. Since the extent of inflammation is proportional to the extent of nonviable tissue in a wound (14), it is reasonable to expect a disruption of optimal wound healing when excessive nonviable tissue is present in the wound. Therefore, minimizing nonspecific thermal damage following resurfacing should promote faster wound healing. This can be accomplished through the use of Er:YAG vaporization of the residual layer of nonspecific thermal damage left from CO2 laser resurfaced skin. It has also been theorized that other forms of abrasive surgery such as dermabrasion with a wire brush, diamond fraise, or sand paper will accomplish an effect similar to Er:YAG laser vaporization by removing the residual thermally damaged layer (15). However, at the time of this writing, clinical studies have not yet been performed. We formally studied the effects of treating one-half of a patient’s face with three passes of the ultrapulse CO2 (UPCO2; Coherent Laser Corp., Palo Alto, CA) laser and the other half of the face with two passes of the CO2 laser followed by two passes with the Er:YAG laser as described subsequently to test this hypothesis (1). Immediately

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after UPCO2 laser resurfacing with three passes at 300 mJ with a computer pattern generated (CPG) density setting of 6 for the first pass, followed by 5 and then 4 for the second and third passes, respectively, the average extent of nonspecific thermal damage was 80 mm (+20 mm) (Fig. 29.1). On the side that was treated with two passes of the UPCO2 laser (as described earlier) followed by two passes with the Er:YAG laser at 15 J/cm2, there was a significantly smaller layer of thermal damage of only 20 mm (+10 mm) (Fig. 29.2). Thus, the Er:YAG laser removed 75% of this nonviable tissue that is present after UPCO2 laser resurfacing. At 48 –72 h, a mixed inflammatory infiltrate with polymorphonucleoctyes (PMNs) and eosinophils was present with nuclear debris (Fig. 29.3); however, less inflammation was noted on the combination UPCO2/Er:YAG treated side (Fig. 29.4). This decrease in inflammation did not appear to affect angiogenesis, as a similar density of superficial blood vessels was observed in histologic samples from both treatment sides at 48 h. However, the epidermis re-formed 1 – 2 days faster with combination UPCO2/Er:YAG treatment than with UPCO2 treatment alone, as determined through additional biopsies of patients at days 4, 5, and 6 postoperatively. At 1 week, biopsy specimens from both sides showed complete re-epithelialization and a mild mixed inflammatory infiltrate that was more pronounced in the skin treated with UPCO2 laser alone compared with combination UPCO2/Er:YAG (Table 29.1). The density of blood vessels in the superficial papillary dermis was also greater in the UPCO2 laser group (Figs. 29.5– 29.7). These histologic findings were compatible with the clinical observations of decreased facial erythema in patients treated with the combination technique. In our patient population, this combination is now our standard laser-resurfacing regimen.

3.

RESURFACING WITH UPCO2 FOLLOWED BY THE Er:YAG LASER

The skin is first resurfaced with the UPCO2 with two passes with the CPG at 300 mJ at settings of 596 and 595 [where 5 is the rectangular pattern, 9 is the size of the pattern, with 1 being smallest and 9 being largest, and the last number (6 and 5) represent the

Figure 29.1 Immediately after laser resurfacing with three passes of the UPCO2 laser as previously described. The epidermis is completely vaporized. A zone of nonspecific thermal damage extends 80 mm beneath the vaporized layer (hematoxylin– eosin 200). [Reproduced with permission from Goldman et al. (1).]

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Figure 29.2 Immediately after laser resurfacing with two passes of the UPCO2 laser and two passes of the Er:YAG laser as previously described. The epidermis is completely vaporized. A zone of nonspecific thermal damage extends 10 mm beneath the vaporized layer (hematoxylin – eosin 200). [Reproduced with permission from Goldman et al. (1).]

Figure 29.3 Forty-eight hours after resurfacing with three passes of the UPCO2 laser, a mixed inflammatory infiltrate with PMNs and eosinophils was present with nuclear debris (hematoxylin – eosin 200). [Reproduced with permission from Goldman MP, Manuskiatti W, Fitzpatrick RE. Combined laser resurfacing with the UPCO2 þ Er:YAG Lasers. In: Fitzpatrick RE, Goldman MP, eds. Cosmetic Laser Surgery. St. Louis: Mosby, 2000.]

Figure 29.4 Forty-eight hours after resurfacing with two passes of the UPCO2 laser and two passes of the Er:YAG laser, a sparse mixed inflammatory infiltrate with PMNs and eosinophils was present with nuclear debris (hematoxylin– eosin 200). [Reproduced with permission from Goldman MP, Manuskiatti W, Fitzpatrick RE. Combined Laser Resurfacing with the UPCO2 þ Er:YAG Lasers. In: Fitzpatrick RE, Goldman MP, eds. Cosmetic Laser Surgery. St. Louis: Mosby, 2000.]


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Figure 29.5 At 2 weeks, complete re-epithelialization with a mild mixed inflammatory infiltrate is present in this specimen of UPCO2 laser 3. The density of blood vessels in the superficial papillary dermis is increased. A dense infiltration of fibroblasts with hyperchromatic nucleoli and hyperchromatic cytoplasm is present (hematoxylin – eosin 200). [Reproduced with permission from Goldman MP, Manuskiatti W, Fitzpatrick RE. Combined Laser Resurfacing with the UPCO2 þ Er:YAG Lasers. In: Fitzpatrick RE, Goldman MP, eds. Cosmetic Laser Surgery. St. Louis: Mosby, 2000.]

density overlap of the individual spots as explained subsequently]. The first pass at a density of 6 (30 – 35% overlap) results in complete removal of the epidermis with minimal vaporization of the superficial papillary dermis (Fig. 29.8). Some collagen contraction may occur with the first pass in thin-skinned areas like the periorbital region. The charred epidermal debris is then wiped off with saline-soaked cotton gauze. A moderate amount of pressure is necessary to completely remove the proteinaceous debris (Fig. 29.9). The second pass at a density of 5 (25 – 30% overlap) produces collagen contraction. The treated area is again wiped clean of any additional debris with salinesoaked gauze, but little debris is present except in areas skipped by the first laser pass (Fig. 29.10).

Figure 29.6 At 2 weeks, complete re-epithelialization with a mild mixed inflammatory infiltrate is present in this specimen of UPCO2 laser 2 þ Er:YAG laser 2. The density of blood vessels in the superficial papillary dermis is less than that seen in Fig. 29.5. A dense infiltration of fibroblasts with hyperchromatic nucleoli and hyperchromatic cytoplasm is present (hematoxylin– eosin 200). [Reproduced with permission from Goldman MP, Manuskiatti W, Fitzpatrick RE. Combined Laser Resurfacing with the UPCO2 þ Er:YAG Lasers. In: Fitzpatrick RE, Goldman MP, eds. Cosmetic Laser Surgery. St. Louis: Mosby, 2000.]

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Figure 29.7 (a) Six weeks after laser resurfacing with the UPCO2 laser 3, there is still a mild inflammatory infiltrate with increased dermal vessels (hematoxylin– eosin 200); (b) 6 weeks after resurfacing with UPCO2 laser 2 þ Er:YAG laser 2, there is sparse inflammation without excessive angiogensis (hematoxylin – eosin 200). [Reproduced with permission from Goldman MP, Manuskiatti W, Fitzpatrick RE. Combined Laser Resurfacing with the UPCO2 þ Er:YAG Lasers. In: Fitzpatrick RE, Goldman MP, eds. Cosmetic Laser Surgery. St. Louis: Mosby, 2000.]

If more significant photodamage is present in some areas, such as the glabellar, perioral areas and cheeks, or in areas of acne scarring, an additional CO2 pass may be performed selectively in these areas at a density of 4 or 5 to achieve deeper ablation as well as further collagen tightening. The 3 mm diameter spot may also be used cautiously

Figure 29.8

Appearance after one pass of UPCO2 with CPG setting of 596, before removal of debris.


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Figure 29.9 A moderate amount of pressure is necessary to remove the proteinaceous debris completely after one pass of the UPCO2 laser 300 mJ with the CPG at a setting of 596. [Reproduced with permission from Goldman MP, Manuskiatti W, Fitzpatrick RE. Combined Laser Resurfacing with the UPCO2 þ Er:YAG Lasers. In: Fitzpatrick RE, Goldman MP, eds. Cosmetic Laser Surgery. St. Louis: Mosby, 2000.]

to achieve further tightening in small areas as well as to better define the vermilion border at a fluence of 300 –500 mJ. The Er:YAG laser is then used at maximal power settings with a focused 4 mm diameter spot-size and 1.7 J (16 J/cm2). We have found that two passes at these setting are necessary to vaporize the nonspecific thermal damage left by the UPCO2 laser as described earlier (Fig. 29.11). We do not wipe the treated areas between passes since proteinaceous debris is not apparent. In addition, we have found that it is easier to treat the area in surface units of 2 – 4 cm by 2 –4 cm (Fig. 29.12). This dermabrasionlike method maintains focus on the treated area so that the entire surface area can be evenly resurfaced (16). The focused handpiece when moved away from the skin will give a larger spot-size that will decrease the energy fluence. (The same energy is distributed onto a larger area of the skin.) When the handpiece is moved closer to the skin, a smaller spot-size is produced that increases the relative energy density on the skin. Therefore, controlling the diameter

Figure 29.10 After the second pass there is only a slight amount of debris present except in areas skipped by the first laser pass. [Reproduced with permission from Goldman MP, Manuskiatti W, Fitzpatrick RE. Combined Laser Resurfacing with the UPCO2 þ Er:YAG Lasers. In: Fitzpatrick RE, Goldman MP, eds. Cosmetic Laser Surgery. St. Louis: Mosby, 2000.]

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Figure 29.11 After two passes with the UPCO2 laser as described in Figs. 29.7– 29.10, the Er:YAG laser is then used at maximal power settings with a 4 mm diameter spot-size and 1.7 J (16 J/cm2). [Reproduced with permission from Goldman MP, Manuskiatti W, Fitzpatrick RE. Combined Laser Resurfacing with the UPCO2 þ Er:YAG Lasers. In: Fitzpatrick RE, Goldman MP, eds. Cosmetic Laser Surgery. St. Louis: Mosby, 2000.]

of the laser spot-size on the skin allows for both feathering at the borders of the treated area as well as sculpting of individual lesions. Next, additional passes with the Er:YAG laser permits the surgeon to sculpt acne scars (Fig. 29.13) as well as sculpt a cupids bow on the upper lip (Fig. 29.14) and more completely plane deeper wrinkles (Fig. 29.15). These can be done with a 0.2 mm diameter focusing handpiece that allows the surgeon to vary the fluence from 5 to 50 J/cm2 as necessary. This method for sculpting scars has been reported by others as well (17). Cho and Kim treated 158 patients with atrophic facial scars with a full face laser resurfacing using the UPCO2 laser. After one to three passes of the entire face with the UPCO2 laser, the acne, and surgical and varicella scars were treated with the Er:YAG laser until the surface of the scar and surrounding skin was equal. Although the Korean patients with Type IV skin in this study developed erythema that lasted an average of 84 days and 13.9% of these patients developed posttreatment hyperpigmentation, this percentage was less than similar

Figure 29.12 The Er:YAG laser is easily used to uniformly vaporize a given area through the use of a dermabrasion-like technique treating the area in surface units of 2 – 4 cm by 2 – 4 cm. [Reproduced with permission from Goldman MP, Manuskiatti W, Fitzpatrick RE. Combined Laser Resurfacing with the UPCO2 þ Er:YAG Lasers. In: Fitzpatrick RE, Goldman MP, eds. Cosmetic Laser Surgery. St. Louis: Mosby, 2000.]


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Figure 29.13 Additional passes with the Er:YAG laser allow the surgeon to sculpt acne scars. (a) Before treatment; (b) sculpting acne scars after first removing the epidermis as described in the text; (c) clinical appearance 11 months after treatment with resolution of acne scarring. [Reproduced with permission from Goldman MP, Manuskiatti W, Fitzpatrick RE. Combined Laser Resurfacing with the UPCO2 þ Er:YAG Lasers. In: Fitzpatrick RE, Goldman MP, eds. Cosmetic Laser Surgery. St. Louis: Mosby, 2000.]

patients treated with the UPCO2 laser alone. The authors also saw faster healing with the combination Er:YAG/CO2 laser treated patients than with their historical controlled CO2-laser treated patients. Scars that occurred after treatment occurred in areas treated aggressively with the Er:YAG laser in prelaser scarred areas, especially the upper lip region. We have previously reported similar results in a split face study (1). The combination UPCO2/Er:YAG laser treated side had erythema that resolved within 2– 3 weeks when compared with 8 weeks when treated with the UPCO2 laser alone. Clinically, there was no difference in the extent or duration of edema between the two techniques. There was also no difference in the improvement rating between the two treatment

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Figure 29.14 A cupids bow can be sculpted on the upper lip with the Er:YAG laser. (a) Diagram of the technique; (b) appearance before sculpting; (c) immediately after sculpting as described in text; (c) appearance 2 months after cupids bow sculpting. [Reproduced with permission from Goldman (16).]

sides at the 8 week follow-up time of the first study. We have since evaluated our initial 20 patients who had one-half of the face treated with CO2 laser alone and the other half with the combination UPCO2/Er:YAG laser treatment over a year after treatment and have found that .75% of the combination CO2/Er:YAG treated side maintained their improvement as good or better than the noncombination UPCO2 laser side (Fig. 29.16) (18). In addition to increasing the efficacy of UPCO2 laser resurfacing alone (by minimizing erythema and increasing wound healing), another advantage of combination laser

Figure 29.15 Further passes with the Er:YAG laser can more completely plane wrinkles. [Reproduced with permission from Goldman MP, Manuskiatti W, Fitzpatrick RE. Combined Laser Resurfacing with the UPCO2 þ Er:YAG Lasers. In: Fitzpatrick RE, Goldman MP, eds. Cosmetic Laser Surgery. St. Louis: Mosby, 2000.]


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Figure 29.16 Combination UPCO2/Er:YAG (right side) showed equal improvement as the left side treated with the UPCO2 laser alone. (a) Before treatment; (b) immediately after treatment as described in the text; (c) 7 days after laser resurfacing; (d) 3 weeks after resurfacing; (e) 2 months after resurfacing. [Reproduced with permission from Goldman MP, Manuskiatti W, Fitzpatrick RE. Combined Laser Resurfacing with the UPCO2 þ Er:YAG Lasers. In: Fitzpatrick RE, Goldman MP, eds. Cosmetic Laser Surgery. St. Louis: Mosby, 2000.]

treatment is that the usual demarcation line between cheek and neck at the mandibular angle is less apparent when the Er:YAG laser is used. This is due to the ability to extend laser resurfacing onto the upper neck with the Er:YAG laser and to blend the resurfaced skin more gradually onto non-resurfaced areas (19).

4.

DERMA-K LASER RESURFACING

At present, one laser manufacturer has combined the CO2 laser with the Er:YAG laser in a near-simultaneous beam (ESC-Sharplan, Needham, MA). The Er:YAG portion is identical to all other Er:YAG lasers in its fluence and pulse-duration which can be varied based both on the energy output as well as on the beam diameter. The CO2 portion is composed of a standard, low power continuous CO2 laser that does not operate within the microseconddomain pulse mode. Thus, the CO2 laser is not utilized to vaporize tissue, but to heat tissue

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Figure 29.17 Schematic representation of the energy profile for the Derma-K laser. (Courtesy of ESC-Sharplan, Inc.)

beneath the Er:YAG laser-ablated tissue and thus provide better hemostasis by coagulating superficial vessels (Fig. 29.17). A multicenter study presently underway is helping to define the optimal parameters for this laser system. Specifically, the optimal fluence and pulse duration of the CO2 laser portion are under investigation. We have found excellent safety and efficacy when using Derma-K at the following parameters: Er:YAG at 1.7 J with a 4 mm diameter spot (16 J/cm2) and the CO2 at 5 W with a 50 ms pulse at a rate of 10 Hz. At this setting, we have found efficient vaporization of skin to a similar depth as when the Er:YAG is used alone, but with better hemostasis. Four passes at this setting does not produce the excessive bleeding usually seen when performing four passes with the Er:YAG alone at these fluences (Fig. 29.18).

Figure 29.18 (a) Immediately after four passes with the Er:YAG laser alone at 1.7 J with a 4 mm diameter spot and 10– 20% overlap. Note bleeding from superficial papillary vessels. (b) Immediately after four passes with the Derma-K at identical Er:YAG settings but with the addition of the CO2 laser at 5 W and 50 ms pulse duration. There is much less, if any, bleeding. [Reproduced with permission from Goldman MP, Manuskiatti W, Fitzpatrick RE. Combined Laser Resurfacing with the UPCO2 þ Er:YAG Lasers. In: Fitzpatrick RE, Goldman MP, eds. Cosmetic Laser Surgery. St. Louis: Mosby, 2000.]


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We evaluated 10 patients treated with four passes at these parameters described earlier (9). Clinical photoaging scores, as well as thermal damage, were evaluated immediately after treatment and new collagen formation at 2 weeks and 3 months postoperatively. The average pretreatment periorbital score was 6.2 (scale of 1– 9 with 1 being minimal and 9 the most severe photodamge). We found 32 –44% improvement in the average posttreatment periorbital, perioral, forehead, and cheek scores. The average thermal damage immediately posttreatment was 20 mm. An average increase of 25 mm or an 86% increase in collagen (p ¼ 0.006) was noted on biopsies taken at 3 months. This limited study demonstrated that the Derma-K at these settings was comparable at four passes to the UPCO2 laser used at three passes (1) or the UPCO2 at two passes followed by two passes with the Er:YAG (1,20). At the settings mentioned, there appears to be a decreased depth of nonspecific thermal damage than when the UPCO2 laser is used alone (14.8 mm with the Derma-K vs. 27– 59 mm with the UPCO2 laser) or in sequence with the Er:YAG laser 23 – 37 mm) (Figs. 29.19 and 29.20). In addition, the duration of erythema is also longer than when the Er:YAG laser is used alone to vaporize to a similar depth, but shorter than the UPCO2 laser at similar depths of vaporization. It also appears that the efficacy is also at a level between the Er:YAG and UPCO2 lasers. Thus, the Derma-K appears to be a unique laser with properties of both previous systems, including both their advantages and disadvantages.

Figure 29.19 Histologic examination immediately after (a) eight passes with the Er:YAG laser alone at 1.7 J with a 4 mm diameter spot and 10–20% overlap; (b) three passes with the Derma-K at identical Er:YAG settings but with the addition of the CO2 laser at 10 W and 50 ms pulse duration; (c) four passes with the Derma-K at identical Er:YAG settings but with the addition of the CO2 laser at 5 W and 50 ms pulse duration (hematoxylin–eosin 200). Note minimal amount of nonspecific thermal damage at these laser fluences. [Reproduced with permission from Goldman MP, Manuskiatti W, Fitzpatrick RE. Combined Laser Resurfacing with the UPCO2 þ Er:YAG Lasers. In: Fitzpatrick RE, Goldman MP, eds. Cosmetic Laser Surgery. St. Louis: Mosby, 2000.]

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Figure 29.20 Comparison of three patients treated to a similar vaporization depth with similar pretreatment wrinkle scores. (a) Er:YAG6 at 1.7 J, 4 mm diameter spot (1, before; 2, after). (b) Derma-K with 4 at identical Er:YAG settings but with the addition of the CO2 laser at 5 W and 50 ms pulse duration. (c) UPCO2 3 at 300 mJ with the CPG at settings of 596, 595, and 584, respectively. [Reproduced with permission from Goldman MP, Manuskiatti W, Fitzpatrick RE. Combined Laser Resurfacing with the UPCO2 þ Er:YAG Lasers. In: Fitzpatrick RE, Goldman MP, eds. Cosmetic Laser Surgery. St. Louis: Mosby, 2000.]

5.

CO3 LASER RESURFACING

The CO3 laser (Cynosure, Chelmsford, MA) contains a single Er:YAG laser head that has been optimized to provide extended pulse durations from 0.5 to 10 ms. Long-pulse


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treatment combines both ablation as well as thermal effects. This laser has an average power of 15 W with an energy of each pulse of 2 J. The repetition rate can be adjusted from 2 to 10 Hz. Three handpieces are available 3, 5, and 7 mm in diameter. It can also be operated with a scanner. The scanner provides a variable overlap with a 5 mm spot-size and a 1 1 in. scanning area. The scanner also has the usual number of scanning shapes. Thermal effects are reported to be 30 – 40 mm with the long 10 ms pulses vs. ,10 mm with a short pulse at 5 J/cm2. This allows the CO3 laser to be used by combining short and long pulse passes to ablate and provide thermal effects relatively independently. Adrian (21) reported a side by side comparison with the UPCO2 laser on periorbital and perioral areas. He compared the UPCO2 laser set at a density of 53 passes with ten, 10 ms pulses of the Er:YAG at 5 J/cm2 with a 5 mm diameter spot-size on the other side. Postoperative discomfort, erythema, and time to re-epithelialization were similar. Patients treated with the UPCO2 laser had a better response for deeper wrinkles. We have evaluated 15 patients in a side-by-side comparison with the UPCO2/ Er:YAG combination treatment performed on one-half of the face and the CO3 laser performed on the other half. The CO3 laser was used at 10.2 J/cm2 with a 10 ms pulse and a 5 mm diameter spot-size for two passes followed by two passes at the 0.5 ms pulse duration at 6.1 J/cm2 (Fig. 29.21). The UPCO2/Er:YAG combination treatment was at the same parameters as described previously. At 3 months posttreatment, there was no statistical difference between each laser treatment. The CO3 side had a tendency toward some increased immediate postoperative bleeding and faster healing. The UPCO2/Er:YAG combination side had a tendency toward increased postoperative edema for 48 h and a significantly increased incidence of erythema up to 4 weeks. Overall improvement in skin texture and wrinkle resolution was exactly the same with each treatment (Fig. 29.22). Final evaluation and publication of this study is pending at the time of this writing. An in vitro study to evaluate changes in collagen caused by the CO3 laser when fluence and pulse duration are varied was recently published (22). Fresh poultry skin was treated with the CO3 laser and tissue contraction was documented. An increased tendon contraction with elongation of the CO3 pulse duration occurred. With increasing fluence, the depth of irreversible bovine collagen change reached a maximum of

Figure 29.21 Intraoperative appearance of UPCO2 and CO3 lasers: (a) following one pass of UPCO2 laser at CPG settings of 595 on left side of face, and one pass of CO3 laser at 10.2 J/cm2, 10 ms pulse duration and 5 mm diameter spot on the right; (b) after removal of debris from one pass; (c) after wiping debris following two passes. (Photos courtesy of Richard Fitzpatrick.)

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Figure 29.22 Comparison of UPCO2 laser on left side of face vs. CO3 on right side. (a) Preoperative appearance; (b) 2 weeks after resurfacing; (c) 1 month after resurfacing; (d) 3 months after resurfacing. (Photos courtesy of Richard Fitzpatrick.)

4.904 mm at a fluence of 2.4 J/cm2 and dropped at higher fluences. With a constant fluence of 6.1 J/cm2 and increasing pulse duration, this irreversible change reached a maximum of 3.25 mm at the highest pulse duration of 10 ms. With a constant fluence of 6.1 J/cm2, the maximum depth of reversible collagen change was 9.52 mm with a pulse duration of 7 ms and the mean maximum fibril diameter was 0.191 + 0.019 mm with a pulse duration of 10 ms. When fluence was varied, using a 10 ms pulse duration, the maximum depth of reversible collagen changes was 9.52 mm with a fluence of 5 J/cm2 and the mean maximum fibril diameter was 0.194 + 0.011 mm with a fluence of 7.7 J/cm2. These results are consistent with a previous study evaluating the effects of pulsed CO2 exposure on bovine tendon collagen (23). 6.

SCITON CONTOUR LASER RESURFACING

This Er:YAG laser combines two separate laser heads to combine independent thermal and ablative effects by having one laser head operate in a short-pulse (0.5 ms) pulse


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with the other head operating in a long-pulse mode (1 – 10 ms). This laser provides 45 W of power with a 50 Hz repetition rate. At 50% overlap of 3 mm diameter spots, fluences of up to 100 J/cm2 can be generated. The ablative mode has a short 200 ms supra threshold pulse. A coagulative pulse immediately follows the ablative pulse. In this manner, the Sciton Contour laser ablates tissue with a sequential thermal seal. The Sciton Contour pattern generator gives a 4 mm spot diameter with a variable scanning field of 3.5 3.5 cm. Spots can be overlapped from 10% to 50%. The pattern has an autorepeat mode of 0.5– 2.5 s delivering 1– 50 pulses/s in the single-pulse mode. All of the standard patterns are available. Typical settings that we have found useful are two passes with a 30% overlap at 16 J/cm2 and coagulative settings of 100 mm coagulation (machine presets that lengthen the pulse width and adjust fluence to achieve measured coagulation depth). The third pass is given as an ablative pass only at 6 J/cm2. In a side-by-side comparative study of 18 patients with one side treated with these settings and the other side treated as described earlier with the UPCO2 followed by Er:YAG laser, we found no apparent clinical difference between the two sides of the face (Fig. 29.23). Patients had the same healing rate, same degree of erythema and other postoperative effects, and same degree of new collagen

Figure 29.23 Comparison of UPCO2 laser resurfacing on left side of face vs. Sciton Contour resurfacing on right. (a) Preoperative appearance; (b) immediately after resurfacing; (c) 48 h after resurfacing; (d) 3 weeks after resurfacing; (e) 3 months after resurfacing.

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formation as well as immediate nonspecific thermal effects. Thus, we believe that the Sciton Contour laser functions as two separate lasers. These observations are similar to those reported by Chris Zachary and Roy Grekin who perform resurfacing with the Contour at varying parameters ranging from 25 to 100 mm of coagulation and 10 – 16 J/cm2 with 50% overlap (LaserNews.net, 1999). Thus, the ideal parameters are not yet apparent. What is apparent is the safety and efficacy of this laser.

7.

RECOMMENDATIONS

The goal of laser resurfacing is to replace the photodamaged epidermis with nonphotodamaged cells and the elastotic dermis with healthy collagen and elastin fibers. CO2 laser resurfacing and now long-pulsed Er:YAG laser resurfacing have been demonstrated to result in both contraction of existing collagen fibers and formation of new dermal collagen. Unfortunately, many patients develop prolonged erythema, pigmentary changes, and delayed healing with aggressive CO2 laser resurfacing. We have shown that the beneficial effects of laser resurfacing can be maintained with a reduction of adverse sequelae through minimizing the extent of nonspecific thermal damage by using a combination of UPCO2 laser followed by Er:YAG laser. Using the Sciton Contour or Cynosure CO3 lasers first with thermal necrosis settings approximating that of pulsed CO2 laser resurfacing and then following passes with pure ablative Er:YAG settings approximates the clinical results seen with sequential CO2/Er:YAG resurfacing. There appears to be a slightly superior efficacy of combining the UPCO2 laser with the Derma-K laser. However, patients must be prepared to live with a few more weeks of erythema. We therefore reserve the combination CO2 laser/Derma-K laser for severely photodamaged and wrinkled patients and/or those with severe acne scars and/or for neck resurfacing. All other patients are treated with the combination UPCO2 laser/ Er:YAG laser, except those with minimal photodamage, who can be treated with the Er:YAG laser alone, single pass UPCO2 laser alone, or single to double pass Derma-K laser alone. Other techniques using the Er:YAG laser alone an ultra-short pulse CO2 laser (Truetouch), or the Derma-K laser, which all produce a decrease in nonspecific thermal damage, have been found to result in a decreased extent and duration of erythema and pigmentary changes with quicker re-epithelialization. Unfortunately, these laser procedures are more time consuming and tedious to perform than standard CO2 laser resurfacing with the UPCO2 or other short-pulsed CO2 laser systems. Therefore, the combination technique for resurfacing appears superior and yields the best and most predictable results in our practice. This technique takes advantage of the predictable thermal effects of the UPCO2 laser, resulting in heating dermal collagen to 60– 658C to induce contraction, and adds to this the highly specific effect of the Er:YAG laser to reduce the resulting nonspecific thermal damage. Combination laser systems and/or long-pulsed Er:YAG lasers may also work as well as the UPCO2 laser followed by the Er:YAG laser without the need to purchase or rent two laser systems. There has been some theoretical concern (24) that definding portion of the thermally damaged tissue may compromise the long-term clinical improvement after laser resurfacing. It is possible that increased collagen deposition may occur in a matrix of increased thermal damage. Long-term follow-up of almost 50 patients undergoing combination laser resurfacing procedures, however, has demonstrated no diminishment in the degree of wrinkle improvement.


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REFERENCES 1. 2. 3.

4. 5. 6. 7. 8.

9.

10. 11. 12. 13. 14. 15. 16. 17.

18. 19. 20. 21. 22.

23.

24.

Goldman MP, Manuskiatti W, Fitzpatrick RE. Combined laser resurfacing with the UPCO2 þ Er:YAG Lasers. Dermatol Surg 1999; 25:160– 163. Fitzpatrick RE, Goldman MP, Satur NM et al. Pulsed carbon dioxide laser resurfacing of photoaged skin. Arch Dermatol 1996; 132:395– 402. Cotton J, Hood AF, Gonin R et al. Histologic evaluation of preauricular and postauricular human skin after high-energy, short-pulse carbon dioxide laser. Arch Dermatol 1996; 132:425 – 428. Stuzin JM, Baker TJ, Baker TM et al. Histologic effects of the high energy pulsed CO2 laser on photoaged facial skin. Plast Reconstr Surg 1997; 99:2036 – 2050. Walsh JT Jr, Deutsch TF. Er:YAG laser ablation of tissue: measurement of ablation rates. Lasers Surg Med 1989; 9:327 – 337. Tse Y, Manuskiatti W, Detwiler SP et al. Tissue effects of the erbium:YAG laser with varying passes, energy, and pulse overlap. Lasers Med Surg 1998; (suppl 10):70. Goldman MP, Manuskiatti W. Combined laser resurfacing with the 950-msec pulsed CO2 þ Er:YAG lasers. Lasers Surg Med 1998; (suppl 10):70. McDaniel DH, Lord J, Ash K, Newman J. Combined CO2/erbium:YAG laser resurfacing of peri-oral rhytides and side-by-side comparison with carbon dioxide laser alone. Dermatol Surg 1999; 25:285 –293. Kauvar ANB, Lou WN, Quintang AT. Equivalent depth resurfacing: a clinical and histologic evaluation of erbium:YAG, carbon dioxide and combined laser procedures. Laser Surg Med 1999; (suppl 11):63. Kauvar ANB. Laser skin resurfacing: perspective at the millennium. Dermatol Surg 2000; 26(2):174– 178. Woodley DT, O’ Keefe EJ, Prunieras M. Cutaneous wound healing: A model for cell – matrix interactions. J Am Acad Dermatol 1985; 12:420 – 433. Clark RA. Biology of dermal wound repair. Dermatol Clin 1993; 11:647 – 666. Pollack SV. Wound healing 1985: an update. J Dermatol Surg Oncol 1985; 11:296 –300. Brody HJ. Chemical Peeling and Resurfacing. 2nd ed. St. Louis: Mosby-Year Book, Inc., 1997:29 – 38. Monheit G. Presentation at the 15th Annual Meeting of the American Academy of Cosmetic Surgery, Orlando, Florida, Jan 2000. Goldman MP. Techniques for erbium:YAG laser skin resurfacing: Initial pearls from the first 100 patients. Dermatol Surg 1997; 23:1219– 1225. Cho SI, Kim YC. Treatment of atrophic facial scars with combined use of high-energy pulsed CO2 laser and Er:YAG laser: a practical guide of the laser techniques for the Er:YAG laser. Dermatol Surg. 1999; 25:12:959 – 964. Goldman MP, Nikoliades G. Long-term follow-up of laser resurfacing with the combination UPCO2 followed by Er:YAG laser. Dermatol Surg 2000. Goldman MP, Fitzpatrick RE, Manuskiatti W. Laser resurfacing of the neck with the erbium:YAG laser. Dermatol Surg 1999; 25:163 – 168. Goldman MP, Marchell N, Fitzpatrick RE. Laser resurfacing of the face with a combined CO2/ erbium:YAG laser. Dermatol Surg 2000; 26:102 – 104. Adrian R. Pulsed carbon dioxide and erbium-YAG laser resurfacing:a comparative clinical and histologic study. J Cutan Laser Therapy 1999; 1:29 –35. Kirsch KM, Zelickson BD, Zachary CB et al. Ultrastructure of collagen thermally denatured by microsecond domain pulsed CO2 laser. Presented at the 17th Annual Meeting of the American Society for Laser Medicine and Surgery, Phoenix, April 6, 1997. Kirsch KM, Zelickson BD, Zachary CB, Tope WD. Ultrastructure of collagen thermally denatured by microsecond domain pulsed carbon dioxide laser. Arch Dermatol. 1998; 134: 1255– 1259. Alster TS. Cutaneous resurfacing with Er:YAG lasers. Dermatol Surg 2000; 26:73 – 75.

30 Combining Laser Resurfacing with Facial Surgery Cynthia Weinstein 174, Victoria Parade East Melbourne, Victoria, Australia

1. 2. 3. 4. 5.

Introduction and Background Components of Facial Aging Procedures to Correct Facial Aging Laser Resurfacing in the Treatment of Photoaging Combining Laser Resurfacing with Other Facial Surgical Procedures 5.1. Combining Laser Resurfacing with Blepharoplasty 6. Preoperative Assessment 7. Technique of Laser Blepharoplasty Combined with Laser Resurfacing 7.1. Upper Eyelid 7.2. Lower Eyelid 7.3. Technique 7.4. Resurfacing Periocular Region 7.5. Crow’s Feet and Infrabrow Skin 8. Results and Complications 9. Adjunctive Procedures 10. Endoscopic Forehead Lift Combined with Laser Resurfacing 11. Technique: Important Aspects 12. Combination of Endoscopic Forehead Lift, Laser Blepharoplasty, Transblepharoplasty Frown Muscle Resection, and Laser Resurfacing 13. Neck Liposuction, Platysmaplasty, and Laser Resurfacing 13.1. Liposuction and Platysmaplasty 13.2. Jowls 13.3. Laser Resurfacing 14. Face and Neck Lift Combined with Laser Resurfacing 15. Laser Resurfacing Combined with Filling Agents 16. Combination of Botox and Laser Resurfacing 17. Results of Combined Procedures References

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INTRODUCTION AND BACKGROUND

Facial rejuvenation is a complex process which requires careful analysis and correction of the various components of facial aging. Consumers are nowadays more sophisticated and discerning when seeking cosmetic improvement of their appearance, so that procedures need to be increasingly individualized. The cosmetic surgeon or dermatologist must be able to comfortably offer a range of treatment options, and in many cases a combination of laser and other surgical procedures. Many patients wish to undergo facial rejuvenation in one operation, as it is more economical in time and cost, so combined procedures will continue to have great appeal. 2.

COMPONENTS OF FACIAL AGING

Facial aging has three main components: gravity, photoaging, and atrophy. Gravity leads to descent of the soft tissues, resulting in brow ptosis, hooding of the upper eyelids, “bags” under the lower eyelids, descent of the malar fat pads, development of jowls, and looseness of the neck. Chronic sun exposure leads to solar elastosis of the skin, which leads to wrinkling, loss elasticity, dyschromias, telangiectasia, and solar keratoses. Aging produces fat atrophy which is most noticeable in the cheek area. All three components of facial aging need to be considered when evaluating patients who seek rejuvenation. The degree of each component varies from one individual to the next. 3.

PROCEDURES TO CORRECT FACIAL AGING

There are many procedures available to correct facial aging and can be divided into antigravity procedures, correction of photoaging, and replacement of atrophic soft tissue. (1) Anti-gravity procedures include brow lift (endoscopic or traditional), blepharoplasty (laser or traditional), rhytidectomy (endoscopic or open including skin only, SMAS, and deep plane), and neck lift (liposuction, platysmaplasty, and open face and neck lift). (2) Correction of photoaging includes, abalative laser resurfacing (CO2 and Erbium:YAG), nonablative laser resurfacing chemical peeling (1), and dermabrasion (2). (3) Replacement of atrophic soft tissues includes fat grafting and filling agents (collagen, hyaluronic acid, silicone, artecoll, and gortex). (4) Reduction of movement related aging botox. 4.

LASER RESURFACING IN THE TREATMENT OF PHOTOAGING

Over the past decade, there has been great interest in the use of lasers for the treatment of photoging, with the introduction of high energy pulsed, and scanning CO2 lasers (3 – 10). Although there was initial excitement with this new treatment modality, it soon became clear that the morbidity and complications associated with carbon dioxide laser resurfacing were considerable (11 –14). This led to the introduction of newer lasers including Erbium:YAG, variable pulse duration Erbium:YAG, and nonablative lasers. The longterm results associated with CO2 lasers for the treatment of photoaging have been encouraging with correction of fine reduction to coarse wrinkles lasting at least 5 years. Histologic changes with new collagen formation suggest that the improvement in photoaging may last up to 20 years in the same manner as deeper phenol peels (15,16). The high morbidity associated with CO2 lasers including prolonged erythema, hyperpigmentation, acne exacerbation, and unpredictable scarring can be attributed to

Laser Resurfacing with Facial Surgery

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the thermal injury produced with CO2 lasers. Although CO2 lasers ablate epidermal tissue efficiently due to its high water content, ablation of the dermis is relatively inefficient due to its low water content. This leads to heat-induced coagulation necrosis of dermal tissues that increases with each laser pass (17). As greater experience was gained with CO2 laser resurfacing, long-term delayed hypopigmentation became more apparent in 15% or more of patients (11). Although there is much debate as to the mechanism of delayed hypopigmentation, the author believes it is due to dermal fibrosis, which is irreversible. The Erbium:YAG laser (wavelength 2940 nm) on the other hand is more strongly absorbed by water than the CO2 laser (wavelength 10,600 nm) and consequently produces less thermal injury (Fig. 30.1). The Erbium:YAG laser can ablate both epidermal and dermal tissues efficiently without producing significant heat-induced coagulation necrosis (18 – 20) (Fig. 30.2). Furthermore, there is no increase in thermal injury with successive laser passes into the dermis (Fig. 30.3). As a result, the Erbium:YAG laser produces less erythema and lower morbidity compared with the CO2 laser. When the Erbium:YAG laser was introduced, it was believed that this laser was only suitable for superficial wrinkles and sun damage. However, with the newer high energy scanning and variable pulse Erbium:YAG lasers, deeper rhytids can also be successfully treated. Both clinical and histologic studies confirm the longevity of these improvements (21 –27). The problem of delayed hypopigmentation may also occur when deeper resurfacing is performed with the Erbium:YAG laser, but the incidence and severity are significantly less than the CO2 laser for equivalent improvement. 5.

COMBINING LASER RESURFACING WITH OTHER FACIAL SURGICAL PROCEDURES

Both the Erbium:YAG and CO2 lasers may be combined with many other procedures used to rejuvenate the face. Including: 1. 2.

Blepharoplasty, Endoforehead lift,

Figure 30.1

Erbium:YAG laser is 10 times more strongly absorbed by water than CO2 laser.

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Figure 30.2 (a) Histology showing clean ablation with the Erbium:YAG laser with insignificant thermal injury. (b) Histology showing significant thermal injury produced with CO2 laser at an equivalent depth of resurfacing. Note the coagulative necrosis at the opening of the hair follicle.

3. 4. 5. 5.1.

Face lift, Liposuction (neck and jowles) and facial Lipoinjection Botox injections, filling agents, and chemical peels.

Combining Laser Resurfacing with Blepharoplasty

Combining blepharoplasty with laser resurfacing of the lower eyelids has contributed greatly to rejuvenation of the upper face. Traditional transcutaneous lower eyelid blepharoplasty was associated with a high risk of complications and patient dissatisfaction. The main problems being lower eyelid malposition, scleral show, and ectropion (28,29). Transconjunctival lower eyelid blepharoplasty, while removing the fat pads, does not solve the problem of loose and wrinkled skin. Combining transconjunctival lower eyelid blepharoplasty with laser resurfacing allows for the simultaneous removal of fatty deposits, with correction of nondynamic periocular wrinkles (30,31). There are many indications for combining blepharoplasty with laser resurfacing including: hooding upper eyelids with periocular wrinkles, bags under the lower eyelids


Figure 30.3

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Erbium:YAG laser resurfacing into the dermis.

with “excess” or loose skin and wrinkles, festoons (malar bags) (32), and glabellar frown lines (transblepharoplasty resection of frown muscles) (Figs. 30.4 – 30.7) (33,34). Although there are no absolute contraindications to laser resurfacing with blepharoplast, there are relative contraindications including severe lower eyelid laxity, previous trancutaneous lower eyelid blepharoplasty, and darker skinned patients. Special precautions are necessary for some patients undergoing this combined procedure. Patients undergoing laser resurfacing must be aware of the morbidity associated with this procedure especially the time to re-epithelialization and the duration of erythema. This is a particular problem for male patients. They must also be aware that the resurfaced skin may be paler in the long term.

Figure 30.4 (a) A 51-year-old woman with “bags” and “loose skin” under her lower eyelids who underwent transconjunctival laser blepharoplasty combined with UltraPulse CO2 laser resurfacing. (b) Postoperative result after 3 months.

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Figure 30.5 (a) A 46-year-old woman with hooding of the upper eyelids and periocular wrinkles secondary to sun damage who underwent laser upper eyelid blepharoplasty combined with UltraPulse CO2 laser resurfacing. (b) Postoperative result after 6 months.

Before undergoing this combined procedure, patients must be assessed for lower eyelid laxity, as resurfacing may precipitate scleral show or ectropion. A Snap test must be performed on all patients preoperatively, and if delayed should alert the operator as to the need for a canthopexy prophylactically. Patients who have previously undergone transcutaneous lower eyelid blepharoplasty may already have a degree of scleral show. Resurfacing of the lower eyelid skin especially with the carbon dioxide laser may precipitate frank ectropion. In this situation, resurfacing should be performed extemely conservatively and preferably with the Erbium:YAG laser. Patients with darker skin are likely to develop postresurfacing hyperpigmentation, which in most cases is temporary. These patients will require the prophylactic use of bleaching creams early in the postoperative period, as soon as the skin has fully re-epithelialized. Bleaching creams often produce a greater intensity and longer lasting erythema. In many patients, full-face resurfacing is a preferred option to prevent the “panda bear” appearance.

6.

PREOPERATIVE ASSESSMENT

A full preoperative assessment should include visual fields and acuity. The amount of redundant upper eyelid skin vs. brow ptosis is assessed. Many patients who present for

Figure 30.6 (a) A 64-year-old woman with hooding of her upper eyelids, “bags” under her lower eyelids and periocular wrinkles who underwent upper and lower eyelid laser blepharoplasty combined with laser resurfacing using the Erbium:YAG laser. Total tissue fluence of 120 – 160 J/cm2 was used in the periocular zone. (b) Postoperative results at 6 months.


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Figure 30.7 (a) A 45-year-old woman with hooding of the upper eyelids and wrinkles who underwent laser blepharoplasty (upper and lower) combined with full-face laser resurfacing using an Erbium:YAG laser with a scanner. (b) Postoperative results at 6 months.

blepharoplasty would actually benefit from brow elevation or may require a combination of blepharoplasty and endoscopic brow lifting. If there is significant lower eyelid laxity, prophylactic canthopexy should be seriously considered. In these cases, it is preferable to use the Erbium:YAG for resurfacing. Laser resurfacing is suitable for fine static lines and loose skin, but is ineffective for dynamic lines such as crow’s feet. The latter is best treated with Botox (Allergan) injections alone or combined with laser resurfacing. Localized laser resurfacing will produce regional redness, which can be difficult to conceal. In many patients with sun damage, it may be best to perform either full-face laser resurfacing or combine regional laser resurfacing with chemical peeling of the remainder of the face. All patients regardless of a past history of herpes infection are prescribed prophylactic antiviral medications.

7. 7.1.

TECHNIQUE OF LASER BLEPHAROPLASTY COMBINED WITH LASER RESURFACING Upper Eyelid

Sand blasted metal eye shields should be used to protect the whole globe. Plastic eye shields can melt and burn the eye, whereas shiny eye shields can reflect the laser beam causing a distal burn. A specially designed protector, the Baker –David clamp, is ideal for upper eyelid blepharoplasty. Local anaesthesia should be administered in a way to avoid rupturing blood vessels, otherwise bruising and hematoma may result. A 30-gauge needle and very superficial placement of the local anesthetic will help to avoid vessel injury. One puncture is sufficient to insert the local anesthetic solution, which may then be spread over the entire upper eyelid by digital pressure.

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The CO2 laser is used in contiuous wave mode to complete the entire procedure. Scalpels and scissors are not required. Occasionally the electrocoagulation is needed, especially if a larger blood vessel (.0.5 mm) is encountered. A focused beam with a 0.1 – 0.2 mm spot size is used. Although some practitioners prefer to use UltraPulse (Lumenis) or superpulse for skin incisions, it has been shown that this is of no advantage compared with continuous wave, as long as the laser is kept strictly in focus at all times (Fig. 30.8). Defocusing the beam will lead to more coagulation and a greater zone of thermal injury. The author usually uses 5 W continuous wave, for the skin incision, carrying the incision through the orbicularis oculi muscle. It is very important to move the laser beam quickly and steadily, to avoid excessively deep upper eyelid incision. An excessively deep incision may lead to injury to the levator aponeurosis, resulting in upper eyelid ptosis. Once the skin and orbicularis have been incised, the skin and muscle are excised on bloc using the same laser settings. A backstop should be used, such as a sand blasted Jaeger plate, to avoid overshoot of the laser beam (Figs. 30.9 and 30.10). Five watts continuous wave is used as the laser setting throughout the entire procedure. If bleeding is encountered, the laser beam is defocused to coagulate the bleeding vessel. Because eyelid vessels are ,1 mm in diameter electrocoagulation is rarely needed. Meticulous hemostasis is important. Once the skin and muscle have been removed, the orbital septum is incised, and any excess fat pads are removed as indicated. The fat pads can be excised against a wet applicator stick or a metallic nonreflecting instrument. Care must be taken not to place any traction on the fat pad during the procedure. It is also important to avoid excessive fat excision, as this can caused a skeletonized appearance (Figs. 30.11 and 30.12). Transblepharoplasty resection of glabella frown muscles, depressor supercilii, may be performed through this incision. The upper eyelid is sutured with 60 simple interrupted mild chromic catgut suture, taking care not to puncture any blood vessels to minimize bruising (Fig. 30.13).

Figure 30.8 CO2 laser used in incisional mode for upper eyelid blepharoplasty. Note eye protection with sand blasted Baker – David clamp.


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Figure 30.9 Skin and muscle are resected en bloc from the upper eyelid using a CO2 laser. A sand-blasted Jaegar plate is used as a backstop.

7.2.

Lower Eyelid

In most situations, lower eyelid rejuvenation may be accomplished using the transconjunctival approach for fat removal combined with laser resurfacing of the skin, in order to “tighten” the lower eyelid skin and remove fine lines. Although a resurfacing CO2 laser can be used, the author has found the Erbium:YAG laser to be as effective without the prolonged erythema and risk of ectropion. If the transcutaneous approach is used on the lower eyelid, it may not be safe to combine with simultaneous skin resurfacing, as the blood supply to the skin is compromised and normal healing may not occur. It would be prudent to delay skin resurfacing until at least 6 weeks to 6 months after the blepharoplasty. Before performing lower eyelid blepharoplasty and resurfacing, it is most important to assess the degree of lower eyelid laxity. If it is present, prophylactic canthopexy may be performed at the same time as resurfacing. In such a situation, it is advisable to first

Figure 30.10 incised.

After skin and orbicularis muscle are resected en bloc, the septum orbiculare is

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Figure 30.11 Preseptal fat pads are excised using the carbon dioxide laser incisional mode. The fat pad is incised over a wet applicator stick.

perform the resurfacing and then the canthopexy. By using this order of procedure, the incision line will not be visible postoperatively.

7.3.

Technique

Local anaesthesia is administered in a similar way to the upper eyelid. It should be given transconjunctivally between the blood vessels to avoid bleeding and bruising. The globe must be protected with a dull metal eye shield and/or a Jaeger plate as needed.

Figure 30.12

Resection of the preseptal fat pads.


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Figure 30.13 Transblepharoplasty resection of the frown muscles. Note branches of the supratrochlear nerve (white arrow).

The CO2 laser is used in the incisional mode at 5 W continuous wave (Fig. 30.14). The incision is placed just distal to the arcade of vessels. The fat pads are released and then excised. Care must be taken to specifically remove the lateral fat pad by applying lateral pressure to the orbital rim. The inferior oblique muscle should be carefully protected from injury during the procedure.

Figure 30.14 Transconjunctival lower lid incision is made using the CO2 laser in incisional mode. The incision is made distal to the blood vessel arcade. Note that the eyeball is protected using a sand blasted Jaegar plate.

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Resurfacing Periocular Region

The periocular region is divided into the thinner eyelid skin and the thicker skin of the crow’s feet and the infrabrow area. The thin skin of the upper and lower eyelids should be resurfaced more conservatively than the rest of the face, to avoid scarring and ectropion. For fine lines, the author no longer uses CO2 lasers for resurfacing of the periocular skin due to the risk of hypopigmentation, scarring, and ectropion. The Erbium:YAG laser is used instead with results that match or resurfacing CO2 laser. It is important to resurface up to the eyelash line by pushing the eyelashes out of the laser field with a applicator stick. Either the scanning Erbium:YAG or single spot is used. Using a scanning laser with 50% overlap pattern 10–15 J/cm2 is selected and two passes are made. This represents a total tissue laser fluence of 62–94 J/cm2 delivered to the surface of the skin (Fig. 30.15). Deeper wrinkles may also be successfully treated with the Erbium:YAG laser but will require slightly higher total tissue energy fluences of 94 –126 J/cm2. These parameters may be safely used unless there is preexisting lower eyelid laxity due to either age or previous lower eyelid surgery. In the latter case, lower energy fluence is used. At all times when performing resurfacing, the tissues must be carefully evaluated. Settings and average number of passes may need to be adjusted, depending on the patient’s skin and response to resurfacing. 7.5.

Crow’s Feet and Infrabrow Skin

As the skin in this region is thicker, greater energy fluence may be used. Total tissue laser energy fluence of 126 – 188 J/cm2 may be necessary to significantly improve wrinkles in this region. The author uses a scanning Erbium:YAG laser with 50% pattern overlap. These guideline settings may be adjusted, depending on the patient’s skin and response to resurfacing. When resurfacing the skin using the Erbium:YAG laser, one can readily visualize the depth reached. In the papillary dermis, there is pinpoint bleeding, small regular pores, and parallel fine collagen bundles. In the reticular dermis, one sees splotchy bleeding, coarse irregularly oriented collagen bundles, and wider pore openings.

Figure 30.15 Transconjunctival removal of fat pads. These are incised over a wet applicator stick.


8.

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RESULTS AND COMPLICATIONS

Results of combined laser blepharoplasty and laser resurfacing have been good to excellent in .90% of patients. The improvement in loose skin and infraocular wrinkles is initially excellent. Some relaxation in the skin occurs and is usually evident after 6 months. However, even after 1 year, there is still considerable correction in this region with both the Erbium:YAG and the CO2 lasers. By combining laser resurfacing with laser blepharoplasty, the different components of aging can be improved with minimal risk of distorting eye shape or producing permanent ectropion. These are major advantages over traditional transcutaneous lower eyelid blepharoplasty. The major disadvantage of the combined procedure is the erythema which may last 6 weeks in the case of Erbium:YAG laser resurfacing or up to 6 months in the case of CO2 laser resurfacing. In the author’s experience with 1000 patients, complications were rare with the combined procedures. Temporary ectropion lasting up to 12 weeks developed in 2% of patients who underwent CO2 laser resurfacing. All of these patients had a degree of lower eyelid laxity preoperatively and some had previously undergone transcutaneous lower lid blepharoplasty. Surgical correction of the ectropion was necessary in 0.1% patients. One patient developed methicillin-resistant Staphylococcus aureus infection. Of the patients who underwent Erbium:YAG resurfacing, none developed ectropion. Regional resurfacing of just the periocular zone led to initial localized erythema producing a “raccoon” appearance. In the long term, localized change in pigment and texture was cosmetically obvious in some individuals, especially in men. It is preferable, in most patients, to consider full-face laser resurfacing to avoid lines of demarcation. Localized erythema was less of a cosmetic problem with Erbium:YAG laser resurfacing compared with the CO2 laser. Localized hyperpigmentation may be a problem in darker skinned patients, so combining laser blepharoplasty with regional laser resurfacing in these patients should only be performed after careful preoperative counseling. In no patient was the hyperpigmentation permanent. Contact dermatitis may occur owing to the use of topical antibiotic ointments. These should be avoided and, instead, semiocclusive dressings or bland topical preparations should be used. Synechiae occurred following Erbium:YAG resurfacing and required minor correction in 1% of patients. 9.

ADJUNCTIVE PROCEDURES

In addition to the combination of laser resurfacing and blepharoplasty, transblepharoplasty corrugator and depressor supercilii resection may also be performed. This is very effective in reducing or eliminating glabellar frown lines with long-lasting improvement. This procedure is performed through the upper eyelid blepharoplasty incision using the carbon dioxide laser in the focused mode. The plane of dissection must be deep to resect the frown muscles but without buttonholing the skin. The frown muscles may be ablated using either the CO2 laser or electocoagulation (Figs. 30.16 and 30.17). Care must be taken to avoid injury to the supraorbital and supratrochlear nerves (33,34). 10.

ENDOSCOPIC FOREHEAD LIFT COMBINED WITH LASER RESURFACING

Combining endoscopic forehead lift with laser resurfacing can greatly enhance upper facial rejuvenation, as it addresses the effects of gravity as well as solar damage. As the

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Figure 30.16 (a) A 63-year-old woman with wrinkles due to sun damage, “bags” under her lower eyelids and glabellar frown lines who underwent laser blepharoplasty (upper and lower) with transblepharoplasty resection of her frown muscles. This was combined with full-face laser resurfacing using the modulated combined Erbium and CO2 laser (Derma K-Lumenis Israel). (b) Postoperative results after 10 weeks.

blood supply to the forehead is excellent, it is possible to combine these two procedures without fear of causing skin necrosis (35 – 37). The purpose of the endoscopic forehead lift is to correct brow ptosis and modify the frowning mechanism. As there is no skin excision, distortion of the forehead –hairline relationship does not occur, ensuring a more natural appearance. Correction of forehead wrinkling is achieved with laser resurfacing, which may also lead to some skin contraction. In younger patients, it may be preferable to use Botox as an alternative to endoscopic forehead lift. Botox is often combined with laser resurfacing. There are a number of advantages of the combined approach compared with the more traditional open forehead-lift including: small scalp incisions, less risk of significant

Figure 30.17 (a) A 49-year-old woman with hooding of the upper eyelids, glabellar frown lines and facial wrinkles due to sun damage who underwent upper eyelid laser blepharoplasty, transblepharoplasty resection of frown muscles combined with full-face laser resurfacing using the scanning Erbium:YAG laser. (b) Postoperative results after 3 months.


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Figure 30.18 (a) A 54-year-old woman with eyebrow ptosis, crowding of the eye complex and wrinkling due to sun damage who underwent endoscopic brow lift, laser blepharoplasty, and full-face laser resurfacing using the Erbium:YAG laser. (b) Postoperative result after 3 months. (c) Preoperative close up view of the eyelid– eyebrow complex. (d) Postoperative close up view of the eyelid– eyebrow complex after 3 months. (e) Preoperative side views. (f) Postoperative side view after 3 months. Note significant improvement of crow’s feet region.

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hair loss, less risk of scalp pruritus, maintenance of forehead – hairline distance, suitable for men with receeding hairlines, and excellent patient acceptance (38 – 41). The endoscopic forehead lift is initially technically more difficult to perform compared with the open forehead lift. However, once familiarity is gained with this procedure, it is relatively easy to perform and may be completed within 1 h. The high cost of endoscopic and laser equipment have to be kept in mind. Laser resurfacing may be associated with prolonged erythema as well as pigmentary and textural changes. These complications may be reduced if the Erbium:YAG laser rather than CO2 is used for resurfacing. As their introduction, the indications for combined forehead lift and laser resurfacing have broadened compared with the traditional open forehead lift (Figs. 30.18–30.20). These include patients with eyebrow ptosis (even elderly patients), men and women with eyebrow ptosis and receding hairlines, patients with prominent vertical glabella creases, and patients with significant horizontal forehead lines and lateral eyebrow ptosis. Many patients use their frontalis muscle to elevate their eyebrow, which will elevate the medial and central eyebrow but not the lateral eyebrow. Once the eyebrow has been elevated to its normal position, the patient will no longer need to use their frontalis

Figure 30.19 (a) A 57-year-old woman with extensive sun damage, brow ptosis, and crowding of the eye complex who underwent endoscopic eyebrow lift, upper eyelid laser blepharoplasty, transblepharoplasty resection of frown muscles combined with full-face resurfacing using the modulated dual mode Erbium:YAG/CO2 laser (Derma K-Lumenis Israel). (b) Postoperative results after 6 months. (c) Preoperative close up view of the eyebrow – eyelid complex. (d) Postoperative close up view of the eyebrow – eyelid complex after 6 months.


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Figure 30.20 (a) A 65-year-old woman with lateral eyebrow ptosis, crowding of the eye complex, lower facial sagging, and sun damage who underwent endoscopic brow lift, SMAS face/neck lift combined with full-face resurfacing using a scanning Erbium:YAG laser. (b) Postoperative results after 3 months.

muscle to provide the elevation, so that horizontal forehead lines will often diminish or disappear. Although there are no absolute contraindications to combining the endoscopic forehead lift with laser resurfacing, relative contraindications do exist. Oral retinoids interfere with wound healing and may lead to atypical scarring. This presents a problem for laser resurfacing, although endoscopic surgery may be performed without additional risk. Regional resurfacing in patients with dark skin may lead to obvious lines of demarcation. This is less of a problem with the Erbium:YAG laser compared with the CO2 laser. Male patients may develop cosmetically obvious lines of demarcation following regional resurfacing. With time, this will usually blend with the surrounding skin.

11.

TECHNIQUE: IMPORTANT ASPECTS

Although details of the technique are beyond the scope of this chapter, some aspects require emphasis. The endoscopic forehead lift is performed via 1 cm incisions behind the hairline. The forehead is divided into central and lateral compartments (Fig. 30.21). Dissection of the forehead is achieved with the use of long periosteal elevators and a 4 mm endoscope (Fig. 30.22). The success of this procedure depends on adequate release of the periosteum and temporal fascias from the entire orbital rim, so that the brow may be elevated to a higher level. Failure of this essential step will lead to recurrence of brow ptosis. The central forehead is dissected in the subperiosteal plane, which is bloodless, and the periosteum is cut and released at the orbital rim. The lateral forehead is dissected in the loose areolar plane between the superficial and deep temporalis fascias until the temporal crest is encountered where the two fascias merge. From this lateral compartment, dissection is carried across the temporal crest to enter the subperiosteal compartment of the central forehead. Inferiorly, the

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Figure 30.21 (a –c) Patient being marked for endoscopic eyebrow lift. (a and c) The arrow points to the position of the supraorbital nerve. (b) The arrow points to the course of the temporal branch of the facial nerve.

lateral dissection is extended to the malar arch with release of attachments to the lateral orbital rim (38 – 40). It is possible to perform the forehead dissection with the carbon dioxide laser, with a special fiber designed for forehead lifting (41). Frown muscle modification may be performed once the periosteum has been incised, although there is much debate as to whether the corrugator muscle should be resected. The depressor supercilii muscle is probably the major muscle responsible for frowning and may be more easily ablated via the upper eyelid incision. It is, however, important to release the corrugator muscle if one wishes to obtain medial brow elevation. Fixation of the forehead is necessary until the periosteum has attached to a


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Figure 30.22 (a) Endoscopic view indicating release of the periosteum at the orbital rim. The arrow indicates the supraorbital nerve. (b) Endoscopic view demonstrating complete release of the periosteum with the supraorbital nerve being preserved (arrow).

higher level. Various methods are used including screw fixation, suture fixation, and various plates. Resurfacing may be achieved with either the CO2 or the Erbium:YAG laser. Using a scanning system with 50% pattern overlap, the total Er:YAG laser energy fluence delivered to the tissue is on the order of 140– 210 J/cm2. It is rarely necessary to use a long pulse Erbium:YAG or combined Erbium:YAG with CO2 to achieve long-term correction in the forehead region, as significant bleeding does not usually present a problem. With Erbium:YAG resurfacing, it is possible to perform regional resurfacing, although there will be some initial demarcation lines. However, unlike carbon dioxide laser resurfacing, this localized erythema will disappear after 6– 8 weeks. The erythema associated with Erbium:YAG resurfacing is less intense in degree compared with resurfacing CO2 lasers.

12.

COMBINATION OF ENDOSCOPIC FOREHEAD LIFT, LASER BLEPHAROPLASTY, TRANSBLEPHAROPLASTY FROWN MUSCLE RESECTION, AND LASER RESURFACING

The combination of all four procedures has a number of advantages. The correct proportion of eye lifting to forehead lifting may be obtained, without exaggeration of either. Most patients have some degree of eyebrow ptosis as well as loose skin on their upper eyelids. By performing laser blepharoplasty, one can remove the preseptal fat pads, leading to a definite upper eyelid crease. This is particularly suitable for patients with heavy or fatty eyelids. The blepharoplasty approach allows ready access to the frown muscles including the depressor supercilii, orbicularis oculi, and corrugator. These may be ablated under direct vision without requiring the endoscope. Many surgeons believe that the depressor supercilii is the major muscle responsible for frowning and the vertical

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glabella furrow associated with this. It is far easier to ablate the depressor supercilii via the upper eyelid than through the forehead. This approach also allows direct release of the periosteum at the orbital rim up to the temporal crest (Fig. 30.19). Fewer and smaller scalp incisions are needed, as frown muscle ablation and orbital release are performed through the eyelid. This is especially suitable for men with receding hairlines and women with thin hair. Endoscopy is not required, as muscle ablation and identification of the supraorbital nerve is performed under direct vision. The remaining subperiosteal dissection may be performed blindly. Permanent eyebrow fixation may be readily performed by placing nonabsorbable sutures through the scalp incisions and basting them into the subcutaneous tissue of the eyebrow. This may be performed accurately by guiding the suture through the blepharoplasty incision. The combination of these procedures has some disadvantages. An upper eyelid incision must be made. Very conservative eyelid resection is important, otherwise lagophthalmos may occur, leading to exposure keratopathy. If the supraperiosteal plane is entered inadvertantly instead of the subperiosteal plane, significant bleeding may occur. More eyelid swelling tends to occur when combining laser blepharoplasty with endoscopic forehead lifting than when using the pure endoscopic approach. Care must be taken to avoid traversing the temporal crest via the upper eyelid, as it is possible to enter the superficial temporalis fascia and injure the temporal branch of the facial nerve.

13.

NECK LIPOSUCTION, PLATYSMAPLASTY, AND LASER RESURFACING

Many patients complain of fullness and looseness in the neck and jowl area, but do not wish to undergo a traditional rhytidectomy. This is particularly true for patients under

Figure 30.23

(a and b) Removal of buccal fat via the oral mucosa.


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50 years of age. By performing neck liposuction with or without a platysmaplasty fullness and a minor degree of looseness in the neck may be significantly improved with minimal incisions. The jowl area may also be improved with judicious liposuction and removal of the buccal fat via the intraoral approach (Fig. 30.23). Generally, the skin of the neck region retracts extremely well, especially when much of the fat has been removed (Fig. 30.24). The face may be rejuvenated at the same time, by performing full-face resurfacing up to the jawline. As with the other combined procedures, the author favors the use of the Erbium:YAG laser for resurfacing owing to its efficacy and low morbidity. It is important to feather the resurfacing procedure toward the jawline beginning 2 cm above and fading toward mandible. To help prevent obvious demarcation lines,

Figure 30.24 (a) A 46-year-old woman with excess fat under the chin and jowls as well as sun damage who underwent liposuction of the neck, buccal fat removal, and full-face Erbium:YAG laser resurfacing. (b) Postoperative results at 8 weeks. (c) Preoperative side view of the patient. (d) Postoperative side view of the patient at 8 weeks.

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resurfacing of the neck itself is a controversial as there is a high risk of scarring and hypopigmentation. If the neck is to be resurfaced, the resurfacing should be very superficial using lower energy fluences than in facial areas. Feathering from the top to the base of the neck is also important. 13.1.

Liposuction and Platysmaplasty

Liposuction of the neck can be achieved using tumescent infiltration, and either regular ultrasonic or power cannula assisted liposuction. It is important to utilize low suction pressures to avoid excessive irregularities. The cannula should be superficial to the platysma muscle so that the marginal mandibular branch of the facial nerve will not be injured. The author has found it particularly helpful to use a flexible cannula for the neck, as more precise contouring can be achieved. When the liposuction has been completed, the submental incision is lengthened to 1.5 cm, and the neck skin is seperated from the platysma muscle using long scissors (Fig. 30.25). The platysma muscle may be plicated in the midline using either absorbable or nonabsorbable sutures down to the level of the thyroid cartilage in men or below in women. The suture may then be threaded below the skin to the post-auricular area and sutured into the mastoid periosteum. This maneuver will produce more definition at the cervico-mental angle. Care must be taken to avoid bunching and creating pleating in the skin surface (Fig. 30.26). 13.2.

Jowls

Liposuction of the jowls should be performed judiciously and conservatively to avoid irregularities and depressions. Very small, ,2 mm, cannulas and low suction pressures are

Figure 30.25 (a– c) Liposuction of neck combined with platysmaplasty. Note improved chin/ neck definition.


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Figure 30.26 (a) A 46-year-old woman with excess fat in the neck as well as wrinkles, and sun damage of facial skin who underwent liposuction of the neck, platysmaplasty, and full-face laser resurfacing using the Erbium:YAG laser. (b) Postoperative results at 3 months. (c) Preoperative side view of the same patient. (d) Postoperative side view at 3 months.

preferable in this region. If a patient has prominent jowls, it may be helpful to remove the buccal fat pads via the oral mucosa by making an incision below the parotid duct opening.

13.3. Laser Resurfacing It is possible to perform full-face laser resurfacing at the same time as neck liposuction. In order to obtain the best aesthetic results, feathering toward the jawline is recommended. This helps to prevent conspicuous hypopigmentation at the jawline. The author’s preference is to use the Erbium:YAG rather than the carbon dioxide laser with fluences ranging from 120 to 200 J/cm2.

14.

FACE AND NECK LIFT COMBINED WITH LASER RESURFACING

Probably the greatest controversy with respect to combined procedures is in rhytidectomy surgery, where skin is undermined to a variable degree. It is safe to resurface the central and medial cheeks in the normal manner, but the lateral cheek must be resurfaced cautiously and conservatively, as there may be significant compromise to the blood supply (42). Deep plane and subperiosteal face lifts are less likely to interfere with the blood supply to the skin so resurfacing can be performed little more deeply. Although

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Figure 30.27 (a) A 72-year-old woman with facial ptosis of soft tissues and extensive solar damage who underwent laser blepharoplasty, face and neck lift as well as full-face laser resurfacing using the Erbium:YAG laser. Very low energy fluence was used on the lateral cheek. (b) Postoperative results after 9 weeks.

Figure 30.28 (a) A 56-year-old woman with facial ptosis and wrinkling who underwent laser blepharoplasty, face and neck lift as well as full-face laser resurfacing using the Erbium:YAG laser. (b) Postoperative results after 4 weeks. (c) Preoperative side view of the same patient. (d) Postoperative side view of the patient after 4 weeks.


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carbon dioxide lasers have been used in combination with face lifting, it is safer and more logical to use the Erbium:YAG laser because of its minimal thermal effects (43). Once the face lift has been completed, the medial and central cheek are resurfaced using similar fluences to the forehead. A square pattern with 50% pattern overlap and 15 – 20 J/cm2 selected. Generally two passes are made, being careful to change the orientation of the pattern after each pass. A total of 90 – 120 J/cm2 is delivered to the tissue. The lateral cheek is treated as a feathering zone, 15 J/cm2 with 0% pattern overlap and one pass only are made producing a total energy fluence at the tissue level of 15 J/cm2. Combining laser resurfacing with face lifting often produces pleasing results with no greater morbidity than laser resurfacing alone (Figs. 30.27 –30.31).

15.

LASER RESURFACING COMBINED WITH FILLING AGENTS

Laser resurfacing may be readily combined with all of the different filling agents. This combination is particularly useful for lip augmentation, nasolabial folds, tear drop deformity, and cheek area. Lip augmentation can be performed using collagen, fat, dermal grafts, GoreTex, silicone parteco, and hyaluronic acid derivatives. Filling agents may be used before cleaning or after resurfacing. Laser resurfacing alone rarely produces significant improvement in the nasolabial fold region. Filling agents may be successfully used with differing degrees of longevity. There is some evidence to suggest that fat grafts may last longer if combined with laser

Figure 30.29 (a) A 73-year-old woman with loose neck skin and sun damage who underwent face and neck lift combined with Erbium:YAG laser resurfacing. (b) Postoperative result after 3 months. (c) Preoperative side view of the same patient. (d) Postoperative side view of the same patient after 3 months.

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Figure 30.30 (a) A 58-year-old patient with dark skin, facial dyschromia and ptosis of the neck and jowls who underwent face and neck lift combined with full-face laser resurfacing using the Erbium:YAG laser. (b) Postoperative view of the patient after 6 months. (c) Preoperative side view of the same patient. (d) Postoperative side view after 6 months.

resurfacing due to the increased collagen production induced by resurfacing. The author has also utilized upper eyelid skin for filling the nasolabial fold if the patient is already undergoing blepharoplasty. The upper eyelid skin, that is, removed during surgery is de-epithelialized and then threaded into the nasolabial fold region.

16.

COMBINATION OF BOTOX AND LASER RESURFACING

Combining Botox (Allergan Inc., Irvine, CA) with laser resurfacing is ideal for the glabellar creases and crow’s feet. Botox injections can be performed before, during, or after the resurfacing procedure (44).

17.

RESULTS OF COMBINED PROCEDURES

In many patients, combining laser resurfacing with surgical procedures provides optimal rejuvenation without increased morbidity. The aging process is complex with effects of gravity producing descent of soft tissue, atrophy of soft tissue and bone, and photoaging. Patients are now becoming increasingly educated about facial rejuvenation, so a more tailored and sophisticated approach is advantageous. It is also more time and cost effective for the patient to undergo combined procedures, if indicated. At the present time with the use of ablative lasers the morbidity associated with resurfacing is greater than the


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Figure 30.31 (a) A 60-year-old woman with extensive sun damage and ptosis of the face and neck who underwent face and neck lift combined with full-face laser resurfacing using the combined Erbium and carbon dioxide machine (Derma-K). The Erbium:YAG laser alone was used on the lateral cheek. (b) Postoperative results at 3 months. (c) Preoperative side view of the patient. (d) Postoperative side view of the patient at 3 months.

corresponding surgical operation. However, if the Erbium:YAG is used for resurfacing rather than the CO2 laser the postoperative morbidity is reduced without compromising the long-term improvement in wrinkles and solar damage.

REFERENCES 1.

Lawrence N, Brody HJ, Alt TH. Chemical peeling. In: Coleman WP, ed. Cosmetic Surgery of the Skin. St. Louis: Mosby, 1997:85 – 111.

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Weinstein Alt TH, Goodman GJ, Coleman WP et al. Dermabrasion. In: Coleman WP, ed. Cosmetic Surgery of the Skin. St. Louis: Mosby, 1997:112– 152. Wheeland RG. Clinical uses of lasers in dermatology. Lasers Surg Med 1995; 16(1):2 – 23. Fitzpatrick RE, Goldman MP, Satur NM et al. Pulsed carbon dioxide laser resurfacing of photoaged facial skin. Arch Dermatol 1996; 132:395 – 402. Weinstein C, Alster TS. Skin resurfacing with high energy pulsed carbon dioxide laser. In: Alster TS, Apfelberg DG, eds. Cosmetic Laser Surgery. Wiley & Sons, 1996:9– 27. Weinstein C. Ultrapulse carbon dioxide laser rejuvenation of facial wrinkles and scars. Am J Cosm Surg 1997; 14:3 – 11. Weinstein C, Roberts TL. Aesthetic skin resurfacing with the high energy ultrapulsed CO2 laser. Clin Plast Surg 1997; 24:379 –405. Chernoff G, Shoenrock L, Cramer H et al. Cutaneous laser resurfacing. Int J Aesthet Rest Surg 1995; 3:57 – 68. Lask GP, Keller G, Lowe NJ et al. Laser skin resurfacing with the SilkTouch flash scanner for facial rhytids. Dermatol Surg 1995; 21:1021 – 1024. Lowe NJ, Lask GP, Griffin ME et al. Skin resurfacing with the ultrapulse carbon dioxide laser. Dermatol Surg 1995; 21:1025 –1029. Weinstein C, Pozner JN, Ramirez OM. Complications of carbon dioxide laser resurfacing and their prevention. Aesth Surg J 1997; July/August. Weinstein C, Ramirez OM, Pozner JN. Post operative care following carbon dioxide laser resurfacing. Avoiding pitfalls. J Dermatol Surg 1998; 24:51 – 56. Nanni CA, Alster TS. Complications of carbon dioxide laser resurfacing. J Dermatol Surg 1998; 24:315 – 320. Bernstein LJ, Kauver AN, Grossman MC, Geronemus RG. The short and long term side effects of carbon dioxide laser resurfacing. J Dermatol Surg 1997; 23:519 – 525. Fitzpatrick RE, Goldman MP, Satur NM et al. Pulsed carbon dioxide laser resurfacing of photoaged facial skin. Arch Dermatol 1996; 132:395 – 402. Minoli JJ, Barton FE. A comparison of the histological effects of chemabrasion, dermabrasion, and laserabrasion in the minipig. Aesthet Surg J 1998; 18:11– 18. Ross VE, Domankevitz Y, Skrobal M et al. Effects of CO2 laser pulse duration in ablation and residual thermal damage: implications for skin resurfacing. Lasers Surg Med 1996; 19:123–129. Hohenleutner V, Hohenleutner S, Baumer W et al. Fast and effective skin ablation with an Er:YAG laser: determination of ablation rates and thermal damage zones. Lasers Surg Med 1997; 20:242 – 247. Kaufmann R, Hartmann A, Hibst R. Cutting and skin ablative properties of pulsed mid-infrared laser surgery. J Dermatol Surg Oncol 1994; 20:112 – 118. Kaufmann R, Hibst R. Pulsed Erbium:YAG laser ablation in cutaneous surgery. Lasers Surg Med 1996; 19:324– 330. Weinstein C. Computerised scanning Erbium:YAG laser for skin resurfacing. J Dermatol Surg 1998; 24:83 – 89. Weinstein C. Erbium laser resurfacing—current concepts. Plast Reconst Surg 1999; 103:602 – 616. Weinstein C. New lasers for skin resurfacing—Erbium:YAG/CO2 systems. Persp Plast Surg 1999; 13(1):57– 81. Weinstein C, Scheflan M. Simultaneous combined Er:YAG and carbon dioxide laser (derma K) for skin resurfacing. Clin Plast Surg 2000; 27:273 – 285. Weinstein C. Modulated dual mode Erbium/CO2 lasers for the treatment of acne scars. J Cutan Laser Ther 1999; 1:204 – 208. Kauvar ANB. Laser skin resurfacing: perspectives at the millennium. Dermatol Surg 2000; 26(2):172– 178. Weinstein C. Erbium skin remodelling. In: Narins RS, ed. Cosmetic Dermatological Surg. NY: Marcel Dekker Inc., 2000. Edgerton MT Jr. Causes and prevention of lower lid ectropion following blepharoplasty. Plast Reconstr Surg 1972; 49:367– 373.

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McCord CD, Shore JW. Avoidance of complications in lower lid blepharoplasty. Ophthalmology 1983; 90(9):1039– 1046. Baker SS, Muenzler WS, Small RG et al. Carbon dioxide laser blepharoplasty. Ophthalmology 1984; 91:238 – 243. Weinstein C. Ultrapulse carbon dioxide removal of periocular wrinkles in association with laser blepharoplasty. J Laser Surg Med 1994; 12(4):205 – 209. Baker SS, Woodward JA. Carbon dioxide laser blepharoplasty, ptosis correction, and treatment of festoons. In: Alster TS, Apfelberg DB, eds. Cosmetic Laser Surgery. Chapter 8. NY: Wiley-Liss, 1999:121– 139. Weinstein C. Carbon dioxide laser resurfacing combined with endoscopic forehead lifting, laser blepharoplasty and transblepharoplasty corrugator muscle resection. J Derm Surg 1998; 24:63 – 67. Knize DM. Transpalpebral approach to the corrugator supercilii and procerus muscles. Plast Reconstr Surg 1995; 95:52– 60. Weinstein C. Endoscopic forehead lift. In: Coleman W et al., ed. Cosmetic Surgery of the Skin. Chapter 27. 2nd ed. St. Louis: Mosby, 1997:421 – 427. Weinstein C. Endoscopic forehead lifting combined with laser resurfacing. In: Coleman W, Lawrence N, eds. Skin Resurfacing. Chapter 24. Baltimore: Williams & Wilkins, 1998:277 – 293. Weinstein C. Laser approach to upper facial rejuvenation. In: Alster TS, Apfelberg DB, eds. Cosmetic Laser Surgery. Chapter 7. 2nd ed. NY: Wiley-Liss, 1999:103 – 120. Ramirez OM. Endoscopic facial rejuvenation. Persp Plast Surg 1995; 9:22. Ramirez OM. Endoscopic subperiosteal browlift and facelift. Clin Plast Surg 1995; 22:639. Ramirez OM, Daniel RK. Endoscopic Plastic Surgery. New York: Springer-Verlag, 1995. Isse NG. Endoscopic laser brow lift. In: Alster TS, Apfelberg DB, eds. Cosmetic Laser Surgery. Chapter 10. 2nd ed. NY: Wiley-Liss, 1999:155 – 167. Mayl N, Felder DS. CO2 laser resurfacing over facial flaps. Aesth Surg J 1997; 17(5):285 – 292. Weinstein C, Pozner JN, Scheflan MS. Simultaneous combination of Erbium:YAG resurfacing with rhytidectomy and forehead lifting. A multidimensional approach to facial aging. Plast Reconstr Surg 2001; 107:586– 592. Carruthers J, Carruthers A. Combining botulinum toxin injection and laser resurfacing for facial rhytids. In: Coleman W, Lawrence N, eds. Skin Resurfacing. Chapter 22. Baltimore: Williams & Wilkins, 1998:235 – 243.

31 Laser Treatment of Scars and Striae Tina S. Alster and H. L. Greenberg Washington Institute of Dermatologic Laser Surgery, Washington, DC, USA

1. Introduction 2. Scar Classification 2.1. Hypertrophic Scars 2.2. Keloids 2.3. Atrophic Scars 2.4. Striae Distensae 2.5. Prescars 3. Patient Considerations for Laser Surgery 3.1. Skin Phototype 3.2. Concurrent Inflammation or Infection 3.3. Medication Use and History of Prior Treatments 3.4. Unrealistic Expectations 3.5. Patient Compliance 4. Laser Practice Essentials and Safety Concerns 5. Treatment of Hypertrophic Scars and Keloids 5.1. Background 5.2. Pulsed Dye Laser 5.2.1. Preoperative Considerations (Pulsed Dye Laser) 5.2.2. Perioperative Considerations (Pulsed Dye Laser) 5.3. Postoperative Considerations (Pulsed Dye Laser) 6. Treatment of Striae 7. Treatment of Atrophic Scars 7.1. Background 7.2. Comparing Resurfacing Lasers: Er:YAG vs. CO2 Laser 7.3. Preoperative Considerations (Er:YAG or CO2 Lasers) 7.4. Perioperative Considerations (Er:YAG or CO2 Lasers) 7.4.1. Perioperative Considerations (CO2 Lasers) 7.4.2. Perioperative Considerations (Er:YAG Lasers) 7.5. Postoperative Considerations (Er:YAG or CO2 Lasers) 7.6. Nonablative Laser Scar Remodeling 8. Prescars 9. Summary References

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1.

Alster and Greenberg

INTRODUCTION

Laser technology has evolved over the past few decades to become the treatment of choice for many types of scars and striae. Various laser treatments have been shown to improve the appearance and symptomatology of hypertrophic scars, keloids, striae, and atrophic scars; but determining the appropriate use of this technology comes with experience. This review will attempt to provide practical guidelines for the physician interested in performing laser scar revision. Integumental injury sets the cascade of wound healing events into motion. In most cases, wound healing results in the restoration of skin which is smooth and normal in appearance. Scars result as a complication of the wound healing process, remnants of a deviation in the orderly pattern of healing. Although pigment and vascular alterations associated with wound healing are typically transient, the textural changes caused by collagen disruption are often permanent. Ultimately, repaired skin will only achieve 70– 80% of its original tensile strength. Wound healing is a process that can be divided into three stages: inflammation, granulation tissue formation, and matrix remodeling (1,2). The inflammation stage is defined by a structured sequence involving inflammatory cells, with the wound healing cascade initiated by neutrophils. Subsequently, a variety of cytokines are elaborated by macrophages creating an environment amicable to granulation tissue formation. Finally, fibroblast migration and proliferation occur with new collagen—first type III and, later, type I. Simultaneously, new capillaries are produced under the influence of angiogenic factors released into the wound environment. A problem arises when this organized process takes a detour. An overzealous healing response may occur, creating a raised nodule of fibrotic tissue. Alternatively, the deleted collagen is not adequately replaced forming a pitted “golf ball” appearance. In either instance, the resultant scar is a visible by-product of skewed wound healing. Patients with scars often present with complaints of associated pruritus or dysesthesia. Although scars rarely pose a health risk, it is imperative that the patient’s perception of aesthetic disfigurement is not overlooked as it can be detrimental to his or her psyche. Pertinent characteristics of the scar and certain patient variables should be taken into consideration prior to laser scar revision.

2.

SCAR CLASSIFICATION

Proper classification of a scar is important. Subtle differences in clinical characteristics define the diagnosis and, subsequently, the treatment protocol. Scar qualities, such as color, texture, morphology, and previous treatment attempts, affect the choice of laser parameters, as well as the number of predicted treatments required for revision (3). 2.1.

Hypertrophic Scars

Hypertrophic scars are typically raised, firm, and erythematous (Fig. 31.1). Over-synthesis of collagen coupled with limited collagenolysis due to decreased expression of collagenase during the remodeling phase of wound healing results in the formation of thick, hyalinized collagen bundles consisting of fibroblasts and fibrocytes. These collagen bundles are arranged in nodules, appearing clinically as hypertrophic scars. Despite excessive tissue proliferation, hypertrophic scars remain within the confines of the original integumental injury. Hypertrophic scars usually form in body areas that exhibit slow wound

Laser Treatment of Scars and Striae

Figure 31.1

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Hypertrophic scar with erythema and located within confines of original wound.

healing or in pressure-associated or movement-dependent areas. The hypertrophic scar usually forms within the first month following injury, but may regress over time. Approximately one-third of patients with hypertrophic scars complain of pruritus and dysesthesia (4,5). 2.2.

Keloids

Keloids are raised, reddish-purple, nodular scars that result from a prolonged proliferative phase during the wound healing cascade due to an inherited metabolic alteration in collagen (Fig. 31.2). Keloids are palpably firmer than hypertrophic scars, containing hyalinized collagen bundles and an increased amount of hyaluronidase (6). In contrast to hypertrophic scars, keloids extend beyond the margins of the inciting wound and do not regress over time (6,7). Their formation varies from weeks to years after the initial trauma and occur most frequently in patients with darker skin tones. 2.3.

Atrophic Scars

Atrophic scars are dermal depressions most commonly caused by collagen destruction during the course of an inflammatory skin disease such as cystic acne or varicella

Figure 31.2

Keloids proliferate far beyond original sites of trauma.

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Figure 31.3

Atrophic scars with typical dermal depressions.

(Fig. 31.3). Surgery and trauma may also result in the formation of atrophic scars. Most patients attempt to camouflage the disfiguring pitted lesions with makeup; however, the appearance is often accentuated by cosmetic application due to enhancement of the “golf ball” surface texture. 2.4.

Striae Distensae

Striae or “stretch marks” are linear bands of atrophic or wrinkled skin. They form as a result of rapid weight fluxes (loss or gain) in areas that have been excessively stretched, such as the abdomen, hips, breasts, and around joints (Fig. 31.4). Dermal inflammation and dilated capillaries mark the initial erythematous presentation of striae with characteristic pink, lavender, and purple hues. Late in their course, striae appear hypopigmented and fibrotic. The pathogenesis of striae remains unclear, but it has been hypothesized that besides mechanical (stretch) factors leading to elastin fiber damage, estrogen and mast cell degranulation with elastolysis may also play a significant role (5).

Figure 31.4

Striae distensae located at sites of excessive and rapid growth.


2.5.

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Prescars

Skin that is scar-prone may respond to early or prophylactic laser treatment in an effort to pre-emptively strike at scar formation Laser irradiation of skin during or soon after cutaneous wounding or repair has been shown to reduce or even prevent scar formation in patients who are at a high risk for scar development (3,8).

3.

PATIENT CONSIDERATIONS FOR LASER SURGERY

Certain “patient factors” should be considered in order to establish a patient’s candidacy for laser surgery. Although not necessarily contraindications to laser surgery, these factors serve to identify appropriate treatment candidates. Proper patient selection is imperative in ensuring the best outcome for both patient and physician. Full knowledge of the surgical indications and contraindications help to determine preoperative, intraoperative, and postoperative management of the patient. 3.1.

Skin Phototype

Ethnic background is an important consideration when assessing the likelihood of a wound developing into a keloid or hypertrophic scar. Hypertrophic scars and keloids affect approximately 4.5% to 16% of the African-American and Hispanic populations. Caucasians are less susceptible, with a white-to-black susceptibility ratio estimated at 1:3.5 to 1:15 (6). Likewise, ethnic background must be considered when contemplating laser outcomes. The presence of an increased amount of epidermal pigment in patients with darker skin tones (phototypes III or greater) interferes with the targeted hemoglobin absorption of pulsed dye laser energy. As a result, the amount of energy effectively delivered to dermal scar tissue is diminished. This phenomenon raises two concerns: (1) the efficacy of laser scar treatment may be reduced and (2) epidermal melanin destruction may eventuate in postoperative hypopigmentation. When considering cutaneous laser resurfacing with the CO2 or erbium laser in darker skin tones, the patient and the treating physician must also be prepared for the possibility of transient posttreatment dyspigmentation. 3.2.

Concurrent Inflammation or Infection

Patients with infectious or inflammatory processes must await resolution before proceeding with laser surgery. In the case of bacterial or viral infection (e.g., impetigo, herpes simplex, and verrucae), the possibility that the infection will koebnerize by laser irradiation must be taken into account. Concurrent inflammatory skin disorders (e.g., cystic acne, psoriasis, and dermatitis) may be exacerbated with laser treatment, and dermal inflammation may impede postoperative healing and clinical effect. 3.3.

Medication Use and History of Prior Treatments

Patients with atrophic acne scars who present for laser skin resurfacing are likely to report prior use of isotretinoin (Accutane). Isotretinoin can foster the development of hypertrophic scars with dermal resurfacing procedures due to its effect on collagen metabolism and wound repair (9). Therefore, it is customary for patients to wait a minimum of 6 months after completion of a course of isotretinoin before undergoing cutaneous laser resurfacing. It is also important to obtain a complete history of previous treatments to

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the affected areas. Phenol peeling or dermabrasion may have resulted in tissue fibrosis which could potentially limit laser-tissue vaporization. Alternately, these treatments may have eventuated in some degree of hypopigmentation which could appear worse once the overlying skin has been vaporized. Lastly, prior injections with silicone or other nonabsorbable fillers may preclude laser surgery. 3.4.

Unrealistic Expectations

Patients who would not consider laser therapy successful with any outcome short of total elimination of their scars have unrealistic expectations and are not good candidates for laser surgery. It should be made clear to the patient that some degree of scarring will persist, and that even with re-treatment, it may not be possible to achieve complete scar eradication. 3.5.

Patient Compliance

Because strict patient compliance is necessary to achieve optimal clinical results, a noncompliant patient is a poor treatment candidate. The role of proper postoperative skin care must be fully described and understood. Thorough review of instructions in both written and verbal form is a necessary part of the treatment process.

4.

LASER PRACTICE ESSENTIALS AND SAFETY CONCERNS

The American Academy of Dermatology suggests laser surgery training during residency or at a CME-accredited laser course. The laser surgeon should be knowledgeable in basic laser physics, laser safety, and have had hands-on experience under the supervision of an appropriately trained and experienced laser surgeon (10). Confidence in one’s own skills is just as imperative in laser as in other types of surgery. Numerous safety measures should be instituted before using the laser, including preventative maintenance, daily equipment testing, and daily logs. For both legal and safety reasons, the academy suggests that “Appropriate nursing and technical staff have documentation of laser training and safety training” (10). Having both an understanding and plan for fire prevention and safety, including the avoidance of flammable drapes and skin preparations, as well as nearby availability of a fire extinguisher and running water, are mandatory. In addition, proper use of portable smoke evacuators and room suction reduces the risk of plume-related complications (e.g., ocular and upper respiratory tract irritation and visual problems) generated by these surgical devices. According to the CDC, “during surgical procedures using a laser, the thermal destruction of tissue creates a smoke plume that can contain toxic gases and vapors such as benzene, hydrogen cyanide, and formaldehyde, bioaerosols, dead and live cellular material (including blood fragments), and viruses” (11). The smoke evacuator should thus be activated at all times during laser resurfacing procedures. Operating room personnel and the patient must all wear protective eyewear appropriate to the laser wavelength being used. Systematically, following a standardized preoperative checklist for both physician and patient will help to decrease bad outcomes and avoid accidental injury. Both pre- and postoperative instructions concerning safety and treatment should be given and explained to each patient and caregiver as appropriate.


5. 5.1.

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TREATMENT OF HYPERTROPHIC SCARS AND KELOIDS Background

Traditional treatments of hypertrophic scars and keloids often involve numerous patient “unfriendly” techniques, including topical and intralesional corticosteroids, topical retinoic acid, surgical excision and/or grafting, cryosurgery, radiotherapy, pressure therapy, intralesional interferon, occlusion, and silicone gel sheeting (6,7,12). Often painful and inconvenient, these traditional treatments result in side effects, including atrophy and dyspigmentation. In addition, scar recurrence rates remain high. The first laser used in the treatment of hypertrophic scars and keloids was a continuous-wave argon laser (13). Although initial reports were encouraging, subsequent studies failed to confirm the treatment’s efficacy (14 –16). Use of the continuous-wave neodymium:yttrium-aluminum-garnet laser (1064 nm) which selectively inhibits collagen production by a direct photobiological effect and creates tissue infarction with subsequent charring and sloughing of the treated area, also showed initial clinical improvement; however, the results were transient, and scar recurrences were common (17 –19). Similarly, continuous-wave CO2 laser vaporization of hypertrophic scars and keloids universally recurred within 1 year of treatment (20 – 24). A revolution in laser technology occurred in the early 1980s with the publication of Anderson and Parrish detailing the theory of “selective photothermolysis,” whereby specific absorption of laser energy to achieve temperature-mediated localized injury is produced in a target (25). Their theory led to the invention of pulsed lasers that were target-specific and highly selective. Increased selectivity limited the degree of thermal damage to healthy tissue, thereby decreasing scarring and other untoward side effects. By the late 1980s, the effectiveness of the vascular-specific 585 nm pulsed dye laser in treating a variety of vascular lesions (e.g., port-wine stains and telangiectasias) was widely known. Some clinicians were starting to use the pulsed dye laser to reduce persistent erythema associated with both hypertrophic scars and keloids. However, the improvement in skin texture, bulk, and pliability of pulsed dye laser-treated scars by Alster et al. (26) had not been expected. Initial testing of the pulsed dye laser system in the treatment of argon laser-induced port-wine stain scars produced improved skin texture and color without the evidence of worsening or recurrence at the 6 month end-study evaluation (26) and even at remote examination 4 years later (4). Subsequent studies have shown significant clinical improvement (e.g., improved texture, pliability, color, and bulk) in the treatment of surgical and traumatic hypertrophic scars within one or two treatments with the pulsed dye laser system (27 – 30) [Fig. 31.5(a) and (b)]. Hypertrophic and keloid median sternotomy, as well as burn scars, have also been proven responsive to pulsed dye laser therapy without evidence of recurrence (31,32). 5.2.

Pulsed Dye Laser

There is no consensus on the mechanism by which pulsed dye lasers achieve these additional clinical effects on hypertrophic and keloid scars. Plausible explanations include laser-induced tissue hypoxia (leading to collagenesis from decreased microvascular perfusion), collagen fiber heating with dissociation of disulfide bonds and subsequent collagen realignment, selective photothermolysis of vasculature (33), and mast cell factors (including histamine, interleukins, and various immunofactors) that could affect collagen metabolism (31). Most hypertrophic scars have an average at least a 50 –80% improvement after two laser treatments. Keloid and more fibrotic hypertrophic scars usually require additional laser or other ancillary treatments to achieve desired results (34,35).

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Figure 31.5 Hypertrophic scars before (a) and 2 months after two consecutive 585 nm pulsed dye laser treatments (b) at 6 week time intervals.

5.2.1.

Preoperative Considerations (Pulsed Dye Laser)

Performing laser treatment of hypertrophic or keloid scars as early as a few weeks following cutaneous injury may produce enhanced clinical results (8). Early intervention in patients known to have a tendency toward hypertrophy (as evidenced by pronounced scarring from earlier injuries) may help forestall keloid formation. This indication for early intervention varies from atrophic scar treatment, which can be effectively undertaken years or even decades after the initial injury with no discernable difference in outcome. Pulsed dye laser therapy is usually performed as an outpatient. There is no need for general or intravenous anesthesia because the snapping sensation caused by the pulsed dye laser produces only minimal discomfort. In addition, concomitant use of a cooling device (e.g., cryogen spray and contact chill tip) aids in reducing pain. If anesthesia is desired, topical lidocaine preparations such as EMLA cream (Astra Pharmaceuticals, Westborough, MA) or LMX cream (Ferndale Laboratories, Inc, Ferndale, MI) with occlusion for 30 – 90 min prior to treatment can be applied. All creams, powders, and makeup should be completely removed with wet gauze prior to laser irradiation. Patients with scars in sensitive body locations (e.g., lips, breasts, perineum, and fingertips) may benefit from the use of intralesional anesthetic injections or nerve blocks. Hair-bearing areas within the treatment site should be moistened with water or saline in order to reduce thermal conduction through singed surface hairs. The use of flammable substances such as alcohol or acetone should always be avoided. 5.2.2.

Perioperative Considerations (Pulsed Dye Laser)

The surgical technique for the pulsed dye laser entails a series of adjacent, nonoverlapping laser pulses delivered across the entire breadth of the scar (Fig. 31.6). During each session, the entire scar is treated; however, treatment technique usually necessitates repetition of the procedure in future sessions either to reach those areas missed by avoidance of pulse overlap or to re-treat those regions that were less responsive to the initial treatments. Scar size, thickness, location, color, and patient’s skin type determine energy density selection. Less fibrotic and paler scars in sensitive skin areas (e.g., anterior chest and periorbital tissue) require lower energy densities, whereas thicker or more erythematous scars can be treated with slightly higher fluences. In general, treatments should begin at lower fluences, allowing for the flexibility of upward adjustment depending on scar response. If the initial treatment session produces good results, the energy density should remain the same on subsequent treatments. However, if only minimal results were achieved, the treatment fluences should be increased by 10%. These views complement the academy


Figure 31.6

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Purpura produced within scar immediately after 585 nm pulsed dye laser treatment.

guidelines that state “The lowest power density or energy fluence that is consistent with a good clinical result is strongly encouraged” (11). 5.3.

Postoperative Considerations (Pulsed Dye Laser)

Postoperative purpura seen with the use of the vascular-specific pulsed dye laser usually resolves within 7– 10 days. Postoperative vesiculation or crusting should prompt the physician to use a lower fluence, placing special attention on operative technique (avoidance of overlapping pulses). During the healing process, the patient should be instructed to avoid extraneous manipulation of the treatment area. Showers are permitted, but care should be taken to gently pat-dry treated areas. Gentle cleansing of the treatment area with water and a mild fragrance-free soap followed by the application of a topical antibiotic ointment is the daily postoperative care protocol. A nonstick bandage should cover the treatment area. The lased area should be evaluated in 6 –8 weeks, at which time another laser treatment can be delivered, if deemed necessary. Hyperpigmentation of the irradiated skin is the most common side effect observed following the use of the pulsed dye laser. This pigmentation will fade spontaneously with avoidance or protection from sun exposure. If hyperpigmentation is present, however, subsequent laser treatments should be postponed until its resolution in order to avoid interference with overlying tissue melanin (a competing chromophore for vascular-specific laser energy). A hydroquinone-containing cream or other topical lightener applied once or twice a day can be prescribed to hasten the fading process. Occasionally, patients may develop an allergic contact dermatitis secondary to a topical antibiotic or an irritant dermatitis from an adhesive bandage. If vesiculation is present, it is imperative to determine whether it is merely the normal purpuric response or nonpurpuric and unrelated to laser irradiation. Concurrent pruritus should increase one’s suspicion of contact dermatitis. In the case of contact dermatitis, the offending agent, ointment, or bandage should be discontinued immediately and a mild topical corticosteroid cream applied until the dermatitis resolves. 6.

TREATMENT OF STRIAE

Striae are treated similarly to hypertrophic scars and keloids, but with the best responses produced at lower energy densities (3.0 J/cm2) (5,36,37). Adjacent, nonoverlapping laser

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pulses of 585 nm pulsed dye laser irradiation are delivered, such that each individual stria is covered. Irradiated striae do not typically exhibit the characteristic purpura seen after treatment of hypertrophic scars and keloids. Due to the lower fluences used, striae usually only appear mildly pink, representing mild postoperative tissue hyperemia and edema. Vesiculation and crusting should not be encountered when proper fluences and operative technique are used. Typically, only one or two treatment sessions are necessary in order to obtain the desired results [Fig. 31.7(a) and (b)]. Postoperative management of striae treated with the pulsed dye laser is basically the same as the protocol followed by patients treated for hypertrophic and keloid scars. Patients are instructed to gently cleanse the treatment areas with water and a mild fragrance-free soap. A topical antibiotic should be applied daily and the treatment area covered with a nonstick bandage. Avoidance of sun exposure to the involved areas during the course of treatment is also advised.

7. 7.1.

TREATMENT OF ATROPHIC SCARS Background

In the past, injection with various filler materials and dermabrasion were the only viable treatment options for atrophic scars. Dermal injection of such filler materials as collagen, fat, and fibrin, produced only transient results due to their rapid re-absorption, committing the patient to a series of ongoing treatments in order to maintain desired clinical results. More permanent injections of liquid silicone were fraught with concerns of material migration, granuloma formation, and systemic disease. Dermabrasion, a highly operatordependent procedure, was limited in its ability to treat delicate tissue areas (e.g., periocular and upper lip skin) and often produced tissue fibrosis and hypopigmentation. Re-contouring atrophic facial scars with CO2 and erbium:yttrium-aluminum-garnet (Er:YAG or erbium) laser vaporization has become popularized in recent years, with the CO2 laser becoming the “Gold Standard” for scar resurfacing (achieving up to 80% clinical improvement in moderate to severe acne scars) [Fig. 31.8(a) and (b)] (38 –44). Through their selective ablation of water-containing tissue, both laser systems offer the advantage of predictable, reproducible vaporization of skin yielding better control when compared with dermabrasion (43 –51). In a study comparing the histologic depths of ablation after laser resurfacing, dermabrasion, and chemical peels, Fitzpatrick et al. (52) demonstrated that skin vaporization and residual necrosis depths secondary to CO2 laser

Figure 31.7 Striae distensae before (a) and 6 weeks after one 585 nm pulsed dye laser treatment (b) at 3.0 J/cm2 (7 mm spot).


Figure 31.8

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Atrophic scars before (a) and 1 year after CO2 laser resurfacing (b).

resurfacing were directly proportional to the pulse energy, as well as the number of laser passes delivered. During laser resurfacing, the epidermis and a variable portion of the dermis are destroyed, allowing for re-epithelialization from adjacent pilosebaceous units. 7.2.

Comparing Resurfacing Lasers: Er:YAG vs. CO2 Laser

Pulsed Er:YAG lasers are 10 times more selective for water-containing tissue than their CO2 counterparts and, thus, result in enhanced tissue vaporization and reduced residual thermal damage (42). Pulsed or scanned CO2 lasers employ pulse durations shorter than 1 ms, thereby not exceeding the skin’s “thermal relaxation time” (above which potential nonselective tissue heating occurs). With the use of the CO2 laser, in particular, the production of increased numbers of myofibroblast and matrix proteins is enhanced as a result of controlled collagen denaturation (heating) (53). Long-term collagenesis and clinical improvement have been demonstrated up to 18 months following surgery (42). Residual thermal damage produced by the CO2 laser in the dermis results in collagen shrinkage that clinically “tightens” the skin and augments collagen remodeling. Because Er:YAG laser resurfacing produces relatively little residual thermal damage compared with the CO2 , decreased postoperative erythema is noted; however, the limited photothermal effect on tissue and collagen remodeling leads to an overall decrease in clinical improvement (54). The Er:YAG may be the preferred method of treatment for mild atrophic scars, offering comparable, although not as pronounced clinical effects with shorter postoperative recovery times. When treating extensive and more severe areas of scarring, the CO2 laser remains preferable-requiring fewer laser passes than is often required with the erbium laser (43). 7.3.

Preoperative Considerations (Er:YAG or CO2 Lasers)

Laser resurfacing, especially when involving the full face, can be a major undertaking and patients need to be prepared in advance. Adequate education entails what should be expected before, during, and after laser treatment. Handouts, videos, counseling, and close follow-up are all important components for increasing patient awareness and compliance, leading to a more palatable experience. On the day of surgery, the patient should be instructed to arrive with a caretaker who understands the patient’s special needs. Makeup and hair products should not be used, and contact lenses and other unnecessary items should be left at home. Discussions concerning

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anesthesia should review all available options including topical lidocaine, nerve blocks, local injections, and intravenous and general anesthesia. The extent of the laser resurfacing procedure will often dictate the anesthetic of choice, with more extensive procedures requiring intravenous or general sedation. Depending on the case and anesthetic, a nurse anesthetist or anesthesiologist should be on hand to deliver the medications and to monitor patient progress intraoperatively. A defibrillator and blood pressure, pulse, and oxygen saturation monitors are necessary for these latter procedures. 7.4.

Perioperative Considerations (Er:YAG or CO2 Lasers)

Regardless of the system chosen, the goals of laser scar resurfacing are 2-fold: (1) to soften the transition between the atrophic indentation and the intact (normal) skin surrounding it and (2) to stimulate collagen production within the atrophied area. The entire cosmetic unit must be treated in order to minimize textural or color mismatch. If treating an isolated scar, spot resurfacing may be considered. In an effort to decrease treatment time when lasing large cutaneous areas, a scanning handpiece should be used. Once de-epithelialization has been achieved (typically requiring one pass with the CO2 laser at 300 mJ and two to three passes with the Er:YAG laser at 5 J/cm2), the scar edges or “shoulders” can be further sculpted with additional vaporizing laser passes. Partially desiccated tissue should be completely removed with saline- or water-soaked gauze after each laser pass in an effort to prevent charring. According to the CDC, a smoke evacuator or room suction hose nozzle inlet must be kept within 2 in. of the surgical site to effectively capture airborne contaminants generated by these surgical devices (the laser plume). At the completion of the procedure, all tubing, filters, and absorbers must be considered infectious waste and be disposed of appropriately (11). 7.4.1. Perioperative Considerations (CO2 Lasers) Many CO2 laser options are available. In general, these systems are used at fluences of 5 J/cm2, thereby reaching the critical irradiance threshold of skin required for successful resurfacing. Laser treatment parameters of 300 mJ energy and 60 W power with variablesized and shaped patterns are used with the computer pattern generator scanning device (Lumenis Ultrapulse, Santa Clara, CA). Scanning devices attached to other CO2 laser systems (ESC/Sharplan FeatherTouch or Luxar NovaPulse) can be used at 5 –20 W per scan, depending on the system and severity of scarring. Scan sizes ranging from 4 to 10 mm in diameter are delivered to the treatment area. Treatment usually requires two to three laser passes with care taken to remove all partially desiccated tissue between passes. Individual scar edges can be further sculpted using smaller diameter spots or scans after treatment of the entire cosmetic unit has been achieved. 7.4.2. Perioperative Considerations (Er:YAG Lasers) The Er:YAG laser is used with a 5 mm spot size at 1.0 –3.0 J (5 –15 J/cm2) to de-epithelialize and sculpt individual scars. A laser technique similar to that described with the CO2 system is used with the Er:YAG. However, because erbium laser vaporization does not typically produce a significant quantity of partially desiccated tissue, wiping the skin between laser passes is often not necessary except in hair-bearing areas (in order to reduce thermal conduction to skin through singed surface hairs). Bleeding is typically seen by the third laser pass as a result of dermal penetration and the inability of the Er:YAG laser to photocoagulate blood vessels. There are several Er:YAG lasers currently available, including those manufactured by Continuum Biomedical, Candela, ESC,


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HGM, MDLT, and SEO (Schwartz Electrooptics), all of which yield comparable clinical and histologic effects. Long-pulsed Er:YAG technology either alone (Sciton Contour, Palo Alto, CA) or in combination with CO2 laser treatment (ESC Derma-K, Needham, MA) has been shown to enhance clinical results and effect better hemostasis (44).

7.5.

Postoperative Considerations (Er:YAG or CO2 Lasers)

Whether CO2 or Er:YAG laser resurfacing is performed, treated skin will appear erythematous and edematous immediately following the procedure, worsening over the ensuing 48 hours. Symptomatic palliation may be achieved with the application of topical ointments, semi-occlusive dressings, or cooling masks (55). The first postoperative week is a critical time for wound healing. Patients should be monitored closely for appropriate healing responses and evaluated for complications (e.g., dermatitis and infection). In the case of Er:YAG laser resurfacing, re-epithelialization typically takes 4 –7 days, whereas CO2 laser resurfacing requires 7 –10 days. Full-face procedures or large treatment areas necessitate the use of appropriate prophylactic antimicrobials (e.g., oral antibacterial and/or antiviral medications) during the re-epithelialization process. The use of topical antibiotics on acutely irradiated skin is avoided due to the high rate of allergic or irritant contact dermatitis. Erythema is most intense and prolonged after CO2 laser resurfacing (3 –4 months average), whereas treatment with the Er:YAG laser leads to minimal erythema usually lasting 4 –6 weeks postoperatively. Laser irradiation of skin with the CO2 or Er:YAG laser systems may provoke a number of immediate and long-term side effects, even when proper protocols have been followed (56 –58). A significant side effect of treatment is transient hyperpigmentation. Although observed more frequently in patients with darker skin tones, hyperpigmentation may occur in any skin type. Transient hyperpigmentation is seen early in the postoperative course, typically becoming apparent 3– 6 weeks after treatment. The process is self-limiting, but resolution may be hastened with the use of bleaching agents (e.g., hydroquinone and arbutin) or acid preparations (e.g., glycolic, retinoic, azelaic, ascorbic, and kojic). Hypopigmentation is a relatively late sequela of treatment, typically seen 6 or more months postoperatively, and appears to be permanent. Fortunately, true hypopigmentation (with total loss of pigment) is rare. Rather, relative hypopigmentation is most frequently observed due to the obvious color difference seen when compared with adjacent nontreated (actinically bronzed) skin. Infection is another concern postoperatively as re-epithelializing skin is more vulnerable to bacterial (e.g., Pseudomonas and Staphylococcus), viral (e.g., herpes simplex), and fungal (e.g., Candida) infections. Prophylactic antivirals and aggressive postoperative wound care lower the incidence of infection (59,60). If infection is suspected, it must be diagnosed and treated early. The most severe complications of laser resurfacing include hypertrophic scarring and ectropion formation which may both be due, in large part, to aggressive intraoperative laser technique. Hypertrophic burn scars can be treated effectively with the 585 nm pulsed dye laser irradiation as described earlier (32), whereas ectropion typically requires surgical reconstruction. Cutaneous laser resurfacing of moderate atrophic scars with the CO2 laser yields a mean clinical improvement of 50– 80% (38 – 40). Collagen remodeling with further scar improvement has been documented up to 12 – 18 months postoperatively (42), so re-treatment of residual scars should be postponed for at least 1 year in order to accurately gauge clinical improvement. The Er:YAG laser system, although effective in the treatment of atrophic scars, does not potentiate the same degree of collagen remodeling as does the

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CO2 laser system and should, thus, be reserved for sculpting of individual scar edges and in the treatment of mild acne scarring unless a long-pulsed system is used (44). 7.6.

Nonablative Laser Scar Remodeling

As a consequence of the risks associated with ablative laser resurfacing, great interest has been shown for less invasive methods to effectively treat atrophic facial scars. Several nonablative laser devices have demonstrated efficacy in the treatment of atrophic facial scars; however, the most popular and widely used are the 1320 nm neodymium: yttrium-aluminum-garnet (Nd:YAG) and 1450 diode lasers (61,62). Each system combines epidermal surface cooling with deeply penetrating infrared wavelengths that selectively target water-containing tissue, thereby creating a discrete thermal injury in the dermis without damage to the epidermis. Protocols for treatment often include three consecutive monthly laser sessions with the greatest clinical improvement noted 3 to 6 months after the final laser procedure. Improvement of scars by 40– 50% has been observed after 1320 nm Nd:YAG or 1450 nm diode laser treatment, with results being substantiated by clinical assessments, patient satisfaction surveys, histologic evaluation, and skin surface texture (profilometry) measurements (61). Although a series of nonablative laser treatments can effect modest improvement in atrophic scars with minimal side-effects, the degree of clinical improvement does not equal that of ablative laser resurfacing. Therefore, it is critical to identify those patients best suited for non-ablative procedures in order to optimize patient satisfaction.

8.

PRESCARS

Treatment of potential scars with lasers as a pre-emptive strike against scar formation is not yet a universally accepted practice; however, in the coming years, it may become a popular adjunct to simple closure and wound treatment. A CO2 or erbium laser is used to vaporize the wound edges with typical resurfacing parameters prior to cuticular suture closure (63). It is conceivable that in the future, patients will come to expect laser assisted wound closure in order to avoid or reduce scar formation. Physicians may also advocate their use in operating and emergency rooms, because physician competency is often based on the patient’s perception of the external scar.

9.

SUMMARY

Current laser technology permits successful treatment of various types of scars and striae. Properly classifying the type of scar and striae will determine which laser system will provide optimum results. The 585 nm pulsed dye laser is best used to treat hypertrophic scars, keloids, and striae; whereas the pulsed CO2 and Er:YAG laser systems effectively resurface atrophic scars. Continued advances in laser technology will serve to further shape the management of scars and striae.

REFERENCES 1. 2.

Clark RAF. Biology of dermal wound repair. Dermatol Clin 1993; 11:647– 666. Kirsner RS, Eaglstein WH. The wound healing process. Dermatol Clin 1993; 11:629 – 640.

Laser Treatment of Scars and Striae 3. 4. 5. 6. 7. 8.

9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31.

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Alster TS. Laser treatment of scars and striae. In: Alster TS, ed. Manual of Cutaneous Laser Techniques. Philadelphia: Lippincott-Raven Publishers, 2000:89– 107. Lupton JR, Alster TS. Laser scar revision. Dermatol Clin 2002; 20:55 – 65. Groover IJ, Alster TS. Laser scar revision of scars and striae. Dermatol Ther 2000; 13:50– 59. Alster TS, Tanzi EL. Hypertrophic scars and keloids: etiology and management. Am J Clin Dermatol 2003; 4:235 – 243. Alster TS, West TB. Treatment of scars: a review. Ann Plast Surg 1997; 39:418 – 442. McCraw JB, McCraw JA, McMellin A, Bettancourt N. Prevention of unfavorable scars using early pulsed dye laser treatments: a preliminary report. Ann Plast Surg 1999; 42:7 – 14. Zachariae H. Delayed wound healing and keloid formation following argon laser treatment or dermabrasion during isotretinoin treatment. Br J Dermatol 1988; 118:703– 706. Dover JS. Guidelines of care for laser surgery. American Academy of Dermatology. Guidelines/Outcomes Committee. J Am Acad Dermatol 1999; 41(3 Pt 1):484– 495. Moss CE. Control of Smoke From Laser/Electric Surgical Procedures. National Institute for Occupational Safety and Health (NIOSH) Publication No. 96 – 128, March 2, 1998. O’Sullivan ST, O’Shaughnessy M. Aetiology and management of hypertrophic scars and keloids. Ann R Coll Surg Engl 1996; 78:168 – 175. Ginsbach G, Kohnel W. The treatment of hypertrophic scars and keloids by argon laser: clinical data and morphologic findings. Plast Surg Forum 1978; 1:61 – 67. Apfelberg DB, Maser MR, Lash H et al. Preliminary results of argon and carbon dioxide laser treatment of keloid scars. Lasers Surg Med 1984; 4:283– 290. Henderson DL, Cromwell TA, Mes LG. Argon and carbon dioxide laser treatment of hypertrophic and keloid scars. Lasers Surg Med 1984; 3:271 – 277. Hulsbergen-Henning JP, Roskam Y, van Gemert MJ. Treatment of keloids and hypertrophic scars with an argon laser. Lasers Surg Med 1986; 6:72 – 75. Abergel RP, Dwyer RM, Meeker CA et al. Laser treatment of keloids: a clinical trial and an in vitro study with Nd:YAG laser. Lasers Surg Med 1984; 4:291– 295. Apfelberg DB, Smith I, Lash H et al. Preliminary report on the use of the neodymium-YAG laser in plastic surgery. Lasers Surg Med 1987; 7:189 – 198. Sherman R, Rosenfeld H. Experience with the Nd:YAG laser in the treatment of keloid scars. Ann Plast Surg 1988; 21:231– 235. Kantor GR, Wheeland RC, Bailin PL et al. Treatment of earlobe keloids with carbon dioxide laser excision: a report of 16 cases. J Dermatol Surg Oncol 1985; 11:1063 – 1067. Stern JC, Lucente FE. Carbon dioxide laser excision of earlobe keloids. Otolaryngol Head Neck Surg 1989; 115:1107– 1111. Apfelberg DB, Maser MR, White DN, Lash H. Failure of carbon dioxide laser excision of keloids. Lasers Surg Med 1989; 9:382 –388. Lim TC, Tan WT. Carbon dioxide laser for keloids. Plast Reconstr Surg 1991; 88:1111. Norris JE. The effect of carbon dioxide laser surgery on the recurrence of keloids. Plast Reconstr Surg 1991; 87:44– 49. Anderson RR, Parrish JA. Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science 1983; 220:524 – 527. Alster TS, Kurban AK, Grove GL et al. Alteration of argon laser-induced scars by the pulsed dye laser. Lasers Surg Med 1993; 13:368 – 373. Alster TS. Improvement of erythematous and hypertrophic scars by the 585 nm flashlamppumped pulsed dye laser. Ann Plast Surg 1994; 32:186– 190. Dierickx C, Goldman MP, Fitzpatrick RE. Laser treatment of erythematous/hypertrophic and pigmented scars in 26 patients. Plast Reconstr Surg 1995; 95:84 – 90. Goldman MP, Fitzpatrick RE. Laser treatment of scars. Dermatol Surg 1995; 21:685 –687. Alster TS, McMeekin TO. Improvement of facial acne scars by the 585 nm flashlamp-pumped pulsed dye laser. J Am Acad Dermatol 1996; 35:79 – 81. Alster TS, Williams CM. Improvement of keloid sternotomy scars by the 585 nm pulsed dye laser: a controlled study. Lancet 1995; 345:1198 – 1200.

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41. 42. 43. 44. 45. 46. 47.

48. 49.

50. 51. 52.

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Alster and Greenberg Alster TS, Nanni CA. Pulsed dye laser treatment of hypertrophic burn scars. Plast Reconstr Surg 1998; 102:2190 – 2195. Reiken SR, Wolfort SF, Berthiaume F et al. Control of hypertrophic scar growth using selective photothermolysis. Lasers Surg Med 1997; 21:7 – 12. Alster TS. Laser scar revision: comparison study of 585 nm pulsed dye laser with and without intralesional corticosteroids. Dermatol Surg 2003; 29:25 –29. Fitzpatrick RE. Treatment of inflamed hypertrophic scars using intralesional 5-FU. Dermatol Surg 1999; 25:224 –232. Alster TS. Comparison of pulsed dye laser and CO2 laser vaporization in the treatment of striae. Dermatol Surg 2000. In press. McDaniel DH, Ash K, Zukowski M. Treatment of stretch marks with the 585-nm flashlamppumped pulsed dye laser. Dermatol Surg 1996; 22:332 – 337. Alster TS, West TB. Resurfacing atrophic facial scars with a high-energy, pulsed carbon dioxide laser. Dermatol Surg 1996; 22:151 – 155. Apfelberg DB. A critical appraisal of high-energy pulsed carbon dioxide laser resurfacing for acne scars. Ann Plast Surg 1997; 38:95– 100. Bernstein LJ, Kauvar ANB, Grossman MC, Geronemus RG. Scar resurfacing with highenergy, short-pulsed and flashscanning carbon dioxide lasers. Dermatol Surg 1998; 24:101 – 107. Alster TS, Lewis AB, Rosenbach A. Laser scar revision: comparison of CO2 laser vaporization with and without simultaneous pulsed dye laser treatment. Dermatol Surg 1998; 24:1299 – 1302. Walia S, Alster TS. Prolonged clinical and histological effects from CO2 laser resurfacing of atrophic scars. Dermatol Surg 1999; 25:926 – 930. Alster TS. Cutaneous resurfacing with CO2 and erbuim:YAG laser: preoperative, intraoperative, and postoperative considerations. Plast Reconstr Surg 1999; 103:619 – 632. Tanzi EL, Alster TS. Treatment of atrophic facial acne scars with a dual-mode Er:YAG laser. Dermatol Surg 2002; 28:551 –555. Alster TS, Nanni CA, Williams CM. Comparison of four carbon dioxide resurfacing lasers: a clinical and histopathologic evaluation. Dermatol Surg 1999; 25:153 – 159. Alster TS, Kauvar ANB, Geronemus RG. Histology of high-energy pulsed CO2 laser resurfacing. Semin Cutan Med Surg 1996; 15:189– 193. Smith KS, Skelton HG, Graham JS et al. Depth of morphologic skin damage and viability after one, two, and three passes of a high-energy, short-pulse CO2 laser (TruPulse) in pig skin. Dermatol Surg 1997; 37:204 –210. Stuzin JM, Baker TJ, Baker TM, Kligman AM. Histologic effects of the high-energy pulsed CO2 laser on photoaged facial skin. Plast Reconstr Surg 1997; 99:2036 –2053. Ross EV, Grossman MC, Duke D, Grevelink JM. Long-term results after CO2 laser skin resurfacing: a comparison of scanned and pulsed systems. J Am Acad Dermatol 1997; 37:709 – 718. Ross E, Naseef G, Skrobel M et al. In vivo dermal collagen shrinkage and remodeling following CO2 laser resurfacing. Laser Surg Med 1996; 18:38. Alster TS. Clinical and histological evaluation of six erbium:YAG lasers for cutaneous resurfacing. Laser Surg Med 1999; 24:87 – 92 Fitzpatrick RE, Tope WD, Goldman MP, Satur NM. Pulsed carbon dioxide laser, trichloroacetic acid, Baker –Gordon phenol, and dermabrasion: a comparative clinical and histologic study of cutaneous resurfacing in a porcine model. Arch Dermatol 1996; 132:469 – 471. Alster TS. Increased smooth muscle actin, factor XIIIa, and vimentin-positive cells in the papillary dermis of carbon dioxide laser-debrided porcine skin [commentary]. Dermatol Surg 1998; 24:155. Alster TS. Cutaneous resurfacing with Er:YAG lasers. Dermatol Surg 2000; 26:73 – 75. Horton S, Alster TS. Preoperative and postoperative considerations for cutaneous laser resurfacing. Cutis 1999; 64:399 – 406. Nanni CA, Alster TS. Complications of carbon dioxide laser resurfacing: an evaluation of 500 patients. Dermatol Surg 1998; 24:315 – 320.

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Bernstein LJ, Kauvar ANB, Grossman NC, Geronemus RG. The short and long-term side effects of carbon dioxide laser resurfacing. Dermatol Surg 1997; 23:519 – 525. Tanzi EL, Alster TS. Side effects and complications of variable-pulsed erbium:yttriumaluminum-garnet laser skin resurfacing: extended experience with 50 patients. Plast Reconstr Surg 2003; 111:1524 – 1529. Walia S, Alster TS. Cutaneous CO2 laser resurfacing infection rate with and without prophylactic antibiotics. Dermatol Surg 1999; 25:857 – 861. Alster TS, Nanni CA. Famciclovir prophylaxis of herpes simplex virus reactivation after cutaneous laser resurfacing. Dermatol Surg 1997; 25:242 –246. Tanzi EL, Alster TS. Comparison of a 1450 nm diode laser and a 1320 nm Nd:YAG laser in the treatment of atrophic facial scars: a prospective clinical and histological study. Dermatol Surg 2004; 30:152 – 157. Rogachefsky AS, Hussain M, Goldberg DJ. Atrophic and mixed pattern of acne scars with a 1320 nm Nd:YAG laser. Dermatol Surg 2003; 29:904 – 908. Greenbaum SS, Rubin MG. Surgical pearl: the high-energy pulsed carbon dioxide laser for immediate scar resurfacing. J Am Acad Dermatol 1999; 40:988– 990.

32 Nonablative Skin Rejuvenation and Acne Therapy David J. Goldberg Mount Sinai School of Medicine, New York, New York and New Jersey Medical School, Newark, New Jersey, USA


1. Introduction 2. Nonablative Skin Rejuvenation 3. Lasers that Target Hemoglobin and Melanin 3.1. Pulsed Dye Laser 3.2. KTP Laser 4. Devices that Target Hemoglobin, Melanin, and Water 4.1. Intense Pulsed Light 4.2. Q-Switched Nd:YAG Laser 4.3. Diode Laser (980 nm) 4.4. Long Pulsed Nd:YAG Laser 5. Lasers That Target Tissue Water 5.1. 1320 nm Nd:YAG Laser 5.2. 1450 nm Diode Laser 5.3. 1540 nm Erbium:Glass Laser 6. Photodynamic Therapy for Skin Rejuvenation 7. Laser and Light-Based Treatment for Acne 7.1. Introduction 7.2. Targeting P. acnes 7.3. Targeting Sebaceous Glands 8. Conclusions References

1.

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INTRODUCTION

The treatment of the skin signs of aging including facial rhytides, telangiectasias, and dyschromias is a great concern to many individuals. Until recently, most approaches to the 637

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treatment of photodamage have required the destruction of the epidermis and portions of the dermis to diminish the epidermal signs of aging and remodel the dermis. These techniques include chemical peels, dermabrasion, carbon dioxide (CO2), and erbium:YAG (Er:YAG) lasers. For over a decade, the CO2 and Er:YAG lasers have been the devices of choice for restoration of photodamaged skin because of their capability to remove precisely and/or heat tissue in specified micron thicknesses while obviating the operator dependency of dermabrasion and the inconsistencies of depth of penetration associated with chemical peels (1 –10). The ability to be strongly absorbed by the tissue’s water content enables these lasers to remove superficial layers of skin in a primarily ablative process. Laser irradiation induces a rapid rise in temperature in a thin layer of tissue until boiling of water occurs, and microscopic tissue fragments are ejected from the skin. Most of the laser energy produces tissue vaporization, with little energy remaining to thermally damage the underlying tissues. The Er:YAG laser at 2940 nm has a significantly higher absorption coefficient for water than does the CO2 laser at 10,600 nm. Consequently, the depth of thermal damage in the underlying tissue is much less for the Er:YAG laser (10 –30 mm) when compared to the CO2 laser (80 – 150 mm). The differences in ablative and coagulative properties of these lasers (reviewed elsewhere in this chapter) can be advantageous depending on the clinical situation being addressed. Skin rejuvenation with CO2 and Er:YAG lasers improves rhytides and textural abnormalities by several mechanisms including dermal ablation, immediate collagen denaturation, and contraction, and long-term wound repair with fibroplasia and dermal remodeling. The observed improvement in dyspigmentation and dysplasia is a direct result of tissue damage and subsequent repair. Despite the dramatic clinical outcomes achieved with laser resurfacing techniques, epidermal destruction produces an open wound with a risk for bacterial, viral, and fungal infections. These procedures require tedious postoperative wound care and convalescent periods from 1 to 2 weeks. Conscious sedation or general sedation is usually required for pain management. Additional drawbacks include prolonged postoperative erythema, transient or long-term pigmentary alteration, and the remote possibility of infection and scarring. 2.

NONABLATIVE SKIN REJUVENATION

Nonablative laser rejuvenation refers to laser and light-based techniques that impart thermal injury to the papillary and superficial reticular dermis while preserving the epidermis (11 – 13). The dermal heat injury induces fibroblast activation and synthesis of new collagen and extracellular matrix material. Two different mechanisms are employed in nonablative rejuvenation. Either discrete melanin or hemoglobin-rich chromophores are targeted with visible wavelengths, or mid-infrared wavelengths in the range of 1.3 – 1.5 mm are used to heat selectively tissue water. 3.

LASERS THAT TARGET HEMOGLOBIN AND MELANIN

Hemoglobin has absorption peaks at 542 nm and from 577 to 595 nm. Melanin absorbs strongly throughout the visible light region. Lasers and pulsed light sources that emit in this region of the electromagnetic spectrum can be used to heat selectively hemoglobin and melanin-containing structures. These isolated foci of heat damage produced at the dermoepidermal junction or in the superficial dermis lead to a “microscopic” wound healing response with fibroblast activation, collagen deposition and remodeling without

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the need to “wound” or ablate the epidermis. Furthermore, laser or light-induced heating and subsequent removal of dermal vessels and pigment-containing cells leads to the resolution of clinically apparent telangiectasia and dyschromia, the pigmentary irregularities associated with photoaging.

3.1.

Pulsed Dye Laser

Pulsed dye lasers, emitting at 585– 600 nm, selectively target hemoglobin and melanin. Until recently, the pulse durations for these systems ranged from 0.45 to 1.5 ms, but newer models deliver pulse trains up to 40 ms. Pulse durations ,6– 10 ms produce a transient purpuric response immediately following laser treatment, but the longer pulse durations enable purpura-free treatment. Zelickson et al. (14) used a 0.45 ms, 585 nm pulse dye laser to treat cosmetic units in 20 patients with mild to severe wrinkles. Spot sizes of 7 and 10 mm were used with fluences of 3 –6.5 J/cm2. One treatment was performed, and the subjects were followed for 6 months. Side effects included purpura and edema in all subjects. Two subjects developed transient post-inflammatory hyperpigmentation. Ninety percent of the subjects with fine wrinkling showed 50% or more clinical improvement. Scanning electron microscopy demonstrated fibroblast activation and increased concentrations of normalappearing collagen and elastic fibers, and an increase in extracellular matrix proteins (15) (Fig. 32.1) Bjeering (16) studied a 585 nm, 3.35 ms pulsed dye laser for treatment of periorbital rhytides in 30 patients. Single treatments were performed at a fluence of 2.4 J/cm2. Mild improvement was noted in class II and III wrinkles. The same protocol was used to treat forearm skin which then used for suction blister induction. Analysis of the blister fluid revealed an increase in the amino terminal peptide of procollagen III. Another ultrastructural study of preauricular skin treated with this laser demonstrated changes consistent with an increase in both type III and type I collagen (17).

3.2.

KTP Laser

A long pulsed KTP laser (Verapulse, Coherent/Lumenis) has been used extensively for treatment of telangiectasias and photodamage-associated dyschromias. Bernstein (18) performed a bilateral comparison study, treating one side of the perioral region in 11 women with mild to deep rhytides. The laser was used with a 3 mm spot, 2 ms pulse duration, and a fluence of 4– 7 J/cm2. Three treatments were performed at an average of 3 –6 weeks intervals. The improvement averaged 51.4% by patient chose the treated side in 8 of 11 subjects. A subsequent study by Lee (19) evaluated a long pulsed KTP laser (Aura, Laserscope) in combination with a long pulsed Nd:YAG laser (Lyra, Laserscope) for photorejuvenation. Patients were treated with either the KTP laser alone, the Nd:YAG laser alone or a combination of both for a series of three to six treatments. The KTP laser was used with a 4 mm headpiece at 30 –50 ms, with fluences of 6 –15 J/cm2. Treatment with the KTP laser alone showed a 70– 80% reduction in redness and pigmentation, 30 – 40% improvement in texture, and 20 –30% reduction in fine wrinkling. Treatment with the 1064 nm laser demonstrated similar improvements in skin texture and wrinkling but minimal improvement in redness and pigmentation. Results from the combined treatment with both lasers were superior to either laser alone.

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Figure 32.1 (a) Before nonablative dermal remodeling with a 595 nm pulsed dye laser and (b) after nonablative dermal remodeling with a 595 nm pulsed dye laser.

4.

DEVICES THAT TARGET HEMOGLOBIN, MELANIN, AND WATER

Devices that emit in the near-infrared region are absorbed to some degree by hemoglobin, melanin, and water. Hence, these devices can be used to target discrete chromophores as well as to heat tissue water. 4.1.

Intense Pulsed Light

Intense pulse light (IPL) devices emit broadband light 500– 1200 nm. The shorter wavelengths can be blocked with cutoff filters. The range of wavelengths emitted enables absorption by all the skins natural chromophores, hemoglobin, deoxyhemoglobin, melanin, and water, as well as deeper tissue penetration by the near-infrared wavelengths. In a study (20), evaluating the effect of IPL in the treatment of rhytides, 30 female subjects, aged 35– 65, Fitzpatrick types I-II and classes I-II skin phenotypes, were treated. Treatment areas included the perioral and forehead regions. One to four treatments were performed over a period of 10 weeks. Noncoherent intense pulsed light was delivered to the skin using a 645 nm cutoff filter. This leads to emission of light with wavelengths between 645 and 1100 nm. Light


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was delivered through a bracketed cooling device, in triple 7 ms pulses, with 50 ms inter-pulse delays between the pulses. Delivered fluences were between 40 and 50 J/cm2. Goldberg evaluated the degree of improvement 6 months after the last treatment. Complications were also evaluated at that time. Clinical improvement was divided into four quartiles: (a) no improvement, (b) some improvement, (c) substantial improvement, and (d) total improvement. Six months after the final treatment, five subjects were noted to have no improvement. Similarly, no subjects were noted to have total improvement. Sixteen subjects showed some improvement while nine subjects showed substantial improvement. All subjects were evaluated for pigmentary changes, post treatment blistering, erythema, and scarring. Three of the 30 subjects were noted to have blistering immediately after treatment. All 30 subjects had post treatment erythema. Six months after treatment, no pigmentary changes, erythema, or scarring were noted. Goldberg concluded that intense pulsed light could improve some rhytides. New collagen formation and improvement of agerelated vascular and pigmented lesions can follow treatment with non-laser technology (10). However, the dermal changes appeared to be subtler than those seen with ablative techniques (Fig. 32.2).

Figure 32.2 (a) Extensive telangiectases of the face before treatment with the intense pulsed light source and (b) improvement in clinical appearance of facial photodamage after treatment with an intense pulsed light source.

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Bitter (22) used an IPL with 550 and 570 nm cutoff filters to treat 49 subjects. Full face treatments were performed at 3 weeks intervals. Bitter found improvements in telangiectasias, dyspigmentation, as well as in fine lines and skin texture. He attributed improved results to the use of a lower cutoff filter to target pigment and telangiectasia. Histological analysis of biopsies taken 4 weeks after four full face treatments demonstrated new collagen in the papillary and reticular dermis, as well as a resolution of the superficial dermal metaphases. Zelickson and Kist (6) described evidence of dermal remodeling in biopsies from two subjects and an increase in type I and type III collagen and elastin 6 weeks after IPL treatment.

4.2.

Q-Switched Nd:YAG Laser

In one of the first studies evaluating a nonablative approach to dermal remodeling, a 1064 nm Q-Switched Nd:YAG laser was used in an attempt to improve rhytides (23). Eleven subjects with perioral rhytides were evaluated using a Q-Switched Nd:YAG laser at 5.5 J/cm2 and a 3 mm spot size. All subjects were of skin phototypes I and II; all had class I and II rhytides. Treatment was delivered until a nonspecific clinical end point of pinpoint bleeding was observed. Subjects were treated only once and were evaluated 7, 30, 60, and 90 days after treatment. At follow-up each subject was evaluated for improvement of rhytides, healing, pigmentary changes, and erythema. In three patients (two perioral and one periorbital), the authors noted improvement that was thought to be comparable to that following ablative resurfacing. In six patients (three perioral and three periorbital), clinical improvement was noted. No pigmentary changes or scarring was noted in any of the treated subjects. At 1 month, 3 of 11 subjects showed persistent erythema at the treated sites. At 3 months, all erythema was resolved (Fig. 32.3). Dermal remodeling was thought to occur through increased collagen I deposition with collagen reorganizing into parallel arrays of compact fibrils. Such an effect can occur with nonablative as well as ablative laser systems. Of note, the greatest improvement seen in this study, occurred in those individuals who had most persistent erythema. This suggested that the degree of improvement following any dermal wounding approach might be directly related to the induction of wound or inflammation. The aforementioned study was expanded when the nonablative, dermal remodeling, effects of a Q-Switched Nd:YAG laser were potentiated by the use of a topical carbon assisted solution (24). Two hundred and forty-two solar damaged anatomic sites on 61 human subjects were treated with three 1064 nm Q-Switched Nd:YAG laser treatments. Parameters of treatment included a fluence of 2.5 J/cm2, a pulse duration of 6 –20 ns, and a spot size of 7 mm. The treatment sites were evaluated at baseline, 4, 8, 14, 20, and 32 weeks for skin texture, skin elasticity, and rhytid reduction. All sites were treated at a base-line visit, and later at 4 and 8 weeks. Adverse events were recorded throughout the study. In this study, a low fluence Q-Switched Nd:YAG laser was utilized for treating mildly solar-damaged skin. Unlike the previous study, there was no epidermal disruption when the lower fluences were used. The Q-Switched Nd:YAG laser energy is not well absorbed by tissue water; it is nonselectively placed within the dermis. The 1064 nm wavelength results in relatively deep penetration into the skin, which is indicative of minimal chromophore-specific laser-tissue interaction. As a result, (a) cellular damage is localized to the tissue immediately adjacent to the carbon, (b) nontargeted tissue is minimally affected, and (c) ,10% of the typical energy output from CO2 lasers is required for the treatment. At 8 months, the investigators reported improvement in skin texture and


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Figure 32.3 (a) Before nonablative dermal remodeling with a Q-switched Nd:YAG laser and (b) after nonablative dermal remodeling with a Q-switched Nd:YAG laser.

skin elasticity, as well as rhytid reduction compared to baseline. The majority of adverse events were limited to mild, brief erythema. Friedman et al. (25) recognized the inherent limitations of photographic and clinical evaluation of improvement after nonablative treatment. They looked at the results in two subjects after five treatments with a low fluence Q-Switched Nd:YAG laser. Clinical results were analyzed using a three-dimensional microtopography imaging system (PRIMOS, GFM, Teltow, and Germany). Six-month results, as measured by this threedimensional method, showed a decrease in skin roughness of 26%.

4.3.

Diode Laser (980 nm)

A 980 nm diode laser equipped with contact cooling was used by Muccini et al. (28) to irradiate skin samples, ex vivo, from eyelid and breast skin, and for in vivo treatment of eyelid skin in 2 subjects. Laser treatment of the ex vivo samples produced a zone of denatured collagen and tissue shrinkage. Biopsies taken from the in vivo laser treated eyelid skin revealed trace denatured collagen and a modest amount of new collagen. On

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day 4, the biopsies revealed a thicker band of new collagen and new elastic fibers. These changes persisted for 1 year. 4.4.

Long Pulsed Nd:YAG Laser

At 1064 nm, there is absorption by hemoglobin, melanin, and water. When fluences lower than those required for hair reduction or vessel treatment are used, there is gentle heating of a large volume of tissue. The epidermal surface can be protected with various methods of skin cooling. A study was performed with a Nd:YAG laser using fluences of 100– 130 J/cm2, pulse durations of 3 –80 ms, and up to five treatments over an 8-week period (26). Ten subjects with Fitzpatrick types II –III skin were followed for 6 months after their final treatment. Side effects were minimal with only one subject showing post-treatment blistering. This healed without scarring. Most patients showed some degree of clinical improvement. In another study, using a 300 ms Nd:YAG laser, Schmults et al. (27) noted not only the clinical improvement but also the electron microscopic evidence of new collagen formation after laser treatment. Lee (19) demonstrated that full face treatment with a long pulsed Nd:YAG laser and contact cooling with a sapphire-cooled plated could improve skin texture and fine lines. Using the same device, Dayan et al. (29) found an overall improvement in wrinkles and skin laxity following up to seven full face treatments in 51 subjects.

5.

LASERS THAT TARGET TISSUE WATER

A variety of devices, including the 1320 nm Nd:YAG lasers, 1450 nm diode laser and 1540 nm ER:Glass laser, heat tissue water. The absorption coefficients for the 1320, 1450, and 1540 nm lasers are 3, 20, and 8 cm21, respectively, with corresponding penetration depths of 1500 nm, 300 nm, and 700 nm. All of these lasers will create deep thermal tissue injury extending from the epidermis, unless epidermal skin cooling is utilized. Using the appropriate laser parameters and skin cooling, all of these devices can be used to heat the papillary and reticular dermis. 5.1.

1320 nm Nd:YAG Laser

The first specifically nonablative laser to be solely marketed to the physician community is a 1320 nm Nd:YAG laser. The goal of this system, similar to that of the previously described systems, is an improvement of rhytides without the creation of a wound. The 1320 nm wavelength is advantageous in its high scattering coefficient. Thus, the laser irradiation scatters throughout the treated dermis after nonspecific absorption by dermal water. In the study by Nelson et al. (30), one or more passes of a 1320 nm Nd:YAG laser were used on photoaged skin. The waveform consisted of 200 ms laser pulsed at a repetition rate of 100 Hz. Laser energy was delivered through a 5 mm spot size with fluences upto 10 J/cm2. A dynamic cryogen cooling technique was applied immediately prior to laser treatment in order to produce selective subsurface skin heating without epidermal damage. Immediately after treatment, mild edema and erythema appeared in the treated skin. These side effects resolved within 2 days. At 2 months after treatment, facial rhytides improved. There was no persistent erythema or pigmentary changes. The currently available model of this 1320 nm Nd:YAG laser is accompanied by a unique handpiece


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with three portals. One portal contains the cryogen spray that cools the epidermis prior to and during treatment, one portal emits 1320 nm Nd:YAG laser irradiation, and one portal contains a thermal sensor. Patients are usually treated at 2– 4 week intervals and can be expected to show the degree of improvement from a nonablative approach (31 – 33). Consistent with the observed clinical improvement is the histologic replacement of the irregular collagen bands with organized new collagen fibrils. Because this laser produces new collagen formation, it has been used as part of a full-face antiaging approach (34) (Fig. 32.4). 5.2.

1450 nm Diode Laser

The 1450 nm diode laser targets tissue water and penetrates to a depth of 500 mm. The laser uses pulse durations in the range of 150 –250 ms, divided into 4 pulses of equal duration, interspaced with three cryogen sprays to avoid epidermal damage. Heating of a 400 – 500 nm zone of the superficial dermis produces a wound healing response followed by collagen deposition and remodeling. Goldberg (35) first studied this laser using a pulse duration of 160– 260 ms and a 4 mm spot size. Twenty subjects, 19 women and 1 man, skin types I– IV, age range 42 – 70 years, were enrolled in the study. Classes I and II rhytides were treated in 12 subjects with periorbital rhytides. One side was treated with the laser and cryogen while the contralateral side was treated with the cryogen alone. Pre-laser, intermediate, and

Figure 32.4 (a) Before nonablative dermal remodeling of the neck with a 1320 nm Nd:YAG laser and (b) after nonablative dermal remodeling of the neck with a 1320 nm Nd:YAG laser.

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post-laser cryogen cooling ranging from 40 to 80 ms in total was provided. Choice of treated sides was randomized. Two to four laser treatment sessions were performed, separated by monthly intervals. Clinical improvement of rhytides was designated as non, mild (same number of rhytids, but lessened in depth), moderate (decreased number of ryhtids), or significant (no rhytids after treatment). Optical profilometry molds were undertaken before and 6 months after the final treatment. Immediate erythema was seen in 19 of 20 treated subjects. It was subjectively evaluated as either mild or severe and was noted on both the laser/cryogen treated site as well as the cryogen-only treated site. No immediate post-treatment blisters were noted; posttreatment edema, usually seen as small edematous papules, was observed at various times in 6 of 20 laser/cryogen treated subjects. The duration was anywhere between 1 and 7 days. Six-month post-treatment post-inflammatory hyperpigmentation was noted only in one subject and only at the laser/cryogen site. No hypopigmentation, erythema, or scarring was noted 6 months after the final treatment. Of the 20 laser/cryogen treated sites, 7 showed no obvious clinical improvement, 10 showed mild improvement, and 3 sites had more than mild improvement. None of the cryogen-alone treated sites demonstrated any improvement 6 months following the final treatment. Clinical improvement was consistent with optical profilometry findings. No perioral sites showed more than mild improvement. Recently, this laser has also been shown in several studies to be effective in the treatment of acne scars. In a series of 20 treated subjects (36), mild to moderate improvement in acne scars was noted after three sessions of 1450 nm diode laser treatment. 5.3.

1540 nm Erbium:Glass Laser

The Er:Glass laser is another device in the mid-infrared class of lasers being used for nonablative improvement in skin textural irregularities. At 1540 nm, water is the only significant chromophore and the depth of penetration lies between the 1320 and 1450 nm lasers. Early animal studies in domestic pigs (37) demonstrated bands of denatured collagen in the dermis and wound shrinkage immediately after treatment. A human study (37) was performed in nine subjects. Punch biopsies taken 2 months after treatment showed change in collagen at a depth of 400– 1300 mm (mean depth 703 mm), measuring 513 mm. Similar results (38) were documented in another human study where biopsies at 2 months after treatment showed fewer elastotic fibers and a new band of collagen.

6.

PHOTODYNAMIC THERAPY FOR SKIN REJUVENATION

Photodynamic therapy (PDT) is a method of destroying cells using a combination of a photosensitizing drug, light, and oxygen. PDT was introduced at the beginning of the 20th century as an experimental method used to destroy cancer cells. PDT uses the biosynthetic pathway for heme where precursor compounds are metabolized into phototoxic compounds. Early treatment applications used systemic photosensitizing drugs which resulted in prolonged phototoxicity. Topical photosensitizers for PDT were first introduced in 1990 in an effort to limit generalized phototoxicity reactions (39). There are currently two topical photosensitizers being used for cutaneous PDT applications: 5-aminolevulinic acid (5-ALA) and the methyl ester of ALA (mALA). These lipophillic compounds are taken up by epithelial cells and metabolized to protoporphyrin IX (PpIX), the precursor of heme. PpIX accumulates in the membranes of intracellular organelles such as lysosomes and mitochondria in epidermal cells, and in


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pilosebaceous units. Topical ALA may directly enter hair follicles, where sebaceous glands actively synthesize and retain PpIX. Selectivity of photosensitization may relate to the ability of photodamaged cells or rapidly proliferating cells to convert more ALA to PpIX than normal epidermal cells, and differences in cutaneous permeability caused by aberrantly differentiated keratinocytes. The tissue specific phototoxic effects of topically applied ALA provide the basis for its clinical indications. Intense visible light delivered to ALA-treated skin excites PpIX into a triplet state, which reacts with tissue oxygen to produce singlet oxygen, inducing membrane damage and cellular destruction. With a sufficient dose of light, the PpIX is completely photobleached in the treatment field with no further phototoxicity. In the absence of light activation, PpIX is metabolized to heme in 24 –48 h. Topical 5-amino levulinic acid has been FDA approved for the treatment of actinic keratoses. The ALA is preferentially absorbed by neoplastic cells and sebaceous glands. In the epidermis, the ALA is converted to PpIX which can be activated by a number of visible wavelengths to produce reactive oxygen species and cell death. The initial studies performed on actinic keratoses were for the treatment of individual lesions, using a narrow band blue light source (40). Approximately 70% of actinic keratoses resolved after one treatment session. In subsequent studies (41), treatment of confluent skin areas demonstrated reductions in actinic keratoses comparable to 5-fluorouracil treatment, as well as significant cosmetic benefits. There was a reduction in telangiectasia, lentigines, enlarged pores, and an overall improvement in skin texture. ALA treatment with the narrow band blue light sources may be complicated by phototoxicity responses, with the development of erythema and crusting. This problem has been obviated with the use of shorter incubation times and other light sources including millisecond-duration pulsed dye lasers and IPL sources.

7. 7.1.

LASER AND LIGHT-BASED TREATMENT FOR ACNE Introduction

Acne is the most common skin disease in the world and affects over 80% of the population. Acne can have profound psychological and emotional effects owing to its onset during adolescence and its potential for permanent scarring (42). The etiology of acne is multifactorial (43). Mechanisms leading to acne include (a) defective follicular keratinization and plugging, (b) the enlargement of sebaceous glands and an increase in sebum production, (c) the proliferation of Propionobacterium acnes (P. acnes), and (d) resultant inflammation. The basic lesion of acne is the comedo. Defective keratinization and plugging of the follicular duct with sebum and keratinous debris blocks egress from the follicular canal. The follicular wall dilates and thins. When the keratin plug is forced to the surface, an open comedo is formed. Closed comedones have a narrower follicular orifice. Comedones may evolve into inflammatory papules, pustules, nodules, or cysts. Increased androgen levels that occur with puberty cause an enlargement of the sebaceous glands and an increase in sebum production. The anaerobic diptheroid, P. acnes, proliferates in the sebum-rich environment of the sebaceous gland and produces chemotactic factors for neutrophils, leading to localized inflammation. Acne therapies have therefore been aimed at reversing these various abnormalities, including (a) removing and preventing the keratin plugs, (b) decreasing the size and output of sebaceous glands, (c) reducing the numbers of P. acnes, and (d) reducing

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inflammation. To date, there is no ideal therapy for acne. Topical and systemic medications, with the exception of oral isotretinoin, require long-term use to achieve results, rarely produce adequate control and treatment programs are often complicated by compliance issues. Systemic isotretinoin is highly effective in improving or eliminating acne in 95% of patients, but is associated with risks and side effects that continue to limit its widespread use. Recently, lasers and light sources have been investigated as alternative or adjunctive therapies for acne. These devices can be used to reduce P. acnes and to alter the sebaceous gland with a decrease in sebum production. 7.2.

Targeting P. acnes

In its normal course of reproduction and metabolism, P. acnes synthesizes large amounts of endogenous intracellular porphyrins (44). When porphyrins absorb light, free radical singlet oxygen is produced by a photochemical reaction. Singlet oxygen is a potent oxidizer, and kills the tissues or organisms that possess activated porphyrins by means of attacking the cell membranes. Several light devices, including broadband blue light, pulsed potassium-titanyl-phosphate (KTP) lasers, and pulsed dye lasers have been shown to be effective in improving acne. The blue light acts solely by means of inducing porphyrinmediated destruction of P. acnes, but the other devices, when used at high power, are thought to also have a secondary effect on sebaceous gland activity, possibly via vascular-mediated damage to the gland. The Clearlight (Lumenis) was the first blue light source (405 – 420 nm) investigated for the treatment of acne. A multicenter study (45) using this device consisted of two 15 min treatments per week for a total of 4 weeks. There was a significant reduction in P. acnes counts at the end of the treatment sessions. Eighty percent of patients responded to therapy with a mean reduction of 60% in acne lesions. There is a gradual return of lesions over 3 – 6 months. Similar results have been found with the DUSA Blue U device. The pulsed KTP laser, emitting at 532 nm has also been explored for the treatment of acne based on preliminary data showing improvement with broadband green light (46). Bowes et al. (47) performed a prospective, split-face study using a 532 nm laser, 4 mm spot, 20 ms pulse duration, and fluence of 7–9 J/cm2 (Aura and Laserscope) twice weekly for 2 weeks. There was a 35.9% decrease in mild to moderate acne on the treated side vs. 1.8% on the control side. At one month, there was a 28.1% reduction in sebum production but no significant decrease in P. acnes as measured by fluorescence photography. The pulsed dye laser was first studied by Seaton et al. (48) who found a 49% reduction in inflammatory lesions vs. a 10% reduction in controls 12 weeks after one treatment. A 585 nm laser was used with a 5 mm spot size, 0.35 ms pulse duration and fluence of 1.5 – 3.0 J/cm2 (N-Light, ICN Pharmaceuticals). Almost half of the treated patients had a 50% reduction in inflammatory acne lesions at 12 weeks. Another study (49), using the same device in a split face, controlled study, showed no difference between the treated and untreated side. Both of these studies used low fluence pulsed dye laser with varying results. Anecdotal reports from many investigators show that the pulsed dye laser, when used at parameters effective for the treatment of vascular lesions, also produce a reduction in inflammatory acne lesions. 7.3.

Targeting Sebaceous Glands

The therapies that reduce P. acnes appear to result in only transient benefit. Longer term remissions are possible when laser and light-based technologies are used to damage selectively the sebaceous glands.


649

PDT using topically applied ALA has also been explored for acne treatment due to the preferential accumulation of ALA in sebaceous glands. ALA was applied under occlusion for 3 h and irradiated with 550 –700 nm broadband red light (50). There was clinically and statistically significant clearance of acne lesions 10 weeks after a single treatment and 20 weeks after multiple treatments. The subjects developed superficial exfoliation, crusting, and transient hyperpigmentation. More recent studies have demonstrated improvement using the pulsed dye laser and IPL to activate the ALA with few side effects (51,52). The mid-infrared lasers that were developed for nonablative facial rejuvenation were recently explored for treating acne due to their ability to heat selectively and to damage sebaceous glands. In histological studies (53), the 1450 nm diode laser (Smoothbeam and Candela) caused sebaceous gland necrosis while preserving the epidermis. On the basis of these results, a number of clinical studies were undertaken exploring this device for acne therapy. In a pilot study (53), 14 of 15 patients treated with an average fluence of 18 J/cm2 had a significant reduction in inflammatory lesions that persisted for 6 months. Clinically and statistically, significant reductions in acne lesions have been demonstrated in other studies after a series of 1450 nm diode laser treatments (54,55) (Fig. 32.5). The 1320 nm Nd:YAG (56) and 1540 erbium:Glass (57) lasers have also been demonstrated to improve acne. Like the 1450 nm diode laser, these mid-infrared lasers impart selective thermal damage to the sebaceous glands while preserving the epidermis. Side effects following such treatments are limited to transient urticarial papules, unless improper skin cooling techniques are applied.

8.

CONCLUSIONS

As laser and device-based technology continues to improve, we are moving closer to achieving the goal of the “lunchtime” facelift. An increasing array of techniques are

Figure 32.5 A female with inflammatory acne, before (a) and after (b) three treatments with the 1450 nm diode laser using a 6 mm spot and a fluence of 13 J/cm2 with a cryogen spurt of 33 ms.

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available that will remove visible signs of aging, including telangiectasias, dyschromias, and skin textural irregularities without any real recovery time. PDT offers the ability to treat skin dysplasia in addition to the cosmetic benefits of laser procedures. In just a few years of intense investigational activity, many new options for acne therapy have been developed. Improvements in device-based therapies in the years ahead may eliminate the need for systemic medications. The future also holds promise for tightening of skin using radiofrequency devices and deep tissue tightening with infrared-based technologies, obviating the need for early surgical intervention.

REFERENCES 1.

2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20.

Fitzpatirck RE, Ruiz-Espara J, Goldman MP. The depth of thermal necrosis using the CO2 laser: a comparison of the superpulsed mode and convent ail modes. J Dermatol Surg Oncot 1991; 17:340 – 344. Kauvar ANB, Waldorf HA, Geronemus RG. A hispathological comparison of “char-free” carbon dioxide lasers. Dermatol Surg 1996; 22:343 – 348. Weistein C. Carbon dioxide laser resurfacing: long-term follow up in 2123 patients. Clinical Plast Surg 1998; 25:109 – 130. Goldberg DJ, Cutler KB. The use of the erbium:YAG laser for treatment of class III rhytides, Dermatol Surg 1999; 25:713 –715. Fitzpatrick RE, Rostan EF, Marchell N et al. Collagen tightening induced by carbon dioxide laser versus erbium:YAG laser. Lasers Surg Med 2000; 27:395– 403. Fulton JE, Barnes T. Collagen shrinkage (selective dermaplasty) with high-energy pulses carbon dioxide laser. Dermatol Surg 1998; 24:37 – 41. Bernstein LJ, Kauvar ANB, Grossman MC, Geronemous RG. The short and long-term side effects of carbon dioxide laser. Dermatol Surg 1998; 24:37 – 41. Nanni CA, Alster TS. Complications of carbon dioxide laser resurfacing: an evaluation of 500 patients. Dermatol Surg 1998; 24:315 – 320. Kauvar ANB, Grossman MC, Bernstein LJ et al. Erbium:YAG laser resurfacing: a clinical histopathologic evaluation. Lasers Surg Med 1998; 10(suppl):33. Kauvar ANB. Laser skin resurfacing: perspectives at the millennium. Dermatol Surg 2000; 26(2):174– 177. Hardaway C, Ross EV. Nonablative laser skin remodeling. Dermatologic Clinics 2002; 20(1):97– 111. Nelson JS, Majaron B, Kelly KM. What is nonablative photorejuvenation of human skin? Sem Cut Med Surg 2002; 21(4):238– 250. Alam M, Tye-Shao H, Dover JS et al. Nonablative laser and light treatments: histology and tissue effects—a review. Laser Surg Med 2003; 33:30– 39. Zelickson B, Kilmer S, Bernstein E et al. Pulsed dye laser therapy for sun damaged skin. Lasers Surg Med 1999; 25:229 – 236. Zelickson B, Kist D. Effect of pulsed dye laser and intense pulsed light source on the dermal extracellular matrix remodeling. Lasers Surg Med 2000; 12(suppl):68. Bjerring P, Clement M, Heickendorff L et al. Selective non-ablative wrinkle reduction by laser. J Cutan Laser Ther 2000; 2:9 –15. Hsu TS, Zelickson B, Dover JS et al. Multicenter study of the safety and efficacy of a 585 nm pulsed-dye laser for the nonablative treatment of facial rhytides. Dermatol Surg 2005; 1:1– 9. Bernstein E. Nonablative skin rejuvenation. Controversies in Cutaneous Laser Surgery. Woodstock, VT, 2000. Lee MW. Combination 532-nm and 1064-nm lasers for noninvasive skin rejuvenation and toning. Arch Dermatol 2003; 139(10):1265– 1276. Goldberg DJ, Cutler KB. Nonablative treatment of rhytids with intense pulsed light. Lasers Surg Med 2000; 26:196 – 199.

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Goldberg DJ. Histologic changes after treatment with an intense pulsed light. J Cutan Laser Ther 2000; 2:53– 56. Bitter PJ. Noninvasive rejuvenation of photoaged skin using serial, full-face intense pulsed light treatments. Dermatol Surg 2000; 26:835 – 843. Goldberg DJ, Whitworth J. Laser skin resurfacing with the Q-switched Nd:YAG laser. Dermatol Surg 1997; 23:903 –907. Goldberg DJ, Metzler C. Skin resurfacing utilizing a low-fluence Nd:YAG laser. J Cutan Laser Ther 1999; 1:23– 27. Friedman PM, Skover GR, Payonk G et al. 3D in-vivo optical imaging for topographical quantitative assessment of non-ablative laser technology. Dermatol Surg 2002; 28:199 – 204. Goldberg DJ, Samady J. Comparison of intense pulsed light and Nd:YAG laser for nonablative treatment of facial rhytids. Lasers Surg Med 2001; 28:141– 144. Schmults CD, Phelps R, Goldberg DJ. Non-ablative facial remodeling: erythema reduction and histologic evidence of new collage formation using a new 300 microsecond, 1064-nm Nd:YAG laser. Arch Dermatol 2004; 140:1373 –1376. Muccini J, O’Donnell F, Fuller T et al. Laser treatment of solar elastosis with epithelial preservation. Lasers Surg Med 1998; 23:121 – 127. Dayan SH, Vartanian AJ, Menaker G et al. Nonablative laser resurfacing using the long pulse (1064 nm) Nd:YAG laser. Arch Facial Plast Surg 2003; 5(4):310 – 315. Nelson JS, Millner TE, Dave D et al. Clinical study of non-ablative laser treatment of facial rhytides. Lasers Surg Med 1998; 17(suppl 9):150. Goldberg DJ. Non-ablative subsurface remodeling: clinical and histologic evaluation of a 1320-nm Nd:YAG laser. J Cutan Laser Ther 1999; 1:153– 157. Goldberg DJ. Subdermal resurfacing. Oper Tech Oculoplast Orbital Reconstr Surg 1999; 2:188 – 193. Goldberg DJ. Nonablative resurfacing. Clin Plast Surg 2000; 27:287– 292. Goldberg DJ. Full-face nonablative dermal remodeling with a 1320 nm Nd:YAG laser. Dermatol Surg 2000; 26:915 –918. Goldberg DJ, Rogachefsky AS, Silapunt S. Non-ablative treatment of facial rhytides: a comparison of 1450 nm diode laser treatment with dynamic cooling as opposed to treatment with dynamic cooling alone. Lasers Surg Med 2002; 30:79 – 81. Tanzi EL, Alster TS. Comparison of a 1450 nm diode laser and a 1320 nm Nd:YAG laser in the treatment of atrophic facial scars. Dermatol Surg 2004; 33:152– 157. Dahan S, Lagarde JM, Turlier V et al. Treatment of neck lines and forehead rhytids witha nonablative 1540 nm Er:glass laser: a controlled clinical study combined with the measurement of the thickness and the mechanical properties of the skin. Dermatol Surg 2004; 30:872 – 879. Ross EV, Sajben FP, Hsia J et al. Nonablative skin remodeling: selective dermal heating with a mid-infrared laser and contact cooling combination. Lasers Surg Med 2000; 26:186– 195. Kennedy JC, Pottier RH, Pross DC. Photdynamic therapy with endogenous protoporphyrin IX: basic principles and present clinical experience. J Photochem Photobiol B 1990; 6:143– 148. Piacquadio DJ, Chen DM, Farber HF et al. Photodynamic therapy with aminolevulinic acid topical solution and visible blue light in the treatment of multiple actinic keratoses of the face and scalp: investigator-blinded, phase 3, multicenter trials. Arch Dermatol 2004; 1:41– 46. Touma D, Yaar M, Whitehead S et al. A trial of short incubation, broad-area photodynamic therapy for facial actinic keratoses and diffuse photodamage. Arch Dermatol 2004; 1:33– 40. Mulder MM, Sigurdsson V, van Zuuren EJ et al. Psychosocial impact of acne vulgaris. Evaluation of the relation between a change in clinical acne severity and psychosocial state. Dermatology 2001; 203:124 – 130. Pawin H, Beylot C, Chivot M et al. Physiopathology of acne vulgaris: recent data, new understanding of the treatments. Eur J Dermatol 2004; 14:4 – 12. Kjeldstad B. Photoinactivation of proprionibacterium acnes by near-ultraviolet light. Z Naturforsch 1984; 39:300 – 302. Shalita A. International Multicenter Clearlight acne phototherapy study. EADV Annual Conference, Munich 2002.

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Goldberg and Kauvar Sigurdsson V, Knulst AC, van Weelden H. Phototherapy of acne vulgaris with visible light. Dermatology 1997; 194:256– 260. Bowes LE, Manstein D, Anderson RR. Effects of 532 nm KTP laser exposure on acne and sebaceous glands. Lasers Surg Med 2003; 18:S6 – S7. Seaton ED, Charakida A, Mouser PE et al. Pulsed-dye laser treatment for inflammatory acne vulgaris: randomized controlled trial. Lancet 2003; 362:1347 –1352. Orringer JS, Kang S, Hamilton T et al. Treatment of acne vulgaris with a pulsed dye laser. A randomized controlled trial. JAMA 2004; 291:2834 – 2839. Hongcharu W, Taylor CR, Chang Y et al. Topical ALA-photodynamic therapy for the treatment of acne vulgaris. J Invest Dermatol 2000; 115:183 – 192. Alam M, Dover JS. Treatment of photaging with topical aminolevulinic acid and light. Skin Therapy Lett 2004; 9(10):7 – 9. Alster TS, Tanzi EL, Welsh EC. Photorejuvenation of facial skin with topical 20% 5-aminolevulinic acid and intense pulsed light treatment: a split-face comparison study. J Drugs Dermatol 2005; 4(1):35 –38. Paithankar DY, Ross EV, Saleh BA et al. Acne treatment with a 1450 nm wavelength laser and cryogen spray cooling. Lasers Surg Med 2002; 31:106 – 114. Friedman PM, Jih MH, Kimyai-Asadi A et al. Treatment of inflammatory facial acne vulgaris with the 1450-nm diode laser: a pilot study. Dermatol Surg 2004; 30:147 – 151. Lupton JR, Fitzpatrick RE. Nonablative cutaneous laser resurfacing using a 1450 nm diode laser for the treatment of mild atrophic scars and inflammatory acne. Lasers Surg Med 2003; 32:S29. Chernoff G. The utilization of 1320 nm Nd:YAG energy for the treatment of active acne vulgaris. White Paper 2004; Cooltouch Inc. Boineau D, Angel S, Nicole A et al. Treatment of active acne with an Er:glass (1.54 um) laser. Lasers Surg Med 2004; 34:S55.

33 Laser Treatment of Leg Veins Arielle N. B. Kauvar New York Laser and Skin Care, New York; New York University School of Medicine, New York; and Suny Downstate Medical Center, New York, New York, USA

1. 2. 3. 4.

Leg Vein Anatomy and Physiology Theoretical Considerations for Laser Treatment of Leg Veins Continuous Wave Lasers Pulsed Lasers and Light Sources 4.1. KTP Lasers 4.1.1. Treatment Technique 4.2. Flashlamp-Pumped Pulsed Dye Laser 4.2.1. Treatment Technique 4.3. Long-Pulsed Dye Lasers 4.3.1. Treatment Technique 4.4. Intense Pulsed Light 4.4.1. Treatment Technique 5. Near-Infrared Lasers for Leg Veins 5.1. Long-Pulsed Alexandrite Lasers 5.1.1. Treatment Technique 5.2. Diode Lasers 5.2.1. Treatment Technique 5.3. Long-Pulsed Neodymium:Yttrium –Aluminum –Garnet Lasers 5.3.1. Treatment Technique 6. Studies Comparing Sclerotherapy and Laser treatment of Leg veins 7. Complications and Their Management 7.1. Purpura 7.2. Vesiculation and Crusting 7.3. Hyperpigmentation 7.4. Hypopigmentation 7.5. Scarring 7.6. Thrombus Formation 8. Conclusions References

654 655 657 658 658 659 659 659 660 662 663 665 665 665 666 667 668 668 670 670 671 671 671 672 672 672 672 672 673 653

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Primary venous insufficiency, presenting as telangiectasia, reticular veins, and varicose veins, affect up to 80% of the population (1). Approximately one-half of these patients may experience symptoms from their disease, but the vast majority seek treatment for cosmetic purposes (2). Until recently, sclerotherapy has been the standard treatment for leg veins up to 4 mm in diameter, and surgical excision for leg veins .4 mm in diameter (3 – 5). As a result of technological advances, lasers and light sources (Table 33.1) can now be safely and effectively used to treat leg telangectasia, venulectasia, and reticular and varicose veins in the appropriately selected patient. Bare fiber diode lasers and radiofrequency devices are now used to treat greater saphenous vein insufficiency. Sclerotherapy remains a highly effective modality for telangiectasia, venulectasia, and reticular veins in the majority of patients (6,7). Nevertheless, there are limitations to this technique (8). Multiple treatment sessions are necessary with sclerotherapy injections, and vessel clearance can take months. Needle phobias are not uncommon. Sclerotherapy-related side effects include telangectatic matting, post-treatment hyperpigmentation, skin ulceration secondary to sclerosant extravasation, and rarely, deep-venous thrombosis, and allergic reactions to sclerosant solutions. For optimal results, considerable experience is required to adequately perform this technique-sensitive procedure. Laser and light source technology provide alternative techniques that may be simpler to perform and provide improved efficacy with limited side effects (Table 33.1). To date, there is no ideal therapy for unwanted leg veins that provides complete vein clearance in one treatment with no associated side effects. Most patients with visible leg veins have a heterogeneity of vessels and often require treatment with multiple modalities. Arborizing telangiectasia, in the absence of elevated venous pressure, may be treated with sclerotherapy or laser therapy. Lasers are ideally suited for the treatment of diffuse, fine superficial linear telangiectasia that are typically difficult to canullate with even a 30 g needle. Venulectasia may be treated with sclerotherapy or laser technology. Reticular veins are usually easily treatable with sclerotherapy, but respond well to the near-infrared lasers. These lasers also play a useful role in the treatment of foot and ankle vessels, where there is a higher incidence of sclerotherapy-induced skin ulceration due to arterio-venous communication. Lasers and light sources are the preferred modalities for the treatment of sclerotherapy-induced matting.

1.

LEG VEIN ANATOMY AND PHYSIOLOGY

Physicians must have a basic understanding of the superficial venous anatomy for successful treatment of leg veins.

Table 33.1

Laser and Light Sources for Leg Veins

Laser or light source

Wavelength (nm)

Pulse duration (ms)

Pulsed KTP Pulsed dye Tunable pulsed dye Long pulsed alexandrite Diode Long pulsed Nd:YAG Intense pulsed light

532 585 585, 590, 595, 600 755 800, 810, 940 1064 510– 1200

1 – 100 0.45 1.5 3 – 20 1 – 250 1 – 100 2 – 25

Laser Treatment of Leg Veins

655

The venous system of the lower extremities consists of a superficial and deep channel [reviewed in Ref. (9)]. The superficial channel runs within the skin and subcutis, and interconnects with the deeper channel by epifacial perforating veins. The three important superficial venous systems include the greater saphenous vein, the lesser saphenous vein, and the lateral sub-dermic venous system. The deep channel runs within the muscular system. Most leg telangectasia communicate directly or indirectly with larger reticular or varicose feeding veins. Superficial leg telangectasia measure 0.03 – 0.3 mm in diameter, and appear as hair-fine pink or red linear or branching vessels. They connect with post-capillary venulectasia that measure 0.4– 2.0 mm in diameter, and are usually branching and purple-blue in color. The post-capillary venulectasia connect to reticular veins measuring 2.0– 4.0 mm in diameter, which appear as wider nonpalpable greenish-blue vessels beneath the skin surface, and to larger varicosities. Telangiectasia are often a sign of abnormal physiology of the venous system or venous insufficiency (10,11). When telangiectasia are associated with larger varicose veins, the elevated hydrostatic pressures must often be eliminated for successful treatment of the smaller vessels. Malfunctioning valves in the venous system result in sequestration and congestion of blood in the lower extremity vessels; smaller surface veins such as telangiectasia, venulectasia, and reticular veins expand with pressure and produce symptoms. Visual inspection and ultrasound of the legs aid in determining whether the surface telangiectasia or varicosities originate from elevated pressures in the superficial venous systems. Most younger patients presenting in their third or fourth decades have telangiectatic patches resulting from reflux in the lateral venous system (12). Reverse flow from the greater or lesser saphenous vein systems must be considered when there is a family history of varicose veins. The presence of reflux may be confirmed with the use of Doppler ultrasound, plethysmography, or duplex ultrasound (12 – 14).

2.

THEORETICAL CONSIDERATIONS FOR LASER TREATMENT OF LEG VEINS

Telangectasia, venulectasia, and reticular veins are excellent targets for laser and light source therapy, because they are located superficially in skin and contain a natural chromophore, such as hemoglobin. Lasers were first used to treat leg telangiectasia as early as the 1970s, but it was not until the development of the millisecond-duration pulsed dye laser in the late 1990s that effective treatment could be delivered with a minimal risk of side effects. The development of the pulsed dye laser in the mid-1980s based on the principles of selective photothermolysis revolutionized the treatment of cutaneous vascular lesions and set the stage for the creation of modern day laser technology. According to this theory (15), chromophore-containing skin structures, such as blood vessels, can be selectively damaged and destroyed using (1) wavelengths of light preferentially absorbed by the targeted chromophore, (2) pulse durations less than or equal to the thermal relaxation time of the treated vessel, and (3) sufficient laser energy density to irreversibly damage the vessel. On the basis of dramatic successes achieved using pulsed dye lasers for the treatment of facial telangiectasia and capillary vascular malformations, these devices were soon applied to the treatment of leg veins. The optimal treatment parameters depend on the vessel type, size, and depth in tissue (16). In general, larger vessel diameters require longer pulse durations for even heating of the entire vessel (17,18). Dierickx et al. (17) demonstrated that telangiectasia

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require millisecond pulse durations. When too-short a pulse duration is used, thermal coagulation is limited to the superficial-most portion of the vessel, and incomplete coagulation results. Deeper vessels require longer wavelengths of light because of their greater depth of penetration into tissue (20) (Fig. 33.1). Spot size can also influence the tissue effect of the laser (21,22). Larger spot sizes are used when deeper penetration is required, but matching the spot size to the vessel diameter minimizes laser thermal effects on the surrounding tissue. In the 1990s, pulsed dye lasers, pulsed potassium titanyl phosphate (KTP) lasers, and the intense pulse light source were optimized for the treatment of leg telangectasia. The role of these devices was limited to the treatment of superficial vessels measuring ,1.0 mm in diameter. Most individuals, however, have vascular webs with a range of vessel diameters and depths. In the past few years, improvements in existing laser technology and the development of additional wavelengths have enabled clearance rates and side-effect profiles comparable to sclerotherapy techniques. Longer wavelengths, including 755, 800, 940, and 1064 nm, can target deeper blood vessels with larger diameters. Millisecond-duration pulses provide slow, even heating of larger diameter blood vessels. Skin cooling techniques are used to selectively cool and protect the epidermis during delivery of light energy (23). Skin cooling techniques are now generally used with all laser and light source treatment of lower extremity vessels. Skin cooling during laser treatment prevents epidermal and collateral dermal damage, and reduces treatment-associated discomfort. Bulk cooling can be achieved using ice applications, but over-cooling the skin may result in reduced efficacy. Water-cooled chambers (sapphire, quartz or copper) can be applied directly to the skin during, before, or after laser pulse application (Fig. 33.2). Cooling gels extract heat from the surface of the skin and are used alone or in conjunction with contact cooling devices. Refrigerated cryogen cooling systems apply brief, millisecond spurts of refrigerated spray to the skin surface, before, during, or after laser pulse impact to extract heat from the epidermis (Fig. 33.3). Skin cooling methods spare the

Figure 33.1 Deeper skin penetration is achieved with longer wavelengths. Courtesy of Lumenis.


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Figure 33.2 (a) Water-cooled sapphire tip on the Laserscope Lyra. (b) Water-cooled copper plate on the Altus Coolglide.

epidermis from damage, and enable the safe use of higher fluences to provide greater lesional clearing.

3.

CONTINUOUS WAVE LASERS

The first lasers to be used in medicine and dermatology were continuous wave lasers. Argon (488 and 514 nm) and continuous wave dye lasers (515 – 590 nm) penetrate to the depth of mid-dermal vessels and are well-absorbed by hemoglobin. These lasers do not produce selective damage of blood vessels because of their long exposure times. When exposure times greatly exceed the thermal relaxation time of the treated vessels, nonspecific thermal injury can damage adjacent tissue. In studies of the argon and continuous wave dye lasers by Apfelberg et al. (24) and Dixon et al. (25), greater than half the patients treated had either no results or poor results from treatment. Experience with the

Figure 33.3 Cryogen spray cooling selectively cools the epidermis, while permitting heating of dermal vessels.

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continuous mode Nd:YAG laser at 1064 nm was also disappointing. The combination of poor hemoglobin absorption, a deeply penetrating wavelength (to a depth of 3.7 mm), and continuous exposure times produced nonspecific tissue damage. The carbon dioxide laser at 10,600 nm also produced poor results for leg telangiectasia. Nonspecific thermal damage resulted from the high absorption by water in the epidermis and dermis, which led to scarring, hypopigmentation, and neovascularization (24,26,27).

4. 4.1.

PULSED LASERS AND LIGHT SOURCES KTP Lasers (Table 33.2)

Pulsed KTP lasers have been used to treat superficial leg telangectasia with good results (28,29). At 532 nm, absorption by hemoglobin is comparable to that of 585 nm light, and the penetration depths in tissue are similar. Green light at 532 nm is produced by passing a 1064 nm Nd:YAG laser beam through a KTP crystal which doubles the frequency. Lasers available at this wavelength use grouped Q-switched pulses for effective exposure times of 1– 50 ms or diode pumped KTP crystals to produce individual laser pulses. Epidermal cooling is achieved with the use of cold gels, ice application, cold air cooling, or contact cooling using sapphire lasers tips or quartz plates. With the use of larger spot sizes (3 –5 mm), longer pulse durations (10 – 15 ms), and fluences of 14 – 20 J/cm2, excellent results are achieved for the treatment of isolated blood vessels ,1 mm in diameter in the absence of feeding reticular veins (28,29) (Fig. 33.4). Good clearance of leg veins 0.5 – 1.0 mm in diameter was achieved with another 532 nm KTP laser using a multi-pulse mode emission (30). The nonuniform pulse sequence was comprised of three stacked pulses of 100, 30, and 30 ms with an interpulse delay of 250 ms. A fluence of 60 J/cm2 was used with a 0.75 mm collimated spot. One treatment produced 53% vessel clearing, two treatments resulted in 78% lesional clearing, three treatments produced 85% clearance, and four treatment resulted in 93% Table 33.2

Pulsed KTP Lasers Diolite 532

Laser type

Manufacturer Wavelength (nm) Pulse duration (ms) Pulse rate Spot sizes Maximum fluence Other features

Aura

Gemini

VersaPulse

Viridis derma

532

Nd:YAG frequency doubled Lumenis/ Coherent 532

Nd:YAG frequency doubled Quantel Medical 532

1 – 50

1 – 100

2 – 50

15 – 150

1 – 10 Hz 0.5– 5 mm 240 J/cm2

Up to 4 Hz 1 – 5, 10 mm Up to 100 J/cm2

Single to 10 Hz 1 – 10 mm 0.26 – 38 J/cm2

110 J/cm2

Scanner contact cooling

Contact cooling

Contact cooling

Nd:YAG frequency doubled Iridex

Nd:YAG frequency doubled Laserscope

Nd:YAG frequency doubled Laserscope

532

532

1 – 100

200– 1400 mm 0.2 – 1.4 J/cm2

Scanner


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Figure 33.4 Resolution of leg veins following treatment with a long-pulsed KTP laser. (Courtesy of Robert Adrian, M.D.)

vessel resolution. Adverse effects were limited to edema, crusting, and transient hypopigmentation. At a wavelength of 532 nm, there is strong absorption by melanin. Patients with sun-tanned skin or darker phototypes are at increased risk for blistering, crusting, and hypopigmentation. The KTP lasers are best used for individuals with skin phototypes I –III without evidence of actinic bronzing or a sun tan. 4.1.1.

Treatment Technique

Depending on the manufacture, pulse durations in the range of 10 –35 ms are used with fluences of 10 –20 J/cm2 and laser beam diameters of 2 – 5 mm. The individual vessels are traced with contiguous laser pulses. The clinical endpoint should be vessel spasm or blanching. Pulse stacking should be avoided because of the increased risk of epidermal damage. Additional laser pulses may be applied to the lesion to achieve the desired endpoint. Proper contact with cooling devices is essential to avoid epidermal damage. The application of a cold coupling gel improves the cooling efficiency, and aids in patient comfort.

4.2.

Flashlamp-Pumped Pulsed Dye Laser (Table 33.3)

In the early 1990s, the first generation pulsed dye lasers, with wavelength of 585 nm and pulse duration of 0.45 ms, were investigated for the treatment of leg veins (31,32). They were found to be effective only for vessels measuring ,0.2 mm in diameter. Hyperpigmentation and hypopigmentation occurred in up to 50% of subjects, but were usually transient in nature. Vessels associated with 2 – 3 mm reticular feeding veins responded poorly. Post-sclerotherapy matting responded well to fluences of 6.5 –7.5 J/cm2 using a 5 mm spot. Hyperpigmentation developed in fewer than 10% of their subjects, but hypopigmentation occurred in a sun-tanned subject. In general, the sub-millisecond pulse durations are effective for only fine caliber leg telangiectasia measuring ,0.2 mm in diameter. The very short pulse durations produce heating of blood limited to the uppermost layers of the vessel, resulting in partial vessel coagulation. Without full-thickness photocoagulation, hydrostatic pressure will dislodge the coagulum, and allow the vessel to recover. The sub-millisecond pulsed dye lasers are now rarely used for leg veins. Low flow matted telangiectasia, in the absence of rapid refill, may be treated successfully with these laser systems.

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Table 33.3

Flashlamp-Pumped Pulsed Dye Laser

Laser type Manufacturer Wavelength (nm) Pulse duration (ms) Pulse rate Spot sizes (mm) Maximum fluence (J/cm2) Other features

SPLT-1b

Cbeam

PhotoGenia V

Flashlamp-pumped pulsed dye laser Candela 585 450 Single or 1 Hz 2 7, 3, 5, 7, 10 10

Flashlamp-pumped pulsed dye laser Candela 585 450 1 Hz 5, 7, 10 16

Flashlamp-pumped pulsed dye laser Cynosure 585 500 Single or 1 Hz 5, 7, 10 20 Air cooling

4.2.1. Treatment Technique Matted telangiectasia are treated with larger spot sizes (7 or 10 mm) used to apply contiguous laser pulses with 10% overlap. Fluences vary depending on the laser manufacturer, and whether cooling devices are being used. Post-treatment hyperpigmentation is relatively common and may require 2 –3 months to fade. Treatment should be limited to patients with phototypes I– III, with the absence of a suntan. Two to three treatments sessions may be required. 4.3.

Long-Pulsed Dye Lasers

Candela Sclerolaser, a tunable 1.5 ms pulsed dye laser, was the first laser specifically designed for the treatment of leg telangiectasia. Long-pulsed dye lasers were developed on the basis of theoretical considerations that treatment of deeper, larger caliber veins would improve with longer, deeper penetrating wavelengths, and longer pulse durations. The longer pulse duration of 1.5 ms compared with 0.45 ms provides improved vessel heating. Although purpura is still produced, it is diminished in intensity and duration compared with the 0.45 ms laser systems. The Scleroplus (Candela, Wayland, MA) and the Photogenica VLS (Cynosure, Chelmsford, MA) have a fixed pulse duration at 1.5 ms and can be tuned to deliver wavelengths of 585, 590, 595, or 600 nm. The V-beam (Candela) and the V-star Photogenica (Cynosure) are fixed at a wavelength of 595 nm and have variable pulse durations from 1.5 to 40 ms. Several studies of these laser systems have been performed for the treatment of leg veins, with varying results (Tables 33.4 and 33.5). In a study of 20 patients with the Candela 595 nm, 1.5 ms laser showed .50% clearance in 45% of patients who were treated at a fluence of 18 J/cm2 with a 2 7 mm elliptical spot size, without cooling (33). At 5 month follow-up, 50% clearance of telangiectasia was noted in 65% of patients. Transient hyperpigmentation occurred in 31% of the treatment sites and transient hypopigmentation developed in 15% of the treatment sites. All pigmentary alterations resolved by the 5 month follow-up visit. In another study using this laser system, without epidermal cooling, up to three consecutive treatments were delivered at 15 and 20 J/cm2 in 29 patients, using a 2 7 mm elliptical spot (34). Clearance of .50% of telangiectasia was achieved at 24 weeks following treatment in 80% of the sites treated at a fluence of 15 J/cm2, and a 100% of the sites treated at a fluence of 20 J/cm2. A range of 20 –40% of the sites developed transient hyperpigmentation and hypopigmentation, which completely resolved by the 24 week follow-up visit.

Laser Treatment of Leg Veins Table 33.4

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Tunable Pulsed Dye Lasers ScleroLaser/ScleroPlus

Laser type Manufacturer Wavelength (nm) Pulse duration (ms) Pulse rate Spot sizes (mm) Maximum fluence (J/cm2) Other features

Flashlamp-pumped pulsed dye laser Candela 585, 590, 595, 600 1.5 Single or 1 Hz 2 7, 3, 5, 7, 10 20 Dynamic cooling

PhotoGenica LV Flashlamp-pumped pulsed dye laser Cynosure 585, 590, 595, 600 1.5 Single or 1 Hz 3, 5, 7, 10 20

Twenty-five patients with leg telangiectasia up to 1.5 mm in diameter were treated three times at 6 week intervals, using a 2 7 mm spot and fluences of either 15 or 20 J/cm2 (35). Six weeks following the last treatment, 84% of vessels treated at 15 J/cm2 and 76% of vessels treated at 20 J/cm2 were resolved. Transient hyperpigmentation (40%) and hypopigmentation (20%) were common. Twenty-five women with leg telangiectasia ,1 mm in diameter were treated with the Candela 595 nm, 1.5 ms pulsed dye laser without cooling (36). A total of four areas were treated in each patient. Two areas were treated at a wavelength of 595 nm with fluences 15 or 20 J/cm2, and two areas were treated at 600 nm with fluences of 15 or 20 J/cm2. Up to three treatments were performed at 6 week intervals. The best vessel clearance was achieved at 595 nm and 20 J/cm2. Although all patients had some clearance of their vessels, the responses were variable with regard to the degree of resolution. Hyperpigmentation occurred in more than 50% of the treated sites, but resolved completely within several months. Superficial scabbing occurred in three patients, but resolved without textural changes. A total of 250 sites of leg telangiectasia ranging in size from 0.1 to 1.2 mm in diameter in 80 patients were treated using a 595 nm, 1.5 ms pulsed dye laser without cooling (37). In this study, refluxing reticular veins were not present or were previously treated by the investigators. Treatment sites were cooled with ice packs prior to and after laser application, and compression wraps were used for 72 h following treatments. Vessels ,0.5 mm in diameter were treated at a wavelength of 590 nm and larger diameter, blue vessels were treated at wavelengths of 595 –600 nm. Vessels with diameters up to

Table 33.5

Variable Pulse-Width Pulsed Dye Lasers

Laser type Manufacturer Wavelength (nm) Pulse duration (ms) Pulse rate (Hz) Spot size (mm) Maximum fluence (J/cm2) Other features

V beam

V star

Flashlamp-pumped pulsed dye laser Candela 595 0.5– 40 1.5 3 10, 5, 7, 10 25 Cooling cryogen

Flashlamp-pumped pulsed dye laser Cynosure 585, 595 0.5 – 40 2 2 7, 5, 7, 10, 12 28 Air cooling

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0.5 mm cleared in all patients after one to two treatments, 6 weeks apart. Eighty percent of vessels ranging in size from 0.5 to 1.0 mm in diameter cleared after up to four treatments. Transient hyperpigmentation and hypopigmentation occurred in 50% of cases, but scarring and telangiectatic matting were not observed. The addition of skin cooling methods has improved the treatment of leg telangiectasia with long-pulsed dye lasers. The dynamic cooling device (DCD, Candela, Wayland, MA) is a method using cryogen spray cooling, first developed by Stuart Nelson at the Beckman Laser Institute (38). This device produces millisecond duration spurts of cryogen that are applied to the skin milliseconds prior to each laser pulse. Cryogen spray cooling used in conjunction with the 585 nm, 0.45 ms pulsed dye laser significantly decreased discomfort during treatment of capillary vascular malformations (39). Kauvar et al. demonstrated decreased pain, purpura, and crusting when cryogen spray cooling was used with a 1.5 ms, 595 nm pulsed dye laser for the treatment of capillary vascular malformations (40). The overall healing times were also reduced from an average of 9 – 5 days. In addition to providing analgesia and epidermal protection, the use of cryogen spray cooling in conjunction with long-pulsed dye laser treatment enables the safe use of higher fluences, resulting in faster clearing of capillary vascular malformations. The use of higher fluences is to produce improved clearance of PWS with long-pulsed dye lasers in adults and infants (41,42). Kauvar et al. (43) treated leg vessels up to 1.2 mm in diameter in 19 patients using a 595 nm, 1.5 ms pulse dye laser (Candela) at fluences up to 23 J/cm2, in conjunction with cryogen spray cooling (Fig. 33.5). Greater than 75% clearance of vessels was noted in 83% of patients 3 months after just one treatment session. With the addition of the cryogen spray cooling, treatment discomfort was reduced, and results appeared to be better than historical controls. To date, there is one published study (44) using the long-pulsed dye laser at a pulse duration of 40 ms for leg telangiectasia. Resolution of leg veins required high enough fluences to produce transient purpura, and the incidence of hyperpigmentation was 55%. In the author’s experience, the best results for leg telangiectasia are achieved using pulsed dye lasers at 595 nm with a pulse exposure time of 1.5– 3.0 ms, in conjunction with skin cooling techniques. 4.3.1.

Treatment Technique

The long-pulsed dye lasers are best used for isolated, linear pink telangiectasia, in the absence of refluxing feeder veins. Treatment is usually performed with a wavelength of 595 nm and a pulse duration of 1.5 ms. An elliptical beam is used with fluences of 15– 18 J/cm2. Higher fluences may be

Figure 33.5 Leg telangiectasia before (a) and 3 months after (b) one treatment with a 595 nm, 1.5 ms pulsed dye laser with cryogen cooling.


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used in conjunction with skin cooling devices. Contiguous laser pulses are applied to the vessels with minimal overlap. Purpura develops immediately after treatment and lasts 7– 10 days. Vessel resolution occurs over a period of 2– 3 months. Two to three treatment sessions may be required. The 595 nm, 1.5 ms laser is also useful for the treatment of post-sclerotherapy matting. Larger spot sizes (10 mm) are most effective. If a central perforating feeder vein is present, it should be treated first with either sclerotherapy or near-infrared laser. Hyperpigmentation can be expected in 20% of patients, and may last up to 3 months. Posttreatment hypopigmentation is less common and resolves over several weeks. Due to the high absorption coefficient for melanin at 595 nm, long-pulsed dye lasers should not be used for the treatment of leg telangiectasia in patients with darker phototypes, the presence of a sun tan, or chronic actinic bronzing.

4.4.

Intense Pulsed Light (Table 33.6)

The intense pulsed light (IPL) was developed in the early 1990s by Energy Systems Corporation (now Lumenis, Santa Clara, CA) specifically for the treatment of lower extremity telangiectasia. There are now several other IPL systems that are being used for vascular indications. Unlike a laser, the IPL uses a filtered flashlamp to produce pulses of noncoherent light in the visible to near-infrared spectrum. The potential advantages of this system over a single wavelength laser are for broad absorption by oxygenated and deoxygenated hemoglobin across the emission spectrum, and the ability to target vessels located deeper within the tissue. The optical absorption properties of hemoglobin vary depending on its state of oxygenation and the size and depth of the blood vessels in tissue. As the diameter and depth of a blood vessel increases, light absorption increases for wavelengths 600 – 1000 nm. At these wavelengths, there is deeper penetration of laser light into tissue, and greater absorption by deoxyhemoglobin. Most IPL devices deliver wavelengths of 515 – 1000 nm, and fluences up to 90 J/cm2, using sequential, synchronized pulse durations of 1 – 25 ms separated by rest intervals of 1 – 100 ms. Confinement of thermal energy is achieved by matching the pulse durations to the thermal relaxation time of the treated blood vessels, and by using a series of filters to remove the lower wavelengths of visible light. Early clinical trials investigating the ESC/Lumenis IPL for the treatment of lower extremity telangiectasia demonstrated clearance rates up to 70% for vessels 0.5 –1 mm in diameter (45), 80% for vessels 0.2– 0.5 mm in diameter, and 90% for vessels ,0.2 mm in diameter (29). Vessels ,0.2 mm in diameter were treated with either a single 3 ms pulse at J/cm2, or a double pulse of 2.4 and 4.0 ms with a 10 ms delay, at 35 to 40 J/cm2. Vessels from 0.2 to 0.5 mm in diameter were treated with double pulses of 3.0 and 6.0 ms pulses, a 20 ms delay, and fluences of 35 –45 J/cm2. Patients with sun tans and skin phototype III or darker were at risk for blistering and erosions, followed by hypopigmentation. Although results from subsequent studies have varied (46,47), Schroeter and Neumann (48) reported clearances of 84.3% of leg telangiectasia 1 month after treatment. Weiss and colleagues (49) found improved results using a combination of pulse durations. They combined the use of 2.4 – 3.0 ms pulses with a 7 ms pulse, separated by a 10 –20 ms delay, using a 570 nm filter, and achieved responses of 74% after two treatments. Their rationale was that smaller and larger diameter vessels overlying one another could be targeted with a combination of shorter and longer pulse durations.

Contact cooling

10– 50 J/cm2 3– 20 J/cm2

Energy range Other features

10 30

10 20, 20 25

2 – 500 ms

Flashlamp Medical BioCare 515 –920

Omnilight

1 – 500 ms

400 – 1200

Flashlamp Palomar

StarLux

400– 1200

Flashlamp Palomar

Estelux

400– 1400

Flashlamp Sciton

Profile

580– 980

Flashlamp Syneron

Aurora

Combined with bipolar RF

10– 30 J/cm2

10– 100 ms 10– 100 ms Up to 200 ms Up to 100 ms

400 –1200

Flashlamp Palomar

MediLux

0.11– 0.33 Hz Single, double, Up to 1 Hz 1 Hz 1 Hz 1 Hz or triple pulses 16 46, 16 46, 8 15, 8 35, 16 46, 8 35, 8 15 13 15 12 12, 10 45 12 12, 12 12, 12 28 12 28 12 21 3– 90 J/cm2 Up to Up to Up to Up to Up to Up to 30 J 90 J/cm2 50 J/cm2 45 J/cm2 40 J/cm2 90 J/cm2 Contact Contact Contact cooling cooling cooling

1 –25 ms

2– 25 ms

0.8 Hz

515 – 1200

515 –1200

600–850

Vasculight Flashlamp Lumenis

Photderm VL

Flashlamp Flashlamp Cutera/Altus Lumenis/ESC

Cool Glide Xeo

Spot sizes (mm)

Laser type Flashlamp ManufacAlderm turer Wavelength 550– 900 (nm) Pulse duration Pulse rate

Prolite

Table 33.6 Intense Pulsed Light Source

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4.4.1. Treatment Technique Although leg telangiectasia clearance can be achieved with the IPL, considerable experience is required on the part of the operator to achieve consistent results. A 2– 3 mm layer of gel should be applied to the skin surface to avoid making skin contact with the crystal. Contiguous laser pulses are applied to the treatment area. A second pass may be performed if there is no evidence of vessel blanching or edema; the crystal is then oriented 908 from the original direction to avoid foot-printing. New contact epidermal cooling devices permit the use of higher fluences, while minimizing the risk of epidermal injury. A thin layer of gel is used with the cooled crystals. In the author’s experience, the IPL is an excellent modality for the clearance of matted telangiectasia, using a 550 nm filter, double pulses of 7 ms, a 10 ms delay, and fluences of 30 – 40 J/cm2. Treatment parameters vary depending on the manufacturer and model being used. Due to the high absorption by melanin throughout the visible light spectrum, there is an increased risk of epidermal damage and pigmentary alteration in darker phototypes and sun-tanned skin.

5.

NEAR-INFRARED LASERS FOR LEG VEINS

The KTP and long-pulsed dye lasers produce excellent results for the treatment of isolated leg telangiectasia 1.0 mm in diameter in the absence of associated refluxing reticular veins. Most patients seeking treatment of their leg veins have arborizing vascular webs of varying size, color, depth, and flow rates. The KTP and long-pulsed dye lasers cannot treat larger diameter, deeper vessels because of their limited depth of penetration. More recently, near-infrared lasers have been developed to treat deeper venulectasia and reticular veins of the legs. These longer wavelengths provide deeper penetration of laser light into tissue, and can preferentially target hemoglobin based on a small peak of absorption in the 700 –900 nm range. Lasers used for this purpose include alexandrite, diode, and Nd:YAG lasers. The alexandrite lasers with wavelength of 755 nm are used with pulse durations of 3 –20 ms. Diode lasers with wavelengths of 800, 810, and 940 nm are used with pulse durations of 10 –250 ms. Lower extremity vessels are treated with 1064 nm Nd:YAG lasers at pulse durations of 15 – 30 ms for telangiectasia, and 50 ms or greater for venulectasia or reticular veins.

5.1.

Long-Pulsed Alexandrite Lasers

Long-pulsed alexandrite lasers were first developed for hair removal and then explored for the treatment of leg veins, based on their deeper penetrating wavelength and adequate absorption by hemoglobin. With sufficiently high fluences, venulectasia and reticular veins show an excellent response to laser therapy (Table 33.7). McDaniel et al. (50) used a 755 nm alexandrite laser (Cynosure) to treat 28 subjects with red vessels measuring up to 3 mm in diameter. Three consecutive treatments were performed at 4 week intervals, using a 10 mm spot size, a pulse duration of 20 ms, and a fluence of 20 J/cm2. The vessels measuring 0.4 – 1.0 mm in diameter responded best with a clearance rate of 48%. Twenty-three percent of leg telangiectasia measuring ,0.4 mm and 32% of vessels 1.0 –3.0 mm in diameter cleared. Kauvar and Lou (51) used a 755 nm, 3 ms alexandrite laser (Genalase, Candela) with higher fluences and cryogen spray cooling for the treatment of leg telangiectasia and reticular veins up to 2 mm in diameter. Fifty-four patches of leg veins were treated

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Table 33.7

Long-Pulsed Alexandrite Lasers

Laser type Manufacturer Wavelength (nm) Pulse duration (ms) Pulse rate Spot size (mm) Maximum fluence Other features

GentleLase

Apogee 6200/9300

Alexandrite, flashlamp excited Candela 755 3 1.5 Hz 6, 8, 10, 12, 15, 18 100 J/cm2 Dynamic cooling device

Alexandrite, solid state Cynosure 755 5, 10, 20, 40 Up to 5 Hz 10, 12.5, 15 Up to 50 J/cm2 Cryogen cooling

in 20 adult females. Each patch of vessels was treated with 1 –3 laser passes using an 8 mm spot and fluences of 60– 80 J/cm2 in conjunction with cryogen cooling. At 12 week follow-up, there was .75% clearance in 65% of the leg veins and .50% clearance in an additional 22% of the treatment sites. Hyperpigmentation occurred in 35% of the treated sites, but resolved over 3 months. This study demonstrated that the combination of longer, more deeply penetrating wavelengths, and millisecond duration pulses at high fluences, can effectively photocoagulate larger diameter telangiectasia and reticular veins. Treatment discomfort was reduced with cryogen spray cooling, which enabled the safe delivery of fluences up to 80 J/cm2, while protecting the epidermis. The long-pulsed alexandrite lasers may be safely used for skin phototypes I– III in the absence of a sun tan (Fig. 33.6). Vessels from 0.4 to 2.0 mm in diameter respond well. Foot and ankle veins and reticular veins can be cleared with this wavelength. Treatment of vessels .2.0 mm in diameter is more painful. Post-treatment hyperpigmentation can be expected in up to 20% of patients, but usually resolves within 3 months. For effective clearance of leg telangiectasia, higher fluences (.50 J/cm2) are necessary in conjunction with proper skin cooling techniques.

5.1.1.

Treatment Technique

Alexandrite lasers can be used to treat lower extremity vessels in patients with phototypes I –III and no sun tan. In the author’s experience, shorter pulse durations (,10 ms) are most effective. Epidermal side effects are possible in darker skin. The individual vessels are treated with contiguous, nonoverlapping laser pulses to an endpoint of intravascular thrombus formation. Additional laser passes may be performed, but pulse stacking should be avoided. Compression is useful when larger veins are treated.

Figure 33.6 Telangiectasia and venulectasia of the ankle, before (a) and after (b) one laser treatment with a 3 ms, 755 nm alexandrite laser (Candela) at 80 J/cm2 with cryogen cooling.


5.2.

667

Diode Lasers (Table 33.8)

Diode lasers emitting at 800, 810, and 940 nm with millisecond pulse durations have been used to treat leg telangiectasia and reticular veins. At these wavelengths, there is selective absorption by hemoglobin, which has a tertiary peak at 915 nm, and there is relatively poor absorption by melanin. The combination of longer wavelengths and millisecond pulse duration enables the treatment of larger leg vessels. Dierickx et al. (52) evaluated an 800 nm diode for the treatment of lower extremity vessels up to 1.5 mm in diameter. Twenty-five subjects underwent a series of one to three treatments at 4 week intervals, and were evaluated 2 months after the last treatment. Fluences of 15–40 J/cm2 were used with pulse durations of 5–30 ms. Double or triple pulses were stacked with a 2 s delay time. The vessels measuring .0.4 mm in diameter cleared better than the smaller diameter ones. It is likely that the lower response rate observed in the smaller diameter vessels related to either the lack of sufficient fluence or the loss of chromophore caused by vessel compression with the contact cooling handpiece. There was 50% clearing in 32%, 75% clearing in 42%, and total clearing in 22% of patients treated. Garden et al. (53) treated 12 patients with 58 vessels ranging from 0.2 to 0.5 mm in diameter with an 810 nm diode, a 0.75 mm spot size, and a 50 ms pulse duration at 40 W for a fluence delivery of 453 J/cm2. Three to four laser passes were performed until vessel spasm was achieved. Patients were treated at an interval of 2– 4 weeks to a maximum of four treatment sessions. After an average of 2.2 treatments, the mean vessel clearance was 60%. A 940 nm diode laser (Medilas D Skinpulse, Dornier, Germering, Germany) is available in Europe and has been investigated for the treatment of leg telangiectasia. This system delivers pulse durations of 10 –100 ms and fluences of 20– 1000 J/cm2 with variable spot sizes from 0.5 to 1.5 mm in diameter. The 940 nm diode laser was studied in 31 patients with leg telangiectasia, who underwent a series of three treatments at 4 week intervals, with the final evaluation 4 weeks after the last treatment. Twenty-six patients were treated with a 1.0 mm handpiece, 40 – 70 ms pulse durations, and fluences of 300 – 350 J/cm2. Another five patients were treated with a 0.5 mm handpiece, 50 ms pulse duration, and fluence of 815 J/cm2. In the 26 patients treated with the 1.0 mm handpiece, there was .75% vessel clearance in 12 and .50% clearance in 20 patients. All five patients treated with the 0.5 mm handpiece showed .75% clearance of telangiectasia. Epidermal cooling was not provided during laser treatment, but ice packs were applied following treatment to relieve discomfort. Transient hyperpigmentation occurred in three patients, and transient hypopigmentation developed in one patient (54). Passeron et al. (55) studied the 940 nm diode laser in 60 patients. In this study, a total of 60 patients with skin phototypes I–IV underwent up to three treatment sessions at

Table 33.8

Diode Lasers

Laser type Manufacturer Wavelength (nm) Pulse duration (ms) Pulse rate (Hz) Spot size (mm) Maximum fluence Other features

940 nm

Featherlite

SLP 1000

LightSheer

Diode Dornier Medilas 940 10– 100

Diode Laserlite 805 + 25 50–250 5 2, 5, 2 4 60 W

Diode Palamar 810 50 –100 3 4, 8, 12 575 J/cm2 Contact cooling

Diode Star Medical Tech 800 5 – 30 0.5 99 10 – 40 J/cm2 Contact cooling

0.5, 1.0, 1.5 200– 1000 J/cm2

668

Kauvar

4 week intervals. Vessels than 0.4 mm in diameter showed a poor response. Vessels between 0.8 and 1.44 mm in diameter showed the best response. Vessels between 0.8 and 1.44 mm in diameter showed the best response with .75% clearance in 88% of patients. To date, all of the studies of diode lasers for the treatment of lower extremity telangiectasia have been performed in patients with phototypes I– III. The safety profile of these devices has not been established for the treatment of darker skin types. 5.2.1. Treatment Technique Diode lasers may be used to treat vessels up to 2– 3 mm in diameter. Lower power devices will provide insufficient fluence to treat vessels ,0.4 mm in diameter. Laser pulses are applied contiguously along the length of the vessel. Additional passes may be performed until an endpoint of vessel spasm or blanching is reached. For devices that are equipped with contact cooling, care should be taken not to apply the handpiece with excessive pressure. This may result in expulsion of blood from the treatment site and loss of the chromophore target. 5.3.

Long-Pulsed Neodymium:Yttrium – Aluminum –Garnet Lasers

Millisecond domain Nd:YAG lasers were introduced for the treatment of leg veins because of their deep penetration and relative absence of absorption by melanin. The longer absorption coefficient for hemoglobin at this wavelength requires the use of very high energy fluences, on the order of 100 –400 J/cm2, depending on the laser beam diameter. Various skin cooling techniques are used to facilitate heat dissipation, prevent epidermal damage, and provide analgesia. Treatment of larger caliber vessels at this wavelength may be painful (Table 33.9). Multiple laser systems are presently available with skin cooling systems. The Altus Coolglide, Laserscope Lyra, Sciton Profile, and Lumenis Vasculight all have contact cooling devices. Cryogen spray cooling is used with the CoolTouch Varia and the Candela GentleYag. The Nd:YAG laser is currently the most versatile wavelength for treating leg veins. Telangiectasia can be treated with small spot sizes and high fluences; larger spot sizes and larger fluences are used to treat venulectasia and reticular veins (Fig. 33.7). Weiss and Weiss (56) investigated a long pulse Nd:YAG laser (Vasculight, Lumenis) in 30 subjects with 0.5 – 3.0 mm diameter vessels. Single, double, and triple synchronized 10 – 16 ms duration pulses were used at fluences of 80– 130 J/cm2. After a single treatment, 75% of the veins cleared at 3 months. In 50% of the treatment sites, there was bruising associated with immediate vessel rupture. Hyperpigmentation was common, but transient. There was no occurrence of epidermal injury. Immediate closure of two varicosities of 3 mm diameter was confined by duplex ultrasound visualization. A study of 20 patients (57) with reticular veins measuring 1.0– 3.0 mm in diameter, using the Coolglide Nd:YAG laser (Altus) showed clearing of .75% of vessels in twothirds of subjects 3 months following one laser treatment. Contiguous laser pulses were applied using a 50 ms pulse duration and a fluence of 100 J/cm2. A topical anesthetic cream was used in 11 patients, and did not appear to alter the treatment efficacy. In a 12 month follow-up study of 25 patients treated with the Vasculight 1064 nm laser (58), 64% of patients achieved 75% vessel clearance after a maximum of three treatment sessions. A 6 mm spot was used with double pulses of 7 ms at 120 J/cm2 for vessels 0.2 –2.0 mm and a single 14 ms pulse at 130 J/cm2 for veins 2.0 –4.0 mm. No increased risk of side effects was observed in patients with types IV and V skin.

Maximum fluence Other features

Laser type Manufacturer Wavelength (nm) Pulse duration Pulse rate Spot size (mm)

Nd:YAG Cynosure 1064

Acclaim 700

Cryogen cooling

1.5, 3, 6, 8, 10, 12, 15, 18 600 J/cm2

Up to 100 ms Up to 6 Hz 2.5, 4, 5, 7, 10

Nd:YAG Cynosure 1064

Smartepil II

50 ms

Nd:YAG HGM 1064

VeinLase

60 W

Up to 10 Hz 3, 5, 7, 10, 12 2

0.1 –300 ms

Nd:YAG Cutera/Altus 1064

CoolGlide Vantage

Up to Up to 300 J/cm2 300 J/cm2 200 J/cm2 Cold air Scanner cold Contact cooling air cooling cooling

5 Hz 3, 5, 7, 10, 12

Up to 300 ms 4–300 ms

Nd:YAG Candela 1064

GentleYAG

Table 33.9 Long-Pulse Nd:YAG Lasers

Up to 4 Hz 1 –5, 10

10 –100 ms

Nd:YAG Laserscope 1064

Gemini

0.33 Hz 6

2–16 ms

Nd:YAG Lumemis 1064

Vasculight

3, 10

10 –90 ms

Nd:YAG Mydon 1064

Wavelength

1 Hz 1.5, 3, 6, 10

1 –300 ms

Nd:YAG Palomar 1064

StarLux

150 J/cm2 60 –300 J/cm2 500 J/cm2 500 –900 J/cm2 Up to 990 J/cm2 Contact Contact Synchronized Air cooling Contact cooling cooling double or cooling triple pulses

Up to 10 Hz 1–5, 10

20 –100 ms

Nd:YAG Laserscope 1064

Lyra

Nd:YAG Quantel

Athos

Contact cooling

400 J/cm2

Scanner

400 J/cm2

0.1 –200 ms 3.5 ms

Nd:YAG Sciton 1064

Profile

Laser Treatment of Leg Veins 669

670

Kauvar

Figure 33.7 Telangiectasia and venulectasia of the thigh before (a) and 3 months after (b) treatment with an Nd:YAG laser (Laserscope) using a 3 mm spot, 50 ms pulse at 250 J/cm2.

Studies of leg telangiectasia with a long-pulsed Nd:YAG laser equipped with contact cooling (Coolglide, Altus) by Rogachefsky et al. (59) and Kauvar (60) showed good clearing using a 7 mm spot, pulse duration of 10 –50 ms, and fluences of 10 –160 J/cm2. Similar results were achieved by Kauvar et al. using the 1064 nm Lyra laser (Laserscope) equipped with contact cooling. The Varia (CoolTouch) is a long-pulsed Nd:YAG laser equipped with cryogen cooling. In a study (61) using a 6 mm spot, pulse durations of 25– 100 ms, and a fluence of 150 J/cm2 with 30 ms of post-contact cryogen spray cooling, there was .75% clearing in 88% of the treatment sites. Type IV and type V patients were treated with cryogen cooling before and after laser pulse impact to avoid epidermal damage. The GentleYAG (Candela) is a 1064 nm laser equipped with cryogen cooling and produces excellent results for telangiectasia and venulectasia (Fig. 33.8). 5.3.1.

Treatment Technique

Long-pulsed Nd:YAG lasers can be used to treat vessels up to 3 mm in diameter, but using this modality to treat vessels .2 mm is hampered by the pain experienced by patients during treatment. The application of topical anesthetic creams prior to treatment is only somewhat beneficial. At 1064 nm, there is a fair amount of energy absorption by water, with resultant skin heating. Active skin cooling is therefore an absolute necessity with the use of these lasers. Pulse stacking, poor apposition of the skin with contact cooling devices, or failure of cryogen spray devices can lead to vesiculation and skin sloughing. In general, less pain is experienced with the use of the smallest possible spot size. For the treatment of telangiectasia, a 1.0–1.5 mm spot size is preferred. A 3 mm spot can be used for venulectasia, and larger spot sizes may be required for reticular veins. Individual laser pulses are applied contiguously, without overlap, for the treatment of vessels up to 1.5 mm. For larger diameter vessels, pulses may be separated out further along the length of the vessel to reach a threshold of vessel spasm or blanching. A second pass may be preformed after the skin has cooled sufficiently. When larger vessels (.2.0 mm in diameter) are treated, compression therapy is used for 2–3 days to avoid intravascular thrombus formation.

6.

STUDIES COMPARING SCLEROTHERAPY AND LASER TREATMENT OF LEG VEINS

Several studies have been recently undertaken to directly compare treatment outcomes with sclerotherapy and laser treatment. Coles et al. (62) compared the use of a long-pulsed


671

Figure 33.8 Leg telangiectasia before (a) and after (b) treatment with a 1064 nm laser equipped with cryogen cooling (GentleYAG, Candela). Courtesy of Vic Ross, M.D.

Nd:YAG laser with contact cooling to sotradecol sclerotherapy in 20 patients with vessels ranging from 0.25 to 3.0 mm, at two comparable sites. A second treatment was performed, if necessary, at 8 weeks, and follow-up was performed 3 months after the second treatment. Mean clearance scores were 2.5/4.0 for laser-treated sites and 2.3/4.0 for sclerotherapy-treated sites. A survey of the subjects found 35% preferred laser and 45% preferred sclerotherapy. Similar results were found by these same authors comparing sclerotherapy with treatment to a 3 ms alexandrite laser. Levy et al. (63) also found no statistical difference in their comparison of sclerotherapy and Nd:YAG laser treatment.

7. 7.1.

COMPLICATIONS AND THEIR MANAGEMENT Purpura

Purpura is an expected treatment outcome when shorter pulse durations are used with the pulsed dye lasers (0.45 –1.5 ms) or alexandrite laser at 3 ms. It is a transient phenomenon, and resolves within 1 – 2 weeks.

7.2.

Vesiculation and Crusting

Vesiculation followed by ulceration or crusting may occur with the use of overly aggressive laser parameters, improper skin cooling techniques, treatment of darker phototypes, or sun-tanned skin. The immediate development of tissue whitening after laser pulse

672

Kauvar

impact is an indication of epidermal damage. Ice packs should be applied immediately, and the laser treatment parameters and patient’s skin pigmentation should be reassessed before continuing with therapy. A topical antibiotic ointment is used until crusting is completely resolved.

7.3.

Hyperpigmentation

Hyperpigmentation is most common following laser treatment of leg veins with the pulse dye lasers, less so with the alexandrite systems, and least with the Nd:YAG lasers. Hyperpigmentation may result from melanin or hemosiderin deposition. Hydroquinones and sunscreen use speed the clearing of melanin-related hyperpigmentation, but do not improve hemosiderin deposition. Generally, laser-induced hyperpigmentation will fade over a period of 1 –3 months. Laser-induced hyperpigmentation is usually responsive to Q-switched alexandrite or Q-switched ruby laser treatments.

7.4.

Hypopigmentation

Hypopigmentation is often a direct consequence of epidermal damage, and usually follows the development of laser-induced vesiculation or crusting. In most cases, the hypopigmentation is transient and resolves in 2– 3 months.

7.5.

Scarring

Atrophic or hypertrophic scar is a rare occurrence, but is possible following laser-induced epidermal necrosis. Laser-induced scarring can often be improved with pulsed dye laser treatment.

7.6.

Thrombus Formation

When near-infrared lasers are used to treat vessels .2.0 mm in diameter, thrombus formation may occur, as it does with sclerotherapy treatment. To avoid thrombus formation, compression garments should be used following laser treatment of larger veins, as with sclerotherapy. The thrombi are evacuated with an 18g needle, and compression is applied for 2 –3 days.

8.

CONCLUSIONS

Lasers now play a greater role in the treatment of lower extremity vessels, due to the availability of innovative systems and technological advances. Telangiectasia, venulectasia, and reticular veins respond well to laser treatment. Although sclerotherapy remains the gold standard of treatment, recent studies demonstrate that comparable results can be achieved with lasers. Lasers should be considered a first line treatment option for the following indications: (1) diffuse, fine caliber, nonarborizing telangiectasia, (2) foot and ankle vessels, (3) sclerotherapy-resistant lesions, (4) post-sclerotherapy matting, and (5) patients with needle phobias. As many patients have webs of heterogeneous vessels, adjunctive use of sclerotherapy and laser treatment often provides the best clinical outcomes.


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34 Laser Hair Removal Christine C. Dierickx Beukenlaan 52, 2850 Boom, Belgium

1. 2. 3. 4. 5.

6.

7. 8. 9.

10. 11.

Introduction Anatomy and Growth Cycle of the Hair Follicle Reasons for Removal of Excessive Hair Traditional Methods of Hair Removal Mechanisms for Hair Removal with Light 5.1. Photothermal Destruction 5.2. Photomechanical Destruction 5.3. Photochemical Destruction of Hair Follicles Laser and Light Source Technology 6.1. Endogenous Chromophore 6.1.1. The 694 nm Ruby Lasers 6.1.2. The 755 nm Alexandrite Lasers 6.1.3. The 800 nm Diode Lasers 6.1.4. Q-Switched 1064 nm Nd:YAG Laser 6.1.5. Long Pulsed 1064 nm Nd:YAG Lasers 6.1.6. Pulsed, Noncoherent Broadband Light Sources 6.1.7. Electro-Optical Synergy (ELOSTM) Technology 6.1.8. Microwave Delivery System 6.2. Exogenous Chromophore 6.2.1. Carbon Suspension – Q-Switched Nd:YAG Laser 6.2.2. Photodynamic Therapy Terminology Clinical Results and Histology Treatment Guidelines 9.1. Preoperative Considerations 9.2. Technique 9.3. Postoperative Changes 9.4. Treatment Interval Side Effects Safety

678 678 680 680 681 681 682 682 683 683 683 687 687 687 687 688 688 689 689 689 689 690 690 691 691 692 693 693 693 694 677

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12. Ethnic Considerations 12.1. Hair Color 12.2. Skin Color 13. Conclusion References

1.

695 695 695 695 696

INTRODUCTION

Unwanted hair is a major cosmetic problem. Many temporary hair removal methods exist, including shaving, bleaching, tweezing, cold and hot wax epilation, and chemical depilatories (1–3). Only electrolysis has offered the potential for permanent hair removal, but the technique is tedious, highly operator dependent, and impractical for the treatment of large numbers of hair (4). Recently, a number of lasers and other light sources have been developed specifically to target hair follicles. These devices offer the potential for rapid treatment of large areas and long-lasting hair removal. Physicians and patients alike have embraced this technology, although published studies assessing the permanency of hair removal have emerged only recently. With the proliferation of devices targeting hair and unsubstantiated claims by manufacturers, significant confusion exists in this field. This chapter will discuss the scientific background of laser hair removal, examine the specifics of different laser systems, and describe the technique of laser hair removal. 2.

ANATOMY AND GROWTH CYCLE OF THE HAIR FOLLICLE

The hair follicle consists of three regions in vertical section: the infundibulum, isthmus, and inferior segment (5). The infundibulum is the uppermost portion of the follicle, extending from the skin surface to the sebaceous duct entrance. The isthmus is a short section that extends from the entrance of the sebaceous duct to the insertion of the arrector pili muscle. The inferior segment of the follicle lies below the arrector pili muscle insertion and includes the hair bulb and dermal papilla. The hair bulb represents an expansion of the lowermost portion of the follicle during its growing, or anagen phase. It is made up of germinative matrix cells along with interspersed melanocytes. The hair bulb surrounds a core of richly vascularized connective tissue known as the dermal papilla, which is continuous with the fibrous sheet that envelops the entire follicle. Hair follicles show a cyclical pattern of growth, progressing from the growing (anagen) phase to the resting (telogen) phase via the intermediary (catagen) phase (6,7). During anagen, matrix cells proliferate and move upward, giving rise to the hair shaft and inner root sheath. Anagen follicles of terminal hair extend deeply into the subcutaneous fat, lying 2 –7 mm below the skin surface (8). During catagen, cell division and melanin production in the bulb cease and the entire lower portion of the hair follicle undergoes apoptosis [9]. Only a thin cord of epithelial cells remains, which shrinks and retracts upward to become the secondary germ. The ensuing telogen phase represents a stage of follicular quiescence. When a new anagen phase begins, a burst of epithelial cell division occurs near the insertion of the arrector pili muscle and hair growth resumes as the secondary hair germ grows downward to form a new bulb. It was initially thought that follicular stem cells resided within or near the matrix of the hair bulb (7,10). However, in mouse follicles, a population of slow cycling stem cells

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has been found in a bulge coming off the outer root sheath (11). The bulge is located at the site of attachment of the arrector pili muscle, 1 mm below the skin surface. This represents the lower end of the “permanent” portion of the hair follicle. Recently, follicular stem cells expressing cytokeratin 15 and b1 integrin have been identified (12). It is now believed that, during late telogen or early anagen, the bulge stem cells are activated by dermal papilla cells and proliferate briefly to form the epithelial downgrowth before returning to their normally dormant state. The duration of anagen and telogen phases, as well as the ratio of anagen to telogen hairs, is dependent on body location (Table 34.1). At any given time, 84% of scalp hairs are in anagen, 2% in catagen, and 14% in telogen (7,13 – 15). In contrast, .50% of leg or arm hair is in telogen at any given time (15,16). Since duration of anagen is the primary determinant of hair length, body sites with long hair have a prolonged anagen phase while sites with shorter hair have a shorter anagen phase and a somewhat longer telogen phase. The anagen phase of scalp hair lasts up to 6 years while the telogen phase lasts about 3 months (14). In contrast, hairs on other body sites such as the extremities or trunk have anagen phases lasting from 4 to 7 months and telogen phases lasting up to 9 months (16). This implies that long-lasting hair loss can be achieved by any method of hair removal that can induce telogen. In order to assess permanency of hair removal, it is necessary to follow patients for at least the duration of one complete hair cycle. Because injury can cause a prolonged delay of hair regrowth, it has been suggested that the follow-up period should include a period of recovery from injury (6 months) in addition to that of one complete hair cycle (3). Hair color is dependent upon the type and amount of melanin within the hair shaft (17 –19). Melanin is produced by melanocytes within the bulb which transfer melanin granules to matrix cells. Melanin production occurs only during anagen, as melanocytes within the bulb degenerate during catagen. Follicular melanocytes produce two distinct types of melanin: eumelanin and pheomelanin. Dark hair contains abundant, heavily melanized eumelanin granules, while red hair contains primarily pheomelanin granules. In gray hair, melanocytes show degenerative changes such as vacuolization and poorly melanized melanosomes, while in white hair melanocytes are greatly reduced in number or absent. The diameter and length of hair is variable, ranging from fine, nonpigmented vellus hairs to coarse terminal hairs. Hair shaft diameter is determined by the size of the dermal

Table 34.1

Duration and Percentage of Different Growth Cycles for Various Body Parts

Body site

% Telogen

% Anagen

Duration of telogen (months)

Duration of anagen (months)

Scalp Eyebrows Upper Lip Beard Axillae Chest Back Arms Legs Pubic area

15 90 35 30 70 70 70 80 80 70

85 10 65 70 30 30 30 20 20 30

3 –4 3 –4 1.5 2 –3 3 2.5 N/A 2 –4 3 –6 2 –3

24 – 72 1–2 2–5 12 4 N/A N/A 1–3 4–6 1–2

Note: N/A, not available.

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papilla and hair bulb (20). Vellus hair is arbitrarily defined as having a cross-sectional diameter of 30 mm (21), while the diameter of terminal hair varies from 40 to 120 mm (22). The type of hair produced by any particular follicle can change. The most striking example is the replacement of vellus by terminal hairs at puberty (23). On the other hand, in male pattern baldness, the terminal hairs are replaced by fine, short hair, resembling vellus hairs. These secondary vellus hairs, or miniaturized or hypoplastic terminal hairs, have a similar diameter as a vellus hair but are still pigmented (24). Prior to the final transition to vellus status, there is a reduction in size of both the papilla and the matrix. Therefore, early baldness appears to be largely due to a progressive diminution in the size of terminal hairs (24).

3.

REASONS FOR REMOVAL OF EXCESSIVE HAIR

Unwanted hair falls into four main categories. Each one of them can be a reason for seeking a method for hair removal. 1.

2.

3.

4.

4.

Hypertrichosis. This is defined as an increase in hair growth that is not androgen dependent (25). The cause of hypertrichosis is most commonly genetic or ethnic. It can also occur secondary to endocrine disturbances, malnutrition, porphyria, medications, and rarely tumors. Hirsutism. This is the term that is reserved for excess hair in women at androgen dependent sites, primarily facial hair. It can be idiopathic or occur secondarily to endocrine disorders, medications, or virilizing tumors (25,26). Aesthetic reasons. Most of the individuals who seek consultation for unwanted hair do so primarily because of cosmetic reasons: facial or body hair in excess of the cultural norm set by society, can be very distressing to some people. Certain areas, including the axilla, bikini line, legs, and face in women, as well as chest or back in men, have to be hairless to be cosmetically accepted by today’s society. Medical reasons. Hair-bearing flaps, used for reconstruction of any kind, may contain unwanted hair that interferes with proper function. Epilation of hair-bearing flaps before surgery is therefore indicated (27 –29). For example, myocutaneous flaps used in urethral reconstruction may cause urinary obstruction, calcification, or infection (30,31).

TRADITIONAL METHODS OF HAIR REMOVAL

Many different methods have been used to treat unwanted hair, including shaving, plucking, waxing, bleaching, and the use of chemical depilatories (32,33). Although shaving is effective, simple, and inexpensive, it is a daily chore that is unacceptable to many women with facial hair. Hair removal by plucking and waxing can last up to several months but treatment is painful and may be complicated by hyperpigmentation, ingrown hairs, folliculitis, or scarring. Chemical depilatories most commonly contain thioglycolates mixed with either NaOH or CaOH and dissolve hair structure by hydrolyzing disulfide bonds. Although they can provide results that last up to 2 weeks by dissolving part of the hair shaft below the skin surface, they are messy and commonly cause irritant dermatitis (3). Antiandrogenic medications such as spironolactone and cyproterone acetate may provide modest improvement to hirsute women. However, results are temporary as

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treatment is suppressive rather than curative (33) and undesirable side effects are not uncommon. Until recently, electrolysis was the only method capable of producing permanent hair removal. There are several types of electrolysis, although all utilize a needle to carry current deep into the follicle. In galvanic electrolysis, direct electric current acts on tissue saline to produce sodium hydroxide, which chemically destroys the follicle. In contrast, thermolysis passes a high-frequency alternating current down the needle to thermally destroy the follicle (34). Although it is generally accepted that electrolysis can provide permanent hair removal, there is little scientific data on which to base efficacy. Potential side effects include pain, hyperpigmentation, hypopigmentation, and scarring. Both efficacy and side effects are highly operator dependent. The technique is most useful for epilation of a few stubborn hairs but is impractical for the treatment of large areas or amounts of excessive hair.

5.

MECHANISMS FOR HAIR REMOVAL WITH LIGHT

There are three means by which light can destroy hair follicles: thermal (due to local heating), mechanical (due to shockwaves or violent cavitation), and photochemical (due to generation of toxic mediators like singlet oxygen or free radicals). Removal of hair has been attempted by all three means (Table 34.2).

5.1.

Photothermal Destruction

Recently, lasers and noncoherent light sources have been introduced to induce selective damage to hair follicles. The mechanisms by which these systems induce selective damage to hair follicles are based on the principles of selective photothermolysis (35). This principle predicts that selective thermal damage of a pigmented target structure will result when sufficient fluence at a wavelength, preferentially absorbed by the target, is delivered during a time equal to or less than the thermal relaxation time of the target (35). In the visible to near-infrared region, melanin is the natural chromophore for targeting hair follicles. Lasers or light sources that operate in the red or near-infrared wavelength region (694 nm ruby laser, 755 nm alexandrite laser, 800 nm diode laser, 1064 nm Nd:YAG laser) and noncoherent light sources with cut-off filters, all lie in an optical Table 34.2 Different Means for Light-Based Hair Removal Photothermal destruction Normal mode ruby lasers (694 nm) Normal mode alexandrite lasers (755 nm) Pulsed diode laser (800 nm) Long pulsed Nd:YAG lasers (1064 nm) Intense pulsed light source (590 – 1200 nm) Photomechanical destruction Carbon suspension– Q-switched Nd:YAG laser Q-switched Nd:YAG lasers Photochemical destruction Photodynamic therapy

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window (36) of the spectrum, where selective absorption by melanin is combined with deep penetration into the dermis. Deep, selective heating of the hair shaft, hair follicle epithelium, and the heavily pigmented matrix is therefore possible in the 600– 1100 nm region. However, melanin in the epidermis presents a competing site for absorption. Selective cooling of the epidermis has been shown to minimize epidermal injury. Cooling can be achieved by various means, including a cooled gel layer, a cooled glasschamber, or cooled sapphire window and a pulsed cryogen spray. Laser pulse width also appears to play an important role, as suggested by thermal transfer theory (37). Thermal conduction during the laser pulse, heats a region around each microscopic site of optical energy absorption. To obtain spatial confinement of thermal damage, the pulse duration should be shorter than or equal to the thermal relaxation time of the hair follicle. Thermal relaxation of human terminal hair follicles has never been measured, but is estimated to be 10 –50 ms (35 – 38), depending on size. Devices for hair removal therefore have pulse durations in the millisecond domain region. The normal mode 694 nm ruby (39 –57), normal mode 755 nm alexandrite (58 – 68), 800 nm pulsed diode lasers (69 –75), long pulsed Nd:YAG lasers (76 – 83), and filtered flashlamp technology (84 – 88) all employ this mechanism. However, sometimes the actual target is not pigmented and is at some distance from a pigmented structure. For example, the follicular stem cells, which line the outer root sheath, are not pigmented and are at some distance from the pigmented hair shaft. These cells appear to be an important target for permanent hair destruction. The concept of thermal damage time (TDT) has therefore been proposed in the case of the hair follicle (89,90). Pulses longer than the thermal relaxation time of the hair shaft allow propagation of the thermal damage front through the entire volume and better damage of the follicular stem cells. Super long pulse heating (.100 ms) appears to allow for long-term hair removal (91,92). 5.2.

Photomechanical Destruction

The spatial scale of thermal confinement and resulting thermal or thermomechanical damage is strongly related to laser pulse width. Q-switched (nanosecond domain) laser pulses effectively damage individual pigmented cells within hair follicles by confinement of heat at the spatial level of melanosomes (93), leading, in animals, to leukotrichia but not to hair loss after Q-switched ruby laser pulses (94). Consistent with this behavior, permanent hair loss has not been reported in humans after Q-switched laser treatments, despite a decade of using Q-switched ruby and Nd:YAG lasers widely for tattoo removal. Photomechanical destruction of hair has been attempted by the so-called Softlight technique (Thermolase Corporation). The method uses a proprietary suspension of carbon particles applied to the skin, with relatively low energies (2 –3 J/cm2) of Q-switched Nd:YAG laser light (1064 nm, 10 Hz, 10 ns pulse duration, 7 mm spot size) (95,96). Higher powered, 1064 nm Q-switched Nd:YAG lasers are also being studied for hair removal (97,98). However, when these very short pulses are used to target hair follicles, there is extremely rapid heating of the chromophore (melanin). This generates photoacoustic shock waves that cause focal photomechanical disruption of the melanocytes in the bulb but no complete follicular disruption. It is therefore unlikely that the Q-switched Nd:YAG lasers will produce long-term hair removal. 5.3.

Photochemical Destruction of Hair Follicles

Photodynamic therapy (PDT) is the use of light and a photosensitizer to produce therapeutic effects. Hair removal with topical aminolevulinic acid (ALA) has been reported

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in a pilot study (99). A mean hairloss of 40% was reported in 12 volunteers after a single exposure to 630 nm light, 3 h after application of 20% ALA to the skin. ALA is a precursor in the porphyrin synthesis and is rapidly and selectively converted to protoporphyrin IX (PPIX) by cells derived from the epidermis and follicular epithelium (100,101). Upon absorption of a photon, PPIX efficiently crosses into an excited triplet state, which in turn generates singlet oxygen by collision with ground-state oxygen. Singlet oxygen is a potent oxidizer that damages cell membranes and protein. This is a so-called photodynamic reaction (102 –104). A host of other porphyrins, chlorins, phthalocyanines, purpurins, and phenothiazine dyes can act as photodynamic agents and are under development as drugs for PDT. It is likely that ALA or one of these other drugs will prove useful for hair removal.

6. 6.1.

LASER AND LIGHT SOURCE TECHNOLOGY Endogenous Chromophore

6.1.1. The 694 nm Ruby Lasers Three normal-mode, 694 nm ruby lasers are available for hair removal (Table 34.3). These include the E2000, EpiPulse Ruby, and RubyStar. The E2000 has been approved by the food and drug administration (FDA) for permanent hair reduction. Because of high melanin absorption at 694 nm, the ruby lasers are best indicated in light skinned (Fitzpatricks’s skin type I– III) individuals with dark hairs (8,39 – 57). The E2000 (Palomar, Burlington, MA) uses a sapphire cooled handpiece (EpiwandTM) to protect the epidermis (105,106). The sapphire lens is actively cooled to 08C or 2108C and put in direct contact with the skin. Compared with air as an external medium, the sapphire provides heat conduction from the epidermis before, during, and after the laser pulse. It permits beam coupling into the skin and internal reflection is reduced by index matching. In addition to surface cooling, the EpiwandTM sapphire handpiece has other distinct advantages. The sapphire lens provides a convergent beam to maximize delivery of light into the dermis. Its surface allows for application of pressure on the skin surface, which deforms the dermis and decreases the distance from the epidermis to the deeper follicular structures. In addition, the pressure blanches the underlying blood vessels, minimizing absorption of laser energy by hemoglobin. Light is delivered through a fiber and two different spot sizes are available (10 and 20 mm). A retroreflector is build into the handpiece, which allows for photon recycling and therefore sufficient energy delivery (107,108). Depending on skin type or hair thickness, a single pulse (3 ms) or twin pulse (100 ms, i.e., two 3 ms pulses, delivered with a delay of 100 ms) can be chosen. The EpiPulseTM long pulsed Ruby (Sharplan, Santa Clara, CA) employs a triple pulse technology with a 10 ms interval between pulses. It keeps the follicle temperature at a sufficient level to cause destruction while the epidermis temperature remains below damage threshold. This synchronized pulsing technology should make treatment of darker skin types possible. Cooling of the epidermis is achieved by applying a thick layer of cooled transparent gel on the skin. A thin, patented, laser aligning sheet can be placed on top of the cooling gel, which enables the proper positioning of the laser beam and helps to insure uniform laser application to all intended areas (57). The RubyStar (Asclepion-Meditec, Jena, Germany) is a dual-mode ruby laser and uses a contact skin cooling method. It can operate in the conventional Q-switched mode for the treatment of tattoos and pigmented lesions, as well as in the normal mode for hair removal.

694

755

800

Long pulse alexandrite

Diode laser

Wavelength (nm)

Long pulse ruby

Light source

5 –60

10 –100 10 –25

3 –50 ms

3 ms 2 ms

Twin Lase (Depilase)

Gentlelase (Candela) Epitouch ALEX (Sharplan) LightSheer (Lumenis) Apogee 100 (Cynosure) 50 – 500 ms

10 –60 (2900 W) Up to 60

5 –70

1 –50 ms

5 –100 ms

12 –100

3 –40 ms

EpiCare (Light Age) Arion (WaveLight)

Up to 3 Hz

10

12 12

5, 10

Up to 2 Hz

Up to 2 Hz

1 – 5 Hz

8, 10, 12, 15, 18 1 Hz

2 –12

1.5, 3, 5, 10

7, 9, 12, 15

10, 12.5, 15

1 Hz

8, 10, 12, 14

25 –40

2 ms 5, 10, 20, 40 ms 5 –50

1.2 Hz

3–6

10 –40

1 Hz

Repetition rate

1.2 ms

10, 20

Spot size (mm)

Epitouch Ruby (Sharplan) Ruby Star (Asclepion) Apogee (Cynosure)

10 –40

Fluence (J/cm2)

3, 100 ms

Pulse duration

E2000 (Palomar)

System name

Table 34.3 Lasers and Light Sources for Hair Removal

Cooling handpiece

Skin cooling Large area scanner (9 8 cm) Combined with 1064 nm YAG laser and cooling Dynamic cooling device Scanner option

Cooling handpiece 0 – 108C Fiber delivery Photon recycling Triple pulse technology Dual mode: may also be Q-switched SmartCoolTM handpiece Scanner option

Other features

684 Dierickx

1064

1064

Q-switched Nd:YAG

Long-pulsed Nd:YAG

Up to 200 ms

0.1– 300 Up to 60

Up to 500 5 –500 15 –400

10 – 100 ms 3 ms 5 –200 ms 3, 5 ms 5 –200 ms 0.3– 200 ms 3 –100 ms 20 – 140 ms

GentleYAG (Candela) Image (Sciton) Athos (Quantel) Dualis (Fotona)

Varia (ICN Photonics) YAG LASE Plus (Depilase) Mydon (Wavelight)

10–70 10 –400 Up to 80 Up to 400

2 –3 12

1 –300 ms

10 ns 5 –7 ns

MedioStar (Asclepion) Softlight (Telstar) Medlite IV (ConBio) CoolGlide (Altus) Lyra (Laserscope) Up to 60

Up to 50 (up to 60 W) Up to 100

10 – 100 ms

Up to 100 ms

10 –40

50 – 250 ms

200 – 1000 ms

Up to 60 (up to 600 W) Up to 60 W

5 –100 ms

SLP1000TM (Palomar)

Apex-800 (Iridex) LaserLite (Diomed) F1 Diode laser (Opus) EpiStar (Nidek)

1.5, 3, 5, 10

2 –12

3 –10

Up to 3 Hz

1

Up to 4 Hz

1.5, 3, 5, 10 12 3, 10 4 2–8

Up to 2 Hz

10 Hz 1, 2.5 and 10

4 Hz

Up to 3 Hz

4 Hz

Up to 5 Hz

Up to 4 Hz

3, 5, 7, 10

7 3–8

12 12

10

4, 7

5, 7, 10

2, 4

7, 9, 11

(continued )

Optional scanner (35/60 mm)

Contact cooling Photon recycling Dynamic cooling Scanner (70 70 mm)

Contact precooling

Integrated active cooling handpiece SheerCoolTM triple contact cooling, photon recycling Integrated contact cooling Carbon

Cooling handpiece Scanner Air cooling

Cooling handpiece

Laser Hair Removal 685

ProLite (Alderm) Spatouch (Radiancy) Aurora DS (Syneron)

550– 900 400– 1200

600– 950 500– 1200

Quantum HR (Lumenis) Ellipse (DDD) Estelux (Palomar)

SmartEpi II (Cynosure) VascuLight (Lumenis) EpiLight (Lumenis)

System name

695– 1200 nm

590– 1200

Wavelength (nm)

Optical energy (680 – 980 nm) combined with electrical energy radio frequency) Microwave technology 2.2 1021 cm MDS (MW Medical)

ELOS technology

Intense pulsed broadband light source

Light source

Table 34.3 Continued

25 – 30 ms

35 ms

0.2– 50 ms 10– 100 ms

15 – 100 ms

20 –28

10 –30 optical energy & 5 – 20 RF energy

10 –50 Up to 7

Up to 21 4 –40

25 –45

Up to 45

Up to 65

1 –14 ms 15 – 100 ms

16 –200

Fluence (J/cm2)

Up to 100 ms

Pulse duration Up to 6 Hz

Repetition rate

0.25 Hz Up to 1

0.5 Hz

64

12 25

0.7 Hz

10 20, 20 25 0.5 Hz 22 55 0.25 Hz

10 48 16 46

34 8 mm

10 45, 8 35 0.5 Hz

6

2.5,5,7,10

Spot size (mm)

Cooling spray

Cooling (5 – 208C on skin surface) combined with skin impedance control

Multiple pulsing Fast coverage rate CoolrollerTM cooling

Contact cooling Multiple pulsing

Contact cooling

Other features

686 Dierickx

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An integrated cooling device consisting of a cooled contact handpiece precools the skin prior to laser pulse delivery. 6.1.2.

The 755 nm Alexandrite Lasers

Several long pulsed alexandrite lasers (755 nm) have been recently introduced for hair removal (58 – 68). At this longer wavelength, the ratio of energy deposited in the dermis to the epidermis is greater because of greater depth of penetration. The risk for epidermal damage in darker skintypes is therefore reduced. Three different alexandrite lasers are available (Table 34.3). These include Apogee (Cynosure, Chelmsford, MA), Epitouch ALEX (Sharplan, Santa Clara, CA), and GentleLase (Candela, Wayland, MA). The Apogee provides pulse durations between 5 and 40 ms and fluences up to 50 J/cm2. A cooling handpiece (SmartCoolTM) allows a continuous flow of chilled air to the treatment area. Epitouch ALEX has a rapid repetition rate (5 Hz) and a scanner that can cover a 40 40 mm2 area within 6 s. GentleLase employs a dynamic cooling device (DCD) to protect the epidermis. This DCD cooling method uses short (5 –100 ms) cryogen spurts, delivered on the skin surface through an electronically controlled solenoid valve; the quantity of cryogen delivered is proportional to the spurt duration. The liquid cryogen droplets strike the hot skin surface and undergo evaporation. Skin temperature is reduced as a result of supplying heat for vaporization. This cooling method allows for fast and selective cooling of the epidermis (109). 6.1.3. The 800 nm Diode Lasers An extremely high-powered (2900 W) diode laser (LightSheer XC, Coherent, Santa Clara, CA) has been approved by the US FDA for permanent hair reduction. Long-term results suggest that the pulsed, 800 nm diode laser is very effective for removal of dark, terminal hair: permanent hair reduction can be obtained in 89% of patients (69 –71). This laser operates at 800 nm, has pulse widths between 5 and 100 ms, a 12 12 mm spot, a 2 Hz repetition rate, fluences between 10 and 60 J/cm2, and a patented contact cooling device (ChillTipTM). Because of the longer wavelength, the active cooling, and the longer pulse widths, darker skin types can be treated more safely (110). Several other 800 nm diode lasers (Apex-800, Iridex, Mountain View, CA; Apogee 100, Cynosure, Chelmsford, MA; F1 diode laser, Opus Medical Inc, Montreal, Canada; Mediostar, Asclepion-Meditec, Jena, Germany; LaserLite, Diomed, Andover, MA; SLP1000, Palomar, Burlington, MA; and EpiStar, Nidek, Gamagori, Japan) have recently been approved by the FDA (Table 34.3). 6.1.4.

Q-Switched 1064 nm Nd:YAG Laser

A high powered, 1064 nm Q-switched Nd:YAG laser (MedLite IV, Conbio, Santa Clara, CA) is now available for hair removal (97,98). It has a very short pulse duration in the nanosecond range, a 4 mm spot, a repetition rate of 10 Hz, and fluences up to 8 – 10 J/cm2. The high repetition rate (10 Hz) delivers the laser pulses very rapidly and therefore larger areas can easily be covered and operative time is significantly shortened. The longer wavelength (1064 nm) makes it useful for darker skin types. Although capable for inducing a growth delay, they appear to be ineffective for long-term hair removal. 6.1.5. Long Pulsed 1064 nm Nd:YAG Lasers Several long pulsed Nd: YAG lasers (1064 nm wavelength), which deliver pulses in the millisecond domain, have been approved by the FDA for hair removal laser treatment

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on all skin types (Table 34.3). These lasers include the Lyra (Laserscope, San Jose, CA), the CoolGlide (Altus Medical, Burlingame, CA), the YagLase (Depilase, Irvine, CA), the Image (Sciton, Palo Alto, CA), the VascuLight (Lumenis, Santa Clara, CA), SmartEpiII (Cynosure, Chelmsford, MA), Athos (Quantel, Les Ulis Cedex, France), Dualis (Fotona, Ljubljana, Slowenie), Varia (ICN Photonics, Llanelli Wales, UK), Mydon (Wavelight, Erlangen, Germany), and the GentleYAG (Candela, Wayland, MA). The long pulsed Nd:YAG have deeply penetrating 1064 nm wavelengths. The reduced melanin absorption at this wavelength necessitates the need for high fluences in order to adequately damage hair. However, the poor melanin absorption at this wavelength coupled with an epidermal cooling device makes the long pulsed Nd:YAG a potential safe laser treatment for patients who are phototypes III– VI (76 – 83). The Nd:YAG laser is also often used for treatment of pseudofollicultis barbae, a skin condition commonly seen in darker skin types (111 –113). 6.1.6.

Pulsed, Noncoherent Broadband Light Sources

Intense pulsed, nonlaser light sources, emitting noncoherent, multiwavelength light has been approved for the claim of permanent hair reduction (84 – 88,114 –116) (EpiLight, Lumenis, Santa Clara, CA; Ellipse, Danish Dermatologic Development, Hørsholm, Denmark). By placing appropriate filters on the light source, wavelengths ranging from 590 to 1200 nm can be generated. Cut-off filters are used to eliminate short wavelengths so that only the longer, more deeply penetrating wavelengths are emitted. Pulse durations vary in the millisecond domain. A single or multiple pulse mode (2 –5) with various pulse delay intervals can be chosen. The wide choice of wavelengths, pulse durations, and delay intervals makes this device potentially effective for a wide range of skin types. The devices come with software that guides the operator in determining treatment parameters depending on the patient’s skin type, hair color, and coarseness. One of the newest emerging hair removal technologies are the lower-price, small, pulsed light hair removal systems, like IPL Quantum HR (Lumenis, Santa Clara, CA), the PlasmaLite (Medical Bio Care, Newport beach, CA), the SpaTouch photoepilation system (Radiancy, Orangeburg, NY), and the Estelux (Palomar, Burlington, MA). These systems have been optimized for hair removal with wavelengths preferentially absorbed by melanin, long pulse widths, and large spotsizes. The Spatouch only weighs 12 pounds and the operating parameters include a 400 – 1200 nm wavelength range, a single pulse duration of 35 ms, a 22 55 mm treatment spot, and up to 7 J/cm2 output energy. The complexity has been far reduced since the operation requires only selection of one parameter, the fluence. The Estelux offers multiple pulsewidth/fluence settings for versatility, depending on the skintype being treated and on whether the goal is longer term hair removal or faster treatments. The system also features a high pulse rate and large spotsize with an unrivaled coverage rate of 7.4 cm2 for fast treatments, photon recycling, and large beam for increased efficacy and a contact sapphire handpiece for extraction of heat for additional comfort and protection. Preliminary clinical evaluation has demonstrated that a significant growth delay effect, similar to the lasers, was achieved (117). Further clinical work, including longterm follow-up, are currently beeing conducted. 6.1.7. Electro-Optical Synergy (ELOSTM) Technology ELOSTM technology utilizes the synergy between electrical [conducted radiofrequency (RF)] and optical (laser or light) energies. The electrical energy causes heat, which is

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focused on the hair follicle and the bulge area, while the optical energy heats mainly the hairshaft. Combined, a uniform temperature distribution across the hairshaft and the follicle should be obtained to achieve effective hair removal. Based on this ELOSTM technology, Syneron (Yokneam Illit, Israel) has developed two families of medical devices: the Aurora systems combine RF energy with light and the Polaris systems combine RF energy with diode laser. Both devices are equipped with cooling. The Aurora line received FDA clearance for hair removal. The use of the RF energy should also allow for treatment of all skin types, since this form of energy is not absorbed by epidermal melanin. 6.1.8.

Microwave Delivery System

A new microwave based hair removal system has been developed for hair removal (Table 34.3). The MDS device (Microwave Delivery System, MW Medical, Scottsdale, AZ) delivers pulses of microwave energy in conjunction with a spray of coolant to the skin. FDA clearance for hair removal for all skin types and for any body part, except the face, was recently obtained. Studies are currently being conducted to collect data on facial hair removal. 6.2.

Exogenous Chromophore

For persons with very dark skin and blonde or gray hair, an effective permanent laser hair removal treatment is still lacking. Potentially, the exogenous chromophore approach could solve this problem. Rather than targeting endogenous melanin, an exogenous chromophore (like dyes, photosensitizers, or carbon particles) can be introduced into the hair follicle and then irradiated with light of a wavelength that matches its absorption peak. The main problem is reliable penetration of the chromophore into all depths of the hair follicle. Therefore, the technique, in its present form, is apparently inadequate for inducing permanent hair loss. However, in vitro testing has recently shown that a new method could increase the quantity and the penetration depth of dyes in follicular ducts (118). 6.2.1. Carbon Suspension –Q-Switched Nd:YAG Laser In this method, an exogenous chromophore (carbon suspension) with a peak absorption in the near-infrared portion of the spectrum, is used in combination with a Q-switched Nd:YAG laser (95,96). The so-called Softlight system (Telstar, Wood River, IL) uses a proprietary suspension of 10 mm diameter carbon particles applied to wax-epilated skin, which is then wiped off, and the skin is irradiated with relatively low energies (2 – 3 J/cm2) of Q-switched Nd:YAG laser light (1064 nm, 10 Hz, 10 ns pulse duration, 7 mm spot size). However, the short pulse duration of the laser used in the Softlight technique (carbon particles þ Q-switched Nd:YAG laser) limits the extent of follicular damage. This technique successfully induces a delay in hair growth, but fails to produce long-lasting hair removal. Alternatively, a dye other than carbon could be used, which stains the viable follicular epithelium and absorbs red or near-infrared wavelengths (118). 6.2.2.


PDT, which has been used primarily for treatment of malignant skin tumors, involves the use of a photosensitizer and light to produce therapeutic effects. The mechanism of action is presumed to involve the generation of toxic reactive oxygen species, subsequent to the photochemical activation of the photosensitizer by light. The recent introduction of 5-ALA as a topical photosensitizer has opened up a variety of potential therapeutic options (99–104).

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In a small pilot study of 12 subjects, 5-ALA was applied topically to hair-bearing skin after wax epilation (99). Test sites were irradiated 3 h later with 630 nm light from an argon-pumped tunable dye laser. At 6 months following a single treatment, a dosedependent decrease in hair regrowth was observed, with the greatest loss (40%) occuring in areas that received the highest doses of light (200 J/cm2). Temporary hyperpigmentation was the only adverse effect noted. PDT may be a useful approach for hair removal. Since photosensitizers tend to localize in the follicular epithelium, photochemical destruction of all hair follicles, no matter what hair color, could potentially be obtained. The technique does not require a laser light source, making it potentially less costly than laser treatment. Long-term data and largescale studies are needed to determine the safety and long-term efficacy of this modality.

7.

TERMINOLOGY

Hair removal is a vague term that has recently been defined (42). “Temporary hair loss” is defined as a delay in hair growth, which usually lasts for 1– 3 months, consistent with the induction of telogen. “Permanent hair reduction” refers to a significant reduction in the number of terminal hairs after a given treatment, which is stable for a period of time longer than the complete growth cycle of hair follicles at the given body site. Recently, it has been suggested to add another 6 months to this posttreatment observation time, that is, the time it takes for a damaged follicles to recover from the laser injury and reenter a normal growth cycle (3). A distinction needs to be made between permanent and complete hair loss. Complete hair loss refers to a lack of regrowing hairs (i.e., a significant reduction in the number of regrowing hairs to zero). Complete hair loss may be either temporary or permanent. Laser treatment usually produces complete but temporary hair loss for 1– 3 months, followed by partial but permanent hair loss.

8.

CLINICAL RESULTS AND HISTOLOGY

Expectations and goals can be very different for each patient: temporary vs. permanent, partial vs. complete hair removal. All responses are clinically significant and may be separately desirable to different patients. Growth delay, which provides a few months of hairless skin, is far more reliable. All laser systems have been shown to temporarily reduce hair growth. It occurs for all hair colors and at all fluences. Blonde-, red-, or gray-haired patients are unlikely to experience a permanent reduction, but hair loss in these patients can be maintained by treatment at 1 – 3 month intervals. Effectiveness for permanent hair reduction is strongly correlated with hair color and fluence. Research has shown that in the ideal patient with fair skin and dark hair, the probability for long-term hair removal after a single treatment is 80 –89% depending on the device used. A critical threshold fluence is also needed to obtain this effect. Long-term, controlled hair counts indicate an average of 20 – 30% hairloss with each treatment, indicating the need for multiple treatments to obtain complete hair removal (42). Differences in efficacy between different anatomical sites are not yet known, as is the number of treatments to obtain complete, permanent hair removal for these different sites. Exceptionally, a patient can obtain long-term complete hair removal after a single treatment, while others respond poorly, for yet unknown reasons. However, most patients (80 –89%) respond favorably.

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Animal studies have shown that the hair growth cycle affects the hair follicle destruction by ruby laser pulses: actively growing and pigmented anagen stage hair follicles were sensitive to hair removal by normal mode ruby laser exposure, whereas catagen and telogen stage hair follicles were resistant to laser irradiation (119). However, in humans, the efficacy of laser hair removal is not influenced by the hair growth cycle (120,121). Unlike the animal model, there is enough melanin present in each growth cycle of the human hair follicle to obtain selective damage to the hair. Often, regrowing hairs are thinner and lighter in color, as indicated by measurements of diameter and color of regrowing hairs (122). This also contributes to the overall cosmetic outcome since the clinical impression of hairiness is not only defined by the absolute number of hairs, but also by the color, the length, and the diameter of the hairs. Histological observations show damage predominantly in hair follicles with large, pigmented shafts, while hair follicles with small (,25 mm), hypopigmented shafts did not demonstrate any morphological change. Immediately after laser treatment, the hair shaft shows fragmentation with focal rupture into the follicular epithelium and thermal damage to the surrounding follicular epithelium (40,42,123). The extent of thermal damage is dependent on the pulse width, but retains confinement on the spatial scale of the follicle itself. One month later, most follicles are in telogen phase while others are being replaced by fibrosis and a foreign body giant cell reaction with phagocytosis of melanin (124,125). At 1 year, most follicles are replaced by miniaturized hair follicles (dominant mechanism) and some are replaced by a fibrotic remnant. Both of these histological findings produce permanent reduction in hair clinically (42,126).

9. 9.1.

TREATMENT GUIDELINES Preoperative Considerations

History Prior to laser treatment the following history is obtained: 1.

2. 3. 4. 5. 6.

Presence of conditions that may cause hypertrichosis a. Hormonal b. Familial c. Drug d. Tumor History of herpes simplex, especially perioral History of herpes genitalis, important when treating the pubic or bikini area History of keloids/hypertrophic scarring Previous treatment modalities—method, frequency and date of last treatment, as well as response Present medications a. photosensitizing medications b. accutane intake within the past year

Preoperative care 6 Weeks before laser treatment .

Sunscreen: A broad spectrum sunscreen is recommended and sun avoidance must be practiced if hair removal is planned in exposed sites.

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. .

.

Bleaching cream: A bleaching cream such as hydroquinone (Solaquin Forte) is prescribed to patients with darker skin types or a suntan. No plucking, waxing, or electrolysis: Research has shown greater hair loss at shaved vs. epilated sites, suggesting that light absorption by the pigmented hair shaft itself plays an important role. Shaving and depilatory creams: Shaving and depilatory creams may be used.

Day before laser treatment .

. .

The patient is instructed to shave the area to be treated. It is important not to irritate the area. If the patient is uncomfortable with the idea of shaving the area, a depilatory cream can be used instead. Start prophylactic antiviral such as Famvir or Zovirax when indicated. Start oral antibiotic when indicated (e.g., nasal and perianal skin).

Day of treatment . .

9.2.

Area to be treated should be clean and free of make-up If needed, 1 –2 h before the scheduled laser treatment, apply a thick layer of a topical anesthetic cream and cover with plastic wrap.

Technique

The procedure for hair removal using all of the aforementioned devices can be summarized as follows: . .

.

.

.

.

Skin preparation: Remove the anesthetic cream, make-up, or skin creams Anesthesia: Although less-sensitive areas (back, legs, arms) can frequently be treated without anesthesia, topical anesthesia is generally used (e.g., EMLAw) on more sensitive areas. When treating the upper lip, local or regional anesthesia with Lidocaine is sometimes required. Visibility: A treatment grid can be applied in order to provide the operator with an outline of the area to be treated. In the absence of a grid, careful attention must be paid to prevent double treatment and skipped areas. Visibility can also be increased by the Seymour lightTM , a polarized headlamp with magnifying loupe. Treatment fluence: The ideal treatment parameters must be individualized for each patient and possibly tested at inconspicuous sites in the area to be treated. The fluence is carefully increased while observing the skin for signs of acute epidermal injury, such as whitening, blistering, ablation, or Nikolsky’s sign (forced epidermal separation). In general, the treatment fluence should be at 75% of the Nikolsky’s threshold fluence. Technique: Slightly overlapping laser pulses are delivered with a predetermined spot size. It is recommended that the largest spot size and the highest tolerable fluence be used to obtain the best results. Cooling of the epidermis Cooling gel: If the device is not equipped with a cooling device, a thick layer of cooled gel is applied before delivery of the laser pulses. Dynamic cooling: With the dynamic cooling device (Gentlelase, Candela), short bursts of cryogen spurts (5 – 100 ms) are delivered automatically on the skin surface, prior to delivery of the laser pulse. Contact cooling: The Epilaser (Palomar) and Lightsheer (Lumenis) use a sapphire cooled handpiece (EpiwandTM and ChilltipTM , respectively) that is

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placed in direct contact with the skin. Prior to pulse delivery, the handpiece is pressed firmly against the skin. After delivery, the handpiece is picked up and placed firmly on an adjacent site, until the entire area is covered. The sapphire cooling tip should be wiped clean every 5 – 10 pulses to remove debris. Between patients, disinfection of the handpiece with Virex II (Johnson & Johnson) is mandatory. 9.3.

Postoperative Changes

The ideal immediate response is vaporization of the hair shaft with no other apparent effect. After a few minutes, perifollicular edema and erythema appear. The intensity and duration depends on the hair color and hair density. If there is a sign of epidermal damage, the fluence should be reduced. Postoperative care . . . . . . . . .

9.4.

Ice packs: reduce postoperative pain and minimize swelling. Analgesics: are not usually required unless extensive areas are treated. Prophylactic courses of antibiotic or antiviral: should be completed. Topical antibiotic ointment: applied twice daily is indicated if epidermal injury occurred. Mild topical steroid creams: may be prescribed to reduce swelling and erythema. Avoid any trauma such as picking or scratching of the area. Avoid sun exposure: use sunblock with SPF 30. Make-up may be applied on the next day unless blistering or crusts developed. Shedding of hair casts: especially on the face, the damaged hair follicle is often shed during the first week after treatment. Patients should be reassured that this is not a sign of hair regrowth.

Treatment Interval

Research has shown that laser hair removal requires the presence of a pigmented hair shaft (119 –121). Retreatment can therefore be performed as soon as regrowth appears. Regrowth is based on the natural cycle, which varies by anatomic location (Table 34.1), but on average, the timing is 6– 8 weeks. More research regarding this is currently being conducted.

10.

SIDE EFFECTS .

.

. .

Laser hair removal is not a painless procedure. Most patients experience some discomfort during and immediately after treatment. One can use a topical or local anesthetic before performing the treatment. Perifollicular erythema and edema are expected in all patients treated if threshold fluences were used. The intensity and duration depend on hair color and hair density. This usually lasts a few hours. Epidermal damage occurs if excessive fluences were used. It is also more common in patients with a tan. Herpes simplex outbreaks are uncommon but may occur. There is a higher risk among patients with a previous history of herpes simplex and when the perioral, pubic, or bikini area are treated.

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. .

. . . .

. .

. .

. .

11.

The risk of bacterial infection is extremely low. However, it may occur following epidermal damage. Transient pigmentary changes such as hypopigmentation or hyperpigmentation can be prevented if the ideal patient and treatment fluence are chosen. This is mostly seen in patients with darker skin types or when patients had recent tan (127 – 131). Permanent pigmentary changes are unlikely except in dark skinned individuals (132). Scarring is unlikely except in cases of overaggressive treatment or postoperative infection. Loss of freckles or pigmented lesions is not uncommon. Patients should be aware of this possibility. Lasering nevus cells may produce clinically atypical nevi. Laser treatment of nevi, present in areas for hair removal, should therefore be avoided, especially in patients with a history of dysplastic nevi or malignant melanoma (133). Temporary or permanent leucotrichia may develop following laser or IPL hair removal (134). A case of lichen planus, being triggered by long pulsed ruby laser treatment for hair removal, has been reported. All patients with a history of skin diseases known to show an Koebner phenomenon like psoriasis vulgaris, vitiligo, lichen planus, Darier disease, should be clearly informed about this possible adverse effect of treatment (135). The induction of Pili Bigeminy by low fluence therapy for hair removal with alexandrite and ruby lasers has been reported (136). A statistically significant increase in sebum excretion occuring 4 –12 months after ruby laser hair removal treatment was observed. The hypothesis was raised that decreased resistance to sebum outflow may explain this result, following miniaturization or absence of hair shaft after ruby laser treatment. Further study is needed to assess mechanisms for this interesting response (137). Urticaria vasculitis induced by diode laser photoepilation has been reported (138). Several cases of induction of hair growth following laser hair removal in young female patients with darker skin types have been reported. Two different phenomena have been observed: either conversion of fine vellus hair to dark, coarse terminal hair at the site of treatment or induction of growth of long fine hairs in the immediate vicinity of the treatment area. Further study is ongoing to assess the mechanisms for this response.

SAFETY .

.

The systems are designed for strong absorption by melanin and deep tissue penetration. They are therefore capable of causing retinal injury. Proper eye protection must be worn by the patient and operating personnel. Treatment near or on the surface of an eye is not recommended. All other body sites can be treated safely. When using contact cooling devices, there is a small but real risk of infection. In between patients, disinfection of the handpiece with Virex or its equivalent, is mandatory.

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. 12.

695

The “plume” generated by the vaporized hair shafts has a typical sulfur smell and in large quantities, can be irritating to the respiratory tract. A smoke evacuator and good ventilation are recommended. Electrical and fire hazards are minimal but exist.

ETHNIC CONSIDERATIONS

12.1. Hair Color Temporary hair loss (1 –3 months) always occurs after laser treatment, regardless of hair color or device used. On the other hand, the ability to induce long-lasting hair reduction is strongly correlated with hair color. Patients with dark hair are most likely to obtain longlasting hair removal. Blonde-, red-, gray-, or white-haired patients are unlikely to experience a permanent reduction, because melanin is low or lacking in the hair follicles. The solution would be a chromophore that is absorbed selectively by the hair follicle and provides a temporary target for laser treatments, such as MeladineTM. MeladineTM is a topical melanin encased phosphatidylcholine-based liposome solution which, when sprayed on the desired area, selectively deposits melanin directly into the hair follicle without staining surrounding skin. The proprietary liposome molecules are small enough to effectively penetrate the infundibulum, but are not taken up by the bloodstream. The result is temporarily melanin rich follicles, which allows patients with lighter hair colors to now benefit from laser hair removal. In European clinical studies, 90% of the patients pretreated with MeladineTM experienced permanent hair reduction of 75% as compared with 0% of patients who did not receive MeladineTM treatment. The effectiveness of the treatment was directly proportional to the amount of MeladineTM used. In fact, those patients who used 86 mL in their pretreatment regime experienced hair reduction of 95%. (J. De Leeuw, presented at the 2002 EADV meeting) 12.2. Skin Color The maximum tolerated fluence is determined by the epidermal pigmentation. Fairskinned patients with dark hair are most easily treated. While dark skin types are not readily treated with any of the ruby lasers because of melanin interference, the alexandrite, diode, Nd:YAG lasers and the intense pulsed light source, operating at longer wavelengths (near-infrared) and longer pulse durations, have been shown to treat darker skin types (IV –VI) more safely, if combined with cooling devices (105,106,110,139 – 147). A Q-switched Nd:YAG laser, with or without an external chromophore, has been shown to be very useful for treatment of dark skin types but appears to be ineffective for permanent hair removal. For patients presenting with a tan, pretreatment with a bleaching agent, sunscreen and sun avoidance for at least 6 weeks is recommended prior to laser treatment.

13.

CONCLUSION

The role of lasers and filtered flashlamps in hair removal has been determined over the last few years. Several controlled studies have demonstrated the efficacy and safety of light based hair removal. The procedure is also very attractive because of its noninvasive nature, the ability to cover a large treatment area, and the speed of treatment. Recently, smaller and less expensive light based devices have become available. It remains to be

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seen if any of these systems will be shown to be more effective. Practitioner and patient have to be cautious and see how this area evolves.

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Alster TS, Bryan H, Williams CM. Long-pulsed Nd:YAG laser-assisted hair removal in pigmented skin: a clinical and histological evaluation. Arch Dermatol 2001; 137(7):885– 889. Goldberg DJ, Silapunt S. Hair removal using a long-pulsed Nd:YAG laser: comparison at fluences of 50, 80, and 100 J/cm2. Dermatol Surg 2001; 27(5):434 – 436. Goldberg DJ, Silapunt S. Histologic evaluation of a millisecond Nd:YAG laser for hair removal. Lasers Surg Med 2001; 28(2):159– 161. Goldberg DJ, Samady JA. Evaluation of a long-pulse Q-switched Nd:YAG laser for hair removal. Dermatol Surg 2000; 26(2):109 –113. Bencini PL, Luci A, Galimberti M, Ferranti G. Long-term epilation with long-pulsed neodimium:YAG laser. Dermatol Surg 1999; 25(3):175 – 178. Sadick NS, Weiss RA, Shea CR, Nagel H, Nicholson J, Prieto VG. Long-term photoepilation using a broad-spectrum intense pulsed light source. Arch Dermatol 2000; 136(11): 1336– 1340. Weiss G, Cohen B. The efficacy of long-term epilation of unwanted hair by noncoherent filtered flashlamp. Lasers Surg Med 2000; 26(4):345. Schroeter CA, Raulin C, Thurlimann W et al. Hair removal in 40 hirsute women with an intense laser-like light source. Eur J Dermatol 1999; 5:374– 379. Sadick NS, Shea CR, Burchette JL et al. High-intensity flashlamp photoepilation: a clinical, histological, and mechanistic study in human skin. Arch Dermatol 1999; 6:668 –676. Weiss RA, Weiss MA, Marwaha S et al. Hair removal with a non-coherent filtered flashlamp intense pulsed light source. Lasers Surg Med 1999; 24(2):128 – 132. Manstein D, Dierickx CC, Koh W et al. Effects of very long pulses on human hair follicles. Lasers Surg Med 2000; 12(suppl):86. Altshuler GB, Anderson RR, Manstein D et al. Extended theory of selective photothermolysis. Lasers Surg Med 2001; 29(5):416 – 432. Suthamjariya K, Battle E, Manstein D et al. Super long pulsed diode for hair removal on all skin types. Lasers Surg Med 2001; 13(suppl):87. Rogachefsky AS, Silapunt S, Goldberg DJ. Evaluation of a new super-long-pulsed 810 nm diode laser for the removal of unwanted hair: the concept of thermal damage time. Dermatol Surg 2002; 28(5):410– 414. Anderson RR, Margolis RJ, Watanabe S et al. Selective photothermolysis of cutaneous pigmentation by Q-switched Nd-YAG laser pulses at 1064, 532 and 355 nm. J Invest Dermatol 1989; 93:28 – 32. Dover JS, Margolis RJ, Polla LL et al. Pigmented guinea pig skin irradiated with Q-switched ruby laser pulses: morphologic and histologic findings. Arch Dermatol 1989; 125:43 – 49. Goldberg DJ, Littler CT, Wheeland RG. Topical suspension-assisted Q-switched Nd:YAG laser hair removal. Dermatol Surg 1997; 23:741 – 745. Nanni CA, Alster TS. Optimizing treatment parameters for hair removal using a topical carbon-based solution and 1064-nm Q-switched neodymium:YAG laser energy. Arch Dermatol 1997 Dec; 133(12):1546– 1549. Kilmer SL, Chotzen VA. Q-switched Nd-YAG laser (1064 nm) hair removal without adjuvant topical preparation. Lasers Surg Med 1997; S9:145. Kilmer SL, Chotzen VA, Calkin J. Hair removal study comparing the Q-switched Nd-YAG and long pulse ruby and alexandrite lasers. Lasers Surg Med 1998; S10:203. Grossman MC, Dwyer P, Wimberley J, Flotte TJ, Anderson RR et al. PDT for hirsutism. Lasers Surg Med 1995; S7:44. Kennedy JC, Pottier RH. Endogenous protoporphyrin IX, a clinically useful photosensitizer for photodynamic therapy. J Photochem Photobiol B 1992; 14:275– 292. Divaris DXG, Kennedy JC, Poittier RH. Phototoxic damage to sebaceous glands and hair follicles of mice after systemic administration of 5-aminolevulinic acid correlates with localized protoporphyrin IX fluorescence. Am J Pathol 1990; 136:891 – 897. Henderson BW, Dougherty TJ. How does photodynamic therapy work? Photochem Photobiol 1992; 55:145 – 157.

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Weishaupt KR, Gomer CJ, Dougherty TJ. Identification of singlet oygen as the cytotoxic agent in photo-inactivation of a murine tumor. Cancer Res 1976; 36:2326 – 2329. Kennedy JC, Pottier RH, Pross DC. Photodynamic therapy with endogenous protoporphyrin IX: basic principles and present clinical experience. J Photochem Photobiol B 1990; 6:143 – 148. Altshuler GB, Zenzie HH, Erofeev AV, Smirnov MZ, Anderson RR, Dierickx CC. Contact cooling of the skin. Phys Med Biol 1999; 44:1003 – 1023. Zenzie HH, Altshuler GB, Smirnov MZ, Anderson RR. Evaluation of cooling methods for laser dermatology. Lasers Surg Med 2000; 26:130– 144. Ross EV, Rathyen JS, Gaudet T, Farinelli WA, Naseef GS, DiMarzio CA, Anderson RR. Recycling wasted photons: a device to increase laser energy used in surgery. Lasers Surg Med 1996; S8:87. Anderson RR, Dierickx CC, Altshuler GB, Zenzie HH. Photon recycling: a new method of enhancing hair removal. Lasers Surg Med 1999; S11:190. Nelson JS, Milner TE, Anvari B, Tanenbaum S, Kimel S, Svaasland L, Jacques S. Dynamic epidermal cooling during pulsed laser treatment of port-wine stain. Arch Dermatol 1995; 131:695 – 700. Battle E, Kittisak S, Alora B, Palli K, Anderson R. Very long pulsed diode laser for hair removal on all skintypes. Lasers Surg Med 2000; S12:85. Kauvar AN. Treatment of pseudofolliculitis with a pulsed infrared laser. Arch Dermatol 2000; 136(11):1343– 1346. Ross EV, Cooke LM, Timko AL, Overstreet KA, Graham BS, Barnette DJ. Treatment of pseudofolliculitis barbae in skin types IV, V, and VI with a long-pulsed neodymium:yttrium aluminum garnet laser. J Am Acad Dermatol 2002; 47(2):263 – 270. Ross EV, Cooke LM, Overstreet KA, Buttolph GD, Blair MA. Treatment of pseudofolliculitis barbae in very dark skin with a long pulse Nd:YAG laser. J Natl Med Assoc 2002; 94(10):888– 893. Smith SR, Goldman MP, Fitzpatrick RE. Long-term results of hair photo-epilation. Lasers Surg Med 998; S10:205. Fitzpatrick RE, Goldman MP, Sriprachya-anunt S. Hair removal utilizing the ESC Epilight device. Lasers Surg Med 1997; S9:165. Troilius A, Troilius C. A long term follow-up of hair removal with a second generation of broad band spectrum intense pulsed light source. Lasers Surg Med 2000; S11:87. Goldberg DJ, Silapunt S. Hair removal with a combined light/heat based photo-epilation system. J Cutan Laser Ther 2001; 3(1):3 – 7. Sumian CC, Pitre FB, Gauthier BE, Bouclier M, Mordon SR. A new method to improve penetration depth of dyes into the follicular duct: potential application for laser hair removal. J Am Acad Dermatol 1999; 41:172– 175. Lin TY, Manuskiatti W, Dierickx CC, Farinelli WA, Fisher ME, Flotte T, Baden HP, Anderson RR. Hair growth cycle affects hair follicle destruction by ruby laser pulses. J Invest Dermatol 1998; 111(1):107– 113. Dierickx CC, Campos VB, Lin DT, Farinelli WA, Anderson RR. Influence of hair growth cycle on efficacy of laser hair removal. Lasers Surg Med 1999; S11:84. Liew SH, Grobbelaar AO, Gault D, Green C, Linge C. Ruby laser-assisted hair removal: a preliminary report of the correlation between efficacy of treatment and melanin content of hair and the growth phases of hair at a specific site. Ann Plast Surg 1999; 42(3):255 – 258. Lin D, Dierickx C, Campos V, Farinelli W, Anderson R. Reduction of regrowing hair shaft size and pigmentation after ruby and diode laser treatment. Lasers Surg Med 1999; S11:86. Ono I, Tateshita T. Histopathological changes in the hair follicle after irradiation of longpulse alexandrite laser equipped with a cooling device. Eur J Dermatol 2000; 10(5):373 – 378. Dierickx C, Leszynski D, Farinelli WA, Campos V, Anderson RR. Mechanism for induction of temporary hair loss. Lasers Surg Med 1999; S11:60. McCoy S, Evans A, James C. Histological study of hair follicles treated with a 3-msec pulsed ruby laser. Lasers Surg Med 1999; 24(2):142– 150.

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35 Laser Assisted Hair Transplantation Marc R. Avram Weill-Cornell Medical Center, New York, New York, USA

1. 2. 3. 4.

The Consult The Donor Region Graft Size Hairline Design 4.1. Men 4.2. Women 5. Current Challenges 6. Erbium Laser Introduced 7. Future References

703 705 706 707 707 708 709 712 713 714

The carbon dioxide laser has been used in medicine since for over three decades. Its wavelength of 10,600 nm in the infrared spectrum makes it an ideal tool to vaporize and cut tissues. It has been used to treat keloids, warts, and many other cutaneous lesions over the past three decades (1). The chief disadvantage of the laser is the non-specific heat it produces beyond the treated target, which can create extensive scarring in the skin. From the 1960s into the 1990s, 15– 20 hair 3 – 4 mm punch grafts were the standard size grafts used in hair transplantation. They produced long-term hair growth but were often a “pluggy” cosmetic failure (Fig. 35.1). The non-selective spread of heat from the CO2 laser produced hundreds of microns of peripheral necrotic tissue, which prevented it from ever being used to create recipient sites in hair transplantation. In the 1990s, there were three revolutionary changes in the technique in hair transplantation: (1) donor harvesting, (2) graft size, and (3) hairline design. These changes allow trained hair transplant teams to consistently produce natural appearing transplanted hair (Figs. 35.2 and 35.3) 1.

THE CONSULT

All patients undergoing hair transplantation should expect natural appearing transplanted hair. Anything less is unacceptable with the changes that have occurred in technique over 703

704

Figure 35.1

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Large graft, pluggy hair transplant.

the past decade. Plugs and “cornrows” should never happen. All skin types and hair colors are candidates for the surgery. The density of donor hair will help determine the amount of expected density of transplanted hair. Patients with below average donor density will have natural but thin transplanted hair. Those with above average density can expect greater density over a larger portion of the scalp. The physical characteristics of hair-color, caliber, and curl will also help determine the expected density of the transplant. Patients with fine, straight hair will not achieve the perceived density as will patients with thick curly hair with an equal number of transplanted hairs. In addition, the density of a hair transplant will be affected by the rate of hair loss and/or postsurgery telogen effluvium which may occur. For most patients, two or three 800–1400 graft sessions will provide a natural long-term frame of hair on the scalp even if they loose most of their hair. Patients with a lot of remaining hair but rapid hair loss may have less hair 6 months after surgery. A bald patient on the other hand can expect a major increase in density 6 months after surgery. The extent and rate of hair loss varies from person to person. When planning a transplant, the surgeon must emphasize the ongoing nature of hair loss. Other criteria whether that determine a patient is a candidate for surgery is if a transplant will make a cosmetic difference over the next 1 or 2 years and whether the transplanted hair will be cosmetically

Figure 35.2

Loss of frontal hairline due to male pattern alopecia.

Laser Assisted Hair Transplantation

Figure 35.3

705

800 1 – 4 hair grafts.

appropriate 10 or 20 years after surgery. Patients who have tried medical treatments for hair loss which failed are anxious to “nip the problem in the bud” by transplanting hair at the earliest stages of hair loss. These are patients who will return for corrective surgery 10 years later, angry they ever had surgery because of the receding tide of hair left the transplanted hair exposed too low in the scalp. Explaining the ongoing loss of hair with or without transplantation, limited donor hair, realistic density based on donor hair and type, and long-term cosmetic considerations will help create realistic expectations for patients and produce happy patients.

2.

THE DONOR REGION

The donor region is the only limiting factor in hair transplantation. Punch harvesting with 3 – 4 mm steel trephines was performed from the 1960s into the 1990s. It is now obsolete because it produced extensive scarring in the donor region and was an inefficient method of harvesting valuable donor hair (Fig. 35.4). Scalpel harvesting of donor hair in an ellipse offers (1) less scarring of the donor region, (2) less transection of donor hair, and

Figure 35.4

Extensive scarring due to punch harvesting.

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Figure 35.5

Donor scar following elliptical harvesting of donor tissue.

(3) a more efficient method to utilize the maximum donor hair (Fig. 35.5). The ellipse is harvested with the patient in the prone position. On average a 15 cm 0.8 cm strip is harvested after anesthetizing the tissue with lidocaine and using 30– 50 cc of saline to tumesce the region (Fig. 35.6). Tumescence of the donor ellipse reduces transection of hair follicles and provides improved hemostasis. Either staples or sutures used to close the site and are left in for 7 –10 days. The remaining scar is far less noticeable than steel punch sites.

3.

GRAFT SIZE

Hair grows in natural groups of 1 –4 hairs on the scalp. Traditional hair transplant grafts contained 15– 25 hairs. When implanted in recipient bald skin, this often resulted in “corn rows” and a pluggy unnatural appearance. Over the past several years, surgeons have started creating grafts in groupings of 1 –4 hairs (Fig. 35.7). The hair follicles are separated from the donor ellipse by skilled assistants, using a variety of different blades. Some physicians prefer to use a stereomicroscope or loupes to assist in graft creation (1). By mimicking nature’s natural groupings of follicles, surgeons can now consistently create undetectable transplanted hair (Fig. 35.8).

Figure 35.6

Tumescence in donor tissue.


Figure 35.7

4. 4.1.

707

1– 4 hair graft vs. standard plug.

HAIRLINE DESIGN Men

The hairline is what defines the cosmetic success of a hair transplant. As with hair graft creation, the trend in hairline design has been toward mimicking as closely as possible what occurs in nature. The goal of a hairline is to frame the face in an undetectable manner. For decades surgeons creating hairlines took the name hairline literally, resulting in straight, sharp demarcation between skin and thick hair bearing skin (Fig. 35.9). “Hairlines” do not exist, but a natural transition zone of gradually increasing density from skin to terminal hair bearing skin occurs. This ill-defined “feathering zone” is created by randomly placing, in an irregular pattern, 1 –3 hair grafts along the newly created hairline (2). The level at which the hairline is created varies from individual to individual. It is important for a surgeon to look at each patient in a global 3608 view before deciding upon where to place the hairline. Androgenetic alopecia is progressive but transplanted hair will grow long-term. Therefore, when viewing patients, surgeons must assume all patients will progress to cosmetically significant hair loss. A newly created hairline must look equally natural 1 year and 20 years after surgery.

Figure 35.8

(a) Before surgery and (b) After 1000 1 – 4 hair grafts.

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Figure 35.9

Blunt straight hairline.

The height of the hairline varies from person to person. Hard and fast rules of how many centimeters a hairline should be placed above the glabella should not be followed, but the shape of a patient’s head and, forehead and level of temporal hairline recession will determine the ideal aesthetic placement of grafts to produce a natural frontal hairline. The posterior hairline should mimic the natural semicircle that expands as hair loss progresses in the vertex of the scalp. It should, as with the frontal hairline, appear be designed anticipating ongoing hair loss in the future. To avoid future aesthetic complications, the posterior hairline should be placed in the same plane as the frontal hairline. This will avoid “chasing” the ever expanding ring of hair loss on the vertex of the scalp with valuable donor grafts.

4.2.

Women

The advent of 1– 4 hair grafts has created a highly effective natural solution for the millions of women suffering from androgenetic alopecia. Unlike men, hair loss is not socially acceptable for women. It is also often dismissed by a spouse and/or physicians. In women, the natural hairline thins but is not entirely lost as with men. The “see through” appearance of hair can be a source of anxiety for women (Fig. 35.10). The

Figure 35.10

Female pattern alopecia with typical intact frontal hairline.


Figure 35.11

709

The intact frontal hairline of female pattern hair loss.

goal for women is not to create a new hairline but to place hundreds of 1– 4 hair grafts behind the frontal hairline in order to re-create the natural density that occurs behind the hairline. The majority of transplanted grafts are placed in a 3 –5 cm zone behind the frontal hairline in order to maximize density and minimize the risk of a postsurgical telogen effluvium. The increased density in the frontal hairline gives women the freedom to style their hair and not fear a gust a wind (Figs. 35.11 and 35.12). The 1 –4 hair grafts also produce natural appearing hair for women with significant loss of hair in the temporal hairline following face-lift or endoscopic forehead surgery. It once again gives women the option to pull their hair back over their ears (Fig. 35.13).

5.

CURRENT CHALLENGES

Patients should expect natural appearing transplanted hair today. While exciting for both patients and hair transplant surgeons, the process of creating and placing 1 –4 hair grafts has produced new obstacles. Creating natural and dense appearing hair for patients has become a leading challenge for surgeons. Traditional punch grafts containing 12 –25 hairs produced density by transplanting 50– 100 grafts per procedure for an average of

Figure 35.12

600 1– 4 hair grafts along the frontal scalp.

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Figure 35.13 (a) Alopecia secondary to face lift and (b) restored hair line after 600 1 – 4 hair grafts.

1500 total hair follicles per procedure. In order to create comparable density, today’s procedure requires 800 –1500, 1 – 4 hair grafts per procedure. To meet these challenges, new instruments to harvest grafts from donor strips and place into 0.8 –1.2 mm recipient sites now exist. The era of a physician and one assistant performing a hair transplant procedure have disappeared and has been replaced by highly trained staff of three to five members per team. One of the technical challenges for the transplant team is adequate hemostasis in the hundreds of recipient sites. Poor hemostasis can make the procedure frustrating for even the most experienced teams, in addition to increasing operating time for the patient. With pulsed and scanned CO2 lasers, many of these problems may be avoided or minimized. Bleeding is controlled because the CO2 laser seals small vessels in the dermis and superficial subcutaneous fat through its thermal effects. The laser offers the potential for making the procedure more efficient and available to surgeons who do not have several skilled assistants. The theory of selective photothermolysis revolutionized the treatment of vascular and pigmented lesions in the 1980s (3). In the 1990s, it has been applied to the CO2 laser and to treat dermatoheliosis and acne scarring (4). These new pulsed and scanned CO2 lasers vaporize ,100 mm of skin with each pass over the skin (5). These separate revolutions of 1 –4 hair grafting and resurfacing CO2 laser allowed the role of lasers in hair transplantation to be investigated. The potential advantages of laser hair transplantation include (1) complete hemostasis in recipient sites resulting in (2) shorter operative time for physician and patient. The CO2 laser can be used to harvest donor strips, but is much slower than a scalpel, and hemostasis is easily controlled with electrocoagulation and therefore is not used in the donor region. Recipient sites vary in size between 0.6 and 1.2 mm wide for 1 –4 hair grafts and need to be 4– 5 mm deep for the bulb of the transplanted hair (Fig. 35.14). Initial histology on scalp tissue revealed peripheral necrosis in the dermis of 80 –120 mm and 40 W laser systems (6) (Fig. 35.15). Between 1994 and 2000, several clinical trials were conducted and the trend over the years has been toward higher energy and shorter pulse times (5) (Fig. 35.16). Clinical trials did demonstrate the ability to consistently grow 1 –2 hairs in laser produced recipient sites (7 – 11). The settings for each laser varies and can be found in


Figure 35.14

711

Depth of hair bulb in tissue 4 – 5 mm below skin surface.

published peer reviewed articles and from manufactures of each lasers. The yield in laser and steel created sites was equal for 1 –2 hair grafts but less in laser produced sites for larger grafts (Fig. 35.17). Laser assisted procedures were quicker due to the excellent hemostasis in recipient sites and some report a more natural appearance of laser transplanted hair (12). Clinical trials have also revealed disadvantages in CO2 laser assisted hair transplantation. (1) For 3–4 hair grafts, the yield of laser created sites was less than steel in an unpredictable minority of patients; (2) the laser de-epithelializes the epidermis around recipient sites creating more and longer postoperative crusting and erythema; and (3) the heat produced by the laser can precipitate a telogen effluvium in some patients with thinning of existing hair (13) (Fig. 35.18). Another unanswered question is how closely CO2 laser sites can be placed without affecting the growth and density of transplanted hair (14). The scanners developed for hair transplantation are efficient in patients with extensive hair loss but in patients with viable existing hair, the scanner can cause unnecessary loss of existing hair. Another challenge to the CO2 laser is the ability to create recipient sites at the appropriate angle (Fig. 35.19). The direction of hair growth changes in the scalp and laser handpieces can be cumbersome to make the sites. Despite initial skepticism in the laser and hair transplant community, clinical trails did demonstrate consistent growth of 1–2 hair grafts and the FDA approved the laser for hair transplantation, although concerns

Figure 35.15

Histology of CO2 sites with 50 microns of necrosis in dermis.

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Figure 35.16

CO2 laser assisted hair transplantation.

have limited the role of the CO2 laser in hair transplantation. As of 2003, steel needles remain the standard instrument for creating recipient sites for hair transplants.

6.

ERBIUM LASER INTRODUCED

Erbium:YAG lasers vaporize water more efficiently than CO2 lasers do (15). This results in less residual thermal damage of skin with each pulse of the laser. Clinically this has resulted in less postoperative edema, crusting and erythema with laser resurfacing (16). With less tissue necrosis, the erbium laser could overcome some of the limitations in graft spacing and size associated with the CO2 laser. Histology of scalp tissue with the erbium laser reveals 5– 10 mm of peripheral necrosis in the dermis (Fig. 35.20). This is far less than the highest energy pulsed CO2 laser produced 30– 40 mm of damage. The minimal necrosis in the dermis and reduced spread of heat in tissue should allow closer placement of erbium:YAG sites than CO2 laser sites, with less risk of telogen effluvium, less postoperative crusting and erythema, and a greater yield of 3 –4 hair grafts. A challenge of erbium:YAG laser hair transplantation is the ability to create a 4 – 5 mm deep and 0.8 – 1.2 mm wide recipient site with a single pulse. With 1 and 2 J/cm2 lasers, 3 –5 pulses are necessary to go to the appropriate depth for implanting

Figure 35.17

Steel punch vs. laser created recipient sites in controlled clinical trial.


Figure 35.18

713

Increased hemorrhagic crusting in laser produced recipient sites.

hair. New generation 3 and 4 J/cm2 erbium lasers are able to produce recipient site with 1 – 2 pulses. A 2 year clinical trial using the erbium laser concluded erbium assisted transplantation is safe and produced .95% yield of 1 –4 hair follicular units with no reported side effects (17).

7.

FUTURE

The role of lasers in hair transplantation continues to slowly evolve. Carbon dioxide laser parameters, scanners, and handpieces are now standard options with lasers. Although possibly an effective tool, there is only a limited role for CO2 lasers in hair transplantation. The erbium laser continues to be investigated. Preliminary histology and clinical trials are encouraging. Over the next several years, erbium lasers with scanners and handpieces will be available that may greatly reduce the time of a hair transplant procedure and may decrease the need for large hair transplant teams. This will allow physicians who do not perform hair transplantation regularly to perform 1000 – 1500 graft sessions. It will allow more physicians to perform safe procedures that produce natural appearing dense transplanted hair efficiently and cost-effectively. The chief challenge of lasers in hair transplantation is the ability to consistently produce natural appearing transplanted hair

Figure 35.19

Bulky CO2 handpiece making recipient sites.

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Figure 35.20

Histology erbium recipient sites with 5 microns peripheral damage.

as we can with steel needles. When the puled dye laser, YAG, ruby, and other lasers were introduced they quickly became the standard tool for treating blood vessels, tatoos, lentigos, and hair removal because the alternative procedures were clearly inferior. In hair transplantation, the nonlaser method is safe and highly effective which makes the bar for lasers higher than for other cutaneous applications. We do know, at the beginning of the 21st century, that laser produced recipient sites can consistently grow 1– 2 hair grafts, something thought of being impossible in the late 1990s. As technology continues to evolve, lasers will become a standard instrument in hair transplantation, which will make the procedure even safer and more efficient and more widely available to physicians.

REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13.

Sloan K, Haberman H, Lynde CW. Carbon dioxide laser-treatment of resistant verrucae vulgaris: a retrospective analysis. Cutan Med Surg 1998; 2(3):142 – 145. Limmer BL. Elliptical donor stereoscopically assisted micrografting as an approach to further refinement in hair transplantation. J Dermatol Surg Oncol 1994; 20(12):789– 793. Stough DB. Hair transplantation by the feathering zone technique. Am J Cosmet Surg 1993; 10:243 – 248. Anderson RR, Parrish JA. Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science 1983; 220(4596):524 –527. Bernstein EF, Brown DB, Kenkel J, Burns AJ. Residual thermal damage resulting from pulsed and scanned resurfacing lasers. J Dermatol Surg 1999; 25(10):739– 744. West TB. Laser resurfacing of atrophic scars. Dermatol Clin 1997; 15(3):449 – 457. Grevelink JM. Laser hair transplantation. Dermatol Clin 1997; 15(3):479 – 486. Smithdeal CD, Carbon dioxide laser assisted hair transplantation—the effect of laser parameters on scalp tissue: a histologic study. Dermatol Surg 1997; 23(9):835 – 840. Ho C, Nguyen Q, Lask G, Lowe N. Mini-slit graft hair transplantation using the ultrapulse carbon dioxide laser handpiece. Dermatol Surg 1995; 21(12):1056– 1059. Villnow MM, Ferduni B. Update on laser-assisted hair transplantation. Dermatol Surg 1998; 24(7):749– 754. Fitzpatrick RE. Laser hair transplantation—tissue effects of laser parameters. Dermatol Surg 1995; 21:1042 – 1046. Tsai RY, Chen DY, Chan HL, Ho YS. Experience with laser hair transplantation in orientals. Dermatol Surg 1998; 24(10):1065– 1068. Unger WP. Laser hair transplantation II. Dermatol Surg 1995; 21(9):759 – 765.

Laser Assisted Hair Transplantation 14. 15. 16. 17.

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Bernstein RM, Rassman WR. Laser hair transplantation: is it really state of the art? Lasers Surg Med 1996; 19(2):233– 235. Khatri KA, Ross V, Grevelink JM, Magro CM, Anderson RR. Comparison of erbium:YAG and carbon dioxide lasers in resurfacing of facial rhytides. Arch Dermatol 1999; 135(4):391– 397. Alster TS. Clinical and histologic evaluation of six erbium:YAG lasers for cutaneous resurfacing. Lasers Surg Med 1999; 24(2):87–92. Uebel C. The use of erbium:YAG laser in hair micro-transplant surgery. Clin Applic Notes 1999; 7(1).

36 Treatment of Nonwhite Skin with Lasers Woraphong Manuskiatti Siriraj Hospital, Mahidol University, Bangkok, Thailand

Mitchel P. Goldman University of California San Diego, San Diego, California, USA

1. Differences Between Pigmented and White Skin 2. Clinical Applications 3. Microvascular Lesions 4. Pigmented Lesions 5. Benign Epidermal Pigmented Lesions 6. Mixed Epidermal and Dermal Pigmented Lesions 7. Dermal Pigmented Lesions 8. Tattoo Removal 9. Skin Resurfacing 10. Hair Removal 11. Prevention and Management of Complications 12. Sun Avoidance 13. Preoperative and Postoperative Treatment Regimen 14. Epidermal Cooling 15. Summary References

718 719 720 724 725 727 727 728 731 735 737 738 738 739 740 740

The approximately 3.5 billion nonwhite people in India, China, northeast and southeast Asia, the Middle East, Spain, Central and South America, and the black population of African countries, the United States, and elsewhere represent the majority of the world’s population. Racial differences in skin pathophysiology have been well documented (1,2). The high risk of pigmentary alterations and scarring following any procedure that produces inflammation of the skin continues to influence physicians to exercise caution with this group of patients. This caution also applies to laser therapy. Even with the highly selective characteristic of current laser therapy, when results are expected to 717

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be similar between the races, they are not. Both genetic background and environmental factors are involved in these differences. The effects of light, including laser light on skin, begins with the absorption of incident laser light by chromophores (3). Melanin, deoxyhemoglobin, oxyhemoglobin, and water are the dominant natural chromophores in the skin, which are used to deposit the energy necessary for laser – tissue interactions in laser therapy (4). Non-Caucasian skin is often more pigmented than Caucasian skin resulting in interference with epidermal melanin when using lasers to treat dermal lesions. This presents a significant challenge for laser surgery. This chapter reviews approaches to laser treatment in nonwhite population.

1.

DIFFERENCES BETWEEN PIGMENTED AND WHITE SKIN

The surgeon who considers performing laser surgical procedures in non-Caucasian patients should have an understanding of the morphologic differences between white and nonwhite skin, especially in patients of black and Asians descent. The major determinant of differences in skin color between white and nonwhite skin is the amount of epidermal melanin. Although there is no difference in the quantity of melanocytes between the two groups, the larger and more melanized melanosomes in nonwhite skin compared with white skin have been well documented (5). In addition, the degradation rate of melanosomes within the keratinocytes of dark skin is slower than that of white skin. The larger and more melanized melanosomes of black skin absorb and scatter more energy, thus providing a higher photoprotection. Conversely, the melanocytes and mesenchyma in darker skin seem to be more vulnerable to trauma and inflammatory conditions than those in white skin (6). The majority of cutaneous laser wavelengths have significant overlap with the absorption spectrum of melanin (see Chapter 2). Therefore, nonwhite skin presents a significant challenge because of greater absorption of laser energy and resulting damage to melanin-containing cells, producing hypopigmentation, hyperpigmentation, and depigmentation (Table 36.1). Interestingly, alterations in pigmentation may not be apparent for several months after laser therapy. Thus, when treating nonwhite skin, test sites and long-term follow-up should be considered. Increased mesenchymal reactivity may result in hypertrophic scars and keloids. Asian and black skins has thicker dermis than white skin, the thickness being proportional to the intensity of pigmentation. This increased dermal thickness along with photoprotection from an increase in size and number of melanosomes, may account for a lower incidence in facial rhytides in Asians and blacks. Similar to black skin, Asian skin has a greater tendency toward hypertrophic scarring. Asians may also have a greater tendency toward prolonged redness during scar maturation than white skin (7). Fitzpatrick (8) developed the classification of skin phototypes based on response to ultraviolet irradiation of the Caucasian population. However, it has often been found that a patient with skin phototype I or II may have genetic origin of skin phototypes III, IV, V, and VI. Given the same clinical expertise in a specific cosmetically sensitive procedure such as laser surgery, the results would be significantly different in clinically similar patients if one had considered more distant ancestry. Lancer (9,10) proposed the socalled “Lancer Ethnicity Scale” (LES) factoring in this additional historical information to provide a method to presurgically skin type the patients and more clearly predict outcome (Table 36.2).

Treatment of Nonwhite Skin with Lasers

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Table 36.1 Risk of Pigmentary Changes of the Current Laser and Intense, Pulsed Light Systems in Nonwhite Skin Target Microvascular lesions

Pigmented lesions and tattoo removal

Skin resurfacing Hair removal

Laser or light systems Flashlamp-pumped pulsed-dye laser (585, 590, 595, and 600 nm) Long-pulsed KTP (532 nm) Diode (532 nm) Copper vapor (511, 578 nm) Krypton (532 nm) Argon (488, 514 nm) Intense, pulsed light system (.515 nm) Copper vapor (511, 578 nm) 510 nm pulsed dye Potassium titanyl phosphate (KTP, 532 nm) Q-switched Nd:YAG (532 nm) Q-switched ruby (694 nm) Q-switched alexandrite (755 nm) Q-switched Nd:YAG (1064 nm) Erbium:YAG (2940 nm) Pulsed or scanned carbon dioxide Q-switched Nd:YAG with topical suspesion Long pulsed ruby Long pulsed alexandrite Diode (800 nm) Long pulsed Nd:YAG Intense pulsed light

Risk of pigmentary changes þþ to þþþ þþ to þþþ þþ to þþþ þþ to þþþ þþ to þþþ þþþ þþ þþ to þþþ þþ to þþþ þþ to þþþ þþ to þþþ þþ to þþþ þþ þ þ to þþ þþþ þ þþ to þþþ þþ þ to þþ þ þþ

Note: þ, low; þþ, moderate; þþþ, high.

Recently, Goldman (11) has proposed a “Universal Classification of Skin Type” that considers genetic racial heritage in the response of melanocytes to both ultraviolet light and inflammation.

2.

CLINICAL APPLICATIONS

Laser use in dermatology has been expanding rapidly since the last decade. Medicine routinely uses “magic bullet” agents that seek their target selectively. Essentially every drug is an example. Drugs cause selective activation and inactivation of specific metabolic pathways. In surgery, lasers are the only example of “magic bullets.” On the basis of the principle of selective photothermolysis (12), pulsed selectively-absorbed lasers have transformed our ability to treat a variety of cutaneous conditions including vascular and pigmented lesions, tattoos, photoaged skin, scars, and unwanted hair. Current laser or light source systems can be classified according to the desired target of destruction (see Chapter 2). Similar to those clinical applications on white complexions, the indications of laser therapy in nonwhite skin include microvascular lesions, pigmented lesions, tattoos, scars, rhytides, and unwanted hair (13). The increase in epidermal melanin in nonwhite skin compared with that of white skin has been claimed to be a limiting factor for obtaining beneficial results in dermatological laser treatment.

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Table 36.2

Lancer Ethnicity Scale (LES)

LES skin type European LES type 3 LES type 1 LES type 2 LES type 1 LES type 1 – 2 LES type 3 – 4 North American LES type 3 Asian LES type 4 LES type 4 Latin/Central/South American LES type 4 African LES type 5 LES type 5 LES type 5 LES type 4

Fitzpatrick skin phototype

Type Type Type Type Type Type

II I III I– II I III

Background geography

Ashkenazy Jewish Celtic Central, Eastern European Nordic Northern European (general) Southern European, Mediterranean

Type II

Native American (including Inuit)

Type IV Type IV

Chinese, Korean, Japanese, Thai, Vietnamese Filipino, Polynesian

Type IV

Central, South American Indian

Type Type Type Type

Central, East, West African Eritrean and Ethiopian North African, Middle East Arabic Sephardic Jewish

V V V III

Note: The Lancer Ethnicity Scale (LES) is a system used to calculate healing efficacy and times. To calculate an individual’s skin type on the LES, find the LES skin type numbers for each of his or her four grandparents. Add the numbers together and divide this total by four. The lower the LES skin type, the better the skin healing after laser surgery and the lesser the risk of scarring, keloids, erythema, discoloration, and uneven pigmentation. Risk factors: LES type 1, very low risk; LES type 2, low risk; LES type 3, moderate risk; LES type 4, significant risk; LES type 5, considerable risk. Source: Modified from Lancer (9).

Patients with nonwhite skin are generally less responsive to treatment because of competition from epidermal melanin for the laser energy.

3.

MICROVASCULAR LESIONS

The indications for laser treatment of microvasular lesions in nonwhite skin are similar to white skin (Fig. 36.1). Oxyhemoglobin, with its major absorption peaks at 418, 542, and 577 nm, is the major chromophore in cutaneous microvessels (12). There are a variety of lasers and intense-pulsed light systems available, producing a spectrum of wavelengths that can be selectively absorbed by oxyhemoglobin. These include argon laser (AL) (488 and 514 nm), copper vapor laser (CVL) (511 and 578 nm), potassium titanyl phosphate (KTP) laser (532 nm), tunable dye lasers (577, 585, 590, 595, and 600 nm), neodynium: yttrium –aluminum – garnet laser (1064 nm) and intense pulsed light system (.515 nm). In nonwhite skin, melanin competes strongly for laser light absorption. Melanin has strong absorption in the 350– 1200 nm wavelength region, being strongest in the ultraviolet range, and decreasing exponentially through visible and into the near infrared wavelengths. In dark-skinned individuals the abundance of this chromophore in relation to


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Figure 36.1 (a) Nevus flammeus, before treatment. (b) After five PDL treatments using a fluence of 7 – 7.5 J/cm2 with a 5 mm diameter spot size at a treatment interval of 2 – 3 months. (Courtesy of K.B. Park, Seoul, Korea.)

oxyhemoglobin in cutaneous blood vessels acts as a total barrier to light from microvascular lasers and intense-pulsed light system (4). Epidermal melanin has been reported to be a main limitation to the final outcome after microvascular laser therapy in clinical (14,15) and histological studies (Fig. 36.2) (16,17). It has been demonstrated that more laser energy is required at the 577-nm (yellow) wavelength to produce the clinical threshold of purpura as skin pigmentation is increased (17,18). However, this morphologic endpoint was not clinically detected in a skin type V subject after irradiating the skin with an energy fluence of 2.75 J/cm2. In contrast, a mean fluence of 1 J/cm2 was sufficient to produce clinically detectable purpura on skin of type I

Figure 36.2 Hypopigmentation secondary to 585-nm PDL treatment (6 months after two treatments using a fluence of 7 J/cm2). (Courtesy of K.B. Park, Seoul, Korea.)

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subjects. Ultrastructural examination revealed the presence of degenerated keratinocytes and melanocytes in type V skin at fluences well below those required to produce clinical purpura even when the skin appeared clinically normal. Interestingly, selective vascular effects also occurred in skin type V at exposures insufficient to cause clinically detectable purpura. Therefore, it is apparent that vascular selectivity is no longer achieved at 577 nm in darker skin (type V) and that the treatment of vascular lesions using this wavelength will result in concurrent epidermal damage. Similarly, a study on the treatment of port-wine stains using a 585-nm flashlamppumped pulsed dye laser (PDL, SPTL-1; Candela Laser Corp., Wayland, MA) has shown that patients with skin types IV and V responded to treatment more slowly and required more treatment sessions to reach the same degree of clearing than patients with skin types I– III (19). In addition, patients with skin types IV – V had a higher overall percentage of none to poor, and slight responders than those of the skin types I and III group (30% vs. 16%). In contrast, when using the 585-nm PDL to treat facial telangiectasia, the same investigators found that skin type have no measurable influence on treatment response. The influence of preoperative skin pigmentation on side effects following treatment with CVL, AL, and 585-nm flashlamp-pumped PDL has been well documented (20 – 22). Studies have shown that the risk of inducing clinically visible pigmentary alterations and textural changes increases with higher preoperative skin pigmentation, and with the application of increasing laser energy. However, pigmentary alteration (hyper- and hypopigmentation) was found to occur at a significantly lower intensity level than scarring (texture change, atrophy, hypertrophy, and skin shrinkage). Darkly pigmented individuals obtained more severe wounding than fair-skinned subjects from AL and CVL treatment (14). In addition, the immediate histological outcome after these laser treatment has been found to depend on the pretreatment pigmentation content (17,18). Side effects after laser treatment of vascular malformations are theoretically due to three different mechanism, all of which result in nonspecific energy deposition: (a) direct and competitive absorption by epidermal melanin, (b) thermal diffusion away from the absorbing chromophores, primarily melanin and hemoglobin, and (c) scattering effects that indirectly increase epidermal and dermal nonspecific injury (4,21). Ashinoff and Geronemus (15) reported ineffective treatment of a port-wine stain in a black patient with a 585 nm PDL. Skin biopsy performed immediately following laser irradiation showed full-thickness necrosis of the epidermis. The ecstatic vessels appeared unaffected. Persistent hyperpigmentation without textural change, and no improvement in the treated area were noted at 8 months posttreatment. However, another study (22) following pigmentary changes after PDL treatment in black patients noted a gradual resolution of side effects. The 585 nm PDL has also been used as a treatment of choice for hypertrophic scars and keloids in fair-skinned individuals (23,24). The efficacy of the PDL in treatment of scars in darker-skinned patients remains variable. A study on the efficacy of the PDL performed in patients with skin phototypes I– VI demonstrated no improvement of the scars on the laser-treated sites compared with untreated control. In contrast, our recent study (25) noted clinical improvement of scars in skin types IV– VI patients following multiple treatment sessions with the PDL. We found the response rate to be lower, and the incidence of epidermal damage increased, when compared with fair-skinned patients (Fig. 36.3). Treatment of stretch marks is another application of the 585-nm PDL that improves the appearance of these lesions (26,27). An increase in dermal elastin noted following PDL treatment was speculated to be the mechanism of improvement. In contrast,


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Figure 36.3 (a) Linear hypertrophic scar of a patient with skin phototype VI; before treatment with a 585 nm PDL with a 5-mm diameter spot size; AI, treated with 3 J/cm2; AII, treated with 5 J/cm2; AIII, treated with 7 J/cm2; E, untreated control. (b) One week following the first PDL treatment; note epidermal necrosis over all laser-irradiated segments. (c) Four weeks following the second PDL treatment; note erythema and hypopigmentation on the laser treated areas. (d) Twelve weeks after the sixth treatment, note flattening of the scar without dyspigmentation.

several studies by other investigators noted no clinical improvement of striae (28,29) and no increase in dermal elastin content histologically (29). A study on the treatment of striae in skin types IV and VI patients has demonstrated no noticeably clinical improvement, with a higher risk of pigmentary alterations (29). In summary, treatment with hemoglobin-targeting lasers and intense-pulsed light systems in dark-skinned patients should be performed with great caution. To be effective, the starting energy density has to be higher than that used on fair Caucasian skin. However, the improvement following this procedure seems to be less effective and with a higher incidence of epidermal damage than those seen in white-skinned patients. The introduction of long-pulsed 1064 lasers with epidermal cooling has also allowed for the treatment of vascular lesions in darkly pigmented skin. We have found that telangiectasias, both on the face and the other body areas, can be successfully treated using a 1064-nm laser with a pulse duration of 25 ms, a 3.5-mm spot size and fluences between 200 and 250 J/cm2. This is usually given in combination with dynamic cooling where a 30-ms cooling spray is used coincident with the laser pulse

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Table 36.3

Protection Efficacy of Various Cooling Devices

Cooling system Ice cube Gel at room temperature Water and sapphire at 58C Water and glass at 58C Cryogenic spray (2308C, 30 ms burst)

Projected tolerable fluence increase for skin phototype II for 700 nm Add 5 – 10 J/cm2 Add 5 J/cm2 Add 10 – 15 J/cm2 Add 5 – 7 J/cm2 Add 10 – 15 J/cm2

Source: Modified from Ross et al. (121) and Dierickx et al. (118).

(Table 36.3). Utilizing these parameters, we have not found epidermal hypopigmentation to occur. As with the treatment of unwanted hair (as discussed later in this chapter), the 1064-nm long-pulsed laser with epidermal cooling has become the laser of choice for the treatment of darkly pigmented skin (11).

4.

PIGMENTED LESIONS

Selective destruction of melanosomes has been well demonstrated by exposing skin to submicrosecond, Q-switched, laser pulses (30,31). A wide range of these are available including a PDL (510 nm), Q-switched frequency-double Nd:YAG laser (532 and 1064 nm), Q-switched ruby laser (QSRL) (694 nm), and Q-switched alexandrite laser (QSAL) (755 nm). All of these Q-switched lasers are useful for treating superficial epidermal lesions such as lentigines and nevus spilus, and dermal pigmented lesions such as nevus of Ota, nevus of Ito, and congenital nevi (Figs. 36.4 and 36.5). Melanin absorption is stronger at shorter wavelengths, whereas longer wavelengths penetrate better into the skin (4). Several factors are involved in using Q-switched lasers for treating benign pigmented lesions in dark-complected individuals. First, the greater amount of epidermal melanin results in greater damage to lesional and adjacent normal skin pigment during laser irradiation. This increased absorption may lead to posttreatment hyperpigmentation (Fig. 36.6), hypopigmentation (Fig. 36.7), depigmentation, and even scarring. Second, larger amounts of epidermal melanin in persons with dark skin tones act as a competing chromophore for laser light while using these Q-switched lasers for treating

Figure 36.4 (a) Lentigines, before treatment. (b) After one treatment with 532-nm Q-switched Nd:YAG laser using a fluence of 2.5 J/cm2 with a 3 mm spot size.


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Figure 36.5 (a) Nevus of Ota pretreatment. (b) After five treatments with Q-switched Nd:YAG laser using an average fluence of 8 – 10 J/cm2 and a 3 mm spot size at treatment intervals of 3 –4 months. (Courtesy of K.B. Park, Seoul, Korea.)

dermal pigmented lesions. Thus, a larger number of sequential treatments are required for complete clearing compared to those of white-complected persons. In addition, the adverse effects resulting from injury to epidermal melanin and the melanocytes responsible for producing normal skin color should be anticipated.

5.

BENIGN EPIDERMAL PIGMENTED LESIONS

Benign epidermal pigmented lesions include lentigines, ephelides, nevus spilus, cafe´-aulait macules (CALMs), and seborrheic keratosis. In dark-skinned patients, these pigmented lesions have been successfully treated with the argon (488 and 515 nm), continuous wave (CW) laser (32), 510-nm short PDL (33), CVL (511 nm, CW) (34), the Q-switched frequency doubled Nd:YAG (532 nm) laser (35), QSRL (32,36 –38), QSAL (755 nm), and the low-fluence CO2 (10,600 nm, CW) laser (39). All of these lasers carry a small risk of depigmentation, hypopigmentation, and hyperpigmentation. However, when treating darkly pigmented skin, pulsed lasers with appropriate energy density provide a more

Figure 36.6 Postinflammatory hyperpigmentation following treatment of nevus of Ota with Q-switched ruby laser. (Courtesy of C. Vibhagool, Bangkok, Thailand.)

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Figure 36.7 (a) Nevus spilus, before treatment. (b) Hypopigmentation secondary to QSRL treatment using a fluence of 9 J/cm2 with a 5 mm spot size. (Courtesy of C. Vibhagool, Bangkok, Thailand.)

selective destruction with a lower incidence of hyperpigmentation and scarring as compared to CW lasers (40). The nonspecific injury to adjacent normal skin caused from CW lasers may result in “laser tanning” (also seen with subthreshold Q-switched laser pulses), which has been hypothesized to result from feedback inhibition of melanogenesis, stimulation of tyrosinase activity, and/or release of intracellular or extracellular melanocyte-stimulating factors. This phenomenon is independent of postinflammatory hyperpigmentation, which remains another effect of the nonspecific damage caused from CW laser energy. Alster and Williams (33) successfully treated a type V skin boy presenting with a CALM, with six 510-nm short PDL treatment at an energy fluence of 2.5 J/cm2, at 2-month intervals. Hypopigmentation or textural changes did not occur. No lesional recurrence was noted at a 2-year follow-up. The exact mechanism whereby this melanin-specific laser destroys lesional pigment without damaging normal skin pigment remains unknown. Repigmentation is most likely due to repopulation by melanocytes in adnexal structures. The injury induced by the 510 nm PDL causes pigmented keratinocyte and melanocyte necrosis. The epidermis sloughs off and is replaced with normal epidermis from adnexal structures. Treatment of CALMs with a CVL (511 nm) also provides favorable results in Thai patients (skin type V) (34). With a mean follow-up period of 22 months after 1 treatment, 9 of 16 (60%) patients achieved 90– 100% clearance, whereas the remainder of the 16 improved 40 –80%. Repigmentation to normal skin color was complete within 1 –2 months with slight hyperpigmentation at the periphery of the treated area, which responded favorable to topical hydroquinone. Transient hypopigmentation recovering after 2 –3 months was observed in most cases. A hypertrophic scar developed in 1 of the 16 patients in the study. In essence, CALMs variably respond to laser treatments and may recur within a few weeks and up to years after complete clearance. Retreatment often results in rapid clearing (40). Studies on treatment of CALMs with lasers in white (41,42) and Asian (38) populations demonstrated a similar variable degree of repigmentation following


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Figure 36.8 (a) Solar lentigines of a skin phototype V patient, before treatment. (b) After one treatment with a 510-nm PDL at a fluence of 2.25 J/cm2.

a long-term follow-up period of up to 50%. This variable behavior of treated lesions implies a subset of lesions with unique biologic behavior. Lentigines have shown excellent response to Q-switched Nd:YAG (QSYAG) (532 nm) laser (35,43), QSRL (694 nm, 40 ns) (36,38), QSAL, and low-fluence carbon dioxide (CO2 laser) (39) (Fig. 36.8). Our experience in treating dark-complected patients shows that the pulsed dye (510 nm) laser, QSYAG laser (532 nm, 5 – 10 ns), QSAL, and QSRL provide excellent results, usually with a single treatment. Transient hypopigmentation is the most common adverse effect of these lasers, whereas the QSYAG laser is associated with purpura and more erythema, secondary to its increased absorption by oxyhemoglobin. A low fluence CO2 laser has been successfully used to remove lentigines in fair-skinned patients without posttreatment hyper- and hypopigmentation (39). In contrast, when treating lentigines in our patients with pigmented complexion using the high energy, pulsed CO2 laser, long-term posttreatment hyperpigmentation is the most common adverse sequelae noted in as much as 50% of patients.

6.

MIXED EPIDERMAL AND DERMAL PIGMENTED LESIONS

Mixed epidermal and dermal lesions such as postinflammatory hyperpigmentation and melasma respond variably and unpredictably to Q-switched and resurfacing lasers (43 –45). In addition, most of the lesions tend to recur without ongoing topical bleaching medications.

7.

DERMAL PIGMENTED LESIONS

Nevus of Ota, a dendritic melanocytosis of the papillary and upper reticular dermis that involves the eye and surrounding skin innervated by the first and second branches of the trigeminal nerve, is a cosmetic problem commonly found in Asians but is also seen in blacks and whites. An incidence of 0.6% has been noted in the Japanese (46). Malignant degeneration has occasionally been reported (47,48). Studies in fair and dark-skinned populations have demonstrated that red (Q-switched ruby) (49–51), near infrared (Q-switched alexandrite) (52–54), and Q-switched Nd:YAG (43,54) lasers are very useful for treating nevus of Ota with fading over several months following each treatment session.

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The “threshold” radiant exposure response defined as immediate whitening of pigmented lesions after short pulse laser exposure is a useful clinical end point with any Q-switched laser, because the whitening correlates directly with melanosome rupture and pigment cell injury. Geronemus treated nevus of Ota in 15 patients of skin phototypes II – V with the QSRL and noted that this threshold response was based on the patients’ skin phototype. Asian patients (skin types IV and V) required slightly lower energy fluence of 7.5 – 8.5 J/cm2 to achieve immediate whitening compared with white and Hispanic patients (skin types II – IV) (8.5 –10 J/cm2). When treating nevus of Ota with Q-switched lasers, lightening of the lesion is noted after the first session with additional clinical improvement noted after every session. Multiple, sequential treatments appear to increase the response rate and may be required for complete clearing of the lesion. The response of nevus of Ota to Q-switched laser treatment also appears to depend on the color of the lesion. The maximum response rate is found in the brown color, and gradually decreases in the brown-violet, violetblue, and blue-green colors, respectively (51). When treating dark-complected patients, using a resurfacing CO2 or Er:YAG laser first to ablate the epidermis will eliminate competing epidermal melanin and melanocytes and remove the epidermis itself, thereby reducing scattering of the beam and physically placing it closer to the dermal target. Thus, a higher delivered energy fluence will impact on the target—dermal melanin. To improve the response rate of treating nevus of Ota, a study using a combination of scanned CO2 and QSRLs was performed (55). A significantly higher percentage of clearing was noted on the side treated with a combination of CO2 and QSRLs, compared with QSRL alone. As red (Q-switched ruby) and near-infrared (Q-switched alexandrite and Q-switched Nd:YAG) wavelengths can be selectively absorbed by dermal pigment, the use of these lasers in the treatment of other melanocytic process with dermal involvement including nevus of Ito (40), Becker’s nevus (56), nevus spilus (57), blue nevus (58), and congenital melanocytic nevus (59 – 62) may be effective (Fig. 36.9). The cafe´-au-lait background of nevus spilus and Becker’s nevus frequently recurs after treatment (40). The short pulsewidth and low energy fluence of these Q-switched lasers are probably not able to damage clusters or nests of nevomelanocytic components. The development of dermalpigment targeting lasers (63 –65) and intense-pulsed light systems (66) with long pulsewidths shows encouraging results on the treatment of these lesions.

Figure 36.9 (a) Congenital melanocytic nevus, before treatment. (b) After treatment with 510 PDL at 3 J/cm2 with a 5 mm diameter spot size followed by treatment with the QSAL at 7 J/cm2 with a 3-mm diameter spot size.


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Figure 36.10 (a) Tattoo removal in a patient with skin phototype V, preoperative. (b) Twelve weeks after two treatments with QSRL at a fluence of 8 – 10 J/cm2 with a 5-mm spot size, 8 weeks between each treatment session.

8.

TATTOO REMOVAL

In fair-skinned individuals Q-switched lasers have been proven effective in removing pigmented lesions and tattoos with minimal risk of adverse sequelae (67 – 70). Laser tattoo removal in darkly pigmented patients has often been presumed to have a greater risk of complication such as hypertrophic scar and keloid formation, and pigmentary alterations, as compared with fair-skinned patients. The efficacy of the Q-switched lasers on tattoo removal in dark-skinned patients is comparable to that of light-skinned patients. Studies on tattoo removal in dark-skinned patients (skin phototypes III–VI) with Q-switched lasers have shown favorable results without scarring or significantly permanent pigment changes (Figs. 36.10 and 36.11) (71–78). Grevelink et al. (73) determined the efficacy and side effects of Q-switched lasers on a small series of skin phototypes V and VI patients. The QSRL at 694 nm, with a pulse duration of 20 ns using a 5 mm spot size at an energy fluence ranging from 4.5 to 6.0 J/cm2, and the QS Nd:YAG laser at 1064 nm, with a pulse duration of 10 ns using a 3 mm spot size at an energy fluence ranging from 4.5 to 7.3 J/cm2 were used to treat four of five patients presenting with charcoal-injected tattoos on the face or neck, and one of five patients having a multicolor tattoo on the mid-chest region. Two of five patients

Figure 36.11 (a) Amateur tattoo of skin phototype VI patient, before laser treatment. (b) After three treatments with Q-switched Nd:YAG (1064 nm) laser at a fluence of 6 –7 J/cm2 with a 3-mm diameter spot size. Source: From Goldman et al. Cutaneous Laser Surgery, 2nd ed. St. Louis: Mosby, 1999.

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(40%) cleared by .90% after six treatments. Lesions of the other three patients were 50% and 60% cleared after four to eight treatments, respectively. A similar study on laser treatment of tattoos in skin phototype VI patients using a QSYAG laser demonstrated that after three to four treatments at 8-week intervals, 8 of 15 (53%) tattoos were 75– 95% cleared, 5 of 15 (33%) were 50%, and 2 of 15 (13%) were only 25% cleared (74). A study on lightskinned patients using a QSYAG laser for tattoo removal (72) demonstrated that in 77% of patients, lesions cleared by .75% in four treatments, and in 28% of patients, lesions cleared by .95% in four treatments. The QSAL (755 nm, 100 ns) has also been proven to be effective for removal of various traumatic tattoos in Asian (skin phototypes III – V) (77) and Spanish (skin phototypes III –IV) (78) skin. When treating patients with dark skin types, pigmentary changes are the most common encountered side effect. Scarring can occur but is very rare when appropriate laser energy (the energy that produces nonexplosive effects on the skin) is selected (71 –77). However, transient textural alterations associated with the healing response can occur during multiple treatments. The lack of clinical scarring noted with Q-switched lasers, even when epidermal damage is noted, is most likely due to the lack of thermal injury to collagen, as evidenced by the absence of histologic fibrosis in areas treated multiple times with both the QSRL and the QSYAG laser (71,72). Transient pigmentary changes including hypopigmentation and hyperpigmentation have been noted in the early healing phase but commonly resolved in 4 –6 weeks. As with treatment of all other pigmented lesions in pigmented races, the incidence of hypopigmentation appears to be a wavelength-dependent phenomenon. The shorter the wavelength, the greater the incidence of hypopigmentation. The incidence of hyperpigmentation is comparable between QSRL and QSYAG laser, which is mostly transient, and has been reported only in darker-skinned patients (skin phototypes II – V) (71,72). A dose – response study on the treatment of tattoos by QSRL noted hypopigmentation at all doses .1.5 J/cm2. This persistent hypopigmentation was apparent in 4 of 10 tattoos followed up 1 year after treatment (71). In contrast, hyperpigmentation was seen in only 1 of 13 skin phototype V patients. QSRL treatment typically results in blistering at the dermoepidermal junction (79), transient hypopigmentation and, less frequently, hyperpigmentation (Fig. 36.12) (80).

Figure 36.12 Blistering secondary to tattoo removal with QSRL in a skin phototype V patient using a fluence of 7 J/cm2 with a 5-mm spot size. (Courtesy of C. Vibhagool, Bangkok, Thailand.)


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As previously noted by others (71 – 74), we find that when treating tattoos in darkskinned persons, the QSRL commonly causes hypopigmentation, whereas the QSYAG laser at appropriate fluences has a lower incidence of hypopigmentation. At the wavelength of 1064 nm, the QSYAG laser light penetrates deeper and therefore might provide less injury to the unintentionally targeted melanosomes (3). We therefore agree with the recommendation of others (67,72,73) that the longer wavelength (1064 nm) QSYAG laser is preferable to the QSRL in the treatment of deeper dermal and blue/ black tattoo pigments in dark-skinned patients.

9.

SKIN RESURFACING

The use of pulsed or scanned carbon dioxide (CO2) lasers for skin resurfacing is a popular procedure for similar indications as dermabrasion and chemical peels. The same principles of thermal confinement used in selective photothermolysis also apply to minimizing the thermal injury from CO2 laser vaporization. In fair-skinned patients, the most common indication for skin resurfacing is to treat chronic sun-damage, wrinkles, traumatic scars, surgical scars, and acne scars. In nonwhite-skinned patients, acne scarring is the most common indication for this procedure. Unfortunately, the risk of prolonged or permanent dyspigmentation, especially postinflammatory hyperpigmentation parallels the degree of the patient’s constitutive skin color or pigment: the darker the color, the greater the potential (81,82). Postinflammatory hyperpigmentation, the most common complication seen following cutaneous CO2 laser resurfacing in nonwhite patients, usually develops around the first month after treatment (Fig. 36.13). An incidence of 25% was reported in a laser resurfacing study in Hispanic patients (skin phototypes II–V) (83). This is compared to a 3–7% incidence of hyperpigmentation after CO2 laser resurfacing in skin phototypes I–IV. In this study, hyperpigmentation occurred only in patients with skin phototypes III and IV (81,82). Although it is transient, the pigmentary alterations remain a major concern in resurfacing nonwhite skin (84). The incidence of postlaser hypopigmentation is higher after a longer follow-up period: 16% in an 8 month follow-up (81) and 19% in a 2 year follow-up study (82), and this seems to be a permanent complication. The incidence of hypertrophic scar and keloid is comparable to that of fair-skinned patients. These later complications are usually the results of poor technique, postoperative infection, or intrinsic patient factors. Studies on CO2 (83,85 –89) and Er:YAG (88,90 –94) laser resurfacing in nonwhite skin (skin phototypes III– V) have shown that these procedures can be performed effectively and safely when proper preoperative and postoperative management is implemented (Figs. 36.14 and 36.15). Pre- and postoperative treatment regimens are necessary to achieve optimum results and to reduce the incidence of postinflammatory hyperpigmentation (81,83,85,95,96). In addition to topical retinoic acid applied each night, patients with skin phototypes III –VI are given topical preparations of hydroquinone, kojic acid, azelaic acid, or vitamin C to be used for 1 – 2 months preoperatively. Although an arbitrary minimum preoperative treatment time of 2 weeks is often recommended, achieving maximum benefit requires months of use. The mechanism of action of each agent is summarized in Table 36.4. These agents are restarted as soon as possible postoperatively (2 –4 weeks). Reinstitution of these topical preparations too early may induce inflammation on the newly regenerated treated skin and should be avoided (84). Although we believe in its efficacy, the advantage of the preoperative treatment remains debatable. A study by West and Alster (97) noted no significant difference in the incidence of post-CO2 laser resurfacing hyperpigmentation between subjects who

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Figure 36.13 (a) Melesma, before two passes laser resurfacing with an UPCO2 laser delivered through a computerized pattern generator (CPG). The pulse energy for the first passes was 300 mJ at a setting pattern 3, size 9, density 6 (3-9-6) except for the periorbital area, where a setting of 5-9-5 was used. The pulse energy for the second pass was 200 mJ with a CPG setting of 3-9-5. (b) Three weeks after CO2 laser resurfacing. (c) Six weeks after treatment with topical hydroquinone, azelaic acid, and vitamin C together with a broad-spectrum sunscreen. (d) Ten months follow-up. Source: From Sriprachya-anunt et al. Lasers Surg Med 2002; 30:90.

received pretreatment with either topical glycolic acid cream or a combination tretinoin/ hydroquinone creams and those who received no pretreatment regimen. In our experience, postinflammatory hyperpigmentation may occur in spite of careful preoperative treatment. However, a recent survey of physician members of the American Society of Laser Medicine and Surgery found that 80% of 106 respondents pretreat skin resurfacing patients with tretinoin, whereas 69% prescribe hydroquinone, and 34% use glycolic acid cream (98). The application of broad-spectrum sunscreen and sun avoidance pre- and postoperatively are also necessary to minimize hyperpigmentation. The advantage of sun avoidance has been demonstrated in a study showing that preoperative and postoperative ultraviolet exposure on laser-treated skin resulted in a poor cosmetic appearance including textural change and hyperpigmentation (99).


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Figure 36.14 (a) Dermatosis papulosa nigra in a patient with skin phototype VI, before treatment. (b) After ultrapulse CO2 laser treatment at 300 mJ with a 2 mm diameter spot size and 0.1 s pulses. Multiple passes were given until the lesion was vaporized to normal skin. Usually each lesion was treated with three to four passes. After each pass/pulse, the epidermal char was wiped away with normal saline.

Despite the favorable results seen with CO2 resurfacing, the enthusiasm for these systems has been limited by the prolonged recovery time, the long-lasting erythema, and dyspigmentation (hypo- and hyperpigmentation). In 1996, the introduction of the Er:YAG laser represented an intriguing and exciting alternative to the pulsed and scanned CO2 resurfacing lasers. Er:YAG laser resurfacing requires a shorter, less painful recovery time, and fewer long-term adverse effects. In general, the recovery time and the incidence of adverse sequelae are proportional to the extent of tissue injury including the total anatomic depth of necrosis, ablation, and residual thermal damage (100 –102). A layer of residual thermal damage observed after a typical Er:YAG laser resurfacing procedure is ,50 mm vs. the 80 – 200 mm typically observed after multiple passes of pulsed CO2 laser resurfacing (101). Therefore, one advantage of Er:YAG laser over CO2 laser is that it appears to offer a higher margin of safety when treating patients with darker complexion (skin phototypes III and higher), because the resultant inflammatory reaction caused by less extensive thermal trauma stimulates less melanocytic activity (90). The incidence of transient hyperpigmentation following CO2 laser resurfacing ranges from 3% to 7% for all patients and nearly 100% among those with skin type IV and higher. Although postoperative hyperpigmentation and prolonged erythema seem to occur at roughly the same rate among patients with darker skin after Er:YAG laser resurfacing, it is often less severe and resolves more quickly compared with CO2 laser treatment (92). The Er:YAG laser therefore appears to be better suited for resurfacing of nonwhite skin. With equal energy fluence and number of passes, the Er:YAG laser produces less total depth of tissue necrosis and hence less effective treatment of deeper wrinkles. The greater immediate collagen contraction effect and the hemostasis property provided by the CO2 laser are the advantages of this laser resurfacing system over the Er:YAG laser. To combine the beneficial properties of these two systems, Goldman et al. (103) successfully developed a resurfacing technique using combined CO2 and Er:YAG lasers on the same treatment session. By using the Er:YAG laser to vaporize a portion of the layer of residual thermal damage created by the CO2 laser, one can achieve a better cosmetic response and get faster healing time, shorter duration of postlaser erythema and hence a decreased incidence of adverse sequelae. The favorable result of this combined

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Figure 36.15 (a) Adenoma sebaceum, pretreatment. (b) One month post 3 passes resurfacing with a CO2 laser coupled with a flashscanner operated at 16 W (on/off time: 0.2/0.4 s) using a 200 mm handpiece at repeat mode. (c) 6 months follow-up. (Courtesy of K.B. Park, Seoul, Korea.) Source: From Song et al. Dermatol Surg 1999; 25:971.

treatment method has also been confirmed by a study on treatment of atrophic scars in Korean patients with skin phototypes IV – V (104). In summary, laser resurfacing is effective in treating photo-damaged skin and acne scars in patients with skin phototypes III –V. However, it must be performed with great caution, together with proper preoperative and postoperative treatment regimens, and sun avoidance. A test patch may be used when considering skin resurfacing for this group of patients. However, this is not always a reliable predictor of postoperative complications.


10.

735

HAIR REMOVAL

The use of laser and pulsed light sources for hair removal is increasing because the treatment is relatively safe and effective in removing large areas of unwanted hair. Although it has been well documented that the ideal patients for this procedure are individuals with dark hair and fair-skin, unwanted or excessive hair is also a cosmetic concern for the darker-complected population. Most of the available laser and light systems with wavelengths in the red and nearinfrared regions have been designed to cause selective photothermal damage to pigmented hair follicles. Improved efficacy is accomplished by the high specificity and selectivity contributed by the accurate selection of an appropriate wavelength and pulse duration to maximize follicular damage and minimize unwanted injury to the epidermis. To target the follicle, these lasers and light sources either count on endogenous melanin within the follicular epithelium or hair shaft. When using light to target these endogenous chromophores, there is also risk of epidermal injury when laser light penetrates to the target. Melanin-containing structures including melanocytes, melanosome-containing keratinocytes, or nevus cells may also be thermally injured when irradiated by red and near-infrared lasers. Consequently, epidermal injury due to the absorption of laser energy by epidermal melanin may occur to a certain degree during the laser impacts. Most clinical studies on the efficacy of laser and intense-pulsed light systems in removing unwanted hair have been performed in fair-skinned individuals because it was theoretically postulated that a larger amount of epidermal melanin in nonwhite individuals may result in a decrease in clinical efficacy and cause an increase in the incidence of adverse effects; especially pigmentary and textural changes, and scarring (Fig. 36.16). Currently, several reports on these light-assisted hair removal systems performed on

Figure 36.16 Four months follow-up, postinflammatory hyperpigmentation after hair removal with a normal-mode ruby laser at a fluence of 20 J/cm2 with a 5-mm diameter spot size and no epidermal cooling.

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darker skin persons have shown comparable results to those of fair-skinned persons with a slightly increased risk of complications (105 – 117). It is difficult to compare the efficacy and side effects of light-assisted hair removal systems because of the variability in the treated anatomical sites and in the types, pulsewidths, spot sizes, and repetition rates of the light sources used, as well as differences in the treatment regimens. All laser and intense-pulsed light systems have been shown to temporarily remove hair. Reduction of hair growth occurs for all hair colors and at all fluences. Blonde, red, or white-haired individuals are unlikely to experience permanent hair reduction, but hair loss in these persons can be sustained by treatment at 3 month intervals (118). We note a similar response rate when treating Asian and black patients. Studies have demonstrated that in the ideal patients with fair skin and dark hair, the possibility for long-term hair removal after a single treatment is 80%. A critical threshold fluence is needed to obtain this result. This fluence is determined as the lowest fluence that can produce perifollicular swelling and erythema appearing a few minute after laser irradiation. If there is a sign of acute epidermal injury including whitening, blistering, or Nikolsky’s sign (forced epidermal separation), the fluence should be reduced. Generally, the treatment fluence should be at 75% of the Nikolsky’s threshold fluence (118). A 2 year follow-up study on the efficacy of normal-mode ruby laser hair removal notes that sites treated with highest fluence (60 J/cm2) obtained the greatest hair reduction (64.3%) (119). Epidermal injury is an anticipated consequence when treating a darker-complexioned patient. Whereas the goal of light-assisted hair removal is permanent follicular destruction, there is also a risk of epidermal damage during hair removal, especially in nonwhite individuals whose epidermis contains larger amounts of melanin. When treating this group of patients, in order to use the highest tolerable fluence to achieve a better hair reduction while minimizing epidermal damage, three important considerations including wavelength and pulse duration of the light sources and epidermal cooling methods should be taken into account. The first important determinant is wavelength of the light source. The ideal laser wavelength for hair removal is a wavelength that is preferentially absorbed by melanin but not by surrounding tissue. Lasers emitting longer wavelengths have the advantage of being able to penetrate deeper into the dermis, minimizing the possibility of absorptive interference by epidermal melanin (120). Color contrast between epidermis and the hair shaft (and bulb) is crucial in determining the optimal wavelength. For high contrast (dark hair, light skin), the low range of wavelength (650–700 nm) can be employed without risking serious injury to the epidermis (and subsequent hypo- and hyperpigmentation). For lighter hair and darker skin, longer wavelength (800 nm) should be applied (121). Studies in patients with skin phototypes III –V have shown that temporary hair reduction after treatment with normal-mode ruby (694 nm) laser (105–107,109,110,114), long-pulsed ruby (694 nm) laser (112,117), short- and long-pulsed alexandrite (755 nm) laser (108,111), diode (810 nm) laser (115,120), Q-switched- (112) and long-pulsed Nd:YAG (1064 nm) laser (122), and intense-pulsed light (116,123) hair removal systems were comparable to that in skin phototypes I– II. However, the incidence of undesirable side effects occurred more often compared with those noted in fair-skinned patients. Although most of these side effects including treatment pain, erythema, edema, blistering, crusting, erosion, purpura, folliculitis, and pigmentary changes (hypopigmentation and hyperpigmentation) were transient and self-limited, pigmentary alterations usually required longer to resolve (.3 months). In addition these side effects also often occurred on tanned skin, in patients with skin phototype III and higher, or on sites treated with excessively high energy fluences.


737

In our experience, when treating subjects with dark skin, the ruby laser system seemed to be associated with higher adverse effects, especially, transient hyper- and hypopigmentation. This results from the melanin interface of the 694 nm light pulse of the ruby lasers. However, the alexandrite, diode, and long-pulsed Nd: YAG lasers, and the intense pulsed light source, operating at longer wavelength and longer pulse widths, have been used to treat these patients safely when combined with cooling devices. Permanent pigmentary alterations and scarring were rare except in cases of over-aggressive treatment or postoperative infection. A retrospective study of the side effects of laser-assisted hair removal treatment in skin phototypes I–V found that the Q-switched Nd:YAG laser resulted in the fewest side effects, whereas the long-pulsed ruby and the long-pulsed alexandrite lasers produced equivalent adverse effects but greater than that of Q-switched Nd:YAG laser (112). Long-term adverse sequelae and scarring were not observed with any of the laser systems under study. As anticipated, lasers with longer wavelengths produce lesser adverse effects. A hair removal study using a long-pulsed Nd:YAG laser to treat patients with skin phototypes II–V noted no pigmentary or textural changes after treatment, even in skin phototype V patients (122). However, the disadvantage of the long-pulsed Nd:YAG hair removal system is that the absorption of this laser light by melanin is decreased compared with that of the ruby laser, such that absorption by the completing chromophore, oxyhemoglobin, is substantially increased. Although it caused fewest side effects, the Qswitched Nd:YAG system does not typically produce long-term hair reduction because of its very short pulse nature and use of low treatment energy fluences (124). Pulse duration of hair removal light sources is the second important parameter for effective hair removal without epidermal injury (125). A pulse duration of 10– 50 ms will damage hair follicles with less epidermal injury. However, caution should be exercised when using very long pulse widths to treat dense hair areas because of thermal conduction between closely adjacent hair follicles. The last important factor to be considered is epidermal cooling. Integrating surface cooling into the delivery configuration is one way to protect the epidermis and consequently prevent or minimize the adverse sequelae of the procedure. Presently, four types of cooling are used in conjunction with lasers and intense-pulsed light systems including (1) passive cooling with a chilled aqueous gel; (2) active cooling with water encased in a glass housing; (3) active conductive cooling with water encased in a sapphire window; (4) dynamic active cooling with a cryogenic spray; and (5) air cooling with a refrigerated air stream. These cooling configurations can provide epidermal preservation compared with no surface cooling (Table 36.3) (121,126). In conclusion, in nonwhite-skinned patients, laser- and pulsed light hair removal systems provide comparable clinical efficacy to that of white-skinned patients. Treatment parameters must be individualized for each patient and with each device. When performing this procedure in darker skin individuals, a range of test fluences should be performed in an inconspicuous area prior to performing complete treatment. A delay of at least 1 h should elapse prior to evaluation of test spots. In our practice, darker skin tones can be safely and effectively treated using a light source with a longer wavelength than that of ruby laser (.694 nm) with a pulse duration of 10 –50 ms and an adequate cooling device.

11.

PREVENTION AND MANAGEMENT OF COMPLICATIONS

Various attempts have been made to reduce the occurrence of side effects of laser treatment in nonwhite patients. They include sun avoidance, the use of preoperative and postoperative treatment regimens, and techniques for epidermal protection.

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12.


SUN AVOIDANCE

For patients with microvascular lesions, tanning may have the benefit of hiding their vascular lesions that appear less distinct, whereas in patients with pigmented skin lesions, ultraviolet (UV) irradiation may accentuate the appearance of the pigmentation. UV exposure prior to laser treatment has been shown to interfere with laser treatment by increasing epidermal melanin pigmentation and epidermal thickness leading to a change in the optical property of the skin (127). UV exposure may also interfere with the posttreatment healing process (13,128,129), alter the treatment outcome and occurrence of side effects. Moreover, laser exposure may influence the carcinogenic potential of UV radiation, which serves as a complete carcinogen, as both tumor initiation and promotion are induced by UV (130). In our practice, several recommendations to minimize the effects of UV light have been suggested. Most of the laser treatments are elective surgeries. Thus, the surgery may be performed on winter pale skin. The use of topical sunscreens, protecting both UVA and UVB usually zinc oxide based should be applied regularly at least 6 weeks prior to the treatment in order to obtain the most optimal outcome (131). Patients are also recommended not to visit tanning booths and not to go sunbathing, although the influence of acquired pigmentation compared with constitutional pigmentation for the development of adverse effects remains (87).

13.

PREOPERATIVE AND POSTOPERATIVE TREATMENT REGIMEN

Although the advantage of preoperative treatment regimens with various topical bleaching agents remains controversial, in current practice, we regularly pretreat our nonwhite patients with a minimal 2-week course of topical retinoic acid (132,133) each night combined with any of the following topical preparation including hydroquinone (134), kojic acid (135), azelaic acid (136), arbutin (137), licorice (138), or vitamin C (Table 36.4) (139). On the postoperative visit, these topical preparations are started as soon as possible (2 –4 weeks) depending on the individual healing response. However, we occasionally observe that postinflammatory hyperpigmentation occurred even with careful preoperative treatment, and this complication resolved spontaneously without using any topical preparations other than a broad-spectrum sunscreen and sun avoidance.

Table 36.4

Topical Preparations to Treat Postinflammatory Hyperpigmentation

Agent Alpha-hydroxy acids Arbutin Azelaic acid Beta-hydoxy acids Glucosamine Hydroquinone Kojic acid Tretinoin

Mechanism of action Promotes keratinocyte turnover Inhibits tyrosinase and melanin synthesis Inhibits tyrosinase and melanin synthesis Promotes keratinocyte turnover Inhibits tyrosinase and melanin synthesis Cytotoxic to melanocytes Inhibits tyrosinase and melanin synthesis Promotes melanosome transfer and keratinocyte turnover


14.

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EPIDERMAL COOLING

For treating pathology that is situated beneath either the epidermis or superficial dermis, it may often be necessary to use higher fluences in order to deliver sufficient photons to the intended target. This applies especially to laser surgery of nonwhite skin patients, in whom higher epidermal levels of melanin effectively decrease the number of photons reaching the dermis. Because scarring is related to the generation of excessive heat, which is greatest at or near the skin surface, methods that cool the superficial compartment of the skin should permit the safe use of higher fluences when necessary and minimize epidermal injury when it occurs (Fig. 36.17). When the epidermis and/or superficial dermis are selectively cooled either immediately before or during laser exposure, the peak temperature reached at these sites is insufficient to cause irreversible thermal damage. However, targets that are situated more deeply and that are therefore not cooled are able to reach the thermal threshold necessary for successful treatment. Lowering the temperature of the skin’s surfaces is therefore a method for selectively controlling the depth at which heat is produced in the skin by lasers or light sources. The effect of epidermal cooling has been shown to enhance clinical efficacy and minimize epidermal damage caused by the laser treatment process (112,118,140 –144). The increased efficacy is a consequence of an increase in the depth of penetration (145) and an allowance of higher energy fluence used (140). The depth to which skin cooling protects the skin from excessive superficial heat injury is largely determined by the temperature and contact time of the hand-piece or cryogen with the skin. An appropriate cooling time and technique permits heat extraction from the epidermis before, during, and after each laser pulse. Thus the epidermal can be minimized. In contrast, an overcooled epidermis may cool down the underneath target and hence result in a decrease in the desired clinical response. The commercial cooling methods/devices include passive cooling with aqueous gel, active cooling with water or refrigerated air, and dynamic active cooling with cryogen spray (Table 36.3). Most of these cooling devices have been used in conjunction with vascular lasers, intense pulsed light systems, and laser hair removal. In a less technically sophisticated manner, we find that precooling and postcooling of the skin with ice can also be performed. This method, like water cooling at 08C with a glass window, will decrease the dermal–epidermal junction temperature depending on application time. However, because it is done manually, the

Figure 36.17 (a) Immediate reaction after a 595-nm pulsed dye laser irradiation at a fluence of 10 J/cm2 and pulse duration of 20, 30, and 40 ms, with and without epidermal cooling using dynamic cooling device (DCD); note the degree of epidermal injury on the areas treated with epidermal cooling. (b) Twenty-four hours after laser irradiation.

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efficacy of this method may be unpredictable (studies comparing cooling systems suggest that DCDs are the most effective/efficient followed by glass/water and finally cold gel or ice).

15.

SUMMARY

The majority of laser treatment in nonwhite skin can be performed effectively. However, this treatment must be approached with caution. Careful preoperative and postoperative treatment programs should be used as well as a prudent selection of types of lasers suited to a patient’s treatment purposes. Lasers with longer wavelengths and longer pulse durations cause a lower risk of pigmentary alterations. Epidermal cooling is a useful method to minimize undesirable epidermal damage. Finally, when treating a nonwhite individual with any laser, a conservative approach is best.

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Anderson KE, Maibach HI. Black and white human skin differences. J Am Acad Dermatol 1979; 1:276 – 382. Berardesca E, Maibach HI. Racial differences in skin pathophysiology. J Am Acad Dermatol 1996; 34:667 – 672. Anderson RR. Laser-Tissue Interactions. Vol. 1. 2nd ed. St. Louis: Mosby, 1999. Anderson RR, Parrish JA. The optics of human skin. J Invest Dermatol 1981; 77:13– 19. Jimbow K, Quevedo WC, Prota G, Fitzpatrick TB. Biology of Melanocytes. Vol. 1. 5th ed. New York: McGraw-Hill, 1999. Olson RL, Gaylor J, Everett MA. Skin color, melanin, and erythema. Arch Dermatol 1973; 108:541 – 544. McCurdy JA. Cosmetic Surgery of the Asians Face. Thieme Medical, 1990. Fitzpatrick TB. The validity and practicality of sun reactive skin type I through VI. Arch Dermatol 1988; 124:869 Lancer HA. Lancer Ethnicity Scale (LES) [letter]. Lasers Surg Med 1998; 22:9. Wolbarsht ML, Urbach F. The Lancer Ethnicity Scale [letter]. Lasers Surg Med 1999; 25:105 – 106. Goldman MP. Universal classification of skin type. Cosmetic Dermatol 2002; 15:53– 57. Anderson RR, Parrish JA. Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science 1983; 220:524 – 527. Anderson RR. Laser medicine in dermatology. J Dermatol 1996; 23:778 – 782. Haedersdal M, Wulf HC. Pigmentation dependent, short time skin reactions to copper vapour laser and argon laser treatment. Burns 1994; 20:195 – 199. Ashinoff R, Geronemus RG. Treatment of a port-wine stain in a black patient with the pulsed dye laser. J Dermatol Surg Oncol 1992; 18:147 – 148. Tan OT, Carney JM, Margolis R et al. Histologic responses of port-wine stains treated by argon, carbon dioxide, and tunable dye lasers. A preliminary report. Arch Dermatol 1986; 122:1016 – 1022. Tong AKF, Tan OT, Boll J, Parrish JA, Murphy GF. Ultrastructure: effect of melanin pigment on target specificity using a pulsed dye laser (577 nm). J Invest Dermatol 1987; 88:747 – 752. Tan OT, Kerschmann R, Parrish JA. The effect of epidermal pigmentation on selective vascular effects of pulsed laser. Lasers Surg Med 1986; 4:365 – 374. Fitzpatrick RE, Lowe NJ, Goldman MP, Borden H, Behr KL, Ruiz-Esparza J. Flashlamppumped pulsed dye laser treatment of port-wine stains. J Dermatol Surg Oncol 1994; 20:743 – 748. Haedersdal M, Wulf HC. Pigmentation-dependent side effects to copper vapor laser and argon laser treatment. Lasers Surg Med 1995; 16:351– 358.

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Section IV: Considerations in the Practice of Laser Surgery

37 Legal Considerations in Laser Surgery David J. Goldberg Mount Sinai School of Medicine, New York, New York; New Jersey Medical School, Newark, New Jersey; and Fordham University School of Law, New York, New York, USA

1. Scenario I 2. Scenario II 3. Scenario III 4. Scenario IV 5. Scenario V References

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Laser surgery has evolved from a field with a primary medical orientation to one that is increasingly geared toward the cosmetic patient. Although legal considerations can arise in the performance of any medical procedure, they are increasingly seen in the field of cutaneous laser surgery because of the large numbers of physicians performing cosmetic laser surgery. A full textbook on health care law would be required to adequately cover all the legal aspects as they relate to cutaneous laser surgery. This chapter will therefore deal with only the most common interaction between cutaneous laser physicians and health care law—that of negligence. The first part of the chapter will discuss the elements of negligence and the evolution of a medical malpractice cause of action following cutaneous laser surgery. The second part of the chapter will describe various hypothetical laser surgical complications and the likelihood of a successful malpractice case evolving from such a postoperative complication. Any analysis of physician negligence must first begin with a legal description of the elements of negligence. There are four required elements for a cause of action in negligence. They are duty, breach of duty, causation, and damages. The suing plaintiff must show the presence of all four elements to be successful in her claim (1). The duty of a physician performing cutaneous laser surgery is to perform that cutaneous laser procedure in accordance with the standard of care. Although the elements of a cause of action in negligence are derived from formal legal textbooks, the standard of care is not necessarily derived from some well-known textbook. It is also not articulated by any judge. The standard of care is defined by some, as whatever an expert witness says it 749

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is, and what a jury will believe. In a case against any cutaneous laser surgeon, the specialist must have the knowledge and skill ordinarily possessed by a specialist in that field, and have used the care and skill ordinarily possessed by a specialist in that field in the same or similar locality under similar circumstances. A dermatologist, a plastic surgeon, or an internist performing cutaneous laser surgery will all be held to an equal standard. A failure to fulfill such a duty may lead to loss of a lawsuit by the physician. If the jury accepts the suggestion that the surgeon mismanaged the case and that the negligence led to problem to the patient, then the physician will be liable. Conversely, if the jury believes an expert who testifies for the defendant doctor, then the standard of care in that particular case has been met. In this view, the standard of care is a pragmatic concept decided case-by case on the basis of the testimony of an expert physician. The cutaneous laser surgeon is expected to perform a laser procedure in a manner of a reasonable physician. He need not be the best in his field, he need only perform the procedure in a manner that is considered by an objective standard as reasonable. It is important to note that where there are two or more recognized methods of diagnosing or treating the same condition, a physician does not fall below the standard of care by using any of the acceptable methods even if one method turns out to be less effective than another method. Finally, in many jurisdictions, an unfavorable result due to an “error in judgment” by a physician is not in and of itself a violation of the standard of care if the physician acted appropriately prior to exercising his professional judgment. Evidence of the standard of care in a specific malpractice case includes laws, regulations, and guidelines for practice, which represent a consensus among professionals on a topic involving diagnosis or treatment, and the medical literature including peer-reviewed articles and authoritative texts. In addition, obviously, the view of an expert is crucial. Although the standard of care may vary from state to state, it is typically defined as a national standard by the profession at large. Most commonly for litigation purposes, expert witnesses articulate the standard of care. The basis of the expert witness, and therefore the origin of the standard of care, is grounded in the following: 1. 2. 3. 4. 5.

The witness’ personal practice and/or the practice of others that he has observed in his experience and/or medical literature in recognized publications and/or statutes and/or legislative rules and/or courses where the subject is discussed and taught in a well-defined manner.

The standard of care is the way in which the majority of the physicians in a similar medical community would practice. If, in fact, the expert herself does not practice like the majority of other physicians, then the expert will have a difficult time explaining why the majority of the medical community does not practice according to her ways. It would seem then that in the perfect world, the standard of care in every case would be a clearly definable level of care agreed on by all physicians and patients. Unfortunately, in the typical situation, the standard of care is an ephemeral concept resulting from differences and inconsistencies among the medical profession, the legal system, and the public. At one polar extreme, the medical profession is dominant in determining the standard of care in the practice of medicine. In such a situation, recommendations, guidelines, and policies regarding varying treatment modalities for different clinical situations published by nationally recognized boards, societies, and commissions establish the appropriate standard of care. Even in some of these cases, however, factual disputes may arise because more than one such organization will publish conflicting standards concerning

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the same medical condition. Adding to the confusion, local societies may publish their own rules applicable to a particular claim of malpractice. Thus, in most situations, the standard of care is neither clearly definable nor consistently defined. It is a legal fiction to suggest that a generally accepted standard of care exists for any area of practice. At best, there are parameters within which experts will testify. Unfortunately, owing to the increased reliance on laser technology by the cutaneous laser surgeon and unrealistic expectations by the public, physicians may sometimes run the risk of being held to an unrealistic and unattainable standard of care. But, in the end, it is the physician community that establishes that standard of care. American physicians have in recent years put forth substantial efforts toward standard setting, specifying treatment approaches to various conditions. Clinical practice guidelines have been developed by specialty societies such as the American Academy of Dermatology (2). The Institute of Medicine has defined such clinical guidelines as “systemically developed statements to assist practitioner and patient decisions about appropriate health care for specific clinical circumstances.” Such guidelines represent standardized specifications for performing a procedure or managing a particular clinical problem. Clinical guidelines raise thorny legal issues (3). They have the potential to offer an authoritative and settled statement of what the standard of care should be for a given cutaneous laser treatable condition. A court would have several options when such guidelines are offered as evidence. Such a guideline might be evidence of the customary practice in the medical profession. A doctor acting in accordance with the guidelines would be shielded from liability to the same extent as one who can establish that she or he followed professional customs. The guidelines could play the role of an authoritative expert witness or a well-accepted review article. Using guidelines as evidence of professional custom, however, is problematic if they are ahead of prevailing medical practice. Clinical guidelines have already had an effect on settlement, according to surveys of malpractice lawyers. A widely accepted clinical standard may be presumptive evidence of due care, but expert testimony will still be required to introduce the standard and establish its sources and its relevancy. Professional societies often attach disclaimers to their guidelines, thereby undercutting their defensive use in litigation. The American Medical Association, for example, calls its guidelines “parameters” instead of protocols intended to significantly impact on physician discretion. The AMA further suggests that all such guidelines contain disclaimers stating that they are not intended to displace physician discretion. Such guidelines, in such a situation, could not be treated as conclusive. Plaintiffs usually will use their own expert, as opposed to the physician’s expert, to define the standard of care. Although such a plaintiff’s expert may also refer to clinical practice guidelines, the physician’s negligence can be established in other manners as well. These methods include (1) examination of the physician defendant’s expert witness, (2) an admission by the defendant that he or she was negligent, (3) testimony by the plaintiff, in a rare case where she is a medical expert qualified to evaluate the allegedly negligent physician’s conduct, and (4) common knowledge in situations where a layperson could understand the negligence without the assistance of an expert (4,5). Some laser centers are located within either hospitals or certified ambulatory care centers. In such situations, a plaintiff may seek hospital committee proceeding minutes about the allegedly negligent physician. The plaintiff may request production of a committee’s minutes or reports, set forth “interrogatories” about the committee process and/or outcome, or seek to depose committee members about committee discussions. If the plaintiff is suing the cutaneous laser surgeon, whose work was reviewed by the committee, the discovery process may seek to confirm the negligence of the professional or to uncover

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additional evidence substantiating the plaintiff’s claims. Such “discovery” requests are often met with a claim that information that is generated within or by a hospital committee is not discoverable. Courts have ruled that the discovery protection granted to hospital quality review committee records prevents the opposing party from taking advantage of a hospital’s careful self-assessment (6). The suing plaintiff must utilize his or her own experts to evaluate the facts underlying the incident. It is felt, by the courts, that such immunity of committee proceedings protects certain communications and encourages the quality review process. External access to committee investigations, it is argued, stifles candor and inhibits constructive criticism felt to be necessary for a quality review process. Constructive, objective peer criticism might not occur in an atmosphere of apprehension that one doctor’s suggestion will be used as a denunciation of a colleague’s conduct in a malpractice suit. When a plaintiff seeks discovery of a facility or hospital incident report, rather than a committee proceeding, policy considerations are somewhat different. Incident reports kept in the medical records, and possibly filed by a staff member, are often more directly related to a single claim for malpractice than would general committee investigations. Courts are usually less willing to protect such incident reports. Because the field of cutaneous laser surgery has evolved rapidly over the past decade, physicians are quick to try new innovations and experimental concepts. Such innovations partially explain the excitement of this growing field. New laser surgical procedures and the treatment of conditions that were heretofore-untreatable (i.e., Port-wine stains and Nevus of Ota) may fall into a regulatory gap not covered by the strict regulations for the laser device itself. Licensing through the Food and Drug Administration carefully regulates medical devices such as lasers (7). Most human experimentation is governed by regulations of the Department of Health and Human Services. The regulations require that an institution sponsoring research must establish an institutional review board. Such an organization will evaluate research proposals before any experimentation begins to determine whether human subjects might be “at risk” and if so, how to protect them. It is not usually difficult to determine whether a new laser is being used experimentally. It is, however, very difficult to determine whether an actual given laser procedure is experimental. Laser surgeons often view themselves as artists in addition to scientists, custom tailoring a treatment for a particular condition. Such approaches can lead to a bad result with variable outcomes in the courts. A laser surgeon who chooses to use a carbon dioxide laser, rather than a scalpel, to perform a circumcision procedure, with a resultant complication leading to penile amputation would have problems suggesting that her medical experimentation conformed to reasonable standard of care. However, another surgeon who chooses, after appropriate informed consent, to use the same laser, rather than a scalpel, for excision of a nevus, with resultant significant scarring might be considered an innovator rather than an experimenter. Such a physician would be no more liable for straying from his duty than the surgeon who might use a standard scalpel, with the same complication, for the same procedure. In fact, most clinical innovations fall between standard practice and experimental research. Much of this innovation is unregulated by the government. The National Commission for the Protection of Human Subjects of Biomedical and Behavioral Research has suggested that any “radically new” procedure should be made the object of formal research at an early stage in order to determine whether such a procedure is safe and effective. It could be argued that some of the cutaneous laser procedures that have evolved, using already FDA cleared laser devices, might be considered radical; most clearly are not. It is clear then that in order for the plaintiff to win her negligence cause of action against the cutaneous laser surgeon, she must establish that her physician had a duty of


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reasonable care in treating her and had in fact breached that duty. However, that breach must also lead to some form of damages. A mere inconvenience to the plaintiff, even in the setting of a physician’s breach, will usually not lead to physician liability in a cause of action for negligence. It is often difficult to predict, in any given malpractice cause of action what the ultimate outcome will. The following teaching hypotheticals are designed to be suggestive of potential malpractice cases and the likely results. Any connection between these scenarios and actual malpractice cases is fortuitous.

1.

SCENARIO I

JH is a 48-year-old woman with Class I rhytids and extensive solar telangiectases. She has used a variety of antirosecea medications and has undergone three sessions of electrocautrey for treatment of her telangiectases. These treatment modalities have led to minimal clinical improvement. Her niece had seen a local otolaryngologist (Dr. Nose) for a rhinoplasty procedure and was extremely happy with the cosmetic results. Because of this physician’s expertise in cosmetic surgery, and her niece’s recommendation, JH sought cosmetic treatment from this physician. Dr. Nose, 1 month prior to seeing JH, spent a weekend learning “laser skin resurfacing.” It is his understanding that carbon dioxide lasers seal small blood vessels while leading to skin rejuvenation. He correctly assumes that this laser will thermally destroy many of the telangiectases on the face of JH. Dr. Nose discusses with JH associated risks of cutaneous laser resurfacing, such as scarring and postinflammatory pigmentary changes following the procedure. The physician chooses to rent a laser from a local rental company. This company also rents lasers such as KTP lasers, Q-switched lasers, and “hair removal” lasers. As Dr. Nose has only learned to use the carbon dioxide laser, he chooses to treat his patient with this laser. The full-face procedure is undertaken without any difficulty. Because of the extensive thermal wound, JH is required to stay in her house for 10 days following the procedure. This is not terribly difficult for her as she has a home-based job and need not leave her house on a daily basis. The telangiectases respond nicely to treatment. Unfortunately, the postresurfacing erythema lasts for .6 months. JH had marital difficulties before the laser surgery. Her husband was never supportive of her undergoing the procedure. Because of the prolonged erythema, JH is reluctant to leave her house. This reclusive behavior represents the final strain to her marriage. Her husband leaves her and ultimately files for divorce. Soon thereafter JH finds out that her telangiectases could have been treated with a KTP laser without any significant ablative wound. There would also have been no delayed erythema following the laser procedure. JH files a lawsuit against Dr. Nose. She claims negligence in his use of the carbon dioxide laser to treat her telangiecatases. Did Dr. Nose breach the standard of care? If so, will he be liable for negligence? Dr. Nose has a duty of care to JH. His duty is not more or not less than that of any dermatologist or plastic surgeon performing the identical procedure. His limited weekend training will not be an adequate defense. His lack of knowledge about KTP lasers will also support his choice of a carbon dioxide laser to treat his patient’s telangiectases. Thus, it would appear that he breached his duty of care. He chose to use a laser that is not ideal for the treatment of telangiectases. Is he then liable? His liability would result only if the breach caused “damages.” JH will be hardpressed to prove that her already failing marriage and resultant divorce represented damages caused by Dr. Nose’s inappropriate use of the carbon dioxide laser in the

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treatment of telangiectases. She is not likely to win the case even though Dr. Nose chose an inappropriate laser to treat his patient. 2.

SCENARIO II

Dr. Doc is a well-known dermatologist with .5 years of experience using a variety of lasers. For the last 2 years, he has been performing laser hair removal with millisecond visible and near infrared lasers and light sources. He has seen success with a variety of systems and has used these systems with a variety of cooling gels, cryogen sprays, and sapphire tipped cooling systems. He evaluates a Fitzpatrick Type IV complected individual (PC) with dark hair. He explains to her that the ideal laser hair removal patient is a dark haired – light skinned individual. Because of her complexion, and the potential risk of laser-induced postinflammatory pigmentary changes, Dr. Doc uses a lesser fluence and slightly longer pulse duration in treating her. He also uses a very cold gel on her skin prior to treatment. It is his understanding that such an approach is safer in darker complected individuals. He also provides PC with a laundry list of general risks such as postlaser scarring and textural changes. She is treated three times over the course of 9 months without difficulty. Unfortunately, 2 months after a fourth session, a hypertrophic scar develops at the site of an upper lip herpes simplex infection that appeared to be activated 1 week after a laser hair removal session. PC had not had a herpetic outbreak in 30 years and, when asked about such proclivity prior to the first laser procedure, she denied any history of herpes simplex infections. PC learns from a friend that most cutaneous laser surgeons provide their cutaneous laser-resurfacing patients with a course of oral antiviral agents—even if they provide no personal history of herpes simplex infections. She reasons, and her attorney agrees, that the same logic should apply to other laser procedures of the skin. Is Dr. Doc liable? It is clear that there is permanent damage to JH. If these damages resulted from the laser procedure, Dr. Doc might be liable. However, unfortunately for JH, it will be hard to prove that Dr. Doc breached the standard of care. Just because physicians routinely provide their resurfacing patients oral antiviral agents does not mean that such medications are required following all laser procedures. The fact that PC denied a history of oral herpes simplex would only bolster Dr. Doc’s defense. 3.

SCENARIO III

Dr. Good is a well-trained cutaneous laser surgeon. In fact, she not only learned to use lasers during her residency training, but also undertook a 1 year laser fellowship in 1993. In 1995, she began to perform cosmetic cutaneous laser resurfacing for photodamaged skin. In her patient handouts, she describes the benefits of carbon dioxide laser resurfacing as compared to deeper peeling agents. One advantage, she suggests, is the lack of obvious phenol-induced delayed hypopigmentation seen with these deeper peels. Dr. Good provides a consent form for his patients and does mention the risk of scarring and temporary pigmentary changes following the laser procedure. In 1996, she performs full-face carbon dioxide laser resurfacing on a 55-year-old Fitzpatrick Type II, Class III rhytid individual. The patient, BB, follows all the appropriate wound care instructions and returns to Dr. Good’s office three times during the 6 months after her laserresurfacing procedure. Both doctor and patient are thrilled with the results and the patient is discharged. Unfortunately, 1 year after the procedure, BB begins to notice significant loss of perioral pigmentation. This problem progressively worsens over the


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next year. BB can no longer go out of the house without makeup and is devastated. Soon thereafter, reports begin to appear in the medical literature about the possibility of delayed post-carbon dioxide laser-induced hypopigmentation. BB brings suit against Dr. Good. BB’s attorney produces Dr. Good’s promotional materials suggesting the safety of this procedure, the consent form that makes no mention of delayed permanent hypopigmentation, and copies of the recent journal articles documenting this problem. Will Dr. Good lose in this negligence cause of action? It would seem that she breached her duty by not mentioning the risk of permanent postlaser-induced hypopigmentation. Certainly, the alleged breach of her duty is the cause of the permanent damage to BB’s face. However, Dr. Good can correctly defend her actions by stating that at the time of the incident the standard of care was not to warn about delayed carbon dioxide laser-induced permanent hypopigmentation. Dr. Good cannot be held responsible for laser-induced complications that were not known, nor described, at the time of the laser procedure. 4.

SCENARIO IV

Dr. Laser is well experienced in Erbium:YAG laser resurfacing. He uses this laser for superficial resurfacing; all his patients re-epithelialize in 5– 7 days. He routinely places his patients on 1 week of oral antiviral therapy. Recently, Dr. Laser has become disenchanted with this laser’s efficacy in the treatment of deeper Class III rhytids. He begins to rent a carbon dioxide laser for his more severely rhytid patients. He continues to give these patients 1 week of oral antiviral treatment despite the fact that re-epithelialization usually takes 10 days in these patients. SG represents one such Class III rhytid patient. Dr. Laser performs the carbon dioxide laser procedure, provides a 7 day oral antiviral treatment to his patient, and sees her in the office at day 3 following the laser procedure. At day 3, SG appears to be doing well and Dr. Laser advises her to return 3 weeks after the procedure. At the 3 week follow-up visit, she is well healed except for four erosive areas on her lip and upper forehead. Dr. Laser reassures her and suggests that she continue to use moist dressings. Two weeks later, the erosions are still not healed and SG seeks evaluation by an expert in the field. This new physician performs a viral culture and determines that she has a herpes simplex infection. He re-treats her with antiviral therapy. She eventually heals but is left with hypertrophic scarring. She files a negligence cause of action against Dr. Laser for performing a procedure that led to her scars. She admits that she signed a consent form that warned her about the risks of laser-induced scarring. When challenged in court about the positive herpes simplex infection, Dr. Laser responds by reminding the jury that he did use 7 days worth of antiviral treatment in his patient, something he traditionally did in his Erbium:YAG laser-treated patients. Unfortunately, for Dr. Laser, he is likely to lose his case. It will be argued by SG’s expert that it is not the use of antiviral agents that defines the standard of care after laser resurfacing. Instead, he will contend the standard of care dictates that antiviral agents be used until full re-epithelialization has occurred. Dr. Laser’s duty was not to simply provide his patient with antiviral agents; his duty was to provide such agents for the full 10 days of re-epithelialization. The breach in this duty lead to the scars on the face of his patient. Dr. Laser may be found culpable in a negligence malpractice cause of action. 5.

SCENARIO V

Dr. James, a well-known and respected dermatologist, purchased an old carbon dioxide laser from his medical school roommate, a colon-rectal surgeon in the local community.

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Dr. James undertook extensive training in carbon dioxide laser resurfacing and had a good knowledge of facial anatomy, wound healing, and the use of several good pulsed char-free carbon dioxide lasers. His laser, purchased at a bargain basement price, was a continuous wave carbon dioxide laser. Dr. James performed 20 full-face laser-resurfacing procedures with this machine. All of his patients were happy with the results. When challenged at a recent meeting about the use of such a continuous wave laser for resurfacing, Dr. James responded by suggesting that he was an expert at this technique. In addition, he noted that before the use of pulsed resurfacing lasers, some physicians used such continuous lasers for facial resurfacing. Recently, Dr. James treated his 21st patient, a 55-year-old woman with Class II rhytids and photodamage. The technique was performed in an identical manner to that of the previous procedures. Unfortunately, his patient had a protracted course of healing with resultant significant hypertrophic scarring. The scarred plaintiff brought a lawsuit alleging malpractice by Dr. James. The plaintiff’s expert, a well-respected cosmetic surgeon, testified that Dr. James’ use of a continuous wave, non-pulsed carbon dioxide laser represented a deviation in the standard of care. The expert contended that a reasonable medical practitioner would not use a continuous wave laser for cosmetic laser resurfacing. Dr. James, testifying on his own behalf, set forth numerous manuscripts from 20 years ago, that such lasers could be used for such procedures. He contended that such papers proved that his practice was in accordance with the standard of care, even if such a technique was not used by most. Dr. James’ argument that he is performing within the standard of care is a fallacious one. It may be true that laser resurfacing, with a continuous wave laser, was the standard of care at the time the provided medical literature was written. However, it is uniformly accepted that the standard of care, timewise, is defined at the time a procedure is performed. Dr. James cannot claim that his procedure is in accordance within the standard of care, at the time of the procedure, simply because he may have complied with the standard established many years before the actual performance of the procedure. The scarring produced by the continuous wave laser may very well represent a breach of the standard of care. He is likely to lose in this negligence cause of action. Cutaneous laser surgery involves the use of exciting ever-changing technology. Physicians are increasingly learning to perform a variety of laser procedures. Because such new technology is ever changing, it is important that physicians be aware of their duty of reasonable care. Should they breach that duty, they may be found liable in a medical malpractice cause of action. REFERENCES 1. 2.

3. 4. 5. 6. 7.

Furrow BF, Greaney TL, Johnson SH, Jost TS, Schwartz RL. Liability in Health Care Law. 3rd ed. St. Paul, MN: West Publishing Co., 1997. Joint American Academy of Dermatology/American Society of Dermatologic Surgery Liaison Committee. Current issues in dermatologic office-based surgery. J Am Acad Dermatol 1999; 40:624 – 634. Hyams AL, Shapiro DW, Brennan TA. Medical Practice Guidelines in Malpractice Litigation: An Early Retrospective, 21 J. Health Pol., Pol’cy & Law 289 (1996) Lamont v. Brookwood Health Service, Inc., 446 So.2d 1018 (Ala.1983) Gannon v. Elliot, 19 Cal.App.4th 1 (1993) Coburn v. Seda, 101 Wash.2d 270 (1984) Federal Food, Drug, and Cosmetic Act, 21 U.S.C.A. s301.

38 Establishing a Laser Unit Elizabeth I. McBurney Louisiana State University School of Medicine, Tulane University School of Medicine, New Orleans, Louisiana, USA

1. Introduction 2. Equipment 2.1. Lasers 2.2. Ancillary Laser Equipment 2.2.1. Smoke Evacuation Systems 2.2.2. Ocular Protection 2.2.3. Surgical Instruments 2.2.4. Surgical Masks, Face Shields 2.2.5. Drapes 2.2.6. Warning Sign on Door 3. Laser Procedure Room 3.1. Size of Room 3.2. Table, Trays, Lights 3.3. Electrical, Water, Ventilation 3.4. Controlled Access 3.5. Fire Fighting and Emergency Equipment 3.6. Recovery Area 4. Documentation 4.1. History and Physical 4.2. Operative Report 5. Photography and Computer Imaging 5.1. Photography 5.2. Computer Imaging 6. Accreditation 7. Physician Credentialing 8. Education and Training 9. Quality Control Management and Improvement 9.1. Standards 9.2. Laser Safety Officer 9.3. OSHA 9.4. Procedural Control Measures

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9.5. Safety Program Monitoring 9.6. Quality Improvement Program 10. Laser Economics 10.1. Cost 10.2. Charges 10.3. Reimbursement 11. Malpractice Insurance 12. Marketing References

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INTRODUCTION

Developing and maintaining a laser surgical unit in a small clinic or office can be a challenging and fulfilling endeavor for both physician and staff. There are several reasons to consider such a project. The physician may want to learn a new skill to offer “state of the art” care and therapeutics to current patients and to attract new patients. Cutaneous laser surgery performed in the office can be quite cost-effective by having less overhead expenses for both physician and patients. Having an office-based laser unit allows the physician direct control and responsibility of the equipment and the staff. 2. 2.1.

EQUIPMENT Lasers

When embarking on a laser-based practice, it is important first to conduct an evaluation of the type of lesions one will be treating with the laser. Careful consideration must be given to several factors including the physician’s surgical experience and ability, referral network, economic realities, and community needs (Table 38.1). One of the primary decisions regarding laser systems is determining whether the equipment should be purchased or rented. The acquisition of the laser can be made through outright purchase, lease purchase, or rentals through a national company. Initially, it may be wise to rent a laser that is available through a company. As the volume of laser surgery cases increases, consideration can be given to leasing or Table 38.1

Laser Procurement Factors

Indications Cost Purchase, lease, or rent Reliability Site specifications Reputation of vendor Portability Warranty Service contract Service availability FDA approval Sufficient energy, spot size, pulse duration, scanner

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purchasing. Advantage of 1 day rental includes access to the newest laser technology without a major capital investment or maintenance contracts. On the other hand, there is no daily or immediate availability. It is advisable to rent a laser if it has low reliability, high maintenance costs, or a significant likelihood of soon becoming obsolete. The criteria for a purchased laser should be a reliable system that has multiple treatment indications and would be used frequently. Ideally, a purchased laser should be portable from one room or office to another. The advantage of purchasing is that the equipment is always available in the office for use by the physician. With laser equipment purchase, there is a drawback that the office must bear the cost and responsibility of maintenance. It is absolutely essential that warranty coverage, subsequent maintenance service contracts, and the cost of such contracts be clearly defined and documented by the vendor. Prior to procurement of a laser system, the physician should evaluate several vendors, warranties and maintenance, service, and whether replacement lasers are made available during times that the laser is being repaired or serviced. Other factors to be considered are the delivery time, recommendations of previous purchasers, and FDA approval of the laser equipment. The physician should request a specification sheet, including on site preparation information, from the manufacturer before purchasing any laser. A single recommendation for the initial purchase of a particular laser will not fit all practices so the physician must determine which laser is best for one’s particular office. Before the laser purchase, the physician should ask the vendor to bring the laser into the facility and allow the physician to perform several laser cases. This will ensure that the equipment will be satisfactory with sufficient energy thus averting a potentially costly mistake. To lease purchase, a laser requires the same diligence and research. The advantages are that no major up-front capital outlay is necessary and the full lease payment can be deducted in full for tax purposes. At the end of the lease, there is usually a buy-out option.

2.2.

Ancillary Laser Equipment

2.2.1. Smoke Evacuation Systems Smoke evacuation systems vary in performance, features, and configurations (1). When selecting a system, primary considerations should be given to good performance with minimal noise and panels that indicate when filters should be changed. The unit should provide sufficient power to filter down to 0.1 mm particles for all procedures which generate a plume (2 –4). Smoke evacuation systems should pull 50 cubic ft/min (i.e., air flow for suction) and should have a captive velocity of 100– 150 ft/min at the inlet nozzle (5). All filters should be cleaned, monitored, and replaced regularly and disposed of properly as biohazard us material (5). Currently, there are no federal regulations for the standard use of smoke evacuator systems. At present, the closest thing to the regulation of surgical smoke in the US is the Occupational Safety and Health Administration (OSHA) regulation of staff exposure to a number of substances commonly found within surgical smoke including benzene, formaldehyde, and hydrogen cyanide. Several organizations recommend that smoke evacuation systems be used during laser surgery, these include American National Standards Institute (ANSI), Association of Operating Room Nurses (AORN), and National Institute for Occupational Safety and Health (NIOSH) (6). Removal of laser smoke plume and its odor provides for a better work environment. According to the NIOSH, laser-generated airborne contaminants contain trace

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hydrocarbons including acetone, isopropanol, toluene, formaldehyde, and cyanide (1). Smoke plumes can cause respiratory irritation and are potentially mutagenic and carcinogenic. Removal of the smoke plume reduces inhalation hazards present during laser surgery. Smoke evacuation systems should be used by health care providers as the first line of protection against occupational exposure to laser-generated airborne contaminants (4,5,7) (Fig. 38.1). Free-standing smoke evacuation systems are more effective in removing laser-generated airborne contaminants than wall suction systems. 2.2.2.

Ocular Protection

Ocular protection is essential equipment for all persons present in the laser operating suite. It can be quite expensive costing up to several hundred dollars per pair of goggles or glasses. The goggles are wavelength specific and are not interchangeable with different types of lasers. When several different lasers are used in the same operating room, great caution must be taken that the correct protective eyewear is used. It is vital to ensure that the wavelength and optical density are appropriate for the laser being used. This information is stamped on the arm or faceplate of the safety goggles. An optimal optical density of six or more will attenuate laser light transmission to a safe level. Higher optical densities offer more protection but reduced visibility (8) (Fig. 38.2). With the protection provided, safety glasses and goggles can at times seem a mixed blessing, especially for the anesthesiologist. This is because the tint of the laser eyewear can make it very difficult to see the oximeter gauges and almost impossible to see the red light diodes (LED) readouts. Therefore, extra consideration should be given to purchasing beam-specific lenses that will not limit ambient light or, using monitoring equipment with backlit displays that are easier to read, through tinted safety glasses (8).

Figure 38.1 Protective eyewear, surgical masks, and smoke evacuation system in use by all present in procedure room during a laser procedure.


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Figure 38.2 Wavelength specific ocular protective glasses. Note wavelength and optical density printed on front (figure courtesy of Uvex Safety, Smithfield, RI).

When laser surgery is being performed in the periorbital area, eye goggles must be replaced with laser protective intraocular or scleral eye shields. There are several types available in multiple sizes. These should be stainless steel with nonreflective surfaces. These eye shields are reasonably priced, durable, and low maintenance instruments. 2.2.3. Surgical Instruments Instruments should be anodized, dulled, nonreflective, or have a matte finish. These types of instruments will result in the diffusion or dispersion of incident laser beams and prevent specular reflection of laser light. Such nonreflective instruments will minimize the possibility that a reflected stray beam will cause a burn or fire as it ricochets (8). 2.2.4.

Surgical Masks, Face Shields

At present, there are no surgical masks capable of filtering out all laser-generated plume particles, bacteria, viruses, or other irritants. It is recommended that ultra-high filtration masks that filter out particles up to 0.1 mm in diameter. High-filtration material works only while dry. During a lengthy laser case, the mask may become moist from breathing, defeating the purpose of the surgical mask. Surgical masks are not designed to provide protection from plume contents. Surgical masks are intended to protect the patient from the surgeon’s contaminated nasal or oral droplets. Therefore, appropriate local exhaust ventilation techniques are the first line of protection against laser-generated airborne contaminants (7). Face shields should be used whenever laser surgical activities could result in splattering or spraying (1) (Fig. 38.3). The Q-switched lasers are noted for generation of tissue particulates. 2.2.5.

Drapes

Fire retardant drapes or moist surgical cloth towels are used during all laser procedures. It should be remembered that nonflammable surgical drapes can melt when heated (3). They will not produce a flame but can cause severe burns when over heated. The cloth towels can be reused after cleaning.

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Figure 38.3

Full face shield protects against tissue splashing.

2.2.6. Warning Sign on Door During periods of laser use, ANSI recommends a notice sign be placed conspicuously outside a laser control area to warn those who may enter the operating suite (7). These warning signs are available from the laser manufacturer.

3. 3.1.

LASER PROCEDURE ROOM Size of Room

The actual size of the room must be sufficient to accommodate the surgical table, mayo stand, smoke evacuation equipment, laser(s), patient, and personnel. The minimum size for a procedure room not using general anesthesia is 12 12 ft (9). The surgical table, mayo stand, and lighting used are basically the same as those used in any standard minor surgery room. However, the number of reflective surfaces should be kept to a minimum and all flammable chemicals and materials should be removed. Ideally, there should be no windows in the laser surgical office. If windows are present, protective measures, such as drapes or shades, should be in place to prevent stray laser radiation from leaving the room.

3.2.

Table, Trays, Lights

The most important placement in the surgical suite is the operating table. It should be positioned in such a way that one can easily pass completely around the table. Ideally, all the rest of the equipment is mobile or placed on a mayo stand allowing it to be moved into position when needed. Fixed equipment decreases access to use (9). The laser equipment should be positioned to fire away from the entrance door.


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Electrical, Water, Ventilation

It is essential that the proper electrical connections and water supply be available for the laser. This will need to be carefully ascertained prior to purchase or rental of the laser. New electrical equipment may need to be installed with certain laser units such as a pulsed dye laser. Many lasers generate considerable heat and require additional ventilation or air-conditioning.

3.4.

Controlled Access

All laser suites should be designated a nominal hazard zone and have controlled access. This can be in the form of locks on the doors or laser safety signs placed in plain view on the door when the laser is in use (10). Wavelength specific goggles should be hung next to the laser safety sign outside the room ready for immediate use by anyone entering the room (Fig. 38.4).

3.5.

Fire Fighting and Emergency Equipment

All laser procedure rooms should contain appropriate fire fighting equipment such as fire extinguishers and fire blankets. Fire extinguishers must be approved by the Underwriter’s Laboratory and should be inspected and tagged regularly. Smoking should be prohibited in the procedure room (11,12). Emergency equipment (EE) should be well organized and ready to use. It should include oxygen, IV access equipment, a full range of emergency medicines, a stethoscope, and a blood pressure cuff (9,13).

3.6.

Recovery Area

A small recovery area needs to designated where the patient can rest immediately after a procedure, if necessary (14). The patient can be observed and receive postoperative instructions. Family and/or friends can join the patient in the recovery area.

Figure 38.4 Warning sign notifying personnel that laser is being used and appropriate protective eyewear is needed before entering room.

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DOCUMENTATION

Documentation is important to record patient care and for ongoing quality management and improvement. Written documentation in regard to the patient includes history and pertinent physical examination, informed consents for the laser procedure and photography, operative procedure report, and summary of wound care instructions (9). 4.1.

History and Physical

A patient’s medical history should be taken regardless of the type of anesthesia planned as well as when no anesthesia is given. The history should include documentation of indications and symptoms warranting the laser procedure, a list of current medications, any known allergies, and existing significant medical conditions. Mental status of the patient also should be assessed and documented. The extent of documentation required in the physical exam is reflective of the type of anesthesia planned or given. For no anesthesia, topical, local, or regional anesthesia, the examination may be specific to the procedure proposed to be performed and co-morbid conditions (11). For IV sedation type of anesthesia, additional assessment of cardiovascular and respiratory symptoms by auscultation should be performed. Vital signs of blood pressure, pulse, respiration, and temperature should be taken and recorded prior to surgery (15). For general, spinal, and epidural anesthesia, all of the items above should be performed but additionally there should also be an assessment and written statement about the patient’s general condition. Laboratory, electrocardiogram, and X-rays that are necessary and relevant to the patient’s health status for the procedure being performed should be completely recorded and available at the time of surgery. Informed consent should be obtained on all patients receiving cutaneous laser surgery. The procedure, explanation of the procedure, its risks, and alternative therapeutic options should be reviewed carefully with the patient. This will allow time for the physician to get to know the patient and identify a patient who may not be satisfied with the results provided by laser surgery. Informed consent is best obtained with a witness present. The contents of the informed consent are dependent on local or state regulations and the guidelines of the facility where the procedure is being performed (15). In addition, consent forms for photography should be designed and available for the patient to sign prior to surgery. 4.2.

Operative Report

An operative report should be recorded for each cutaneous laser surgery procedure. The operative report must convey the important information in a brief standard form. Specific points included in each report can make preparation easy (9). An outline of an operative report should include: 1. 2. 3. 4. 5. 6. 7.

Patient’s name. Date of birth or chart identification number. Date of operation. Preoperative diagnosis. Postoperative diagnosis. Operative procedure performed. Anesthesia—including type and name of anesthetist or anesthesiologist (if applicable).


8. 9. 10. 11. 12.

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Surgeon. Assistants. History and indications for the procedure. Informed consent discussed and signed. Procedure in detail. The type of skin preparation, drapes, eye protection, masks, smoke evacuation system used are recorded. It should include accurate laser parameters such as energy, fluency, spot size, pulse duration, and specific wavelength. When used, scanner settings should also be recorded. Narrative of the procedure, complications, estimated blood loss if appropriate, specimen disposition, if appropriate, wound care, condition of patient at conclusion of the procedure, follow up arrangements, and discharge should be recorded.

Written instructions for patient understanding of wound care are essential. Postoperative care contributes as much as, if not more than, the actual laser procedure to attaining good results. Patients often do not remember detailed verbal instructions so that written postoperative care instructions should be provided to each patient. Ideally, this should be reviewed in the presence of a friend or family member. When anesthesia has been used, these instructions should be reviewed with the patient prior to the surgery. Specific instructions for follow up and information and phone numbers for patients to call with questions should be provided to minimize confusion (9). Good records are essential for maintaining high medical care, memorialization of events, and ongoing quality evaluation. The ultimate standard and final word is the written record.

5. 5.1.

PHOTOGRAPHY AND COMPUTER IMAGING Photography

Medical photography is necessary for accurate record-keeping (9). Photographic documentation of presurgical appearance, progress of multiple laser treatments received over time, and final results may be important to the patient, insurance company, third party payors, and for medical/legal records. Prospective patients often request to see photographs of expected results or potential complications and having one’s surgical photographic log available is helpful. The quality of photographs desired will determine the type of equipment selected. Photographs for insurance purposes, litigation, and/or records need to show clear details. High-quality medical photographs are required for photographic case logs or illustrations for publications (9). Prints from instant cameras are adequate for record keeping alone. Thirty five millimeter cameras with appropriate lenses are most often used. Digital cameras are rapidly replacing the standard 35 mm cameras, as clarity and definition are refined.

5.2.

Computer Imaging

Managing patient’s expectations before laser surgery can greatly improve patient satisfaction after surgery. Computer software imaging provides the surgeon with an invaluable communication tool to show the patient realistic results expected. Several companies provide computer imaging software programs to evaluate patients. These types of programs require specific computer equipment and a digital camera to be easily used in the office. The cost of imaging software is considerable, so before purchase, the buyer should contact program users and compare vendors, service availability, and ease of use.

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ACCREDITATION

Accreditation is the voluntary process through which an office facility or organization is able to measure the quality of its service and performance against nationally recognized standards (11). Surgical centers can seek accreditation through several avenues. The American Osteopathic Association (AOA) and the Joint Commission on Accreditation of Health Care Organizations (JCAHO) both accredit a broad spectrum of health care organizations (11,16). The Accreditation Association for Ambulatory Health Care (AAAHC), however, specializes in the accreditation of ambulatory surgery facilities. It is a private, nonprofit organization founded in 1979 to assist ambulatory health care organizations in improving the quality of care they provide to patients. It achieves this by setting standards, measuring performance, providing consultation and education when needed, and ultimately granting accreditation to those organizations that are found to be in compliance with its standards (11). Surveys are scheduled with representatives of AAAHC. There are several advantages to seeking accreditation. Risk managed healthcare organizations, health insurance, and other third parties are strongly encouraging or even mandating the facilities with whom they do business to be accredited. Accreditation may allow the facility to receive Medicare and/or third-party reimbursement for services performed in addition to physician charges. Medicare grants reimbursement for approved services only to those facilities that have successfully attained accreditation through Medicare certification or the AOA’s, JCAHO’s, or AAAHC’s deemed status survey accreditation program (16). Continuous quality improvement (CQI) is another benefit of accreditation through ongoing self-evaluation. By stressing the facility’s strengths and pointing out areas in need of further improvement, data base CQI allows the organization to look at itself in a more critical manner (16). A displayed certificate of accreditation signals to the public, patients, and other health care professionals what the surgery has center’s accomplished. A facility that continues to be successful in maintaining the standards of care highlights the achievements of the organization and demonstrates a desire to deliver quality health care. Public recognition of this visible sign of quality care can serve as an appropriate marketing tool. Insurance companies would have at least one obvious criteria for determining payment. Capital lending bodies can rely on this benchmark of organizational stability. Medical malpractice costs may be reduced through improved risk management, peer review, and consultation (17). The disadvantage of accreditation is real but not discouraging. The cost of improving the facility to meet national standards of care can be significant. For instance, an office may need to make changes in the physical layout of the facility such as modifying doors, walls, and emergency exits. The office also may have to hire additional professionals to adequately staff the accredited facility. Other costs the facility will incur are consultants to prepare for the surgery, the accreditation process application fees, fees for manuals and on-site surveys. Depending on the organization from whom the accreditation is sought, these fees can be several thousand dollars. The accreditation process can require considerable staff time to prepare for the survey. It may also be a stressful period of time for the personnel of the facility. With some facilities, it may take more than 1 year to meet the standards and properly complete the paperwork before an onsite evaluation can occur. Another potential disadvantage of accreditation is the diligence and responsibility required to maintain the standards of care. Once awarded accreditation, the facility must be dedicated to maintaining these standards on an ongoing basis.


7.

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PHYSICIAN CREDENTIALING

In general, the physician should have completed medical training in an appropriate specialty residency such as dermatology which provides training in cutaneous surgery, cutaneous anatomy, and basic factors regarding skin wound healing. There should be a general knowledge of basic laser physics, laser tissue interaction, and laser safety. For specific training, the physician should have laser surgery training in residency or attendance at an appropriate laser course which includes hands-on experience or equipment hands-on experience conducted under the supervision of a skilled laser surgeon (18). Currently, there are no federal or state regulations to mandate physician laser credentialing, but there are ANSI guidelines to assist with developing credentialing policies. The physician should review pertinent literature and audiovisual aids and attend training courses devoted to the teaching of laser principles and safety (7). The courses should include basic laser physics, tissue interaction, hands-on workshop, and discussions related to the use of lasers in the operator’s specialty. ANSI recommends a minimum of 16 h to be completed, depending on the technical skills involved. Following this education, a preceptorship with an experienced laser surgeon in the specialty should be carried out. A preceptorship may consist of several brief periods or a prolonged stay with a minimum of 8– 16 h of observation and hands-on time. This training and experience should be recorded according to the specific wavelengths. In lieu of this training, the physician may have had appropriate laser surgery training in an accredited residency program documented with a letter from the program director (7). Basic cardiac life support certification is recommended. In facilities where intravenous sedation or analgesic drugs and/or general anesthesia are administered, physicians and staff should be trained in advanced cardiac life support.

8.

EDUCATION AND TRAINING

Education and training are essential for everyone using or working with medical lasers (class IIIB –IV) including laser safety officers (LSOs), physicians, technicians, nurses, and all perioperative team members. Each facility or private practice is responsible for establishing its own criteria for this education but it may consult the appendices of ANSI, Z136.3 as well as recognized professional organizations for recommendations and guidance (7,18 – 20). Nursing and assistance staff educations should incorporate didactic and practical sessions. They should emphasize perioperative safety and patient management. According to ANSI, Z136.3, laser safety training for perioperative nursing and support personnel must be comparable with that taught to physicians (7). Continuing education for all staff is recommended. Participation in these educational activities should be documented in each personnel file and indicate new skills acquired as well as number of hours spent in maintaining proficiency (21). A smoothly functioning laser operative team depends on education and training of all members. This will ensure excellent, high-quality patient care and safety for all. Physicians can employ nurses, technicians, physician assistants, or other health care workers to perform minor laser procedures such as hair removal. Each state has different regulations regarding nonphysician use of lasers. Some states only allow physicians to operate lasers whereas others have no regulations or restrictions whatsoever.

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QUALITY CONTROL MANAGEMENT AND IMPROVEMENT

Quality control management and improvement requires establishment and knowledge of standards, identification of hazards risks, problems or concerns with patient care, implementation of appropriate control measures, and consistent program management. Identification of knowledge of deviations gained via quality assessment and improvement process is used to initiate change and corrective actions (22,23). 9.1.

Standards

ANSI is a nonregulatory body that provides thousands of safety standards in the US. The main objective of ANSI is to establish and maintain benchmarks for national safety through consensus documents (7). ANSI Z136.3 publication is the accepted standard for laser safety and health care. It is not regulatory but is used by OSHA and accreditation organizations such as JCAHO. The standard provides a comprehensive guide for development of administrative and procedural control measures necessary for maintenance of a safe laser environment and should be used as the ultimate guide for all clinical laser facilities (7,22). In addition to ANSI Z136.3, a copy of ANSI A136.1 entitled “American National Standard for the Safe Use of Lasers” should be obtained and reviewed (24). This material covers all laser safety issues. 9.2.

Laser Safety Officer

The person responsible for maintenance of laser safety is the LSO. The standard for the safe use of lasers in health care facilities (ANSI A136.3) defines the laser safety office in Section 1.3, as follows: “The laser safety officer (LSO) is an individual with the training, self-study, and experience to administer a laser safety program. This individual (who is appointed by the administration) is authorized and is responsible for monitoring and overseeing the control of laser hazards. The LSO shall affect a knowledgeable evaluation and control of laser hazards by utilizing, when necessary, the most appropriate clinical and technical support staff and other resources” (7). The LSO is the contact person for the laser unit should there be evaluation by accrediting body, an OSHA compliance inspection, or a medical legal situation. There is only one LSO and the person must be available during all uses and must be responsible for safety, regardless of who is operating the system. In a small practice, the physician appears to be the likely candidate for the LSO. In a larger clinic with multiple laser operators, it is often wise to appoint a permanent office professional such as a nurse or a physician’s assistant. There are no strict rules as to who may serve as a LSO, only that the identified person be appropriately trained and empowered to establish procedures and to enforce compliance. A new section of ANSI Z136.3 standards (1.4, the small medical clinic) describes in detail what the private laser user is responsible for: 1. 2. 3. 4. 5.

Safety requirements are no less stringent in private practice than in a hospital. Individual laser users must know all professional standards and regulations and must be thoroughly trained in laser safety. The user must insure that the entire staff is properly trained. There must be an appointed LSO. The user must establish and follow standard-based policies and procedures. A periodic review program is in effect and includes review of adequacy of


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safety protocols for the laser, vacuums, power meters, and procedure manuals for laser use and safety that are available in the facility (7,22). 9.3.

OSHA

Compliance with OSHA is a vital part of laser safety programs. There are no specific OSHA guidelines for assessing a facilities level of compliance but ANSI Z136.3 is used as the benchmark (3,22). OSHA offers responses to requests, complaints, and incident reports. Facilities must demonstrate that they have established policies and procedures, provided personal protective equipment, implemented employee education programs of all employees who may be at risk for exposure to laser hazards, and have documented complete periodic safety audits, ongoing administrative control, and program surveillance. Several states have regulations for the installation, regulation, and operation of medical laser systems in health care facilities. The LSO must check with the State Board of Health for local requirements.

9.4.

Procedural Control Measures

Procedural control manuals for laser use and safety must be available in the facility. Procedure controls must be established for controlled access, ocular hazards, flammability hazards, management of airborne contaminants, electrical hazards, and reflective hazards (14,22). Excellent examples of standard operation procedures are published in ANSI Z136.3 (7). Periodic review programs should be in effect including medical emergency plans, availability and currency of emergency medical supplies, power failure protocol, fire protocol, adequacy of sterilization, and proper functioning of all monitoring equipment (12).

9.5.

Safety Program Monitoring

Safety audits are the measure for regular monitoring. ANSI standards require an audit at least once a year. A laser safety audit must be supervised by the LSO. There are four audit components (22): 1. 2. 3. 4.

Equipment inventory and develop a checklist, Inspect every item on the checklist, Document results, and Identifications based on the audit reports.

Inventory equipment lists should include lasers, laser unit, keys, and instructions, signs, protective eyewear, window barriers, smoke evacuation system, operation manuals, policy and procedure manuals. Audits should also include calibration and output testing which can be delegated to biomedical engineering or to the manufacturer’s laser technician.

9.6.

Quality Improvement Program

At least two physicians are involved in quality improvement activities in order to provide peer-based review. This is ongoing monitoring, development and application of criteria used to evaluate care, evaluation of data, measures implemented to resolve problems, revaluation to determine whether corrective measures are successful. An active integrated

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peer-based quality improvement program is the basis to have continuous improvement of quality care.

10.

LASER ECONOMICS

The three most important elements in measuring the economic status of a laser program are costs, charges, and reimbursement (14). Charges and reimbursements must exceed cost to maintain a laser unit on solid financial ground. 10.1.

Cost

The actual cost of a laser procedure must be calculated before the evaluation of adequacy of charges and reimbursement can be determined. The direct cost of the laser procedure can be estimated by dividing the purchase price of the laser by the total number of anticipated cases (14,25). Cost per procedure ¼ cost of laser=anticipated laser cases per year Cost per procedure ¼ annual laser lease=anticipated laser cases per year Other ancillary costs must also be calculated to portray an accurate financial analysis including service and maintenance contracts, dye replacement, laser fibers, smoke evacuation system, drapes and masks, and special instruments. Staffing, marketing, administrative expenses must also be included in the cost analysis. All this information is used to ascertain the correct cost of each laser procedure. Cost of procedure ¼ cost of laser=anticipated laser cases per year þ annual ancillary costs=anticipated laser cases per year 10.2.

Charges

When a laser program is established, the physician must decide the charge for the laser services. There are three ways to develop a laser charge: a fee per laser use, a fee for time interval, or a fee that is incorporated into the procedure charge (14). 10.3.

Reimbursement

Physician reimbursement is based on the current procedural technology (CPT) codes which are recognized by third-party payers and Medicare (20). There are some CPT codes which are laser specific, there are destructive codes which have been expanded to include lasers as well as a therapeutic modality (Table 38.2). Many laser procedures, such as resurfacing for facial rejuvenation, are not considered medically necessary and require direct patient payment. In recent years, the physical destruction codes (17000, 17003, 17004, 46924, 54065, 56501, 56515) were expanded to include laser as a destruction modality. Many laser procedures, such as resurfacing for rhytides, are not considered medically necessary and require direct patient payment. For patients with red or brown birthmarks, traumatic scars or tattoos, or benign tumors, such as angiofibromas, the physician may have to write a letter of medical necessity for laser treatment to obtain preauthorization. It is often useful to send an accompanying photograph and copies of recent, related medical articles. Facility reimbursement for

Establishing a Laser Unit Table 38.2

Destructive Codes were Expanded to Include Lasers as a Therapeutic Modality

17000 –17003 –17004 17106 –17108

15780 15781 40500 46917 46924 54065 54057 56501 57061 –57065

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Destruction, benign or premalignant lesions, by any method, including laser Destruction of cutaneous vascular proliferative lesions (e.g., laser technique) 17106 ¼ ,10 cm2 17107 ¼ 10.0 2 50.0 cm2 17108 ¼ .50.0 cm2 Dermabrasion, total face (e.g., for acne scarring, fine wrinkling, rhytides, general skin keratosis) Dermabrasion, segmental, face Vermilionectomy for actinic cheilitis (with 22 modifier) Destruction of lesion(s), anus (e.g., condyloma, papilloma, molluscum contagiosum, herpetic vesicle), simple; laser surgery. Destruction of lesions of anus, any method Destruction of lesions of penis, any method Destruction of lesion(s), penis (e.g., condyloma, papilloma, molluscum contagiosum, herpetic vesicle), simple; laser surgery Destruction of lesions of vulva, any method Destruction of vaginal lesions, any method

outpatient procedures is variable. Being an accredited facility with deemed Medicare status or approval by a state agency allows for facility reimbursement on covered procedures. The staff and patient must be informed prior to the laser surgery of the financial payment arrangements. For self-pay cosmetic procedures, payments before the procedure may be appropriate.

11.

MALPRACTICE INSURANCE

Whenever the decision is made to establish a laser unit, the primary physician should contact their malpractice insurance carrier. There could be additional premium fees. In addition, if a nonphysician will be performing laser surgery, it should be confirmed that appropriate malpractice insurance will be in effect.

Table 38.3

Options or Techniques for Enhancing Public Awareness and Education

Word of mouth Information brochures in waiting room Letterhead, professional business cards Telephone book—yellow pages Direct mail, newsletters to patients Direct (paid) advertising—radio, television, billboards, magazines, newspapers Internet—website Booth displays—health fairs Speaking engagements—civic groups, hospital outreach programs, health clubs, medical professional organizations Publication of medical articles TV or local newspaper stories—newsworthy information on lasers Public relations consultants

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MARKETING

After a laser program has been established, its success is dependent on generation of interest and requests for laser procedures by new and existing patients. The objectives are to make patients, colleagues, and the community aware of a practice’s new laser capabilities. There are multiple of ways to promote one’s new laser program (27). The methods selected will depend on the physician’s preference and budget limitations (Table 38.3). Regardless of the route taken to promote the laser unit, the physician should always be certain the information given is accurate and presented in an ethical professional manner.

REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

11. 12.

13.

14. 15.

16. 17. 18. 19.

ECRI. Surgical smoke evacuation systems. Health Devices. Plymouth Meeting. Vol. 26, issue 4. PA: ECRI, 1997:131 – 179. Smith JP, Moss CE, Bryant CJ, Fleeger AK. Evaluation of a smoke evacuator used for laser surgery. Lasers Surg Med 1989; 9:276 – 281. Lanzafame RJ. Editorial. Smoking “guns”. Lasers Surg Med 1997; 20:354 – 355. Recommended practices for laser safety in practice settings. AORN J 1998; 67(1):263 – 269. Romig CL, Smalley PJ. Regulation of surgical smoke plume. AORN J 1997; 65(4):824 – 828. ECRI. Update evaluation surgical smoke evacuation systems. Health Devices. Plymouth Meeting Vol. 28, issue 9. PA: ECRI, 1999:333 – 362. ANSI Z 136.3. For the safe use of lasers in health care facilities. New York: American National Standards Institute, 1996. Ben-zvi S. Laser safety: guidelines for use and maintenance. Biomed Instrum Technol 1989; 360– 368. Maloney ME. The Dermatologic Surgical Suite Design and Materials. NY: Churchill Livingstone, 1991; 105. Food and Drug Administration. Performance standard for laser products, center for devices and radiological health, 21 Code of Federal Regulations, section 1040.10. 21 CFR Ch.1: 556 – 574, 1997. Accreditation Association for Ambulatory Health Care. Accreditation handbook for Ambulatory Healthcare. Inc., Wilmette, IL, 2000. Drake LA, Ceilley RI, Cornelison RL, Dobes WA, Dorner W, Goltz RW, Lewis CW, Salasche SJ, Chanco Turner ML. Guidelines of care for office surgical facilities. J Am Acad Dermatol Part I 1992; 26(5):763– 765. Drake LA, Ceilley RI, Cornelison RL, Dinehart SM, Dorner W, Golta RW, Fraham GF, Hordinsky MK, Lewis CW, Pariser DM, Salasche SJ, Skouge JW, Chanco Turner ML, Webster SB, Whitaker DC, Butler B, Lowery BJ. Guidelines of care for office surgical facilities. Self-assessment checklist. J Am Acad Dermatol Part II 1995; 33(2):265 – 270. Ball KA. Lasers: the Perioperative Challenge. St. Louis: Mosby, 1995:434. Drake LA, Dinehart SM, Goltz RW, Graham GF, Hordinsky MK, Lewis CW, Pariser DM, Skouge JW, Chanco Turner ML, Webster SB, Whitaker DC, Butler B, Lowery BJ. Guidelines of care for local and regional anesthesia in cutaneous surgery. J Am Acad Dermatol 1995; 33(3):504– 509. Brown S. Accrediation of ambulatory surgery centers. AORN J 1999; 70(3):814 – 821. Settles JA. Deemed status accrediation of nonhospital-based ambulatory surgery centers. Sem Perioper Nurs 1995; 4(4):119–204. Dover JS, Arndt KA, Dinehart SM, Fitzpatrick RE, Gonzalez E et al. Guidelines of care for laser surgery. J Am Acad Dermatol 1999; 41(3):484 – 495. American Society for Laser Medicine and Surgery. Guidelines for office based laser procedures. Am Soc Laser Med and Surg, Waussu, WI; April 1999.

Establishing a Laser Unit 20. 21. 22. 23. 24. 25. 26.

27.

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American Society for Dermatologic Surgery. ASDS Adopts Position Statement On Use of Allied Health Professionals. Currents, Schaumburg, IL, 1999. American College of Surgeons. Guidelines for office-Based Surgery: Quality Assurance. Vol. 79, issue 10. ACS, 1994:32– 34. Smalley PJ. Laser safety management: hazards, risks, and control measures. In: Alster TS, Apfelberg DB, eds. Cosmetic Laser Surgery. New York: Wiley-Liss, 1999:305 – 319. Tweedy JT. Health and hazard control and safety management. GR/St. Lucie Press, Boca Raton, 1987:516. ANSI Z 136.1. For the safe use of lasers. Orlando, FL: The Laser Institute of America, 1986. Cunningham JG. Negotiating your laser lease. Skin Aging 2002; May:72 – 76. Kirschner CG, Anderson CA, Dalton JA, Davis SJ, Evans D, Hayden D, Kopacz J, Kotowicz GM, Mindeman ML, O’Hara KE, O’Heron M, Pavloski D, Reyes D, Rozell D, Watkins AA, Young RL, Zacharias J, AMA Editorial Staff. Physician’s Current Procedural Terminology (CPT). Chicago, IL: American Medical Association, 2000. Alster TS, Apfelberg DB. Evaluation, installation, and marketing of a cosmetic laser practice. In: Alster T, Apfelberg D, eds. Cosmetic Laser Surgery, 2nd ed. New York: Wiley-Liss, 1999:1 – 7.

39 Anesthesia Options for Laser Surgery John A. Carucci and David J. Leffell Section of Dermatologic Surgery and Cutaneous Oncology, Yale University School of Medicine, New Haven, Connecticut, USA

1. 2. 3. 4. 5. 6.

Introduction Physiology Ideal Anesthetic Topical Agents Local Infiltration Regional Anesthesia 6.1. Supraorbital Block 6.2. Infraorbital Block 6.3. Mental Block 6.4. Digital Block 7. Intravenous Sedation 7.1. Diazepam 7.2. Midazolam 7.3. Propofol 7.4. Ketamine 7.5. Fentanyl 8. General Anesthesia 9. Management of Discomfort Associated with Specific Procedures 9.1. Treatment of Vascular Lesions 9.2. Tattoo Removal 9.3. Hair Removal 9.4. Ablation of Tumors 9.5. Resurfacing of Scars and Rhytides 10. Postoperative Pain Management 11. Conclusion References

776 776 776 777 777 778 778 778 779 780 780 781 781 782 782 782 782 783 783 783 784 784 784 785 785 786 775

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Carucci and Leffell

INTRODUCTION

The scope and number of laser surgical procedures continues to increase as the prices of the machines decrease and their clinical indications become more broad. A key requirement in achieving patient satisfaction is administration of safe and effective anesthesia. The route and anesthetic will vary with the extent and type of procedure performed. However, the dermatologic surgeon can choose between topical, local, or regional anesthesia or in larger cases, intravenous sedation or general anesthesia. The appropriate choice and use of these options will be discussed in this chapter. It must be stressed that these distinctions are meant as a guide and that modalities are often combined to achieve desired effects. For example, topical agents provide excellent first line analgesia prior to local injection and premedication with an oral benzodiazepine is a useful anxiolytic adjunct for regional block.

2.

PHYSIOLOGY

Pain sensation is carried by larger C fibers and smaller A-delta nerve fibers (1,2). Neural transmission takes place through saltatory propagation of an electrical impulse by the neuronal cell wall or axolemma. The phospholipid bilayer of the axolemma allows for the establishment of an ionic gradient, which is maintained by a Naþ/Kþ ATPase pump. The pump maintains a 10-fold increase in the concentration of intracellular potassium. The axolemmal bilayer is selectively permeable to potassium, which exits the cell at a rate that exceeds the entry of sodium. This selective egress of potassium produces an electrical gradient with a resting membrane potential of 270 mV. Opening of transmembrane, ion-specific exchange channels produce a rapid influx of sodium ions down a concentration gradient resulting in depolarization of the cell and production of an electrical impulse otherwise known as an action potential. Local anesthetics exert their effect by blocking the rapid influx of sodium ions across the axolemma (1,2). This may occur by one of two mechanisms. The membrane expansion theory states that the nonspecific absorption of local anesthetic causes a transient expansion of the bilayer, which results in compression of the sodium channels. On the other hand, the specific receptor theory proposes that local anesthetics block the propagation of the action potential by binding reversibly to the specific receptors within or adjacent to the internal opening of the sodium channel.

3.

IDEAL ANESTHETIC

The ideal anesthetic would show several characteristics (Table 39.1) (2,3). It could be administered without pain and without concern for systemic toxicity, allergic reaction, Table 39.1 Anesthetic

The Ideal

Painless No systemic toxicity Nonallergenic No risk for nerve damage

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or nerve damage. In addition, the ideal anesthetic agent would act rapidly and would continue to be effective for the duration of the procedure. It should be clear from this description that the ideal anesthetic does not exist. Luckily, the dermatologic surgeon has enough options from which to choose in order that acceptable anesthesia is achieved for laser procedures.

4.

TOPICAL AGENTS

Topical agents are among the simplest choices for anesthesia prior to laser procedures (Table 39.2) (4). They are particularly useful in the treatment of vascular lesions by pulsed dye laser (585 nm), tattoo removal using the ruby laser (694 nm), and hair removal using the long-pulsed alexandrite laser (755 nm). The most widely used topical agent is eutectic mixture of local anesthetics (EMLA). It is a combination of lidocaine 2.5% and prilocaine 2.5%. EMLA is applied to the surgical site and covered with an occlusive dressing 1– 2 h prior to surgery. The amount of time should be a function of the thickness of the skin at the surgical site. Immediately prior to the procedure the dressing is removed and EMLA cream is wiped away with alcohol pads. ELA-max (lidocaine 4%) is used in a similar fashion and offers the potential benefit of a higher concentration of anesthetic. Betacaine-LA is another topical anesthetic composed of prilocaine, lidocaine, dibucaine, and the vasoconstrictor phenylephrine. It is used similar to other topical anesthetics in that it is applied to the operative site 1– 2 h prior to the procedure. Some report that occlusion of Betacaine-LA is not required for enhanced efficacy. In one study of the use of EMLA in the treatment of PWS in children by pulsed dye laser, mean pain scores were reduced 66% when compared with control patients (5). Furthermore, pain was abolished in 40% of patients treated with EMLA. As an indication of their effectiveness, both EMLA and ELA-max were shown to decrease the discomfort felt during medium depth combination chemical peel without influencing the clinical or histologic result (6). However, there was no difference in efficacy of these agents. In another study, EMLA and ELA-max were superior to Betacaine-LA ointment in control of pain resulting from treatment on the volar forearms of volunteers with the Q-switched Nd:YAG laser (1064 nm) (7).

5.

LOCAL INFILTRATION

Injectable anesthetics block nerve conduction in a circumscribed area (1). Local injection provides excellent anesthesia prior to resurfacing of scars or rhytides confined to a single cosmetic unit. Injectable anesthetics may belong to either the ester or amide chemical class. Esters include cocaine, procaine, tetracaine, and chloroprocaine (Table 39.3). Amides include mepivicaine, bupivicaine, etidocaine, prilocaine, and lidocaine, the most commonly used local anesthetic in dermatology (Table 39.3). Lidocaine offers the advantage of rapid onset and long duration and thus is appropriate for local infiltration

Table 39.2

Topical Anesthetics

EMLA: Lidocaine and prilocaine ELA-max: Lidocaine Betacaine-LA: Lidocaine, prilocaine, dibucaine, and phenylephrine

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Table 39.3

Local Anesthetics

Esters

Amides

Cocaine Procaine Tetracaine Chloroprocaine

Mepivicaine Etidocaine Prilocaine Lidocaine

prior to laser resurfacing procedures. The use of lidocaine is not without potential hazards. Adverse effects associated with lidocaine include light-headedness, tinnitus, perioral tingling, metallic taste, tremors, slurred speech, seizures, myocardial depression, and eventually cardiovascular collapse. Epinephrine is often included to counteract the vasodilatory effect and provide hemostasis. Use of epinephrine is contraindicated in patients with peripheral vascular disease, acute angle glaucoma, hyperthyroidism, pregnancy, and severe cardiovascular disease. The maximum dosage of lidocaine recommended for a 70 kg adult is 7.5 mg/kg with epinephrine and 4.5 mg/kg without epinephrine. Local injection should be administered through as few puncture sites as possible to decrease pain associated with administration. Application of a topical anesthetic cream prior to injection may also be useful in minimizing pain.

6.

REGIONAL ANESTHESIA

Nerve blocks are used to anesthetize a nerve at a point proximal to the surgical site (8,9). Nerve blocks are particularly useful in anesthetizing cosmetic units prior to laser resurfacing. Commonly used nerve blocks include the supraorbital, infraorbital, mental blocks. The advantages of nerve blocks include a decreased number of punctures, decreased amount of anesthetic agent, and absence of anatomic distortion. Disadvantages include operator dependency, increased time, decreased duration of anesthesia, and risks that include permanent loss of sensation due to nerve transection or compression. 6.1.

Supraorbital Block

The supraorbital nerve exits the supraorbital foramen at a point 2 cm above the orbital rim on a vertical line from the pupil (10). Adequate anesthesia can be achieved by injecting 1 – 2 cc of long-acting anesthetic without epinephrine near the foramen but not directly into it (Fig. 39.1) (11). The anesthetized area should include forehead skin from the superior temporal line to the midline, approximately half of the upper eyelid, and the frontoparietal scalp between the midline and the superior temporal line extending posteriorly to the level of a vertical plane drawn perpendicularly to the posterior edge of the helical rim of ear (9). 6.2.

Infraorbital Block

The infraorbital nerve exits the foramen 1 – 2 cm inferior to the orbital rim on a vertical line extending downward from the pupil (11,12). The infraorbital nerve is blocked by injection of 1– 2 cc of long-acting anesthesia injected near but not into the foramen (Fig. 39.2) (9). The area numbed involves the nose, cheek, lip, and lower eyelid.


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Figure 39.1 Supraorbital block. Adequate anesthesia can be achieved by injecting 1 – 2 cc of long-acting anesthetic without epinephrine near the supraorbital foramen. (Photograph by Marc Brown.)

The nasal sidewall, ala, and base of the columella should be affected. Bilateral infraorbital block should allow adequate anesthesia to perform procedures on the upper lip (9).

6.3.

Mental Block

The mental nerve exits from a foramen below the base of the second bicuspid in a line vertical with the pupil, supraorbital, and infraorbital foramina (13). In order to block the mental nerve, the lower lip is reflected allowing visualization of the likely course of the nerve below the mucosal surface (Fig. 39.3) (9). After blocking the nerve by submucosal

Figure 39.2 Infraorbital block. The infraorbital nerve is blocked by injection of 1 –2 cc of longacting anesthesia injected near but not into the foramen. (Photograph by Marc Brown.)

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Figure 39.3 Mental block. In order to block the mental nerve, anesthetic is injected into the mucosal surface toward the mental foramen. (Photograph by Marc Brown.)

injection, the needle is passed 1 cm in front of the vestibule to the inferior mandibular border to anesthetize the lower lip and chin pad (9).

6.4.

Digital Block

Digital blocks are useful in treatment of recalcitrant verruca by laser ablation. While digital blocks often require additional local anesthesia, especially in the periungual area, they allow for less traumatic introduction of local anesthetic. Local anesthetic without epinephrine is injected into the lateral side of the proximal aspect of the digit (14). Anesthetic is delivered to the dorsal and palmar areas to reach the dorsal and palmar digital nerves. The process is repeated on the contralateral side (Fig. 39.4). In theory the entire finger should be numb, however, local infiltration is usually required to fully anesthetize the nail bed and periungual area. Care is taken to avoid excessive injection of anesthetic, which may result in compression. Epinephrine is avoided to reduce the possibility of arterial spasm that could result in necrosis of the digit.

7.

INTRAVENOUS SEDATION

Intravenous sedation may be required with larger procedures such as full face resurfacing. This procedure is not without serious potential complications and should not be attempted by those not properly trained in the use of systemic anesthesia or by those not certified in and qualified to perform advanced cardiac life support. In cases where IV sedation is required, it should be administered by an anesthesiologist or under the direct supervision of an anesthesiologist. The following is a discussion of some of the agents available for intravenous sedation for laser surgery. Some of the more commonly used agents include diazepam, midazolam, propofol, ketamine, and fentanyl.


781

Figure 39.4 Digital block. Local anesthetic without epinephrine is injected into the lateral side of the proximal digit and delivered to the dorsal and palmar areas. The process is repeated on the contralateral side. (Photograph by Marc Brown.)

7.1.

Diazepam

Diazepam is a benzodiazepine that is useful as a premedication, sedative, amnestic, or induction agent (15). Its mechanism of action for sedation involves facilitation of the activity of the inhibitory neurotransmitter gamma amino butyric acid (GABA). Benzodiazepines enhance the chloride channel gating function of GABA, which results in a hyperpolarized cell that is more resistant to neuronal excitation. Diazepam is highly lipid soluble, which results in rapid entry into the CNS. When administered intravenously the onset of action is ,2 min with peak effect observed in 3– 4 min. Effects last for 15 min to 1 h. Diazepam is metabolized in the liver to active metabolites oxazepam and desmethyldiazepam, which may contribute to prolonged half life. In the event of overdose or untoward response, the effects may be antagonized by flumazenil (16). Adverse reactions may include circulatory, respiratory, and CNS depression while paradoxical excitement may be observed. 7.2.

Midazolam

Midazolam is another benzodizepine that can be used for premedication, conscious sedation, or in supplementation of other agents (15,17,18). As it is also a benzodiazepine, midazolam exerts its sedative effect by facilitating effects of GABA. Midazolam acts more rapidly than diazepam with onset of activity within 30 s of intravenous administration. Peak activity is observed within 3 –5 min and effects last for 1 h. As with diazepam, reversal can be achieved with administration of the benzodiazepine antagonist flumazenil (16). Overall, midazolam shows greater amnestic effect and a fourfold increase in sedative potency when compared with diazepam. Potential adverse effects include respiratory and

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cardiac arrest. We recommend that midazolam only be administered by those familiar with its use and potential adverse effects. We further recommend the immediate availability of flumazenil for reversal. 7.3.

Propofol

Propofol is a lipid soluble isopropylphenol hypnotic agent that has the advantage of rapid induction and rapid awakening (19 – 21). Rapid awakening with minimal residual CNS effects makes this an attractive agent for brief procedures. Onset is observed within 30 s with peak effect achieved in about 1 min. The duration of activity is 5 –10 min. These advantages aside, propofol carries the risks of respiratory and circulatory depression as well as an increased risk of seizures. Thus, the use of propofol is not recommended for patients with a history of seizures. 7.4.

Ketamine

Ketamine is a phencyclidine derivative that produces dissociative anesthesia. EEG performed under anesthesia with ketamine shows evidence of dissociation between the thalamus and the limbic system (22,23). Induction of anesthesia is achieved in 60 s when ketamine is administered intravenously. Amnesia and analgesia are achieved through use of ketamine. Cardiac stimulation may adversely increase myocardial oxygen demand in patients with ischemic heart disease. Airway secretions may be increased by ketamine as is intracranial pressure. Ketamine rarely if ever produces allergic reaction, however, emergence from ketamine may be accompanied by visual, auditory, and proprioceptive hallucinations. The incidence of emergence illusions after ketamine approaches 30%, thus limiting its utility in office based procedures. 7.5.

Fentanyl

Fentanyl is a phenylpiperidine derivative and a potent opioid antagonist (24). It is approximately 100 times more potent as an analgesic than morphine. It is highly lipid soluble and therefore has a short duration as well as a rapid onset. Respiratory depression may last longer than analgesia. Fentanyl decreases cerebral blood flow and metabolic rate but does not depress cardiovascular stability. Onset of activity occurs within 30 s and peak effects are achieved in 5 –15 min when administered intravenously. Duration of action is 30 – 60 min. In addition to central respiratory depression, potential adverse effects include muscle rigidity sufficient to interfere with ventilation. In any case, regardless of choice of anesthetic agent, we recommend that the administration of intravenous sedation be performed by an anesthesiologist who can appropriately monitor cardiac and respiratory status during the procedure.

8.

GENERAL ANESTHESIA

The use of general anesthesia for dermatologic laser surgery is rarely required. However, one instance where general anesthesia has been required is for treatment of port wine stains (PWS) in infants and young children (25). In these cases, the procedure, usually pulsed dye laser surgery, is performed in a pediatric operating room with an anesthesiologist who is an expert in adminstration of anesthesia to infants and children.


9. 9.1.

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MANAGEMENT OF DISCOMFORT ASSOCIATED WITH SPECIFIC PROCEDURES Treatment of Vascular Lesions

The majority of our experience with vascular lesions involves treatment of hemangiomas and vascular malformations using the pulsed dye laser (585 nm) (Table 39.4; Fig. 39.5). Patients note that treatment is similar to the sensation of “being splattered by grease from a frying pan” or “being hit by a snapping rubber band.” For smaller lesions, ice packs applied for several minutes before the procedure may suffice. In some cases, no anesthesia may be required. For larger lesions, we have found that application of EMLA or ELA-max 1– 2 h prior to treatment is usually sufficient to minimize discomfort associated with PDL therapy. Treatment of PWS in children may be challenging. If the child is unable or unwilling to cooperate to allow for treatment, general anesthesia may be required. In one study, 86% of children with vascular lesions treated by PDL required some form of pain management ranging from topical to general anesthesia. Despite concerns about vasoconstriction caused by topical anesthetics, it has been shown that application of EMLA cream prior to pulsed dye treatment of PWS has no adverse effect on efficacy (26). In another study performed to evaluate the use of general anesthesia, it was found that the combination of propofol and fentanyl offered excellent anesthesia with and low risk of complication (27). In this study, propofol was chosen to achieve early discharge and to reduce the incidence of postoperative emesis. Fentanyl was added to propofol for analgesia. The authors state that this combination offers the benefit of rapid onset and awakening, excellent analgesia, and an immobile patient. Volatile anesthetics have been used in the treatment of PWS in children. In one study comparing the use of four volatile anesthetics in the treatment of PWS, it was found that patients treated with sevoflurane experienced significantly greater degree of fading than patients treated with halothane, enflurane, or isoflurane (28). The authors surmised that fading caused by sevoflurane might decrease effectiveness of treatment.

9.2.

Tattoo Removal

Patients with black ink tattoos who are treated with the Q-switched ruby laser (694 nm) liken the discomfort associated with the procedure to “being splattered with hot grease.” Patients who have experienced both PDL and Q-switched ruby laser treatments seem to agree that there is more discomfort associated with treatment by ruby laser. We have found that treatment with a topical anesthetic under occlusion applied 2 h prior to treatment helps minimize discomfort associated with tattoo removal (Table 39.4; Fig. 39.6). It should be stressed that longer application times are necessary when treating the skin of the extremities and trunk, which tends to be thicker.

Table 39.4

Management of Discomfort Associated with Laser Surgery

PDL for vascular lesions: No anesthesia or topical agent; consider general anesthesia in infants and young children Ruby for tattoo removal: Topical agent with postoperative acetominophen Alexandrite or diode for hair removal: No anesthesia or topical agent Ablation of rhytides: Premedicate with bezodiazepine, local injection, regional block, or IV sedation for procedure, centrally acting oral agent postoperatively

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Figure 39.5 Anesthesia for pulsed dye laser treatment of vascular lesions. Options range from no anesthesia to general anesthesia depending on the size of the lesion and the age of the patient.

9.3.

Hair Removal

The cooling devices associated with hair removal lasers such as the alexandrite (755 nm) or diode (810 nm) laser sufficiently reduce discomfort so that pain is not a deterrent to treatment. A topical anesthetic 1– 2 h prior to treatment may be used (Table 39.4; Fig. 39.7). This approach is similar to that for anesthesia for epilation by electrolysis (29,30). 9.4.

Ablation of Tumors

Treatment of benign and malignant tumors with the carbon dioxide laser requires proper anesthesia. Depending on size and anatomic location, a combination of topical anesthetics, local injections, and regional blocks are effective. In addition, prescription of a centrally acting oral analgesic for short-term use during the postoperative period is often required. 9.5.

Resurfacing of Scars and Rhytides

In resurfacing scars and rhytides the pain management protocol should be based on the anatomic location and area (Table 39.4; Fig. 39.7). For small scars, local injection is sufficient for perioperative pain management. Postoperative discomfort is usually easily managed with acetaminophen. For resurfacing of cosmetic units, a combination approach is required. We prescribe a benzodiazepine, usually diazepam (5 mg) to be taken orally prior to the procedure. The main benefits are derived from its anxiolytic properties.

Figure 39.6 Anesthesia for tattoo removal. Options range from no anesthesia to local injection depending on the size of the area to be treated.


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Figure 39.7 Anesthesia for laser resurfacing. Although local injection or regional blockade is sufficient for resurfacing of a single cosmetic unit, IV sedation or general anesthesia may be required for larger cases.

In some cases a topical anesthetic is applied 1 h prior to the procedure to minimize pain associated with injection of local anesthetic. For the postoperative period, we generally prescribe a centrally acting oral analgesic. Increasingly, physicians are relying upon total intravenous anesthesia (TIVA) for facial resurfacing. In one study, a technique using propofol with midazolam and fentanyl administered supplementally as needed was described (31). In this study, all anesthetics were administered by board-certified anesthesiologists, and American Society of Anesthesiologists (ASA) Standards for Anesthesia Monitoring were followed. Patients were premedicated with glycopyrrolate. An induction dose of propofol was followed by laryngeal mask airway insertion. TIVA was maintained with a propofol infusion with supplemental midazolam, fentanyl, and oxygen administered as needed. Mean time to discharge after the procedure was 16 min and TIVA was well tolerated without complications. In another study, the propofol – ketamine technique was reviewed as a means of providing anesthesia for laser resurfacing in an office-based environment (32). In this retrospective chart review of 95 patients, all patients were reported to have received adequate anesthesia. No hallucinations, postoperative nausea or vomiting (PONV), cardiovascular instability, or seizures were reported. The authors of that study propose that the propofol – ketamine technique may be an excellent alternative anesthetic approach to EMLA cream, tranquilizer-opioid regimens, or general inhalational anesthesia for facial laser resurfacing.

10.

POSTOPERATIVE PAIN MANAGEMENT

Postoperative pain in most cases is minimal to moderate and is usually easily managed with acetaminophen 650 mg taken orally every 4– 6 h as needed for several days. Aspirin and NSAIDs are generally avoided due to their anticoagulant effects, which may result in increased purpura. Acetaminophen (300 mg) with codeine (30 mg) is prescribed for patients in whom discomfort is not relieved by acetaminophen alone. Tramadol (50 mg) is an alternative to acetaminophen with codeine (33). It is a centrally acting opioid receptor antagonist that is generally well tolerated, effective, and nonaddictive.

11.

CONCLUSION

The number of dermatologists performing laser procedures continues to rise. The dermatologic surgeon must become familiar with the numerous anesthetics currently available

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and be proficient on their use in order to achieve desired results with minimal discomfort. The choice of anesthesia and postoperative pain management are dictated by the procedure itself and the patient’s disposition. Short procedures such as treatment of smaller vascular lesions by pulsed dye laser may require no anesthesia or application of a topical agent, whereas laser ablation of rhytides requires premedication with an anxiolytic agent, local or regional injection, and postoperative pain management with a centrally acting agent (Table 39.4).

REFERENCES 1. 2. 3. 4. 5. 6.

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13. 14. 15. 16. 17. 18. 19. 20. 21.

Skidmore RA, Patterson JD, Tomsick RS. Local anesthetics. Dermatol Surg 1996; 22(6):511– 522. Grekin RC, Auletta MJ. Local anesthesia in dermatologic surgery. J Am Acad Dermatol 1988; 19(4):599– 614. Epstein RH, Halmi B, Lask GP. Anesthesia for cutaneous laser therapy. Clin Dermatol 1995; 13(1):21– 24. Lener EV et al. Topical anesthetic agents in dermatologic surgery. A review. Dermatol Surg 1997; 23(8):673– 683. Sherwood KA. The use of topical anesthesia in removal of port-wine stains in children. J Pediatr 1993; 122(5 Pt 2):S36 – S40. Koppel RA, Coleman KM, Coleman WP. The efficacy of EMLA versus ELA-Max for pain relief in medium-depth chemical peeling: a clinical and histopathologic evaluation. Dermatol Surg 2000; 26(1):61– 64. Friedman PM et al. Comparative study of the efficacy of four topical anesthetics. Dermatol Surg 1999; 25(12):950– 954. Zide BM, Swift R. Addendum to “How to block and tackle the face”. Plast Reconstr Surg 1998; 101(7):2018. Zide BM, Swift R. How to block and tackle the face. Plast Reconstr Surg 1998; 101(3):840– 851. Knize DM. A study of the supraorbital nerve. Plast Reconstr Surg 1995; 96(3):564 – 569. Jenkins DB, Spackman GK. A method for teaching the classical inferior alveolar nerve block. Clin Anat 1995; 8(3):231– 234. Prabhu KP, Wig J, Grewal S. Bilateral infraorbital nerve block is superior to peri-incisional infiltration for analgesia after repair of cleft lip. Scand J Plast Reconstr Surg Hand Surg 1999; 33(1):83– 87. Smith JS, Dwyer BE, Rigg DL. Mental nerve block revisited—a simplified technique for surgery of the lower lip. Anaesth Intensive Care 1985; 13(4):407 – 409. Ferrera PC, Chandler R. Anesthesia in the emergency setting: Part I. Hand and foot injuries. Am Fam Physician 1994; 50(3):569– 573. Finder RL, Moore PA. Benzodiazepines for intravenous conscious sedation: agonists and antagonists. Compendium 1993; 14(8):972, 974, 976 –980. Whitwam JG. Flumazenil and midazolam in anaesthesia. Acta Anaesthesiol Scand Suppl 1995; 108:15 – 22. Nordt SP, Clark RF. Midazolam: a review of therapeutic uses and toxicity. J Emerg Med 1997; 15(3):357– 365. Rosen DA, Rosen KR. Intravenous conscious sedation with midazolam in paediatric patients. Int J Clin Pract 1998; 52(1):46– 50. Bryson HM, Fulton BR, Faulds D. Propofol. An update of its use in anaesthesia and conscious sedation. Drugs 1995; 50(3):513– 519. McNeir DA, Mainous EG, Trieger N. Propofol as an intravenous agent in general anesthesia and conscious sedation. Anesth Prog 1988; 35(4):147 – 151. Bauman LA et al. Pediatric sedation with analgesia. Am J Emerg Med 1999; 17(1):1 – 3.

Anesthesia Options for Laser Surgery 22. 23. 24. 25. 26. 27. 28. 29.

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Gruber RP, Morley B. Ketamine-assisted intravenous sedation with midazolam: benefits and potential problems. Plast Reconstr Surg 1999; 104(6):1823– 1825, discussion 1826– 1827. Bergman SA. Ketamine: review of its pharmacology and its use in pediatric anesthesia. Anesth Prog 1999; 46(1):10– 20. Peng PW, Sandler AN. A review of the use of fentanyl analgesia in the management of acute pain in adults. Anesthesiology 1999; 90(2):576 –599. Scheepers JH, Quaba AA. A two-year review of pain control during laser therapy using the flashlamp pulsed dye laser. Br J Plast Surg 1994; 47(2):112 – 116. Ashinoff R, Geronemus RG. Effect of the topical anesthetic EMLA on the efficacy of pulsed dye laser treatment of port-wine stains. J Dermatol Surg Oncol 1990; 16(11):1008– 1011. Vischoff D, Charest J. Propofol for pulsed dye laser treatments in paediatric outpatients. Can J Anaesth 1994; 41(8):728– 732. Tanaka K et al. The influence of volatile anesthetics on portwine stain. Clin Ther 1993; 15(3):567– 569. Hjorth N, Harring M, Hahn A. Epilation of upper lip hirsutism with a eutectic mixture of lidocaine and prilocaine used as a topical anesthetic. J Am Acad Dermatol 1991; 25(5 Pt 1):809– 811. Wagner RF Jr, Flores CA, Argo LF. A double-blind placebo controlled study of a 5% lidocaine/prilocaine cream (EMLA) for topical anesthesia during thermolysis. J Dermatol Surg Oncol 1994; 20(2):148 –150. Blakeley KR et al. A total intravenous anesthetic technique for outpatient facial laser resurfacing. Anesth Analg 1998; 87(4):827– 829. Friedberg BL. Facial laser resurfacing with the propofol-ketamine technique: room air, spontaneous ventilation (RASV) anesthesia. Dermatol Surg 1999; 25(7):569 – 572. Lee CR, McTavish D, Sorkin EM. Tramadol. A preliminary review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in acute and chronic pain states. Drugs 1993; 46(2):313– 340.

Index

Ablation efficacy Er:YAG laser, 183 Absorption curve hemoglobin, 358 Absorption process, 68– 69 Absorption spectrum melanin, 490 Accreditation laser unit, 766 Accreditation Association for Ambulatory Health Care (AAAHC), 766 Acne diode laser, 328– 329 keloidalis nuchae, 152– 156 pyogenic granuloma, 152– 153 PDT dermatology applications, 396– 398 perioral area, 564 scars, 710 Er:YAG lasers, 193, 577 focal laser ablation, 28 Acoustic hazards, 95 Acquired melanocytic nevi pigmented lesions removal, 277 Acquired vascular lesions laser treatment, 475– 485 Actinic cheilitis, 153– 154, 525 laser performance applications, 153– 154 preoperative view, 155 technique treatment, 528 Actinic damage full-face, 561, 562 Actinic keratoses (AK), 427, 428 ALA-PDT, 391, 393

PDT dermatology applications, 396 – 398 red light sources, 392 Actinic porokeratosis lesion treatment, 162 Active skin cooling PWS treatment, 452 Acute contact dermatitis, 422 – 425 development, 424 Adenoma sebaceum, 523, 734 laser performance applications, 147 – 148 Air precooled (AC), 75 Alcohol laser impact, 92 Alexandrite lasers, 687 light pulses, 287 Q-switched lasers, 510 – 511 selective photothermolysis, 286 targets side effects and complications, 289 TRT, 286 Alexandrite rod primary, 286 Allergic dermatitis tattoos, 292 Allergic reaction, 281 Allergic skin reaction, 425 Alopecia secondary to face lift, 710 Alpha-hydroxy acids postinflammatory hyperpigmentation, 738 Aluminum. See neodymium: yttriumaluminum-garnet (Nd:YAG) laser American National Standard for Safe Use of Lasers, 80 789

790 American National Standard for Safe Use of Lasers in Health Care Facilities, 80 American National Standards Institute (ANSI), 16, 80 laser safety, 16– 18 risk classification, 83 standards, 93 American Osteopathic Association (AOA), 766 American Society for Laser Medicine and Surgery (ASLMS), 10, 15– 16 cosmetic surgeons, 29 laser industry, 23 Amides, 778 Aminolevulinic acid (ALA), 329, 388 application, 391, 392 PDT AK, 391 BCC, 395 facial AK, 391 melanin absorption, 393 Ancillary laser equipment laser unit, 758– 761 Anderson, R. Rox, 24–25 Androgenetic alopecia, 708 Anesthesia, 775– 786 discomfort, 783– 784 Er:YAG laser, 189 clinical treatment, 558 general, 782 hair removal, 784 ideal, 776 laser resurfacing, 785 local infiltration, 777 physiology, 776 pulsed dye laser treatment of vascular lesions, 784 rhytides resurfacing, 784 scar resurfacing, 784 tattoo removal, 783, 784 tumor ablation, 784 upper eyelid, 595 vascular lesions, 783 Angel kiss, 442 Ankle telangiectasia, 666 venulectasia, 666 Antigravity procedures, 590 Antioxidants dermal structures, 536 Arbutin postinflammatory hyperpigmentation, 738 Argon laser (AL), 9 – 12, 720 continuous wave, 106– 112, 476– 477

Index cutaneous treatment disease, 17 –18 lesions telangiectasias, 109 scaring, 106 surgery flat opaque scars, 18 hypertrophic scars, 23 test area, 19 treatment, 10 clinical indications, 111 linear ectatic vessels, 111 preoperative, 107, 110, 111 vascular lesion treatment, 106 Argon-pumped tunable dye laser (APTDL), 476 continuous and quasicontinuous, 112 – 117 continuous wave lasers, 477 CW, 477 PDL, 482 pigmented lesions, 114 treatment preoperative, 113 –118 Atoms energy transition characteristics, 62 Atrophic scars, 621, 622 before and after, 629 Er:YAG vs. carbon dioxide laser, 629 laser treatment, 472 – 473 linear telangiectasias, 480 nonablative laser scar remodeling, 631 perioperative considerations, 630 postoperative considerations, 631 preoperative considerations, 629 PWS complications and management, 455 skin resurfacing, 473 treatment, 628 – 632 Azelaic acid postinflammatory hyperpigmentation, 738 Bags lower eyelid, 593, 594, 602 Bare fiber diode lasers, 326 –327 saphenous vein closure, 326 –327 Basal cell carcinoma (BCC), 36, 139 ALA-PDT, 395 lesion treatment, 159 PDT dermatology applications, 396 – 398 SCC, 427 Basov, Nikolai, 8 Beckman lab, 24 – 25 Beer’s law, 267

Index Bellina, Joseph, 13 Benign cutaneous appendage tumors, 429 Benign epidermal pigmented lesions, 727– 727 Benign melanocytic tumors, 430 Benign pigmented lesions QSRL treatment, 261 Benign vascular disorders pulsed dye lasers, 209–210 Benzodiazepine, 781– 782, 784 Betacaine-LA, 777 Beta-hydroxy acids postinflammatory hyperpigmentation, 738 Blepharoplasty, 595, 612 with laser resurfacing, 592– 593, 595– 600 Blistering tattoo removal, 730 Blood vessels selective thermal destruction, 201 Blunt straight hairline, 708 Botox and laser resurfacing, 613 Bowen’s disease lesion treatment, 159 PDT dermatology applications, 396– 398 Brow ptosis, 604 Buccal fat removal, 608, 609 Butterfly rash, 232 Cafe-au-lait macules (CALM), 275, 494 lentigo, 276 QSRL treatment, 495 treatment, 726 Candela PDPL Q-switched lasers, 511 Candela’s Dynamic Cooling Device, 451 Candela V-beam treatment guidelines, 238– 239 Candidal infections promotion, 557 Capillary vascular malformations, 442 Carbon dioxide laser, 12– 15, 554, 703, 710 ablation, 521 assisted hair transplantation disadvantages, 711 histology, 711 clinical advantages, 537 combined laser resurfacing techniques, 582– 584

791 comparison, 582 complications, 544 – 549 cutaneous conditions, 15 defocused CW mode, 146 dermatology, 165 early clinical use, 520 epidermal and dermal lesion treatment advantages and limitations, 524 clinical indications, 520 – 525 complications, 528 – 529 cutaneous laser surgery, 519 – 530 laser safety, 524 – 525 technique, 525 – 527 erbium:YAG laser, 30, 155, 184, 591 comparison studies, 192 HPV, 150 hypertrophic scars treatment, 507 intraoperative appearance, 583 legal scenario, 753, 755 morbidity, 590 new developments, 164 pioneers, 13 postoperative care, 165 pre- and postoperative considerations, 164 – 165 preoperative regimen, 165 relative contraindications, 164 – 165 results, 542 – 544 resurfacing, 38, 537 – 539 collagen remodeling and regeneration, 539 collagen shrinkage, 538 – 539 legal scenario, 754 single pulse vaporization, 537 – 538 safety issues, 163 – 164 scanners, 20 skin resurfacing, 535 – 540, 731 – 733 studies, 28 superficial resurfacing, 549 – 550 surgery, 69 port-wine stain, 14 temperature profiles, 138 technique, 539 – 542 tissue, 524 interaction, 134 – 135 vaporization, 535, 554 wound healing, 144 – 145 Carbon suspension Q-switched Nd:YAG laser, 689 LPA treatment, 301 Cellular debris ejected, 98 Center for Devices and Radiological Health (CDRH), 82

792 Central upper lip hemangioma, 472 Chemical depilatories, 680 Chemical hazards, 95 protection, 95 Cherry angioma, 250, 434 Children port-wine stain, 12 Chilling, 22 Chilling and wrinkles, 33– 34 laser technologies, 33 Chloroprocaine, 778 Chondrodermatitis nodularis helicus lesion treatment, 160 Chromophores diameters, 72 in skin, 718 Civatte Poikiloderma, 250 Clean ablation histology, 592 Clinical guidelines, 751 Cocaine, 778 Coherent UltraPulse laser, 29 Collagen biochemical studies, 538 hypertrophic scars, 225 keloids, 225 remodeling and regeneration, 539 shrinkage, 538–539 Combination Er:YAG laser treatment, 579 Combined laser resurfacing techniques, 569– 586 carbon dioxide lasers, 582– 584 derma-K laser, 579– 582 Er:YAG lasers, 571– 579 Sciton contour laser resurfacing, 586 – 587 theoretical considerations, 570– 571 Common acquired nevi melanocytic lesions removal, 279– 280 Compound nasal tip hemangioma infant, 463 Compound or deep lesions proliferating hemangiomas, 470– 471 Computerized pattern generator (CPG), 538 Condyloma acuminata laser performance applications, 150 Confocal microscopy (CM), 417– 419 advances, 433 cross-polarized image, 433 human skin imaging, 435 illustration, 417 images, 423 appearance difference, 419 dysplasia, 429

Index formation and contrast, 418 melanocytic lesions, 431 sequence frames, 424 superficial epithelial cell layer, 421 superficial folliculitis, 427 vertical and converse sections, 420 lesion diagnosis, 435 normal skin, 419 – 422 image interpretation, 419 – 421 morphometric analysis, 421 – 422 optimal design and imaging parameters, 418 – 419 psoriasis, 422 range parameters, 418 reflectance, 417, 435 clinical dermatology, 415 – 435 reflectance principles, 417 – 418 skin lesion applications, 422 – 432 inflammatory skin diseases, 422 – 426 skin tumors, 426 – 432 skin surgery applications, 432 – 433 dermatologic surgery, 432 laser treatment evaluation, 432 – 433 Congenital melanocytic nevus, 728 Congenital nevi long-pulsed ruby laser, 498 pigmented lesions removal, 277 Contact cooling (CC), 75 device manufacturers, 408 skin cooling methods, 405 – 406 Contact dermatitis (CD), 422 Continuous and quasicontinuous argonpumped tunable dye laser, 112 – 114 facial telangiectasias, 113 – 114 laser parameters, 112 perioperative considerations, 113 port-wine stains, 112 – 113 Continuous quality improvement (CQI), 766 Continuous wave (CW), 65, 476 APTDL, 477 argon laser, 106 – 113 laser parameters, 106 port-wine stains, 106 – 108 defocused mode carbon dioxide laser, 146 lasers, 105 – 124, 476 – 484 argon lasers, 476 –477 argon-pumped tunable dye laser, 477 cooper vapor laser, 477 –478 copper bromide laser, 478 – 479 krypton laser, 479 leg vein laser treatment, 657 PWS treatment, 446

Index and pulsed carbon dioxide lasers, 129– 165 beam profiles, 131– 132 history, 131– 134 physical properties, 131 pulsed lasers, 65– 66 RSP modes differences, 132 vaporization pearls technique, 162– 163 Convective cooling skin cooling methods, 407– 408 Cooling dermatologic laser systems, 411 nonablative laser skin rejuvenation, 411 skin cooling, 411–412 Cooling devices protection efficacy, 734 Cooling plates, 406 Cool Touch Varia, 348 treatment, 348– 349 Copper bromide laser (CBL), 114– 118 continuous wave lasers, 478–479 laser parameters, 114– 115 Copper vapor laser (CVL), 26, 114– 118, 720 CALM, 726 continuous wave lasers, 477–478 facial telangiectasia, 117 laser parameters, 114– 115 manufacturers, 115 PWS treatment, 116 treatment preoperative, 116, 119 Corneal eye shields, 90 Corneal injury, 87– 88 Corneal scarring, 84 Cornrows, 704 Cosmetic cutaneous laser resurfacing legal scenario, 754 Cosmetic surgeons ASLMS, 294 Cosmetic tattoos laser treatment, 514 Cowden’s disease, 523 Crow’s feet, 600 region, 603 Crusting leg vein laser treatment, 671 Cryogen atomization CSC, 406 Cryogen spray (CS), 75, 657 Cryogen spray cooling (CSC), 406, 407 cryogen atomization, 407 vascular lesion treatment, 410 Cryogen treated sites, 646

793 Current procedural technology (CPT) codes, 770 Cutaneous allergic reactions tattoos, 292 Cutaneous cooling, 249 Cutaneous laser resurfacing cosmetic legal scenario, 754 Cutaneous laser surgeon legal scenario, 754, 756 Cutaneous laser surgery clinical innovations, 752 epidermal and dermal lesions, 519 – 530 evolved, 752 historical perspectives, 1 – 39 timeline development, 38 Cutaneous lesions SLE, 232 Cutaneous photosensitivity PDT, 398 Cutaneous T-cell lymphoma (CTCL), 396 PDT dermatology applications, 397 Cutaneous treatment disease argon laser, 17 – 18 Cylindromas, 523 Cynosure’s photogenic laser, 408 Cynosure V-star treatment process, 240 Darier’s disease lesion treatment, 161 Darier-White’s disease, 425 Darier-White’s papule, 426 Deep focal hemangioma infant, 462 Deep lesions proliferating hemangiomas, 470 – 471 Defocused CW mode carbon dioxide laser, 146 Delivery system, 133 Depressor supercilii, 596 Derma-K laser, 580 combined laser resurfacing techniques, 579 – 582 Dermal depth ablation, 559 Dermal-epidermal (DE) junction, 149 Dermal lesions, 523 – 524 ablation, 523 carbon dioxide lasers, 529 advantages and limitations, 524 complications, 528 laser safety, 524 – 525 technique, 525 – 527

794 Dermal lesions (Contd.) pigmented, 496– 500, 727– 728 side effects and complications, 500 treatment, 69 QSRL treatment, 261 treatment, 523 Dermal melanocytic nevi melanocytic lesions removal, 279 Dermal remodeling, 638 Dermal structures antioxidants, 536 Dermatitis PWS complications and management, 455 Dermatoheliosis, 710 Dermatologic laser systems cooling, 411 Dermatologic surgery CM skin surgery applications, 432 Dermatologic surgery lasers history, 4 Dermatologist legal scenario, 754, 755 Dermatology carbon dioxide lasers, 165 lasers, 64– 65, 76 lasers and laser-tissue interactions, 59– 76 PDT acne, 396– 397 applications, 391– 398 BCC, 394– 395 Bowen’s Disease, 395– 396 melanoma, 396 psoriasis, 397 recalcitrant warts, 396 squamous cell carcinoma (SCC), 396 phototherapy, 384 Dermatology Online Journal, 37 Dermatosis papulosis nigra (DPN), 140 lesion treatment, 157 Dermis resurfacing erbium:YAG, 593 Desferrioxamine (DFO), 395 Destruction modality, 770 Destructive codes, 771 Diazepam, 781, 784 Dibucaine, 777 Diffuse reflections, 86 Diffuse telangiectasia preoperative Krypton laser treatment, 122 Digital block, 780, 781 Digital videomicroscopic photos LPA laser treatment, 301

Index Dihydroxyphenylalanine (DOPA) melanin, 246 Dimethyl sulfoxide (DMSO), 395 Diode laser, 327 – 329, 687 acne, 328 – 329 efficacy, 328 – 329 crucial components, 318 hair removal, 323 mechanism, 320 laser tissue soldering, 329 –330 efficacy, 329 – 330 mechanism, 329 leg veins, 667 – 668 nonablative rejuvenation, 327 – 328 efficacy, 327 – 328 potential complications, 328 PDT, 329 research applications, 329 – 330 imaging, 330 SCC, 330 SLP, 323 wound healing, 330 Direct current (DC) power supplies, 133 Direct laser energy, 66 Discoid lupus erythematosis (DLE), 233 prior treatment, 233 Disseminated superficial actinic porokeratosis (DSAP), 162 Donor density, 704 Donor ellipse tumescence, 706 Donor region laser assisted hair transplantation, 705 Donor scar, 706 Dosimetry, 67 Drake, Ellet, 15 Drapes, 761 Dry gauze ignition, 92 Dye lasers, 65 Dynamic Cooling Device (DCD), 451 Dysplasia confocal images, 429 Earlobe keloids laser performance applications, 151 Eccrine poroma, 429 Ectatic vessels preoperative copper vapor laser treatment, 119 Einstein, Albert, 4, 6 Electrical and mechanical hazards, 93 – 95 controlled access, 93 – 95 Electromagnetic radiation, 60 – 61 spectrum, 60

Index Electromagnetic spectrum (EMS), 85 diagrammatic representation, 85 Electro-optical synergy (ELOS), 688 Elliptical harvesting, 706 Emission spectrum IPL, 357 Endogenous chromophore, 683– 689 Endogenous cutaneous pigment, 287 Endoscopic eyebrow lift, 604 patient being marked, 606 Endoscopic forehead lift with laser blepharoplasty, 607 with laser resurfacing, 601, 604– 607 Endoveneous laser therapy (EVLT), 327 Energy conservation law, 87 Ephelides, 495 Epidermal melanocytic lesions removal, 279 Epidermal absorption laser energy, 403 Epidermal cooling, 75, 322, 739 nonwhite skin laser treatment, 739 Epidermal lesions, 521– 523 carbon dioxide lasers, 529– 530 advantages and limitations, 524 complications, 528– 529 laser safety, 524– 525 technique, 525– 527 pigmented, 495– 496 clinical treatment, 493– 496 skin carbon dioxide lasers, 529– 530 treatment, 69 Epidermal melanin, 724 Epidermal neoplasms, 426– 427 Epidermal nevi laser performance applications, 155– 156 Epidermal ulceration, 353 Epidermis combined laser resurfacing techniques, 571 Erbium:glass laser, 646 Erbium recipient sites histology, 714 Erbium:YAG laser, 29– 30, 181– 194, 553– 566 ablation efficacy, 183 acne scars, 193, 577 alternative, 554 anesthesia, 189 assisted transplantation, 31 carbon dioxide combination manufacturer, 579 carbon dioxide laser, 30, 155, 184, 591 comparison studies, 192

795 clinical treatment, 556 – 562 anesthesia, 558 patient selection, 556 – 557 postoperative care, 560 – 562 preoperative procedure, 557 – 558 pretreatment regimen, 557 treatment technique, 558 – 560 combination treatment, 579 combined laser resurfacing techniques, 571 – 579 commercially available, 186 complications, 562 – 565 dermis resurfacing, 593 facial resurfacing, 194 four passes, 580 histologic examination, 581 laser assisted hair transplantation, 713 laser plume and noise, 184 – 186 maximal power settings, 576 nuclear debris, 572 photoaging treatment, 590 physics laser-tissue interaction, 182 – 183 pigmentory abnormalities, 192 – 193 postoperative care, 189 – 190 pre- and perioperative care, 189 problems, 186 publications, 186 residual thermal damage, 183 – 184 resurfacing, 555 legal scenario, 755 nonfacial skin, 556 studies, 191 superficial ablation and thermal damage, 556 systems, 38 thermal damage, 555 rhytides resurfacing, 558 perioral, 561 periorbital, 560, 565 scalp tissue, 712 side effects, 190 skin lesions, 193 – 194 skin resurfacing, 190 – 192, 731 – 733 surgery, 69 technique diagrams, 578 thermal damage, 30 treatment, 186 – 187 considerations and contraindications, 187 – 188 indications, 187 results, 190 – 194 techniques, 188 – 189 vaporization, 576

796 Erbium:YAG laser (Contd.) wound healing, 190 wrinkles, 578 Erythema, 352 postoperative, 563 prolonged pigmentation, 352 Esters, 778 Ethylenediamine tetraacetic acid (EDTA), 395 Etidocaine, 778 Eutectic mixture of lidocaine (EMLA, Elamax), 260, 558, 777 LMX, 453 Evaporative cooling skin cooling methods, 406– 407 Excimer lasers, 375– 384 laser phototherapy, 377– 381 hypopigmented scars, 380 psoriasis, 377– 380 vitiligo, 380– 381 laser-tissue interactions, 376 medicinal uses, 375 psoriasis, 382– 383 safety considerations, 381 technology, 375– 376 tissue ablation, 377 treatment guidelines, 382 UVB lasers and light sources, 381–382 vitiligo and hypopigmented scars, 383 Exogenous chromophore, 689 Exogenous cutaneous pigments, 287– 288 Extensive segmental hemangioma, 470 Eye anatomic structure, 84 anatomy, 84– 85 hazards lasers, 83– 84 protection, 88– 91 medical surveillance, 90– 91 patients, 90 Eye and Face Protection Standard, 88 Eyebrow ptosis, 603 Eyebrow lift endoscopic, 604 patient being marked, 606 Eyebrow ptosis lateral, 605 Eyelids. See also lower eyelid; upper eyelid laser treatment, 90 Fabrikant, V.A., 5 Face laser resurfacing and neck lift, 611– 612, 613, 615

Index Face shields, 761 Facial PWS, 448 Facial aging, 590 correction, 590 Facial AK ALA-PDT, 395 Facial photodamage after treatment pulsed light source, 641 Facial ptosis of soft tissue, 612 Facial PWS infant, 452 Facial resurfacing Er:YAG laser, 194 Facial sagging lower, 605 Facial surgery and laser resurfacing, 589 – 615 adjunctive procedures, 601 complications, 601 preoperative assessment, 594 results, 601, 615 technique, 605 – 606 Facial telangiectasia, 251 – 252, 483 argon pumped tunable dye laser continuous and quasicontinuous, 113 – 114 preoperative, 117 treatment, 117 CVL, 117 IPL specific indications, 362 –363 KTP PDL, 480 leg telangiectasias, 306 rosacea, 229 view, 252 Facial vascular lesions, 363 Fat pads preseptal excised, 598 resection, 598 transconjunctival removal, 600 Feathering zone, 707 Federal Laser Product Performance Standard (FLPPS), 82 Female pattern alopecia, 708 Female pattern hair loss intact frontal hairline, 709 – 710 Fentanyl, 782 Filling agents and laser resurfacing, 613 Fire containment, 92 – 93 Fire hazards, 91 Fire prevention, 91 – 92

Index Fitzpatrick Type III rhytides individual legal scenario, 754 Fitzpatrick Type IV complicated individual legal scenario, 754 Flashlamp-pumped pulsed dye laser leg vein laser treatment, 659– 660 PWS, 446– 449 early vs. later treatment, 448 prognostic indicators, 447– 448 recurrence, 448– 449 Flat opacification, 19 Flat opaque scars argon laser surgery, 18 Fluence, 67 PDL, 241 RTD, 138 Fluorescence, 76 Focal hemangioma, 471 infant, 463 Focal laser ablation acne scars, 28 Food and Drug Administration (FDA), 355 gallium-arsenide laser, 35 laser hair removal, 32 Photofrin, 35 Forehead lift endoscopic with frown muscle resection, 607 with laser resurfacing, 601, 604– 607 Free-electron lasers, 65 Frequency doubling, 65 Fresnel reflection, 404 Frown muscles, 602, 607 modification, 606 transblepharoplasty resection, 599 Full-face laser resurfacing and neck lift, 615 Full face shield, 762

Gallium-arsenide laser FDA, 35 Garnet. See neodymium: yttriumaluminum-garnet (Nd:YAG) laser Gaussian beam profile, 131 General anesthesia, 782 General operating principles, 134 Glabellar frown lines, 602 Glucosamine postinflammatory hyperpigmentation, 738 Glycosaminoglycan (GAG), 236 Goldman, Leon, 8, 9, 10, 13, 16, 18, 22, 23, 27 Gould, Gordon, 8

797 Graft size hair transplantation, 703 laser assisted hair transplantation, 706 Green argon laser, 26 Grenz layer, 536 Gunpowder traumatic tattoos, 275 Gynecologic laser, 13 Hailey-Hailey disease lesion treatment, 161 Hair bulb depth, 711 Hair color, 679 ethnic, 695 Hair follicles anatomy, 678 growth cycle, 678 – 679 laser hair removal, 31 treatment QS Nd:YAG laser, 271 Hair grafts, 704 before and after, 707 vs. standard plug, 707 Hairline design laser assisted hair transplantation, 707 –708 Hair loss temporary, 690 Hair reduction long-term, 367 Hair removal, 277, 280, 319, 735 – 737 anesthesia, 784 candidate, 320, 321 diode lasers, 323 IPL, 368 lasers, 409 technology, 683 – 689 light sources pulse duration, 737 technology, 683 – 689 long term IPL, 366 LPA laser, 300 – 305 eye safety, 305 medical history, 303 – 304 patient expectation, 303 physical examination, 304 protocol, 304 – 305 telangiectasia treatment, 305 treatment parameters, 305 noncoherent light source, 365 – 367 treatment techniques, 368 photochemical destruction, 682 photomechanical destruction, 682 photothermal destruction, 681

798 Hair removal (Contd.) pigmentary changes risk, 719 postinflammatory hyperpigmentation, 735 pseudofolliculitis barbae, 308– 309 pulsed diode lasers efficacy, 322– 325 reasons, 680 techniques improvements search, 300 thermal damage, 321 traditional methods, 680 treatment parameters, 322, 324 TRT, 321 usage long-pulsed Nd:YAG lasers, 347 Hair transplantation creating natural and dense, 709– 710 graft size, 703 thickness expectation, 704–705 time frame, 704– 705 Heat, 71 Hemangiomas, 110– 111, 254, 471 KTP lasers, 121– 122 laser therapy criteria, 209 laser treatment, 461– 473 lip, 469 preoperative copper vapor laser treatment, 119 proliferating, 463– 473 pulsed dye lasers, 208– 209 superficial proliferating, 464 pulsed dye laser, 464 superficial segmental infant, 462 Hematoporphyrin derivative (HPD), 388 Hemoglobin absorption curve, 268, 358 light, 69 Nd:YAG laser, 479 targeting lasers treatment, 723 Hemorrhage crusting, 713 Hexascan scanner, 21 Hidradenitis suppurativa lesion treatment, 159 High-efficiency particulate air (HEPA) filter, 97 Hirsutism, 680 Histiocytoma lesion treatment, 160– 161 Hooding and upper eyelid, 594, 595, 602

Index Human immunodeficiency virus (HIV), 96 Human papillomavirus (HPV), 96, 149, 522 – 523 carbon dioxide laser, 150 Human skin ablation, 71 – 72 laser choice, 71 chromophores, 70 chromosomes, 69 – 71 imaging CM, 435 Hydrocystoma lesion treatment, 160 Hydroquinone postinflammatory hyperpigmentation, 738 Hyperpigmentation, 352 leg vein laser treatment, 671 periorbital area, 563 PWS complications and management, 455 Hyperpigmented solar lentigines, 290 Hypertrichosis, 680 Hypertrophic PWS, 449 Hypertrophic scars, 20, 620, 718 before and after, 626 argon laser surgery, 23 carbon dioxide laser treatment, 507 with erythema, 621 linear, 723 prevention, 38 PWS complications and management, 455 traumatic, 226 treatment, 625 – 626 Hypopigmentation, 721 leg vein laser treatment, 671 PWS complications and management, 455 Hypopigmented scars excimer lasers, 383 laser phototherapy, 380 Ideal anesthetic, 776 Indocyanine green (ICG), 328 Industrial lasers, 23 Infant compound nasal tip hemangioma, 463 deep focal hemangioma, 462 facial PWS, 452 focal compound hemangioma, 463 segmental VI hemangioma, 464 superficial segmental hemangioma, 462 Infection, 623 Inflammation, 623

Index Infrabrow skin, 600 Infraorbital block, 778, 779 Infraorbital hyperpigmentation, 499 Intense pulsed light (IPL), 346, 347 concepts, 359–360 device, 355–360 manufacturers and brand names, 356 emission spectrum, 357 hair removal, 368 long term, 366 VascuLight, 369– 370 indications, 361– 368 facial telangiectasias, 362–363 leg telangiectasias, 361– 362 leg vein laser treatment, 665 photoepilation, 365 parameters, 366 pulse duration, 360 sclerotherapy, 370 source, 484– 485 system, 370, 719, 723 International Congress on Applicants of Lasers and Electro-Optics (ICALEO), 15 International Laser Safety Conference (ILSC), 15 International Society for Laser Medicine Surgery, 15 Interstitial laser therapy (ILT), 467 Intravenous sedation, 780– 781 Involuting hemangiomas laser treatment, 468– 471 John A. Hartford Foundation, 8 Joint Commission on Accreditation of Healthcare Organizations (JCAHO), 80, 766 Jowls, 610 Kaplan, Isaac, 15 Kaposi’s sarcoma lesion treatment, 161 Keloidal fibroblasts Nd:YAG laser, 34 Keloids, 621, 718 and hypertrophic scars, 225– 227 collagen fibers, 225 treatment, 226 and nonearlobe keloids laser performance applications, 151– 152 treatment, 227 Ketamine, 782 Klippel-Trenaunay syndrome, 443, 444

799 Kojic acid postinflammatory hyperpigmentation, 738 Krypton laser, 26, 123 – 124 continuous wave lasers, 479 laser parameters, 123 operative considerations, 123 – 124 preoperative treatment telangiectasia, 122 telangiectasia, 123 – 124 wavelength, 478

Lancer Ethnicity Scale (LES), 720 factoring, 718 Large focal hemangioma, 470 Large lip hemangioma, 469 Large nasal tip hemangioma, 468 Large parotid hemangioma, 468 Laser, 24 – 25. See also specific types action schematic, 63 assisted hair removal selective photothermolysis, 74 assisted hair transplantation, 30 – 31, 703 – 714 consult, 703 –704 current challenges, 712 donor region, 705 erbium laser, 713 future, 714 graft size, 706 hairline design, 707 – 708 available listings, 318 basic advantages, 14 beam reflectance, 67 beam variables, 67 biostimulation, 34 – 35 blepharoplasty, 595, 612 with laser resurfacing, 592 – 593, 595 – 600 cooling skin cooling, 408 – 409 delivering energy, 66 delivery, 66 dermatology, 64 – 65, 76 skin cooling, 403 – 412 developments, 27 – 28 energy epidermal absorption, 403 transmission, 66 excisions histology and electron microscopy, 145 eye hazards, 83 – 84 foot pedals, 94

800 Laser (Contd.) hair removal, 31– 33, 409, 678–696 clinical results, 690 ethnic considerations, 695 FDA, 32 hair follicles, 31 histology, 690 legal scenario, 754 melanin, 299 safety, 694– 696 side effects, 693 terminology, 690 thermokinetics, 32 treatment guidelines, 691–692 treatments, 323 hazard classification, 82– 83 impact alcohol, 92 injury thermokinetics, 22 instrumentation and properties Q-switched Nd:YAG laser, 266 irradiation, 71 and laser-tissue interactions dermatology, 59– 76 light characteristics, 61 fundamental physical laws, 67 light amplification, 62 light bulb, 61– 62 light sources near infrared lasers, 453 pulsed KTP lasers, 453 PWS, 452– 453 major classification, 318 masks laser plume hazards, 98 medicine and surgery, 9 noise Er:YAG laser, 184– 186 nonablative skin rejuvenation, 410 and nonlaser photothermal devices vascular lesions treatment, 245 parameters copper vapor lasers/copper bromide lasers, 114–115 Krypton laser, 123 KTP lasers, 119– 120 pulsed dye lasers, 202– 203 PDT polychromatic light source, 389– 390 performance applications, 146– 152 actinic cheilitis, 153– 154 adenoma sebaceum, 147– 148 condyloma acuminata, 150

Index earlobe keloids, 151 epidermal nevi, 155 – 156 keloids and nonearlobe keloids, 151 –152 nail matrixectomy, 150 – 151 sebaceous hyperplasia, 154 – 155 syringoma, 156 trichoepitheliomas, 147 warts, 148 xanthelasma, 156 phototherapy excimer lasers, 377 – 381 hypopigmented scars, 380 vitiligo, 380 – 381 physics, 250, 260 parameters, 241 plume and noise Er:YAG laser, 184 – 186 plume hazards, 95 laser masks, 98 organic compounds, 95 – 96 particulate debris, 96 pathogenicity, 96 – 97 protection and evacuation, 97 principles, 62 – 64 procedure room laser unit, 762 – 763 procurement factors, 758 protective eyewear, 88 Q-switching, 66 resurfacing, 29 – 30, 138, 574 adjunctive procedures, 601 anesthesia, 785 with blepharoplasty, 592 – 593, 595 – 600 and Botox, 614 capabilities, 141 comparison, 585 complications, 601 crow’s feet, 600 with endoscopic forehead lift, 601 – 604 with face and neck lift, 611 – 612 with facial surgery, 589 – 615 with filling agents, 613 infrabrow skin, 600 jowls, 610 legal scenario, 753 lower eyelid, 597 and neck liposuction, 608 – 611 periocular region, 600 photoaging, 590 and platysmaplasty, 610 preoperative assessment, 594 results, 601, 615 technique, 605 – 606

Index techniques, 569– 586 upper eyelid, 595–596 safety American National Standards Institute, 16 – 17 measures, 79– 98 organizations and regulations, 80 skin disease, 403 spot size, 133 sterilization, 162 surgeons, 752 surgery legal considerations, 749–756 patient considerations, 623– 624 tattoo removal, 278– 279 cosmetic, 278– 279 dark skin, 279 medicinal and traumatic, 279 professional and amateur, 278 technique, 251– 256 Photofrin, 35 technique and parameters, 278– 280 technology expansion, 4 therapeutics skin cooling, 412 tissue interaction, 67– 68, 134– 141, 182– 186, 246– 250, 260, 266– 267 clinical examples, 138– 141 Er:YAG laser physics, 182 excimer lasers, 376 high PD with small spots, 140– 141 long exposures in CW low-medium PD defocused mode, 139– 140 low PD and short exposure, 140 patients, 67 PDL, 481 physics, 134– 135 pigmented lesions, 490– 491 selective photothermolysis theory, 266– 267 target chromophore specificity, 267– 268 target destruction, 268– 269 tissue soldering diode laser research applications, 329– 330 treated sites, 642 treatment, 506– 507 acquired vascular lesions, 475– 485 atrophic scaring, 471–473 clinical objectives, 74–75 CM skin surgery applications, 432– 433 cosmetic tattoos, 514 evaluation, 432– 433

801 eyelids, 90 goals, 71, 450 hemangiomas, 461 – 473 involuting hemangiomas, 471 – 472 leg vein, 654 – 674 pigmented lesions, 489 – 500 principles, 260 –261 PWS, 441 – 455, 449 scars, 619 – 632 side effects, 722 skin cooling methods, 75 striae, 619 – 632 surgical correction, 473 tattoos, 288, 505 – 515 thermal tissue destruction, 506 – 507 vascular component, 463 – 464 vascular malformations, 722 unit, 757 –772 accreditation, 766 ancillary laser equipment, 758 – 761 documentation, 764 education and training, 767 equipment, 758 – 761 laser economics, 770 laser procedure room, 762 – 763 lasers, 758 malpractice insurance, 771 marketing, 772 photography and computer imaging, 765 physical credentialing, 767 quality control management, 768 – 769 utilizing cooling skin cooling, 408 – 409 veins sclerotherapy vs. laser treatment, 670 warning signs, 94 wavelength, 250 treatment, 288 Laser Aesthetics Cool Touch Varia, 348 Laser Institute of America, 15 Laser protective eyewear (LPE), 88 types, 89 Laser safety officer (LSO), 768 Laser Safety Resources, 81 Laserscope vein treatment parameters, 342 – 343 Laserscope Lyra, 348, 350, 657 lower-extremity venulectasia, 345 Lateral eyebrow ptosis, 605 Leg telangiectasias, 252 cooling, 410 facial telangiectasias, 306 IPL specific indications, 361 – 362 LPA laser, 306 oxyhemoglobin, 306

802 Leg veins anatomy and physiology, 654 biopsy versapulse laser, 248 diode lasers, 667– 668 laser treatment, 654– 674 complications, 671– 674 continuous wave lasers, 657 crusting, 671 Flashlamp-pumped pulsed dye laser, 659– 660 hyperpigmentation, 671 hypopigmentation, 671 intense pulsed light, 665 KTP lasers, 658– 659 long-pulsed dye lasers, 660– 662 pulsed lasers and light sources, 658– 665 purpura, 671 scarring, 671 theory, 655– 656 thrombus, 671 vesiculation, 671 long-pulsed alexandrite lasers, 665–667 long-pulsed diode laser, 325– 326 complications, 325– 326 efficacy, 325 long-pulsed Neo:YAG, 668– 670 near-infrared lasers, 665– 669 parameters, 362 pretreatment LPA laser treatment, 307, 308 sclerotherapy, 308 telangiectasia, 655, 662 therapy advances, 310 versapulse laser treatment, 253 Leiomyomas, 523 Lenticular injury, 88 Lentigines, 493– 494, 724, 726 Lentigo CALM, 276 Lesional lightening degree PWS, 204– 205 Lesions biological nature, 289 compound or deep proliferating hemangiomas, 464– 466 diagnosis CM, 435 QSRL treatment, 261– 262 treatment, 157– 162 actinic keratosis, 162 basal cell carcinoma, 159 Bowen’s disease, 159

Index chondrodermatitis nodularis helicus, 160 Darier’s disease, 161 dermatosis papulosis nigra, 157 disseminated superficial actinic porokeratosis, 162 Hailey-Hailey disease, 161 hidradenitis suppurativa, 159 histiocytoma or xanthoma disseminatum, 160 – 161 hydrocystoma, 160 Kaposi’s sarcoma, 161 lymphangioma circumscriptum, 160 neurofibromas, 157 – 158 nevus sebaceous, 160 pearly penile papules, 158 Q-switched alexandrite lasers, 293 scar revisions, 159 – 160 seborrheic keratoses, 157 steatocystomas, 158 tattoos, 161 – 162 Leukotrichia, 31 Lidocaine, 558, 706, 777, 778. See also eutectic mixture of lidocaine (EMLA, Elamax) Light amplification laser, 62 assisted hair removal, 736 bulb laser, 61 – 62 delivery PDT, 389 – 390 dosimetry PDT, 390 polychromatic light source, 389 features, 61 lasers characteristics, 61 pulses alexandrite lasers, 287 Light amplified stimulated emission of radiation (laser), 8 Linear ectatic vessels preoperative argon laser treatment, 111 Linear hypertrophic scar, 723 Linear telangiectasias atrophic scar, 480 Lip hemangioma, 469 Lipid soluble isopropylphenol hypnotic agent, 782 Litigation, 750 Local anesthetics, 778

Index Long-pulsed alexandrite (LPA) laser, 297– 310 carbon suspension-assisted Q-switched Nd:YAG treatment, 301 future applications, 310 hair removal, 300–305 eye safety, 305 medical history, 303– 304 patient expectation, 303 physical examination, 304 protocol, 304– 305 telangiectasia treatment, 305 treatment parameters, 305 history, 297– 299 leg telangiectasias, 306, 307– 308 leg veins, 665– 667 long-term efficacy, 301 photothermolysis, 298– 299 pretreatment, 302 safety, 301 studies, 302 scientific history, 298– 300 selective photothermolysis, 298– 299 treatment carbon suspension Q-switched Nd:YAG laser, 301 digital videomicroscopic photos, 301 leg veins pretreatment, 307, 308 telangiectasia histology, 309 TRT, 299 Long-pulsed diode laser, 317– 330 complications, 319– 330 efficacy, 319– 330 history and scientific basis, 318– 319 indications, 319– 330 leg veins, 325– 326 complications, 325– 326 efficacy, 325 pigmented lesions, 326 efficacy, 326 potential complications, 326 technique, 319– 330 vascular lesions, 326 efficacy, 326 mechanism, 326 Long-pulsed dye lasers leg vein laser treatment, 660– 662 Long-pulsed lasers, 479– 484, 723 KTP and frequency doubled ND:YAG laser, 479–480 Nd:YAG lasers, 337– 353, 479, 687 advantages and disadvantages, 338 clinical protocol/studies, 342– 343 hair removal usage, 349– 351

803 laser physics, 338 – 340 laserscope, 347 leg veins, 668 – 670 lower-extremity vessels, 353 Lumenis VascuLight, 350 popularity, 347 presently available technologies, 347 safety, 338 Sciton Image, 347 side effects, 352 Long-pulsed ruby laser congenital nevus, 498 Long pulse duration pulsed dye laser, 225 clinical uses, 219 – 240 developments, 241 PWS, 220 – 225 Long term hair reduction, 367 Long term hair removal IPL, 366 Loose neck skin, 613 Loose skin lower eyelid, 593 Lower-extremity telangiectasias, 231 – 233 Lower-extremity veins TRT, 339 Lower-extremity venulectasia Laserscope Lyra, 343 Lower-extremity vessels long-pulsed Nd:YAG laser, 347 treatment, 349 – 351 Lower eyelid bags, 593, 594, 602 laser resurfacing with blepharoplasty, 597 loose skin, 593 Lower facial sagging, 605 Low-fluence Q-switched Nd:YAG laser, 645 Lumenis, 342 Lumenis VascuLight long-pulsed Nd:YAG lasers clinical protocol/studies, 342 – 347 treatment parameters, 348 – 351 Lupus erythematosis, 233 Lymphangioma circumscriptum lesion treatment, 160 Magic bullet agents, 719 Magnetic resonance imaging (MRI), 416 Maiman, Theodore, 7 Male pattern alopecia, 704 Malignant melanoma, 432 Malpractice, 750 Malpractice insurance laser unit, 771

804 Marketing laser unit, 772 Maser, 5, 6 Massachusetts General Hospital (MGH), 25 Matted telangiectasia preoperative Krypton laser treatment, 122 Maximal thermal content, 445– 446 Maximum permissible exposure (MPE), 88 Mechanically shuttered pulses and superpulsing, 132–133 Medical lasers identification, 64 Medication, 623 Melanin, 679 absorption, 509, 510, 512, 724 ALA-PDT, 393 curve, 268 spectrum, 490 wavelengths, 70 laser hair removal, 299 major chromophore, 224 Melanocytic lesions confocal images, 431 QSRL histology, 270 Melanocytic lesions removal, 279– 280 common acquired nevi, 279– 280 dermal melanocytic nevi, 279 epidermal, 279 Melanocytic nevi, 430, 497– 498 melanocytic lesions removal, 279 Melanocytic skin tumors, 429– 432 Melanoma PDT dermatology applications, 396 treatment, 27 Melanosomes absorption, 508 destruction, 724 Melesma, 732 Mental block, 779, 780 Mepivicaine, 778 Mesenchymal reactivity, 718 Mester, E., 34 Microvascular lesions, 720– 723 pigmentary changes risk, 720 Microwave amplified stimulated emission of radiation (MASER), 5 Microwave delivery system, 689 Midazolam, 781 Millisecond Nd:YAG, 645 Minimal erythema dose (MED), 378 possible combination treatment, 383 psoriasis treatment, 379

Index Mixed epidermal and dermal pigmented lesions, 727 Molecules energy level structure, 69 Morphometric analysis CM normal skin, 421 – 422 Motor vehicle accident traumatic tattoos, 506 Mucosal lesions, 521 – 522 ablation, 526 Multiple pulsing concepts noncoherent light source, 359 – 360 Nail matrixectomy laser performance applications, 150 – 151 Nasal hemangioma, 469 Nasal tip hemangioma, 468 National Institute of Health and Occupational Medicine, 8 Nd:YAG. See neodymium: yttriumaluminum-garnet (Nd:YAG) laser Near infrared lasers PWS lasers and light sources, 453 Neck lift, 613 with full-face laser resurfacing, 615 with laser resurfacing, 611 – 612 Neck liposuction, 608 – 611 platysmaplasty, 610 with platysmaplasty, 610 Neodymium: yttrium-aluminum-garnet (Nd:YAG) laser, 25, 33, 720 after nonablative dermal remodeling, 645 commercially available, 185 hemoglobin absorption, 479 injury, 87 keloidal fibroblasts, 34 long-pulsed lasers, 479 before nonablative dermal remodeling, 645 photon, 70 pigment removal, 509 Q-switched lasers, 509 – 510 scarring, 509 systems available, 342 vascular lesions, 492 Neurofibromas, 523 lesion treatment, 157 – 158 Nevus flammeus, 721 Nevus of Ota, 276, 287, 496 – 497, 725, 727 Nevus sebaceous lesion treatment, 160

Index Nevus spilus, 726 Nidek Unipulse laser, 143– 144 Nominal hazard zone (NHZ), 88 Nonablative lasers facial rejuvenation, 649 near-infrared, 640 photoaging treatment, 590 rejuvenation diode, 327– 328 skin rejuvenation, 410 cooling, 411 Nonablative skin remodeling PDL, 236– 241 Noncoherent intense pulsed light, 640– 642 Noncoherent light source adverse reactions, 368– 369 hair removal, 365–367 multiple pulsing concepts, 359– 360 photorejuvenation, 365 poikiloderma, 363– 365 pulse duration, 359 spot size, 357 treatment techniques, 367– 368 hair removal, 368 vascular lesions, 367– 368 wavelength, 356 Nonfacial skin Er:YAG laser resurfacing, 556 Nonlaser photothermal devices and lasers vascular lesions treatment, 246 Nonmelanocytic skin tumors, 426– 429 Nonneoplastic skin lesions, 425 Non-Q-switched millisecond Nd:YAG laser with fluences, 642– 643 Nonspecific thermal damage zone, 572 Nonwhite skin laser treatment, 717–740 clinical applications, 719– 720 complications, 737 epidermal cooling, 739– 740 sun avoidance, 738 teaching, 738 NovaPulse laser, 143 Nuclear debris Er:YAG laser, 572 inflammatory PMNs, 572 removal, 574, 575 Occupational Safety and Health Administration (OSHA), 82, 769 Ocular protection, 760 Optical coherence tomography (OCT), 416 Optical density (OD), 88

805 Otolaryngologist legal scenario, 753 Oxygenated hemoglobin, 340 Oxyhemoglobin, 720 leg telangiectasias, 306

Pain management postoperative, 785 Palmar capillary hemangioma, 208 Palomar Medical Corporation, 405 cooling handpiece, 405 Paradoxical darkening, 262 Paranasal hemangioma surgical resection, 472 Parotid hemangioma, 468 Patel, C.K.N., 12 Pathologic process treatment, 16 Patient compliance, 624 Patient safety-scar, 17 – 22 Pearls technique, 162 –163 cutting, 163 CW vaporization, 162 – 163 Pearly penile papules, 523 lesion treatment, 158 Perifollicular edema, 324 Periocular region resurfacing, 600 Periocular wrinkles, 594 Perioperative considerations, 108 – 109 sunlight, 108 Perioral area acne, 564 Perioral rhytides Er:YAG laser resurfacing, 561 Periorbital area hyperpigmentation, 563 Periorbital rhytides Er:YAG laser resurfacing, 560, 565 Periungal wart preoperative view, 527 Periungal wart preoperative surgery, 148 Periungal warts, 149 Permanent hair reduction, 690 Personnel and patient safety-plume, 17 Phencyclidine derivative, 782 Phenylephrine, 777 Phenylpiperidine derivative, 782 Photoaging correction, 590 laser resurfacing, 590 topical treatments, 536

806 Photoaging (Contd.) treatment erbium: YAG, 590 nonablative lasers, 590 variable pulse duration erbium: YAG, 590 Photochemistry, 76 Photodamage legal scenario, 756 Photodynamic diagnosis (PDD), 391 Photodynamic therapy (PDT), 35–36, 76, 329, 387– 399, 689 cosmic results, 398 cutaneous photosensitivity, 398 dermatology applications, 391– 398 acne, 396– 397 actinic keratoses (AK), 389 BCC, 394– 395 Bowen’s Disease, 395– 396 complication prevention and management, 398 cutaneous T-cell lymphoma, 397 melanoma, 396 psoriasis, 397 recalcitrant warts, 396 squamous cell carcinoma (SCC), 396 diode laser research applications, 329 future, 35– 36 light delivery, 389– 390 photoinduced destruction, 390 photosensitizers, 388– 389 polychromatic light source, 389 lasers, 389– 390 light dosimetry, 390 skin cancer, 36 skin cancers, 330 Photofrin FDA, 35 laser technique, 35 Photofrin (porfimer sodium), 35 Photography and computer imaging laser unit, 765 Photoinduced destruction PDT, 390 Photokinetic selectivity, 360 Photon, 61 energy, 76 Nd:YAG lasers, 70 tissue entrance, 68 Photorejuvenation, 366 noncoherent light source, 365 Photosensitizers modern studies, 35 PDT, 388–389

Index Phototherapy dermatology, 384 skin lesions, 384 Photothermolysis alexandrite lasers, 286 LPA laser, 298 – 299 theory, 710 laser-tissue interactions, 266 –267 Physical credentialing laser unit, 767 Physical destruction codes, 770 Pigment allergic responses tattoos, 513 Pigmentary alteration, 274 – 275, 281 risk, 719 Pigmentary scarring, 281 Pigmentation prolonged erythema, 349 types, 498 Pigment-containing cells destruction, 491 Pigmented lesions, 112, 724 clinical treatment, 493 –500 epidermal pigmented lesions, 493 –496 laser tissue interactions, 490 – 491 laser treatment, 489 – 500 long-pulsed diode laser, 326 pigmentary changes risk, 719 postoperative care, 290 Q-switched and pulsed lasers and light sources, 491 – 493 removal, 37, 275 – 277 acquired melanocytic nevi, 277 congenital nevi, 277 selective photothermolysis, 74 treatment, 492, 494 treatment considerations, 288 – 289 Pigmented skin vs. white skin, 718 Pigment laser Q-switched alexandrite lasers, 285 Pigment lasers, 26 – 27 Pigment removal Nd:YAG laser, 509 Plantar verruca, 210 Plantar Warts technique treatment, 527 Platysmaplasty and neck liposuction, 610 Pluggy hair transplants, 704 Plugs, 704 vs. hair grafts, 707 Poikiloderma Civatte, 254

Index Poikiloderma IPL, 364 neck, 364 noncoherent light source, 363– 365 treatment, 364 Polychromatic light source PDT, 389 Polymorphonucleocytes (PMNs), 571 nuclear debris, 572 Porfimer sodium, 35 Port-wine stain (PWS), 18, 200, 220, 253–254 carbon dioxide laser surgery, 14 children, 12 clinical conditions, 220 comparative studies, 37 complications and management, 454–455 atrophic and hypertrophic scars, 455 dermatitis, 455 hyperpigmentation, 455 hypopigmentation, 455 reticulation, 454 skin graying or whitening, 455 continuous wave argon laser, 106– 108 continuous wave laser treatment, 446 CVL treatment, 116 darkening, 204 diagnosis, 442 facial, 448 Flashlamp-pumped pulsed dye laser, 446– 449 early vs. later treatment, 448 prognostic indicators, 447– 448 PWS recurrence, 448– 449 histologic evidence, 481 KTP lasers, 120– 121 lasers and light sources, 452– 453 near infrared lasers, 453 pulsed KTP lasers, 453 laser tissue interaction, 445– 446 pulse duration and thermal relaxation time, 445 selective photothermolysis, 445 spot size, 445– 446 wavelength, 445 laser treatment, 441– 455, 449 lesional lightening degree, 204– 205 long pulse duration pulsed dye laser, 220–225 lower extremity, 224 patents response, 205 pathogenesis, 444– 445 patient energy dosages, 206 PDL, 408 treatment, 221, 223 pediatric studies, 206

807 preoperative argon laser treatment, 107 preoperative argon pumped tunable dye laser treatment, 113, 114, 116 – 117 preoperative copper vapor laser treatment, 116 prior PDL treatment, 222 pulsed dye lasers, 203 –207 pulsed dye laser treatment, 448 radiotherapy, 11 related symptoms, 443 – 444 skin grafting, 11 studies, 116 Sturge-Weber syndrome, 443 therapeutic challenge, 252 – 253 treatment, 404, 446, 722, 782 active skin cooling, 452 improvements, 449 purpura, 454 techniques, 107, 454 vascular anomalies, 442 – 443 vascular ectasia, 447 Versapulse laser treatment, 253 view, 205 Postinflammatory hyperpigmentation (PIH), 27, 275, 498, 557 alpha-hydroxy acids, 738 arbutin, 738 following treatment of nevus of Ota, 725 hair removal, 735 treatment, 738 Postoperative erythema, 563 Postoperative pain management, 785 Postoperative wound care, 22 dressings, 22 Postprocedure considerations complications, 281 wound care, 280 Postsurgery telogen effluvium, 704 Potassium titanyl phosphate (KTP) lasers, 119 – 123, 720 crystal, 26, 65 and frequency doubled ND:YAG laser long-pulsed lasers, 479 – 480 hemangioma, 121 – 122 laser parameters, 119 – 120 leg vein laser treatment, 658 – 659 PDL facial telangiectasias, 480 perioperative considerations, 121 port-wine stains, 120 – 121 preoperative treatment spider veins, 121 pulsed, 245 – 255 telangiectasias, 120 – 121

808 Preoperative argon laser treatment linear ectatic vessels, 111 port-wine stain, 107 telangiectasias, 110 Preoperative argon pumped tunable dye laser treatment facial telangiectasia, 117 perioperative considerations, 117 pigmented lesions, 118 port-wine stain, 113, 114, 116– 117 telangiectasias, 115 vascular lesions, 117– 118 Preoperative copper vapor laser treatment ectatic vessels, 119 hemangioma, 119 port-wine stain, 116 telangiectasias nose, 118 Preoperative Krypton laser treatment diffuse telangiectasia, 122 matted telangiectasia, 122 venous lake lip, 123 Preoperative KTP laser treatment spider veins, 121 telangiectasias, 120 Preoperative view warts, 149 Prescars, 623, 632 Preseptal fat pads excised, 598 resection, 598 Prilocaine, 558, 777, 778 Primary alexandrite rod, 286 Primary rod Q-switched alexandrite lasers, 285 Principle of selective photothermolysis, 719 Procaine, 778 Procedural control measures, 769 Programmed cell death skin aging, 553 Prokhorov, Aleksander, 8 Proliferating hemangiomas, 464– 471 compound or deep lesions, 470– 471 ulcerated lesions, 467– 469 Prolonged erythema pigmentation, 346 Propionibacterium acnes, 396 Propofol, 782 Pseudofolliculitis barbae, 308– 309, 325 permanent hair removal, 308– 309 Psoriasis, 235– 236 CM, 422 excimer laser, 382– 383 excimer lasers laser phototherapy, 377– 380

Index PDL treatment, 235 PDT dermatology applications, 397 topical treatment, 384 treatment MED, 379 Ptosis of face and neck, 615 Public awareness and education, 771 Pulsed carbon dioxide lasers and continuous wave, 129 – 165 Pulsed diode lasers, 245 – 255, 319 – 326 complications, 324 –325 hair removal efficacy, 322 – 325 Pulsed dye laser (PDL), 199 – 213, 220, 454, 477, 480 – 484, 639 after nonablative dermal remodeling, 640 applications, 210 APTDL, 482 basic concepts, 199 – 202 benign vascular disorders, 209 – 210 clinical effectiveness, 203 clinical use, 221 controversy, 209 – 210 development, 221 fluence, 240 hemangiomas, 208 – 209 increased risks, 482 – 483 irradiation immediate reaction, 739 laser parameters, 201, 202 – 203 laser-tissue interaction, 481 limitations treatment, 212 long pulse duration clinical uses, 219 – 240 new generation, 220 before nonablative dermal remodeling, 640 nonablative skin remodeling, 236 – 241 nonvascular lesions, 210 perioperative considerations, 626 postoperative considerations, 211 – 212, 627 preoperative considerations, 211 – 212, 626 pulse duration, 200 pumped development, 112 – 113 PWS, 200, 203 – 207, 408 test sites, 204 rhytides, 211 safety, 202 side effects, 212 superficial hemangiomas, 464 systems, 202 telangiectasias, 207 – 208, 236 test site placement, 207

Index telangiectasias treatment, 483 telangiectatic lesions, 481 tissue response, 200 treatment, 226, 446– 452, 465 anesthesia, 784 efficacy study, 228 psoriasis, 235– 236 pulse duration, 449– 450 PWS, 221, 223, 448 rosacea, 230 skin cooling, 450 spot size and overlap, 449 of vascular lesions, 784 verrucae, 227 wavelength, 449 variety, 212 Pulsed KTP lasers, 245– 255 PWS lasers and light sources, 453 Pulsed lasers, 65 continuous wave, 65– 66 and light sources leg vein laser treatment, 658– 665 treatment tattoos, 507– 508 Pulsed light source, 31 facial photodamage after treatment, 641 telangiectases of face, 641 Pulsed noncoherent broad band light sources, 688 Pulse duration effect, 136 hair removal light sources, 737 IPL, 360 noncoherent light source, 359 Pulsed dye laser treatment, 449– 450 Q-switched alexandrite laser, 286 –287 and thermal relaxation time laser tissue interaction, 445 PWS, 445 TRT, 268 Pulse flashlamp-excited dye laser (PLDL), 26 Candela Q-switched lasers, 511 Pulse overlap, 369 Punch harvesting, 704 Purpura, 627 leg vein laser treatment, 671 PWS treatment, 454 Pyogenic granulomas (PG), 152– 154 acne keloidalis nuchae, 152– 153 preoperative lesion, 153 Pyrolysis, 136

809 Q-switched alexandrite laser (QSAL), 285 – 293 complications and side effects, 293 lesion treatment, 293 pigment specific laser, 285 primary rod, 285 pulse duration, 286 – 287 QS Nd:YAG laser, 276 systems and specifications, 293 tattoo removal, 729 – 731 textural changes and scarring, 291 treatment guidelines, 290 nevus of Ota, 728 pearls, 289 –291 side-effects and complications, 291 – 292 tattoo, 291 wavelength, 510 Q-switched and pulsed lasers and light sources pigmented lesions, 491 – 493 Q-switched lasers, 508 – 511 Alexandrite laser, 510 – 511 Candela PDPL, 511 comparative studies, 514 – 515 Nd:YAG laser, 509 – 510 ruby laser, 508 – 509 side effects, 512 –513 treatment, 511 – 512 intervals, 512 numbers, 512 parameters, 511 – 512 tattoo, 500 Q-switched Nd:YAG (QSYAG) laser, 34, 265 – 282, 687, 724 after nonablative dermal remodeling, 643 disadvantages, 274 hair follicle treatment, 271 laser instrumentation and properties, 266 before nonablative dermal remodeling, 643 QS alexandrite laser, 276 tattoo, 270 removal, 729 treatment, 273 nevus of Ota, 725 traumatic tattoo, 275 Q-switched ruby laser (QSRL), 259 – 264, 490, 724 histology, 269 depth of penetration, 269 melanocytic lesions, 270 tattoo removal, 269

810 Q-switched ruby laser (QSRL) (Contd.) history, 259– 260 tattoo removal, 271– 275, 729– 731 treatment, 260, 493, 495, 496 benign pigmented lesions, 261 CALM, 495 complications, 262 danger, 262 dermal lesions, 261 indications, 271– 277 lesions, 261– 262 nevus of Ota, 725 Q-switched ruby laser-resistant tattoo removal QSRL treatment indications, 272 Q-switching, 25– 26, 66 lasers, 66 selective photothermolysis, 26 tattoos, 25 Quality control management laser unit, 768– 769 Quasicontinuous argon-pumped tunable dye laser, 112–114

Radiation amplification, 5 stimulated emission, 63 therapy postoperative, 152 PWS, 11 tissue damage, 69 Radiation Control for Health and Safety Act of 1969, 16 Radiofrequency (RF) powers supplies, 133 Razor bumps, 325 Recalcitrant warts PDT dermatology applications, 396 Red lip liner tattoo, 513 Red vessel clinical treatment, 360 Reepithelialization, 573 wound, 570 Reflectance laser beam, 67 Reflectance confocal microscopy, 417 clinical dermatology, 415–435 Reflections diagrammatic representation, 86 Regional anesthesia, 778– 779 Relaxation, 68 Residual fibro-fatty tissue, 466 Residual telangiectatic matting, 362

Index Residual thermal damage (RTD), 135 – 138 cutaneous studies, 29 Er:YAG laser, 183 – 184 various parameters, 135 Resurfacing, 28 – 30, 607 laser comparison, 141 – 144 periocular region, 600 studies Er:YAG laser, 191 system, 144 Reticulation PWS complications and management, 454 Retina division, 83 injury, 87 Retin-A, 536 Rhinophyma, 523, 530 preoperative surgery, 146 technique treatment, 529 Rhytides, 277, 280 Er:YAG laser resurfacing, 558 Fitzpatrick Type III legal scenario, 754 legal scenario, 753, 755, 756 pulsed dye lasers, 211 Rhytides resurfacing anesthesia, 784 erbium:YAG laser, 558 perioral, 561 periorbital, 560, 565 Robotized hexagonal scanners, 20 Rosacea, 363 facial telangiectasias, 229 PDL treatment, 230 Rosacea and facial telangiectasias, 228 – 230 Ruby laser, 683 – 686 inventor, 7 long-pulsed congenital nevus, 498 optical, 9 Q-switched lasers, 508 – 509 Ruby optical maser, 7 Safety, 624 carbon dioxide laser, 163 – 164, 524 – 525 excimer lasers, 381 eye safety, 305 International Laser Safety Conference (ILSC), 15 laser American National Standards Institute, 16 – 17 measures, 79 – 98 organizations and regulations, 80

Index laser safety officer (LSO), 768 Laser Safety Resources, 81 long-pulsed alexandrite (LPA) laser, 301, 302 long-pulsed Nd:YAG lasers, 344 Occupational Safety and Health Administration (OSHA), 82, 769 patient safety-scar, 17– 22 PDL, 202 personnel, 17 Radiation Control for Health and Safety Act of 1969, 16 Salmon patch, 442 Saphenous vein closure bare fiber diode lasers, 326– 327 Scalpel harvesting, 704 Scalp tissue erbium laser, 712 histology, 712 Scanner-driven SilkTouch laser, 29 Scanners, 20 carbon dioxide lasers, 20 Scars, 704. See also specific type argon laser, 106 classification, 620– 622 laser treatment, 619– 632 leg vein laser treatment, 671 Nd:YAG laser, 509 resurfacing anesthesia, 784 revisions lesion treatment, 159– 160 Scattered energy tissue damage, 67 Schawlow, Theodore, 7 Sciton contour laser resurfacing combined laser resurfacing techniques, 586– 587 Sciton Image long-pulsed Nd:YAG lasers clinical protocol/studies, 342– 347 Sciton Profile, 348, 351 Sclerotherapy IPL, 370 vs. laser treatment laser veins, 670 leg veins pretreatment, 308 Sebaceous gland hyperplasia, 234– 235, 429 histopathology, 430 laser performance applications, 154– 155 Seborrheic keratosis, 158 lesion treatment, 157 Segmental VI hemangioma infant, 464

811 Selective epidermal cooling, 404 Selective photothermolysis, 23, 24, 72 – 73, 445 achievement, 445 cutaneous blood vessels, 73 laser assisted hair removal, 74 pigmented lesions, 74 PWS laser tissue interaction, 445 Q-switching, 26 skin cooling, 74– 76 tattoos, 74 treatment, 507 theory, 710 Seminal events and personae, 5 Septum orbiculare incised, 597 Sequential carbon dioxide erbium laser resurfacing, 549 Sharplan microslad scanner, 21, 28 Shorter pulses advantages, 137 SilkLaser, 142 – 143 Single pulse vaporization carbon dioxide laser resurfacing, 537 – 538 Skin ablation, 71 – 72 laser choice, 71 aging programmed cell death, 553 cancer PDT, 330 photodynamic therapy, 36 chromophores, 70 chromosomes, 69 – 71 color ethnic, 695 cooling, 656 –657 contact cooling, 405 – 406 convective cooling, 407 – 408 cooling future, 411 – 412 evaporative cooling, 406 – 407 laser dermatology, 403 – 412 lasers utilizing cooling, 408 – 410 laser therapeutics, 412 laser therapy, 75 methodology development, 76 methods, 405 – 408 pulsed dye laser treatment, 450 selective photothermolysis, 74 – 76 vascular lesions, 409 disease lasers, 403

812 Skin (Contd.) grafting PWS, 11 graying or whitening PWS complications and management, 455 hazards, 91 imaging CM, 435 laser beam variables, 67 lesion CM applications, 426– 432 nonneoplastic, 425 phototherapy, 384 and orbicularis muscle resected, 597 phototype, 623 classification, 718 pigmentation absorption spectra, 246 non-Caucasian vs. Caucasian, 718 rejuvenation topical agents, 553 resurfacing, 731– 734 atrophic scaring, 472 carbon dioxide lasers, 535– 540, 731– 733 Er:YAG laser, 190– 192, 731– 733 pigmentary changes risk, 719 surgery applications, 432– 433 dermatologic surgery, 432 laser treatment evaluation, 432– 433 tumors CM, 426– 432 nonmelanocytic, 426– 429 SmartCool cold air blower, 465 Smoke evacuation systems, 759 Smoke evacuators, 97 Society for Laser Medicine and Surgery, 15 Solar lentigines, 727 Solar lentigo, 276 Solar telangiectases legal scenario, 753 Solid-state lasers examples, 64 Spider angioma, 484 Spider telangiectasia, 250 Spider veins, 232 development, 229 Spot size wavelength, 358 Squamous cell carcinoma (SCC) BCC, 427

Index diode laser, 330 research applications, 330 PDT dermatology applications, 396 Standard plug vs. hair grafts, 707 Steatocystomas lesion treatment, 158 Steel punch vs. laser, 712 Stretch marks treatment, 722 Striae, 233 – 234 distensae, 622 before and after, 628 laser treatment, 619 – 632 Sturge-Weber syndrome, 443 PWS, 443 Sun avoidance nonwhite skin laser treatment, 738 Sun burn, 384 Sun damage, 615 Superficial ablation Er:YAG laser resurfacing, 556 Superficial epithelial cell layer CM image, 421 Superficial folliculitis confocal images, 427 Superficial hemangiomas pulsed dye laser, 464 Superficial proliferating hemangiomas, 467 Superficial resurfacing carbon dioxide lasers, 549 – 550 Superficial segmental hemangioma infant, 462 Super long pulse (SLP) diode lasers, 323 Superpulsed (SP) technology, 132 Supraorbital block, 778, 779 Surgical correction laser treatment, 473 Surgical instruments, 761 Surgical masks, 761 standard, 98 Surgical resection paranasal hemangioma, 472 Svelto, Orazio, 8 Swiss Patent Office, 6 Syringomas, 523 laser performance applications, 156 preoperative view, 156 technique treatment, 528 Systemic lupus erythematosis (SLE), 233 cutaneous lesions, 233

Index Target chromophore specificity laser-tissue interactions, 267– 268 Tattoo, 496– 500 allergic dermatitis, 292 amateur, 499 blue-black, 510 categorization, 287 cutaneous allergic reactions, 292 gang related, 506 ink darkening, 274, 281 laser treatment, 505– 515 pulsed, 507– 508 QS Nd:YAG, 270 Q-switched, 500 Q-switched alexandrite, 291 wavelength, 288 pigment allergic responses, 513 pigment explosion, 26 postoperative care, 290 Q-switching, 25 selective photothermolysis, 74 side effects, 512–514 allergic reactions, 513 and complications, 500 epidermal debris, 513– 514 ink darkening, 513 pigmenting and textural changes, 513 treatment lesion, 161–162 selective photothermolysis, 507 Tattoo removal, 729– 731 anesthesia, 783, 784 blistering, 730 immune system, 288 laser technique and parameters, 278– 279 cosmetic, 278– 279 dark skin, 279 medicinal and traumatic, 279 professional and amateur, 278 pigmentary changes risk, 719 QSAL, 730 QSRL, 729 cosmetic, 273– 274 dark pigmentation, 272– 273 disadvantages, 274– 275 histology, 269 medicinal and traumatic, 272– 273 treatment indications, 271– 275 QSYAG, 730 session number, 512 Teeth hazards, 91 Telangiectases of face pulsed light source, 640

813 Telangiectasias, 109, 254 ankle, 666 argon lasers lesions, 109 histology LPA laser treatment, 309 Krypton laser, 123 – 124 KTP lasers, 120 – 121 leg veins, 655, 662 linear atrophic scar, 480 lower extremity treatment, 231 lower-extremity, 231 – 233 nose preoperative copper vapor laser treatment, 118 PDL, 207 – 208, 236 treatment, 483 perinasal, 208 preoperative argon laser treatment, 110 pumped tunable dye, 115 preoperative KTP laser treatment, 120 prior PDL treatment, 237 thigh, 670 Telangiectatic lesions PDL, 481 Temporary hair loss, 690 Tetracaine, 778 Tetrafluoroethane (TFE), 75, 451 Theory of selective photothermolysis, 710 Thermal damage Er:YAG laser resurfacing, 555, 556 specific to nonspecific, 72 Thermal destruction time (TDT), 300 Thermal injury, 87 histology, 592 Thermal necrosis, 559 Thermal quenching, 342 Thermal relaxation time (TRT), 267, 445 alexandrite lasers, 286 hair removal, 321 long-pulsed alexandrite lasers, 299 lower-extremity veins, 339 pulse duration, 268 Thermal tissue destruction laser treatment, 506 – 507 Thermokinetic selectivity (TKS), 299 Thigh telangiectasia, 670 venulectasia, 670 Threshold radiant exposure, 727 Thrombus leg vein laser treatment, 671

814 Tissue ablation excimer lasers, 377 characteristics, 68 damage radiation, 69 scattered energy, 67 entrance photons, 68 vaporization, 72 carbon dioxide lasers, 554 Topical agents skin rejuvenation, 553 Topical anesthesia, 777 Townes, Charles H., 5, 6 Transblepharoplasty resection frown muscles, 599 of glabella frown muscles, 602, 596, 604 Transconjunctival lower lid incision, 599 Transconjunctival removal fat pads, 600 Transient pigmentary changes, 730 Transient postinflammatory hyperpigmentation, 494 Traumatic tattoos motor vehicle accident, 506 treatment QS Nd:YAG laser, 275 Tretinoin postinflammatory hyperpigmentation, 738 Trichloroacetic acid, 28 Trichoepitheliomas laser performance applications, 147 TruPulse laser, 144 beam profile, 132 Tuberous sclerosis preoperative surgery, 148 Tumescence donor ellipse, 706 Tumor ablation anesthesia, 784 Tunable dye lasers, 720. See also argon-pumped tunable dye laser (APTDL) Ulcerated lesions proliferating hemangiomas, 466– 470 Ulceration, 466 Ultra-long pulse duration PDL, 229 Ultra-low particulate air filter, 97 Ultra-low penetration air filter, 163 UltraPulse laser, 30, 142– 143 UltraPulse mode, 133 Ultrastructure carbon dioxide LSR, 145

Index Ultraviolet (UV) irradiation, 738 lasers and light sources excimer laser, 381 – 382 Unger, Walter, 30 Upper eyelid anesthesia, 595 blepharoplasty carbon dioxide laser, 596 hooding, 595, 602 with hooding, 594 laser blepharoplasty, 602, 604 laser resurfacing with blepharoplasty, 595 – 596 US Federal Laser Product Performance Standard, 82 US Food and Drug Administration, 355, 484. See also Food and Drug Administration (FDA)

Vaporization, 582 carbon dioxide lasers, 535 Er:YAG laser, 576 single pulse carbon dioxide laser resurfacing, 537 – 538 Variable pulse duration erbium: YAG photoaging treatment, 590 Vascular abnormalities, 73 Vascular anomalies PWS, 442 – 443 Vascular component laser treatment, 463 – 464 Vascular ectasia PWS, 447 Vascular lesions, 110 anesthesia, 783 laser treatment, 108 long-pulsed diode laser, 326 Nd:YAG lasers, 492 noncoherent light source treatment techniques, 367 – 368 post-laser treatment patient care sheet, 109 preoperative argon pumped tunable dye laser treatment, 117 – 118 pulse durations, 247 skin cooling, 409 treatment argon laser, 106 CSC, 410 laser and nonlaser photothermal devices, 245

Index Vascular malformations laser treatment side effects, 722 VascuLight IPL hair removal, 369– 370 long-pulsed Nd:YAG lasers clinical protocol/studies, 342– 347 treatment parameters, 346 V-beam long PDL, 483, 484 Veins. See also leg veins lower-extremity TRT, 359 saphenous vein closure bare fiber diode lasers, 326–327 spider, 232 development, 229 Venous lake lip preoperative Krypton laser treatment, 123 Venous lakes, 254 Venulectasia ankle, 666 lower-extremity Laserscope Lyra, 348 thigh, 670 Verrucae, 227– 228 PDL treatment, 227 Versapulse laser leg vein biopsy, 248 treatment leg veins, 249 PWS, 253 Vesiculation leg vein laser treatment, 671 Vessels lower-extremity long-pulsed Nd:YAG laser, 337– 353 Vitiligo excimer lasers, 383 laser phototherapy, 380– 381 topical treatment, 384

815 Warning sign, 763 door, 762 – 763 Warts laser performance applications, 148 preoperative view, 149 Water absorption vs. laser wavelength, 591 Wavelengths krypton laser, 478 melanin absorption, 70 noncoherent light source, 356 pulsed dye laser treatment, 449 PWS laser tissue interaction, 445 specific laser eye protection, 89, 761 spot size, 358 Weber, Joseph, 5 Wellman lab, 24 – 25 Wound reepithelialization, 570 Wound care postoperative, 22 postprocedure considerations, 280 Wound healing carbon dioxide lasers, 144 – 145 diode laser research applications, 330 Wrinkles Er:YAG lasers, 578 Xanthelasma laser performance applications, 156 preoperative view, 157 Xanthoma disseminatum lesion treatment, 160 – 161 XRT. See radiation, therapy

Yttrium. See neodymium: yttriumaluminum-garnet (Nd:YAG) laser

Zimmer cold air blower, 408

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