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Clinical Procedures in Laser Skin Rejuvenation
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SERIES IN COSMETIC AND LASER THERAPY Published in association with the Journal of Cosmetic and Laser Therapy
Already available 1. David Goldberg. Fillers in Cosmetic Dermatology. ISBN: 1841845094 2. Philippe Deprez. Textbook of Chemical Peels. ISBN: 1841844950 3. C William Hanke, Gerhard Sattler, Boris Sommer. Textbook of Liposuction. ISBN 1841845329
Of related interest 1. Robert Baran, Howard I Maibach. Textbook of Cosmetic Dermatology, 3rd edition. ISBN: 1841843113 2. Anthony Benedetto. Botulinum Toxin in Clinical Dermatology. ISBN: 1842142445 3. Jean Carruthers, Alistair Carruthers. Using Botulinum Toxins Cosmetically. ISBN: 1841842176 4. David Goldberg. Ablative and Non-Ablative Facial Skin Rejuvenation. ISBN: 1841841757 5. David Goldberg. Complications in Cutaneous Laser Surgery. ISBN: 1841842451 6. Nicholas J Lowe. Textbook of Facial Rejuvenation. ISBN: 1841840955 7. Shirley Madhere. Aesthetic Mesotherapy and Injection Lipolysis in Clinical Practice.ISBN: 1841845531 8. Avi Shai, Howard I Maibach, Robert Baran. Handbook of Cosmetic Skin Care. ISBN: 1841841793
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Clinical Procedures in Laser Skin Rejuvenation Edited by
Paul J Carniol MD FACS Cosmetic Laser and Plastic Surgery Summit, NJ USA
Neil S Sadick MD FAAD FAACS FACP FACPh Sadick Aesthetic Surgery and Dermatology NewYork, NY USA
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© 2007 Informa UK Ltd First published in the United Kingdom in 2007 by Informa Healthcare,Telephone House, 69–77 Paul Street, London EC2A 4LQ. Informa Healthcare is a trading division of Informa UK Ltd. Registered Office: 37/41 Mortimer Street, London W1T 3JH. Registered in England and Wales number 1072954. Tel: +44 (0)20 7017 5000 Fax: +44 (0)20 7017 6699 Website: www.informahealthcare.com All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior permission of the publisher or in accordance with the provisions of the Copyright, Designs and Patents Act 1988 or under the terms of any licence permitting limited copying issued by the Copyright Licensing Agency, 90 Tottenham Court Road, London W1P 0LP. Although every effort has been made to ensure that all owners of copyright material have been acknowledged in this publication, we would be glad to acknowledge in subsequent reprints or editions any omissions brought to our attention. A CIP record for this book is available from the British Library. Library of Congress Cataloging-in-Publication Data Data available on application ISBN-10: 0 415 41413 X ISBN-13: 978 0 415 41413 5 Distributed in North and South America by Taylor & Francis 6000 Broken Sound Parkway, NW, (Suite 300) Boca Raton, FL 33487, USA Within Continental USA Tel: 1 (800) 272 7737; Fax: 1 (800) 374 3401 Outside Continental USA Tel: (561) 994 0555; Fax: (561) 361 6018 Email:
[email protected] Distributed in the rest of the world by Thomson Publishing Services Cheriton House North Way Andover, Hampshire SP10 5BE, UK Tel: +44 (0)1264 332424 Email:
[email protected] Composition by C&M Digitals (P) Ltd, Chennai, India Printed and bound in India by Replika Press Pvt Ltd
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Contents
List of contributors Note on outcomes 1 Laser safety William Beeson 2 Evaluation of the aging face Philip J Miller 3 Carbon dioxide laser resurfacing, Fractional resurfacing and YSGG resurfacing Dee Anna Glaser, Natalie L Semchyshyn and Paul J Carniol 4 Erbium laser aesthetic skin rejuvenation Richard D Gentile 5 Complications secondary to lasers and light sources Robert M Adrian 6 Nonablative technology for treatment of aging skin Amy Forman Taub
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11 Management of vascular lesions Marcelo Hochman and Paul J Carniol
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12 Laser treatment for unwanted hair Marc R Avram
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11
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14 Treatment of leg telangiectasia with laser and pulsed light Mitchel P Goldman
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15 Photodynamic therapy Papri Sarkar and Ranella J Hirsch 45
16 Adjunctive techniques I: the bioscience of the use of botulinum toxins and fillers for non-surgical facial rejuvenation Kristin Egan and Corey S Maas
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181
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8 Treatment of acne scarring Murad Alam and Greg Goodman
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10 Laser treatment of pigmentation associated with photoaging David H Ciocon and Cameron K Rokhsar
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7 Lasers, light, and acne Kavita Mariwalla and Thomas E Rohrer
9 Nonsurgical tightening Edgar F Fincher
13 Non-invasive body rejuvenation technologies Monica Halem, Rita Patel, and Keyvan Nouri
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17 Adjunctive techniques II: clinical aspects of the combined use of botulinum toxins and fillers for non-surgical facial rejuvenation Stephen Bosniak, Marian Cantisano-Zilkha, Baljeet K Purewal and Ioannis P Glavas 18 Adjunctive techniques III: complementary fat grafting Robert A Glasgold, Mark J Glasgold and Samuel M Lam Index
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Contributors
Robert M Adrian MD FACP Center for Laser Surgery Washington, DC USA Murad Alam MD Departments of Dermatology, Otolaryngology, and Surgery Northwestern University Chicago, IL USA Marc R Avram MD Department of Dermatology New York Presbyterian Hospital-Weill Medical College at Cornell Medical Center New York, NY USA William Beeson MD AAFPRS AACS Beeson Aesthetic Surgery Institute Carmel, IN USA Stephen Bosniak † MD Marian Cantisano-Zilkha MD Manhattan Eye, Ear and Throat Hospital New York, NY USA Paul J Carniol MD Cosmetic Laser and Plastic Surgery Summit, NJ USA David H Ciocon MD Department of Dermatology Albert Einstein College of Medicine New York, NY USA
Kristin Egan MD Department of Otolaryngology UCSF San Francisco, CA USA Edgar F Fincher MD PhD The David Geffen School of Medicine at UCLA and Moy-Fincher Medical Group Los Angeles, CA USA Richard D Gentile MD Facical Plastic and Aesthetic Laser Center Youngston, OH USA Dee Anna Glaser MD Dermatology Department St Louis University St Louis, MO USA Mark J Glasgold MD Department of Surgery Robert Wood Johnson Medical School University of Medicine and Dentistry of New Jersey Piscataway, NJ USA Robert A Glasgold MD Department of Surgery Robert Wood Johnson Medical School University of Medicine and Dentistry of New Jersey Piscataway, NJ USA
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List of contributors
Ioannis P Glavas MD Oculoplastic Surgery Manhattan Eye, Ear and Throat New York, NY USA
Kavita Mariwalla MD Department of Dermatology Yale School of Medicine New Haven, CT USA
Mitchel P Goldman MD LaJolla Spa LaJolla, CA USA
Philip J Miller MD FACS Department of Otolaryngology New York University School of Medicine and The NatraLook ProcessTM and East Side Care New York, NY USA
Greg Goodman MD Department of Dermatology Minash University Melbourne Australia Monica Halem MD Department of Dermatology Miller School of Medicine University of Miami Miami, FL USA Ranella J Hirsch Skin Care Doctors Cambridge, MA USA Marcelo Hochman MD The Facial Surgery Center Charleston, SC USA Samuel M Lam MD Willow Bend Wellness Center Lam Facial Plastic Surgery Center and Hair Restoration Institute Plano,TX USA Corey S Maas MD Department of Otolaryngology UCSF and The Maas Clinic San Francisco, CA USA
Keyvan Nouri MD Department of Dermatology Miller School of Medicine University of Miami Miami, FL USA Rita Patel MD Department of Dermatology Miller School of Medicine University of Miami Miami, FL USA Baljeet K Purewal MD Department of Opthalmology Lutheran Medical Center Brooklyn, NY USA Thomas E Rohrer MD Department of Dermatology Boston University School of Medicine and Skin Care Physicians of Chestnut Hill Chestnut Hill, MA USA Cameron K Rokhsar MD FAAD FAACS Department of Dermatology Albert Einstein College of Medicine New York, NY USA
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List of contributors Neil S Sadick MD Sadick Aesthetic Surgery and Dermatology New York, NY USA Papri Sarkar MD Department of Dermatology Harvard Medical School Boston, MA USA
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Natalie L Semchyshyn MD Dermatology Department St Louis University St Louis, MO USA Amy Forman Taub MD Advanced Dermatology Northwesten University Department of Dermatology Lincolnshire, IL USA
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Note on outcomes
Although every effort has been made to ensure that information about techniques and equipment is presented accurately in this publication, the ultimate responsibility rests with the practitioner physician. Use of these techniques or items of equipment does not guarantee outcomes or that they are the optimal procedures available. Procedure results and potential complications frequently vary between patients: physicians must evaluate their patients individually and make appropriate decisions about treatment based on each analysis. Although it is not always necessary, when a physician initiates any new therapy on a patient the use of ‘test spots’ or other tests of limited
areas should be considered for patient response before initiating the full treatment itself. Neither the publishers, nor the editors, nor the authors can be held responsible for errors or for any consequences arising from the use of information contained herein. For detailed instructions on the use of any product or procedure discussed herein, please consult the instructional material issued by the manufacturer. Some of the use of technology and procedures described in this text may be ‘off label’ as regards the FDA in the USA and may also not have EC approval in Europe, and are described as such, to be used at the discretion of the physician.
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1. Laser safety William Beeson
INTRODUCTION Surgical lasers have opened a new vista for aesthetic surgery. Laser skin resurfacing is commonplace, as is laser treatment for vascular lesions, varicosities, and laser hair removal. Laser blepharoplasty and facelifts, as well as the employment of the laser in endoscopic facial surgery, are becoming commonplace. With the increasing varieties of lasers and the numerous wavelengths available, laser safety has become a more complex issue.1 It is incumbent upon the surgeon to consider the safety of not only his or her patient, but also the entire operating room staff. With the increasing trend for more and more procedures to be performed in an ambulatory surgical setting, we find that medical lasers are commonly being employed in small clinics or office surgical settings. Not only physicians, but podiatrists, dentists, and others use lasers on a daily basis in their office clinical practices.The requirements and principles for the safe use of lasers are no less stringent in this setting than when the lasers are employed in a large metropolitan hospital. Laser safety standards apply equally in all of these settings. When a physician utilizes a medical laser, they have a medical, legal, and ethical responsibility to be aware of the requirements for the safe use of lasers in healthcare facilities.This means that the physician should be trained in laser safety and be knowledgeable as to local and federal regulations, as well as the advisory standards and professional recommendations for the use of lasers in their applicable speciality.
CLASSIFICATION OF LASERS Medical lasers are classified in the USA in accordance with the Federal Laser Product Performance Standard,
which essentially classifies lasers based on the ability of the laser beam to cause damage to ocular and cutaneous structures. The Food and Drug Administration (FDA) Center For Devices and Radiologic Health (CDRH) has the responsibility for implementing and enforcing the Federal Laser Product Performance Standard and Medical Device Amendment to the Food, Drug, and Cosmetic Act. In general, medical lasers are of class III-B or class IV. Medical lasers can be divided into two broad categories: those in the visible and mid-infrared range (roughly 400–1400 nm), in which the focal image on the retina presents the primary ocular hazard; and those in the ultraviolet and infrared regions, in which the main ocular hazard is to the cornea and skin. In general, class IV laser systems present a fire hazard in addition to the ocular and cutaneous hazards associated with class III-B lasers. A class I laser is considered to be incapable of producing damaging levels of laser emission. Class II applies only to visible laser emissions, which may be viewed directly for time periods ≤ 0.25 s: the aversion response time (aversion response is defined as movement of the eyelid or head to avoid exposure to a noxious stimulant or bright light). This is essentially the blink reflex time. Only if one purposely overcomes one’s natural aversion response to bright light can a class II laser pose a substantial ocular hazard. Class III lasers may be hazardous by direct exposure or exposure to specific reflection. A subcategory of class III (class III-A) consist primarily of lasers of 1–5 nW power. These pose a moderate ocular problem under specific conditions where most of the beam enters the eye. The aiming beam or alignment beam for a laser usually falls within this range, and can be hazardous when viewed momentarily if the beam enters the eye. For this reason, one must take particular caution when
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using the alignment beam and be aware that ocular damage can occur with misuse. Class III-B lasers comprise those in the 5–500 mW output range. Even momentary viewing of class III-B lasers is potentially hazardous. Class IV lasers are those emitting > 500 mW (0.5 W) radiant power. Most surgical lasers fall within this class, and pose a potential hazard for skin injury, ocular injury, and fire hazards.
REGULATIONS In addition to FDA enforcement, other rules and regulations apply to the use of lasers in the medical setting. In recent years, the Occupational Safety and Health Administration (OSHA) has stressed the need for employers to inform and educate workers on workplace risks. This has been of particular importance with regard to the use of lasers in the workplace. The Department of Labor has developed guidelines for Laser Safety Hazard Assessment, which pertain to the use of medical lasers.2 Compliance with OSHA rules is an important component of a laser safety program.
HAZARD CLASSIFICATION There are no specific OSHA guidelines for assessing the level of compliance of a facility providing laser facelifts and laser blepharoplasty. However, the American National Standards Institute (ANSI) standard ‘Safe Use of Lasers in Health Care Facilities’ (Z136.3) is used as a benchmark. All assessments by the OSHA are made under the ‘general duty clause’, which states that there is a shared duty between the employer and employee for establishing and maintaining a safe working environment. The employer has a duty to provide the proper safety equipment, appropriate education and training, and a work environment free of known potential risks and hazards. The employee has a duty to attend the training, use of personal protective equipment, and follow safe work practices at all times. OSHA compliance officers respond to requests, complaints, and accidents reported. Facilities must demonstrate that they have established policies and procedures, identified proper personal protective equipment, implemented a
program for education of all employees who might be at risk for exposure to laser hazards, performed and documented periodic safety audits, and assured ongoing administrative control in program surveillance.3 In addition to governmental agencies such as the FDA, OSHA, and state departments of health, nongovernmental accrediting and review organizations also have guidelines and recommendations for the laser safety in healthcare facilities. The ANSI is a nonregulatory body that promulgates thousands of safety standards in the USA.Working committees have representation from industry, the military, regulatory bodies, user groups, research and educational facilities, and professional organizations. The ANSI also participates in international standard work through groups such as the International Organization for Standardization (ISO).The main objective of the ANSI is to establish and maintain benchmarks for national safety through consensus documents. ANSI Z-136.3 has become the expected laser safety standard in healthcare. Although it is not regulatory, it has taken on the impact of regulations through its wide acceptance. It is used by the OSHA and many accrediting organizations such as the Joint Commission (previously the Joint Commission on Accreditation of Healthcare Organizations, JCAHO) and the Accreditation Association of Ambulatory Healthcare (AAAHC), and it is exhibited as reference during litigations. The standard provides a comprehensive guide for the development of administrative and procedural control measures that are necessary for maintaining a safe laser environment and should be used as the cornerstone for all clinical laser programs. It is important to develop a risk management process regarding the safe use of lasers, consisting of written policies and procedures, as well as ongoing evaluations of compliance, and demonstrating timely and appropriate responses to incidents or accidents that could occur. Typically, the person responsible for the management of the laser safety–risk management program will be the laser safety officer. The ANSI Z136.3 standard defines the laser safety officer as ‘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 laser safety officer shall effect the knowledgeable evaluation and control of
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Laser safety laser hazards by utilizing, when necessary, the appropriate clinical and technical support staff and other resources.’4 The laser safety officer should be responsible for verifying the classifications of the laser systems, hazard analysis, ensuring appropriate control measures are in effect, approving all policies and procedures, ensuring that protective equipment is available, overseeing instillation of equipment, ensuring that all staff are properly trained, and maintaining medical surveillance records. In private practice in small clinical settings, the physician who owns and runs the practice or clinic is very likely to serve as the laser safety officer. All laser users must adhere to the following principles: • Laser safety requirements are no less stringent in private practice than in a hospital setting. • The individual laser user must know all professional standards and regulations and be thoroughly trained in laser safety. • The user must ensure that the entire staff are properly trained in the safe use of lasers. • There must be an appointed laser safety officer. • The user must establish and follow standard-based policies and procedures. It is important that safety audits be utilized in a routine manner to be sure that laser safety programs are being adhered to. ANSI standards require an audit at least annually. A laser safety audit is an assessment of all equipment, supplies, and documents involved in performing laser treatments in a facility. It is supervised by the laser safety officer and consists of four basic components: 1. 2. 3. 4.
Inventory all equipment and develop a checklist. Inspect every item on the checklist. Document results. Identify action items based on audit results.
In addition to the ANSI, voluntary healthcare accrediting organizations such as the Joint Commission and the AAAHC all have standards that apply to the use of lasers in the medical environment, including the office surgical setting. Laser regulation at state and local government levels has increased significantly in recent years. Regulations vary from state to state. The current trend is for state
3
regulatory bodies, such as medical licensing boards and departments of health, to address laser safety issues by setting standards for credentialing and training. Regulations will usually dictate the type of individual or individuals who are qualified to perform laser treatments and prescribe levels of training to document current competency with each type of laser being used. Almost all require personnel using lasers in healthcare arenas to be cognizant of basic laser safety issues. Some states allow only physicians to perform laser surgery, while others allow physician assistants and advanced practice nurses to perform laser treatments. Some will allow nurses and other allied health personnel to perform laser treatments, but only with the direct supervision of a trained physician. Still other states permit the use of lasers by paramedical personnel and ‘others’ in less supervised situations. However, the current trend is for increased supervision and training. While some states may not directly address laser surgery, they do so indirectly by requiring accreditation of ambulatory surgical or office surgical units. In these cases, the medical licensing board has subrogated authority to a national accrediting organization such as the Joint Commission, the AAAHC, or the American Association for Accreditation of Ambulatory Surgery Facilities (AAAASF). Each of these organizations has developed specific standards that can be applied to laser use in the medical setting. In 2005, the Joint Commission, currently in its sentinel event program, adopted measures for its accredited organizations to utilize in an attempt to reduce the likelihood of patient injury from fire resulting from the use of lasers in the operating room. Since the Joint Commission accredits the vast majority of hospitals in the USA and since all Joint Commission-accredited organizations using medical lasers must adhere to these recommended standards, one could argue from a legal standpoint that these are de facto ‘community standards’. The legal implications of not meeting the accepted ‘community standards’ if a patient has an injury when being treated with a medical laser are significant. It is imperative that any person in a medical practice who treats with a laser adhere to strict regulations regarding scope of practice, licensing requirements, and standardized procedures. It is also extremely important for the physician’s malpractice insurance carrier to determine who is covered under the physician’s policy. It is essential to know if the person doing the laser
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treatments is outside his or her scope of practice, as an insurance company will not insure someone who is illegally practicing outside the scope of his or her license, etc. Health practitioners cannot ignore the importance of this issue for overall success and safety. At present, there are no national, state, or local certifications or licensing agencies to qualify the competency of surgeons, nurses, or technicians in the safe use of lasers. There is no standardized or universally accepted certification or training organization. It is, therefore, important to consider the ANSI guidelines as well as the recommendations of various professional medical societies in this regard (Boxes 1.1 and 1.2). Box 1.1 Recommendations for establishing laser program and clinical setting 1. Check with medical licensing board in your state regarding laser regulations 2. Develop laser safety protocols for your facility. Document training for yourself and your staff 3. Consider formal laser safety officer training and appoint a laser safety officer 4. Monitor changes in accreditation standards and ANSI Z-136.3 guidelines 5. Check with your medical liability carrier. Obtain delineation of coverage for yourself and your staff regarding the use of lasers in your practice
Box 1.2 Information resources for laser safety guidelines • American National Standards Institute (ANSI), 11 West 42nd Street, New York, NY 10 036 • Laser Institute of America, 12424 Research Parkway, Suite 125, Orlando, FL 32826 • US Food and Drug Administration (FDA), Center for Devices and Radiologic Health (CDRH), 9200 Corporate Boulevard, Rockville, MD 20850 • US Department of Labor, Occupational Safety and Health Administration (OSHA), 200 Constitution Avenue, NW,Washington, DC 20210 • Joint Commission (formerly JCAHO), 1 Renaissance Boulevard, Oak Brook Terrace, IL 60181 • Accreditation Association of Ambulatory Healthcare (AAAHC), 5250 Old Orchard Road, Suite 200, Skokie, IL 60077
BIOLOGICAL HAZARDS OF LASERS Laser hazards can essentially be divided into nonbeam-related hazards and beam-related hazards. The latter are unique to lasers, and pose the need for special attention and safety requirements when using lasers in the medical setting.This relates to the optical radiation hazard, which can result in damage to both eyes and skin. Because the eye is considered to be most vulnerable to laser light, the ocular hazards are considered of paramount importance. In most cases, the eye has a natural protective mechanism that limits retinal exposure to irritants. The blink reflex occurs at about every 0.25 s and accounts for the aversion response previously described. However, the intensity of some laser beams can be so great that injury can occur before the protective lid reflex. This usually happens with lasers operating at 400–1400 nm. It is commonly referred to as the ‘retinal hazard region’. Because of acoustic effects and heat flow, significant tissue damage can occur, leading to severe retinal impairment. For this reason, it is not uncommon to lose all visual function when exposed to even minimal amounts of laser energy when that energy is focused on critical areas of the retina such as the fovea. Such visual loss is generally permanent, since the neural tissue of the retina has minimal ability to replicate. Injury to the cornea and the anterior segment of the eye is possible from wavelengths in the ultraviolet and in the infrared beyond 1400 nm. When injury occurs to the cornea, it is usually superficial and involves the corneal epithelium. Re-epithelization usually occurs within 1–2 days, and total recovery of vision usually results. However, deeper penetration can result in corneal scaring and permanent loss of vision. Carbon dioxide (CO2) laser wavelengths pose such a potential risk. Excimer lasers operate in the ultraviolet range and pose a potential hazard to the cornea. Ocular injury can occur from direct penetration of a focused beam. However, it is more likely that injury will occur due to accidental ocular exposure to a reflected beam. Protection from reflected laser beams can be difficult. The most commonly employed surgical laser today is the CO2 laser. Since the CO2 laser wavelength of 10.6 µm is in the far-infrared region, it is invisible, and so this potential hazard can go unnoticed. For this
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Laser safety reason it is imperative that precautions be taken at all times when using CO2 lasers.This is also true of Ho:YAG and Nd:YAG lasers.This is in contrast to KTP and argon lasers, whose emissions are in the visible region. Reflections most commonly occur from flat metallic mirror-like surfaces such as nasal speculums or surgical instruments. Black anodized or abraded–roughened surfaces can reduce (but not totally eliminate) the potential for beam reflection. Roughening a surface is generally thought to be more effective than ebonizing it, since the beam is diffused to a greater degree.5 Because of the potential for ocular injury secondary to beam reflection, it is imperative that proper protection be afforded to the patient and all operating room personnel at all times when lasers are in use. Ordinary optic glass protects against all wavelengths shorter than 300 nm and longer than 2700 nm. Polycarbonate safety glasses with sideshields are suitable for use with the CO2 lasers if the power is < 100 W.The glass should have an optical density of 4. While polycarbonate glasses may be adequate, there can be burn-through with higher-power lasers. Thus, even when wearing protective eyewear, one should not focus the laser beam directly on the shield for any length of time. Laser safety glasses should always have sideshields. The optical density rating should be listed on the sidebar of the eyeglasses. It is important to realize that many lasers radiate at more than one wavelength. For this reason, eyewear of appropriate optical density for a particular wavelength could be completely inadequate at another wavelength radiated by the same laser. This is particularly important for lasers that are tunable over broad wavelength bands. When a patient is within a nominal hazard zone (NHZ), patient eye protection is imperative.The NHZ is a space within which the level of the direct, reflected, or scattered radiation during normal operation exceeds the acceptable maximal permissible exposure (MPE). Proper eye protection may range from wet eye pads to laser-protective eyewear. In most cases, corneal protectors provide the best protection. Plastic corneal protectors have become popular. However, in some cases, plastic shields can transfer thermal energy to the cornea, with resultant injury. This is especially true with darker-colored shields.6
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CUTANEOUS INJURY While ocular injury is the most devastating direct beam laser injury, cutaneous hazards do exist.The skin can be injured either through a photochemical mechanism or by a thermal mechanism. First-, second-, and third-degree burns can be induced by visible and infrared laser beam exposure. Such injuries have been noted to occur in < 1% of patients, with 10% of surgeons reporting unintentional burns to either patients or operating room personnel.7,8 In most cases, moist towels draped around the operative site and fireresistant surgical drapes will provide proper protection.
NON-BEAM-RELATED HAZARDS In addition to direct laser beam hazards to the eye and skin, there are non-beam laser hazards that need to be considered. These include electrical hazards, lasergenerated airborne contaminants (laser plume), waste disposal of contaminated laser-related materials such as filters, and laser-generated electromagnetic interference. All medical lasers must operate in compliance with the National Electric Code (NFPA-70) and with state and local regulations. Electrical hazards can be related to damaged electrical cords and cables, inadequate grounding, and the use of conductive liquids in the vicinity of the laser when it is in operation. These problems can usually be minimized with an appropriate laser maintenance program by qualified biomedical engineers and adherence to appropriate laser safety guidelines when operating electrical equipment in the surgical environment. Laser-generated airborne contaminants present a significant problem. Studies have shown the presence of gaseous compounds, bio-aerosols, dead and live cellular materials, and viruses in the laser plume. The laser plume can cause ocular and upper respiratory tract irritation. The unpleasant odors of the laser plume can cause discomfort to both the physician and the patient.The laser plume can cause ocular irritation, and may be even more of a problem for individuals who wear soft contact lenses, as the particles can permeate the lenses and cause prolonged irritation.
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However, of greatest concern is the mutagenic and carcinogenic potential of the compounds contained in the plume.At a time when the threat from bloodborne pathogens has led to enhanced awareness of the risks of contact with blood and blood byproducts, the practice of universal precautions has taken on a new meaning. The use of a laser smoke evacuator is imperative. If the evacuator is held 2 cm from the source of the laser plume, aerosolization of the particles is minimal. The suction created in the evacuator tubing is important. This results in the creation of a vortex that removes mutagenic debris and prevents aerosolization of the carbonized particles. (The latter impregnate the tubing, which should therefore be treated as a biohazard when it comes to disposal.) In most cases, routine operating room suction and suction tubing do not provide adequate evacuation of the laser plume. While surgical masks may help reduce laser exposure, their use alone is not adequate. At present, there is no mask respirator on the market that excludes all laser-generated plume particles, such as viruses, bacteria, and other hazards. Surgical masks are not designed to protect from plume contents. Rather, they are intended to protect patients from the surgeon’s contaminated nasal or oral droplets. Specialized surgical masks that filter out particles down to 0.3 µm with high efficiency are available and can help to decrease the inhalation of laser plume particles. While some laser masks are of sufficiently increased density to remove a higher proportion of laser-generated particles, their use alone is not adequate.9 As with smoke evacuator tubing, filters will be impregnated with potentially dangerous materials, and should therefore be treated as hazardous waste. Lasers can create electromagnetic interference. Electromagnetic radiation generated by lasers can interfere with other sensitive electronic equipment present in the facility, such as cardiac telemetry equipment.This can also affect patients who have pacemakers. The electromagnetic interference potential of a laser system is normally described in the manufacturer’s labeling, or it can be determined by a biomedical engineer with laser safety officer experience.
FIRE HAZARD Operating room fires are rare – but when such blazes do occur, they can be lethal. Potentially flammable
materials such as gauze, cotton, paper surgical drapes, and plastic endotracheal tubes can be ignited in the operating room by the laser, and the oxygen-enriched environment can intensify fires. Accidental fires are a well-known hazard associated with laser treatment. It has been estimated that combustion occurs in 0.4–0.57% of CO2 laser airway procedures.10 Others have demonstrated that, in the presence of oxygen concentrations of 21–25%, polyvinyl chloride, red rubber, and silicone endotracheal tubes can rapidly ignite when struck with CO2 laser beam.The threshold for ignition is increased with the addition of helium to the oxygen concentration. This is due to the fact that helium has a higher thermal density and acts as a heat sink, delaying combustion for about 20 s. Laser fires have also resulted from the ignition of polyvinyl chloride endotracheal tubes wrapped in aluminum tape.11 In general, medical lasers are class III-B or IV lasers. Class IV laser systems (emitting > 500 mW radiant power) present a fire hazard in addition to the ocular and cutaneous hazards associated with class III-B lasers. Most surgical lasers fall within this class. The basic elements of a fire are always present during surgery.A misstep in procedure or a momentary lapse of caution can quickly result in a catastrophe. Slow reaction to the use of improper firefighting techniques and tools can lead to damage, destruction, or death. To reduce the threat of a laser fire, it is essential to understand and to employ the principles of the ‘fire triangle’. For a fire to start, three components must be present: heat, fuel, and an oxidizer. The key to laser safety in this regard is to control all three components. ‘Heat’ represents the flame or the spark. It is the ‘ignition’ for the fire.The nature of the heat source can be extremely varied – often something that one would not immediately think of, such as an overhead surgical light, an electrocautery unit, a drill, or a fiberoptic light left on a surgical drape. A ‘fuel’ has to be present for the heat source to ignite. Once again, the potential ‘fuel’ can be an item that one would not likely consider, such as a petroleum-based ophthalmologic ointment. Fuels commonly encountered in surgery can be divided into five categories: the patient, prepping agents, linens, ointments, and equipment. The key ‘oxidizer’ in the operating room is the oxygen-rich environment. An oxidizer can be thought
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Laser safety of in this context as something that facilitates ignition and combustion. Decades ago, anesthesiologists recognized the hazards of flammable anesthetic agents in the operating room and eliminated them.Today, oxygen is one of the key components to deal with in regards to operating room fires. In the great majority of such fires that have been reviewed, an oxygen-rich environment and ineffective management of this ‘oxidizer’ were the key factors in the mishap. Preventing fires in the operating room is dependent on disrupting the fire triangle, as all of its components must be present for a fire to develop. One needs to control the heat source, manage the fuels, and minimize the oxygen concentration. One of the most common errors is inadvertent activation of the laser. Not infrequently, the surgeon thinks that he or she is stepping on the cautery foot pedal when they are actually stepping on the laser pedal, which activates the dangling laser, whose beam is directed on a flammable surgical drape (the ‘fuel’). One of the most basic – but most effective – safety measures is to eliminate the clutter of multiple foot pedals for the laser, cautery, liposuction unit, etc. Removing all of the foot pedals and having only the foot pedal of the equipment one is using in access range is extremely important. ANSI standards dictate that there be a laser-designated operator trained in the safe use of any particular laser.The responsibility of the laser operator is to release the laser from standby setting mode when the surgeon requests its activation and to immediately place the laser back on standby mode when the surgeon is finished.This markedly reduces the likelihood of inadvertent laser activation. It is essential that the laser operator ensure that there is an appropriate ‘environment’ before activating the laser.They should scan the room to ensure that no flammable agents such as acetone or cleaning agents are present, that all personnel are wearing appropriate eye protection, that the patient’s eyes are protected, and that the oxygen has been reduced to room air levels before the laser, is activated. Managing the potential ‘fuel’ source is important, and requires delegation and advanced planning. Proper prepping techniques are critical. If possible, the use of alcohol-based prepping solutions should be avoided. It is important that flammable prep solutions be removed and not allowed to drip and ‘pool’ on the drapes under the patient, enabling fumes to accumulate and possibly be ignited. It is also important to be
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alert for potential fire risks on the patient, such as eye mascara, perfume, and hairspray, of all which can be flammable. Minimizing the oxygen environment is extremely important and must be done in concert with the anesthesiologist.This requires presurgical discussion regarding how one plans to perform the procedure, the type of anesthetic to be used, etc. In many cases, monitored anesthesia care can be used. It may be possible to reduce the oxygen concentration being delivered to room air levels during the time the laser is being activated and to return immediately to supplemented levels when the laser is deactivated.This requires coordination between the surgeon and the anesthesiologist and the ability of the surgeon to immediately terminate the laser use if the anesthesiologist notes a precipitous drop in FiO2 on the pulse oximeter. If a nasal cannula or a face mask is used to deliver oxygen, one has to be sure that surgical drapes are not tented, such that oxygen can pool under them. In cases where higher levels of oxygen are required by the patient, and alternating from supplemented oxygen to room air is not possible, a helium and oxygen combination may serve to increase the safety margin when oxygen has to be utilized. Helium acts as a heat sink. It can delay combustion for up to 20 s. The oxygen concentration should be maintained below 40%. Recommendations regarding anesthesia are summarized in Box 1.3. Box 1.3 Recommendations regarding anesthesia • Oxygen should be used at the lowest possible concentration • Oxygen (or other gases) should never be directed toward the laser field • Any mixture of nitrous oxygen and oxygen should be treated as if it were pure oxygen • Helium can be used to increase the ignition threshold • Laryngeal airways (with spontaneous respiration) are preferred over face masks; if a mask is used, an oxygen analyzer can be utilized to ensure minimal leakage • If an endotracheal tube is used, the cuff should be filled with saline rather than air. The tube should be wrapped in aluminum or copper tape • Collared masks, nasal cannulas, or airway materials should be avoided. • Anesthetics that are administered either by inhalation or topically should be nonflammable.
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PREPARING FOR FIRES It is imperative to develop a laser-fire protocol. Being prepared for fire is an inexpensive insurance and will minimize the cost in dollars, loss in time, emotional shock, injury, and possibly death. Preparation involves a number of steps. The most important is practicing fire drills to teach all staff about their responsibility during a laser fire. This should be done similarly to what is done for medical codes and other routine disaster drills. It is surprising how many individuals do not know how to select a proper fire extinguisher or how to use one. Most fire extinguishers operate according to the mnemonic ‘PASS’: Pull the activation pin, next Aim the nozzle at the base of the fire, next Squeeze the handle to release the extinguishing agent, and Sweep the stream over the base of the fire. There are three classes of fire extinguishers: A, B, and C. Class C is used for electrical equipment. With the demise of Halons as fire-extinguishing agents, CO2 is the best all around fire extinguisher for the use in the operating room. Halons (bromofluorohydrocarbons) are damaging to the environment and are no longer made or sold. However, if a Halon fire extinguisher is available, it is the optimal one to use. Small CO2 fire extinguishers have five-pound charges and weigh approximately 15 pounds. This is easily enough for most people to handle and small enough to mount unobtrusively on the wall in the operating room near the door. CO2 fire extinguishers are rated for use against class B and class C fires in the operating room setting, although they can be used effectively against the kinds of class A fires that are likely to occur. CO2 fire extinguishers emit a fog of CO2 gas with liquid and solid particles that rapidly vaporize to cool and smooth the fire, while leaving no residue to contaminate the patient. Dry powder fire extinguishers employ primarily of ammonium sulfate, which is emitted in a stream against the fire. The powder smothers, cools, and to some extent disrupts the chemical reaction of the fire. During use, the powder limits visibility and covers everything in the surrounding area, which can damage delicate equipment. The powder irritates the mucous membranes and its long-term toxicity has not clearly been determined. Using a powder fire
extinguisher in the operating room will make the room and much of the equipment unusable for a period of time. For these reasons, dry powder should not be used as the first line of defense against operating room fires. Pressurized-water fire extinguishers are available, but are heavy and chiefly effective against only class A fires. If a laser fire should inadvertently occur, quick action is imperative.Ventilation should be stopped and anesthetic gases discontinued.Then the tracheal tube, mask, and nasal cannula should be removed.The fire should be extinguished with normal saline.The patient should then be mask-ventilated with 100% oxygen.The anesthesia should be continued in order to facilitate injury assessment to allow the patient to be stabilized. Iced saline compresses should be applied to areas of burn.A flexible nasal pharyngoscope or bronchoscope should be used to survey the upper airway and laryngeal tissues to evaluate the extent of injury. Foreign bodies and carbonized debris should be removed. Copious irrigation with normal saline and Betadine soap can be used to remove carbonized debris from cutaneous burned areas. Xeroform gauze and bacitracin ointment can be applied to areas of minor cutaneous burns. If thermal injury has occurred in the nasal airway, a light nasal packing with Xeroform gauze can be used to stent the airway to treat thermal damaged tissues. Depending on the severity of injury, it may be important to consider the use of intravenous steroids. High-humidity environments should be provided and oxygenation monitored. Patients may require ventilatory support for laryngeal edema as a potential problem. A chest X-ray should be considered in order to obtain a baseline evaluation to monitor for ‘shock lung’. Evaluation by other consultants such as a pulmonologist or ophthalmologist should be considered when appropriate. Systemic antibiotics such as cephalosporins should be considered. In all but the most minor cases, the patient should be observed overnight.12
ENVIRONMENT OF CARE Medical lasers should be used in the appropriate environment.There should be proper electrical grounding
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Laser safety to minimize potential electrical shock. There should be proper ventilation and the room should be of sufficient size to enable the use of smoke evacuators, laser equipment, and additional personnel needed for proper laser instrumentation. Treatment should be performed in a controlled area, which should limit entry by unauthorized personnel. Proper warning signs should be displayed at the entry and within the controlled area. Only those properly trained in laser safety should be admitted to the controlled area. All open portals and windows should be covered or restricted in such a manner as to reduce the transmission of laser radiation to levels at or below the appropriate ocular MPE for any laser used in the treatment area. It should be noted that normal window glass has an optical density in excess of 5.0 and therefore should be appropriate for CO2 lasers at 10:600 µm. Other lasers require the facility windows to have additional coverings or filtering. While it is important that the entryway to the laser room or treatment area be secured, it is equally important that emergency entry be permitted at all times. For this reason, internal locks are not advisable. If a laser, fire, or explosion should occur, an internally locked door could prevent appropriate emergency response. It is important to have proper safety equipment within the treatment environment.This includes proper eye protection for all staff, as well as the patient, a fire blanket, and a fire extinguisher available. Of equal importance is an appropriate laser plume evacuation device. In most cases, standard surgical wall suction does not suffice.
TRAINING It is imperative that all personnel using medical lasers be properly trained and that appropriate laser safety protocol exist within each facility. Acceptable standards dictate that an individual designated as a laser safety officer be in charge of developing criteria and authorizing procedures involving the use of lasers within the facility, and ensuring that adequate protective measures for control of laser hazards exist and that there exist a mechanism for reporting accidents or incidents involving the laser.
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It is also important that accurate records be maintained for lasers, as well as laser-related injuries.
SUMMARY Lasers can be employed in a variety of medical settings.When used properly, lasers can provide dramatic improvements in the quality of patient care. However, as with any medical procedure, complications can and do occur. Close adherence to standard accepted laser safety protocols can dramatically reduce that risk and improve the quality of patient care.
REFERENCES 1. Sliney DH,Trokel SL. Medical Lasers and Their Safe Use. New York: Springer-Verlag, 1992. 2. ANSI Z-136.3-2004: American National Standard for Safe Use of Lasers in Health Care Facilities –. New York: American National Standards Institute, 2004. 3. Smalley P. Laser safety management; hazards, risks, and control measures. In: Alster T, Apfelberg D, eds. Cutaneous Laser Surgery. New York:Wiley-Liss, 1999. 4. ANSI Z-136.3:The Standard For the Safe Use of Lasers in Health Care Facilities. New York: American National Standards Institute, 2004. 5. Sliney DH. Laser safety. Lasers Surg Med 1985;16:215–25. 6. US Department of Labor, Title 29: Codes of the Federal Regulations, Occupational Health and Safety. 7. ANSI Z-136.3-1996: American National Standard for Safe Use of Lasers in Healthcare Facilities. New York: American National Standards Institute. 8. Wood RL, Sliney DH, Basye RA. Laser reflections from surgical instruments. Lasers Surg Med 1992;12:675–8. 9. Ries WR, Clymer MA, Reinisch L. Laser safety features of eye shields. Lasers Surg Med 1996;18:309–15. 10. Olbricht SM, Stern RS, Tany SV, Noe JM, Arndt KA. Complications of cutaneus laser surgery. A survey. Arch Dermatol 1987;103:345–9. 11. Baggish MS. Complications associated with CO2 laser surgery in gynecology. Am J Obstet Gynecol 1981; 139:658. 12. Fretzin S, Beeson WH, Hanke CW. Ignition potential of the 585nm pulse dye laser; Review of the Literature and Safety Recommendations. Dermatol Surg 1996;22: 699–702.
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2. Evaluation of the aging face Philip J Miller
INTRODUCTION In this chapter, we will explore the algorithm involved in analyzing the aging face. But before we even begin that journey, we must ask the question ‘What is an aged face?’ While the answer may seemingly be self-apparent, further contemplation reveals a complexity not first appreciated. For starters, when is the face considered ‘aged’? Secondly, are all ‘aged features’ that we would typically list a result of aging? And finally, do we have a comprehensive and detailed understanding of the pathophysiology of facial aging, which serves as the foundation for our analysis?
WHAT IS AN AGED FACE While the jury may still be out regarding when life actually begins, one could argue that death begins at the moment of conception! Life is nothing more than the balance between anabolic activities and catabolic activities. Throughout our life, the ratio of anabolic and catabolic states simply switches. Somewhere along that continuum, we begin to demonstrate findings on the outside of our body, particularly the face, where the catabolic process has increased its relative strength compared with the anabolic process. From that movement on, at different rates and in different ratios, mixed with different environmental exposures, these processes determine the resulting ‘aged appearance’ of any one person. What is considered an aged face in one society may not in fact be so in another society.We are quite aware of the tremendous respect and honor awarded to
seniors in the Asian community – and, sadly, not so present in the Western world.Typical features that we would readily find people wanting to correct in the West may in fact be worn as a badge of honor in the East. Nevertheless, those features are still a result of the aging process, and identifying them is the purpose of this chapter.
ARE ALL FEATURES OF AN AGED FACE DUE TO THE AGING PROCESS? As Fig. 2.1 demonstrates, a typical aged face will consist of a myriad of features. However, further inspection reveals that these features can be divided into two different categories. One category is chronological aging alone.These are the features that are never seen in youthful individuals, they occur as one ages, and almost everyone who is aged has them. The second
Aged features
Chronological features:
Morphological features:
Those features that appear in nearly all aged individuals, and are not present in the young
Those features that appear in nearly all aged individuals, but are also present in some youthful individuals
Fig. 2.1 The breakdown of aged features into chronological and morphological features.
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Table 2.1 Example of age-specific and non-age-specific features Aged features
Youthful features
It depends!!!!
• • • • • • •
• • • • •
• • • • •
Wrinkles, fine and coarse Malar depressions Furrows Skin excess Actinic changes Mandibular teeth showing Submental fat accumulation
Overall facial fullness/volume Prominent cheeks Plump lips Smooth, unblemished skin Maxillary teeth visible
category, I would like to refer to as morphological features.These are features that, although possessed by all aged people, are present in some individuals even in their youth. Examples of these two categories are listed in Table 2.1. It is interesting to note that features such as a nasojugal groove or a low-hanging upper lid crease or even a deepened nasolabial groove are present in some 6-year-olds. These individuals are certainly not chronologically aged, nor do they appear to appear old. Nevertheless, they certainly possess some of the very features that we readily admit to appearing in the aged face.
PATHOPHYSIOLOGY OF AGING A thorough analysis of the aging face begs us to ask us how it got that way. My impression is that the current pathophysiological model of facial aging is in its infancy, and we will see a rapid, indeed exponential, rise in our understanding of the pathophysiology of facial aging over the next two decades. Prominent in this model will be an ever-increasing role of facial volume depletion as contributing to – if not primarily responsible for – the ultimate contour irregularities and transformations that occur in the aged face. The old model of loss of elasticity, and sagging due to gravity, will be replaced by a more detailed and comprehensive understanding of the individual role of and complex interaction among • skin aging • skeletal remodeling • fat pad atrophy
Low lid crease Low brows Thin lip Nasojugal groove Nasolabial folds
• subdermal fat loss • fat deposition Furthermore, we will find that these processes inevitably exerts their effects on two anatomical components that are fixed: the muscle attachments to the bone and the osseocutaneous ligaments.This complex reaction of changes and exertions is subject to gravitational forces, resulting in a more typical aged facial appearance. Adding to that an increase in muscle tone in order to maintain facial function, particularly in the periorbital region, so that decreased visual fields are eliminated by contracting the frontalis, gives the characteristic superficial skin findings associated with the aged face.
YOUTH VERSUS BEAUTY Where do we begin the aging facial analysis? Do we start from the surface and proceed sequentially with our assessment layer after layer? Do we begin at the scalp and then proceed inferiorly towards the neck? Do we start at the nasal tip and work posteriorly? Do we make a global assessment and then work to the specific areas? Does it matter? I believe that the analytical algorithm that one uses is not nearly as important as the ‘ideal’ with which the patient is being compared. Thus, the real question in ‘aging face analysis’ is not so much ‘Why do they look old?’ as ‘with what are we comparing the patient’s face?’Are we trying to restore the patient to their own youthful appearance or to an idealized youthful appearance? Do most patients wish to be ‘restored’ to a prior
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Fig. 2.2 Twins with very different upper eyelid formations. The female’s upper lids are age-appropriate and beautiful, but could be considered ‘aged’ if these very same features presented themselves in a 40-year-old.
age, or to look more refreshed and rejuvenated, but still look their ‘age’. Is there not a component of their desire, in fact, that struggles with the desire to improve their appearance while maintaining their essential features? Here it is worthwhile to explore the concept of ‘ageless beauty’ – which is ultimately the goal of the aging face surgery that we perform. ‘Aging face surgery’ is really a poor term, because it is not really youthfulness alone that we are attempting to achieve. Age does not necessarily make one less or more attractive – although it does play a role. Therefore, beauty and youth are not necessarily one and the same.Youth, in my opinion, is not our goal as much as an ageless appearance, not a particular time period in the patient’s past. The best result is a face whereby you cannot tell the patient’s age. One looks at the postoperative face (not compared with the preoperative face) and cannot tell whether the patient is 25 or 40. They possesses volume and fullness. Their face is ageless. It should be kept in mind that youth is not necessarily attractive. If we were capable of magically restoring our patients to their most desirable youthful state, would they be completely satisfied? Some patients would be, but others would not. For these patients, ‘aging face procedures’ means not only correcting an
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aging face or features, but also aesthetic facial features by which we are asked to alter their appearance to make them more attractive.Therefore, ‘aging face analysis’ may mean a collection of aged and not necessarily aged features that the patient possesses to make them more attractive and appear more youthful. It should be kept in mind that we want to do that without altering those characteristics that are essential to the person’s uniqueness – those essential features that make us look undeniably who we are.These features may consist of the slight slant of the palpebral aperture, the position of the malar fat pad, the dimple on the cheek, the cleft in the chin, or the fullness of the upper lid. Over the years, some of these features have been routinely and erroneously thrown in with the list of aging face features. Consequently, we are quick to identify them as ‘aged’ and to eradicate them or modify them in an effort to create an idealized youthful appearance by removing all that is considered aged. Obviously, those features that are essential to one’s uniqueness should not be tampered with. A wonderful example of this is seen in my twins (Figure 2.2). My son has a very prominent upper eyelid crease, whereas my daughter has a much fuller upper eyelid crease with a lower brow. While typically a lower brow and upper eyelid fullness is deemed to be a classic sign of an aging face, requiring intervention, I submit that this particular feature in my daughter is her ‘essence’ and should not be at all manipulated now or 40 years from now. We have seen this as well in two classical examples, one being Mr Robert Redford and the second Mr Burt Reynolds. Both of their periorbital procedures resulted in what would be considered a youthful appearance. But their results occurred at the expense of removing their essential upper eyelid features.Those essential features for decades had been their ‘brand’; a masculine hooded upperlid with a low brow. Therefore, it is important to recognize that in performing aging face analysis, one needs to separate the analysis performed on a patient’s features that most likely were a result of the aging process and those that were never present at all and would in fact make this individual appear perhaps more attractive. For the sake of this chapter, we will focus exclusively on those features that are a result of the chronological process.
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Table 2.2 Fitzpatrick skin types Type
Color
Reaction to UVA
Reaction to sun
I
Very sensitive
III
Caucasian; blond or red hair, freckles, fair skin, blue eyes Caucasian; blond or red hair, freckles, fair skin, blue or green eyes Darker Caucasian, light Asian
Sensitive
IV
Mediterranean,Asian, Hispanic
Moderately sensitive
V
Middle Eastern, Latin, light-skinned black, Indian Dark-skinned black
Minimally sensitive
Always burns easily, never tans; very fair skin tone Usually burns easily, tans with difficulty; fair skin tone Burns moderately, tans gradually; fair to medium skin tone Rarely burns, always tans well; medium skin tone Very rarely burns, tans very easily; olive or dark skin tone Never burns, deeply pigmented; very dark skin tone
II
VI
Very sensitive
Least sensitive
Table 2.3 Glogau wrinkle scale Skin type
Age (years)
Findings
1. no wrinkles 2. wrinkles in motion
Early 20s or 30s 30s to 40s
3. wrinkles at rest
50 plus
4 only wrinkles
60 or 70s
Early photoaging: early pigmentary changes, no keratoses, fine wrinkles Early to moderate photoaging: early senile lentigines, no visible keratoses, smile wrinkles Advanced photoaging: dyschromia and telangiectasia, visible keratoses, wrinkles at rest Severe photoaging: yellowish skin color, previous skin malignancy, generalized wrinkling
SKIN Among the absolute hallmarks of an aging face are the changes associated with the skin. The most common changes associated with facial skin aging are those due to photoaging (skin damage related to chronic sun exposure). This results in dyspigmented, wrinkled, inelastic skin, with associated redness and dryness. Furthermore, mild to moderate facial wrinkling and laxity with benign and malignant lesions round out the skin changes that should be addressed through many of the techniques presented in this book. See Tables 2.2 and 2.3, which show the Fitzpatrick and Glogau classifications of skin types and wrinkles respectively.
VOLUME LOSS It is easy to overlook this particular component of facial aging. Since surgical procedures reposition and lift, it is
only natural, but incorrectly, assumed that the cause of that descent is skin laxity and gravity. However, on further examination, evaluation, and analysis, it is clear that descent and laxity can result from volume loss. As illustrated in Figure 2.3(a), a fully inflated balloon appears robust and lacks contour abnormalities. However, as seen in Figure 2.3(b), a deflated balloon has the potential to not only descend, but also become deformed.The difference between Figure 2.3(a) and 2.3(b) is nota general laxity of the balloon’s tarp, but rather the volume inside the balloon. Reinflating the balloon, as opposed to repositioning the tarp, is responsible for eliminating all of those identifiable features. Likewise, many of the features that we will discuss below are in part due to a loss of volume, and one should train one’s eyes to appreciate that volume loss in the following areas: the temporal fossa, the lateral brow, and the malar eminence. Furthermore, volume loss may be seen in the lips and perioral region. Finally, it should be appreciated that overall loss of volume in
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a
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b
Fig. 2.3 Two identical balloons.The one in (a) is inflated and is rigid and wrinkle-free.The one in (b) is partially deflated, its surface contains ripples, like wrinkles, and it is lax and subject to deformation from wind or gravity. Human skin is like the tarp on these balloons. Fully inflated skin appears youthful and robust. Deflated skin sags and reveals wrinkles and furrows.
the subcutaneous tissue can make certain bony features much more prominent along the infraorbital rim, as well as the submandibular triangle, wherein the submaxillary gland appears quite prominent.
CHIN POSITION The next step in the facial analysis process is to assess the location of the chin in relationship to the patient’s lower lip as well as the surrounding tissue. One should look for the appearance of jowling, chin ptosis, chin retrusion, submental fat accumulation and severe neck skin laxity. Following the path of the mandible
posteriorly, the next assessment is the general protuberance and width of the angle of the mandible. Atrophy and medial displacement of the angle of the mandible or atrophy of the masseter muscle can in fact contribute to a narrow and withdrawn facial contour. The nasolabial lines are now assessed for their presence and degree, as well as for the contribution made to these lines by ptotic skin and subcutaneous tissue superior to them. In my experience, the presence of a nasolabial fold is less due to ptosis of the malar fat pad than to atrophy of the malar fat pad with resulting ptosis (see the balloon concept illustrated in Figure 2.3) of the resulting subcutaneous tissue. Elevation of the malar tissue superiorly and slightly posteriorly assesses
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the degree of laxity, as well as the overall effect of repositioning this tissue to efface the nasolabial line and to reinflate the malar mound.
PERIORAL REGION The lips are now evaluated for the prominence of the white roll, the philtral ridge, and robust red lips. The maxillary teeth should be visible and the mandibular teeth hidden.White lip wrinkles are also assessed.
PERIORBITAL REGION Finally, attention is then directed towards the periorbital region. Signs of upper lid ptosis are identified and documented. Lower lid laxity and position are identified and documented. Brow position is similarly considered. Unlike the current trend of repositioning the brow cephalically, I find that a lower placed brow in both women and men, in combination with a more robust lateral brow fullness, provides a sophisticated and ageless appearance. An overly elevated brow does not convey youth. It conveys surprise.The absence and presence of forehead, glabellar, and periorbital rhytids are evaluated and documented. Lower lid pseudoherniation of fat is noted, as is the presence of an infraorbital hollow. The degree of nasojugal depression is documented, and photographs taken at an earlier age are reviewed to ascertain which of the facial features were present in youth and which were subsequently acquired with aging.
SUMMARY Technical expertise, however important to obtaining excellent and consistent results, is only part of the equation. The wrong technique performed flawlessly will typically reveal a result that is below par, while the correctly chosen procedure performed just satisfactorily typically results in acceptable if not extraordinary results. We can only recommend the most suitable procedure if we perform a thorough and accurate analysis, and that analysis includes not only an assessment of the patient’s facial features, but also their desires, expectations and their notions on which procedures they feel most comfortable with to get there.Therefore, proper and thorough analysis is paramount for it will lead us to selecting the most appropriate treatment plan and consequent results for any individual patient and thus predictable and consistent outcomes. Nevertheless, analysis cannot be learned in a vacuum. Analysis inevitably requires that we compare it with an idealized version, and even then it requires us to understand the pathophysiology by which we got to that point, and then we must correlate those findings with a suitable treatment.
PLAN Knowledge in all of these domains and re-exploring all of these disciplines are essential parts of our growth as physicians.
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3. Carbon Dioxide Laser Resurfacing, Fractionated Resurfacing and YSGG Resurfacing Dee Anna Glaser, Natalie L Semchyshyn and Paul J Carniol
INTRODUCTION Although skin resurfacing has been performed for centuries in the forms of chemical peels, sanding, and dermabrasion, it was not until the 1990s that lasers were safely and effectively used as a resurfacing tool. Initially, carbon dioxide (CO2) lasers with a wavelength of 10 600 nm (1006 µm) were used as a destructive tool. Technology advanced quickly in the 1990s from continuous-wave CO2 lasers to pulsed CO2 lasers to help minimize the thermal damage produced by the older CO2 lasers. Ultrashort pulse technology emerged, as did computerized pattern generator (CPG) scanning devices that allowed for a more standardized delivery of the laser pulses. Because of the prolonged healing required and the risks associated with CO2 lasers, the erbium :yttrium aluminum garnet lasers (Er:YAG) lasers with stronger water absorption (2940 nm) and less thermal damage were developed. Er:YAG lasers proved to be excellent ablative tools, with shorter healing times, but did not provide the same tightening that was achievable with CO2 resurfacing. The next advance came in the form of erbium lasers with longer pulse widths that could provide more heating and thermal damage in the skin. The short-pulsed erbium lasers were combined with CO2 lasers and long-pulsed Er:YAG lasers to try to blend the benefits of shorter healing times with more substantial skin tightening. Attempts to improve the laser resurfacing technique continue to be studied, with a concentrated effort now looking at nonablative options to induce
dermal remodeling and fractionated skin resurfacing to minimize the risks from skin ablation and to shorten the healing times for patients. This chapter will focus on ablative resurfacing, with an understanding that the principles behind good patient selection and care will remain paramount despite continued changes in the lasers that might be developed.
INDICATIONS The most common uses for laser skin resurfacing are to treat wrinkles and acne scars of the face. Any epidermal process should improve with laser resurfacing, including lentigines, photoaging, actinic keratosis, and seborrheic keratosis (Box 3.1). Some dermal lesions, such a syringomas, trichoepitheliomas, and angiofibromas, will improve with laser resurfacing, but results will vary with the histologic depth of the process. In our experience, there is a high recurrence rate with dermal lesions. Actinically induced disease, including actinic keratosis (AK) and actinic cheilitis, can respond very well to laser resurfacing. Superficial and nodular basal cell carcinomas have been successfully treated with the UltraPulse CO2 laser. The cure rates achieved by Fitzpatrick’s group was 97% in primary lesions (mean follow-up 41.7 months).1 In addition, the use of laser resurfacing may be used prophylactically to reduce the risk for the development of future AK and AK-related squamous cell carcinoma.2 Prevention of some basal cell carcinomas may be achieved, although this has not been definitively demonstrated.3
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Box 3.1 Indications for laser skin resurfacing • • • • • • • • • •
Photodamage Rhytids Acne scars Benign adenexal tumors Benign epidermal growths Rhinophyma Actinic cheilitis Actinic keratosis Basal cell carcinoma Scar revision
Despite the multiple uses, by far the prime use in our office is for the improvement of facial photoaging, rhytids, and acne scars.To date, ablative laser resurfacing is the most efficacious technique we have to treat perioral rhytids (Fig. 3.1). a
b
Fig. 3.1 Significant reduction in perioral rhytids at 4 months.
PATIENT SELECTION The key to successful laser resurfacing is proper patient selection (Table 3.1). Potential candidates need to have a realistic expectation of the outcome, risks, and significant amount of time required to heal, as well as the time to see the final results. The ‘ideal’ patient has fair skin with light eyes, has no history of poor wound healing, and is comfortable with wearing make-up during the postoperative healing period.The history should specifically address issues that relate to wound healing, such as immunodeficiency, collagen vascular diseases, anemia, diet, scarring history, keloid formation, recent isotretinoin usage, and past radiation therapy to the area. The history should include the patient’s general health, current or past medications, and mental health issues. Diseases known to koebnerize are also a relative contraindication – these include psoriasis, vitiligo, and lichen planus. Diseases that reduce the number of adenexal glands or alter their function are relative contraindications and need to be reviewed – these include collagen vascular diseases such as systemic lupus erythematosus and scleroderma. A history of herpes, frequent bacterial infections, or frequent vaginal candidiasis is not a contraindication, but should be noted to better plan how to treat the patient during the perioperative period. Equally important is to ascertain the pigment response of the patient (in terms of hyperpigmentation or hypopigmentation) to sun exposure or injuries. In our experience, patients with Fitzpatrick skin type IV are some of the most challenging to treat due to their risks of postoperative dyschromias. Patients will need to avoid sun exposure for several months after the surgery, and the physician needs to document the patient’s ability to do so along with their ability to use broad-spectrum sunscreens daily. In the Midwest of the USA, with four distinct seasons, it is preferable to perform deep resurfacing procedures during the winter months to minimize sun exposure. However, a thorough review of a patient’s travel plans during the 3- to 4-month healing period then becomes important. Although most patients recognize the risks of a trip to a warm sunny destination, many may underestimate the risks with higher altitudes such as with snow skiing.
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Table 3.1 Patient selection Absolute contraindications
Relative contraindications
Unrealistic expectations Unable/unwilling to perform wound care Isotretinoin therapy within prior 6–12 months
Tendency to keloid formation Tendency to poor wound healing/scar History of radiation therapy in area History of collagen vascular disease History of vitiligo Diseases that koebnerize (e.g., psoriasis) Pregnancy/breastfeeding Unable/unwilling to avoid sun exposure postoperatively
PROCEDURE Preoperative care The preoperative care should begin at the time that the patient decides to undergo laser skin resurfacing. Photoprotection and prevention of tanned skin should be maximized before surgery. Melanocyte stimulation before the laser resurfacing may increase the risk of postinflammatory hyperpigmentation after the procedure.A sunscreen with a sun protection factor (SPF) of 30 or higher should be used daily, along with an ultraviolet A (UVA) blocker such as zinc oxide, titanium dioxide, or avobenzone. We advise patients to supplement sunscreen use with physical measures such as large sunglasses and hats. The use of topical therapy before surgery is common – this might include topical tretinoin, hydroquinone and antioxidants. It is clear that the use of a topical retinoid is quite valuable before skin resurfacing with chemical peels through its action on the stratum corneum and epidermis. The use of topical tretinoin can increase the penetration of the peel, provide a more even peel and enhance healing.4,5 Due to the high affinity for water with the CO2 and Er:YAG lasers, these lasers are very capable of evaporating the epidermis without the use of tretinoin. There may be other effects that could theoretically improve the laser resurfacing process and healing. Retinoids regulate gene transcription and affect activities such as cellular differentiation and proliferation. They can induce vascular changes of the skin and a reduction and redistribution of epidermal melanin.6 Retinoids (at least theoretically) can speed healing and perhaps
reduce pigmentary changes. Thus, it is our practice to begin a topical retinoid at least 2 weeks prior to the procedure – even earlier if possible. Because of the relatively common development of postinflammatory hyperpigmentation after laser resurfacing, especially in the darker skin tones, many physicians will pretreat with a bleaching agent such as hydroquinone (HQ). HQ works by inhibiting the enzyme tyrosinase, which is necessary for melanin production within the epidermis. It can also inhibit the formation of melanosomes. There is a clear role for HQ products after laser resurfacing to treat hyperpigmentations; this will be discussed later in the chapter. HQ may not have any clinical effect when used prior to laser surgery, since the melanocytes that it is working on are all removed during the laser procedure. It is certainly not unreasonable to initiate HQ in a 3–5% cream for those patients at high risk for developing hyperpigmentation after their procedure. Like the topical retinoids, it can be irritating and should be discontinued if it is causing an irritant dermatitis. A rare side-effect of HQ is exogenous ochronosis, but this usually occurs only with prolonged use of higher concentrations and should not develop even in predisposed individuals within just a couple of weeks.7 There is no proven role for the use of topical antioxidants, alpha-hydroxy acids, or beta-hydroxy acids, but they are often in the skin care regimen of patients and we do not discontinue their use prior to laser resurfacing. Tobacco smoking can delay wound healing, and patients are strongly encouraged to stop tobacco use.As an alternative, if the patient is unable or unwilling to stop smoking at least 2 weeks prior to the
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procedure, he or she is encouraged to switch to a tobaccoless product such as a patch or gum. The use of oral antiviral therapy is standard practice, even if the patient does not have a history of herpes simplex virus (HSV) infections. Typically, famciclovir or valacyclovir is used in prophylactic doses such as famciclovir 250 mg twice daily or valacyclovir 500 mg twice daily. Doses need to be adjusted for renal dysfunction.The patient begins therapy the day before the procedure and continues until re-epithelialization is complete. It can be helpful to keep antiviral therapy in the office to administer to the patient if he or she forgot to initiate therapy before the procedure. The use of prophylactic systemic antibiotics is of questionable value prior to surgery and remains controversial.8 A first-generation cephalosporin is typically used by one of us (NLS), while no antibiotics are routinely used by the other (DAG). Interestingly, recent animal studies have shown that CO2 laser resurfacing reduces microbial counts of most microorganisms on lasered skin compared with skin treated using mechanical abrasion.9 On the other hand, nasal mupricin is routinely prescribed (by DAG) for healthcare workers due to the current high rates of methicillin-resistant Staphylcoccus aureus (MRSA) in hospitals and nursing homes. Unfortunately, the incidence of MRSA in the community is also increasing, and MRSA may be encountered in non-healthcare workers.10,11 Surgeons should monitor their local communities for recommendations regarding community-acquired MRSA. There have been no published studies on the use of antifungal therapy prior to laser resurfacing, although Candida infections can develop during the postoperative period, especially when occlusive dressings are used. It has been our practice, and that of others, to treat women with a known history or frequent or recurrent vaginal candidiasis with oral fluconazole after the procedure, even when using open healing techniques.9 Botulinum toxin is routinely administered to our patients prior to laser resurfacing of the face. Placebocontrolled studies have demonstrated improved results when compared with laser resurfacing alone.12,13 Preoperative use of botulinum toxin type A can diminish rhytids as well as textural, pigmentational and other features of skin aging when used in conjunction with
laser resurfacing.13 Our preference is to treat at least 2 weeks prior to laser surgery and repeat at approximately 3 months postoperatively. Patients are given instruction sheets listing skincare items they will need after the procedure along with their prescriptions for postcare medications. These will be discussed later in the chapter.
Laser resurfacing Before coming into the office for their procedures, patients are instructed to wash their face well. After drying, they apply a topical anesthetic cream such as EMLA (a eutectic mixture of lidocaine 2.5% and prilocaine 2.5%) under occlusion with a plastic wrap. This is left intact for 2–2.5 hours. One of us (NLS) will reapply the topical anesthetic 45 minutes prior to the procedure. The EMLA not only helps to provide cutaneous anesthesia, but also hydrates the skin, which decreases the procedure’s side-effect profile.14 Further anesthesia or analgesia can be obtained with nerve blocks, local infiltration of lidocaine, tumescent anesthesia or diazepam, and, in our office, intramuscular meperidine and midazolam, or ketorolac, is used.The topical agents are removed prior to beginning the laser procedure. When using the UltraPulse CO2 laser (Lumenis, Santa Clara, CA), the face is treated at 90 mJ/45 W, and the first pass is usually performed at a density of 7 for central facial areas (periorbital, glabellar, nose, and perioral): the upper and lower eyelids are treated at a density of 6 with the energy setting at 80 mJ.The density should be decreased to 6 and then 5 when feathering to the hairline and jawline. The first pass is intended to remove the epidermis, which is wiped free with a wet gauze in the central facial areas only, and a second pass is performed to central facial areas at a density of 4–5 (90 mJ), depending on the tightening needed. If required, the second pass on the eyelids is performed at a density of 4. Energies are decreased towards the periphery of the face. A third pass may be needed in areas of acne scarring or in the perioral area with deeper wrinkles. As with any laser procedure, careful monitoring of tissue response during treatment is performed to determine the necessity of any additional passes and energy level used.
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Carbon dioxide laser resurfacing, fractionated resurfacing and YSGG resurfacing A similar approach is taken when using one of the combined Er:YAG lasers such as the Sciton laser (Palo Alto, CA).The first pass is used to remove the epidermis and frequently 25 J/cm2 (100 µm ablation, zero coagulation) with 50% overlap is used. A second or third pass is used to heat and hopefully to induce skin tightening. Ablative and coagulative settings are used with a typical second, pass and a commonly used setting would have 50% overlap with 10 µm ablation and 80 µm coagulation. Where there are very deep rhytids or scars, the erbium laser in just the ablative setting can be used in a single spot to help sculpt the edges. It is important to remember that when used in the ablative mode, there is very little (if any) hemostasis, and pinpoint bleeding can help identify the depth of resurfacing. Laser resurfacing is best done to the entire face to avoid lines of demarcation between treated and untreated skin.The procedure should be carried into the hairline and at the jaw and chin; a feathering technique should be used. This includes a zone of decreased energy, decreased density, or pulse overlap.When treating a patient with moderate to severe photodamage, it is important to blend into the neck as much as possible. One approach is to lightly resurface the neck with a chemical peel; in our office, a Jessners and/or glycolic acid peel is used. Another option is to laser the neck, which will be reviewed later in the chapter.
Postoperative care Wound care is critical, and regimens vary among physicians. Occlusive and nonocclusive dressings are available. Occlusive dressings cover the skin and are usually removed in 1–3 days. These can decrease patient discomfort, but may promote infection by harboring bacteria or yeast. When opaque, the dressings can mask visualization of the wound, thus delaying the detection of an infection. Clear dressings (e.g., Second Skin) allow the patient and medical team to look at the lasered skin. When used in our office, they are most commonly removed on the second day postoperatively and the patient is switched to open healing. Open dressings or nonocclusive dressings are usually petroleum-based ointments. Frequent soaking and
21
cleaning are necessary (at least 4 times daily), followed by frequent application of petroleum jelly, Aquaphor ointment or one of the many wound care ointments that are available. Additives, fragrances, or dyes will increase the chance of contact allergic or irritant dermatitis developing and should be limited as much as possible. In very sensitive individuals, pure vegetable shortening can be used. Dilute vinegar can be used to soak and debride the wound, promote healing, and inhibit bacterial growth. Wound care needs to be performed until reepithelialization is complete. Depending on the type of laser used and how aggressive the surgeon was with his or her settings, re-epithelialization should be complete within 5–10 days. Prolonged healing times can indicate an infection, contact dermatitis, or other problem, and increases the risks of complications.
COMPLICATIONS AND THEIR MANAGEMENT Complications following laser surgery are relatively infrequent, but when they do occur, they need to be treated quickly and efficiently to minimize patient anxiety and long-term morbidity.15 Obviously, good patient selection, surgical management, and postoperative care are necessary to help prevent complications, but, even in the best of cases, complications do occur (Box 3.2).
Box 3.2 Complications of ablative laser resurfacing • • • • • • • • • • • •
Activation of herpes simplex virus (HSV) Bacterial infection Candidal infection Delayed healing Prolonged erythema Hyperpigmentation Hypopigmentation Acne Milia formation Contact dermatitis Scarring Line of demarcation with untreated skin
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Table 3.2 Causative agents encountered in CO2 laser infections16 Organism
Pseudomonas Staphylococcus aureus S. epidermidis Candida Enterobacter Escherichia coli Proteus Corynebacterium Serratia Herpes simplex virus (HSV)
a
Percent
41.2 35.3 35.3 23.5 11.8 5.9 5.9 5.9 5.9 5.9
b
The most common complications seen immediately postoperatively are swelling and exudative weeping related to the degree of wounding. If facial swelling is severe, oral or intramuscular steroids, and non steroidal anti-inflammatory agents (NSAIDs) can be administered. Milia formation is common, with the development of small white papules, usually < 1mm in size, which need to be distinguished from pustules. Papules are an occlusive phenomenon, and will resolve without treatment. Infections can occur, and may be bacterial, viral, or fungal in nature (Table 3.2).16 Signs and symptoms include pain, redness, pruritus, drainage (usually not clear), yellow crusting, and sometimes erosions, vesicles or pustules may develop (Fig. 3.2). Pruritus, especially, should alert the physician to a possible infection. Appropriate evaluation may include tzanck smear, potassium hydroxide (KOH) prep, gram stain, and cultures to accurately diagnose the causative agent. Treatment should begin early, pending culture results. Fitzpatrick’s group found that half of their patients who developed a post-laser infection had more than one microorganism. Thus, broad coverage should be initiated, and should generally include an agent that will cover Pseudomonas aeruginosa. Acne is another complications that can be seen relatively early in the course. Oral antibiotic therapy and discontinuation of petroleum-based ointments usually suffice. Topical acne therapies are not generally well
Fig. 3.2 A postoperative infection at day 3, with redness, edema, yellow drainage and crusting, and pustules.The patient noted increasing discomfort and pruritus. tolerated, due to skin sensitivity, and need to be used judiciously. Contact dermatitis can occur, and may be due to an allergic reaction or an irritant reaction. It may occur within the first few weeks or months after laser resurfacing. Redness, pruritus, and delayed healing may be noted, but vesiculation is rare. Topical antibiotics are a common cause of allergic contact dermatitis, and should be avoided. Patients may be using them without the knowledge of their physician. Topically applied agents should be reviewed and discontinued. Dyes and fragrances that are added to laundry detergents, fabric softeners, and skincare items are also potential causes. Discontinuation of the offending agent(s) and topical corticosteroids should be initiated early.17
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PIGMENTARY ABNORMALITIES Hypopigmentation Lightening of the skin is desirable for most patients undergoing facial rejuvenation. Patients who undergo resurfacing of cosmetic units such as the perioral area or periocular area may exhibit a noticeable difference between the ‘new’ treated skin and the untreated skin that exhibits the various dyschromias associated with photoaging.This should be avoided as indicated previously, but when faced with such a patient, treating the remaining skin will lighten the hyperpigmentation and help to blend in the differences.Although topical agents such as retinoids and hydroquinones can be used, visible results take months and are not practical for most patients. Resurfacing is the fastest way to improve patients’ appearance in these cases. Depending on the severity, a chemical peel such as a Jessner’s/35% trichloroacetic acid (TCA) peel may be sufficient, or laser resurfacing can be performed. Superficial resurfacing is all that is required for most, and the Er:YAG laser is an excellent device.The goal is to remove the epidermis, and one or two passes maybe all that is required. This heals rapidly and with minimum risks. In the very sun-damaged patient, it may be difficult to find a good stopping point. In these instances, treating the full face may only accentuate the discoloration of the neck. Light rejuvenation of the neck can be done, but may accentuate the damage to the chest. Light resurfacing can be performed down the neck and chest area, extending onto the breast – but this may then accentuate the damage to the arms and forearms, etc. In these patients, a combination of modalities can be used: topical agents as described above for the entire area; laser resurfacing of the face; lighter resurfacing of the neck and chest (we generally use chemical agents such as 20–30% TCA or 70% glycolic acid, but Er:YAG laser resurfacing is used successfully by many physicians); and chemical resurfacing of the arms, forearms, and hands with 20–30% TCA or 70% glycolic acid. Another option is the use of nonablative laser technology such as the ‘Photofacial’ technique. Several intense pulsed light (IPL) systems are now available, which use a broad-spectrum intense pulsed light source with changeable crystals attached to the hand-
Fig. 3.3 Persistent depigmentation 2½ years following CO2 laser resurfacing that was performed in the perioral area only.
piece to filter out undesirable wavelengths. This modality has been applied to the face, neck, chest, and upper extremities. Numerous treatment sessions are required, but are generally well tolerated, with little to no ‘healing-time’ for the patient.The fluence varies with skin type and area, but the neck is generally treated more conservatively and using lower fluences. It is important that the operator carefully place the filters to avoid overlapping and also to prevent skipped areas or ‘footprinting’.
Depigmentation True depigmentation of the skin following laser resurfacing is more difficult to treat than the pseudohypopigmentation described above. The skin acquires a whitish coloration and does not flush or change color with normal sun exposure (Fig. 3.3). A slight textural change can even be noted at times such that make-up does not ‘stick’ to the skin well or does not last as long as make-up applied to other areas. The latter represents superficial scarring or fibrosis. It can occur after any form of resurfacing, but it is more commonly encountered with CO2 laser resurfacing and is much less common with Er : YAG resurfacing. Like pseudohypopigmentation, depigmentation seems to be more
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evident when cosmetic units are treated individually or when a cosmetic unit such as the upper lip is treated more aggressively than the surrounding skin. Depigmentation has been considered a permanent complication of CO2 laser resurfacing.When evaluated histologically, there is a varying quantity of epidermal melanin present. Residual epidermal melanocytes are present, indicating that repigmentation should be possible. Mild perivascular inflammation has been noted in 50% of biopsies, and superficial dermal fibrosis was present in all biopsies.18 This suggests that the pathogenesis of the laser-induced hypopigmentation may be related to a suppression of melanogenesis and not complete destruction of the melanocytes. Grimes et al18 have reported successful treatment of hypopigmentation following CO2 laser resurfacing using topical photochemotherapy twice weekly.18 Seven patients were treated with topical 8-methoxpsoralen (0.001%) in conjunction with UVA therapy. Moderate to excellent repigmentation was demonstrated in 71% of the patients. Using the same reasoning, narrowband UVB and an eximer laser may both be effective. Narrowband UVB, which emits at 311–312 nm, has been reported to be efficacious for vitiligo, while excimer lasers emit at 308 nm and can be targeted to a given site.19 Alexiades-Armenakas et al 20 have reported two patients who were treated for laserinduced leukoderma using an excimer laser. They speculate that repigmentation is related to the stimulation of melanocyte proliferation and migration, along with the release of cytokines and inflammatory mediators in the skin. Potential disadvantages of any of these therapies, however, include the time necessary to see repigmentation, cost, erythema and pruritus during therapy, and hyperpigmentation of skin immediately surrounding the treated skin, which can take months to return to normal. Unfortunately, the results are mixed, and return to baseline can occur after therapy is discontinued. Repigmentation has been an unrealistic goal, and until more data are available on investigative tools such as phototherapy, an honest discussion must take place with the patient. Additional resurfacing of the unaffected skin may be helpful to reduce any hyper pigmentation or dyschromia if present, but will only help to reduce the differences with adjacent areas. Once again, care should be taken not to re-treat too aggressively.
Scarring The development of scarring following laser surgery is perhaps the most feared and distressing complication encountered. Deeper wounds are more likely to result in scarring, which is not usually encountered unless the wound extends into the reticular dermis. However, since this is the level that is generally targeted with the CO2 laser to eradicate wrinkles, acne scars, and varicella scars, cosmetic surgeons will be faced with scarring if they perform enough procedures. Hypertrophic scars can develop anywhere, but are most likely to occur around the mouth, chin, mandibular margin, and less often over other bony prominences such as the malar and forehead regions. Nonfacial skin is also more likely to develop scarring due to the relative paucity of pilosebaceous units and adenexal structures. It has been the experience of one of us (DAG) that patients with a history of acne scarring, regardless of prior isotretinoin use, are more likely to develop delayed wound healing and hypertrophic scarring when compared with the average patient. The surgeon should be alerted to possible scarring when there is delayed wound healing for any reason. Infections need to be treated early and aggressively. Candidal, bacterial, and herpetic infections can delay healing, prolong the inflammatory stage, and increase the chance that the wound will heal with scar development. Likewise, contact dermatitis that is not controlled early and poor wound care are potential precursors for postoperative scarring. Early on, the treated skin may appear redder than the surrounding skin. As the process continues, textural changes can be discerned with palpation of the area (Fig. 3.4), and, as time progresses, a mature scar will develop. In the early stages, topical steroids may have a role.A medium to potent steroid should be used twice daily, but should be applied only to the area of concern and not to the entire lasered area. If prolonged erythema alone is noted without any discernible textural changes, a class II or III steroid may suffice but if thickening or induration is present, a class I steroid should be considered.The patient needs to be monitored closely so that steroid-induced atrophy, stria, or telangectasia do not develop and so that progression of the scarring can be followed.
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a
b
Fig. 3.4 (a) Persistent erythema with textural changes at 6 months post CO2 laser resurfacing. (b) Scar development present at the lip 6 months post CO2 laser resurfacing. Intralesional glucocorticosteroids are probably more effective than topical steroids if textural changes and induration have developed.We typically use triamcinolone acetonide diluted to a concentration of 2.5–5 mg/cm3 for facial scars, but will use 7.5–10 mg/cm3 for very thick or indurated scars. A 30-gauge needle is used to minimize further trauma to the area, and the injection is given into the superficial dermis of the scar. Injections can be repeated every 2–4 weeks, depending on the response or progression of the scar. Treatment should be continued until the skin returns to the same texture and consistency as the surrounding tissue. Overtreatment can result in atrophy, and telangectasia can develop. Some surgeons use occlusion therapy in the early stages of scarring. A very large number of silicone gel dressings have become available over the past few years. If utilized, they should be applied to the scar daily and worn for 12–24 hours per day as tolerated. A mild dishwashing detergent can be used to clean the
25
dressing. An onion skin extract, Menderma gel (Merz Pharmaceuticals, Greensboro, NC), is also marketed to improve and prevent scarring. Its efficacy in not known, and patients using any such product need to be monitored for irritant and allergic contact dermatitis. Another treatment used after laser surgery to treat scars is 5-fluorouracil (5-FU).21 This antimetabolite is a pyrimidine analog and works by inhibiting fibroblast proliferation. A concentration of 50 mg/cm3 is injected into the scar and a total dose of 2–100 mg is used each injection session. Although effective, the injections are quite painful. The addition of Kenalog should be considered and is mixed such that 0.1 cm3 of Kenalog 10 mg/cm3 is added to 0.9 cm3 of the 5-FU (45 mg 5-FU). Less pain and potentially greater efficacy are associated with the latter solution. Approximately 0.05cm3 is injected per site, separated by approximately 1 cm. Injections should be performed two or three times weekly initially, and only the indurated portions of the scar should be injected. Side-effects include pain with injection, purpura, and rarely superficial tissue slough. Flashlamp-pumped dye laser (FLPDL) therapy is effective, and was first described by Alster.22 The settings typically used with the 585 nm FLPDL are 5–7.5 J/cm2 with a 7 mm spot size or 4–5J/cm2 with a 10 mm spot size. Newer vascular lasers and intense pulsed light sources are also being used to treat surgical scars. The V Beam (Candela Corp., Wayland, MA) has a wavelength of 595 nm and a cryogen spray to help cool the epidermis is our preferred laser for scars. Broad-spectrum, intense pulsed light such as the VascuLight (Lumenis, Santa Clara, CA) has been effective with a 570 nm filter. Treatments are administered at 3- to 4-week intervals, and generally will require a minimum of 2–4 treatment sessions. Patients may develop anxiety about having ‘more laser surgery’ if they have already developed a scar from previous laser surgery, but these techniques are generally well tolerated and with minimal risks. Because of the low fluences used, purpura generally does not develop. Although well accepted as an effective treatment, not all studies have demonstrated good results using the pulsed dye laser for scars. In a study by Wittenber et al,23 the flashlamp pulsed dye laser and silicone gel sheeting showed improvement in scar
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blood flow, volume, and pruritus, but the results were no different than the controls. Combining modalities will ensure the best results in reduction of scar volume and erythema and improvement of texture. Laser therapy can be added to the regimen after the scar has begun to show flattening with 5-FU or steroids. Thus, fibroblast activity is suppressed by 5-FU, inflammation is suppressed by corticosteroids, and pulsed dye laser suppresses angiogenesis and endothelial cell growth factors. Concomitant use of the CO2 laser and the pulsed dye laser has been described for nonerythematous scars.24 The CO2 laser is used to de-epithelialize the scar; total vaporization of the scar is not suggested. Then the 585nm pulsed dye laser is used with fluences of 6–6.5 J/cm2 with a 7 mm spot. Finally, resurfacing can be tried for scars that have not responded to the treatment modalities already described. This, however, can result in further scarring, and should be used judiciously.The patient needs to be counseled extensively regarding the potential risks. The scarred area and a small amount of normal appearing skin surrounding the scar should be anesthetized with local anesthesia. Either a CO2 Er:YAG laser can be used, but we prefer the Er:YAG system since it provides ablation with little thermal injury.The scarred area should be ablated superficially with an additional pass to blend with the surrounding skin. Wound care is performed in the standard fashion. Less commonly, hypertrophic scars are hyperpigmented. In these cases, either a pulsed dye laser or a pigment-specific pulsed dye 510 nm laser and a 532 nm frequency-doubled neodymium (Nd):YAG laser can be used to lighten the scar. The immediate endpoint is the production of an immediate ash-white color. ‘Significant’ or ‘average’ improvement can be achieved in approximately 75% of scars.25
SPECIAL CONSIDERATIONS Resurfacing cosmetic units For patients who are not willing to undergo entire face resurfacing and who have deep rhytids limited to the perioral area, CO2 laser resurfacing can be combined with more superficial resurfacing. The preoperative
care is the same, but the face is first resurfaced or peeled to the desired depth. When using chemical peeling, the face is first degreased with alcohol or acetone. Jessner’s peel is applied and then TCA is applied directly onto the skin in concentrations of 20–35%, depending on the desired results. Application of the TCA is performed one cosmetic unit at a time to decrease discomfort and to monitor for the desired level of frost. A hand-held fan or cooling device will enhance the patient’s comfort. Once the peel or superficial laser resurfacing has been performed, the perioral area can be treated with the more aggressive CO2 or Er:YAG lasers as described above. The peeled skin will be red and clearly identifiable to the laser surgeon.Wound care is the same as previously described. Due to the smaller surface area that is more deeply treated, there is less total swelling and exudative drainage. This approach is especially popular in our patients who are ready to undergo a second resurfacing procedure for the mouth area but have retained satisfactory results to the rest of their face.
Neck resurfacing Due to the relative paucity of adenexal structures in the neck, rejuvenation procedures need to be performed judiciously. The use of the Er:YAG laser to improve photoaging was established in the late 1990s, but only modest improvements were seen.26 The desire to improve results led to the use of the CO2 laser, but with mixed results. In 2001, Fitzpatrick and Goldman27 published a study on 10 subjects using the UltraPulse CO2 laser. Despite no complications being seen at the initial neck test areas, 40% of the patients had complications observed at 3–6 months, including patchy hypopigmented scarring (with and without textural changes) in the lower portions of the neck. Despite some obvious improvements noted in the color and texture of the skin (although no improvement in wrinkling was observed), it was concluded that the risks outweighed the potential benefits, at least at the three different parameters studied. In 2006, Kilmer et al28 reported their experience in performing CO2 neck resurfacing in over 1500 patients. Only 2 patients developed hypopigmentation. Over 99% of the neck cases in this study were treated concomitantly with facial resurfacing. Any patient who had undergone
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Carbon dioxide laser resurfacing, fractionated resurfacing and YSGG resurfacing prior neck radiation was excluded from neck CO2 resurfacing. Topical EMLA was used as previously described in this chapter with a second application 45 minutes before the procedure. Lower energy densities were used as the treatment proceeded down the neck. Epidermal debris was not wiped off the neck, in order to minimize additional trauma.
Fractional CO2 resurfacing Carbon dioxide laser resurfacing can give the most dramatic improvements, in terms of smoothing skin, decreasing rhytids, removing lentigines and tightening facial skin. However, due to the typical associated length of recovery it remains unpopular with patients. Other lasers have been developed to try to achieve a more carbon dioxide laser resurfacing type of improvement with a relatively brief recovery period. One of these is fractional CO2 laser resurfacing and the other is the new YSGG resurfacing laser. Although fractional lasers are now available in several different wavelengths, the fractional 10 600 nm carbon dioxide laser can offer some of the beneficial ablative and tightening effects associated with traditional Carbon dioxide laser resurfacing. In fractional photothermolysis, a fraction of the skin surface is treated with the laser, resulting in small zones of thermal injury bridged by surrounding areas of untreated skin.29 Since, only a fraction of the skin is treated, reepithelialization occurs relatively quickly by migration of epithelial elements from the adjacent untreated skin, into the lasered areas. The fractional CO2 laser (Active Fx, Lumenis, Inc., Santa Clara, CA, USA), produces small spots (approximately 1.3 mm) that are scanned using the computerized pattern generator. Between the spots there are areas of untreated skin. This laser is designed to decrease the possible lateral thermal effects of the laser, while allowing the deeper thermal heating effects in each of the treated areas for stimulation of neocollagen production and inducing skin contraction. Since the laser treatment is fractionated the lateral heating effects are decreased by leaving adjacent untreated areas which allow for heat dissipation. Furthermore the device’s CoolScanTM setting allows
27
the spots to be placed in a “random” pattern, which skips from one region to the next rather than treating sequential adjacent areas. This allows for additional thermal relaxation between pulses resulting in less overall thermal injury, and quicker recovery. Posttreatment erythema resolves more rapidly. The treated areas are smaller and placed in a less dense manner than in traditional CO2 laser resurfacing. Settings are variable and are based on patient need in terms of acceptable downtime and degree of photodamage or acne scarring. Initially, post treatment patients develop area of punctate crusting surrounded by areas of unlasered skin. As could be anticipated this also becomes pink and develops mild swelling. Typically, the third author has the patients keep the area moist until it completely reepithelializing. This can be achieved by application of Aquaphor (Beiersdorf,) every 8 hours or other dressings with a moisturizing effect. The third author also routinely gives antivirals starting twenty four hours prior to the laser treatment. Each physician, must decide in their own prophylaxis and after care regimens. Typically patients can resume their regular activities 4–7 days post treatment. Although the results are not as dramatic as with traditional carbon dioxide laser resurfacing the third author’s patients have been pleased with the results of these treatments.They have noted improvement in their skin texture, wrinkles, and lentigines as well as some mild skin tightening. More aggressive settings can also be used for more dramatic results dramatic results with a consequent increase in patient downtime. Patients with deep rhytids and significant skin laxity who are willing to deal with the healing process associated with CO2 resurfacing can have a non-fractionated resurfacing. A different type of fractional CO2 laser is currently under development (Reliant Technologies, Mountain View, CA USA). This laser penetrates the skin more deeply than the traditional CO2 laser and may allow a greater tightening effect. (presented at American Society of Dermatologic Surgery Annual meeting, palm Desert, CA, October 2006) Another alternative to fractional CO2 resurfacing is the 2790 nm laser. (the Pearl, Cutera, Brisbane, California.) This laser is designed to resurface similar to an erbium laser but to provide deeper associated thermal effects to create greater collagen stimulation
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and skin tightening.The effect is between the effect of the typical erbium laser and the carbon dioxide laser. It is used to improve skin smoothness, reduce mild wrinkles and decrease hyperpigmentation.
THE FUTURE Fractional laser, contiguous laser and plasmakinetic resurfacing will undoubtedly continue to advance and improve. Further improvements in patient outcomes may be obtainable with combination therapy including using nonablative lasers, fillers, neurotoxins, and cosmeceuticals.The push continues for less invasive, more efficacious tools with added predictability and safety. The key is to a successful resurfacing practice hower, still involves proper patient selection, good technique and wound care, and the early identification and management of complications.
REFERENCES 1. Iyer S, Bowes L, Kricorian G, Friedli A, Fitzpatrick RE. Treatment of basal cell carcinoma with the pulsed carbon dioxide laser: a retrospective analysis. Dermatol Surg 2004;30:1214–18. 2. Iyer S, Friedli A, Bowes L, Kricorian G, Fitzpatrick RE. Full face laser resurfacing: therapy and prophylaxis for actinic keratoses and non-melanoma skin cancer. Lasers Surg Med 2004;34:114–19. 3. Kilmer SL, Semchyshyn N. Ablative and nonablative facial resurfacing. In: Goldberg DJ, ed. Laser Dermatology. Berlin: Springer-Verlag 2005:83–98. 4. Hevia O, Nemeth AJ, Taylor JR. Tretinoin accelerates healing after trichloroacetic acid chemical peel. Arch Dermatol 1991;127:678–82. 5. Vagotis FL, Brundage SR. Histologic study of dermabrasion and chemical peel in an animal model after pretreatment with Retin-A. Aesth Plast Surg 1995;19:243–6. 6. Kang S, Leyden JJ, Lowe NJ, et al Tazarotene cream for the treatment of facial photodamage. Arch Dermatol 2001;137:1597–604. 7. Penneys NS. Ochronosis-like pigmentation from hydroquinone bleaching creams. Arch Dermatol 1985; 121:1239–49. 8. Nester MS. Prophylaxis for and treatment of uncomplicated skin and skin structure infections in laser and cosmetic surgery. J Drugs Dermatol 2005;4:20–5.
9. Manolis E, Tsakris A, Kaklamanos I, Siomos K. In vivo effect of carbon dioxide laser skin resurfacing and mechanical abrasion on the skin’s microbial flora in an animal model. Dermatol Surg 2006;32:359–64. 10. Crum NF, Lee RU,Thornton SA, et al. Fifteen-year study of the changing epidemiology of methicillin-resistant Staphylococcus aureus. Am J Med 2006;119:943–51. 11. Fritsche TR, Jones RN. Importance of understanding pharmacokinetic/pharmacodynamic principles in the emergence of resistances, including community-associated Staphylococcus aureus. J Drugs Dermatol 2005;4:4–8. 12. Zimbler M, Holds J, Kokoska M, et al. Effect of botulinum toxin pretreatment on laser resurfacing results: a prospective, randomized, blinded trial. Arch Facial Plast Surg 2001;3:165–9. 13. West T, Alster T. Effect of botulinum toxin type A on movement-associated rhytides following CO2 laser resurfacing. Dermatol Surg 1999;25:259–61. 14. Kilmer SL, Chotzen VA, Zelickson BD, et al. Full-face laser resurfacing using supplemented topical anesthesia protocol. Arch Dermatol 2003;139:1279–83. 15. Fitzpatrick RE, Geronemus RG, Grevelink JM, Kilmer SL, McDaniel DH. The incidence of adverse healing reactions occurring with UltraPulse CO2 resurfacing during a multicenter study. Lasers Surg Med 1996; Suppl 8:S34. 16. Sriprachya-Anunt S, Fitzpatrick RE, Goldman MP, Smith SR. Infections complicating pulsed carbon dioxide laser resurfacing for photoaged facial skin. Dermatol Surg 1997;23:527–35. 17. Railan D, Kilmer SL. Ablative treatment of photoaging. Dermatol Ther 2005;18:227–41. 18. Grimes P, Bhawan J, Kim J, Chiu M, Lask G. Laser resurfacing-induced hypopigmentation: histologic alterations and repigmentation with topical photochemotherapy. Dermatol Surg 2001; 27:515–20. 19. Hong S, Park H, Lee M. Short-term effects of 308-nm xenon-chloride excimer laser and narrow-band ultraviolet B in the treatment of vitiligo: a comparative study. J Kor Med Sci 2005;20:273–8. 20. Alexiades-Armenakas MR, Bernstein LJ, Friedman PM, Geronemus RG. The safety and efficacy of the 308-nm excimer laser for pigment correction of hypopigmented scars and striae alba. Arch Dermatol 2004;140:955–60. 21. Fitzpatrick R. Treatment of inflamed hypertrophic scars using intralesional 5-FU. Dermatol Surg 1999;25:736–7. 22. Alster T. Improvement of erythematous and hypertrophic scars by the 585-nm flashlamp-pumped pulsed dye laser. Ann Plast Surg 1994;32:186–90. 23. Wittenberg G, Fabian B, Bogomilsky J, et al. Prospective, single-blind, randomized, controlled study to assess the efficacy of the 585-nm flashlamp-pumped pulsed-dye
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24.
25.
26.
27.
laser and silicone gel sheeting in hypertrophic scar treatment. Arch Dermatol 1999;135:1049–55. Alster T, Lewis AB, Rosenbach A. Laser scar revision: comparison of CO2 laser vaporization with and without simultaneous pulsed dye laser treatment. Dermatol Surg 1998;24:1299–302. Bowes LE, Nouri K, Berman B, et al. Treatment of pigmented hypertrophic scars with the 585 nm pulsed dye laser and the 532 nm frequency-doubled Nd : YAG laser in the Q-switched and variable pulse modes: a comparative study. Dermatol Surg 2002;28:714–19. Goldman MP, Fitzpatrick RE, Manuskiatti W. Laser resurfacing of the neck with the erbium : YAG laser. Dermatol Surg 1999;25:736–7. Fitzpatrick RE, Goldman MP, Sriprachya-Anunt S. Resurfacing of photodamaged skin on the neck with
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an UltraPulse carbon dioxide laser. Lasers Surg Med 2001;28:145–9. 28. Kilmer SL, Chotzen VA, Silva SK, McClaren ML. Safe and effective carbon dioxide laser skin resurfacing of the neck. Lasers Surg Med 2006;38:653–7. 29. Manstein D, Herron GS, Sink RK,Tanner H,Anderson R. Fractional photothermolysis: a new concept for cutaneous remodeling using microscopic patterns of thermal injury. Lasers Surg Med 2004; 34:426–38. 30. American Society of Dermatologic Surgery Annual Meeting, Palor Desert, CA, October 2006.
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4. Erbium laser aesthetic skin rejuvenation Richard Gentile
MODALITIES OF SKIN REJUVENATION Aesthetic skin rejuvenation (ASR) is certainly not a new process, and historical accounts date back as many as four millennia (2000 BC). For thousands of years, humans (both male and female) have been utilizing treatments to improve the appearance of a poor complexion or to enhance the beauty of a natural complexion. Throughout the ages, humans have sought out simple, elective cosmetic methods to improve highly visible and undesirable permanent cutaneous signs: facial wrinkles and residual facial scars that may follow ailments such as acne, smallpox, and chickenpox.1 The first examples of such ‘treatments’ were apparently noted in ancient Egypt and recorded in the famous Edwin Smith Surgical Papyrus, the oldest medical document in existence.2 The description of the wrinkleremoval recipe prepared from hemayet fruit included the composition and the technique for application. Ancient Greece and the Roman Empire are both well represented in the quest for more beautiful skin, and Cleopatra (whose name has been synonymous with beauty through the ages) wrote a book on beautification that was quoted by Galen and other medical writers. Her recipes were quoted well into the Middle Ages. Due to the lack of sophisticated medical technology, many of these treatments relied on what we would now call homeopathic ‘spa’ products and abrasives. The transition to utilizing chemicals for ASR occurred in the early to mid 1800s. Phenol was first prepared in 1842 by the French chemist August Laurent and presented at the 1867 Paris Exhibition.The mid to late 1800s also found Hebra3 utilizing various acids, alkalis, and other corrosives to treat freckles and melasma. It is not clear whether Hebra treated wrinkles with these chemical agents. Chemical agents facilitating ASR (particularly phenol) became more widely utilized in the early 1900s,
and George Miller MacKee4 became a proponent of chemical ASR after first experimenting on himself. In 1953, Abner Kurtin5 published ‘Corrective surgical planing of the skin’, capturing the imagination of plastic surgeons and dermatologists. He proposed dermabrasion as a better method to improve acne pits and scars. Kurtin’s description of dermabrasion actually reintroduced Ernst Kronomayer’s dermabrasion procedure, which Kronomayer had introduced in Germany in 1905. Dermabrasion, chemical peeling (trichloroacetic acid (TCA) and phenol) were considered standards for ASR until the 1990s. The last decade has seen unprecedented technological development of lasers, other light sources, and radiofrequency (RF) approaches for ASR. They have dominated the ASR arena, although a reverse trend towards a return to chemical exfoliation exists in some practices. Currently lasers, other light sources, and RF devices are generally classified as ablative and nonablative. Goldberg6 has reviewed the four different tissue interactions of laser, light, and RF with regard to the biological effects of ASR devices on skin and adjacent structures. The description traces the evolutionary development of these devices: 1. The initial devices ablated the epidermis, caused dermal injury, and provided a significant thermal effect (carbon dioxide (CO2) lasers). 2. Subsequent devices caused highly selective epidermal ablation, with minimal thermal effects (erbium : yttrium aluminum garnet (Er:YAG) short pulsed lasers). 3. Later devices ablated the epidermis, caused dermal injury, and provided variable thermal effects (dualmode and long- or variable-pulsed Er:YAG lasers). 4. The more recent evolution of devices do not ablate the epidermis, wound the dermis and provide
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The fifth generation of devices (not mentioned by Goldberg) are nonablative or subablative devices that produce a more substantial thermal effect for skin tightening and rejuvenation, and include mono- and bipolar RF devices, with or without optical energy, and infrared and fractionated devices.Variable-pulsed Er:YAG lasers are also included in this category, as these devices have been developed to provide higher degrees of thermal effects at the level of the dermis and perhaps below as one function of their clinical application.
EVOLUTION OF USE OF ERBIUM LASERS IN AESTHETIC AND MEDICAL DERMATOLOGY As reviewed by Ronel,7 laser technology applied to skin resurfacing was discovered to yield more predictable depths of injury when compared with chemical peels or dermabrasion.The first laser used for laser-assisted skin rejuvenation (LASR) was a pulsed CO2 laser that Fitzpatrick and colleagues modified from a device that had been developed for otolaryngological and gynecological use. It was initially utilized for periorbital and perioral LASR, but initial appraisals of substantial aesthetic improvement led to its use for full facial rejuvenation.The CO2 laser quickly became the workhorse for LASR, and its advantages and limitations became well recognized. Although the long-term skin rejuvenation and tightening provided by this device are unparalleled, marked erythema persisting for weeks or months and permanent (sometimes delayed) hypopigmentation occur at a rate that is not acceptable for many patients. In some patients, as with a deep phenol peel, the recovery ‘downtime’ can approach 2 weeks, which may be unacceptable for those with active lifestyles or work obligations. Subsequent to the laser boom of the early to mid 1990s, further research led to the development of other lasers for LASR.The aim was to employ a more precise laser beam, resulting in less intense adverse sideeffects and a shorter recovery period. In 1990, Kaufman and Hibst8 reported on the cutaneous laser ablative effects of the mid-infrared Er:YAG laser utilized in short pulses.They employed the laser on pig skin and on
experimental patients, treating superficial lesions such as epidermal nevi. Precise control of epidermal ablation was achieved, with small ablation depths and also thermal necrosis rates that did not exceed 50 µm. Kaufman and Hibst8 concluded that the laser should have potential for LASR, but also noted that, due to the limited dermal thermal depths of action, bleeding could be a problem. The Er:YAG laser was first introduced as a bonecutting tool in the USA in 1996, but commercial availability for LASR followed the completion of Food and Drug Administration (FDA) studies of photodamage. Initial enthusiasm for the Er:YAG laser was high due to its ability to operate at a more superficial level and with greater precision. Collagen contraction was noted to be 1–2% during lasing, reaching 14% in the long term. Concurrent with its introduction, some short comings of the Er:YAG laser became apparent. A major disadvantage of the superficial and fleeting energy absorption of the Er:YAG laser is its poor ability to maintain hemostasis.There is not much ‘heat sink’ in the wound, so thermal necrosis does not significantly impair the laser’s subsequent ablation, but blood in the wound bed does make controlling wound depth difficult.The blood spatter also creates more of a biological hazard to the surgeon and assistants.The other limitation of the Er:YAG laser is that there is less collagen contraction, although this may be due to the fact that comparable depths of resurfacing are not being accomplished due to the lack of hemostasis.The shortcomings of the short-pulsed Er:YAG laser led to some technological modifications, which included a longer variable pulse duration as well as the development of lasers with ‘dual-mode’ capabilities.These dual-mode capabilities allow the operator to dial in the depths of ablation as well as the thermal effects (coagulation) desired.
ERBIUM LASER PHYSICAL PROPERTIES AND LIGHT–TISSUE INTERACTION Erbium laser physical properties Solid state lasers have lasing material distributed in a solid matrix.Yttrium aluminum garnet (YAG,Y3Al2(ALO4)3) is a synthetic crystalline material of the garnet group
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Fig. 4.1 Yttrium aluminum garnet (YAG,Y3 Al2 (AlO4 )3 ) is used for synthetic gemstones.When doped with neodymium (Nd3) or erbium (Er),YAGs are used as the lasing medium in lasers.
(Fig. 4.1) used as the active laser medium in various solid state lasers.YAG is commonly ‘doped’ with other elements to obtain a specific laser wavelength. In the Nd:YAG laser, the dopant is the rare earth element neodymium. In the Er:YAG laser, it is another rare earth element, erbium (Fig. 4.2). Er:YAG lases at a wavelength of 2940 nm. Its absorption bands suitable for pumping are wide and are located between 600 and 800 nm, allowing for efficient flashlamp pumping (Fig. 4.3).The dopant concentration used is high: about 50% of yttrium atoms are replaced. The Er:YAG laser emission couples well with water and bodily fluids, making these lasers especially useful in medicine and dentistry: Er:YAG lasers are used for treatment of tooth enamel as well as aesthetic dermatological applications. Er:YAG lasers are also used for noninvasive monitoring of blood sugar.The mechanical properties of Er:YAG are essentially the same as those of Nd:YAG. Er:YAG lasers operate at relatively eye-safe wavelengths (radiated incident through the lens is absorbed in the eye and does not damage the retina), work well at room temperature, and have high slope efficiency. Er:YAG laser light is pale green.
Erbium laser light–tissue interaction (biophotonics) There are four primary interactions of laser light with tissue (Fig. 4.4). The first interaction is surface reflection. There may also be scattering. This is then
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Fig. 4.2 Elemental erbium is a rare silvery rare earth metal. Erbium is associated with several other rare earth elements in the mineral gadolinite fromYtterby in Sweden (from which both the names yttrium and erbium are derived).
followed by absorption by the target, and some of the light may be transmitted through the tissues on the other side of the target.The absorption of laser light in tissue is a remarkably strong function of wavelength.The result is that lasers of different wavelengths have qualitatively and quantitatively different interactions with tissue (Fig. 4.5). The thermal relaxation time depends very strongly on the absorption length.The absorption length is the distance the laser light travels in tissue before it is 63% absorbed.Taken together, these two parameters determine a critical power density. This is the minimum power density that must be used to limit thermal damage to a depth equal to one absorption length (Table 4.1). For the Er:YAG laser, the absorption length is 0.001 mm, the thermal diffusion time is 4 µ, the critical power density is 600 W/mm2, and the critical pulse energy is 0.0025 J/mm2. In addition to the initial interactions of light with the target, subsequent interactions can be summarized as having photothermal, photochemical, or photoacoustic effects on the target. As is widely recognized, the Er:YAG wavelength of 2940 nm is absorbed 12–18 times more efficiently by superficial (water-containing) cutaneous tissue than is the CO2 laser emission at 10 600 nm. Considering the typical short-pulse erbium pulse duration of 250 µs, a cutaneous ablation depth of 10–20 µm is accomplished at a fluence of 5. The vaporization threshold of the Er:YAG laser is 0.5–1.7 J/cm2. The fluence and depth of tissue ablation are directly related.
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Flashlamp (pump source)
Partially reflective mirror
Laser output
Highly reflective mirror Er:YAG crystal
(Laser medium)
Optical resonator
Fig. 4.3 Laser pumping is the act of energy transfer from an external source (flashlamp) into the laser gain medium (the Er:YAG crystal). Stimulated emission occurs when a population inversion occurs, with more members in an excited state than in lower-energy states.
Backward scattering
Forward scattering
Transmission Laser beam Absorption Direct reflection
For every 1 J/cm2, 2–4 mm of tissue depth is ablated. This allows for precise control of tissue ablation. It occurs with minimal residual thermal damage and can be compared with the 20–60 µm of tissue damage per standard pass of the CO2 laser with 150 µm of residual thermal damage per standard pass. Pulsed laser energy causes controlled vaporization of the skin according to the principles of selective photothermolysis. Target tissues contain chromophores with absorption peaks that selectively absorb the particular wavelength of the laser pulse. Tissue adjacent to the chromophore absorbs the energy to a much lesser degree. The interaction of target tissue with the CO2 laser is predominantly a thermomechanical reaction that leads to target destruction of dermal vessels and proteins. The Er:YAG laser interacts with tissue via a photomechanical reaction.
Fig. 4.4 Biophotonics examines the interface of laser and human tissue and is characterized by reflection, absorption, scatter, and transmission.
Absorption of the optical laser energy causes immediate ejection of the dessicated tissue from its location at supersonic speeds. This popping sound (like a cap gun) is audible and represents the microexplosion taking place at the tissue level.The translation of Er:YAG laser energy into mechanical work is an important factor that protects the surrounding tissue: minimal thermal energy remains to dissipate and cause collateral damage.
COMMERCIALLY AVAILABLE ERBIUM LASERS While it is beyond the scope of this chapter to detail every Er:YAG laser manufactured, we do want to review some models that are or have been commercially
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Erbium laser aesthetic skin rejuvenation a
105
104
Absorption coefficient (cm−1)
103
Melanin
102
Water Hemoglobin
101
100 Protein 10−1 10−2 Scatter
10−3
10−4 0.1
1
10
Wavelength (µm)
Penetration depth (mm)
Nd:YAG
0
Diode
CO2
Alexandrite
Ho: Er: YAG YAG
Pulse dye
Nd: YAG
KTP
KTP
CO2
Excimer
Er:YAG
Type of laser
b
Pigmented tissue
1 2
3
Unpigmented tissue
4 0 −1
Depth of Penetration 1
10
Wavelength (µm) Ultraviolet
Visible
Infrared
Fig. 4.5 Biophotonics also examines laser absorption (a) and tissue penetration (b) as functions of wavelength, pulse duration, and thermal relaxation time. Selective photothermolysis describes the process of wavelength-specific target destruction.
available so that the laser’s unique specifications and design can be understood.These will be listed as shortpulsed systems, dual-mode systems, and variablepulsed systems.
Short-pulsed Er:YAG systems The prototype of the Er:YAG short-pulsed systems, and one of the first to market in 1996, was the
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Table 4.1 Critical power densities and minimum coagulation depths a
Laser
Absorption length (minimum damage zone) (mm)
Thermal diffusion time (s)
Critical power density (W/mm2)
Critical pulse energy (J/mm2)
0.1 pigmented ∞ unpigmented 0.1 pigmented ∞ unpigmented 5 0.4 0.001 0.02 2
0.4 — 0.4 — 100 1 4 × 10−6 0.002 16
0.6 — 0.6 — 0.1 1 600 50
0.25 — 0.25 — 13 1.0 0.0025 0.040
Argon ion Doubled Nd:YAG (KTP) Nd:YAG Hol:YAG Er:YAG CO2 Electrocautery
a Wavelength and thermal relaxation time determine the critical power density. This is the minimum power density that must be used to limit thermal damage to a depth equal to one absorption length. Short-absorption-length lasers such as Er:YAG are capable of producing less thermal damage than lasers with long absorption lengths. In order to achieve this desirable effect, these strongly absorbed lasers must be operated at high power density. When laser energy is delivered in a pulsed mode, it is possible to limit the tissue damage to one absorption length while working at an average power density less than the critical value. This result is only possible if the pulsed energy exceeds the critical value shown in the last column.
Coherent Ultrafine Erbium (Fig. 4.6). At the time of its release in 1996, the UltraFine Erbium was advocated for incision, excision, ablation, vaporization, and coagulation of soft tissue, including superficial skin resurfacing, precision microplaning, etching, and tissue sculpting. The laser vaporizes 20–50 µm of tissue with very little thermal effect. It is equipped with a computerized pattern generator as well as a variablewidth handpiece. The laser has a maximum output of 3000 mJ and pulse variability from 200 to 600 µs. We have used this laser for 10 years, and it has been very reliable. Others like it include the ConBio CB Erbium/2.94 and the recently introduced Friendlylight portable laser, which is highly transportable. The Nexgen Pixel is a short-pulsed Er: YAG laser that utilizes a pixel grid pattern of 49 or 81 ablations, sparing intervening epidermis.The planned ablation is 20–50 µm per pass for epidermal ablation.
Dual-mode Er:YAG systems Dual-mode, different laser type Recent developments in Er:YAG lasers have led to the combination of ablative and coagulative pulses (hence
Fig. 4.6 The Coherent UltraFine Er:YAG laser was one of the first to be available commercially, in 1996.
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Erbium laser aesthetic skin rejuvenation the term dual-mode), which allow much deeper vaporization with significant control of hemostasis. One of the earliest dual-mode systems was the Sharplan DermaK. (Both Coherent and Sharplan brands are now owned by Lumenis.) Both the CO2 laser and Er:YAG laser are clinically proven to be effective technologies for ablative skin rejuvenation.Yet, alone, each laser has its limitations. In order to provide physicians access to the best characteristics of each laser wavelength, Sharplan combined a high-power Er:YAG laser and a subablative CO2 laser in the blended DermaK system. DermaK has the unique capability to deliver both Er:YAG and CO2 beams simultaneously (K blend mode) to the same tissue area for skin rejuvenation. The Er:YAG laser carries out accurate ablation of superficial layers, opening the way for the CO2 laser to affect the deeper tissue layers. DermaK combines the best of both the Er:YAG and CO2 lasers for improved clinical efficacy. It replicates the precise tissue ablation and minimal necrosis found in Er:YAG systems and significantly controls the heating of deeper tissue layers, typical of CO2 systems.The concurrent delivery of both wavelengths provides the physician with enhanced control over hemostasis (dry erbium technique), thereby increasing the range of applications of the Er:YAG laser. The CO2 mode of the DermaK delivers sufficient thermal energy to seal small blood vessels throughout the surgical procedure, creating the benefit of a clean, dry surgical field. Simultaneous operation of both the Er:YAG and CO2 lasers minimizes the number of passes required for a given procedure, thereby minimizing erythema and decreasing the recovery time. At the same time, the dual wavelengths allow more overall energy to be transferred to the tissue, increasing the ablation depth and controlling thermal impact. DermaK can also perform many standard CO2 laser surgical and aesthetic incisional procedures, such as blepharoplasty. There is generally no need for deep sedation when treating most body areas in LASR. Same laser type, variable pulse duration Another dual-mode system is the Sciton Contour (Fig. 4.7) The Contour Er:YAG contains not one but two Er:YAG lasers providing 45 W of power.The engineers use a technology called optical multiplexing to
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Fig. 4.7 The Sciton Profile is an example of a second-generation Er:YAG laser. Such lasers are known as dual-mode devices.
generate multiple variable-length ‘macropulses’ to generate high tissue fluence.At 50% overlap, fluences of up to 100 J/cm2 can be generated for aggressive vaporization. Sufficient energy can be delivered to remove the epidermis in one pass. The optical multiplexing also allows the laser to be used in an ablative mode, a combined ablative/coagulative dual mode, or a pure coagulative mode. The ablative mode is characterized by a short (200 µs) suprathreshold pulse. The dual-mode ablation/coagulation is achieved by an ablative pulse immediately followed by a relatively long subablative pulse.The coagulative mode consists simply of a series of subablative pulses.The Sciton Contour is the model for many current lasers featured below.
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Table 4.2 Dermatological conditions treatable with the Er:YAG laser Becker nevi Compound nevi Naevi spili Verrucae Epidermal nevi Xanthelasma Syringomas Milia palpebrarum Seborrhoic keratoses Darier’s disease
• • • • • • • • •
• • • • • • • • •
Trichoepitheliomas Sebaceous hyperplasia Eruptive hair cysts Xanthelasma Adenoma sebaceum Angiofibroma Hidradenoma Morbus Favre–Racouchot Lentigines
Introduced in 2002, the Fontona laser systems feature a proprietary VSP (Variable Square Pulse) technology. This allows the practitioner to accommodate the laser pulse duration and its fluence according to the needs of the specific application (Fig. 4.8). By means of digital online energy regulation, the energy of each pulse is actively controlled to match the required value while the laser is in operation.This enables the practitioner to treat selected tissues without heating the surrounding tissue unnecessarily.With a short pulse width, the VSPshaped Er:YAG laser induces minimal thermal effects to underlying tissue while rejuvenating the superficial skin layers through ablation of the epidermis.This allows the practitioner to offer effective skin rejuvenation treatments with higher comfort levels and shorter recovery. By increasing the pulse duration, more heat is diffused in the skin and a resulting collateral thermal effect is achieved. Long-pulsed lasers characteristically have pulse durations of the order of milliseconds, in contrast to short-pulse durations of the order of microseconds. These thermal effects produce pronounced collagen contraction and new collagen stimulation in the dermis. Clinical trials have proven a light ablative effect on the epidermis, relatively noninvasive stimulation of new collagen formation, and no post-treatment downtime. Fotona’s stacked pulse technology provides a purely nonablative Er:YAG laser SMOOTH mode for skin rejuvenation treatments.The thermal SMOOTH mode allows dermal remodeling and rejuvenation without affecting the epidermis. The Cynosure CO3 laser has a similar variable-pulse technology, featuring pulse durations of 0.5, 4, 7, and 10 ms.
Ablation speed
Variable-pulse Er:YAG systems
0
Miliary osteomas Papillomas Café-au-lait spots Syringomas Basal cell carcinoma Squamous cell carcinoma Telangiectasia Rhinophyma Hailey–Hailey disease (familial benign pemphigus)
High power
Low power
Short pulse
Long pulse
0.5
1.0
Thermal effect
• • • • • • • • • •
1.5
Pulse duration (ms)
Fig. 4.8 Biophotonics has also resulted in understanding dosimetry of pulse duration and fluence in an attempt to achieve more collateral thermal damage with the Er:YAG laser in order to achieve better hemostasis as well as collagen contraction. The FDA has recently given approval for use in the USA of the BURANE XL Er:YAG laser, which also features variable triple-pulse technology.The BURANE XL features a specially designed and patented pulse sequence for each application (coagulation, scars, and wrinkles) that heats the deeper skin layers to a specific temperature while protecting the epidermis by allowing it to cool down during the pauses of the pulse sequences.All these dosimetry models are based on longer pulse duration and subablative laser energies for subablative dermal heating.
CLINICAL DERMATOLOGICAL APPLICATIONS OF ERBIUM LASERS Due to its superficial action and tendency to not promote dermal scarring, the Er:YAG laser is well adapted to ablating and etching superficial cutaneous neoplasms and cutaneous blemishes (Fig 4.9). The high ablative
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a
b
c
d
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Fig. 4.9 This patient presented for removal of an irritated seborrheic keratosis, as shown in the preoperative photograph (a).The lesion is excised by sharp intradermal excision (b).The underlying dermal components are ablated and the edges are ‘feathered’ (c).The final result is shown in (d). potential results in microexplosive destruction of the skin lesions without the associated scarring that would result from epidermal or dermal excisions. Numerous clinical applications are listed in Table 2.
CLINICAL AESTHETIC APPLICATIONS OF ERBIUM LASERS LASR with a short-pulsed Er:YAG laser is most commonly used for the improvement of fine rhytides. In patients with moderate photodamage and rhytides, modulated Er:YAG laser skin resurfacing results in greater collagen contraction and improved clinical
results compared with short-pulsed Er:YAG systems. The clinical improvement of severe rhytides treated with a modulated Er:YAG laser can be impressive (Fig. 4.10).There are conflicting reports as to whether or not the endpoints of CO2 LASR can be reached even when ablating to similar depths. Newman and colleagues compared a variable-pulse Er:YAG laser with traditional pulsed or scanned CO2 laser resurfacing for the treatment of perioral rhytides.9 Although a reduced duration of re-epithelialization was noted with the modulated Er:YAG laser (3.4 days vs 7.7 days with a CO2 laser), the clinical results observed were less impressive than those following CO2 laser resurfacing. Er:YAG laser systems may greatly improve atrophic scars caused by acne,
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c
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Fig. 4.10 This treatment took place over two sessions. (a) Preoperative photograph. (b) Following excision/ablation of seborrheic keratosis with basal cell carcinoma.The patient then elected to have aesthetic full-face LASR 1 year postoperatively and is shown 4 days (c) and 12 days (d) post LASR, with multiple excision ablations.
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Erbium laser aesthetic skin rejuvenation trauma, or surgery. In a series of 78 patients,Weinstein reported 70–90% improvement of acne scarring in the majority of patients treated with a modulated Er:YAG laser10. Pitted acne scars may require ancillary procedures, such as subcision or punch excision, for optimal results.These procedures can be performed either prior to or concomitant with Er:YAG laser resurfacing.
ERBIUM LASER TECHNIQUES Cutaneous ablative surgery In treating superficial epidermal lesions such as irritated seborrheic keratoses, the primary lesion can be ablated or an epidermal shaving of the lesion followed by ablative pulses can be performed. On most treatments with the short-pulsed laser system, the fluence is set to 5, which corresponds to about 20 µm of ablation. The lesion ablation is continued until the entire lesion is vaporized. The adjacent dermis is ‘feathered’ to taper the cutaneous margins of the lesion.
‘Dry erbium’ This is a fairly new term, with the ‘dry erbium’ representing an epidermal ablation that does not extend into the papillary dermis, where bleeding is encountered. Often, this treatment is done with subablative levels of laser energy and is associated with rapid recovery and a result that is intermediate to microdermabrasion or photorejuvenation but not as significant as superficial laser resurfacing.
Superficial LASR The technique used for superficial LASR is to set the fluence to 5 and use three passes.This equates to about 40–60 µm of ablation. After the inititial ablation, the same settings are maintained until punctuate bleeding is encountered.
Medium-depth LASR The techniques utilized for medium-depth LASR will be influenced by the Er:YAG laser technology available
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and by other techniques that the laser surgeon can call upon. With longer-pulsed or dual-mode systems and progression beyond 60–80 µm, there may be bleeding from the dermal plexus, which will slow the procedure down. It is our preference to change our technique if we wish to accomplish a deep LASR for moderate to deep rhytides.When employing a combination technique for the full face, we generally perform the CO2 laser resurfacing in the first pass, followed by Er:YAG laser ablation of the char. When using ablative bipolar RF (BPRF) (Visage, Arthrocare Corp.), we ablate the epidermis and then heat the dermis (Fig. 4.11) with several passes of ablative BPRF.This technique serves to contract dermal collagen without excessive thermal damage to the deeper dermal layers.When treating acne scarring, we sometimes convert to dermal sanding in the deeper dermal layers.
Deep LASR Essentially the same techniques are utilized as in medium-depth treatment, but the deeper dermal treatment is performed with more passes. This is frequently necessary for deeply creased upper lip rhytids. It is important to always use a graduated approach for deeper techniques and to treat the facial skin with an appreciation of the skin thickness in each facial area as well as the depth or degree of the rhytids. We occasionally utilize a fractionated CO2 laser pass after completing the medium-depth LASR. This involves spatially separated pulses of the CO2 laser over the treatment area. The smallest possible spot size is utilized, with no overlapping of pulses.
PATIENT SELECTION AND PERIOPERATIVE MANAGEMENT As with most aesthetic facial procedures, appropriate patient selection and reasonable patient expectations are the cornerstones of any successful intervention. A complete medical and surgical history should be obtained prior to any recommendations. The contraindications to laser resurfacing are unrealistic patient expectations, a tendency toward keloid or hypertrophic scar formation, isotretinoin use
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Fig. 4.11 Combination resurfacing techniques utilize other modalities to achieve the same endpoint that multiplexing pulse duration achieves. Ablative bipolar radiofrequency or fractional CO2 laser treatment to the upper dermis enhances hemostasis and collagen contraction.
within 6 months prior to surgery, and a lack of patient compliance with postoperative instructions. Other medical considerations include identifying patients with reduced numbers of adnexal skin structures, such as those with scleroderma, burn scars, or a history of prior ionizing radiation to the skin. These patients should be approached with caution. Long-term use of skin pharmaceuticals such as glycolic acid products or retinoids may thin the dermis and alter the depth of penetration of the LASR. A history of previous skin rejuvenation procedures is noteworthy, because these procedures could potentially slow the wound healing process due to the presence of fibrosis. Patients who have undergone prior transcutaneous lower lid blepharoplasty or have limited infraorbital elasticity may be at increased risk for postoperative ectropion.When applicable, patients who smoke should be discouraged from doing so before and after surgery to reduce the risk of delayed or impaired wound healing. Physical examination of the treatment area includes careful attention to Fitzpatrick skin type and specific areas of scarring, dyschromia, and rhytid formation. For patients desiring periorbital laser treatment, the eyes must be examined for scleral show, lid lag, and ectropion. Other epidermal pathology should also be noted, including seborrheic keratoses, solar lentigines, actinic keratoses, and cutaneous carcinomas.The author prefers to address this during the LASR, but some lesions may need to be addressed prior to the LASR.
LASR can lead to reactivation of latent herpes simplex virus (HSV) infection or predispose the patient to a primary infection during the re-epithelialization phase of healing. Prophylactic antiviral medication should be prescribed during the postoperative period, regardless of a patient’s HSV history.11 Currently used regimens include famciclovir 250 mg twice daily, acyclovir 400 mg three times daily, or valacyclovir 500 mg twice daily. The medication may be administered the day before or on the morning of laser resurfacing, and should be continued for 7–10 days or until re-epithelialization is complete. Antibiotics for bacterial prophylaxis may be prescribed; however, little data exist to support their use, because of the relatively low incidence of postoperative bacterial infections reported. The routine use of antibiotic prophylaxis may increase the incidence of antibiotic resistance and predispose patients to organisms of increased pathogenicity. When used, cephalosporin (cephalexin), semisynthetic penicillin (dicloxacillin), macrolide (azithromycin), or quinolone (ciprofloxacin) is administered 1 day before or on the morning of surgery, and is continued until re-epithelialization is complete.The use of topical antibiotics on the laser-induced wound may be recommended, but neomycin-based products should be avoided due to a 10% incidence of sensitivity to this compound. Postoperative wound care can follow an open or closed method.With the closed method, a semiocclusive
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Erbium laser aesthetic skin rejuvenation dressing (Flexan) is placed on the denuded skin.These wound dressings have been shown to accelerate the rate of re-epithelialization by maintaining a moist environment. In addition, decreased postoperative pain has been reported with their use.The closed method may create a low-oxygen environment that may promote the growth of anaerobic bacteria and subsequent infection. As such, many proponents of the closed technique currently endorse removal of the dressing with wound inspection 24–48 hours after the procedure, followed by topical emollients.The open wound technique consists of frequent soaks with cool saline or Domeboro solution.These soaks are followed by the application of ointment to promote re-epithelialization while allowing adequate visualization of the resurfaced wound. Er:YAG laser resurfacing ablates superficial cutaneous tissue and causes a thermal injury to denuded skin.Therefore, some adverse effects are to be expected and should be considered complications. These ‘sideeffects’ of cutaneous laser resurfacing include transient erythema, edema, burning sensation, and pruritus. Short-pulsed Er:YAG laser resurfacing procedures are associated with a significantly shortened period of reepithelialization and erythema when compared with the CO2 laser. However, when equivalent depths of ablation and coagulation are achieved with the aforementioned modulated systems, postoperative healing times are comparable.
LASER RADIATION SAFETY AND ERBIUM LASERS All laser devices distributed for both human and animal treatment in the USA are subject to Mandatory Performance Standards. They must meet the Federal laser product performance standard, and an ‘initial report’ must be submitted to the Center for Devices and Radiological Health (CDRH) Office of Compliance prior to the product being distributed. This performance standard specifies the safety features and labeling that all laser products must have in order to provide adequate safety to users and patients. A laser product manufacturer must certify that each model complies with the standard before introducing the laser into US commerce.This includes distribution
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for use during clinical investigations prior to device approval. Certification of a laser product means that each unit has passed a quality assurance test and that it complies with the performance standard.The firm that certifies a laser product assumes responsibility for product reporting, for record-keeping, and for notification of defects, non-compliance, and accidental radiation occurrences. A certifier of a laser product is required to report the product via a Laser Product Report submitted to the CDRH. Er:YAG lasers belong to safety class IV; i.e., these lasers are high-power lasers (500 mW for continuous-wave and 10 J/cm2 or the diffuse reflection limit for pulsed), which are hazardous to view under any condition (directly or diffusely scattered), and are a potential fire hazard and a skin hazard. Significant controls are required of class IV laser facilities.
AVOIDANCE AND TREATMENT OF COMPLICATIONS Complications of Er:YAG laser resurfacing should be differentiated from temporary ‘side-effects’ of the procedure. Temporary side-effects of Er:YAG laser resurfacing include transient erythema, edema, burning sensation, and pruritus. Healing times are short for the short-pulsed systems, but second- and third-generation models are designed to function more on a par with CO2 laser systems and so the complication profile may be similar, but appears to be intermediate in terms of the most frequent complications of prolonged erythema, hyper- or hypopigmentation, and dermal fibrosis or scarring. In addition to the complications mentioned above, mild complications of Er:YAG laser resurfacing include milia, acne exacerbation, contact dermatitis, and perioral dermatitis. Moderate complications include localized viral, bacterial, and candidal infection. The most severe complications include disseminated infection and the development of ectropion. Diligent evaluation of the patient is necessary during the re-epithelialization phase of healing. This is important, because a delay in recognition and treatment of complications can have severe deleterious consequences, such as permanent dyspigmentation and scarring.As always, patient selection and avoidance of these
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procedures in any patient predisposed to delayed or abnormal cutaneous wound healing will reduce the frequency of severe postoperative sequellae. Although short-pulsed Er:YAG laser resurfacing has a significantly better adverse-effect profile and complication rate when compared with pulsed or scanned CO2 laser resurfacing, long-term data for the modulated Er:YAG laser systems are not yet available. Because the modulated Er:YAG laser systems may be used to create zones of collateral thermal damage similar to those created by the CO2 laser, further studies are necessary to determine the incidence of delayed hypopigmentation.
REFERENCES 1. Goldman MP, Fitzpatrick RE. Cutaneous Laser Surgery: The Art and Science of Selective Photothermolysis, 2nd edn. St Louis, MO: Mosby-Year Book, 1999:339–436. 2. Kotler R. Chemical Rejuvenation of the Face. St Louis, MO: Mosby-Year Book, 1992:1–35.
3. Hebra F, Kaposi M. On Diseases of the Skin, Including Exanthemata. London: New Sydenham Society, 1874: Vol 3:22–23. 4. MacKee GM, Karp FL. The treatment of post acne scars with phenol. Br J Dermatol 1952;64:456–9. 5. Kurtin A. Corrective surgical planing of skin. Arch Dermatol Syph 1953;68:389. 6. Goldberg DJ. Lasers for facial rejuvenation. Am J Clin Dermatol 2003;4:225–34. 7. Ronel DN. Skin resurfacing, laser: erbium YAG. eMedicine. http://www.emedicine.com/plastic/topic 108.htm (accessed November 2006). 8. Kaufmann R, Hibst R. Pulsed 2.94-microns erbium–YAG laser skin ablation – experimental results and first clinical application. Clin Exp Dermatol 1990;15:389–93. 9. Newman JB, Lord JL, Ask 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;26:208–14. 10. Weinstein C. Modulated dual mode erbium CO2 lasers for the treatment of acne scars. J Cutan Laser Ther 1999; 1:204–8. 11. Tanzi EL: Cutaneous laser resurfacing: erbium:YAG. eMedicine. http://www.emedicine.com/derm/topic 554.htm (accessed November 2006).
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5. Complications secondary to lasers and light sources Robert M Adrian
INTRODUCTION The name laser is an acronym for Light Amplification by Stimulated Emission of Radiation. In 1917, Albert Einstein was the first to theorize about the mechanism that makes lasers possible, called ‘stimulated emission’. In 1958, Charles Townes and Aurthur Schawlow theorized about a visible laser system that would use infrared or visible electromagnetic energy. Although some controversy exists regarding the individual who invented the first laser, Gordon Gould, who first used the term ‘laser’, has been credited with inventing the first light laser. In 1965, the carbon dioxide (CO2) laser was invented by Kumar Patel. Since that time, there has been a tremendous increase in theoretical and practical laser knowledge, resulting in an explosion of laser technology used in thousands of everyday applications. One of the first individuals to report on the effects of lasers on the skin was Leon Goldman, whom many consider to be the father of laser medicine. Goldman’s pioneering work using pulsed (ruby) and continuouswave argon lasers serves as the foundation for our present understanding of laser medicine and surgery. The first lasers used to treat skin conditions were continuous-wave CO2 dioxide, argon, and argonpumped tunable dye lasers.The major disadvantage of continuous-wave lasers is that the side-effects are related to how long the beam is in contact with the target (dwell time), and are thus operator-dependent. This resulted in high rates of complications, primarily in the form of scarring. In the late 1980s, the first pulsed lasers became available with the introduction of the flashlamp-pumped pulse dye laser by the Candala Corporation. Pulsed lasers were a major advance in laser medicine, since
energy delivery was now selectable and dwell time on tissue became an independent factor in treatment.The introduction of pulsed lasers greatly reduced the incidence of scarring secondary to laser treatment.The subsequent addition of cutaneous cooling during laser delivery was another significant advance in cutaneous laser surgery. Epidermal protection and increased patient comfort secondary to cooling served to advance the art and science of laser medicine. In the early 1980s, there were few major companies providing lasers for cutaneous application.Today, there are dozens worldwide, and hundreds of laser devices are available for use in the treatment of numerous congenital and acquired skin conditions. Along with the explosion of interest in cosmetic laser surgery came a tremendous number of ‘new’ users of this technology.As a result, we have seen a significant increase in side-effects and complications associated with the use of lasers. Since most laser and light sources ultimately are designed to heat targets, complications secondary to treatment using lasers and light sources is most often related to excessive thermal energy delivered during the procedure. It is this excess thermal energy that most often contributes to unfavorable clinical results. In this chapter, we will not address side-effects of lasers that are common or anticipated and often unique to the laser or light source used, but will rather confine our discussion to complications that are events not generally expected as a result of treatment. Complications secondary to lasers and light sources may be minor or serious, but all need prompt and accurate diagnosis and treatment to prevent further patient morbidity. As shown in Box 5.1, there are numerous potential complications seen as a result of the use of lasers and light sources. Box 5.2 lists some
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of most common causes of complications resulting from the use of lasers and light sources (Figs 5.1–5.3). Box 5.1 Complications of lasers and light sources • Ocular complications: − Corneal − Retinal • Infection of personnel • Hyperpigmentation • Hypopigmentation • Blistering • Crusting • Delayed wound healing • Infection • Cutaneous infarction • Scarring
Box 5.2 Causes of complications from lasers and light sources • Lack of basic knowledge and training on a specific treatment modality • Incorrect choice of laser or light source to treat a clinical condition • Failure to adequately recognize the clinical condition confronting the operator • Failure to anticipate, recognize, and treat common or uncommon postoperative complications • Failure to refer patients with evolving or nonresponding complications to more experienced colleagues − ‘When you’re in a hole, stop digging.’ • Failure to adequately screen and counsel patients prior to the procedure, thus avoiding postoperative disappointment and frustration for both patient and treating individual
LACK OF OPERATOR KNOWLEDGE AND EXPERIENCE The single most important cause of postoperative complications is lack of proper training and experience of the treating individual. The explosion of interest in cosmetic laser treatments has served as a magnet for those who wish to provide such services primarily for the purpose of financial gain. Unfortunately, most of these individuals are not willing to spend the time or
Fig. 5.1 Severe herpes simplex infection post carbon dioxide laser resurfacing (by permission of Jean Rosenbloom)
monetary investment learning the basic science of laser surgery, treatment protocols, and techniques necessary to provide safe and effective laser and light source-based procedures. So-called ‘weekend warriors’ abound.This is a term used to describe ‘laser experts’ who are constantly unleashed on an unsuspecting public after a few hours at an evening or weekend training session. The use of a given laser or light source by any individual should be complemented by a complete understanding of cutaneous structure and function, basic dermatology, laser safety and physics, infectious diseases of the skin, cutaneous wound care, and management of common side-effects and complications. It is inconceivable how any individual without prior knowledge or training in dermatology could reasonably fulfill all of the
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Fig. 5.3 Hypertrophic scarring after long-pulse YAG laser treatment of a tattoo.
Fig. 5.2 Severe hypertrophic scarring secondary to CO2 laser burn
above prerequisites during a single evening or weekend ‘laser seminar’. My views are not meant to suggest that only dermatologists or plastic surgeons are suitable to perform laser- or light-based procedures, but rather that non-dermatologist physician specialists or allied health professionals should spend the necessary time and effort to become properly trained prior to turning themselves loose on their patients or clients.
INCORRECT CHOICE OF LASER OR LIGHT SOURCE FOR A GIVEN CONDITION Despite the fact that there are hundreds of lasers and light sources available to treat cutaneous conditions,
there are relatively few tissue targets or chromophones available within the skin (Box 5.3). Although it may seem intuitive, many individuals will often use a given laser or light source to treat a condition that is not within the technological scope of the device (Figs 5.4–5.6). Although one might conclude that this was related to lack of knowledge and experience, I have found that it is more often related to monetary consideration on the part of the operator. Common sense would suggest that one would choose a laser or light source that would reasonably address the target chromosphere – however, many examples of laser clinical condition mismatches are seen in clinical practice.
Box 5.3 Cutaneous chromophones • • • • • • • •
Melanin Oxygenated hemoglobin Reduced hemoglobin Water Tattoo ink Iron Medication-induced pigment Foreign-body pigments
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a
b
Fig. 5.4 Scarring and pigmentation from improper use of an IPL Device
FAILURE TO RECOGNIZE THE PRESENTING CLINICAL CONDITION Most physicians and allied health professionals with training in cutaneous medicine can properly recognize the clinical condition confronting them. Unfortunately, inexperienced or untrained individuals often fail to recognize the presenting condition, resulting in worsening of the condition or complications from treatment. What excuse could one offer for treating a nodular melanoma as a hemangioma or a linear verrucous nevus, or tuberous sclerosis as warts, other than lack of knowledge on the part of the physician? In addition, many serious medical conditions, such as collagen
Fig. 5.5 Perioral scarring secondary to CO2 laser resurfacing.
Fig. 5.6 Scarring of the chest after CO2 laser resurfacing.
vascular disease, congenital neurocutaneous syndromes, and vascular anomalies, present for cosmetic treatment while actually needing proper diagnosis and treatment rather than simply ‘cosmetic’ improvement.
FAILURE TO ANTICIPATE, RECOGNIZE AND TREAT COMMON POSTOPERATIVE COMPLICATIONS Most laser and light source treatments are accompanied by various postoperative side-effects, which are defined as conditions that are expected and directly related to
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Fig. 5.7 Scarring from smooth laser treatment of a tatoo
the procedure itself. Examples include purpura secondary to pulsed dye laser treatment, pinpoint bleeding and crusting from Q-switch laser treatment, and swelling and weeping of the skin after CO2 or Er:YAG laser resurfacing. Complications, on the other hand, are conditions that may or may not be expected, but are caused by the procedure and are of significant nature to require proper diagnosis and treatment. Such complications can be relatively minor, such as mild hypo- or hyperpigmentation, edema, or minor crusting. Serious complications include bacterial, fungal, or viral infections; severe pigment disturbances; and hypertropic and keloidal scarring. Sepsis and systemic allergic reactions, although less common, may be life-threatening, and need prompt proper diagnosis and treatment by skilled, welltrained individuals. Failure to recognize and skillfully address these complications is a major cause of postlaser morbidity.
FAILURE TO TIMELY REFER PATIENTS WITH EVOLVING OR NONRESPONSIVE COMPLICATIONS TO MORE EXPERIENCED COLLEAGUES IN A TIMELY MANNER All practitioners of laser- and light-based techniques, regardless of experience, have encountered
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postoperative complications. Morbidity secondary to postoperative complications can often be greatly reduced in most cases by arriving at the correct diagnosis and providing prompt treatment. Physicians who fail to refer in a timely manner most often do so because they actually fail to accurately diagnose the presenting condition itself. Most often, I have encountered failure to recognize and treat postoperative viral (herpes) and fungal (Candida) infection. Many patients are treated for weeks with the wrong diagnosis, only to rapidly heal when proper diagnosis and treatment is intiated. Unfortunately, lack of training and lack of experience lead to a failure of proper diagnosis and treatment, causing significant morbidity for patients. Again, proper training and experience are the primary causes of late referral of complications.
FAILURE TO ADEQUATELY SCREEN AND INFORM PATIENTS PRIOR TO THE PROCEDURE The cornerstone of a successful cosmetic and laser practice is informed consent. Why? Because an adequately informed patient will understand the risks, benefits, and possible outcomes prior to the procedure. Preoperative counseling with blunt and honest answers prior to the procedure all but eliminate the likelihood of postoperative patient dissatisfaction and complaints. I have found that patients are much more relaxed post-treatment when they had undergone a detailed discussion covering risks, benefits, and realistic outcomes prior to the procedure. In my opinion, informed consent is the single most important factor leading to a smooth postoperative experience.
SUMMARY There is no doubt that the use of lasers and light sources has been one of the most significant advances in cosmetic medicine and surgery in the last century. Millions of people have benefited from new technologies to treat a wide variety of congenital and acquired medical and cosmetic conditions. Unfortunately, many
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practitioners fail to undergo adequate training, resulting in an unacceptable number of complications secondary to the use of these new technologies. Blame can be placed on all those involved: laser companies who will sell or rent a laser or light source to ‘any willing provider’ regardless of their level of training or experience; practitioners who themselves fail to undergo the necessary training in order to provide safe and effective laser procedures; and finally the patients themselves, who fail to adequately evaluate the training and experience of their provider prior to
the procedure and then complain that they had an unfavorable result or complication. The internet age has given patients powerful tools to ‘interview’ physicians online, narrowing down the list of local experts who will most likely provide more successful and safer outcomes than their inadequately trained colleagues. The explosion of laser day-spas, med-spas and nonphysician-supervised ‘laser centers’ presents a growing challenge to patients to seek out experts in their community and avoid those who may ultimately do more harm than good.
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6. Nonablative technology for treatment of aging skin Amy Forman Taub
ABLATIVE VERSUS NONABLATIVE
Nonablative
To understand nonablative technology, it is important to understand ablative technology, which came earlier. Understanding the difference between the two technologies puts their respective advantages and weaknesses into perspective.
Nonablative lasers attempt to spare the epidermis and to influence the dermis directly with light and/or radiofrequency (RF) energy.With no epidermal wound, there is no recovery period and thus no interruption of life’s daily routines. Although efficacy is less than that of ablative laser procedures, the dermal wound response from nonablative laser treatments stimulates new collagen production and repairs tissue defects.3 Energy is deposited 100–500 µm below the skin surface, where most histological changes (solar elastosis) associated with photoaging occur. Nonablative laser procedures target the dermis and avoid epidermal damage by cooling during treatment,4–10 as well as targeting chromophores other than water: hemoglobin, melanin, and collagen. In addition, the wavelengths utilized for nonablative lasers are in the visible and near-infrared region of the electromagnetic spectrum and penetrate to the upper and mid-dermis – the target zone. A variety of studies5,7,11–19 indicate that skin tightening and wrinkle reduction months after nonablative laser or light therapy are associated with collagen remodeling. This relationship was established by comparing clinical improvement with changes in histological characteristics, ultrastructure, and biochemical constituents known to play a role in wound healing and the production of dermal collagen.
Ablative In ablative skin resurfacing, the outer layers of skin are vaporized and replaced by new collagen and epidermis as wound healing occurs over days to weeks. Ablation is possible because water has a high absorption coefficient in the infrared region. The most widely used lasers for ablative resurfacing are the pulsed 10 600 nm carbon dioxide (CO2) and 2940 nm erbium : yttrium aluminum garnet (Er:YAG) lasers. The Er:YAG wavelength is more efficiently absorbed by water, and thus leaves little residual heat deposition to collateral tissue, whereas the CO2 laser deposits more heat in the surrounding area. This may be an important stimulus to collagen renewal and hence skin tightening and rhytid effacement,1 but leads to more complications. In either case, the mechanism of renewal is epidermal and dermal injury, which denatures collagen and activates fibroblasts, causing the synthesis of new collagen and extracellular matrix material.2 Nonablative lasers were developed in response to the two fundamental problems with ablative lasers: long periods of downtime and the risk of long-term hypopigmentation and scarring.
Microablative Fractional photothermolysis (FP) has recently been introduced for ‘microablative’ resurfacing.20,21
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a
b
c
100 µm
100 µm 0 days
d
100 µm 1 days
3 days
100 µm 7 days
Fig. 6.1 Photomicrograph of skin treated with fractional device, 15 mJ. At 0 days, one can see thermal denaturation of the epidermis and dermis, with no effect to the structural integrity of the stratum corneum (remains intact).At 1 day post treatment, a vacuole is overlying the re-epithelized epidermis and the zone of thermal denaturation in the dermis.The vacuole is known to contain epidermal necrotic debris and dermal contents.At 3 days post treatment, one can see a compacted MEND (‘microscopic epidermal necrotic debris’ – this is actually a misnomer, as there is epidermal and dermal content) overlying the epidermis (which appears almost completely healed) and the thermally denatured dermis.At 7 days post treatment, one can see that the MEND is starting to exfoliate, while the epidermis has regained full thickness.The dermal aspect of the lesion also appears to have started healing, with an influx of cellular activity in and around the vicinity of the lesion. (Photomicrograph courtesy of Reliant Technologies, Inc.) Although FP is associated with limited downtime and usually requires multiple sessions, its main mechanism is via tissue ablation; thus, it has features of both ablative and nonablative techniques. In the novel FP technique, a 1550 nm laser creates a pattern of microscopic thermal wounds rather than uniform thermal damage in the skin.These microthermal zones (MTZs) are typically 100 µm wide and 300 µm deep and are surrounded by undamaged tissue, thus promoting a rapid healing response. The density and space between MTZs can be adjusted for a given energy level, and adverse effects, pain, and discomfort are manageable.20,22 This results in more rapid epithelialization than with ablative therapy, as well as deeper penetration into the dermis, with the possibility of eliminating abnormal dermal deposits and/or breaking up scars mechanically (Fig. 6.1). Clinical examples are shown in Figs 6.2 and 6.3.
NONABLATIVE TECHNOLOGIES FOR PHOTOREJUVENATION Many nonablative devices have been developed over the past 10 years.There are infrared devices targeting superficial collagen with nonspecific heating, pulsed dye lasers (PDLs), which heat the vessels and radiate heat into the other parts of the dermis, long-pulsed neodymium (Nd):YAG lasers, intense pulsed light (IPL) devices, lightemitting diode (LED) devices, photodynamic therapy (PDT), and the new tissue tightening devices designed to cause three-dimensional changes in the skin through nonablative methods. Each of these modalities will be discussed in the following sections.
Laser or visible light technology In photorejuvenation, technologies with wavelengths in the visible spectrum target the upper dermis. Many
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a
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b
Fig. 6.2 Before (a) and after (b) three treatments of a woman with melasma and textural irregularities treated with a fractional device, 6–8 mJ, density level 6, with eight passes. (Photographs courtesy of Amy Forman Taub MD.) lasers and light sources have been developed with the principal use in mind of removing excessive epidermal pigmentation, reducing upper dermal telengiectasia, and improving the texture and tone of the skin. It has been noted by a number of investigators that these modalities also seem to improve superficial wrinkles and cause some skin smoothing and tightening.
Pulsed dye laser As the first laser developed to apply the principle of selective photothermolysis, the 585 nm PDL remains the gold standard for the treatment of vascular lesions.23 Zelickson et al13 reported the first investigation of the PDL for the treatment of sun-induced facial rhytids. Histological examination revealed dermal changes consistent with collagen remodeling. These results were confirmed in 2000 by Bjerring et al24 who, by altering the pulse duration, obtained cosmetic improvement without purpura. Tanghetti et al25 reported similar clinical improvements in facial dyspigmentation and wrinkling after single-pass and double-pass treatment with either 585 nm or 595 nm PDL devices. In a controlled, split-face study, Hsu et al26 reported improvements in surface topography of 9.8% (one treatment) and 15% (two treatments), supported by histological evidence of collagen remodeling. Key studies are summarized in Table 6.1.
Intense pulsed light Generally considered the gold standard for the nonablative treatment of superficial photodamage, IPL therapy achieves selective photothermolysis with noncoherent polychromatic light (about 500–1200 nm). Due to the broad spectrum of visible light, the two main chromophores, hemoglobin and melanin, can be effectively targeted with only one piece of technology.The minimal risk and downtime associated with this procedure have contributed to its success.8 Two key studies were reported in 2000. Bitter11 showed that serial full-face treatments with IPL visibly improved wrinkling, irregular pigmentation, skin coarseness, pore size, and telangiectasias in more than 90% of patients with little downtime.The patient satisfaction rate exceeded 88%. A clinical example and photomicrographs of biopsy specimens are shown in Figs 6.4 and 6.5, respectively. Goldberg and Cutler27 showed that IPL therapy nonablatively improved facial rhytids and skin quality with minimal adverse effects. Other studies are summarized in Table 6.2. Using treatment parameters similar to those used by Bitter, Negishi and colleagues28,29 showed that IPL improved pigmentation, telangiectasias, and skin texture of Asian skin. Goldberg and Samady30 revisited perioral rhytids, using different IPL parameters and comparing results with those of a 1064 nm Nd:YAG laser. Patient
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a
b
c
d
Fig. 6.3 (a,b) A 27-yearold man whose acne scars had been treated three times unsuccessfully with trichloroacetic acid (15%) peels. (c,d).After a single fractional photothermolysis session, the acne scars are markedly improved 4 weeks later. Skin texture was also improved. (Reproduced with permission from Hasegawa T, Matsukura T, MizunoY, Suga Y, Ogawa H, Ikeda S. Clinical trial of a laser device called fractional photothermolysis system for acne scars. J Dermatol 2006;33:623–7.)
satisfaction rates were similar, although blistering and erythema were more common with IPL. In a 93-patient study, Sadick et al31 showed that up to five full-face IPL treatments resulted in significant
improvement in a variety of clinical indications of photoaging. A newer technology combining IPL with RF (electro-optical synergy, or ELOS) was evaluated by Sadick et al31 and found to be at least as efficacious
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Table 6.1 Studies of the use of the pulsed dye laser (PDL) for photorejuvenation Areas/ conditions treated (No. of treatments)
Wavelength (nm)/Fluence 2 (J/cm )/Pulse duration (ms)
Ref
No. of patients
13
20
Mild to severe perioral and periorbital wrinkles (1)
585/3.5–6.5/ 0.45
24
40
Facial wrinkles (1)
25
17
26
58
Adverse effects
Follow-up (months)
9/10 with mild to moderate wrinkling showed 50% or greater improvement at 6 months, 3/10 with moderate to severe wrinkling showed clinical improvement at 3 months
Transient purpura, swelling
Up to 14
585/2.4/ 0.350
Statistically significant decreases in Fitzpatrick class I, II, III wrinkles
None
Up to 6
Facial dyspigmentation and wrinkling (4)
585 or 595/ 3–4/0.5
Clinically observable improvement in dyspigmentation and wrinkling for all subjects
None
6
Periorbital wrinkling (1 or 2)
585/2.4–2.9/ 0.35
Improvements in surface topography of 9.8% (one treatment) and 15% (two treatments)
Minor pain 1, 3 during initial treatment, minimal temporary reddening
a
Efficacy
b
Fig. 6.4 A 54-year-old woman: (a) before and (b) 4 weeks after five full-face intense pulsed light (IPL) treatments. Note the improvement in fine wrinkles and skin texture. (Reproduced with permission from Bitter PH Jr. Noninvasive rejuvenation of photodamaged skin using serial, full-face intense pulsed light treatments. Dermatol Surg 2000;26:835–42. for pigmentation and vascularity but potentially more advantageous for pore size, superficial rhytides, laxity and texture due to the addition of the RF modality which can penetrate more deeply into the dermis to stimulate collagen remodeling.
Potassium titanyl phosphate The 532 nm wavelength of the potassium titanyl phosphate (KTP) laser device is readily absorbed by oxyhemoglobin and melanin,34 making it especially
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a
The efficacy of the KTP laser is comparable to that of IPL.36 The smaller spot size and ergonomic flexibility of the KTP handpiece, however, promote ease of use and allow practitioners to focus on resistant lesions.34 Although fewer treatments are required, the risk of erythema and edema is higher with the KTP laser21 and the treatment is less tolerable.36 The results of key studies are presented in Table 6.3.
Photomodulation
b
Fig. 6.5 Photomicrographs of biopsies of forehead skin from (a) the untreated forehead and (b) the treated forehead 4 weeks after the fifth IPL treatment. (Reproduced with permission from Bitter PH Jr. Noninvasive rejuvenation of photodamaged skin using serial, full-face intense pulsed light treatments. Dermatol Surg 2000;26:835–42).
effective for treating red and brown discolorations due to photodamage35 and inducing growth of collagen and elastin fibers when endothelial damage causes the release of cytokines.34 Combining the KTP laser with the 1064 nm Nd:YAG laser device15,35 makes use of the greater penetration depth of the longer wavelength to create a synergistic effect that further improves skin quality and wrinkle reduction beyond what is achievable by KTP alone (Figure 6.6).15
In photomodulation, a light-emitting diode (LED) is used to manipulate cellular activities without thermal effect.37 McDaniel and colleagues showed37,38 that they could upregulate procollagen synthesis and downregulate matrix metalloproteinase (collagenase) in fibroblast culture with specific pulse sequences and durations of low-energy, narrowband, or coherent light. The effects were strongest when 590 nm LED devices were used. These findings led to a multicenter trial in which 90 patients with photodamaged skin received eight LED photomodulation treatments using a full-panel 590 nm nonthermal full face LED array delivering 0.1 J/cm2 with a specific sequence of pulsing treatments over 4 weeks.12 More than 90% showed improvement in at least one Fitzpatrick photoaging category and 65% showed improvement in facial texture, background erythema, fine lines, and pigmentation, all without pain or adverse effects. Improvements peaked in 4–6 months after the final treatment. The clinical results were supported by post-treatment histological studies that showed increased collagen in the papillary dermis. The use of combination 633 nm and 830 nm LED light therapy for the treatment of photodamaged skin has been reported by two groups.19,39 In a 31-patient study, Russell et al39 treated facial rhytids nine times and noted (1) 25% to 50% improvement in photoaging scores of 52% of patients and (2) significant patient-reported improvement in periorbital wrinkles in 81% of patients 12 weeks after the final treatment. In a similar 36-patient study, Goldberg et al19 reported very similar results. Electron microscopic data of posttreatment tissue showed collagen fibers of increased thickness. Adverse effects were limited to mild erythema in one patient.
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Table 6.2 Studies of the use of intense pulsed light (IPL) for photorejuvenation Areas/ conditions No. of treated (No. Ref patients of treatments)
Cut-off filter (nm)/Fluence (J/cm2)/Pulse duration (ms)
27
30
Perioral rhytids (1–4)
11
49
28
Efficacy
Adverse effects
Follow-up (months)
645/40–50/7
16/30 patients had some improvement, 9/30 substantial improvement
Transient erythema, blistering
6
Full face/overall photorejuvenation (mean 4.94)
550 or 570/ 30–50/ 2.4–4.7
75% of patients reported ≥ 50% overall improvement
Mild, temporary erythema, blisters, darkening of lentigines and freckles
1
97 (Asian skin)
Facial photorejuvenation (3–6)
550 or 570/ 28–32/2.5–5
88.4% of patients reported ≥ 51% improvement in pigmented lesions, 77.7% reported ≥ 51% improvement in telangiectasias, 77.3% reported ≥ 51% improvement in skin texture
30
15
Perioral rhytids (3–5)
590/755/ 40–70, 3–7
On 1–10 scale, mean patient satisfaction scores 6.4 (at 590 nm), 6.2 (at 755 nm) at 6 months
Blistering, erythema with IPL
Up to 6
39
36 (Asian skin)
Facial freckles (1–3)
550–590/ 25–35/4
91.7% of patients reported very or extremely satisfied
Transient erythema, pain, hyperpigmentation, crusting
6
32
47
Facial rhytids, vascularity, dyschromia, pore size
550/570/ 28–34/2.4–4
Long-term improvement in rhytids, vascularity, dyschromia, pore size
Temporary swelling, erythema, crusting, purpura
6
33
23
Midfacial photoaging (3)
500–690, 890–1200/ 24–30/pulse duration not reported
Improvement in surface texture, mottled hyperpigmentation/ solar lentigines, erythema/ telangiectasias
Discomfort during treatment, transient focal vesiculation, crusting, erythema
1
31
93
Wrinkles, elastosis, vascular and pigmented lesions of face (up to 5)
560 or 640/ 20–44/2–7
Significant reduction in wrinkles, elastosis, vascular and pigmented lesions; improvement in 90% of patients at 6 months; patient satisfaction high
Temporary erythema, edema, purpura, hyperpigmentation
6
a
Results were evaluated at the end of the third treatment.
0a
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a
b
Fig. 6.6 A 51-year-old woman: before (a) and (b) 6 months after six treatments with combined potassium titanyl phosphate (KTP) and neodymium : yttrium aluminum garnet (Nd:YAG) lasers. Note the overall improvement in erythema, pigmentation, skin tone and texture, pore tightening, and rhytid reduction. (Reproduced with permission from Lee MW. Combination 532 nm and 1064 nm lasers for noninvasive skin rejuvenation and toning.Arch Dermatol 2003;139:1265–76.)
Table 6.3 Studies of the use of the 532 nm potassium titanyl phosphate (KTP) laser for photorejuvenation
No. of Ref patients
Areas/ conditions treated (No. of treatments)
Fluence (J/cm2)/ Pulse duration (ms)
15
50
Face (3–6)
34
7
36
17
Efficacy
Adverse effects
Follow-up (months)
7–15/7–20
All patients had mild to moderate improvement in appearance of rhytids, moderate improvement in skin toning and texture, great improvement in reduction of pigmentation and redness; KTP results superior to 1064 nm laser results
Mild, temporary erythema, edema; sensitivity to heat and recurrence of flushing and telangiectasias in patients with rosacea; mild to moderate pain during and after treatment
Up to 18
Periorbital and midfacial (4)
10–14/ 13–17
Noticeable overall improvement in all patients, all patients pleased with results
Temporary mild erythema
2
Facial dyschromias and telangiectasias (1)
7–9/30
Average improvement 42%/30% for vascular/ pigmented lesions
Pain during treatment; temporary edema and erythema, crusting of dyschromias
1
LEDs are promising, as they are less expensive to manufacture, they take only seconds of irradiation, and they are painless. They have also been used to reduce
inflammation in sunburn and provide palliation for breast cancer metastatic to the chest wall, and more novel indications for this modality may be discovered in the future.
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59
b
Fig. 6.7 Before (a) and after (b) four monthly treatments with blue light and δ-aminolevulinic acid photodynamic therapy. (Photographs courtesy of Michael Gold MD.)
Photodynamic therapy PDT uses a light-activated photosensitizing agent to create cytotoxic singlet oxygen within abnormal tissue. Because the photosensitizer accumulates preferentially in abnormal cells, PDT selectively destroys these target cells without damaging surrounding tissue.Although PDT with δ-aminolevulinic acid (ALA) is approved by the US Food and Drug Administration (FDA) only for the treatment of actinic keratosis (AK) in the face and scalp, the technique is being used to treat a wide variety of skin conditions (including photorejuvenation) because of its efficacy, safety profile, and minimal downtime.40 Photodynamic rejuvenation denotes the use of PDT to improve the clinical manifestations of photodamage.41 Touma et al42 showed that 1-hour ALA incubation provided approximately the same improvement in photodamage as 14- to 18-hour ALA incubation and that ALA–PDT could be used to treat broad areas of photodamage. A variety of studies have led to the recommendation40 that either IPL (preferred), blue light (alternate), or PDL (other) be used to activate the photosensitizer when ALA–PDT is used for photorejuvenation. One of the advantages of PDT is its ability to be performed with many different technologies. Protoporphyrin IX is the photoabsorbing molecule, and although absorption is greatest at 417 nm (blue light), there are multiple Q-bands of absorption up to about
650 nm. This means that IPL, PDLs, KTP lasers, red light, and LED diodes all will activate the photosensitizer and be able to produce a photodynamic treatment. Another huge advantage of PDT is that it can eradicate precancerous cells while improving photodamage (Fig. 6.7). Blue light, red light, LEDs,43 ELOS,44 PDLs, and IPL have been used in PDT for photorejuvenation.Two topical photosensitizers are currently in use: ALA and methyl aminolevulinate. Studies of the use of IPL or blue light are shown in Table 6.4. Split-face studies45–47 have shown the superiority of PDT with IPL versus IPL alone.
Long-wavelength lasers and light sources for collagen stimulation Collagen remodeling with the use of infrared lasers has been extensively studied. Early studies7,16,17 using the 1320 nm Nd:YAG laser showed minimal to visible clinical improvement in facial rhytids, with histological evidence of dermal collagen 1–6 months after the final of a series of treatments. Results with the 1540 nm Er:glass laser were less encouraging, possibly because collagen denaturation and dermal fibroplasia had occurred too deeply in the dermis to improve wrinkles.5 A 24-patient study52 showed gradual clinical improvement in mild to moderate facial rhytids during and 6 months after a series of three once-monthly treatments with a 1540 nm Er:glass laser device. An
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Table 6.4 Results of photodynamic therapy with δ-aminolevulinic acid (ALA–PDT), using intense pulsed light (IPL) or blue light, for photorejuvenation. Ref
No. of patients
ALA contact time (hours)
Light source
No. of treatments
Improvement, clearance, or response rate (%)
Adverse effects
Follow-up (months)
48
10
1
IPL
3
90 (crow's feet); 100 (tactile skin roughness); 90 (mottled hyperpigmentation); 70 (facial erythema); 83 (actinic keratosis)
—
3
49
32
Short contact
Blue
1
90 (actinic keratosis); 72 (skin texture); 59 (skin pigmentation)
—
—
50
17
1
IPL
1
68 (actinic keratosis); 55 (telangiectasias); 48 (pigment irregularities); 25 (skin texture)
Mild transient erythema, edema
1, 3
45
Not available
—
IPL
3a, 2b
80 (ALA–PDT–IPL) vs 50 (IPL) photoaging; 95 vs 65 (mottled hyperpigmentation); 55 vs 20 (fine lines)
46
13
—
IPL
3a
55 (ALA–PDT-IPL) vs 29.5 (IPL) crow’s feet; 55 vs 29.5 (tactile skin roughness); 60.3 vs 37.2 (mottled hyperpigmentation); 84.6 vs 53.8 (facial erythema); 78 vs 53.6 (actinic keratosis)
Erythema, edema
3
51
10
1
IPL
2a
1.65a (ALA–PDT–IPL) vs 1.28c (IPL)
Temporary erythema, mild edema, desquamation
6
47
20
0.5–1
IPL
3a, 2b
80 (ALA–PDT–IPL) vs 45 (IPL) global score; 95 vs 60 (mottled hyperpigmentation); 80 vs 80 (fine lines); 95 vs 90 (tactile roughness); 75 vs 75 (sallowness)
Mild stinging during treatment; temporary erythema, scaling, edema, oozing, crusting, vesiculation
1
a
—
1
Split face, ALA–PDT–IPL vs. IPL. Full face, IPL alone. c Mean clinical grade (1= 25% improvement, 2= 25–50%; 3 = 51–75%; 4 = 76–100%). Adapted with permission from Nestor M, Gold M, Kauvar A, et al.The use of photodynamic therapy in dermatology: results of a consensus conference. J Drugs Dermatol 2006; 5:140–54. b
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b
Fig. 6.8 Before (a) and after (b) two treatments with electro-optical synergy (ELOS) with pulsed light and ELOS with a diode laser. (Photographs courtesy of Macrene Alexiades-Armenakas MD,PhD.)
increase in dermal collagen was not observed until several months after the final treatment. A recent review of clinical trials with the 1540 nm Er:glass laser53 confirmed that collagen remodeling and improvement were gradual, and emphasized the importance of explaining this to patients. With regard to the 1064 nm Nd:YAG laser, the studies of Lee15,54 revealed subtle and gradual improvements in wrinkles, skin laxity, and overall appearance, supported by histological evidence of collagen remodeling. In another study,55 a series of four treatments with a 1450 nm diode laser (SmoothBeam, Candela Corp.,Wayland, MA) resulted in mild to moderate improvement in facial rhytids in all 25 patients treated and increases in dermal collagen 6 months after the final treatment.The treatment was well tolerated, and adverse effects were transient and limited to erythema, edema, and postinflammatory hyperpigmentation. Two other groups56,57 have reported clinical evaluations of the 1064 nm Nd:YAG laser. Dayan et al56 found an approximately 12% reduction in Fitzpatrick scale scores for coarse wrinkles, a 17% reduction for skin laxity, and a 20% overall improvement. Taylor and Prokopenko57 reported a 30% improvement in wrinkles and skin laxity and an approximately 16% improvement in texture, pores, and pigmentation. Dang et al58,59 focused on head-to-head comparisons on mouse skin. In one study,58 they compared the histological, biochemical, and mechanical responses associated with the Q-switched 1064 nm Nd:YAG laser
and the 1320 nm Nd:YAG laser.The 1064 nm laser produced a 25% greater improvement in skin elasticity, a 6% greater increase in skin thickness, and an 11% greater hydroxyproline synthesis (a measure of collagen content59) by the second month after treatment. Type III collagen increased markedly after 1064 nm laser treatment, while type I collagen increases were greater after treatment with the 1320 nm laser. In another study59 comparing a 595 nm PDL (Vbeam, Candela Corp.,Wayland, MA) with a 1320 nm Nd:YAG laser (Cooltouch II, ICN Pharmaceuticals Inc., Roseville, CA), PDL treatment produced a greater increase in dermal thickness, hydroxyproline levels, and type I and type III collagen, while improvement in skin hydration was greater with the 1320 nm laser. However, none of these differences was statistically significant. Orringer et al60 assessed collagen remodeling after a single treatment of photodamaged skin with either a 585 nm PDL (NLite, ICN Pharmaceuticals Inc.) or 1320 nm Nd:YAG laser (Cooltouch II, ICN Pharmaceuticals Inc.).At 1 week post treatment, histological examination revealed statistically significant increases in type I procollagen messenger RNA expression (47% and 84% above pretreatment levels for the 585 and 1320 nm lasers, respectively), as well as induction of primary cytokines, matrix metalloproteinases, and type III procollagen. Doshi and Alster61 evaluated the combination RF and diode laser (ELOS: Polaris WR, Syneron Medical Ltd, Israel) for the treatment of facial rhytids and skin laxity. This device delivers RF and 910 nm diode laser energy
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Fig. 6.9 Partially denatured collagen after Thermage treatment as 160 microns by electron microscopy. (Reproduced courtesy of Dr. Brian Zelickson and Thermage Corp.) sequentially through a bipolar electrode tip with epidermal cooling. Three treatments were given at 3-week intervals to 20 patients with mild to moderate rhytids and skin laxity. Optical and RF fluences ranged from 30 to 40 J/cm2 and from 50 to 85 J/cm3, respectively. The prospective study showed a mean clinical improvement of superficial rhytids at 6 months of 1.63/4. For skin laxity of the jowl and cheek, improvement scores reached 2.00/4 at 6 months. Patient assessments were similar. Side-effects were mild. In a combined study62 of ELOS with both IPL and a diode laser (Fig. 6.8), overall effectiveness scores in multiple measures of photodamage was approximately 26%.
NONABLATIVE TECHNOLOGIES FOR SKIN TIGHTENING From the evidence that collateral heating of the dermis while targeting vascular and pigmented lesions created new collagen and decreased wrinkles sprang the idea of bulk dermal heating. Bulk dermal heating requires relatively deep energy deposition over a period of seconds as opposed to microseconds, with cooling to protect the epidermis.The intent of tissue tightening is to actually lift or firm tissue in a three-dimensional manner. This is not the same as stimulating collagen to fill in superficial scars or wrinkles, but a deeper shift in tissue
volumes, leading to a remodeling of the entire soft tissue envelope, a completely new aesthetic capability. Collagen fibers consist of protein chains held in a triple helix. When collagen is heated, non-colavent bonds linking the protein strands together are ruptured, producing an amorphous arrangement of randomly coiled chains.63 As the chains rearrange, fibers of the denatured collagen become shorter and thicker. Heat-induced contraction of collagen and long-term fibroblastic stimulation are is the basis for the treatment of skin laxity.64 For exposures lasting several seconds, the denaturation temperature of collagen has been estimated at 65°C.65,66 In practice, however, collagen denaturation has a complex dependence on temperature described by the Arrhenius reaction-rate equation.This relationship may not hold for very short time exposures to heat, because the kinetics of collagen denaturation are not known.66 There are two technologies supported by peerreviewed literature at present for evaluation: RF and broadband infrared (IR) light.
Radiofrequency-based tissue tightening RF energy interacts with tissue to generate a current of ions that, when passed through tissues, encounters resistance. This resistance, or impedance, generates
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Table 6.5 Studies of the use of radiofrequency (RF) for skin tightening Ref
No. of patients
Fluence (J/cm2)
Areas treated
Efficacy
Adverse effects
Follow-up (months)
Face, anterior neck
70% of patients noticed significant improvement in skin laxity and texture at 3 months
Moderate pain during treatment; 3/40 patients experienced superficial blistering
1, 2, 3
73
40
—
74
15
52 (only for 2 patients treated with 1 cm2 tip)
Face
14/15 patients responded; nasolabial folds: 50% of patients had at least 50% improvement; cheek contour: 60% had 50% improvement; mandibular line: 27% had at least 50% improvement; marionette lines: 65% had at least 50% improvement.
Minimal discomfort during treatment in all patients; superficial burn (1 patient)
6–14
69
86
58–140
Periorbital wrinkles, brow position)
Fitzpatrick wrinkle scores improved by 1 point or more in 83.2% of patients; 50% of patients satisfied to very satisfied; 61.5% of eyebrows lifted by 0.5 mm
Minimal erythema, edema, 2nd-degree burn; small residual scar at 6 months in 3 patients
6
70
16
—
Cheeks, jaw line, upper neck
5 of 15 patients contacted were satisfied with results
Mild, transient erythema and edema
6
78
17
125–144
Brow, jowls, nasolabial folds, puppet lines
Gradual tightening
Mild, temporary erythema
4
75
50
97–144 (cheeks) 74–110 (neck)
Mild to moderate skin laxity in neck and cheek
Significant improvement in most patients; patient satisfaction was similar to observed clinical improvement
Mild and temporary edema, erythema, rare dysesthesia
6
68
24
Upper third of face; brow elevation; forehead, temporal regions
Objective data showed non-uniform (asymmetric) improvement; patient satisfaction low; 72.7% said they would not have the procedure again; results not predictable
Pain during treatment; redness
4–14 weeks
57
7
Face; laxity, wrinkles, pores, pigmentation, texture
About 16% median improvement in wrinkles and skin laxity; about 16% improvement in texture, pores, and pigmentation; patients satisfied; improvement maintained 2–6 months
None
2–6
—
73.5
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heat in proportion to the amount of impedance. Tissues with high impedance will be heated more than tissues of low impedance.67 Traditional RF devices used in skin surgery deliver therapeutic energy through the tip of an electrode in contact with skin. The concentrated thermal energy produces heat at the surface of the skin, which injures both the dermis and epidermis.68 To reduce heat-induced epidermal injury while heating the dermis, developed the ThermaCool, a device that delivers RF energy to the skin via a thin capacitive coupling membrane that distributes RF energy over the tissue volume beneath the membrane’s surface (rather than concentrating the RF energy at the skin surface) while cooling the epidermis by cryogen spray.69,70 Although the deep dermal layer can theoretically reach temperatures exceeding 65°C, permitting the heat-sensitive
a
collagen bonds to go beyond their 60° denaturation threshold, the temperature of the epidermis is maintained between 35°C and 45°C.68 A study of the histological and ultrastructural effects of RF energy suggested that collagen fibrils contract immediately after treatment and that production of new collagen is induced by tissue contraction and heat-mediated wounding (Fig. 6.9).71 The first clinical study of the ThermaCool assessed skin contraction, gross pathology, and histological changes for a range of RF doses.70,72 Iyer et al73 reported that 70% of patients noticed skin laxity improvement 3 months after a single RF treatment and that improvement increased with additional treatments. A subsequent report described a prototype device designed to produce heat in the dermal layer of tissue while protecting the epidermis by cryogen spray
b
Fig. 6.10 Before (a) and 8 months after (b) tissue tightening treatments: one radiofrequency treatment on the left side of the face and two broadband infrared light device treatments on the right. Note the decreased depth of the nasolabial folds and marionette lines, the firming of the skin over the mid cheek and the restoration of the shape of the face toward an oval, instead of a rectangle. (Photographs courtesy of Amy Forman Taub MD.)
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Table 6.6 Studies of the use of broadband infrared (IR) light for skin tightening
Ref
No. of patients
79
25
80
42
Device (No. of treatments)
Fluence (J/cm2)
Local anesthesia
Treatment target
1100– 1800 nm (1–3)
20–40
For first 5 patients
Forehead; lower face and neck
1100– 1800 nm (2)
30–38
Sometimes
Face, neck, abdomen
cooling.74 Of the 15 patients,14 responded to a single treatment without wounding or scarring. Pain was used to indicate the tolerability of treatment. Patients resumed normal activities immediately after treatment. Other RF studies that followed are summarized in Table 6.5. In each study, patients had a single treatment, local anesthesia was used during treatment, and results were evaluated by comparing pre- and posttreatment photographs. Improvements with a single treatment were gradual and subtle and lasted for several months. Higher fluences were required with thick skin.69 When low fluences were used, improvements were less pronounced.70,75 Initially, it was believed that the highest fluences would yield the best results. However, this was accompanied by significant patient discomfort and a relatively high rate of significant side-effects,76 such as scars and changes in skin surface textures (e.g., indentation or waffling). A different model based on a lower-fluence, multiple-pass protocol was shown via ultrastructural analysis of collagen fibril architecture to provide much more collagen deposition deeper in the dermis than the high-fluence protocol.77 This is believed to yield more consistent results, higher patient tolerability, and fewer complications. Recent advances include specialized tips for more superficial areas (eyelids) and body areas (arms and abdomen).
Adverse effects
Follow-up (months)
Immediate improvement in 22 patients, persisted for follow-up period; all patients satisfied
Small burns
Up to 12
Improvement moderate or higher in 52.4% of patients
Transient minor swelling and erythema, rare blister
4
Efficacy
Infrared light-based tissue tightening A broadband infrared light tightening device has recently been developed as an alternative technology for tissue tightening (Titan, Cutera, Brisbane, CA). This generates energy of up to 50 J/cm2 energy at 1100–1800 nm wavelengths, with pre- and postcooling being built into the multisecond pulse. The long wavelengths of near- and mid-IR radiation offer three major advantages over shorter wavelengths: (1) deeper penetration into the dermal layer (2) less absorption by melanin, and (3) reduced risk in dark-skinned patients.56 This device targets the dermis at a depth of 1–2 mm, which is more superficial than the RF device. The author has found this to be an advantage for thinner skin, whereas the RF technology may be better for thicker skin with more subcutaneous tissue attached – but these observations are anecdotal. However, in many skin types, the results may be similar (Fig. 6.10). Studies of the use of infrared light in tissue tightening are summarized in Table 6.6.
THE FUTURE AND CONCLUSIONS A major advantage of nonablative techniques is that treatment requires little or no downtime for patients. The importance of this feature is evident from the
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growth and proliferation of nonablative devices since they were introduced in the late 1990s. Disadvantages are that efficacy is modest and multiple treatments are required to achieve results. Future efforts will be focused on increasing efficacy and reducing the number of treatments, making treatment more affordable for more patients.
REFERENCES 1. Fitzpatrick R, Rostan E, Marchell N. Collagen tightening induced by carbon dioxide laser versus erbium:YAG laser. Lasers Surg Med 2000;27:395–403. 2. Nelson J, Majaron B, Kelly K. What is nonablative photorejuvenation of human skin? Semin Cutan Med Surg 2002;21:238–50. 3. Grema H, Greve B, Raulin C. Facial rhytids – subsurfacing or resurfacing? A review, Lasers Surg Med 2003;32: 405–12. 4. Herne K, Zachary C. New facial rejuvenation techniques. Semin Cutan Med Surg 2000;19:221–31. 5. 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; 26:186–95. 6. Kelly K, Nelson J, Lask G, Geronemus R, Bernstein L. Cryogen spray cooling in combination with nonablative laser treatment of facial rhytids. Arch Dermatol 1999; 135:691–4. 7. Goldberg D. Full-face nonablative dermal remodeling with a 1320 nm Nd:YAG laser. Dermatol Surg 2000; 26:915–18. 8. Goldberg D. New collagen formation after dermal remodeling with an intense pulsed light source. J Cutan Laser Ther 2000;2:59–61. 9. 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; 27:111–16. 10. Fournier N, Dahan S, Barneon G, et al. Nonablative remodeling: a 14-month clinical ultrasound imaging and profilometric evaluation of a 1540 nm Er:Glass laser. Dermatol Surg 2002;28:926–31. 11. Bitter P. Noninvasive rejuvenation of photodamaged skin using serial, full-face intense pulsed light treatments. Dermatol Surg 2000;26:835–42. 12. Weiss R, McDaniel D, Geronemus R, Weiss M. Clinical trial of a novel non-thermal LED array for reversal of photoaging: clinical, histologic, and surface profilometric results. Lasers Surg Med 2005;36:85–91.
13. Zelickson B, Kilmer SL, Bernstein E, et al. Pulsed dye laser therapy for sun damaged skin. Lasers Surg Med 1999;25:229–36. 14. Rostan E, Bowes L, Iyer S, Fitzpatrick R. 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;3:129–36. 15. Lee M. Combination 532-nm and 1064-nm lasers for noninvasive skin rejuvenation and toning. Arch Dermatol 2003;139:1265–76 [Erratum: 2004;140:625]. 16. Menaker G, Wrone D, Williams R, Moy R. Treatment of facial rhytids with a nonablative laser: a clinical and histologic study. Dermatol Surg 1999;25:440–4. 17. Goldberg D. Non-ablative subsurface remodeling: clinical and histologic evaluation of a 1320-nm Nd:YAG laser. J Cutan Laser Ther 1999;1:153–7. 18. Sadick N, Alexiades-Armenakis M, Bitter P Jr, Hruza G, Mulholland R. Enhanced full-face skin rejuvenation using synchronous intense pulsed optical and conducted bipolar radiofrequency energy (ELOS): introducing selective radiophotothermolysis. J Drugs Dermatol 2005; 4:181–6. 19. Goldberg D, Amin S. Russell B,et al. Combined 633-nm and 830-nm LED treatment of photoaging skin. J Drugs Dermatol 2006;5:748–53. 20. Manstein D, Herron G, Sink R, Tanner H, Anderson R. Fractional photothermolysis: a new concept for cutaneous remodeling using microscopic patterns of thermal injury. Lasers Surg Med 2004;34:426–38. 21. Weiss R,Weiss M, Beasley K, Munavalli G. Our approach to non-ablative treatment of photoaging. Lasers Surg Med 2005;37:2–8. 22. Geronemus R. Fractional photothermolysis: current and future applications. Lasers Surg Med 2006;38:169–76. 23. Kauvar A, Rosen N, Khrom T. A newly modified 595-nm pulsed dye laser with compression handpiece for the treatment of photodamaged skin. Lasers Surg Med 2006;38:808–13. 24. Bjerring P, Clement M, Heickendorff L, Egevist H, Kiernan M. Selective non-ablative wrinkle reduction by laser. J Cutan Laser Ther 2000;2:9–15. 25. Tanghetti E, Sherr E, Alvarado S. Multipass treatment of photodamage using the pulse dye laser. Dermatol Surg 2003;29:686–90. 26. Hsu T, Zelickson B, Dover J, et al. Multicenter study of the safety and efficacy of a 585 nm pulsed-dye laser for the nonablative treatment of facial rhytids. Dermatol Surg 2005;31:1–9. 27. Goldberg D, Cutler K. Nonablative treatment of rhytids with intense pulsed light. Lasers Surg Med 2000;26: 196–200. 28. Negishi K, Tezuka Y, Kushikata N, Wakamatsu S. Photorejuvenation for Asian skin by intense pulsed light. Dermatol Surg 2001;27:627–631; discussion 632.
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Nonablative technology for treatment of aging skin 29. Huang Y, Liao Y, Lee S, Hong H. Intense pulsed light for the treatment of facial freckles in Asian skin. Dermatol Surg 2002;28:1007–12. 30. Goldberg D, Samady J. Intense pulsed light and Nd:YAG laser non-ablative treatment of facial rhytids. Lasers Surg Med 2001;28:141–4. 31. Sadick N,Weiss R, Kilmer S, Bitter P. Photorejuvenation with intense pulsed light: results of a multi-center study. J Drugs Dermatol 2004;3:41–9. 32. Brazil J, Owens P. Long-term clinical results of IPL photorejuvenation. J Cosmet Laser Ther 2003;5:168–74. 33. Kligman D, Zhen Y. Intense pulsed light treatment of photoaged facial skin. Dermatol Surg 2004;30:1085–90. 34. Carniol P, Farley S, Friedman A. Long-pulse 532-nm diode laser for nonablative facial skin rejuvenation. Arch Facial Plast Surg 2003;5:511–13. 35. Tan M, Dover J, Hsu T, Arndt K, Steward B. Clinical evaluation of enhanced nonablative skin rejuvenation using a combination of a 532 and a 1,064 nm laser. Lasers Surg Med 2004;34:439–45. 36. Butler E, McClellan S, Ross E. Split treatment of photodamaged skin with KTP 532 nm laser with 10 mm handpiece versus IPL: a cheek-to-cheek comparison. Lasers Surg Med 2006;38:124–8. 37. McDaniel D,Weiss R, Geronemus R, Ginn L, Newman J. Light-tissue interactions I: Photothermolysis vs photomodulation laboratory findings. Lasers Surg Med 2002;14:25. 38. Weiss R, Weiss M, Geronemus R, McDaniel D. A novel non-thermal non-ablative full panel LED photomodulation device for reversal of photoaging: digital microscopic and clinical results in various skin types. J Drugs Dermatol 2004;3:605–10. 39. Russell B, Kellet N, Reilly L. Study to determine the efficacy of combination LED light therapy (633 nm and 830 nm) in facial skin rejuvenation. J Cosmet Laser Ther 2005;7:196–200. 40. Nestor M, Gold M, Kauvar A, et al. The use of photodynamic therapy in dermatology: results of a consensus conference. J Drugs Dermatol 2006;5:140–154. 41. Ruiz-Rodriguez R, Sanz-Sanchez T, Cordoba S. Photodynamic rejuvenation, Dermatol Surg 2002;28:742–4. 42. Touma D,Yaar M, Whitehead S, Konnikov N, Gilchrest BA. A trial of short incubation, broad-area photodynamic therapy for facial actinic keratoses and diffuse photodamage. Arch Dermatol 2004;140:33–40. 43. Lowe N, Lowe P. A pilot study to determine the efficacy of ALA–PDT photorejuvenation for the treatment of facial ageing. J Cosmet Laser Ther 2005;7:159–62. 44. Hall J, Keller P, Keller G. Dose response of combination photorejuvenation using intense pulsed light-activated photodynamic therapy and radiofrequency energy. Arch Facial Plast Surg 2004;6:374–8.
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45. Bhatia A, Dover J, et al. Adjunctive use of topical aminolevulinic acid with intense pulsed light in the treatment of photoaging. Paper presented at: Controversies and Conversations in Cutaneous Laser Surgery, Mt Tremblant, Canada, August 2004. 46. Gold M, Bradshaw V, Boring M, Bridges T, Biron J. Splitface comparison of photodynamic therapy with 5aminolevulinic acid and intense pulsed light versus intense pulsed light alone for photodamage. Dermatol Surg 2006;32:795–801. 47. Dover J, Bhatia A, Stewart B, Arndt K.Topical 5-aminolevulinic acid combined with intense pulsed light in the treatment of photoaging.Arch Dermatol 2005;141:1247–52. 48. Gold M. Intense pulsed light therapy for photorejuvenation enhanced with 20% aminolevulinic acid photodynamic therapy. J Lasers Med Surg 2003; 15(Suppl):47. 49. Goldman M, Atkin D, Kincad S. PDT/ALA in the treatment of actinic damage: real world experience. J Lasers Med Surg 2002;14(Suppl):24. 50. Avram D, Goldman M, Effectiveness and safety of ALA– IPL in treating actinic keratoses and photodamage. J Drugs Dermatol 2004;3(1 Suppl):S36-S39. 51. Alster T,Tanzi E,Welsh E. Photorejuvenation of facial skin with topical 20% 5-aminolevulinic acid and intense pulsed light treatment: a split-face comparison study. J Drugs Dermatol 2005;4:35–8. 52. Lupton JR,Williams CN,Alster TS. Nonablative laser skin resurfacing using a 1540 nm erbium glass laser: a clinical and histologic analysis. Dermatol Surg 2002;28:833–5. 53. Fournier N, Mordon S. Nonablative remodeling with a 1,540 nm erbium:glass laser. Dermatol Surg 2005;31: 1227–35. 54. Lee M. Combination visible and infrared lasers for skin rejuvenation. Semin Cutan Med Surg 2002;21:288–300. 55. Tanzi E, Williams C, Alster T. Treatment of facial rhytids with a nonablative 1,450-nm diode laser: a controlled clinical and histologic study. Dermatol Surg 2003;29:124–8. 56. Dayan SH, Vartanian AJ, Menaker G, Mobley SR, Dayan AN. Nonablative laser resurfacing using the long-pulse (1064-nm) Nd:YAG laser. Arch Facial Plast Surg 2003; 5:310–15. 57. Taylor M, Prokopenko I. Split-face comparison of radiofrequency versus long-pulse Nd-YAG treatment of facial laxity. J Cosmet Laser Ther 2006;8:17–22. 58. Dang YY, Ren QS, Liu HX, Ma JB, Zhang JS. Comparison of histologic, biochemical, and mechanical properties of murine skin treated with the 1064-nm and 1320-nm Nd:YAG lasers. Exp Dermatol 2005;14:876–82. 59. Dang Y, Ren Q, Hoecker S, et al. Biophysical, histological and biochemical changes after non-ablative treatments with the 595 and 1320 nm lasers: a comparative study.
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Clinical procedures in laser skin rejuvenation Photodermatol Photoimmunol Photomed 2005;21: 204–9. Orringer JS, Voorhees JJ, Hamilton T, et al. Dermal matrix remodeling after nonablative laser therapy. J Am Acad Dermatol 2005;53:775–82. Doshi S, Alster T. 1,450 nm long-pulsed diode laser for nonablative skin rejuvenation. Dermatol Surg 2005;31: 1223–6. Alexiades-Armenakas M. Rhytides, laxity, and photoaging treated with a combination of radiofrequency, diode laser, and pulsed light and assessed with a comprehensive grading scale. J Drugs Dermatol 2006; 5:731–8. Lennox MA. Febrile convulsions in childhood; a clinical and electroencephalographic study. Am J Dis Child 1949;78:868–82. Ruiz-Esparza J. Near painless, nonablative, immediate skin contraction induced by low-fluence irradiation with new infrared device: a report of 25 patients. Dermatol Surg 2006;32:601–10. Koch D. Histological changes and wound healing response following noncontact holmium:YAG laser thermal keratoplasty. Trans Am Ophthalmol Soc 1996; 94:745–802. Ross E, McKinlay J, Anderson R.Why does carbon dioxide resurfacing work? A review. Arch Dermatol 1999; 135:444–54. Taub A. Harnessing radiofrequency energy. Skin Aging 2003;11:52–8. Bassichis BA, Dayan S, Thomas JR. Use of a nonablative radiofrequency device to rejuvenate the upper one-third of the face. Otolaryngol Head Neck Surg 2004;130:397–406. Fitzpatrick R, Geronemus R, Goldberg D, et al.Multicenter study of noninvasive radiofrequency for periorbital tissue tightening. Lasers Surg Med 2003;33:232–42. Hsu T, Kaminer M.The use of nonablative radiofrequency technology to tighten the lower face and neck. Semin Cutan Med Surg 2003;22:115–23.
71. Zelickson B, Kist D, Bernstein E, et al. Histological and ultrastructural evaluation of the effects of a radiofrequency-based nonablative dermal remodeling device: a pilot study. Arch Dermatol 2004;140:204–9. 72. Kilmer S. A new, nonablative radiofrequency device: preliminary results. In: Controversies and Conversations in Cutaneous Laser Surgery. Chicago: American Medical Association Press, 2002:95–100. 73. Iyer S, Suthamjariya K, Fitzpatrick R. Using a radiofrequency energy device to treat the lower face: a treatment paradigm for a nonsurgical facelift. Cosmet Dermatol 2003;16:37–40. 74. Ruiz-Esparza J, Gomez J.The medical face lift: a noninvasive, nonsurgical approach to tissue tightening in facial skin using nonablative radiofrequency. Dermatol Surg 2003;29:325–32. 75. Alster T, Tanzi E. Improvement of neck and cheek laxity with a nonablative radiofrequency device: a lifting experience. Dermatol Surg 2004;30:503–7. 76. Narins RS,Tope WD, Pope K, Ross E. Overtreatment effects associated with a radiofrequency tissue-tightening device: rare, preventable, and correctable with subcision and autologous fat transfer. Dermatol Surg 2006;32:115–24. 77. Kist D, Burns AJ, Sanner R, Counters J, Zelickson B. Ultrastructural evaluation of multiple pass low energy versus single pass high energy radio-frequency treatment. Lasers Surg Med 2006;38:150–4. 78. Narins D, Narins R. Non-surgical radiofrequency facelift. J Drugs Dermatol 2003;2:495–500. 79. Ruiz-Esparza J. Near painless, nonablative, immediate skin contraction induced by low-fluence irradiation with new infrared device: a report of 25 patients. Dermatol Surg 2006;32:601–10. 80. Taub A, Battle E Jr, Nikolaidis G. Multicenter clinical perspectives on a broadband infrared light device for skin tightening, J Drugs Dermatol 2006;5:771–8.
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7. Lasers, light, and acne Kavita Mariwalla and Thomas E Rohrer
INTRODUCTION Acne vulgaris is an exceedingly common multifactorial disease of the pilosebaceous unit, believed to affect approximately 40 million adolescents and 25 million adults in the USA alone.1 It is thought to be physiologic in adolescence due to its affect on nearly 85% of young people between the ages of 12 and 24 years.2 However, 12% of adult women and 3% of adult men will have clinical acne until the age of 44.3 Many authors have described that, in addition to long-term scarring, which can be disfiguring, patients with acne often carry significant psychosocial morbidity, including anxiety, sleep disturbances, clinical depression, and suicide.4–8 In many cases, acne can be successfully treated using conventional topical or oral medications such as antibacterials, antimicrobials, and retinoids. However, this approach often has drawbacks involving side-effect profiles, length of treatment, and patient compliance.9–13 With oral retinoids, practitioners are faced with federally mandated paperwork that takes not only time, but also several patient visits in order to deliver treatment.14,15 For the subset of patients who have failed these treatment modalities, laser and light-based systems have emerged as standalone and adjunct therapies. These devices work by targeting the components of the pilosebaceous unit that lead to acne lesions, namely either the resident bacterium Propionibacterium acnes, inflammation, or the pilosebaceous unit itself.
THE BUILDING BLOCKS OF ACNE VULGARIS In order to select the appropriate device for treating acne, it is essential to understand the pathogenesis of
the acne lesion itself (Fig. 7.1). Acne vulgaris can be broken down into lesion types based on pathogenesis and severity: comedones, inflamed papules, nodules, and cysts. The majority of data involving laser and light-based therapies are based on the treatment of the non-cystic form of acne vulgaris. Simply put, acne has four main pathophysiological features: hyperkeratinization, sebum production, bacterial proliferation, and inflammation. The early comedone is produced when there is abnormal proliferation and differentiation of keratinocytes in the infundibulum, forming a keratinous plug. This leads to impaction and distention of the lower infundibulum, creating a bottleneck affect.As the shed keratinocytes form concretions, the sebum in the follicle thus becomes entrapped. This stage represents the noninflammatory closed comedone. As accumulation increases, so too does the force inside the follicle itself, eventually leading to rupture of the comedo wall, with extrusion of the immunogenic contents and subsequent inflammation. Depending on the nature of the inflammatory response, pustules, nodules, and cysts can form. One factor in the pathogenesis of acne vulgaris is the role of the resident P. acnes found deep within the sebaceous follicle.16–18 P. acnes is a slow-growing, gram-positive anaerobic bacillus. It contributes to the milieu of acne production in the lipid-rich hair follicle by producing proinflammatory cytokines (e.g., interleukin-1 (IL-1) and tumor necrosis factor α (TNF-α)), as well as many lipases, neuraminidases, phosphatases, and proteases. True colonization with P. acnes occurs 1–3 years prior to sexual maturity, when numbers can reach approximately 106/cm2, predominantly on the face and upper thorax.19 Although some suggest that the absolute number of P. acnes does not correlate with clinical severity,16 it is common belief that the
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Pore
Resident P. acnes
Sebaceous lobule
Sebum
The pilosebaceous unit
Hair shaft
Pore
Retained keratin and lamellar concretions
P. acnes proliferation
Inflammation
Sebaceous lobule regression
Inflammatory papule/pustule
Fig. 7.1 The pathogenesis of acne. Lasers & light based devices target either the pilosebaceous unit, to decrease sebum production or improve sebum flow out of the gland, or the resident Propionibacterium acnes to combat acne vulgaris. Comedones result from hyperkeravatosis at the level of the infundibulum along with increased sebum secretion.As the accumulated keratin and sebum form a plug, inflammation and proliferation of P. acnes produces the clinically inflammatory acne papule.
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Lasers, light, and acne proinflammatory mediators released by these bacteria are at least partially responsible for the clinical acne lesion. In practice, acne is predominantly found on the face and to a lesser degree on the back, chest, and shoulders.The majority of studies using laser and light-based systems target acne on the face, although we present data from a limited number of studies performed elsewhere on the body.
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therapy, some see little to no improvement. Compared with conventional therapy, laser and light devices require no daily routine, are not altered by antibiotic resistance, have few systemic side-effects, and are easy to administer, and some (infrared and radiofrequency devices) offer significant textural improvement of acne scars. On the other hand, these modalities are much more expensive, involve some degree of patient discomfort during treatment, have post-treatment recovery/downtime due to erythema, and require multiple trips to the dermatologist’s office. As with any laser procedure, patients’ skin phototype and underlying psychosocial disturbances should be considered.
Patient screening
Choosing the appropriate laser
As new laser- and light-based systems emerge for the treatment of acne vulgaris, the selection of patients and the type of device to use for each one can seem daunting. In our clinical practice, we use a series of simple guidelines before initiating laser or light-based therapies.
In most practices, the choice of device depends on what is available to the practitioner. When multiple devices are available, it is crucial to keep in mind the area of involvement and the presence of scarring. For example, in large areas such as the chest and back, treatment with infrared lasers with a 4–6 mm spot size is generally too time-consuming and painful for the patient. Instead, for wide treatment areas, light-based therapy with or without δ-aminolevulinic acid can be used. In cases of significant acne scarring, infrared lasers are often used, since these devices are also frequently employed to improve the texture of the skin, including scars. The ultimate decision, however, is up to the individual practitioner and the patient, and should be evaluated in terms of what the treatment is targeting: the sebaceous gland or P. acnes itself.
1. Is the patient a topical or oral medication failure? 2. Has the patient tried isotretinoin or are there circumstances that make isotretinoin a less-thanideal medication for the patient? 3. Is the patient’s acne mainly comedonal or are there inflammatory acne papules as well? To what extent is the patient’s acne nodulocystic? 4. Does the patient have acne and acne scarring? It is important to keep in mind that most laser systems will work to some extent. Topical and oral medications should be optimized and are generally continued during the initial phase of treatment with any of the devices. Occasionally, laser and light-based treatments may be used as first-line therapy, with or without topical and oral medications, in patients presenting with both active acne and acne scars who also want treatment of their scars.
The patient encounter In the initial evaluation of the patient, it is important to set realistic expectations. Although many patients see dramatic improvement with laser and light-based
TARGETING P.ACNES P. acnes produces and accumulates endogenous porphyrins, namely protoporphyrin, uroporphyrin, and coproporphyrin III,20,21 as part of its normal metabolic and reproductive processes. These porphyrins absorb light energy in the near-ultraviolet (UV) and blue regions of the spectrum, and can be visualized by Wood’s lamp (365 nm) examination, under which they fluoresce coral red.22 Porphyrins have two main absorption peaks, the Soret band (400–420 nm) and the Q-bands (500–700 nm), which make them susceptible to excitation by lasers and
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Extinction coefficient Soret band > 2×105
Q-bands L mol−1 cm−1
400
600 Wavelength (nm)
Fig. 7.2 Excitation spectrum of protoporphyrins.The Soret band represents the highest peak of light absorption and thus sensitizer activation, while the Q-bands represent the several weaker absorptions at longer wavelengths. Because the highest peak of absorption of porphyrins is on the blue region (415 nm), this wavelength is used by several light source systems for acne treatment.
light sources emitting wavelengths in the visible light spectrum (400–700 nm) (Fig. 7.2). Once induced, these photosensitizers generate highly reactive freeradical species, which cause bacterial destruction23,24 (Fig. 7.3).The singlet oxygen formed in the reaction is a potent oxidizer that destroys lipids in the cell wall of P. acnes. Although absorption and photodynamic excitation are most efficient between the wavelengths of 400 and 430 nm, with enough light, the reaction may be initiated with a variety of different wavelengths. Porphyrin concentration, effective fluence, wavelength of the emitted photons, and temperature at which the reaction is carried out all play a role in P. acnes photoinactivation.25
Photoinactivation of P. acnes with visible light UVA/UVB After sunlight exposure, as many as 70% of patients report improvement in their acne.26 It is not known whether the UV or visible light component is primarily
Photons
NH
N
Basic porphyrin structure N
HN
Destruction of lipids in cell wall of P. acnes
Reactive oxygen free radicals
Excited porphyrin molecules
Fig. 7.3 Mechanism of P. acnes destruction by visible light interaction with porphyrins.When exposed to absorbed light wavelengths, porphyrins act as photosensitizers and generate highly reactive free-radical species, one of which is singlet oxygen.These radicals are potent oxidizers and destroy the lipids in the cell wall of P. acnes.
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Lasers, light, and acne responsible for this effect. In vitro experiments have shown that P.acnes can be inactivated by low-dose nearUV radiation; however, given the potential carcinogenicity of UVA and UVB therapy, in vivo studies have not been able to justify this means of acne treatment, regardless of the treatment parameters.27,28
Conclusion: While anecdotal evidence of acne improvement over the summer has a rational basis, the potential side-effects of prolonged UV radiation are unacceptable risks, and other modalities should be sought.
Blue light The strongest porphyrin photoexcitation coefficient (407–420 nm) lies in the Soret band. It comes as no surprise, then, that irradiation of P. acnes colonies with blue light (415 nm) leads to bacterial destruction. In vitro, colony counts of P. acnes have decreased by four orders of magnitude 120 minutes after exposure to a metal halide lamp with a wavelength of 405–420 nm (ClearLight, Lumenis Ltd, Santa Clara, CA). Kawada et al29 used this light source on mild to moderate acne lesions in 30 patients and found a 64% mean acne lesion count reduction after 10 Clearlight treatments over a 5-week period with a one- to twoorder decrease in P. acnes colony count in correlated in vitro experiments.The study showed that papules and pustules improved more than comedones, but 10% of patients actually experienced an increase in acne. Another study utilizing the blue light source failed to show bacterial count changes by polymerase chain reaction (PCR) after therapy; however, damaged P. acnes were observed at the ultrastructural level.30 Shalita et al31 used the ClearLight to treat 35 patients with lesions on the face and back using 10-minute light exposures twice weekly over a 4-week period.There was an 80% improvement of noninflammatory and a 70% improvement of inflammatory lesions as assessed 2 weeks after the last treatment. Using the same device, Elman et al32 carried out a split-face double-blind controlled study (n =23) in which patients were treated a total of eight times for 15 minutes (420 nm, 90 mW/cm2). In this group, 87% of the treated sides showed at least a 20% reduction of inflammatory acne lesions with a 60% mean reduction of lesions in responders that remained steady at
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2, 4, and 8 weeks post therapy. In the same trial, Elman et al32 treated 10 patients with papulopustular acne in a split-face dose-response study, exposing them to narrowband visible blue light (90 mW/cm2) for either 8 minutes or 12 minutes. Although there was a more than 50% decrease in inflammatory lesions in 83% of the treatment areas, there was little difference between 8- and 12-minute exposure times (a decrease of 65.9% versus 67.6%, respectively).32 Success in the treatment of acne vulgaris with the blue light may be dependent on the lesion morphology. For example, Tzung et al33 showed a 60% improvement in papulopustular lesions in skin phototypes III and IV with four biweekly treatments (F-36 W/Blue V, Waldmann, Villingen-Schwenningen, Germany) and worsening of nodulocystic acne in 20% of patients (n =28). Using a different blue light source (Blu-U, DUSA Pharmaceuticals, Inc., Wilmington, MA), Gold et al34 found an average 36% reduction in inflammatory acne lesion counts after 4 weeks of biweekly 1000-second light therapy sessions, compared with a 14% reduction in patients using 1% clindamycin solution twice daily. The authors of this study, however, acknowledge that a limiting factor in their trial was sample size (n =13 for the clindamycin arm and n = 12 for the light therapy arm), making it difficult to draw a conclusion regarding diligent topical antibiotic use versus blue light therapy alone. In fact, if all patients entered into the study are considered, there is no difference in the amount of clearing.
Conclusion: Blue light is effective for papules and pustules more than comedones, and carries the risk of worsening nodulocystic acne. It is effective in varying skin types.
Combination blue and red light One of the main restraints of blue light therapy for acne is that it is highly scattered in human skin and thus penetrates poorly. Red light, while less effective in photoactivating porphyrins,35 has increased depth of penetration into the epidermis to reach the porphyrins in the sebaceous follicles. Red light can also potentially induce anti-inflammatory effects by stimulating cytokine release from macrophages.36
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In combination, red and blue light may act synergistically by exerting both antibacterial and anti-inflammatory effects. Papageorgiou et al37 compared the simultaneous use of red and blue light to treat acne vulgaris in a randomized single-blind control study with blue light phototherapy versus 5% benzoyl peroxide in a total of 140 patients with mild to moderate acne. After 84 consecutive treatments of 15 minutes (cumulative doses 320 J/cm2 for blue light and 202 J/cm2 for red light), the authors noted a final improvement of 76% in inflammatory lesions, which was significant compared with the results of blue light or benzoyl peroxide alone.
Conclusion: Combination blue and red light may act synergistically; however, the length of treatment requires patient compliance and diligence.
Yellow light Intense yellow light at 585 nm theoretically penetrates deeper than blue light, and, using the same principle of P. acnes porphyrin excitation, offers another alternative to laser devices. Edwards et al38 studied 30 patients with mild to moderate facial acne and exposed each side of their face to 3.0, 1.5, or 0.1 J/cm2 (sham) twice a week for 4 weeks.At 6 weeks after completion of therapy, patients who received 3.0 J/cm2 had a 23% improvement in Leeds acne score, with a 21% decrease in total lesion count. This system relies on a light-emitting diode (LED) and may offer some benefit to patients with mild acne.
Conclusion: Intense yellow light may improve mild acne, although alternatives exist in the blue light and combined blue and red light modalities that have shown greater efficacy than yellow light alone. Long-term efficacy data are not yet available for the LED.
Intense pulsed light Intense pulsed light sources emit a broad band of light with wavelengths generally ranging from 500 to 1200 nm. Although less selective by nature, these devices emit wavelengths of energy that are absorbed
by many chromophores and therefore can be used to treat a variety of conditions. The Palomar LuxVO (Palomar Co., Burlington, MA) handpiece provides wavelengths of 400–700 nm and 870–1200 nm. Gupta et al39 studied this device in 15 patients with Fitzpatrick skin phototypes I–V. Each patient received three to five treatments spaced 1–2 weeks apart (11 J/cm2, 60–100 ms pulse width, and three to four passes over the entire treatment area) and was followed up 3 months after completion of the last treatment. The authors found no significant difference in noninflammatory lesion counts, but did note a significant reduction in mean comedone, papule, and pustule counts as well as a significant improvement in global severity grade of acne. In the skin type V group, mild crusting associated with postinflammatory hyperpigmentation was noted, but resolved with time.
Conclusion: IPL may be an effective and safe treatment option for mild to moderate inflammatory acne lesions in a variety of skin types.
Pulsed light and heat Knowing that porphyrins have the highest excitation spectrum at lower wavelengths and yet in order to reach P. acnes a greater depth of penetration is required, which can only be accomplished through longer wavelengths, one of the dilemmas of lightbased therapy for acne vulgaris was how to combine these two properties. As a result, Radiancy Inc. designed proprietary technology for the simultaneous delivery of pulsed light and heat energy (LHE) through the ClearTouch system (430–1100 nm, 35 ms, 3–9 J/cm2, and spot size 22 mm × 55 mm). The LHE technology primarily rests on the principle that, like any other photochemical reaction, the efficiency of porphyrin induced P. acnes destruction is determined by the rate of production of excited porphyrins. The rate of porphyrin excitation is related to four factors: (1) the concentration of porphyrins; (2) the photon flux; (3) the temperature of the chemical reaction; and (4) the wavelength of the photons.40 One of the advantages of a pulsed light source compared with continuous-wave mode devices is the ability to provide many more photons at peak power.41 For
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Fig.7.4 Before (a) and after treatment (b) with the ClearTouch system (Radiancy Inc.),a device that emits wavelengths between 430 and 1100 nm in pulses of 35 ms and a low fluence (3–7.5J/cm2).This system,which combines light and heat damage to allow for deeper skin penetration and antibacterial effect for acne treatment,is used biweekly for 1 month with two passes during each therapy session.(Photographs courtesy of Dr Helena Regina de Brito Lima.) example, a 3.5 J/cm2 pulsed wave light source with a 35 ms pulse width delivers 10 000 times more photons than a continuous-wave 10 mW/cm2 light source.The disadvantage of using pulsed light is oxygen (ratelimiting) depletion and therefore rapid reaction saturation. Because the range of emitted wavelengths emitted by this device is broad, both antibacterial and anti-inflammatory effects are induced, since the peak absorption of endogenous porphyrins is covered as well as that of hemoglobin in blood vessels proximal to the inflamed acne papule. The efficacy of a combination of heat and light is also quantitatively justified through the Arrhenius equation, which states that the higher the temperature, the faster a given chemical reaction will proceed.42 Thus, the ability to deposit heat through conduction from a nonoptical, exogenous source may reduce inflammation and even speed up the photodynamic reactions. This was shown by Kjeldstad et al,23 who, using 330–410 nm near-UV light, found that in vitro photoinactivation of P. acnes increased as the temperature increased in intervals of 10°C, 20°C, and 37°C, with reciprocal increase in P. acnes colonies with decreased temperature. Elman and Lask43 studied the efficacy of the ClearTouch system (Radiancy Inc., Orangeburg, NY) in 19 acne treatment-naive patients with inflammatory and noninflammatory acne lesions. Each patient received a total of eight 10-minute treatments (two passes) over a period of 1 month (430–1100 nm, 3.5 J/cm2, 35 ms pulse, and 22 mm × 55 mm spot size). One month after treatment, noninflammatory
acne lesions were 79% ± 22% clear, while inflammatory lesions were 74% ± 20% clear.Two months after the last treatment, noninflammatory and inflammatory lesion counts were reduced by 85% and 87%, respectively. Gregory et al44 also studied the ClearTouch system in a multicenter blinded control trial of 50 patients suffering from mild to severe acne who discontinued all treatment 4 weeks prior to the start of the trial. Patients served as their own control and received two passes biweekly for 1 month. Four weeks later, the authors noted a mean 60% reduction in inflammatory lesion counts, compared with a 32% increase in the control phase, with erythema as the only reported side-effect (Fig. 7.4).
Conclusion:The technological basis of pulsed light and heat makes intuitive sense by allowing practitioners to target both P. acnes and the sebaceous gland. As a result, this device is successful in treating both inflammatory and noninflammatory acne vulgaris.
Laser 532 nm KTP laser The 532 nm (green) potassium titanyl phosphate (KTP) laser has as its target chromophores oxyhemoglobin and melanin.As such, it is typically used to treat telangiectasia and superficial pigmented lesions. However, since this laser has a greater optical penetration depth into skin than blue light, it has the innate
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ability to activate bacterial porphyrins along with some nonspecific collateral thermal injury to sebaceous glands, and is generally well tolerated. Thus, it has also been trialed in the treatment of acne vulgaris. Baugh and Kucaba45 studied the effect of the Aura KTP laser (Laserscope, San Jose, CA) in 21 subjects with mild to moderate facial acne in a split-face singlecenter prospective trial. Patients who had been treated with systemic antibiotics in the 8 weeks prior, topical therapy in the 2 weeks prior, or oral retinoids in the 6 months prior to the start of the trial were excluded. Individual pulses of 12 J/cm2 with a 30–40 ms pulse width and a 1–5 Hz frequency were delivered with the use of a continuous contact cooling tip (Laserscope VersaStat I, which cools the skin to −4°C) twice a week for 2 weeks.The control area was treated with contact cooling alone. Results demonstrated the greatest improvement in acne papules (>45% reduction) at 1 week, which deteriorated by 4 weeks to just over 35% reduction, with no improvement in infiltrated lesions at 4 weeks. Acne pustules showed the most improvement at 4 weeks, while comedone improvement did not exceed 13% reduction at either 1 or 4 weeks post treatment. Total percent improvement in comedones, papules, pustules and infiltrated lesions was 25% 1 week after treatment and 21% 4 weeks after treatment. Subjectively, 47.6% of patients felt 70–79% overall satisfaction with the therapy. Of note, none of the subjects experienced post-treatment redness or irritation. Using the Aura (Iridex, Mountainview, CA) KTP laser (4 mm spot size, 7–9 J/cm2, 20 ms pulse, and 3–5 Hz), Bowes et al46 carried out a prospective splitface study involving 11 patients using 6–10 passes per half-face for 2 weeks. A moderate decrease in mild to moderate acne lesion count was noted after 1 month (36%), versus a 1.8% increase in the control group. Sebum production also decreased (28%), but there was minimal effect on P. acnes as measured by fluorescence photography. Subsequently, Lee47 reported on her experience with the Aura for facial and trunk acne by treating 25 patients with KTP alone, 25 patients with laser followed by topical medications and cleansers, and 125 patients with concomitant laser and topical treatment. A majority (90%) of the 125 patients treated
simultaneously with laser and topical agents had 80–95% improvement, which was similar to the group who followed their laser treatment with topical agents. Fifty percent of the 125 patients maintained results over 4 months without additional treatment. The laser-only group had more flares, less clearance, and slower response times in comparison. These data suggest that although the laser alone induces a limited response, it may be beneficial in combination therapy for acne treatment.
Conclusion: The KTP 532 nm laser can induce a reduction in inflammatory facial acne, although longterm suppression is variable. This laser is less successful in comedone treatment, and may be best used as an adjunctive therapeutic with topicals.
Pulsed dye laser: 585 nm Similar to the KTP, the chromophore for the flashlamp-pumped pulsed dye laser (PDL) is oxyhemoglobin, making it particularly suitable for reducing the ‘red’ component of clinically apparent acne lesions. In addition, as discussed earlier, 585 and 595 nm yellow light can be used to photoexcite porphyrins and reduce P. acnes. Seaton et al48 demonstrated a 49% reduction in inflammatory lesion counts (regardless of severity at baseline) versus 10% in controls 12 weeks after a single pass of the 585 nm PDL (5 mm spot size, 1.5–3.0 J/cm2, and 350 µs pulse; NLite System, ICN Pharmaceuticals Inc., Costa Mesa, CA). Other studies using the same device, however, were less encouraging. In a randomized blinded placebo-controlled trial of 26 patients with mild to moderate acne, Orringer et al49 showed only a trend towards improvement that was not statistically significant in mean papule counts, mean pustule counts, or mean comedone counts. Grading of serial photographs also showed no significant differences in Leeds scores for treated skin at baseline and at week 12 compared with untreated skin at the same time points.49 Although the two groups of investigators used the same device setting, the number of laser pulses used to treat each patient varied. Orringer et al48 used 385 per patient, while Seaton
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Fig. 7.5 a) Patient with acne and post acne erythema before treatment. b) Same patient 6 weeks later, following two treatments with the pulsed-dye laser.
et al50 used at least 500 pulses per patient, which may contribute in part to the difference in results.
In summary: targeting P. acnes
Pulsed dye laser: 595 nm Alam et al51 reported significant acne clearance in 25 subjects using a 595 nm PDL (7 mm spot size, 8–9 J/cm2, 6 ms pulse). These treatment parameters may be more suitable for acne, given the increased depth of penetration as well as longer pulse duration and higher fluence (Fig. 7.5).
The modalities thus far discussed directly or indirectly rely on the biological property of porphyrin as a photosensitizer to induce the destruction of P. acnes colonies in vivo and clinically improve acne vulgaris. Although light therapy in the 400–420 nm range coincides with porphyrin peak excitation, longer wavelengths allow for deeper dermal penetration. Unfortunately, since P. acnes is a rapid regenerator, acne clearance is generally short-lived (at most 3 months), and therefore treatments must be continued on an ongoing basis. Given this limitation, it is questionable whether these laser and light-based systems are a significant enough improvement over topical therapies to justify the expense and time needed to treat.
Conclusion: Because the pulsed dye laser is able to affect the ‘red’ component of acne and has a good depth of penetration, it may be suitable for patients with mildto-moderate inflammatory acne. However, the results have been widely variable – from no improvement to near 50% reduction.
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Glycine + Succinyl CoA → ALA → Prophobilinogen → Hydoxymethylbilane → Uroporphyrinogen III → (Uroporphyrinogen) III → Protoporphyrinogen III → Protoporphyrin IX → Heme ↑ Ferrochelatase
Fig. 7.6 Devices using topical application of δ-aminolevulinic acid (ALA) are effective because they take advantage of the heme synthesis pathway, leading to protoporphyrin IX.When the protoporphyrin IX is photoactivated, the singlet oxygen and free radicals produced are not only cytotoxic to P. acnes but also damage the pilosebaceous unit itself.
TARGETING THE PILOSEBACEOUS UNIT The sebaceous gland is under many influences during adolescence.The ensuing increase in sebum production plays a primary role in acne formation. Although targeting P.acnes is one approach to ameliorating acne vulgaris, another involves targeting the pilosebaceous unit itself. By reducing the size, and therefore the sebum output, of the gland, or by straightening out the tubule by which it drains, several devices have been shown to significantly reduce acne for extended periods of time.
Photodynamic Therapy Photodynamic therapy (PDT) has recently been used in the treatment of acne vulgaris. This method uses a photosensitizer and low-intensity visible light that, together, produce cytotoxic oxygen radicals. One of the advantages of this method is that the photosensitizer can be selectively applied and illumination can be focused. In addition, this system is equally effective on all strains of P. acnes, regardless of antibiotic resistance.52
δ-Aminolevulinic acid Topical δ-aminolevulinic acid (ALA) is preferentially taken up by pilosebaceous units and incorporated into the heme synthesis pathway, resulting in the production of protoporphyrin IX. When photoactivated, protoporphyrin IX produces singlet oxygen molecules and free radicals, which are cytotoxic (Fig. 7.6). In addition, it has been shown that the addition of ALA
actually enhances intracellular porphyrin synthesis itself.53 PDT has also been used in combination with ALA in the treatment of nonmelanoma skin cancer, actinic keratoses, acne vulgaris, viral warts, and other dermatoses.54 The combination of topical ALA application followed by PDT results in cytotoxic free-radical production and death of P. acnes, as well as damage to the pilosebaceous unit itself. ALA application times as brief as 15–60 minutes followed by red, blue, or intense pulsed light, PDL, diode lasers, or LED sources have all been shown to be effective. ALA and red light In a study of 22 patients with chest and back acne, Hongcharu et al55 found that the majority of protoporphyrin IX production was localized in the sebaceous glands and hair follicles after three hours application of ALA under occlusion. Subsequently, these authors used a broad band 550–700 nm red light source at a fluence of 150 J/cm2, and were able to show a persistent decrease in acne lesion counts for 10–20 months following one to four treatments. Histology revealed damaged and even destroyed sebaceous glands. Sebum excretion rate, sebaceous gland size, and follicular bacterial counts also all decreased. Adverse effects, often typical of ALA–PDT treatment, included erythema, crusting, pain, and hyperpigmentation. Itoh et al56 reported an intractable case of acne vulgaris on the face that, after treatment with ALA–PDT (4-hour drug incubation, 635 nm), remained clear at 8-month follow-up. A subsequent study by the same group57
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Lasers, light, and acne evaluated 13 subjects and demonstrated a reduction in new acne lesion counts at 1, 3, and 6 months following PDT treatment. ALA and blue light Pain-free treatments with few side-effects have been described with four weekly treatments using the blue light after short ALA incubation periods (15 minutes).58 In 15 patients with moderate to severe acne, the combination of 1-hour ALA incubation and blue light led to a continued reduction in acne lesion counts in responders up to 72% at 3 months after the last treatment.59 ALA and red light diode laser Pollock et al60 investigated the use of a red light diode laser (CeramOptec GmbH, Bonn, Germany) in combination with 20% ALA cream applied under occlusion for 3 hours. Ten patients with mild to moderate acne of the back were treated weekly for 3 weeks (635 nm, 25 mW/cm2, and 15 J/cm2) and assessed 3 weeks after the last treatment. ALA–PDT-treated areas demonstrated a significant reduction in acne lesion counts, but not in P. acnes concentration as assessed by P. acnes swabs or sebum excretion. It is possible, as Pollock et al60 suggest, that another mechanism of action may play a role in the response of acne to ALA–PDT. They also suggest that perhaps PDT, rather than destroying P. acnes, damages the bacterium so that it is unable to function normally.They speculate that when the bacterium is swabbed and put into an ideal culture environment, it grows normally, thus giving an inaccurate picture of what is occurring deep in the pilosebaceous unit. ALA and polychromatic visible light Oral ALA followed by exposure to polychromatic visible light from a metal halide lamp resulted in marked improvement based on a physician clinical assessment score in 61% of 51 patients treated for intractable acne on the body. Kimura et al61 administered the ALA at a dose of 10 mg/kg, which produced no liver dysfunction. However, adverse effects did occur, and consisted of slight discomfort, burning and stinging during the irradiation.
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ALA and IPL Hwang and Seo62 compared two light spectra of IPL (Ellipse, DDD, Denmark), namely VL (555–950 nm) and HR (600–950 nm) with varying application times of ALA (1 hour vs 4 hours).They followed patients at 1, 4, 14 and 24 weeks after a single treatment, and found no difference in the number of comedones or inflammatory acne lesions when comparing 1-hour and 4-hour ALA incubation times. Of the two, the 600–950 nm applicator was more efficient than the 555–950 nm applicator in reduction of inflammatory acne. Given these data, and the risk of hyperpigmentation, Hwang and Seo62 concluded that ALA should be applied for a short time. Gold et al54 enrolled 15 patients who underwent four weekly treatments (ClearTouch, 3–9 J/cm2) after 1 hour incubation with ALA, and found a 71.8% reduction in inflammatory acne lesions at 12-week follow-up in 80% of the patients.This was an increase from a 68.5% reduction 1 month after treatment. Of note, none of the treated lesions recurred at 3-month follow-up. ALA and PDL In one of the few studies using patients with mild to severe acne including cystic and inflammatory lesions, Alexiades-Armenakas63 used a combination of ALA–PDT with the 595 nm PDL. Topical ALA was applied for 45 minutes on the face, followed by a single minimally overlapping pass with the long-pulsed PDL (595 nm, 7–7.5 J/cm2, 10 ms, 10 mm spot size, and dynamic cooling spray 30 ms) in 14 patients, who were then followed monthly for 13 months. Controls were treated with conventional therapy (oral antibiotics, oral contraceptives, or topicals) or PDL only. Complete clearance occurred in 100% of the patients in the PDL–PDT-treated group, with a mean of 2.9 treatments being required to achieve complete clearance. In the control groups, mean percent lesional clearance rate per treatment was 77%. The mean percent lesional clearance per treatment was 32% in the PDL-only group and 20% in the oral antibiotic and topical group, although the number of patients in these two control groups was small (n = 2 for each). Nonetheless, the PDT–laser combination was well tolerated, with minimal erythema lasting 1–2 days without evidence of crusting, blistering, or dyspigmentation. This pilot study demonstrated that PDL
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Dynamic cooling device spray
Stratum corneum
Laser pulse
Epidermis
Dermis Hair
Sebaceous gland
follicle
Sebaceous gland
Dynamic cooling device pulse cools and protects the epidermis
Laser penetrates the skin to base of the sebaceous gland
Thermal injury to the sebaceous gland
Fig.7.7 Lasers at 1320,1450,and 1540 nm (mid-infrared) have shown impressive clearing of acne lesions.The lasers heat the dermis,in bulk,including the upper and mid-dermis,where sebaceous glands are primarily located.As a result,a potential reduction in the size and sebum output of the sebaceous gland,or a straightening of the infrainfundibular tubule,occurs and there is an improvement in acne.Side-effects associated with these lasers are pain,transient erythema and edema,and a risk of hyperpigmentation.
may be an efficacious combination with ALA to achieve clearance in patients with varying stages of acne from comedones to cysts.
Conclusion: Topical ALA application enhances the production of porphyrins and not only can induce cytotoxic effects on P. acnes but can also target sebaceous glands for destruction. The end-result is a decrease in acne, which varies depending on the light source used for illumination.
Indocyanine green Carotenoids are the natural chromophore in sebum, with an absorption range of 425–550 nm.The problem with using a laser in this wavelength range is the number of unintended components of the skin that will absorb this wavelength, resulting in unwanted side-effects such as blood coagulation.The ideal wavelength to use is in the ‘optical window’, which is 600–1300 nm.64 The only barrier is that local chromophores do not absorb in this wavelength. However, indocyanine green (ICG, a tricarbocyanine dye) is a chromophore with peak absorption at 805 nm, which can be applied topically and is known to be preferentially accumulated by sebaceous glands. In combination with diode lasers, ICG is thought to cause both photodynamic and photothermal effects within P. acnes and the pilosebaceous unit.
Tuchin et al65 treated 22 patients with inflammatory acne lesions on the back and face. An 803 nm (OPC-BO15-MMM-FCTS diode laser, Opto Power Corp., Tucson, AZ) or 809 nm (Palomar Medical Technologies, Inc., Burlington, MA) diode laser was used after occlusive ICG application for 5 or 15 minutes. The combination of ICG and laser produced less inflammation, lesion flattening, and reduction in P. acnes and sebum production compared with no treatment, ICG alone, and laser-only-treated areas. A subsequent pilot study for moderate to severe acne lesions showed that multiple treatments with ICG and a nearinfrared diode laser improved skin for as long as 1 month without side-effects when compared with a single ICG-laser treatment session.66 In one of the select studies to look at body acne, Lloyd and Mirkov67 treated patients with 5% ICG microemulsion for 24 hours under occlusion and then treated them with a 810 nm diode laser (4 mm spot size, 810 nm, 40 J/cm2, and 50 ms pulse; Cyanosure, Inc.). Histology showed evidence of selective necrosis of the sebaceous glands. Using these parameters, the group then treated 10 patients with back acne, and their preliminary clinical results showed a decrease in acne in the treatment area at 3-, 6-, and 10-month follow-up. It should be noted that treatment did not lead to immediate resolution of acne lesions, which cleared through the skin’s own healing process. However, the treated regions remained lesionfree for extended periods of time, leading Lloyd and
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Fig. 7.8 a) Patient with severe acne and acne scarring prior to laser treatment. b) Same patient 6 weeks later, following five treatments with a 595 nm pulsed-dye laser and 1450 nm infrared divide laser (Smoothbeam Laser, Candela Corp., Wayland MA).
Mirkov67 to speculate that ICG-diode laser treatment did cause thermal damage in the sebaceous gland.
Conclusion: ICG and long-pulsed diode lasers are an effective way to target sebaceous glands by applying an exogenous chromophore to the skin, however downsides include incubation time and pain during treatment due to collateral heating.
Infrared lasers Isotretinoin use is known to cause shrinkage of sebaceous glands, with a resultant reduction in sebum output. Interestingly, although sebum concentration returns to normal after therapy discontinuation, many patients remain clear of acne. This has led to the hypothesis that even a temporary alteration of sebaceous glands may be sufficient to induce long-term
acne clearance.The distribution of sebaceous glands is highly variable in the dermis; however, infrared lasers target water, which is the dominant chromophore in the sebaceous gland. Consequently, mid-infrared laser light, which has a depth of penetration into the superficial dermis, is able to produce a zone of injury in the superficial dermal layer that may injure sebocytes and arrest the overproduction of sebum and disrupt the pathogenesis of acne itself. Alternatively, infrared lasers may be affecting the infundibulum of the pilosebaceous unit and improving the sebum flow out of the gland (Fig. 7.7). In any event, infrared lasers have been shown to significantly clear acne for extended periods of time (Fig. 7.8). Infrared lasers encompass the 1320, 1450 and 1540 nm wavelength devices.
1450 nm In a multipart trial, Paithankar et al68 demonstrated that the 1450 nm diode laser with cryogen spray cooling
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(Smoothbeam, Candela Corp., Wayland, MA) could induce thermal injury confined to the dermis histologically after irradiation of ex vivo human skin. Using rabbit ear skin as an in vivo model, treatment with the Smoothbeam produced histological alteration of sebaceous glands within the dermis at day 1 and day 3, with recovery from initial injury by day 7. Next, Paithankar et al68 conducted a human trial, using the 1450 nm diode laser (average fluence 18 J/cm2) for four treatments separated by 3 weeks each, and demonstrated a reduction of acne lesions in 14 of 15 patients at 6-month follow-up. Importantly, only 1 of the immediate post-treatment biopsies yielded sebaceous glands, indicating that selective targeting of the sebaceous gland is possible, as the histology demonstrated thermal coagulation of the sebaceous lobule and follicle with no epidermal alteration. Long-term biopsies taken at 2 and 6 months post treatment showed sebaceous glands that had returned to their pretreatment state. In a blinded multicenter study, 45 patients received four monthly treatments with the 1450 nm diode laser (14 J/cm2), of whom 26 had at least 65% improvement in lesion counts 1 month following treatment.69 At 6 months, 5 patients required no additional intervention. Mazer and Fayard70 reported 18-month remission rates in 29 patients who avoided any additional acne-modifying treatments such as laser or topical or oral therapy after four treatments with the 1450 nm diode laser (12–14 J/cm2, 35-dynamic cooling spray 35 ms, 6 mm spot size, and no overlapping whole-face treatment) every 4–6 weeks.They noted that initially there was an average 74.8% reduction in total acne lesion counts (maximum 88.5%, minimum 49.4%), which showed only a slight deterioration to 71.8% at 18 months (maximum 88.5%, minimum 47.9%). A pilot study demonstrated the safety of the 1450 nm laser in the treatment of inflammatory facial acne in 28 Indian patients with skin type IV or V.71 Each patient was treated with four sessions at 21-day intervals, alternating with glycolic acid peels on the 10th day after laser treatment. The control group of 28 patients was treated with glycolic acid peels only. The results demonstrated a reduction in lesion count of 40% after one treatment, 57% after two treatments, and 85% after four treatments, with recurrence in 7.1% of the group at 6 months. In comparison, lesion counts in the control group decreased by 17.9% after one peel and
51.8% after four peels. However, 96.4% of the patients in the control group experienced recurrence at 6 months. Postinflammatory hyperpigmentation was seen in only 3.6% of patients. This low incidence of postinflammatory hyperpigmentation may have been due to the concomitant use of glycolic acid peels. Jih et al72 compared the dose response of a 1450 nm diode laser (prototype laser supplied by Candela Corp., Wayland, MA) in 20 patients with skin phototypes II–VI and an age range of 18–39 years. Topical lidocaine (5% Ela-Max) was applied to the entire face 1 hour before laser treatment, and patients were evaluated via split face comparisons after treatment with either 14 or 16 J/cm2 for three treatments. At 12month follow-up, similar reductions in inflammatory acne lesion counts were observed (76.1% reduction using 14 J/cm2 vs 70.5% reduction using 16 J/cm2). One of the downsides of 1450 nm diode treatment is the level of discomfort reported by some patients. As a result, widespread use of this laser in younger populations has been limited. Bernstein73 reported his experience in six subjects with active papular acne who were treated in a split-face randomized trial monthly for 4 months. Half of the face was treated with a single pass (12–14 J/cm2), while the other half was treated with a double-pass at a lower energy (8 J/cm2), and subjects were evaluated 2 months after the final treatment. Bernstein73 reports a 78% reduction in acne counts on the single-pass-treated side and a 67% reduction on the half of the face treated with the lower energy. Importantly, patients had an average pain rating of 5.6 on a scale of 1 (minimum) to 10 (maximum) with the high-energy single pass and 1.3 with the lower-energy double pass.
The 1450 nm laser in combination with other therapies Using the 1450 nm laser as an adjunct in patients who were on oral and/or topical acne treatments, Friedman et al74 observed an 83% decrease in inflammatory facial acne lesion counts following three treatments at 4- or 6-week intervals. Side-effects were transient and local, including erythema, edema, and pain during treatment. Similarly, Astner et al75 used the SmoothBeam as an adjunct to conventional acne therapy in 13 patients who continued their
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Fig. 7.9 a) Patient with significant acne and acne scarring prior to treatment. b) Same patient 6 weeks later, following four treatments with a 595 nm pulsed-dye laser and a 1450 nm infrared laser (Smoothbeam Laser, Candela Corp.,Wayland MA).
medications during four treatments spaced 4–6 weeks apart (12–14 J/cm2). They noted a mean 54.6% improvement in lesions counts which persisted for the 6-month follow-up period of the study. The 595 nm PDL has been used in combination with the 1450 nm diode laser in a study of 15 patients with inflammatory facial acne. First, patients were treated with the 595 nm PDL (10 mm spot size, 6.5–7.5 J/cm2, and 6–10 ms pulse; Vbeam, Candela Corp., Wayland, MA) followed by a single pass with the 1450 nm diode (6 mm spot size, 10–14 J/cm2, and dynamic cooling spray at 30–40 ms). Glaich et al76 reported a mean acne lesion count reduction of 52% after one treatment, 63% after two treatments, and 84% after three treatments. This combination may be successful due to the dual targeting of the sebaceous gland (1450 nm laser) and P.acnes (595 nm PDL) (Fig. 7.9). Wang et al77 carried out a study in which 19 patients with Fitzpatrick skin types II–IV and active
inflammatory acne, who had discontinued all topical and systemic anti-acne medications 3 weeks prior to the first treatment and had not used isotretinoin in the previous 6 months, were randomized and controlled to receive a combination treatment on one side of the face and laser only on the other side. Each patient received a total of four treatments 3 weeks apart and attended two follow-up visits at 6 and 12 weeks after the last treatment. In those patients receiving combination therapy, one side of the face was treated with microdermabrasion with six passes at the full setting (Vibraderm, Dermatherm, Irving, TX). Following this, the face was treated with the SmoothBeam 1450 nm laser (Candela Corp, MA; 13.5–14 J/cm2, 6 mm spot size, and dynamic cooling spray at 30–40 ms). Photographs of the patients at baseline and at 3, 6, and 12 weeks post treatment were evaluated by an independent observer, who counted the total number of acne lesions. Wang et al77 found no statistically
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significant difference in acne reduction with the addition of microdermabrasion to the treatment plan (61% clearance with laser alone and 54.4% clearance at 12 weeks for microdermabrasion and laser), nor was there a significant difference in patient pain level or discomfort. Interestingly, there was also no difference in sebum production from baseline compared with 12 weeks post treatment.This is consistent with the notion that thermal damage of the sebaceous glands immediately after treatment is quickly reversed.
Conclusion: Studies suggest that the 1450 nm diode may have clinical utility as primary therapy for inflammatory acne, or as an adjunctive acne treatment in patients needing greater clearance than topicals or systemic antibiotics alone can provide.
1540 nm The 1540 nm erbium (Er) : glass laser (Aramis, Quantel Medical, Med-Surge Technologies, Dallas, TX), induces new collagen formation79,80 and has primarily been used for wrinkle reduction. Studies by Boineau and Kassir80,81 have shown success with this laser wavelength in acne vulgaris as well. Twenty-five patients with lesions on the back and face underwent four treatments with the 1540 nm laser (10 J/cm2, 3 ms pulse, 5–6 pulse train mode, and 2 Hz) at monthly intervals, and experienced a 78% mean lesion count reduction.81 In a separate study evaluating the face only, 20 patients with skin phototypes I–IV had an 82% decreased lesion count at 3 months after four biweekly treatments (8–12 J/cm2 and 3–6 pulse train mode).82 An advantage of this system is the decreased oiliness reported by patients in both trials and the lack of immediate or delayed adverse effects. Angel et al82 found a mean acne count reduction of 78% on 18 patients 2 years following treatment with this device.
Conclusion: The 1540 nm Er : glass laser may be appropriate for back and face acne in varying skin phototypes, although only a few trials have been conducted with this system.
1320 nm Although no studies have been published on the efficacy of the CoolTouch (Laser Aesthetics, Inc., CA) 1320 nm laser system in the treatment of acne, the company was FDA-approved for this use in 2003. Most of the studies involving the 1320 nm device have evaluated its efficacy in acne scar remodeling.The dermal layer is targeted by using water as the primary chromophore.The effect of dermal damage is collagen remodeling and re-epithelialization, leading to a more youthful-appearing epidermis.
Radiofrequency Radiofrequency devices are used to treat moderate and severe acne through volumetric heating. A handheld piece housing a treatment tip containing a coupler allows for an even application of heat while a spray of cryogen is delivered to avoid an epidermal burn; the result is the creation of an inverted thermal gradient such that the surface remains coolest while heat is delivered to the dermis. Ruiz-Esparza and Gomez83 used the ThermaCool (Thermage, Inc., Hayward, CA) device and observed an excellent response in 18 of 22 patients (82%), and a modest response in 9%. Furthermore, they noted clinical improvement in acne scarring.While these results are encouraging, the limited follow-up time (1–8 months), and small study size (n = 22) underscore the need for larger studies with longer follow-up. Avram and Fitzpatrick84 compared the efficacy of SmoothBeam and Thermage (Thermage, Inc., Hayward, CA) in alleviating both acne and acne scars. Twenty patients with moderate acne (more than eight inflammatory lesions) had half the face treated with SmoothBeam (1450 nm and 12–16 J/cm2) and the other half treated with Thermage (settings 13.5–15.0) during a total of three treatments spaced 4 weeks apart. At the 6-month post-treatment follow-up, a 72% improvement in active acne on the half-faces treated with SmoothBeam was found, compared with a 60% improvement in the halffaces treated with Thermage. However, Thermage improved acne scarring by 46%, compared with 38% with SmoothBeam. Ice pick scars were the worst responders.
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Conclusion: Radiofrequency devices can be used for moderate to severe acne, and may also simultaneously help with the texture and appearance of acne scarring.
In summary: targeting the pilosebaceous unit In targeting the sebaceous gland, PDT, infrared lasers, and radiofrequency devices are all effective to varying degrees because they attempt to change a key link in the chain of events leading to an acne lesion. In theory, by damaging enlarged sebaceous glands, sebum overproduction is decreased, if not eliminated, for a period of time. As it stands now, however, this still remains a theory, as only mild sebaceous gland alteration has been proven histologically. Even though this temporary alteration may be sufficient to result in long-term acne clearance, studies have yet to demonstrate sebaceous gland ablation. In those studies where sebocyte alteration was evaluated, return to pretreatment histology was noted in the long term. Further studies are also needed to document histological changes in the infundibular region that would improve the flow of sebum from the gland.
FUTURE TRENDS The idea of a portable handheld device to treat acne vulgaris is becoming one of the emerging technologies in laser and light based therapies.The Zeno (Tyrell, Inc., Houston,Texas, USA) was approved in June 2005 by the FDA as an over-the-counter device for the treatment of mild to moderate acne vulgaris, and is proposed to work through the induction of heat-shock proteins, which then kill resident P. acnes.85 No preliminary results regarding the efficacy of this device have yet been published; however, clinical trials are currently underway and the product is available for consumer purchase.
REFERENCES 1. Leyden JJ. Acne vulgaris is a multifactorial disease. J Am Acad Dermatol 2003;49(3 Suppl):S199.
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2. Zaenglein AL, Thiboutot DM. Acne vulgaris. In:Bolognia JL, Worizzo JL, Rapini RP, eds. Dermatology. Spain: Elsevier, 2003:531–44. 3. Goulden V, Stables GI, Cunliffe WJ. Prevalence of facial acne in adults. J Am Acad Dermatol 1999;41:577–80. 4. Yang C, Su L, Feng W et al. Emotional distress and related factors in patients with acne. Abstract. J Am Acad Dermatol AB1 March 2006. 5. Yang C, Feng W, Chen H et al. Sleep problems and related factors in patients with acne. Abstract. J Am Acad Dermatol AB2. March 2006. 6. Mallon E, Newton JN, Klassen A et al.The quality of life in acne: a comparison with general medical conditions using generic questionnaires. Br J Dermatol 1999; 140:672–6. 7. Gupta MA, Gupta AK. Depression and suicidal ideation in dermatology patients with acne, alopecia areata, atopic dermatitis and psoriasis. Br J Dermatol 1998;139:846–850. 8. 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;203:124–30. 9. Lee DJ,Van Dyke GS, Kim J. Update on pathogenesis and treatment of acne. Curr Opin Pediatr 2003;15:405–10. 10. Gollnick HP, Krautheim A. Topical treatment in acne: current status and future aspects. Dermatology 2003; 206:29–36. 11. Velicer CM, Heckbert SR, Lampe JW et al. Antibiotic use in relation to the risk of breast cancer. JAMA 2004;291:827–35. 12. Gough A, Chapman S, Wagstaff K et al. Minocycline induced autoimmune hepatitis and systemic lupus erythematosus-like syndrome. BMJ 1996;312:169–72. 13. O’Donnell J. Overview of existing reseach and information linking isotretinoin (Accutane®), depression, psychosis, and suicide. Am J Ther 2003;10:148–59. 14. Hill MJ. iPLEDGE: protecting patients or prohibiting access to care? Dermatology Nursing. 18(2):124, 2006 April. 15. Brinker A, Kornegay C and Nourjah P. Trends in adherence to a revised risk management program designed to decrease or eliminate isotretinoin-exposed pregnancies. Arch Dermatol 2005;141:563–9. 16. Leyden JJ, McGinley KJ, Mills OH et al. Propionibacterium levels in patients with and without acne vulgaris. J Invest Dermatol 1975;65:382–4. 17. Holland KT, Aldana O, Bojar RA, et al. Propionibacterium acnes and acne. Dermatology 1998;196:67–68. 18. Leyden JJ, McGinley KJ,Vowels B. Propionibacterium acnes colonization in acne and nonacne. Dermatology 1998;196:55–58. 19. Handa S. Propionibacterium infections. Retrieved from http://www.emedicine.com/med/topic 1917.htm
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20. Lee WL, Shalita AR, Poh-Fitzpatrick MB. Comparative studies of porphyin production in Propionibacterium acnes and Propionibacterium granulosum. J Bacteriol 1978;133: 811–15. 21. Ashkenazi H, Malik Z, Harth Y et al. Eradication of Propionibacterium acnes by its endogenic porphyrins after illumination with high intensity blue light. FEMS Immunol Med Microbiol 2003;35:17–24. 22. Kjeldstad B, Johnsson A. An action spectrum for blue and near ultraviolet inactivation of Propionibacterium acnes; with emphasis on a possible porphyrin photosensitization. Photochem Photobiol 1986;43:67–70. 23. Kjeldstad B. Photoinactivation of Propionibacterium acnes by near-ultraviolet light. Z Naturforsch [C] 1984; 39:300–302. 24. Melo TB. Uptake of protoporphyrin and violet light photodestruction of Propionibacterium acnes. Z Naturforsch [C] 1987;42:123–8. 25. Elman M, Lebzelter J. Light therapy in the treatment of acne vulgaris. Dermatol Surg 2004;30:139–46. 26. Charakida A, Seaton ED, Charakida M et al. Phototherapy in the treatment of acne vulgaris: What is its role? Am J Clin Dermatol 2004;5:211–16. 27. Mills OH, Porte M, Kligman AM. Enhancement of comedogenic substances by UV radiation. Br J Dermatol 1978;98:145–50. 28. van Weelden H, de Gruihl FR, van der Putte SC et al.The carcinogenic risks of modern tanning equipment: is UV-A safer than UV-B? Arch Dermatol Res 1988;280:300–307. 29. Kawada A,Aragane Y, Kameyama H et al.Acne phototherapy with a high-intensity, enhanced, narrow-band, blue light source: an open study and in vitro investigation. J Dermatol Sci 2002;30:129–135. 30. Omi T, Bjerring P, Sato S et al. 420 nm intense continuous light therapy for acne. J Cosmet Laser Ther 2004;6:156–162. 31. Shalita AR, Harth Y, Elman M et al. Acne phototherapy using U.V.-free high intensity narrow band blue light: 3 centres clinical study. Proc SPIE 2001;4244:61–73. 32. Elman M, Slatkine M, Harth Y.The effective treatment of acne vulgaris by a high-intensity, narrow band 405–420 nm light source. J Cosmetic & Laser Ther 2003;5:111–117. 33. Tzung TY,Wu KH, Huang ML. Blue light phototherapy in the treatment of acne. Photodermatol Photoimmunol Photomed 2004;20:266–69. 34. Gold MH, Rao J, Goldman MP et al. A multicenter clinical evaluation of the treatment of mild to moderate inflammatory acne vulgaris of the face with visible blue light in comparison to topical 1% clindamycin antibiotic solution. J Drugs Dermatol 2005;4:64–70. 35. Sigurdsson V, Knults AC, van Weelden H. Phototherapy of acne vulgaris with visible light. Dermatology 1997;194: 256–60.
36. Young S, Bolton P, Dyson M et al. Macrophage responsiveness to light therapy. Lasers Surg Med 1989;9:497–505. 37. Papageorgiou P, Katsambas A, Chu A. Phototherapy with blue (415nm) and red (660nm) light in the treatment of acne vulgaris. Br J Dermatol 2000;142:973–8. 38. Edwards C, Hill S, Anstey A. A safe and effective yellow light-emitting diode treatment for mild to moderate acne: A within-patient half-face dose ranging study. Abstract. J Am Acad Dermatol. AB15; March 2006. 39. Gupta A. Efficacy and safety of intense pulsed light therapy using wavelengths of 400–700 nm and 870–1200 nm for acne vulgaris. J Am Acad Dermatol AB27, March 2006. 40. Elman M, Lebzelter J. Evaluating pulsed light and heat energy in acne clearance. Radiancy White paper, June 2002. Retrieved from http://www.radiancy.com/USA/ appdocs.htm. 41. Herd RM, Dover JS, Arndt KA. Basic laser principles. Dermatol Clinic 1997;15:355–72. 42. International Union of Pure and Applied Chemistry Compendium of Chemical Terminology 2nd edition, 1997. Retrieved from http://www.iupac.org/goldbook/A00446.pdf. 43. Elman M, Lask G.The role of pulsed light and heat energy (LHE) in acne clearance. J Cosmet Laser Ther 2004;6: 91–95. 44. Gregory AN,Thornfeldt CR, Leibowitz KR et al. A study on the use of a novel light and heat energy system to treat acne vulgaris. Cosmet Dermatol 2004;17:287–300. 45. Baugh, WP and Kucaba WD. Nonablative phototherapy for acne vulgaris using the KTP 532 nm Laser. Dermatol Surg 2005;31:1290–6. 46. 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. 47. Lee CMW. Aura 532nm laser for acne vulgaris – a 3 year experience, Annual Combined Meeting of the American Society for Dermatologic Surgery and the American Society for Mohs Micrographic Surgery and Cutaneous Oncology, New Orleans, LA, October 2003. 48. Seaton ED, Charakida A, Mouser PE et al. Pulsed-dye laser treatment for inflammatory acne vulgaris: randomised controlled trial. Lancet 2003;362:1347–52. 49. Orringer J, Kang S, Hamilton T et al. Treatment of acne vulgaris with a pulsed dye laser: a randomized controlled trial.JAMA 2004;291:2834–9. 50. Chu A. Pulsed dye laser treatment of acne vulgaris. JAMA 2004;292:1430. 51. Alam M, Peterson SR, Silapunt S et al. Comparison of the 1450nm diode laser for the treatment of facial acne: a left-right randomized trial of the efficacy and adverse effects. Lasers Surg Med 2003;32:S30.
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Lasers, light, and acne 52. Ortiz A, Van Vilet M, Lask GP,Yamauchi PS. A review of laser and light sources in the treatment of acne vulgaris. J Cosmetic and Laser Therapy 2005;7:69–75. 53. Ashkenazi H, Malik Z, Harth Y et al. Eradication of Propionibacterium acnes by its endogenic porphyrins after illumination with high-intensity blue light. FEMS Immunol Med Microbiol 2003;35:17–24. 54. Gold MH, Bradshaw VL, Boring MM et al. The use of a novel intense pulsed light and heat source and ALA-PDT in the treatment of moderate to severe inflammatory acne vulgaris. J Drugs Dermatol 3(6 Suppl):S15–9, 2004 Nov-Dec. 55. Hongcharu W, Taylor CR, Change Y et al. Topical ALAphotodynamic therapy for the treatment of acne vulgaris. J Invest Dermatol 2000;115:183–92. 56. Itoh Y, Ninomiya Y, Tajima S et al. Photodynamic therapy for acne vulgaris with topical 5-aminolevulinic acid. Arch Dermatol 2000;136:1093–1095. 57. Itoh Y, Ninomiya Y, Tajima S et al. Photodynamic therapy for acne vulgaris with topical delta-amenolevulinic acid and incoherent light in Japanese patients. Br J Dermatol 2001;144:575–579. 58. Goldman MP. Using 5-aminolevulinic acid to treat acne and sebaceous hyperplasia. Cosmet Dermatol 2003;16: 57–58. 59. Gold MH, Bradshaw VL, Boring MM et al. The use of a novel intense pulsed light and heat source and ALA-PDT in the treatment of moderate to severe inflammatory acne vulgaris. J Drugs Dermatol 2004;3:S15–S19. 60. Pollock B,Turner D, Stringer MR et al.Topical amenolevulinic acid-photodynamic therapy for the treatment of acne vulgaris: a study of clinical efficacy and mechanism of action. Br. J Dermatol 2004;151:616–22. 61. Kimura M, Itoh Y, Tokuoka Y et al. Delta-aminolevulinic acid-based photodynamic therapy for acne on the body. J Dermatol 2004;31:956–60. 62. Hwang EJ and Seo K. Topical photodynamic therapy for treatment of acne vulgairs: comparison of two IPL applicators and different application times of ALA. Abstract 290. American Society for Laser Medicine and Surgery Abstracts pg. 86. 63. Alexiades-Armenakas, M. Long-pulsed dye laser-mediated photodynamic therapy combined with topical therapy for mild to severe comedonal, inflammatory, or cystic acne. J of Drugs in Dermatol 5(1); 2006 January 45–55. 64. Parrish JA. New concepts in therapeutic photomedicine: Photochemistry, optical targetings, and the therapeutic windown. J Invest Dermatol 1981;77:44–50. 65. Tuchin VV, Genina EA, Bashkatov AN, et al. A pilot study of ICG laser therapy of acne vulgaris: photodynamic and photothermolysis treatment. Lasers Surg Med 2003;33: 296–310.
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66. Genina EA, Bashkatov AN, Simonenko GV, et al. Lowintensity indocyanine-green laser phototherapy of acne vulgaris: pilot study. J Biomed Opt 2004;9:828–34. 67. Lloyd JR and Mirko M. Selective photothermolysis of the sebaceous glands for acne treatment. Lasers Surg Med 2002;31:115–20. 68. Paithankar DY, Ross EV, Saleh BA, et al. Acne treatment with a 1,450nm wavelength laser and cryogen spray cooling. Lasers Surg Med 2002;31:106–114. 69. Mazer JM.Treatment of facial acne with a 1450 nm diode laser: a comparative study. Lasers Surg Med 2004:34: S67. 70. Mazer JM and Fayard V. Eighteen months results after treatment of facial acne with the 1450 nm diode laser. Abstract 103. American Society for Laser Medicine and Surgery. 71. Santhanam A, Shah A and Kumar P. The 1450-nm diode laser in the treatment of inflammatory facial acne vulgaris in Indian patients – A pilot study. J Am Acad Dermatol. Abstract. P45. 72. Jih MH, Friedman PM, Goldberg LH et al.The 1450-nm diode laser for facial inflammatory acne vulgaris: doseresponse and 12-month follow-up study. J Am Acad Dermatol 2006;55:80–7. 73. Bernstein EF. Lower-energy double-pass 1450 nm laser treatment of acne dramatically decreases discomfort with similar efficacy as compared to standard high-energy treatment. Abstract 104. American Society for Laser Medicine and Surgery Abstracts. 74. 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;30:147–51. 75. Astner S, Anderson R and Tsao S. 76. Glaich A, Friedman P, Jih M, et al. Treatment of inflammatory facial acne vulgaris with combination 595-nm pulsed-dye laser with dynamic-cooling-device and 1450nm diode laser. Lasers Surg Med 2005;Epub. May 2005. 77. Wang SQ, Counter JT, Flor Me and Zelickson BD. Treatment of inflammatory facial acne with the 1,450 nm diode laser alone versus microdermabrasion pluse the 1,450 nm laser: a randomized, split-face trial. Dermatol Surg 2006;32:249–55. 78. Lupton JR,William CM,Alster TS. Nonablative laser skin resurfacing using a 1540nm erbium glass laser: a clinical and histologic analysis. Dermatol Surg 2002;28:833–5. 79. 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. 80. 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.
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81. Kassir M, Newton D, Maris M et al. Er:glass (1.54 um) laser for the treatment of facial acne vulgaris. Lasers Surg Med 2004;34:S65. 82. Angel S, Boineau D, Dahan S, Mordon S. Treatment of active acne with an Er:Glass (1.54 um) laser: A 2-year follow-up study. Journal of Cosmetic and Laser Therapy 2006;8:171–6. 83. Ruiz-Esparza J, Gomez JB. Nonablative radiofrequency for active acne vulgaris: the use of deep dermal heat in the
treatment of moderate to severe active acne vulgaris (thermotherapy): a report of 22 patients. Dermatol Surg 2003;29:333–9. 84. Avram, DK and Fitzpatric RE. Treatment of active acne and acne scars with SmoothBeam (1,450 nm) and Thermage (radio frequency): A comparative study. ASLMS abstracts 56. 85. Retrieved from http://www.myzeno.com.
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8. Treatment of acne scarring Murad Alam and Greg Goodman
INTRODUCTION Optimal treatment of acne scarring is prevention of the same by aggressive treatment of active acne.1,2 Failing that, the treatment of acne scarring may require the sequential application of several corrective procedures. Even so, the degree of improvement is typically incomplete, as scar can be concealed but not removed.
DEFINITION AND CLASSIFICATION OF ACNE SCARS Before appropriate therapies can be selected, acne scarring needs to be qualitatively and quantitatively assessed.3,4 The simplest operational definition of acne scar is a visible textural abnormality that was historically preceded by active acne at the same site, and if biopsied, would reveal histological evidence of a scar. In practice, it may be difficult to confidently assert the provenance of a particular scar, since the active process – acne or something else – leading to its creation may be temporally remote.Yet there are typical configurations of scarring that are usually believed, based on visual inspection alone, to be highly likely to have been caused by acne. Acne scars can be classified based on shape and depth. One recently proposed classification recognizes three types of scars (Fig. 8.1):4 • ice-pick scars are V-shaped nicks with a pinpoint base that may culminate in the shallow papillary dermis or in the deep reticular dermis • boxcar scars are rectangular scars with vertical walls and a flat base, and these may also be shallow or deep
• rolling scars are gently undulating scars that resemble hills and valleys, are less well-demarcated, and tend to be less focally deep Alternatively, acne scars can be considered hypertrophic, atrophic, or a combination thereof:3,5 • grade 1 acne scarring is distinguished by erythematous, hypopigmented, or hyperpigmented macules (Fig. 8.2) • grade 2 is distinguished by mild atrophy or hypertrophy, similar to the rolling scars described previously • grade 3 is distinguished by moderate hypertrophy or atrophy that is visible at social distances of 50 cm or greater, and rolling and shallow box car scars, as well as moderate hypertrophic and keloidal scars • grade 4 is distinguished by severe atrophy or hypertrophy that cannot be flattened by stretching the skin between thumb and forefinger
Fig 8.1 Stylized cross-sectional view of ice-pick, rolling, shallow boxcar, and deep boxcar scars (from left to right).The upper horizontal dashed line denotes the normal depth of ablation with resurfacing procedures, the three lines in a pyramidal array represent fibrous bands securing the rolling scar to the dermal–subcutaneous junction. (Based on the acne classification popularized by Jacob, Dover, and Kaminer.)
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Fig 8.2 Postinflammatory hyperpigmented macules of the cheek after resolution of active acne.
The classification of acne scarring as a function of individual skin type is less well described. It is known that some individuals are more prone to develop scarring following resolution of acne papulopustules or cysts, whereas others may only have transient erosions or discoloration that eventually remits. In general, patients who have previously developed acne scarring remain at risk for further scarring following active acne in the future. Acne scarring of equivalent depth and type may also be more noticeable on patients with darker skin types or pigmentary abnormality. For instance, the light and shadow of darker skin may accentuate the apparent depressions associated with acne scarring; similarly, rosacea or centrofacial redness may demarcate and define the borders of acne scars on the cheeks.
AGE OF ACNE SCARS AND ACTIVE ACNE To some extent, the appropriate treatment for acne scars is predicated on their age. Specifically, if scars are red, a series of laser treatments with pulsed-dye laser or intense pulsed light may be especially useful for
reducing this blush if the scars are not more than a few years old.6,7 In cases when active acne has resolved during the past 6–12 months, caution should be exercised when approaching the treatment of scarring. It is possible that the superficial resolution of acne may not be indicative of a cessation of the deep process, and invasive procedures such as subcision or resurfacing may restimulate cyst formation. It is essential to adequately treat and inactivate all ongoing acne before treatment on any scarring can commence. The presence of active acne strongly militates against the treatment of any coexisting acne scars.These acne scars may either not be mature – and hence may be susceptible to exacerbation or inflammation – or mature themselves but their treatment may trigger nearby active acne. An in-depth consultation with the patient is required to convey this concern. It should be explained that the deferment of acne scar treatment does not indicate reluctance to treat acne scars or lack of expertise in such treatment; rather, the postponement is necessary because immediate treatment may worsen the combined adverse visual effect and symptomatology of the active acne and acne scarring. Active acne cysts may enlarge and drain, or become painful, and the active acne inflamed by manipulation may lead to further acne scarring. A final caveat entails the treatment of acne scarring in patients with pre-existing conditions that may lead to poor scar healing. Such conditions may be managed like acne scarring in the context of active acne: treatment of the scars may be delayed or embarked upon very gingerly so as to preclude inadvertent exacerbation. Most authorities suggest that invasive procedures for acne scarring be undertaken only 1 year after completion of oral isotretinoin treatment for resistant cystic acne. A complete history should elicit information about such treatment; the timing, type and degree of success associated with prior acne scarring improvement procedures; any tendency to produce keloids or hypertrophic scars after surgery or injury; any tendency to hyperpigment after injury; disorders, such as collagen vascular diseases, that impede wound healing; bleeding diatheses; disorders that predispose to infection; recurrent cold sores; allergies to antibiotics and medications; and psychological disorders, including depression, anxiety, factitial disorders (e.g., compulsive
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picking, self-mutilation, etc.) and medication for these. Picking behaviors are exceedingly common, especially in young women who have an obsessive need to ensure the perfection of their skin, and a consequent urge to extirpate pimples and textural abnormalities with their nails and other implements.The physician should carefully explain that picking after procedures to reduce acne scarring will worsen this scarring and be highly counterproductive. If the patient seems unable or unwilling to grasp this concept, or appears unlikely to to adhere to a postoperative regimen, expert consultation with a psychologist or psychiatrist is desirable prior to proceeding with surgery.
Lack of new acne lesions for a few weeks or 1–2 months does not necessarily presage a remission of active acne.This may simply be a cyclical or fortuitous reduction in acne that may not persist. If some degree of active acne remains persistent, continuing efforts to manage this should continue even as invasive treatments for acne scarring are commenced. Sometimes patients will continue to develop one or two small papules every few weeks even when on maximal therapy for acne.At some point, after treatment with topical and oral antibiotics and retinoids, the surgeon may have to decide to proceed with acne scarring treatment despite the occasional occurrence of active acne.
PATHOGENESIS OF ACNE SCARRING
TYPES OF TREATMENTS FOR ACNE SCARRING: RESURFACING, NONABLATIVE THERAPY, INCISIONAL SURGERY, INJECTION, CYTOTOXIC THERAPIES
The pathogenesis of acne scarring is too complex an issue to discuss fully here, but recent research indicates that intensity of scarring may be associated with the extent of inflammation associated with active acne. Specifically, the type and timing of the cell-mediated immune response may be associated with the degree of post-acne scarring.8 In one study, the cellular infiltrate and nonspecific immune response were initially greater but later reduced in patients who did not subsequently develop scars. However, in patients who did develop post-acne scarring, the initially smaller specific immune response later increased.
MANAGEMENT OF ACTIVE ACNE If the patient does have active acne, a brief discussion about treatment of acne scars should be followed by implementation of a plan to stop the production of new acne lesions. Treatment of active acne can take 12–18 months or more before a steady state of nearclearance is reached. If prior measures to control active acne have included the use of isotretinoin, a minimum of 12 months and as much as 18 months should elapse prior to treatment of acne scarring. Once patients understand that treatment of active acne is a necessary prerequisite for treatment of acne scarring, they may be more compliant with acne treatment than in the past.
The number and range of treatments for acne scarring is vast. Indeed, the options are so plentiful that even experienced practitioners need to group and classify therapeutic options to simplify decision-making. One grouping recognizes four major categories: • treatments for altering the color of the acne mark or scar • excisional and incisional surgery, including most punch techniques • augmentation by autologous and nonautologous methods • treatments for increasing or decreasing collagen deposition around the scar The last method, which includes nonablative, partially ablative, and ablative resurfacing by any means, subsumes the largest number of discrete interventions. Notably, since techniques within a given category are similar in terms of invasiveness, downtime, risk, and efficacy, practitioners may need to master only one or two treatments per category to provide patients with a complete range of therapeutic options. Finally, since even the most invasive acne scarring treatments in the hands of experienced physicians are unlikely to result
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in near-total resolution of scarring, a series of treatments that work synergistically should be selected. Some procedures are more risky and may be associated with delayed healing, and the practitioner should determine the level of risk preferred by the patient. In sum, for best outcomes, it is preferable to be (1) expert at a few procedures rather than to be passably familiar with a large number and (2) collaboratively with the patient, develop a rational, sequential treatment plan that cumulatively provides the best possible outcome. ‘Resurfacing’ denotes treatments that entail removal or destruction of the epidermis and partial-thickness dermis. Subsequent to resurfacing procedures, dermal and epidermal re-epithelialization occurs, usually over a period of 1–2 weeks. Post treatment, there is a reduction in acne scars that occurred in the skin strata that were resurfaced. Resurfacing is associated with risk of hypopigmentation and scar, which can occur if the depth of ablation reaches the bulge region of the hair follicle. Common resurfacing procedures can rely on thermal, chemical, or mechanical injury, and include laser ablation, medium to deep chemical peels, dermabrasion, and plasma resurfacing. ‘Nonablative’ therapies are those that do not fully deepithelialize the epidermis and dermis but rather deliver subdestructive energies that induce skin remodeling. Most commonly, nonablative therapies induce thermal injury by application of a range of laser and light sources, but other energy devices, such as bipolar and monopolar radiofrequency (RF), may be used. Between resurfacing and nonablative therapies are an intermediate set of treatments referred to as ‘partially ablative’ or ‘minimally ablative’. Typically, these create a penetrating epidermal and dermal injury only over a small percentage of the treated skin surface area. Downtime is consequently reduced over that of resurfacing, but efficacy may be better than for nonablative treatments. Common examples of partially ablative therapies are fractional resurfacing as well as skin needling and rolling. ‘Incisional surgery’ entails cutting into the skin, and may also include removal of skin, or excision. Pitting or ‘ice-pick’ scarring can be treated by punch excision, punch grafting, or punch elevation. Rolling scarring can be improved by subcision: minute cuts in the skin followed by abrasion of the underside of the dermis.
Large, mixed acne scarring in a linear array can be removed by standard elliptical excision. In some cases, the skin may be pierced but not cut as pre-packaged injectable fillers or autologous fillers are instilled under acne scars to raise them flush to the skin. ‘Injection’ therapy for acne scars has advanced since the introduction of a range of new soft-tissue augmentation materials over the past decade. Such materials include autologous fat, human collagen, hyaluronic acid derivatives, calcium hydroxyapatite, silicone, and other agents. Cytotoxic therapies may be most relevant for hypertrophic acne scars. Either medical or radiation therapies may be used to mitigate the growth of exuberant scars on the chest, face, and back. Intralesional agents such as 5-fluorouracil (5-Fu), bleomycin, and verapamil, topical agents such as imiquimod, as well as radiation treatment may help flatten scars.
ACNE SCAR TREATMENT BY RESURFACING Resurfacing is commonly accomplished by laser, chemical application, or dermabrasion. To some extent, the choice of procedure is a function of the age of the treating dermatologist, and prevailing fashions when he or she trained. Laser resurfacing remains a gold standard for safety in ablative resurfacing. In this procedure, a carbon dioxide (CO2), erbium : yttrium aluminum garnet (Er: YAG), or hybrid laser device is used to vaporize the epidermis and partial-thickness dermis.As a calibrated laser is used, tissue removal is precise, reproducible, and minimally operator-dependent; especially when a computerized pattern generator (CPG) is used, even and consistent skin removal is achieved.The CO2 laser provides the deepest injury, some immediate tissue contraction, hemostasis through its cauterizing effect, and the overall best clinical effect achievable by laser, but downtime with multiple-pass resurfacing can be 1–2 weeks. The Er:YAG laser is associated with less invasive ablation that is more suited to the treatment of fine acne scarring or photoaging, but downtime until complete re-epithelialization can be half as long. Since intraoperative bleeding can complicate and hence limit multiple-pass Er:YAG laser resurfacing, some
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Treatment of acne scarring hybrid devices include a small CO2 laser to facilitate coagulation; alternatively, a low-power and highpower Er:YAG laser can be paired in the same box for this purpose. Hybrid devices may also provide a clinical effect intermediate between classic Er:YAG and CO2 laser resurfacing. Using an Er:YAG laser after CO2 laser resurfacing can remove a thin layer of debris and devitalized tissue, and speed healing. Notably, post-treatment erythema after CO2 laser resurfacing can last 2–3 months, although it can be concealed with make-up. Outcome data indicate that most patients are very pleased with the outcome of their laser resurfacing procedure at 3 months post treatment, and remain so at 18 months; in the immediate postoperative period, the anxiety associated with wound-healing and temporary disfigurement causes mild, transient concern in some.9 In dermabrasion, the skin is smoothened by mechanical abrasion analogous to sanding. The skin is scraped away with a wire brush or a spinning disk-like burr covered with diamond particles; in some cases, true medium- or fine-grit sandpaper that has been autoclaved and wrapped around the finger or instrument like a thimble may be used to treat small areas. Dermabrasion has become less popular since the advent of HIV and other bloodborne infectious diseases that can be spread by aerosolized particles of skin and blood. Unlike laser resurfacing, dermabrasion is more operator-dependent, as the pressure applied can modify the depth of treatment.Acquiring and maintaining adequate anesthesia during dermabrasion can be challenging, and certain areas, including the eyelids, nose, malar prominence, and jawline, can be difficult to treat.There are no controlled studies comparing laser resurfacing with dermabrasion for acne scarring, but in the anecdotal experience of the authors, laser resurfacing appears to be more consistently efficacious. Dermabrasion may, however, be less prone to cause post-treatment erythema than laser resurfacing. Hypopigmented macules associated with acne scars (Fig. 8.3) have in some cases been reported to be improved following needle dermabrasion (using a tattoo gun without pigment) or focal manual dermabrasion.10,11 Medium and deep chemical peels are another resurfacing technique. Medium-depth peels typically consist of sponge application of trichloroacetic acid (TCA), 20–35%, after degreasing of the skin; sometimes, a
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Fig. 8.3 Hypopigmented cheek scars that are slightly atrophic.
prepeel with Jessner’s solution may be performed to improve even peel penetration. Depending on the duration of application and the number of layers of solution, a deeper or shallower effect can be achieved. The benefits of medium-depth peeling are that no expensive machinery, such as a laser, is required. Also, there is no aerosolization of infectious particles. At the same time, peels are relatively operator-dependent, and pooling of solution in facial crevices can result in uneven treatment from less experienced practitioners. In general, medium-depth peels provide a shallower ablation than CO2 laser resurfacing. Deep chemical peels, most notably the Baker–Gordon or phenol peel, are deeper-penetrating but carry two potential risks: (1) the potential cardiotoxicity of phenol requires intraoperative monitoring during full-face peeling; and (2) porcelain-white hypopigmentation will occur after treatment. For patients with focal acne scarring who always wear make-up, deep peels may be a safe option due to the small surface area treated and the ability to conceal depigmentation post-operatively. A special localized case occurs when a toothpick, or the sharp wooden end of a cotton-tip applicator created after the applicator has been deliberately broken, is dipped in a very concentrated solution of 95% or 100% TCA and then applied to the base of an icepick scar. This resurfaces the pinpoint base of the scar, and permits repair by granulation, which can fill in the scar.12
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A more recent variant of resurfacing is plasma resurfacing.This uses the ‘fourth state of matter’ to precisely injure epidermis and underlying dermis without inducing immediate sloughing of the epidermis. As such, plasma resurfacing has similarities to single-pass CO2 laser resurfacing. A plasma cloud of electrons removed by radiofrequency sparking of nitrogen gas is absorbed by the skin, but the epidermis is not truly ablated. In process, it seems to resemble a medium-strength TCA peel, but may give deeper and more impressive results, seemingly without much risk of hypopigmentation and scarring, although it is a comparatively new technique. The gentler approach, and the persistence of partially injured epidermis as a biological dressing, minimizes fluid loss, crusting, and delayed healing. Healing usually occurs within a week. There are some similarities regardless of the resurfacing technique used. Tumescent or local anesthetic, combined with nerve blocks and at least oral sedation, is usually employed. Beyond this, conscious sedation or general anesthetic may be used, especially for laser resurfacing. Post treatment, some method of dressing (either closed or open) is used to protect the deepithelialized skin as it heals. For at least 1 week, the patient cannot be present at work or social engagements. In darker-skinned patients, post-inflammatory hyperpigmentation is a virtual certainty; in Asian and African-American patients, such color change may last a year or longer before gradually resolving.The risk of infection is mitigated by initiating oral antibiotics and antivirals before the resurfacing procedure.
ACNE SCAR TREATMENT BY NONABLATIVE THERAPY During the past 5 years or so, nonablative therapy has largely replaced ablative therapy for the treatment of acne scars. In nonablative therapy, directed energy, usually thermal, is used to induce tissue modification and collagen remodeling in the dermis. The benefits compared with ablative therapy are that skin deepithelialization does not occur, and nonablative therapy is therefore a ‘lunchtime’ procedure that is associated with little or no downtime. Transient erythema and mild edema resolving over hours to days are often the only post-treatment effects. Since
nonablative therapy tends to be a milder procedure than ablation, multiple treatments may be required and/or these treatments may be combined with other acne treatment methods. Since heating of the dermis can induce remodeling of the dermis and improvement of embedded acne scars, a range of laser and light devices can be used. Indeed, virtually any laser or light device, used appropriately, can achieve modest improvement in acne scars.Among those that have been used in this capacity are the pulsed-dye laser, the potassium titanyl phosphate (KTP) laser, and intense-pulsed light. These are vascular-selective machines that, apart from improving surface topography, can also reduce the erythema that may encircle and hence accentuate acne scars of the central face. Multiple treatments, often 3–6 or more about a month apart, are needed to reduce redness and cause some textural change. A class of nonablative lasers has been especially successful at improving acne scars. These mid-infrared lasers include the 1064 nm neodymium (Nd):YAG,13 1320 nm Nd:YAG (Cool Touch),14–18 1450 nm diode (Smoothbeam),19 and 1540 nm Er:glass (Aramis), as well as intense-pulsed light machines with a similar range (Titan, 1100–1800 nm). Such devices have been shown in numerous studies to significantly improve rolling, boxcar, and ice-pick scars of the cheeks, perioral areas, and elsewhere.The main limitation is intraoperative discomfort, which may be sufficient to require topical and oral pain medications. In darker-skinned patients, the risk of postinflammatory hyperpigmentation is significant and may suggest the use of the 1540 nm device. Nonablative therapy can also be performed with RF devices, including those using monopolar and bipolar technologies. RF energy, in cadaver skin, can shrink the fibrous septae,20 and may also have collagen-remodeling effects.While it is typically used for tightening sagging facial or body skin rather than for rectification of acne scars, RF treatment, like treatment with broadband infrared light, may ameliorate acne scars. When acne scars are mild, textural abnormality may be minimal, and the primary visual feature may be a halo of erythema that highlights the scar. Such redness can be removed by a series of treatments with vascularselective lasers or light sources,21 such as the pulsed-dye laser, the KTP laser, and the intense-pulsed light device.
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Treatment of acne scarring Post-treatment effects are minimal erythema and edema, which resolve within a few hours to a day. Such treatments may be also appropriate for patients who desire a very minimal intervention, and can tolerate little or no downtime. Acne excoriée, which may be associated with erythematous macules, has also been successfully treated with vascular laser and psychotherapy.22 It is believed that erythematous acne scars can be treated even when they are immature, by pulsed-dye laser immediately after suture removal.23 Unlike erythematous macules, hyperpigmented and hypopigmented macules are better managed passively. Q-switched lasers for pigment and tattoos are minimally effective in reducing post-inflammatory hyperpigmentation, and may even exacerabate such pigmentation at high fluences;24,25 gentle nonablative glycolic acid, salicylic acid, Jessner’s solution, and retinoic acid peels may be less prone to aggravate brown areas.26,27 In general, pigmentation of scars in olive-skinned patients will fade gradually over 3–18 months, if strict sun avoidance and sun protection are practiced in association with a topical preparation, such as hydroquinone, kojic acid, and azelaic acid.28,29 White macules may be very difficult to treat, and may only be transiently repigmented with repeated treatments with the 308-nm excimer laser, phototherapy, or application of autologous cultured melanocytes. Microdermabrasion, a topical therapy that entails spraying of aluminum oxide crystals on the epidermis, is popular and frequently touted as beneficial for acne scarring.30 However, objective evidence of the efficacy of microdermabrasion for treatment of acne scarring is minimal. What little improvement can be achieved appears to require repeated, intense sessions and the elicitation of pinpoint bleeding, which is seldom induced. Microdermabrasion should not be confused with dermabrasion, a highly effective ablative therapy for acne scars.
ACNE SCAR TREATMENT BY PARTIALLY ABLATIVE THERAPY For treatment of acne scars, resurfacing provides maximal improvement and nonablative therapy offers the promise of convenience and safety. To wed these two desirable outcomes in a single therapy, so-called ‘partially ablative’ treatments have been devised. These
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methods are used to resurface only a portion of the skin area treated, thus allowing maintenance of skin integrity, fewer side-effects, and more rapid healing. One pioneering method of partially ablative therapy is fractional resurfacing. Using a diode-pumped 1550 nm erbium laser, fractional resurfacing (Fraxel, Reliant Technologies, Mountain View, CA) creates a grid pattern of microthermal zones of tissue coagulation but an intact stratum corneum.31,32 Over a period of days after treatment, microscopic epidermal and dermal necrotic debris is expelled, and collagen remodeling occurs at the affected areas. A series of treatments can resurface virtually the entire surface area, but by fractionating treatments, downtime is minimized and the serous crusting of typical resurfacing is avoided. It has been shown that high-energy treatments are more effective for the treatment of acne scarring; such treatments do not ablate more surface area, but provide a greater volume of thermal injury. A simpler, less precise approach to partially ablative therapy is skin rolling or needling. These procedures purport to achieve on a macroscopic level what fractional resurfacing can do on a microscopic level. In needling,11 a fine 30-gauge needle held by a hemostat is used to serially puncture a 2–3 mm deep grid pattern on the skin, including epidermis and dermis. Fibrous bands holding down acne scars are released, and the coagulum resulting from the pinpoint intradermal bleeding can raise depressed scars and instigate granulation tissue. For larger scars, a tattoo gun without pigment11 or a rolling pin may be used. Rolling is performed with a needle-studded rolling pin33 – a metal cylinder implanted with needle-like protrusions – that is pressed against the facial or extrafacial skin and rotated around the long axis to make an array of microperforations until some bruising is observed. In both rolling and needling, pinpoint bleeding occurs and is managed by application of pressure. Epidermal healing occurs with minimal crusting in a few days, and dermal trauma culminates in collagen remodeling. This process, also referred to as ‘collagen induction therapy’ can be repeated a few weeks later.Anatomical areas that respond poorly to this treatment include the nose and periorbital regions. Synergies may accrue if rolling is used in combination with other treatments, such as nonablative laser, vascular laser, subcision, or blood transfer.
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a
Fig. 8.4 Rolling scars amenable to subcision can occur periorally, on the upper and lower cheeks, and at the temples. Subcision can also be highly effective for nasal scars (not shown).
b
ACNE SCAR TREATMENT BY INCISIONAL SURGERY Apart from ablative, partially ablative, and nonablative external smoothening techniques, cutting surgery can be used to treat acne scars. One minimally invasive surgical technique for rolling scars is subcision, which is preceded by instillation at the site of scarring of anesthesia – local for small areas and tumescent for larger areas. Developed by Norman and David Orentreich,34,35 subcision (Figs. 8.4 and 8.5) requires insertion of an 18–26-gauge Nokor or similar needle, or even a blunt canula, into the superficial subcutis. Depth of insertion is contingent on the degree of scar indentation, with intradermal positioning more appropriate for shallow scars and deep dermal placement for deeper scars. The needle is then rotated so that the spearlike tip is parallel to the skin, and the needle is used to tent the skin. Back-and-forth rasping movement of the needle along the underside of the dermis releases fibrous attachments holding down scars and stimulates the growth of reactive fibrosis that gradually fills the deadspace underlying newly loosened scars. In a manner similar to liposuction, fanning movement of the needle and triangulation of each scar from different entry sites helps elevate scars. Especially if widespread treatment is being performed, intraoperative bruising and bleeding is minimized by using tumescent
Fig. 8.5 (a) In subcision, the rasping needle is used to release the fibrous bands connecting rolling scars to the deep skin structures. (b) Simultaneous tenting of the skin with the needle minimizes the risk of injury to neurovascular structures. anesthesia, or copious quantities of a dilute 0.5% lidocaine with 1:200 000 solution, and allowing the anesthesia to sit for 20–30 minutes before commencing
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Table 8.1 Common fillers for acne scarring (USA) Filler type Human-derived Autologous
Heterologous Non-human-derived Temporary
Permanent
Filler name
Method of use
Persistence
Blood aspirate Fat
Can be injected deep or superficially Injected deep for rolling scars
Human collagen
Fine superficial scars, or layering in dermis
Weeks to months Weeks to months, portion of effect may be permanent 2–3 months
Hyaluronic acid Calcium hydroxyapatite Liquid silicone
Versatile, for deep and medium injection Deep, for rolling scars (off-label)
6–9 months 1 year
Rolling scars (not FDA-approved)
Many years
needle insertion. Postoperative ecchymoses and edema can last 1–3 weeks.To avoid a flare of cystic acne after treatment, susceptible patients with some active acne may be treated with oral tetracyclines for several weeks before and after subcision. Individual deep boxcar or ice-pick scars can be resistant to nonsurgical treatment. At times, the best approach can be to cut these out. A time-honored technique uses a biopsy punch to treat such scars. If the targeted scar fits precisely within the punch, circumferential cutting with the punch can cause elevation of the scar as lateral and deep fibrous bands are severed and the plug containing the scar spontaneously elevates.This is referred to as punch elevation. Alternatively, if the scar is very deep and well embedded, the central plug may be removed, as in the case of a punch biopsy.Then the created defect may either be sewn end-to-end, to create a slit-like scar (i.e., punch excision), or filled with a similar shaped plug harvested from an uninvolved scar (i.e., punch grafting). At times, a series of deep scars may be present in a linear or curvilinear array. Such scars may be revised by removal of a strip of epidermis and dermis using the techniques of elliptical excision and bilayered closure with eversion. If a patient requires punch or linear excision as well as resurfacing for treatment of acne scars, it is preferable to perform the excisions first, as the re-epithelialization following the ablative procedure will conceal the excision lines. Perifollicular hypopigmentation of acne scars, especially those of the trunk, remains highly resistant to treatment. If papular and facial, hypopigmented scars
may be treated with fine-needle diathermy, and grafting procedures useful in vitiligo may also be considered. Minigrafting is limited in efficacy, since the spread in pigment from the graft sites to the surrounding scars appears to be restricted,36,37 but epidermal suspensions of cultured and noncultured cells are promising new therapies. Newly available automated commercial kits for trypsin epidermal separation (ReCell) may simplify the grafting process.37,38
ACNE SCAR TREATMENT BY FILLERS Filler injection is a minimally invasive method of scar improvement that can be combined with other treatments. Also known as soft-tissue augmentation materials, fillers can be autologous, heterologous, or synthetic; additionally, they can be prepackaged or harvested prior to use. Until the 21st century, the primary Food and Drug Administration (FDA)-approved prepackaged augmentation material was bovine collagen. Since then, human-derived collagen (Cosmoderm and Cosmoplast), hyaluronic acid derivatives (Restylane, Juvederm, Hylaform, Hylaform Plus, and Captique), calcium hydroxyapatite (Radiesse – pending FDA approval, used off-label), and liquid silicone (used off-label)39 have been used frequently (Table 8.1). While bovine collagen required skin testing to exclude allergy, none of the newer fillers do, although they should not be used in patients with known sensitivity to their
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ZYDERM I ZYDERM II
ZYPLAST
Fig. 8.6 The depth of injection of filler agents is contingent on their viscosity and duration of action, with thicker, longer-lasting materials injected at the dermal–subcutaneous junction (lower arrow), and finer materials like collagens injected higher. constituents. In terms of persistence of action, silicone is near-permanent; calcium hydroxyapatite has a longevity of 1–1.5 years, hyaluronic acid derivatives of 6–9 months, and collagens of 2–3 months. Longerlasting fillers are injected deeper (Fig. 8.6), at the dermal–subcutaneous junction, for correction of deeper acne scars. Liquid silicone must be injected in very small aliquots, using the ‘microdroplet’ technique, to minimize the risk of a delayed immune response. Unless silicone is being used, patients should be advised that the correction provided by fillers is temporary.The first time a filler is used, a short-acting one like collagen or hyaluronic acid should be considered, because it is important to establish that the cosmetic effect is appropriate before this is made longstanding with a more persistent filler. In general, fillers are more successful for improvement of rolling scars rather than bound-down ice-pick or boxcar scars. If rolling scars are being treated, subcision may precede use of fillers.The subcised scars are more mobile and likely to float up after injection of filler material into their bases. Not all fillers are prepackaged. Autologous fillers that can be harvested before injection include blood and fat. Blood can be removed via blood draw and then injected deep into atrophic or depressed acne scars.40 Injection can be repeated at monthly intervals, and can result in raising of the scar both by direct volume
effect and by initiation of a wound-healing cascade that causes reactive fibrosis. For fine, shallow acne scars, injection of blood can be performed using a 1ml syringe and 30-gauge needle to raise a bruised bleb high in the dermis; this can be combined with postinjection vascular laser treatment at approximately 50–75% the normal fluence to activate the hemoglobin chromophore and thus facilitate scar involution while reducing redness. Laser treatments may be repeated at monthly intervals. Another autologous filler is fat.41 Autologous fat can be harvested from the abdomen or hips and then injected via a fine cannula into an area of depressed rolling scars. Excess fat can be frozen for later use, although defrosted cells are not viable but rather serve as a biocompatible filler. Fat transfer with fresh fat can provide some permanent correction, with a fraction of the implanted cells continuing to thrive at the recipient site. Current research indicates that use of adult adipose-derived stem cells can augment the effect of fat transfer. The degree of fat transfer correction, and its persistence, is paradoxically inversely related to the quantity of fat transplanted: filling the defect area to turgidity can reduce fat survival by impairing vascular supply to the living cells. Like blood injection, fat transplantation can be repeated. Unlike blood transfer, fat transfer is inappropriate for shallow superficial scars.
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a
a
b
b
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Fig. 8.7 Lower cheek, chin, and perioral acne scarring before (a) and after (b) fat transfer, subcision, and laser resurfacing.
Fig. 8.8 Chin and jawline area scarring (a) that is diminished after skin rolling and subcision (b).
TREATMENT OF HYPERTROPHIC ACNE SCARS
of 2.5 mg/ml, with 0.5–2 ml per scar.48 Topical imiquimod49 may be an adjunctive prophylactic treatment applied at the surgical site immediately after surgical keloid excision, but treatment efficacy has not been consistently seen. Radiation therapy can successfully shrink keloids; however, in younger patients, and at head and neck sites, the associated long-term risks can preempt this approach.
Acne scars, particularly of the chest and back, can become hypertrophic, and rarely keloidal. Management of such scars is similar to that of hypertrophic scars caused by other phenomena. Recently, it has become evident that intralesional injection of cytotoxic agents may induce remission of selected hypertrophic scars.42,43 Cytotoxic agents may be an alternative to the treatment of hypertrophic and keloidal scars with highstrength intralesional corticosteroids.44–47 5-Fu at a concentration of 50 mg/ml may be combined in an 80:20 ratio with a low-potency intralesional steroid solution. A typical scar is filled with 0.1–0.3 ml of this mixture, and a total of about 1 ml used per injection session. Intralesional verapamil has also been reported to be of some utility when injected at a concentration
CONCLUSIONS Treatment of acne scarring, itself a complex problem, requires a well-organized plan, a willing patient, and a skilled physician. Usually a range of techniques, including more or less ablative resurfacing, surgery, and injection, are required (Figs 8.7 and 8.8). Scarring cannot be entirely erased, and treatment of scarring in a field of active acne can exacerbate the latter; for this
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reason, the best treatment of acne scarring remains the prevention of active acne.
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treatment of acne scarring and photoaging. Dermatol Surg 2006;32:346–52. 15. Bellew SG, Lee C,Weiss MA,Weiss RA. Improvement of atrophic acne scars with a 1320 nm Nd:YAG laser: retrospective study. Dermatol Surg 2005;31:1218–22. 16. Fulchiero GJ Jr., Parham-Vetter PC, Obagi S. Subcision and 1320-nm Nd:YAG nonablative laser resurfacing for the treatment of acne scars: a simultaneous split-face single patient trial. Dermatol Surg 2004;30:1356–9. 17. Sadick NS, Schecter AK. A preliminary study of utilization of the 1320-nm Nd:YAG laser for the treatment of acne scarring. Dermatol Surg 2004;30:995–1000. 18. 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 histologic study. Dermatol Surg 2004;30:152–7. 19. Chan HH, Lam LK,Wong DS, Kono T,Trendell-Smith N. Use of a 1,320 nm Nd:YAG laser for wrinkle reduction and the treatment of atrophic acne scarring in Asians. Lasers Surg Med 2004;34:98–103. 20. Abraham MT, Ross EV. Current concepts in nonablative radiofrequency rejuvenation of the lower face and neck. Facial Plast Surg 2005;21:65–73. 21. 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. 22. Bowes LE, Alster TS. Treatment of facial scarring and ulceration resulting from acne excorie with 585-nm pulsed dye laser irradiation and cognitive psychotherapy. Dermatol Surg 2004;30:934–8. 23. Nouri K, Jimenez GP, Harrison-Balestra C, Elgart GW. 585-nm pulsed-dye laser in the treatment of surgical scars starting on the suture removal day. Dermatol Surg 2003;29:65–73. 24. Bekhor PS.The role of pulsed laser in the management of cosmetically significant pigmented lesions. Australas J Dermatol 1995;36:221–3. 25. Chan H.The use of lasers and intense pulsed light sources for the treatment of acquired pigmentary lesions in Asians. J Cosmet Laser Ther 2003;5:198–200. 26. Cuce LC, Bertino MC, Scattone L, Birkenhauer MC. Tretinoin peeling. Dermatol Surg 2001;27:12–14. 27. Wang CM, Huang CL, Hu CT, Chan HL. The effect of glycolic acid on the treatment of acne in Asian skin. Dermatol Surg 1997;23:23–9. 28. Stratigos AJ, Katsambas AD. Optimal management of recalcitrant disorders of hyperpigmentation in darkskinned patients. Am J Clin Dermatol 2004;5:161–8. 29. Goldman MP. The use of hydroquinone with facial laser resurfacing. J Cutan Laser Ther 2000;2:73–7. 30. Tsai RY, Wang CN, Chan HL. Aluminum oxide crystal microdermabrasion. A new technique for treating facial scarring. Dermatol Surg 1995;21:539–42.
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Treatment of acne scarring 31. Rahman Z, Alam M, Dover JS. Fractional laser treatment for pigmentation and texture improvement. Skin Ther Lett 2006;11:7–11. 32. Geronemus RG. Fractional photothermolysis: current and future applications. Lasers Surg Med 2006;38: 169–76. 33. Fernandes, D. Skin needling as an alternative to laser. Paper delivered at IPRAS, San Francisco, 1999. 34. Orentreich DS, Orentreich N. Subcutaneous incisionless (subcision) surgery for the correction of depressed scars and wrinkles. Dermatol Surg 1995;21:543–9. 35. Alam M, Omura N, Kaminer MS. Subcision for acne scarring: technique and outcomes in 40 patients. Dermatol Surg 2005;31:310–17. 36. Boersma BR, Westerhof W, Bos JD. Repigmentation in vitiligo vulgaris by autologous minigrafting: results in nineteen patients J Am Acad Dermatol 1995;33:990–5. 37. Falabella R, Arrunategui A, Barona MI, Alzate A. The minigrafting test for vitiligo: detection of stable lesions for melanocyte transplantation J Am Acad Dermatol 1995; 33:1061–2. 38. Olsson MJ, Juhlin L. Long-term follow-up of leucoderma patients treated with transplants of autologous cultured melanocytes, ultrathin epidermal sheets and basal cell layer suspension. Br J Dermatol 2002;147:893–904. 39. Barnett JG, Barnett CR.Treatment of acne scars with liquid silicone injections: 30-year perspective. Dermatol Surg 2005;31:1542–9. 40. Goodman GJ. Blood transfer: the use of autologous blood as a chromophore and tissue augmentation agent. Dermatol Surg 2001;27:857–62.
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41. Goodman, GJ. Autologous fat transfer and dermal grafting for the correction of facial scars. In: Harahap M, ed. Surgical Techniques for Cutaneous Scar Revision. New York: Marcel Dekker, 2000:311–49. 42. Meier K, Nanney LB. Emerging new drugs for scar reduction. Expert Opin Emerg Drugs 2006;11:39–47. 43. Saray Y, Gulec AT.Treatment of keloids and hypertrophic scars with dermojet injections of bleomycin: a preliminary study. Int J Dermatol 2005;44:777–81. 44. Lebwohl M. From the literature: intralesional 5-FU in the treatment of hypertrophic scars and keloids: clinical experience. J Am Acad Dermatol 2000;42:677. 45. Uppal RS, Khan U, Kakar S, Talas G, Chapman P, McGrouther AD. The effects of a single dose of 5-fluorouracil on keloid scars: a clinical trial of timed wound irrigation after extralesional excision. Plast Reconstr Surg 2001;108:1218–24. 46. Bodokh I, Brun P. Treatment of keloid with intralesional bleomycin. Ann Dermatol Venereol 1996;123:791–4. 47. Espana A, Solano T, Quintanilla E. Bleomycin in the treatment of keloids and hypertrophic scars by multiple needle punctures. Dermatol Surg 2001;27:23–7. 48. Copcu E, Sivrioglu N, Oztan Y. Combination of surgery and intralesional verapamil injection in the treatment of the keloid. J Burn Care Rehabil 2004;25:1–7. 49. Berman B,Villa A. Imiquimod 5% cream for keloid management. Dermatol Surg. 2003;29:1050–1.
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9. Nonsurgical tightening Edgar F Fincher
INTRODUCTION During the natural course of aging, the face undergoes a series of predictable changes. The skin loses its elasticity through a loss of integrity of both collagen and elastin fibers in the dermis, resulting in visible static rhytids and deeper furrows. Furthermore, a loss of adipose tissue, most notably in the midface, leads to volumetric depletion of the underlying soft tissue support of the facial skin. The result of these two changes is a gravitational descent of the facial tissues that contributes to hollowing of the cheeks, descent of the malar fat pads, and deepening of the nasojugal, malar–palpebral, and nasolabial folds.This can be further compounded by the effects of exposure to ultraviolet radiation, which is known to accelerate the aging process by promoting elastolysis, collagenolysis, and dyschromia. An increased number of patients are seeking consultation for treatment options in an effort to reverse many of these visible signs of aging. Our population is becoming more concerned with its appearance and is becoming more proactive in seeking out procedures that will reverse the aging process. Furthermore, the general trend continues to be for patients seeking less invasive procedures with less downtime. In the past, cervicofacial rhytidectomy, deep chemical peels, or full-face laser resurfacing1,2 were the only options for achieving significant rejuvenation. These procedures delivered excellent results; however, these results came at the cost of significant downtime. Over the past 3–4 years, several new devices have arrived on the market providing alternatives to traditional skin tightening procedures. These newer devices utilize volumetric heating of the dermis, through either radiofrequency
or near-infrared energy, as a non-ablative method to tighten the skin.The physiological basis of the effect is a result of the effects of the heating upon collagen fibers in the dermis. Collagen fibers are triple-helix protein chains, which denature and become an amorphous, random-coil structure upon heating.3 This results in shortening of both the length and diameter of collagen fibrils. Ross et al4 have suggested that after collagen shortening, fibroblasts in the heated region begin the synthesis of new collagen fibers, resulting in tissue remodeling at the cellular level, and skin tightening at the cosmetic level. Currently, there are two significant noninvasive skin tightening devices available on the market. Other devices are available and others are soon to be released; however, none of these has demonstrated reliable results. The first device, the ThermaCool TC, utilizes radiofrequency (RF) energy to heat the dermis and create skin tightening, while the second device, the Titan, uses near-infrared light to achieve the same end. These procedures deliver safe and effective skin tightening with the promise of no downtime. Although the overall results are variable and may be only modest, many patients with only early signs of aging, or those with active lifestyles or busy careers, will often opt for a lesser procedure in exchange for less downtime. For those patients who suffer from extensive skin laxity on deep rhytides or who desire maximal rejuvenation, rhytidectomy and laser resurfacing continue to be the gold standards by which all procedures are compared. Careful patient selection and counseling and establishing appropriate expectations become extremely important when determining the appropriate procedure for the patient.
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MONOPOLAR RADIOFREQUENCY
Treatment Parameters
Background
The use of the ThermaCool TC as a deep-tissue tightening procedure enables patients to experience a safe and effective treatment for mild to moderate skin laxities. Its benefits include a quick recovery period and an excellent safety profile. The major drawback of the procedure, however, is the discomfort experienced by some patients undergoing treatment. Thermal energy can lead to sensations of deep heat, burning, or a sharp stabbing pain. These can often be minimized with the use of topical anesthetics or oral analgesics; however, the use of complete sedation or anesthesia is not recommended as it prevents any patient feedback, which is an important safety measure of this device. Recommendations are for physician operators to adjust energy levels based upon patient feedback. The maximal treatment parameter should be set to a point where the patient experiences moderate, but comfortable, heating. Pain, discomfort, or intense heating should not be allowed, as this lowers the threshold for overheating, burns, or deep-fat atrophy. Current protocols involve performing multiple passes (three to five) at low to moderate fluences instead of the previously recommended single-pass high-fluence protocol. Studies have demonstrated that this multiple-pass lower-fluence protocol provides equivalent collagen contraction and skin tightening as the single-pass high-fluence treatment. The current protocol utilized in our office includes two complete passes at maximal fluence across the entire treatment area. Maximal fluence, in this case, is defined as the highest setting that the patient can comfortably tolerate. We ask the patient to report discomfort on a scale of 1–10, where maximal tolerability means 6–7. The majority of these pulses will elicit only minimal discomfort; however, several areas, such as the malar prominence, the preauricular region, along the mandible, over the sternocleidomastoid, and the supraorbital areas, are reliably the most painful areas to treat, and a decreased fluence or only a limited number of passes may be used in these areas if discomfort is high. Once the two complete passes have been achieved, an additional three or four focal passes are performed along key
Approved by the US Food and Drug Administration (FDA) in the spring of 2003 to elevate the brow, ThermaCool TC (Thermage Inc., Hayward, CA) has been used in a number of different applications to reduce skin laxity in the face and upper neck. The ThermaCool TC is now FDA-approved for treating rhytids on all areas of the body. It works by delivering a safe, alternating-current monopolar RF signal in a nonablative, uniform fashion to tissues. Operating at a frequency of 6 MHz, the ThermaCool TC generates heat in the underlying skin tissues by virtue of resistance (impedance).The amount of resistance will vary depending upon the tissue composition, and studies have shown that the higher tissue resistance, and thus the major thermal effect, is in the dermis and subcutaneous layers. To prevent injury to the epidermis, a direct-contact dynamic cryogen cooling system is incorporated into the handpiece to ensure uniform constant cooling throughout the treatment period.The depth of effect of the ThermaCool TC depends on the geometric size of the treatment tip, while the degree of the effect depends on the conductive properties of the tissue. With the standard medium-depth 1.5 and 3.0 cm2 tips, approximately 60–70% of the energy is delivered to the dermis at a depth of around 2–2.5 mm. The remaining 30% dissipates throughout the surrounding and deeper tissues, providing significant heating at depths of around 4–5 mm. Tissues possessing a higher impedence, such as fat, tend to generate a greater degree of heat, resulting in a deeptissue thermal effect.5,6 A second factor in understanding the clinical effects of the ThermaCool TC is the effect on the fibrous septae within the fat compartment. Studies have demonstrated that a large amount of the RF energy is dissipated or channeled through the fibrous septae that separate the fat compartments. This effect leads to heating of these fibrous bands and their subsequent shrinkage to further contribute to the overall skin tightening effect. Monopolar RF therefore provides not only dermal heating and tightening, but also deep tissue effects that contribute an additive effect to the global skin contraction.
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tightening points. These areas typically include the skin overlying the lateral malar area and zygoma, lateral to the nasolabial fold, and along the mandible. These passes continue until visible tissue tightening is observed (Fig. 9.1).
Clinical effects
Fig. 9.1 This patient was being assessed midway through her treatment. She had undergone two complete passes followed by three focal passes to the left side of the face only. Signs of immediate skin tightening are evident as softening of the nasolabial fold, slight elevation of the malar fat pad, and softening of the jowl.
a
The data compiled from research thus far suggest that this novel RF device provides a safe and effective technique to tighten the skin of the face and upper neck 6–13 (Fig. 9.2). The tissue tightening effects of the Therma Cool TC have also been analyzed in split-face studies, providing direct comparisons between control and experimental treatments in the same patients. This objective, split-face study determined that RF treatment resulted in remarkable improvements in brow position, superior palpebral crease, angle of the eyebrow, and jowl surface area.12 After a single treatment, patients on average exhibited 4.3 mm of brow elevation, 1.9 mm of superior palpebral crease elevation along the midpupillary line, and 2.4 mm of brow
b
Fig. 9.2 A patient before (a) and 3 months after (b) monopolar radiofrequency (ThermaCool TC) treatment to her entire face. Although results are often difficult to appreciate using standard two-dimensional photography, careful examination shows moderate improvement along the nasolabial fold and mandibular line.
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elevation along the lateral canthal line. In addition, the peak angle of the eyebrow became more acute by an average of 4.5°, and there was a mean decrease of 22.6% in the surface area of the jowls.12 Especially noteworthy is that these results were achieved without significant downtime or serious side-effects. An important issue with this device is that it is well recognized that there is some variability in the expected response from patient to patient, with some patients showing only limited improvement. Several studies have been published analyzing criteria for determining which patients are most likely to respond to treatment. In a group of patients evaluated over a 6month period following treatment, it was determined that there was improvement in submandibular and upper neck skin laxity in 17 out of 20 patients. Subjects who did not respond to treatment were found to be older than 62 years.9 This age-dependent response was also supported in a study by Hsu and Kaminer,6 who performed a single RF treatment in the lower face and neck of 16 patients. It was found that younger patients responded better to RF treatment, with the average age of patients not showing satisfactory outcomes from the treatment being 58, compared with 51 in the group of patients showing clinical improvement. The ineffectiveness of the procedure on older patients can theoretically be attributed to the fact that collagen bonds are replaced by irreducible multivalent crosslinks with age. This renders the functional basis of RF tissue tightening ineffective, as the thermal injury caused by RF treatment cannot break collagen bonds held together by multivalent crosslinks. The deep tissue tightening effects after RF treatment, coupled with the low side-effect profile and noninvasive techniques, makes the ThermaCool TC a safe and effective alternative to surgery in patients with mild to moderate skin laxity. Further studies on RF treatment still have to be carried out, however, as the duration of tightening in treated patients has yet to be determined.
Side-effects and limitations The ThermaCool TC device has been on the market for over 3 years at the time of writing. Over that
period of time, it has demonstrated an extremely safe track record. The evolution of the device has included multiple safety updates to the equipment, including the addition of multiple thermal sensors on the treatment tip in order to constantly monitor and adjust epidermal temperature, an enhanced dynamic cooling system to also maintain safe parameters, and modifications to the recommended treatment energies and profiles. RF tissue tightening can also result in temporary side-effects, such as focal erythema, edema, skin tenderness, mild burns, and rare dysesthesia.6–12 Generally, these effects last only a few hours, but have been reported to persist for several days to over a week. The complication of treatment with the ThermaCool TC giving rise to the greatest concern was the rare occurance of focal fat atrophy. Early in the course of the history of the ThermaCool TC, there were several cases of permanent fat atrophy that occurred following treatment. Although these cases were few and restricted to a small number of users, these permanent alterations created a great deal of concern about the safety of this device. Further investigation revealed that these complications were the effects of excessively high energy delivered to areas of high fat content. The net effect of short-pulse high-energy RF energy was necrosis or melting of the underlying fat, with residual permanent defects. The treatment protocols were subsequently modified to ensure that treatments were conducted well within safe limits. The current protocols described above include multiple-pass low to moderate energy levels to achieve the desired effect. Other potential side-effects include the risk of scarring or temporary blisters. The actual incidence of these effects is extremely low when protocols and treatment techniques are followed. If a blister occurs, it is generally very superficial and can be successfully managed by treatment with moist occlusion, with an anticipated recovery time of around 1 week. The biggest attraction of this device, unlike many other technologies available these days, is that it truly meets the zero-downtime claim. Any sort of side-effect is extremely rare, and the vast majority of patients will immediately return to their daily activities without interruption.
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Newer applications and additional uses New treatment protocols are being developed for off-face and eyelid applications with the ThermaCool TC. A new 0.25 cm2 tip is available for treating the upper eyelid. This is intended for use in patients with early blepharochalasis. This ‘eye-tip’ has a different energy profile than the standard 1.5 or 3.0 cm2 medium-depth tips.The heating profile of the ‘eye-tip’ is more superficial, and it is thus appropriate for the thin skin of the upper eyelid. Again, a multiple-pass low-energy treatment protocol is used for the upper eyelid. Appropriate patients for eyelid treatment are young patients with early eyelid laxity. Patients with fat herniation or excessive skin redundancy are better served by surgical blepharoplasty. ‘Tummy by Thermage’ is the latest treatment protocol to be announced by the Thermage Corporation. Although many users have been performing treatments to the abdomen, arms, and legs for years, this new protocol is the first to be approved by the company. This protocol also uses the 3.0 cm2 mediumdepth tips in a multiple-pass low-energy treatment protocol. Fluences are adjusted based upon patient comfort levels, and typically range from 352.0 to 354.5. A new variation in treatment technique is what sets this protocol apart from previous ones. The abdominal treatments are performed using the temporary marking grids; however, the pulses are delivered in a staggered partially overlapped protocol.The operator alternates between squares and circles to provide a 25% overlap. This stacking or partial stacking of pulses prolongs the thermal profile to provide enhanced skin tightening. The ability to stack or partially overlap pulses also raises the question whether similar applications on the face or neck can safely provide greater skin tightening in these areas. The use of RF energy in combination with tumescent liposuction is another area of potential application. Although this treatment combination is not recommended by the Thermage Corporation due to an uncertainty in RF energy distribution through partially undermined or tumesced tissues, many operators have empirically reported enhanced outcomes with this combination. In our practice, we
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routinely utilize this approach with cervicomental liposuction and have performed a limited number of abdominal cases to achieve maximal skin contraction. It must be stressed that there is no patient feedback under tumescent anesthesia and that this procedure should only be performed by experienced operators with fluence settings that are well within the usual and safe limits.
NEAR-INFRARED SKIN TIGHTENING Background A newer device for noninvasive skin tightening is the Titan by Cutera (Cutera, Inc., Brisbane, CA). Currently, the Titan is FDA-approved for dermal heating and is used in an off-label application for cosmetic treatments. The Titan produces dermal heating through the emission of near-infrared light between 1100 and 1800 nm. This near-infrared spectrum of light has water as the target chromophore, thus in turn causing heating of the dermal tissue to a depth of 1–2 mm. Similar to RF tissue tightening, the ultimate effect of dermal heating is thermal modification, leading to secondary collagen synthesis and remodeling of skin tissue. The major difference between these two devices is the thermal profile. As previously mentioned, the monopolar Rf device (ThermaCool TC) focuses the majority of its energy at a depth of approximately 2 mm; however, there is still deeper penetration of approximately 30% of the energy to depths of around 4–5 mm. Furthermore, the RF energy dissipates through other structures such as the fibrous septae that may also contribute to tissue tightening. The Titan device deposits its energy in a very discrete area around 1–2 mm, with little deeper diffusion, thus providing focused tissue heating in the dermis. The Titan XL handpiece has a large spot size (1 cm × 3 cm), and can emit pulses of light up to 8.1 s, making it the only infrared light of its kind. As with RF tissue tightening devices, contact heating of the skin would normally cause damage to the epidermis. As a result, the Titan employs a pre-, parallel, and post-contact cooling system through a sapphire window, providing epidermal protection. Contact
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cooling is employed in combination with a surface gel. The use of refrigerated gel is highly recommended to provide additional cooling, epidermal protection, and nhanced patient comfort. Controlled clinical trials that objectively examine the effects of the Titan are, as yet, unpublished. However, two papers have provided some preliminary evidence that are worth mentioning. In the first, Ruiz-Esparza et al14 reported on a series of 25 patients treated with the Titan for eyebrow lifting only, eyebrow lifting in addition to cheek and neck skin laxity, and lower face only. The shortcomings of this paper were that there was no objective measurement of clinical changes nor was there standardization of the treatment parameters. Patients received a wide range of energy settings, with a large variation in the number of total pulses, and a few patients even received multiple treatment sessions. The results from the series showed that 22 out of 25 patients displayed improvement in at least one of the treated areas. The three patients who did not respond at any treatment site had no similar differences in age, sex, or skin type. In addition, the series also compared the effects of low fluence versus high fluence on the clinical outcome. Patients were divided into two subgroups: the first group of patients received low-fluence (20–25 J/cm2) treatments and less than 150 total pulses. The second subgroup received higher-fluence treatments (≥30 J/cm2) and a higher number of total pulses (150–360). The results demonstrated that although the lower-fluence subgroup experienced significantly less discomfort, they showed relatively little or no response to the treatment. In contrast, groups receiving higher fluences produced beneficial results.14 Side-effects reported in this series included three patients who experienced superficial second-degree burns, which selfresolved. There were no other reported complications. A second study, by Zelickson et al,15 reported on the histological effects of treatment with the Titan device. These authors evaluated the immediate tissue effects of the infrared device on cadaveric forehead skin and live abdominal skin to determine the depth of collagen fibril denaturation. In the cadaveric forehead skin, treatment with fluences of 50 J/cm2 and 100 J/cm2 lasting 5–10 seconds resulted in collagen fibril denaturation in the depth range between 1 and 2 mm. Abdominal skin treatments (with fluences of 30 J/cm2, 45 J/cm2, and 65 J/cm2) showed similar results, as the 0–1 mm and
1–2 mm depth ranges showed a significant amount of collagen fibril denaturation.The 0–1 mm range showed a lesser severity in collagen denaturation, however, as the cooling function of the Titan worked to preserve epidermal integrity. The results from this study show that thermal injury caused by the Titan induces the desired immediate tissue effects at an optimal depth beneath the skin believed to be responsible for producing the beneficial cosmetic effect achieved from deeptissue tightening. A shortcoming of this study was that there was no long-term follow-up on the actual clinical effects of the treatment.
Combination Technology Newer combination technology, such as the ReFirme (Syneron LTD, Yokneam, Israel), combined bipolar radiofrequency with broad spectrum light source and have also shown promising results for skin tightening in a painless fashion.
Treatment parameters Similar to monopolar RF, energy settings with the Titan device are determined based upon patient comfort.The maximal energy is considered to be the level at which the patient experiences mild discomfort.This can be defined as feeling a moderate heating sensation for a split second, or as experiencing 6 out of 10 on a pain scale. It is not recommended that this level be exceeded, as there is potential for overheating of the skin, with subsequent blistering. In our practice, the Titan device has been used to treat the forehead, midface, neck, chest, arms, legs, and abdomen. Energy levels vary depending upon the treatment site and patient tolerance. Regardless of the area treated,Titan treatments consist of multiple nonoverlapping passes delivering low energy. The total number of passes is usually around three to five to achieve visible tightening of the treated area.
Clinical effects As with other nonsurgical skin tightening devices, the exact degree of skin tightening will be variable. This
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b
Fig. 9.3 A patient before (a) and 3 months after (b) a single full-face treatment with near-infrared (Titan) skin tightening. Typical results include moderate tightening along the mandibular line, along with attenuation of the jowls and nasolabial folds. makes the endpoint difficult to predict for both surgeon and patient. Another important factor to note is the delay to achieving the final endpoint. In most of our cases, patients did not achieve maximal correction until 3–5 months post treatment. Even at this point of maximal correction, many of the changes were difficult to perceive without examining preoperative photographs. The most common areas to show improvement with the infrared tightening were the mandibular line, which became more defined with a less prominent jowl area. The second most common area to demonstrate improvement was an elevation of the malar fat pad and concomitant softening of the nasolabial fold (Fig. 9.3). In our hands, this device provided limited improvement in the neck and brow regions. It is extremely important to point out these factors and limitations to patients during preoperative consultation so that realistic expectations can be set appropriately.
Side-effects and limitations The delivery of infrared light to the skin under appropriate guidelines is an extremely safe modality. Reports of adverse events thus far are limited to a very small number of superficial scars. The majority of these have occurred on the upper forehead, and it is believed that reflected energy from the underlying cranium was responsible for thermal injury to the skin. It is important to follow the recommendations for low-energy multiple-pass treatments with extra caution over bony prominences such as the forehead, mandible, and malar prominence. Furthermore,
sufficient contact gel must be used in order to provide adequate coupling for surface cooling.
Future directions A question that is yet to be determined is whether serial treatments provide greater correction than a single treatment. For example, is it beneficial to perform three monthly treatments with infrared skin tightening to enhance the final outcome? Although no published data currently exist, many of our patients believe that they receive extra benefit from their multiple treatments. In theory, one would expect that the amount of collagen contraction achieved with one treatment session is certainly not maximal and that further contraction could be achieved with additional treatments.The ideal energy settings, number of passes, and the treatment interval are all variables that are not known or well understood. The only way to clearly determine this is through careful morphometric analysis in a split-face study and through continued close monitoring and collection of data from patient treatments.
SUMMARY We have discussed two noninvasive devices on the market that are appropriate for treating early skin laxity. Both of these devices provide zero-downtime treatments, and therein lies their true strength. No other treatments available can provide zero downtime
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with the potential for some degree of correction. Although the amount of correction is variable and, at times, limited, many patients cannot afford or are unwilling to spend 2–3 weeks recovering from a surgical procedure.These two devices, therefore, offer alternatives to traditional lifting procedures when patients can not afford the downtime and are willing to accept a lesser degree of lifting. The area of noninvasive skin tightening is still relatively new, and we, as operators, are still learning how to maximize our results. Certainly, the future will bring us further technological advancements and other new devices that will enhance our ability to perform less-invasive and noninvasive rejuvenation.
REFERENCES 1. Alster TS, Garg S. Treatment of facial rhytides with a high-energy pulsed carbon dioxide laser. Plast Reconstr Surg 1996;98:791–4. 2. Khatri KA, Ross EV, Grevelink JM, et al. Comparison of erbium:YAG and carbon dioxide lasers in resurfacing of facial rhytides. Arch Dermatol 1999;135:391–7. 3. Lennox G. Shrinkage of collagen. Biochim Biophys Acta 1949;3:170–87. 4. Ross EV, Naseef GS, McKinlay JR, et al. Comparison of carbon dioxide laser, erbium:YAG laser, dermabrasion, and dermatome: a study of thermal damage, wound contraction, and wound healing in a live pig model: implications for skin resurfacing. J Am Acad Dermatol 2000;42:92–105. 5. Tunnel JW, Pham L, Stern RA, et al. Mathematical model of nonablative RF heating of skin. Lasers Surg Med 2002;14(Suppl):318.
6. Hsu TS, Kaminer MS. The use of nonablative radiofrequency technology to tighten the lower face and neck. Semin Cutan Med Surg 2003;22:115–23. 7. Fitzpatrick R, Geronemus R, Goldberg D, et al. Multicenter study of noninvasive radiofrequency for periorbital tissue tightening. Lasers Surg Med 2003;33: 232–42. 8. Ruiz-Esparza J, Gomez JB. The medical face life: a noninvasive, nonsurgical approach to tissue tightening in the facial skin using nonablative radiofrequency. Dermatol Surg 2003;29:325–32. 9. Alster TS, Tanzi E. Improvement of neck and cheek laxity with a non-ablative radiofrequency device: a lifting experience. Dermatol Surg 2004;30:503–7. 10. Fisher GH, Jacobson LG, Bernstein LJ, et al. Nonablative radiofrequency treatment of facial laxity. Dermatol Surg 2005;31:1237–41. 11. Koch RJ. Radiofrequency nonablative tissue tightening. Facial Plast Surg Clin North Am 2004;12:339–46. 12. Nahm WK, Su TT, Rotunda AM, et al. Objective changes in brow position, superior palpebral crease, peak angle of the eyebrow, and jowl surface area after volumetric radiofrequency treatments to half of the face. Dermatol Surg 2004;30:922–8. 13. Kilmer SL. A new nonablative radiofrequency device: preliminary results. In: Arndt KA, Dover JS, eds. Controversies and Conversations in Cutaneous Laser Surgery. Chicago: American Medical Association Press, 2002:93–4. 14. Ruiz-Esparza J, Shine R, Spooner GJR. Immediate skin contraction induced by near painless, low fluence irradiation by a new infrared device: a report of 25 patients. Dermatol Surg 2006;32:601–10. 15. Zelickson B, Ross V, Kist D, et al. Ultrastructural effects of Titan infrared handpiece on forehead and abdominal skin. Dermatol Surg 2006;327:897–901.
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10. Laser treatment of pigmentation associated with photoaging David H. Ciocon and Cameron K Rokhsar
INTRODUCTION Cumulative exposure to the sun can induce clinical and histological changes in the skin, commonly called photoaging or dermatoheliosis. This occurs primarily in patients with fair skin types (Fitzpatrick 1 to Fitzpatrick 3 skin types) who have experienced repeated solar injuries over the years, such as lifeguards and outdoor laborers.1 Clinically, photoaging represents a polymorphic response to sun damage that manifests variably as wrinkles, skin roughness and xerosis, irregular mottled pigmentation, telangiectasias (poikiloderma of Civatte), actinic purpura, sallowness (also known as Milian citrine skin), and brown macules or solar lentigines. Besides fair skin, other risk factors for the development of photoaging include difficulty in tanning, ease of sunburning, a history of sunburn before the age of 20, advancing age, smoking, male gender, and living in areas with high ultraviolet (uv) radiation (high altitudes).2 Individuals who develop photoaging often have a genetic susceptibility to photodamage and can experience sufficient actinic damage to develop skin cancers such as basal cell cancer or melanoma. The areas primarily affected by photoaging include the face, the V area of the neck and chest, the back and sides of the neck, the backs of the hands and extensor arms, and, in women, the skin between the knees and ankles. Photodamaged skin typically appears attenuated, atrophic, scaly, wrinkled, leathery, and, in some cases, furrowed and ‘cigarette paper-like’. In persons of Celtic ancestry, photoaging can produce profound epidermal atrophy without wrinkling, making the skin appear almost translucent and making dermal structures such as blood vessels more visible.
Because of its predilection for visible parts of the body, photoaging-induced pigmentation can have significant psychosocial impact on affected individuals. Unfortunately, treatment of such pigment alterations has been difficult. Each year, millions of dollars are spent by consumers seeking ‘quick-fix’ solutions for the cutaneous stigmata of aging. In 2002, more than 5 million nonsurgical and 1.5 million surgical cosmetic procedures costing more than $13 billion were performed in the USA.3 We can only expect such numbers to increase in the coming decades as our aging population expands, given increases in life expectancy and growing consumer demand for improvements in cosmetic appearance. While photoprotection with either chemical or physical sunscreens remains the mainstay of care for patients with photoaging-induced pigmentation, additional topical treatments in the form of retinoids, steroids, chemical bleaches such as hydroquinone, hydroxy acids, and chemical peels are also available. Unfortunately, many of these topical treatments are only able to affect changes at the level of the epidermis, while most textural and tinctorial changes in sundamaged skin are caused by alterations in structures in the upper and deep dermis. The introduction of laser and visible-light technology over the past 30 years has revolutionized our understanding and treatment of photoinduced pigmentation by more selectively targeting pigmented molecules and structures in the dermis without damaging the overlying epidermis. They have also proven useful in more directed treatment of epidermal pigmentation. In this chapter, we will review some of the more common pigmented lesions associated with
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photoaging as well as the most current and effective laser modalities available for their treatment.
SOLAR LENTIGINES Solar lentigines are the most common of pigmented lesions induced by photoaging.4 They are macular, hyperpigmented lesions ranging in size from a few millimeters to more than a centimeter in diameter. They tend to be multiple and grouped and bear a predilection for sun-exposed surfaces, including the face, neck, hands, and forearms.Alternative names for solar lentigines include actinic lentigines, liver spots, age spots, and sunspots. As with photoaging, the incidence of solar lentigines increases with time, affecting more than 90% of Caucasians older than 50 years.When evaluating individuals with suspected solar lentigines, clinicians must take care in distinguishing them from ephelides, lentigo simplex, pigmented actinic keratoses, flat seborrheic keratoses, melanocytic nevi, and malignant melanoma. While they can be usually differentiated on the basis of history and clinical appearance, some cases may warrant a biopsy. Although numerous non-laser therapies have been shown to be effective for solar lentigines, including retinoic acid, mequinol, and cryotherapy, many of them require repeat applications over extended periods of time to achieve significant cosmetic improvement. In addition, lightening with topical treatment is usually temporary and incomplete, with the lesions recurring immediately following cessation of therapy.The primary advantage of laser treatment of solar lentigines is that most can be removed completely in one to three treatments, depending on the modality, which provides patients with more immediate satisfaction. The primary target in a solar lentigo is the pigment melanin. Because of the broad absorption spectrum of melanin, which ranges from 351 to 1064 nm, various lasers have been used to treat solar lentigines, most with excellent results. Lasers used in published reports include the pulsed dye (585–595 nm), copper vapor (511 nm), krypton (520–530 nm), frequencydoubled Q-switched neodymium : yttrium aluminum garnet (Nd:YAG) (532 nm), Q-switched ruby (694 nm), Q-switched alexandrite (755 nm), Qswitched Nd:YAG (1064 nm), carbon dioxide (CO2) (10 600 nm), and argon (488–630 nm) lasers.4 For the
purpose of this review, we will concentrate on three laser modalities widely regarded as the safest and most effective for the treatment of solar lentigines: the Qswitched ruby laser, the Q-switched alexandrite laser, and the Q-switched Nd:YAG laser. The Q-switched ruby laser (QSRL) was developed to emit light in very short pulses that is preferentially absorbed by melanin, thereby reducing damage to other skin structures. Q-switched lasers can induce both photothermal and photomechanical reactions. These lasers generate high-energy radiation that leads to a rapid rise in temperature (1000°C), resulting in evaporation of targeted pigments within the skin and vacuolization (photothermal damage). The collapse of the temperature gradient that is created between the target tissue and the surrounding tissue also causes fragmentation of the target (photomechanical damage). The use of the QSRL for the treatment of solar lentigines was described in a study of eight women with 196 solar lentigines on their forearms.5 Therapy was delivered as a single brief pulse of 40 ns to a 4 mm2 area. A single course of treatment resulted in fading of the lesions without scarring and no recurrence within a 6- to 8-week follow-up period. Histopathological examination of biopsy specimens showed vacuolization of superficial pigmentation to a maximum depth of 0.6 mm immediately after treatment. Immunohistochemical examination of specimens stained with anti-melanocyte-specific antibodies did not indicate remaining melanocytic structures in moderately pigmented lesions. Another Q-switched laser that has been also shown to be effective for lentigines is the Q-switched Nd:YAG (QSNd:YAG) laser at 532 nm.A three-center trial evaluated the effectiveness of the frequencydoubled QSNd:YAG laser (532 nm, 2.0 mm spot size, 10 ns) in removing benign epidermal pigmented lesions with a single treatment. Forty-nine patients were treated for 37 lentigines.6 Treatment areas were divided into four quadrants, irradiated with fluences of 2, 3, 4, or 5 J/cm2 and evaluated at 1- and 3-month intervals following treatment. For lentigines, response was dose-dependent, with greater than 75% pigment removal achieved in 60% of those lesions treated at higher energy fluences. Although mild, transient erythema, hypopigmentation, and hyperpigmentation were noted in several patients, they all resolved
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Fig. 10.1 Removal of solar lentigines on the face of a patient with type IV skin after treatment with one session of the Q-Switched Alexandrite laser (Candela Corporation).
spontaneously within 3 months. No other textural changes or scarring were noted. In a subsequent study the safety and efficacy of the QSRL at 694 nm and the frequency-doubled QSNd:YAG (1064 and 532 nm) lasers were compared.7 Twenty patients with pigmented lesions (including lentigines, café-au-lait macules, nevus of Ota, nevus spilus, Becker’s nevus, postinflammatory hyperpigmentation, and melasma) were treated with the QSRL and the frequency-doubled QSNd:YAG lasers. Clinical lightening of the lesion was assessed 1 month after a single treatment. A minimum of 30% lightening was achieved in all patients after only one treatment with either the QSRL or the frequency-doubled QSNd:YAG laser. The QSRL seems to provide a slightly better treatment response than the QSNd:YAG laser. Furthermore, most patients found the QSRL to be more painful during treatment, but the QSNd:YAG laser caused more postoperative discomfort. Neither laser caused scarring or textural change of the skin. At present the QSNd:YAG laser at 532 nm is favored by many clinicians for the treatment of lentigines in light-skinned individuals, while the QSNd:YAG at 1064 nm is favored for individuals with darker skin types.8 One study has recently reported the use of the Nd:YAG laser in medium skin types such as Asian skin. Chan et al9 compared the clinical efficacy and the adverse event profile of three different lasers: the Versapulse Q-switched (VQS) Nd:YAG at 532 nm, the Versapulse long-pulse (VLP) Nd:YAG laser at 532 nm, and a conventional QSNd:YAG laser at 532 nm (Medlite, Continuum Biomedical, Livermore, CA).
The VLP, unlike the VQS laser, causes tissue destruction purely through photothermal effects. Thirty-four Chinese patients with 68 solar lentigines on the face were treated with one of the three lasers. For the VLP laser, the spot diameter was 2 mm, with a pulse duration of 2 ms and fluence of 9–12 J/cm2. For the VQS laser, the spot size was 3–4 mm with a fluence of 1.0–1.5 J/cm2. The Medlite laser system involved a spot size of 2 mm, with a fluence of 0.9–1.0 J/cm2. The mean scores (maximum 10) for the degree of clearing achieved using both patients’ and clinicians’ assessments were 4.751, 4.503, and 4.78 for the Medlite, VQS, and VLP lasers, respectively, indicating no difference in efficacy. Our treatment of choice is the use of the Q-switched alexandrite laser (755 nm), as it removes pigmentation effectively without the purpura commonly associated with the use of the QSNd:YAG at 532 nm (Fig. 10.1). With the alexandrite crystal, the laser wavelength is 755 nm, which is longer than that of the ruby laser (694 nm) and the QSNd:YAG laser at 532 nm. Longer wavelengths penetrate more deeply into the dermis and are absorbed less readily by epidermal melanin. If the skin is irradiated with wavelengths in the 400–600 nm range, oxyhemoglobin will compete strongly with melanin for absorption of photons, and vascular damage will occur, resulting in purpura.With longer wavelengths (> 600 nm), where absorption by oxyhemoglobin is substantially reduced or absent and absorption by melanin over blood pigments dominates, damage is restricted to the melanin pigment-laden structures (Fig. 10.2). In a study by Jang et al,10
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Fig. 10.2 5 days post treatment of lentigines on hands with the Q-Switched Alexandrite laser (Candela Corporation).Typically, crusting is seen, without purpura. The crusted areas typically peel off within 7–10 days.
197 patients with freckles were treated with the Q-switched alexandrite laser at 8-week intervals and clinically analyzed. The Q-switched alexandrite laser was operated at 755 nm, with a pulse width of 100 ns using a 3 mm spot.After a single treatment, all the irradiated freckles in 64% of patients were graded as excellent. More than 76% removal of freckles required an average of 1.5 treatment sessions with 7.0 J/cm2. No scarring, long-standing pigment changes, or textural changes were seen. The superiority of laser therapy over cryotherapy in the treatment of solar lentigines has been well described. Todd et al11 have reported a comparative study of the frequency-doubled QSNd:YAG laser (532 nm), the HGM K1 krypton laser (521 nm) (HGM Medical Systems Inc., Salt Lake City, UT), the DioLite 532 nm diode-pumped vanadate laser (Index Corp., Mountain View, CA), and cryotherapy. A total of 27 patients with a minimum of six lesions on the backs of their hands were enrolled in the study. Each hand was divided into four sectors, and one treatment was applied per sector.Treatment with the frequency-doubled QSNd:YAG laser involved treatment for 30 ns to a 3 mm spot; comparative treatments with the HGM K1 krypton laser and the DioLite 532 nm diodepumped vanadate laser were 0.2 s on/0.2 s off to a 1mm spot and 39 ms to a 1 mm spot, respectively.
At 6 weeks after treatment, the frequency-doubled QSNd:YAG laser was found to provide superior lightening compared with other treatments. This level of response was still maintained at 12-week follow-up. From the patients’ perspective, a survey showed that they considered this form of laser therapy to produce the best results (n = 18), followed by diode-pumped vanadate laser (n = 6), cryotherapy (n = 2), and the krypton laser (n = 1). The fewest adverse events were reported from use of the Qswitched laser, whereas the krypton laser had the highest number of such events. Mild transient erythema was reported for all therapies, with hypopigmentation and/or hyperpigmentation and scarring occurring infrequently. Intense pulsed light systems (IPLs) have been also shown to be effective for the treatment of solar lentigines – although less so compared with Q-switched lasers.8 IPLs emit broadband light containing multiple wavelengths. Using various filters to include or exclude particular wavelengths, one can target various structures in the skin, depending on the wavelength emitted. Like Q-switched lasers, IPLs are also based on the principle of selective photothermolysis. However, IPLs are typically less predictable than Q-switched lasers, due to the wider range of wavelengths being used. Most often, the removal of lentigines by the IPL is incomplete and is an added benefit that occurs during IPL facial photorejuvenation to correct mild wrinkles, poor skin texture, and telangiectasias associated with chronic sunlight exposure. Because light from the IPL must pass through the epidermis in order to reach the dermal fibroblasts in photorejuvenation, focal melanin deposits that cause lentigines are inadvertently treated as well. Once photothermolyzed, these lesions usually turn a dark brown color and then peel off in 7–10 days. Because the wrinkle-improvement aspect of IPL generally takes 6–8 weeks to be seen, and is mild at best, much of the early patient enthusiasm for IPL stems from the eradication of solar lentigines and improvement of telangiectasias (Fig. 10.3). For those individuals seeking to improve pigmentation as well as fine, moderate, and deep rhytides on the face, ablative resurfacing with the CO2 laser (10 600 nm) or Er-YAG laser (2940 nm) remains the gold standard (Fig. 10.4). The chromophore for both lasers is water. The CO2 and erbium lasers operate by
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Fig. 10.3 Improvement in telangiectasias and pigmentation associated with photodamage following three treatment sessions with an intense pulse light (IPL) source: (a) before; (b) after treatment. (Photographs courtesy of Elizabeth Rostan, MD.)
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Fig. 10.4 Significant reduction in pigmentation and rhytids associated with chronic photodamage after a three-pass resurfacing procedure with the Ultrapulse CO2 laser. vaporizing epidermal and dermal tissue. The depth of vaporization depends on the device and number of passes, but in general, in the most aggressive ablative resurfacing procedures, one does not ablate more than 400 µm of skin. One can reverse the pigmentation associated with photoaging rather effectively with
ablative resurfacing, with outstanding results not only in pigmentation and lentigines, but also in deep lines and furrows. One also sees a degree of tissue tightening unparalleled with other laser devices. The downside is the potential risk for scarring and pigmentary alteration, which in the worse-case scenario can be
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Microscopic epidermal necrotic debris (MEND)
Controlled zones of denatured collagen in the dermis
100 µm
Fig. 10.5 Histological evaluation after fractional resurfacing with the Fraxel laser.The coagulated epidermis is referred to as MEND (microscopic epidermal necrotic debris). The MEND are extruded within a week after the procedure. It is thought that the improvement in pigmentation is related to the extruded MEND having a high melanin content. Below each MEND is a denatured column of collagen (bluish in color).These columns serve as a new stimulus for collagen production.
permanent as the raw skin heals. It is important to note that the erbium laser can also be used superficially, with little downtime or erythema. However, these so called ‘microlaser peels’ have very little effect on pigmentation. The newest technology for the improvement of solar lentigines is fractional resurfacing with the Fraxel laser (Reliant Technologies, Mountain View, CA). This is a new concept in laser resurfacing whereby the skin is resurfaced fractionally (15–30%) in one session.12,13 This is accomplished by the placement of an array of numerous microscopic zones of thermal damage in the epidermis and dermis, surrounded by islands of normal tissue. The normal skin left untreated serves as a reservoir for healing, allowing the skin to heal rapidly. This procedure is typically repeated four to six sessions every 2–4 weeks. In this way, one can resurface a large portion of the skin over time. Unlike CO2 or erbium laser resurfacing, the skin is not vaporized during fractional resurfacing, and therefore there are no full-thickness wounds. Rather,
the skin is photocoagulated. These photocoagulated zones of thermal damage range from 80 to 150 µm in diameter and from 300 to 900 µm in depth, depending on the parameters utilized (Fig. 10.5).The percentage of the skin resurfaced at one time depends on the combination of energy and final densities used. In four to six treatment sessions, one can resurface 59–84% of the skin at a setting that resurfaces 20% of the skin at a time, and 76–88% at a setting that resurfaces 30% at a time. The photocoagulated epidermis, which is referred to as MEND (microscopic epidermal necrotic debris), is extruded 3–5 days after the procedure; this is clinically manifested as first bronzing of the skin and later as fine flaking. The columns of photocoagulated collagen in the dermis serve as a stimulus for production of new collagen. One can thus achieve both epidermal and dermal remodeling over time (Fig. 10.6). The advantages to this fractional approach to resurfacing are numerous, from both a theoretical and a practical perspective. First and foremost, patients do not have open wounds, minimizing downtime. Second, anatomical areas that would generally be highly prone to complications of scarring with traditional resurfacing lasers, such as the neck, chest, and hands, can be safely and aggressively treated. Third, potential complications associated with open wounds, such as infection and hyper/hypopigmentation and scarring, are minimized. Fourth, one can potentially treat deeper dermal pathology. Fifth, water is the chromophore, so tissue interaction, both in the epidermis and in the dermis, is relatively uniform. Traditionally, with combined CO2/erbium laser resurfacing, one ablates tissue approximately 200–400 µm during multiple-pass procedures. Any deeper treatment risks the complication of scarring.With Fraxel laser treatment, one can penetrate tissue much deeper safely, as entire epidermal and dermal ablation is not achieved. The diameter of each column of coagulated tissue is small enough to be invisible to the unaided eye and is surrounded by untreated skin, which provides a tremendous reservoir for healing. Because of these two factors, tissue can be coagulated within this small column as deep as 900 µm safely. With the second-generation Fraxel laser (Fraxel SR 1500) employing a variable spot size, penetration as deep as 1.1 mm is possible. The coagulated epidermis is replaced within 24 hours by an influx of cells from the periphery of the treated spot, or column.
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Fig. 10.6 Improvement in pigmentation, actinic keratosis and rhytides after fractional resurfacing with four session of the Fraxel laser: (a) before; (b) after treatment. The current Fraxel laser is a fiberoptic laser utilizing a wavelength of 1550 nm.The laser handpiece is equipped with a so-called intelligent optical tracking device that is able to calculate the speed of the operator’s hand against a background blue dye, adjusting for inconsistencies in hand speed, to place the intended number of microthermal zone in a given area. Other manufacturers have also fractionated the beams of their devices. Palomar manufactures a device that has a fractionated head allowing for delivery of fractionated laser spots in a stamping mode. A few laser manufacturers are in the process of fractionating CO2 or erbium laser beams in hope of decreasing the patient downtime associated with ablative resurfacing while maintaining its superior results. The Fraxel laser is currently FDA-approved for treatment of periorbital wrinkles, acne and surgical scars, skin resurfacing procedures, and dermatological procedures requiring the coagulation of soft tissue, as well as photocoagulation of pigmented lesions such as lentigines and melasma. Solar lentigines on the face, and indeed anywhere on the body, can be treated. Multiple sessions are required. It is important to note that the mechanism of clearance is through nonspecific resurfacing and is not pigment-specific.Therefore, Qswitched lasers remain the gold standard for treatment of distinct lentigines. Fractional resurfacing is useful in those individuals who seek improvement of diffuse
pigmentation or additionally seek improvement in texture, wrinkles, and (acne) scars.
DERMATOHELIOSIS Long-term sun exposure results in wrinkled, inelastic skin that reflects a loss of collagen in the mid to upper dermis, with concomitant accumulation of elastotic material.14,15 This process is referred to as solar elastosis, reflecting these histological changes. The elastotic material is derived largely from elastic fibers, stains with histochemical stains for elastin, and demonstrates marked increased deposition of the protein fibulin 2 and its breakdown products. The mechanism behind collagen loss in photodamaged skin may be the upregulation of matrix-degrading metalloproteinases such as collagenase and gelatinases following UV irradiation of the skin. In addition, UV radiation causes significant loss of procollagen synthesis in the skin.16 Patients with dermatoheliosis present with an overall sallow, wrinkled complexion. Unfortunately, few topical regimens are effective in treating this condition because the pathology lies in the mid to upper dermis. Fortunately, various light-based technologies are available to help improve the appearance of patients with this common condition.
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Fig. 10.7 Significant reduction in wrinkles associated with chronic sun damage after a multipass resurfacing procedure with the Ultrapulse CO2 laser: (a) before treatment; (b) at 6 months’ follow-up.
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Fig. 10.8 Reduction in pigmentation and fine lines after resurfacing with five sessions with the Fraxel laser: (a) before; (b) after treatment. (Photographs courtesy of Elizabeth Rostan, MD.)
The gold standard for treatment of solar elastosis on the face remains ablative resurfacing with CO2 or erbium lasers. Tissue is vaporized from 200 to 400 µm. As the raw skin heals, a wound healing cascade is initiated in which inflammatory cells recruit dermal fibroblasts to produce new dermal collagen. This process results in an improvement of wrinkles associated with photoaging (Fig. 10.7). Both deep lines and pigmentation associated with photoaging can
be drastically improved with this procedure. The potential risks are infection, scarring, and hyper/ hypopigmentation, which can at times be delayed. As mentioned above, fractional resurfacing with the Fraxel laser has been promising in the treatment of fine wrinkles, texture and dermatoheliosis. Fractional resurfacing treats photodamaged skin by targeting only a small fraction of the skin surface in each treatment session. Photodamage to the face (Fig. 10.8), neck,
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Fig. 10.9 Improvement in pigmentation and textural abnormalities associated with sun damage after combination treatment with the Q-switched alexandrite laser (one session) and the Fraxel laser (four sessions): (a) before; (b) after treatment. (Photographs courtesy of Richard Fitzpatrick MD.)
chest, arms (Fig. 10.9), and hands has been treated successfully, as have acne scars, other scars, and various types of dyschromia, including melasma. This treatment regimen has produced more significant improvements in texture, color, and deep lines than are commonly seen with other nonablative technology. In a study conducted by Rokhsar and Fitzpatrick,13 an improvement of 1.5 was seen in the wrinkle score following four to six sessions with the Fraxel laser, utilizing the Fitzpatrick wrinkle score, measuring wrinkles on a scale of 1–9. Dermal remodeling with IPL has been a source of renewed interest. In a study by Goldberg,17 five patients underwent four sessions of dermal remodeling with an intense pulsed light source. All patients received a pretreatment biopsy and a second biopsy 6 months after the initial treatment. Biopsies were evaluated for histological evidence of new collagen formation 6 months after the initial treatment.While pretreatment biopsies showed evidence of solar elastosis, the post-treatment biopsies showed some degree of superficial papillary dermal fibrosis, with evidence of an increased number of fibroblasts in scattered areas of the dermis. Such changes, the author concluded, were evidence of new dermal collagen formation. Recently, investigators have reported better results by combining IPL with δ-aminolevulinic acid (ALA). However, it still appears that improvement in fine lines is subtle at best with IPL treatments.
Various other lasers have been shown to induce nonablative dermal collagen remodeling, including the 1320 nm Nd:YAG laser, the 1450 nm diode laser, and the 1540 nm Er:glass device. However, in reality, the results are often not reproducible – or are subtle at best. Because of their longer wavelengths, these lasers are more deeply penetrating and less damaging to the epidermis, while being minimally absorbed by melanin. They use water as a chromophore and are intended to target dermal collagen. It is generally accepted that this class of lasers is the least effective in treatment of wrinkles associated with photoaging.
POIKILODERMA OF CIVATTE Poikiloderma of Civatte refers to erythema associated with a reticulate pigmentation and telangiectasias usually seen on the sides of the neck, lower anterior neck, and the ‘V’ of the chest. Civatte first described the condition in 1923. It is a rather common, benign condition affecting the skin. Many consider it to be a reaction pattern of the skin to cumulative photodamage, since the submental area, shaded by the chin, is typically spared. It frequently presents in fair-skinned men and women in their mid to late 30s or early 40s.
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The blue–green argon laser was the first laser system used for treating poikiloderma of Civatte. Although it offered improvement, this treatment had significant side-effects, most notably scarring.The 532 nm potassium titanyl phosphate (KTP) laser introduced later was an improvement, although complicated by cases resulting in occasional hypopigmentation. Treatment options for poikiloderma of Civatte were revolutionized with the advent of the pulse dye laser (PDL).18 PDLs were first introduced in 1989, with the first laser emitting light at 577 nm, coinciding with the last peak of the oxyhemoglobin absorption spectrum (418, 542, and 577 nm). Because its target chromophore was hemoglobin, the PDL quickly became the treatment of choice for vascular lesions, including telangiectasias, hemangiomas, and portwine stains. By lengthening the wavelength to 585 nm, the PDL achieved deeper penetration into the dermis without compromising vascular selectivity. Currently available PDLs emit a wavelength of 585 or 595 nm with longer pulse durations.Although there is deeper penetration of energy at 595 nm compared with 585 nm, the absorption of oxyhemoglobin is less after 585 nm.Therefore to compensate for this decreased absorption, the 595 nm PDL requires an additional 20–50% of fluence compared with 585 nm systems. Because telangiectasias are a prominent feature of poikiloderma of Civatte, the PDL provides a superior treatment alternative for this condition. In one study, seven female patients (ages 42–52 years) with clinically typical poikiloderma of Civatte, which they considered to be causing significant cosmetic disfigurement, were treated with a PDL at a wavelength of 585 nm and a pulse duration of 0.45 ms (SPTL-1B; Candela Corp., Wayland, MA).19 All seven patients were of skin type I or II (i.e., they burnt easily, with little or no tendency to tan), and in all of them reticulate telangiectasia was the most prominent component of the condition. In all of the patients, a test patch was treated and reviewed at 3 months. Subsequent treatments were undertaken at intervals of 3 months.The fluences used were 5.0 J/cm2 with a 10 mm beam diameter (five patients) and 7.0 J/cm2 with a 7.0 mm beam diameter (two patients). Topical anesthesia with EMLA cream or cooling with ice was used. Results were assessed by one of the two authors and graded as excellent (vascular component of the
lesion not visible), good (partial clearing of 50% of the vascular component of the lesion), or poor (no visible change). Five patients had an excellent result, one had a good result, and one had a good result with respect to clearing of the vascular component but an overall unsatisfactory cosmetic result due to scarring and hypopigmentation in the treated area. This adverse result is of some interest, since the test patch did not produce any scarring or pigment change, and the changes did not occur until 4 months after the treatment. This patient had been treated at a fluence of 7.0 J/cm2. No other adverse effects were noted – in particular, no pigment changes. Subsequent studies have attempted to delineate further the adverse outcomes associated with PDL treatment of poikiloderma of Civatte, particularly since uniform guidelines for treatment of the condition do not exist. In a study by Meijs et al20 eight patients (seven women and one man, mean age 48 years) with poikiloderma of Civatte were treated with a PDL using a 585 nm wavelength and a fixed pulse duration of 0.45 µs. In all patients, one or two test PDL patches were performed and reviewed after 3 months. All of the patients tolerated the testing without complications. Subsequent treatments were undertaken at intervals of 3 months. All patients were treated with fluences between 3.5 and 7 J/cm2, using a 7 or 10 mm spot size.All had a good result with respect to clearing of the vascular component. Nevertheless, six of them, treated with 5–7 J/cm2, reported severe depigmentation 4–11 months after treatment. Two patients treated with lower fluences (3.5–5.5 J/cm2), however, did not report this depigmentation.Therefore, to avoid depigmentation, the authors recommend using fluences as low as possible when treating dark-skinned individuals for poikiloderma of Civatte with PDL and not exceeding an upper limit of 5 J/cm2, on a 10 mm spot size. Incomplete clearing of poikiloderma of Civatte is typically a result of poor light penetration depths in blood. For example, the light penetration depths in blood at 532 and 585 nm wavelengths are approximately 37 (absorption coefficient approximately 266 cm−1) and 52 µm (absorption coefficient approximately 191 cm−1), while the ectatic blood vessels of poikiloderma of Civatte are approximately 100 µm
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Fig. 10.10 Poikiloderma of the neck and chest is improved after five sessions with the Fraxel laser: (a) before; (b) after treatment. (Photographs courtesy of Richard Fitzpatrick MD.)
in diameter. As a result, large blood vessels cannot be completely coagulated, resulting in incomplete clearing of poikiloderma of Civatte, even with the PDL. A new high-energy PDL (V-Beam; Candela), capable of producing higher fluences with larger spot size, is equipped with a glass slide that is used to physically displace blood in the skin, allowing the energy to be preferentially absorbed by melanin. Although new, this laser holds greater promise in the treatment of pigmentation and telangiectasias associated with poikiloderma. IPL has also been widely used for the treatment of poikiloderma.21, 22 As IPL covers a broad range of wavelengths, it can potentially treat both the vascular and pigmented components of poikiloderma. Usually, three to five sessions are necessary to achieve optimal results. A potential negative outcome that can be associated with the use of IPL in the treatment of poikiloderma is the pin-striping developed by some patients and associated with the use of the rectangular handpieces of IPL devices. Care must be taken to use the IPL handpiece in a vertical manner in one session alternating with a horizontal manner in the next to minimize the potential for pin-striping. Given that one cannot use ablative resurfacing to reverse signs of photoaging in body areas commonly affected by poikiloderma, such as the chest and neck,
due to the risk of scarring, fractional resurfacing has revolutionized the treatment of poikiloderma (Fig. 10.10). Unlike the modalities based on selective photothermolysis, which aim to achieve homogeneous thermal injury in a particular target within the skin, fractional photothermolysis produces an array of microscopic regions of thermal injury surrounded by uninjured dermal tissue. Recent clinical studies indicate that fractional photothermolysis is effective in treating fine wrinkles and epidermal dyschromia, and in remodeling acne scars.23, 24 Fine rhytides improve over time.The improvement in pigmentation is related to the concept of MEND formation and extrusion. As mentioned above, this microscopic epidermal necrotic debris refers to a column of photocoagulated epidermis ranging from 80 to 150 µm in diameter, which sloughs off 3–7 days post treatment. MEND has a high melanin content when examined histologically – a fact that may explain improvement in skin pigmentation. Patients typically need three to five treatment sessions every 2–4 weeks. Besides the face, common treatment areas include the neck, chest, and hands. One distinction between fractional photothermolysis, IPL, and Q-switched laser technology is that its 1550 nm wavelength laser largely targets tissue water and not melanin. Improvement in pigmentation is a byproduct of general resurfacing and is not pigment-specific.
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ACTINIC PURPURA Actinic purpura is a benign clinical entity resulting from sun-induced damage to the connective tissue of the dermis.25 It is characterized by ecchymoses on the extensor surfaces of the forearms and the dorsa of the hands that usually last 1–3 weeks. It is an extremely common finding in elderly individuals, occurring in approximately 11.9% of those older than 50 years. Its prevalence markedly increases with years of exposure to the sun. The effects of chronic sun exposure with the resultant UV-induced skin changes occur more often and are more pronounced in fair-skinned individuals than in others. The purple macules and patches of this condition occur because red blood cells leak into the dermal tissue. This extravasation is secondary to the fragility of the blood vessel walls caused by UV-induced dermal tissue atrophy. This atrophy renders the skin and microvasculature more susceptible to the effects of minor trauma and shearing forces. The insult to the skin is typically so minor that isolating it as a cause of the ecchymoses can be difficult. Notably, no inflammatory component is found in the dermal tissue. The absence of a phagocytic response to the extravascular blood has been postulated to be responsible for delaying resorption for as long as 3 weeks. Given its self-limited course, actinic purpura does not require extensive medical care.To prevent further UV-induced damage to the skin, sunscreens that provide both UVA and UVB protection should be applied daily, especially to areas affected by the purpuric lesions. Patients should also use barrier protection (e.g., clothing). To date, lasers have not been described as a treatment for purpura, probably because of its self-limited course. However laser-mediated photorejuvenation techniques, both ablative (CO2 and Er:YAG lasers) and nonablative, can induce dermal collagen remodeling and may theoretically prevent the formation of actinic purpura in photodamaged skin by strengthening tissue collagen.
CONCLUSIONS The past 20 years has witnessed a dramatic revolution in the approach taken by dermatologists in the treatment
of pigmentation induced by photoaging. Prior to the advent of lasers, most therapies, including topical preparations, could only target pigment in the epidermis, making it difficult to treat those lesions where the responsible pigment lay deeper in the upper to middermis. Although certain technologies such as the CO2 and Er:YAG lasers could induce dermal collagen remodeling to combat rhytides and solar elastosis in addition to treating dermal pigmentation, they could only do so at the expense of epidermal ablation and damage. Newer technologies such as IPL, the Q-switched lasers, and fractional photothermolysis allow less ablative and more targeted treatment of dermal pigmentation, which translates into fewer treatments with shorter recovery times and fewer side-effects such as hyper/hypopigmentation. As our understanding of these technologies evolves, we may better address the cosmetic and psychosocial concerns of our growing aged population.
REFERENCES 1. Stern RS. Clinical practice. Treatment of photoaging. N Engl J Med 2004;350:1526–34. 2. Holman CDJ, Evans PR, Lumsden GJ, Armstrong BK. The determinants of actinic skin damage: problems of confounding among environmental and constitutional variables. Am J Epidemiol 1984;120:414–22. 3. American Society of Aesthetic Plastic Surgery. Cosmetic Surgery National Data Bank. 2002 Statistics. New York: ASAPS Communications. at http://www.surgery.org./ press/statistics-2002.asp (accessed 12 November 2006). 4. Ortonne JP, Pandya AG, Lui H, Hexsel D. Treatment of solar lentigines. J Am Acad Dermatol 2006;54(5 Suppl 2):S262–71. 5. Kopera D, Hohenleutner D, Landthaler H. Qualityswitched ruby laser treatment of solar lentigines and Becker’s nevus: a histopathological and immunohistochemical study. Dermatology 1997;194:338–43. 6. Kilmer SL, Wheeland RG, Goldberg DJ, Anderson RR. Treatment of epidermal pigmented lesions with the frequency doubled Q-switched (532 nm) Nd:YAG laser: a controlled single-impact, dose–response multicenter trial. Arch Derm 1994;130:1515–19. 7. Tse Y, Levine VJ, McClain SA, Ashinoff R. The removal of cutaneous pigmented lesions with the Q-switched ruby laser and the Q-switched neodymium: yttrium– aluminum–garnet laser. A comparative study. J Dermatol Surg Oncol 1994;20:795–800.
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Laser treatment of pigmentation associated with photoaging 8. Schmults CD,Wheeland RG. Pigmented lesions and tattoos. In: Goldberg DJ, Dover JS, Alam M, eds, Lasers and Lights, Vol 3. Philadelphia: Elsevier Saunders, 2005: 41–66. 9. Chan HH, Fung WK,Ying SY, Kono T. An in vivo trial comparing the use of different types of 532 nm Nd:YAG lasers in the treatment of facial lentigines in oriental patients. Dermatol Surg 2000;26:743–90. 10. Jang KA, Chung EC, Choi H, et al. Successful removal of freckles in Asian skin with a Q-switched alexandrite laser. Dermatol Surg 2000;26:231–4. 11. Todd MM, Rallis TM, Gerwels JW, Hata TR. A comparison of three lasers and liquid nitrogen in the treatment of solar lentigines. Arch Dermatol 2000;136:841–6. 12. Manstein D, Herron GS, Sink RK, et al. Fractional photothermolysis: a new concept for cutaneous remodeling using microscopic patterns of thermal injury. Lasers Surg Med 2004;34:426–38. 13. Rokhsar CK, Tse Y, Lee S, Fitzpatrick RE. The treatment of photodamage and facial rhytides with Fraxel (fractional photothermolysis). Lasers Surg Med 2005;36(Suppl 17):21–42(abst). 14. Calderone DC, Fenske NA. The clinical spectrum of actinic elastosis. J Am Acad Dermatol 1995;32:1016. 15. Fisher GJ, Kary S, Vasani J, et al, Mechanisms of photoaging and chronological skin aging. Arch Dermatol 2002;138:1462–70. 16. Fisher GJ, Datta SC, Talwar HS, et al. Molecular basis of sun-induced premature skin aging and retinoid antagonism. Nature 1996;379:335–9.
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17. Goldberg DJ. New collagen formation after dermal remodeling with an intense pulsed light source. J Cutan Laser Ther 2000;2:59–61. 18. Kim KH, Rohrer TE, Geronemus RG. Vascular lesions. In: Goldberg DJ, Dover JS, Alam M, eds. Lasers and Lights, Vol 3. Philadelphia: Elsevier Saunders, 2005: 11–27. 19. Haywood RM, Monk BE. Treatment of poikiloderma of Civatte with the pulsed dye laser: a series of seven cases. J Cutan Laser Ther 1999;1:45–8. 20. Meijs M, Blok F, de Rie M.Treatment of poikiloderma of Civatte with the pulsed dye laser: a series of patients with severe depigmentation. J Eur Acad Dermatol Venereol 2006;20:1248–51. 21. Goldman MP, Weiss RA. Treatment of poikiloderma of Civatte on the neck with an intense pulsed light source. Plast Reconstr Surg 2001;107:1376–81. 22. Weiss RA, Goldman MP,Weiss MA.Treatment of poikiloderma of Civatte with an intense pulsed light source. Dermatol Surg 2000;26:823–7. 23. Rokhsar C, Fitzpatrick RE. The treatment of melasma with fractional photothermolysis: a pilot study. Dermatol Surg 2005;31:1645–50. 24. Rokhsar CK, Lee S, Fitzpatrick RE. Review of photorejuvenation: devices, cosmeceuticals, or both? Dermatol Surg 2005;31:1166–78. 25. Kalivas L, Kalivas J. Solar purpura. Arch Dermatol 1988;124:24–5.
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11. Management of vascular lesions Marcelo Hochman and Paul J Carniol
INTRODUCTION There are multiple types of vascular-related lesions that can be treated with lasers. These include, but are not limited to: hemangiomas, vascular malformations, telangiectasias, rosacea, scar neovascularization, and pyogenic granulomas. Currently, there are a number of lasers available for the treatment of these vascular lesions. These include lasers working at the following wavelengths: 500, 532, 595–600, 940, and 1064 nm. Some of these lasers can also be used to treat other conditions, such as acne and lentigines. Patients who present for treatment fall into two main categories, based on their age. Adults often present with a variety of vascular lesions or rosacea. Children present for treatment of hemangiomas or vascular malformations. Vascular lesions are relatively common. Overall, vascular birthmarks affect approximately 8–10% of births, or nearly 400 000 new cases in the USA alone per year.1 Adults will present with either these lesions or acquired lesions, which have appeared since childhood.
HEMANGIOMAS Infantile hemangiomas are the most common benign tumors occurring in infancy and childhood, being present in about 2% of neonates. They are true tumors, exhibiting the features of all neoplasms, such as increased mitosis and hyperplasia. Although up to 30% of these lesions may present at birth, they usually become apparent in the first weeks of life.1–5 Congenital hemangiomas are completely formed and present at birth, and have a natural history and prognosis very
different from those of infantile hemangiomas. There are additional, rarer related vascular birthmarks, which are beyond the scope of this chapter.6,7 More than 60% of infantile hemangiomas occur in the head and neck, predominantly in Caucasians and somewhat less commonly in those of African or Asian descent. For unclear reasons, female neonates are more likely to be affected than males in a 3–5:1 ratio.They also seem to be more common in premature infants; increased prevalence correlates with both decreasing gestational age and birthweight.8,9 Although most hemangiomas occur sporadically, familial inheritance in an autosomal dominant fashion has been found.10 Recently, infantile hemangiomas have been linked to placental tissue. The leading hypotheses for the etiology of these lesions is the metastasis and implantation of placental cells or placental precursor cells into areas of high blood flow in the neonate, such as the head and neck region. Much is still unknown about the mechanisms of these processes, however, the link between placental and hemangioma cells is irrefutable.11 Hemangiomas always increase in size by proliferation (hyperplasia) during the first year of life, and involve skin, mucosa, and subcutaneous tissues to different degrees. Cutaneous hemangiomas may involve only papillary dermis (superficial), deeper layers of the skin or subcutaneous tissues (deep), or both (compound). They may be focal, well-defined lesions or segmental, involving dermatome-like segments of skin.There seem to be generalized sites of predilection on the face.12 The period of proliferation typically ends within the first 4–8 months, although, rarely, it can last up to 12–14 months.The end of proliferation marks the beginning of the involutional phase. During this phase, which may last for years, the hemangioma undergoes varying amounts of regression in size and
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replacement with fibrofatty tissue over a variable period of time. Approximately 30–40% of hemangiomas involute to a cosmetically and functionally acceptable point and do not require any treatment. Intervention is necessary, and sought by patients, for the remaining majority of cases, even after waiting more than 7 years, and is dependent on multiple factors, such as size, anatomical location, age of the child, and others.13 After involution is complete, superficial hemangiomas leave an atrophic scar with a variable degree of telangiectasia, deep hemangiomas leave a residual mass of fibrofatty tissue covered with a saggy cutaneous envelope, and compound lesions show varying degrees of all the above features. Accurate diagnosis and treatment planning of hemangiomas is made entirely on the basis of clinical history and physical examination, with imaging studies rarely being needed and of limited import. Terms such as ‘strawberry or capillary angioma’ or ‘cavernous hemangioma’ and others are of historic and folkloric interest, and should not be used when communicating about these lesions.
VASCULAR MALFORMATIONS In contrast to hemangiomas, vascular malformations5 are always present at birth (although they may not be apparent), enlarge by hypertrophy, never proliferate, and never involute.They are true developmental anomalies, not tumors, and their rate of hypertrophy, and hence their functional and cosmetic significance, is extremely variable. Vascular malformations may originate from capillaries, veins, venules, lymphatics, arterioles, or any combination of these structures.They may involve skin, subcutaneous tissues, and mucosa. They may also be superficial, deep, compound, as well as focal or diffuse as hemangiomas. Capillary malformations are superficial, pink macules previously known as salmon patch, angel’s kiss, or stork bite.They most commonly involve the midline of the nape of the neck, followed by the forehead. Although they are classified as vascular malformations, these lesions typically do fade with advancing age and are of passing significance.Venular malformations, known as portwine stains, are important lesions made up of ectatic postcapillary venules. Although they may present as flat, pink macules at the beginning of life, they usually darken
and thicken with advancing age, forming a cobblestone appearance as the dermal vessels continue to dilate under the constant hydrostatic pressure. Thus, these lesions enlarge over time by increasing the size of the involved vessels, not by increasing the number of vessels. Their distribution patterns seem to correspond to dermatomes, and the presumed etiology is deficient or inefficient postcapillary venule innervation.14 Venous malformations composed of ectatic veins are usually seen in the lips, the tongue and floor of the mouth, the buccal fat space, and other mucosa.Patients frequently complain of swelling with dependency, pain, limited function of the affected region, and cosmetic deformity. Superficial lesions are visible as purple masses, whereas deeper lesions present as bluish or colorless subcutaneous masses. Arteriovenous malformations are rare vascular lesions originating from arteriovenous channels that failed to regress during fetal development.15 A palpable mass with an obvious well-developed arterial supply and dilated tortuous veins are typical features.A murmur may be heard or a thrill may be palpated over the mass.These must be differentiated from arteriovenous fistulas, which are usually precipitated by trauma. In contrast to hemangiomas, imaging studies are of frequent use for establishing an accurate diagnosis and planning of treatment. Magnetic resonance imaging (MRI), angiography, and ultrasound are important diagnostic tools, and the particulars of differentiating these lesions have been well described.16 Lymphatic malformations (previously known as cystic hygromas) are dilated lymphatic channels arising from congenital blockage or arrest of the normal development of the primordial lymphatic plexus.Although they grow at a slow, steady rate, a sudden increase in size may be seen due to infection, trauma, or hormonal changes. Over 80% of the lymphatic malformations of the head and neck are located in the cervical region, although they may also involve the oral cavity, supraclavicular area, and parotid gland.These can be divided into three categories. Some lesions tend to be well defined, with macrocystic features (>2 cm3), others tend to be interstitial, infiltrating and poorly defined microcystic lesions (< 2 cm3), and the third group consists of mixed lesions. Most lymphatic malformations are diagnosed in infancy, with up to 90% being apparent by 2 years of age. Currently, MRI is the diagnostic tool of choice.
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TREATMENT Hemangiomas17,18 There is no accepted consensus on the treatment of infantile hemangiomas although the prevailing trend is to intervene rather than follow the old dictum of benign neglect (‘leave it alone, it will go away’). Often, the proliferation of the hemangioma can be stopped with early treatment with a vascular laser. Furthermore, the vast majority of hemangiomas involute incompletely and leave a cosmetic defect necessitating intervention regardless of how long patients are willing to wait. Additionally, the psychological literature has documented the effects of facial differences on self-image.‘Success in life’ has been found to correlate with facial self-image of children between the ages of 2 and 5 years.19,20 The goal of therapy in young children is to optimize the chance of normal facial appearance and function by elementary school age. Limited hemangiomas that are not on the face have not been shown to have an effect on self-image. Treatment for hemangiomas varies, depending on anatomical site, functional and cosmetic significance, depth, complicating factors (i.e., ulceration or visual axis impingement), and whether the lesion is proliferating or involuting. As for most medical problems, hemangioma management decisions are made after analyzing the risks as well as the potential benefits. For most cutaneous hemangiomas, the greatest risk is bleeding if the lesion is traumatized. However, depending on location, hemangiomas can cause visual field obstruction or be at risk for causing airway obstruction. Since these are significant risks due to the lesion, they usually outweigh the risks of therapy. One approach to deciding whether to treat a hemangioma is to ask the question: ‘Can we get a result now with this (particular) treatment that is at least as good as if we observe the lesion and allow it to follow its known and presumed natural course?’ If the answer is yes, then that specific intervention is justified at that time. If the answer is no at that time, then observation is continued until a predetermined point of re-evaluation. Serial observation is an active treatment option and very different than telling the parents to wait an
Fig. 11.1 This young child presented with an proliferating superficial hemangioma, which involved the external nasal skin and extended into the nostril opening. It was treated with a 595 nm laser and had an excellent response.After the first treatment, it stopped proliferating and regressed with subsequent treatments. (Photograph courtesy of Paul J Carniol MD.)
indeterminate number of years for the hemangioma to ‘go away’ – particularly as some hemangiomas will never completely regress, and even with regression there can be sequelae. In addition to observation, during the proliferative period, treatment can include steroid therapy, laser treatment, surgical excision, or combination therapy. Lasers play an important role in the treatment of cutaneous hemangiomas.21 Frequently, early treatment of a proliferating hemangioma will either slow or cease proliferation. In some cases, this will even lead to early regression of the lesion, thereby minimizing the chance of scarring or other problems. (Fig. 11.1). Even hemangiomas that have thickened and are still actively growing will respond to vascular laser therapy
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a
b
Fig. 11.2 This child presented with a proliferating hemangioma of the left malar region (a). She had an excellent response to a series of treatments with a 595 nm laser (b). (Photographs courtesy of Paul J Carniol MD.)
(Fig. 11.2). After initial laser therapy, any residual lesion can be treated with lasers or surgical intervention if or as needed in the future. From infancy until over a year of age, this can frequently be performed without the use of general anesthesia. These hemangiomas are usually treated with a 595 nm flashlamp-pumped dye laser (VBeam, Candela, Wayland, MA). Recently, a device has become available that employs both a 595 nm laser and a 1064 nm laser (Cynergy, Cynosure, Westford, MA). As well as allowing separate use of the lasers, this device can also be used in multiplex sequential laser mode to treat vascular lesions.With this technology, it can be used not only to treat 595 nm laser-responsive lesions, but also to treat lesions that are resistant or minimally responsive to the 595 nm laser. This offers an advantage in treating hemangiomas and resistant venular vascular malformations (‘portwine stains’). Rapidly proliferating hemangiomas that pose a functional or serious cosmetic threat can be treated with systemic corticosteroids, although there is a lack of consensus on their use.This lack of consensus is due to the potential for significant sequelae from corticosteroid therapy. Furthermore, corticosteroids are only useful during proliferation. Therefore, their use needs to be carefully justified, and serial observation in cooperation with the child’s pediatrician is necessary. At present, a dose of 4 mg/kg/day oral prednisone or
prednisolone for a period of 4–6 weeks and tapered over 2 weeks is frequently employed. If there is no response within the initial 2 weeks of treatment, the steroid should be tapered over 1 week and discontinued. These protocols may change in the future. Therefore, we recommend that, before initiating therapy, practioners should review the most recent therapeutic recommendations and the criteria for utilization. Appropriate patient evaluation and determining whether corticosteroids are indicated should be undertaken prior to initiating this therapy. Although 75% of patients respond significantly to this regimen, rebound growth may occur as the corticosteroid dose is tapered. If this occurs, then the lowest dose that maintains proliferation in check should be maintained for an additional 3–4 weeks and then tapered again. The patient should be followed cautiously by a pediatrician and monitored for the possible side-effects of steroid treatment. Long-term complications have not been observed, and justify the use of the drug in appropriate cases.22 Intralesional steroid injections are useful for a limited group of very welldefined, focal, deep, and occasionally compound hemangiomas. We use an injection mixture of triamcinolone (40 mg/ml) and betamethasone (6 mg/ml)8 in very select cases of parotid, eyelid, and midcheek lesions. We do not inject auricular or nasal tip hemangiomas,
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Management of vascular lesions since steroid injection can be associated with weakening of the supporting cartilages and white plaque deposits can be seen through the thin soft tissue envelope. The goal of depot injections is to slow proliferation of the deep component. Great care must be taken when using lasers to treat injected lesions, as there appears to be a higher risk for ulceration, particularly in the malar area (personal observations by one of the authors (MH) from 1990 to the present). If the lesion is life-threatening or does not respond to steroid therapy, other medications such as vincristine can be considered. Although initially the first choice for these difficult situations, interferon in children under the age of 1 year should be used very cautiously because of the associated high incidence of spastic diplegia now recognized. Due to this risk, many centers will not use interferon therapy. Other medications, such as imiquimod, a topical immunomodulator, may prove useful for controlling proliferating hemangiomas, although controlled studies are still needed to confirm its efficacy in humans. Recently, intralesional bleomycin has been advocated in the treatment of proliferating hemangiomas, although again further experience is needed to validate its use.23,24 Before initiating systemic therapy, it is important for each physician to review the current recommendations for such therapy. Surgical management of hemangiomas is integral to the overall treatment algorithm.17,18,25 Historical misgivings and misconceptions about the operability of these lesions have been supplanted by experience and better understanding. Surgical planes exist (between the hemangioma and surrounding structures) or can be created (between the superficial and deep components or within the deep component). Hemangiomas are solid tumors with few, isolated feeding vessels. Therefore, meticulous technique and the use of routine micro-unipolar and bipolar devices makes their dissection virtually bloodless. Conservatism is critical when resecting facial tissue in children, and the use of flaps and grafts is avoided as far as possible. The goal is to resect enough tissue and achieve primary closure of the skin. We avoid the use of flaps and grafts. However, in complicated cases, due to the extent of the lesion, primary closure may not be possible. Subtotal excision of the deep component to preserve contour or to set the stage for a further resection
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is common. Every effort is made to obtain a functional and cosmetic result before school age to minimize the potential for psychological sequelae. When considering surgery, the risks of the procedure, including the risk of possible postoperative morbidity, should be considered. Our threshold for excision of nasal tip and periorbital lesions, with a significant associated deformity, is lower than for other sites, because of the obvious severe potential functional and cosmetic sequelae. If the potential benefits of surgical excision (e.g., cosmetic improvement and parents’ peace of mind) outweigh the potential risks, lesions at other sites can also be excised during the proliferative phase. Once the phase of proliferation is ended, the progression of involution of the lesion may be observed for a few months. If there is no significant involution, then treatment should be considered based on the previously discussed principles. If the lesion undergoes involution, lasers and other modalities can be used to treat atrophic scarring, telangiectasia, and residual subcutaneous fibrofatty tissue. Atrophic scarring can be treated with carbon dioxide (CO2) or erbium laser skin resurfacing. More recently, a fractionated CO2 laser has become available that also can be used to treat this scarring (Active Fx, Lumenis, Santa Clara, CA). Residual telangiectasias can be treated with a vascular laser (VariLite, Iridex, Mountain View, CA; Cynergy, Cynosure, Westford MA; VBeam, Candela, Wayland, MA). Residual subcutaneous fibrofatty tissue can be excised and sculpted to obtain better contours.
Capillary and venular vascular malformations Vascular malformations can vary in size and location, from small limited vascular malformations (Fig.11.3) to extensive malformations, with intracranial involvement such as Sturge–Weber syndrome. Laser therapy is the preferred method of treatment for capillary and venular vascular malformations (‘portwine stains’). There are now a number of lasers that can potentially be used to treat these lesions (see the lasers listed above for hemangiomas). Start-safe parameters are used for the initial laser pulses to evaluate the clinical response and set the stage for further treatments.26
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a
b
Fig. 11.3 (a) This young woman had a limited venular vascular malformation of the left side of her neck. (b) She responded well to two treatments with a vascular laser with complete clearing of the visible lesion. (Photographs courtesy of Paul J Carniol MD.) Once the response to the initial laser pulses has been assessed, the laser parameters can be adjusted. Portwine stains are typically treated every 4–6 weeks. The therapeutic endpoint is clearance of the lesion, diminished response to therapy, or the patient deciding that the improvement has reached their personal goal. Venular vascular malformations do not grow new vessels after birth. However, due to the hydrostatic pressure, over time, the blood vessels involved in these malformations increase in diameter. Therefore, after laser therapy, even if the residual vessels are not clinically apparent, over time they may become visible due to increased diameter. Thus, at some time in the future, some of these patients will redevelop visible lesions that will require retreatment.Thickened, ‘cobblestoned’, or purple vascular malformations may not respond to treatment with a 595 nm laser alone. However, these lesions may respond to ‘multiplex’ therapy with the sequential 595 nm–1064 nm Cynergy laser. Some of these lesions have also responded to careful treatment with a neodymium : yttrium aluminum garnet (Nd:YAG) laser.
Venous malformations Venous malformations can be treated with laser photocoagulation, sclerotherapy, or surgical resection,
depending on the depth, extent, and location of the lesion. Due to their blue color, these may not respond to traditional vascular lasers. However, superficial lesions or the superficial component of compound lesions can be treated with a sequential 595 nm–1064 nm laser (Cynergy) or with judicious use of an Nd:YAG laser. Laser photocoagulation diminishes the vascularity of the overlying skin or mucosa, which can then be preserved if surgical resection of the deeper component is performed.The deep component of the lesion should be resected carefully because of the risk of bleeding due to extremely fragile ectatic vessels. In contrast to hemangiomas – and probably the source of misgivings about the role of surgery for vascular lesions – hemostasis during these procedures can be quite challenging. Tedious dissection and hemostasis with vascular clips, peripheral transcutaneous sutures, and topical hemostatic agents are employed to varying degrees. Preparation for blood transfusions should be made preoperatively. Resection of the cutaneous component is imperative to prevent recurrence. Sclerotherapy and embolization are viable alternatives in the treatment of venous malformations. They are also useful as pre- and postoperative adjunctive treatment. Sclerotherapy involves a percutaneous puncture into the malformation, and, under fluoroscopic guidance, an irritant is injected into the malformation to promote
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Management of vascular lesions clotting, inflammation, and eventually fibrosis of the lesion. It is important to note that sclerotherapy can require repeated treatments to maintain control of the lesion, and usually is not considered curative as the lesion may eventually re-expand. Sclerosing agents, such as absolute ethanol, sodium tetradecyl sulfate, sodium morrhuate, polidocanol, sclerosant foam, and ethanolamine, have been reported in the treatment of venous malformations.27 Injection of sclerosing agents has significant associated risks in the upper two-thirds of the face. The veins in the head and neck region lack valves. Therefore, the injection of sclerosing agents in the upper and middle third of the face can cause cavernous sinus thrombosis. The amount of sclerosing agent depends on the agent itself and the extent of venous malformation, but, as a rule, it should not exceed 1 ml/kg of body weight. If the lesion is extensive and more than one treatment is necessary, they should be spaced at 4- to 6-week intervals.
Arteriovenous malformations Treatment with laser, steroids, or irradiation has not been effective in the management of arteriovenous malformations. The most effective treatment of these lesions is complete surgical excision of the lesion with clear margins, followed by immediate reconstruction. If the lesion is extensive, then combined treatment consisting of highly selective embolization followed by complete resection within the next 24–48 hours is indicated. The natural progression of the lesion is inexorable growth over time. Therefore, the main goal of surgery should be complete eradication of the nidus, with clear margins to prevent recurrence. The sacrifice of structures involved by the arteriovenous malformation (e.g., mandible, facial nerve, and muscles of mastication) may be a necessary part of the procedure. The surgical and anesthetic team must be prepared to replace with blood products, and cell-saver technology may be helpful in the most difficult cases. Resection and reconstruction of these and other malformations is more akin to traditional head and neck cancer procedures than those for infantile hemangiomas.
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Lymphatic malformations Surgical excision is the preferred treatment modality for lymphatic malformations. Because of the difficulty of distinguishing involved tissue from normal tissue, complete resection of lesions with microcystic infiltrating features is not always possible. Lesions with well-defined macrocystic features are more likely to be resected completely. Superficial mucosal lesions can be treated with the CO2 laser using 20 W continuous mode until sufficient depth of destruction is obtained. The wound is then left to heal by second intention. Extensive lesions involving both mucosa and deep soft tissue may need to be treated with a combined approach. Recurrence after ‘total’ resection of macrocystic lesions is probably due to infiltrating features of the lesions at the interface with normal tissues. Mass reduction with needle aspiration is reserved for cases with a threatened airway. OK-432 (a lyophilized mixture of a low-virulent group A Streptococcus pyogenes incubated with penicillin G) is not yet approved for general use in the USA, but has been used extensively in Europe and Japan, with results showing up to 96% complete response in macrocystic lesions. Bleomycin has also been used, with similar results. Overall, the literature continues to support good results with sclerotherapy in patients with macrocystic disease only, which is the same entity that traditionally also responds well to surgery. Patients with microcystic disease, especially if it is extensive, will likely require multiple therapies to help control and alleviate their symptoms.28,29
Facial telangiectasias and rosacea Many adults are unhappy with their facial telangiectasias. These frequently appear around the nasal ala, nasal tip, nasal dorsum, chin, and cheeks (Fig. 11.4). The majority of these will respond to treatment with a vascular laser. For some of these lesions, the response to a particular laser wavelength varies with the diameter of the involved vessel.30 Larger-diameter vessels frequently will have a better response to a 940 nm laser than to a 532 nm laser. Besides medical therapy, the redness of rosacea can also be treated with a vascular laser. Patients are often
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b
Fig. 11.4 (a) This patient was unhappy with nasal and cheek telangiectasias. (b) After treatment with a 532 nm and 940 nm laser (VariLite, Iridex, MountainView, CA) she had a significant improvement in her telangiectasias. (Photographs courtesy of Paul J Carniol MD.) very pleased with the lightening and decreased redness from laser therapy.
CONCLUSIONS Correct diagnosis is the major factor in successful treatment of vascular lesions of the head and neck. Hemangiomas must be differentiated from vascular malformations because of the therapeutic implications. Steroids, lasers, and surgical excision all have a place in the management of these lesions. As more information is gained about the pathophysiology of these lesions, the management schema will continue to evolve.
ACKNOWLEDGMENT This work was supported is part by The Hemangioma Treatment Formulation (www.hemangiomatreatment. org).
REFERENCES 1. Marler J, Mulliken J. Vascular anomalies – classification, diagnosis and natural history. Facial Plast Surg Clin North Am 2001;9:495–504. 2. Mulliken JB, Fishman SJ, Burrows PE. Vascular anomalies. Curr Probl Surg 2000;37:519–84 3. Mulliken JB, Glowacki J. Hemangiomas and vascular malformation in infants and children: a classification based on endothelial characteristics. Plast Reconstr Surg 1982; 69:412–20.
4. Bauland CG, van Steensel MA, Steijlen PM, Rieu PN, Spauwen PH. The pathogenesis of hemangiomas: a review. Plast Reconst Surg 2006;117:29e–35e. 5. Waner M, Suen J. Hemangiomas and Vascular Malformations of the head and Neck. New York: WileyLiss, 1999. 6. Krol A, MacArthur CJ. Congenital hemangiomas. Arch Facial Plast Surg 2005;7:307–11. 7. Mulliken JB, Enjolras O. Congenital hemangiomas and infantile hemangiomas: missing links. J Am Acad Dermatol 2004;50:875–82. 8. Powell TG, West CR, Pharoah PO, Cooke RW. Epidemiology of strawberry hemangioma in low birthweight infants. Br J Dermatol 1987;116:635–41. 9. Amir J, Mezker A, Krikler R, Reisner SH. Strawberry hemangioma in preterm infants. Pediatr Dermatol 1986;3:331–2. 10. Blei F,Walter J, Orlow SJ, Marchuk DA. Familial segregation of hemangiomas and vascular malformations as an autosomal dominant trait. Arch Dermatol 1998;134: 718–22. 11. Phung TL, Hochman M, Mihm M. Current knowledge of the pathogenesis of infantile hemangiomas. Arch Facial Plast Surg 2005;7:319–21. 12. Waner M, North P, Scherer KA, Frieden IJ.The non-random distribution of facial hemangiomas. Arch Dermatol 2003;139:869–75. 13. Williams EF 3rd, Starislaw P, Dupree M, et al. Hemangiomas in infants and children: an algorithm for intervention. Arch Facial Plast Surg 2000;2:103–11. 14. Smollen BR, Rosen S. Port wine stains: a disease of altered neural modulation of blood vessels? Arch Dermatol 1986;122:177–9. 15. Kohout MP, Hansen M, Pribaz JJ, Mulliken JB. Arteriovenous malformations of the head and neck: natural history and management. Plast Reconstr Surg 1998;102:643–54. 16. Buckmiller L. Update on hemangiomas and vascular malformations. Curr Opin Otolaryngol Head Neck Surg 2004;12:476–87.
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Management of vascular lesions 17. Hochman M, Williams EF. Management of cutaneous hemangiomas. Facial Plast Surg Clin North Am 2001; 9:621–8. 18. Hochman M, Mascareno A. Management of nasal hemangiomas. Arch Facial Plast Surg 2005;7:295–300. 19. Lande RG, Crawford PM, Ramsey B. Psychosocial impact of vascular birthmarks. Facial Plast Surg Clin North Am 2001;9:561–7. 20. Williams EF 3rd, Hochman M, Rodgers BJ, et al. A psychological profile of children and families afflicted with hemangiomas. Arch Facial Plast Surg 2003;5:220–34. 21. Thomas RT, Hornung RL, Maaning SC, Perkins JA. Hemangiomas of infancy: treatment of ulceration. Arch Facial Plast Surg 2005;7:312–15. 22. Boon L, MacDonald DM, Mulliken J. Complications of systemis corticosteroid therapy for problematic hemangiomas. Plast Reconst Surg 1999;104:1616–22. 23. Adams D. The non-surgical management of vascular lesions. Facial Plast Surg Clin North Am 2001;9:601–8. 24. Pienaar C, Graham R, Geldenhuys S, Hudson DA. Iatralesional bleomycin for the treatment of hemangiomas. Plast Reconst Surg 2006;117:221–6.
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25. Balniji RK, Buckingham E, Williams EF. An aesthetic approach to facial hemangiomas. Arch Facial Plast Surg 2005;7:301–6. 26. Kelly KM, Choi B, McFarlane S, et al. Distribution and analysis of treatment for port-wine stains. Arch Facial Plast Surg 2005;7:287–94. 27. Deveikis JP. Percutaneous ethanol sclerotherapy for vascular malformations in the head and neck. Arch Facial Plast Surg 2005;7:322–5. 28. Fujino A, Moriya Y, Kitajima M, et al. A role of cytokines in OK-432 injection therapy for cystic lymphangioma: an approach to the mechanism. J Pediatr Surg 2003;38: 1806–9. 29. Banieghbal B, Davies MRQ. Guidelines for the successful treatment of lymphangioma with OK-432. Eur J Pediatr Surg 2003;13:103–7. 30. Carniol PJ, Price J, Olive A. Treatment of telangiectasias with the 532 nm and the 940/532 nm diode laser. Facial Plastic Surg 2005;21:117–19.
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12. Laser treatment for unwanted hair Marc R Avram
INTRODUCTION
THE CONSULT
Hair is a physical characteristic that helps distinguish each one of us as individuals. The color, length, and texture of hair on our scalp are among the few physical characteristics that we can control. Hair frames our face. A full head of hair makes any individual appear more youthful. Millions of people try to maintain their hair with medication and surgery.1 While a positive physical characteristic on the scalp, eyebrows, and eyelashes, hair on almost every other part of the skin is perceived as a negative physical attribute. For decades, millions of people sought treatment to remove unwanted hair. The majority of treatment options resulted in a safe but temporary reduction of hair requiring regular maintenance throughout life. In the 1990s, the most significant new treatment option to permanently destroy hair was introduced: laser hair removal.2 Laser hair removal is based on the theory of selective photothermolysis.3 Selective photothermolysis has revolutionized the therapeutic role of lasers in medicine. In the skin, prior to removing hair, it was successfully applied to treating unwanted vascular lesions, pigmented lesions, tattoos and wrinkles.4–6 Laser hair removal has become one of the most popular cosmetic procedures over the past ten years. For millions of patients, it has resulted in a long-term reduction in unwanted hair. As with any procedure, appropriate candidate selection and expectations are vital to its success. Appropriate candidate selection, expectations, choice of laser/light device, and the risks of the procedure and how to minimize them are established during a medical consultation.
All patients undergoing laser hair removal should have a medical consultation before the procedure (Table 12.1). For the vast majority of patients, unwanted hair is the result of a combination of benign hormonal and genetic factors. In a minority of patients, unwanted hair can be a cutaneous sign of an underlying medical condition or a side-effect of medication.7 A medical consultation is needed to help distinguish between the two. The target chromophore for laser/light sources using selective photothermolysis is thought to be melanin.8 This is the reason current technology only works on pigmented hair. Patients with blond, gray, or lightly pigmented hair will see no improvement from laser/light sources, and should not undergo treatment. All skin types can undergo successful hair removal. Since melanin is the target chromophore, the risk of cutaneous hyper- or hypopigmentation in darker skin types is higher with shorter wavelengths such a 694 nm ruby, 755 nm alexandrite or 800 nm diode lasers. Longer wavelengths with longer pulse durations such a 1064 nm long-pulse yttrium aluminum garnet (YAG), penetrate deeper into skin relatively Table 12.1 Candidate selection Good candidate
Poor candidate
Pigmented thick hair All skin types Realistic expectations
Unpigmented hair Vellous hair Persistent sunburn Unrealistic expectations
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sparing epidermal pigment and reducing (but not eliminating) the risk of hyper/hypopigmentation.9 The caliber of the hair follicle also helps determine the success of the procedure. Thick hair tends to respond better than thin vellous-like hair. In a small minority of patients with a lot of vellous hair, a paradoxical growth of hair may even occur.10 The reason for this remains unknown. The laser works best on follicles in an anagen phase of growth. This results in the need for multiple treatments to achieve a clear clinical hair reduction. Since follicles in the anagen phase are the target, treatments should be spaced between 4 and 12 weeks depending on the location on the body.There is variability on how well each patient will respond. Most patients will have a majority of hair removed after 5–10 treatments. A minority will have near complete removal and a small minority little or no improvement. Patients should also be aware of the potential need for future maintenance treatments. It is unclear whether such maintenance treatments are needed as a result of hair follicles emerging from a prolonged laser-induced telogen phase or of newly generated hair follicles. At the end of the consult, patients should be encouraged to ask questions or contact the office with any questions or concerns prior to scheduling the procedure.The overwhelming majority of patients with realistic expectations of what lasers can and cannot due for removing hair will be happy with their result.
PREOPERATIVE All patients should be given a written informed consent to review. Common potential side-effects, posttreatment protocol, current medications, past medical history, and questions regarding the procedure and consent should be discussed. An active sunburn or inflammatory dermatosis increases the risk of blistering resulting in potential dyschromia or textural changes in the skin. Sunscreen use and sun protection prior to treatment and in the first 48 hours after treatment need to be emphasized to lower the risk of sideeffects. A patient presenting to the office with a sunburn or active inflammatory dermatosis should be rescheduled.
Fig. 12.1 All individuals wear protective eye shields.
The amount of pain associated with the procedure is a reflection of the density and caliber of hair follicles on the treated skin. Patients with thick, dense hair will experience pain with the procedure, while those with less density and finer hair will experience less pain. The perception of pain varies from individual to individual. The majority of patients undergo treatment with no anesthesia and tolerate the procedure well. Some require or request a topical anesthetic to reduce discomfort. Topical anesthetics should be used in safe quantities and as directed to minimize the risk of lidocaine toxicity.11 Local anesthetics should not be used in the region to be treated by a laser or light source, because the water in the dermis from the local anesthetic will be heated by the energy from the laser light, thereby increasing the risk of a blistering reaction, dyschromia, and textural changes in the skin.
THE PROCEDURE Safety is paramount in the operation of all lasers (Fig. 12.1). Everyone in the procedure room should wear protective shields or goggles. Hair should be trimmed in the treated region to reduce the risk of epidermal changes secondary to thermal injury of follicles above the skin and to reduce the plume in the room. Careful attention should be paid to treat the entire surface of
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Fig. 12.3 Larger spot sizes allow greater penetration of laser light.
Fig. 12.2 Poor cosmetic result secondary to lack of overlap of spot size when treating the back.
the desired treatment zone by slightly overlapping each pulse (Fig. 12.2). It is vital that the appropriate use of the laser and cooling device be followed to reduce the risk of side-effects.12 Many lasers require firm contact with the skin for optimal efficacy and safety. Any operator of a laser should be thoroughly trained in the appropriate technique. Larger spot sizes will allow for a more rapid treatment and greater penetration of energy into the skin, and should be used wherever possible13 (Fig. 12.3). Immediately following the treatment, erythema and perifollicular edema are visible, which typically resolve in 30–60 minutes (Fig. 12.4). Postoperative instructions should be reviewed. Patients should be encouraged to contact the office if there is any crusting, blistering, dyschromia, pain after the procedure, or any questions or concerns.
Fig. 12.4 Perifollicular edema immediately after treatment.
COMPLICATIONS All medical procedures are associated with potential side effects. Laser hair removal is no exception. Every physician’s goal is to minimize any risk of sideeffects.The majority of complications can be avoided by a proper physical examinations, medical history, and appropriate preoperative instructions during the consultation. Common side-effects includes
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Clinical procedures in laser skin rejuvenation Table 12.2 Complications from laser hair removal Common
Unusual
Transitory acne/folliculitis Transitory crusting Transitory dyschromia
Permanent dyschromia Scarring Paradoxical increase in hair Ocular damage Vascular changes Viral or bacterial infection
REFERENCES Fig. 12.5 Dyschromia secondary to inappropriate power and technique.
transitory, crusting, superficial erosions and pseudofolliculitis and temporary dyschromia (Figs. 12.5 and Table 12.2). Unusual complications include permanent dyschromia, scarring and paradoxical increased hair growth, ocular damage from operator error, infection, and vascular changes in the skin. All patients should be encouraged to contact the office and be seen as soon as possible if they believe they are having any side-effects after a procedure. Rapid medical intervention can often eliminate or substantially reduce the long-term effects of a complication.
THE FUTURE Currently, laser hair removal is a safe, effective procedure. With appropriate candidate selection, expectations, and laser device, the vast majority of patients are happy with the results. A challenge remains to permanently remove unpigmented or lightly pigmented hair follicles. Several different technologies have been tried without consistent effective long-term permanent reduction of hair.14 Photodynamic therapy may become a treatment option. Effective, safe, affordable home devices may be another development in the field over the next several years. Ultimately, safe selective genetic manipulation of hair follicles where we want and where we do not want it on our skin will become a reality.
1. Avram MR, Cole JP, Gandelman M, et al. The potential role of monoxidil in hair transplantation setting. Dermatol Surg 2002;28:894–900. 2. Grossman MC, Dierickx C, Farinelli W, Flotte T, Anderson RR. Damage to hair follicles by normal-mode ruby laser pulses. J Am Acad Dermatol 1996;35:889–94. 3. Anderson RR, Parrish JA. Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science 1983;220:524–7. 4. Anderson RR, Margolis RJ, Watenabe S, et al. Selective photothermolysis of cutaneous pigmentation by Qswitched Nd:YAG laser pulses at 1064, 532, and 355 nm. J Invest Dermatol 1989;93:28–32. 5. Astner S.Anderson RR.Treating vascular lesions. Dermatol Ther 2005;18:267–81. 6. Bernstein EF. Laser treatment of tattoos. Clin Dermatol 2006;64:850–5. 7. Azziz R. The evaluation and management of hirsutism. Obstet Gynecol 2003;101:995–1007. 8. Wanner M. Laser hair removal. Dermatol Ther 2005; 18:209–16. 9. Battle EF, Hobbs LM. Laser assisted hair removal for darker skin types. Dermatol Ther 2004;17:177–83. 10. Alajlan A, Shapiro J, River JK, et al. Paradoxical hypertrichosis. J Am Acad Dermatol 2005;53:85–8. 11. Brosh-Nissimov T, Ingbir M,Weintal I, Fried M, Porat R. Central nervous system toxicity following topical skin application of lidocaine. Eur J Clin Pharmacol 2004;60:683–4. 12. Klavuhn KG, Green D. Importance of cutaneous cooling during photothermal epilation: theoretical and practical considerations. Lasers Surg Med 2002;31:97–105. 13. Baumler W, Scherer K, Abels C, et al.The effect of different spot sizes on the efficacy of hair removal using a longpulsed diode laser. Dermatol Surg 2002;28:118–21. 14. Sadick NS, Laughlin SA. Effective epilation of white and blond hair using combined radiofrequency and optical energy. J Cosmet Laser 2004;6:27–31.
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13. NonInvasive body rejuvenation technologies Monica Halem, Rita Patel, and Keyvan Nouri
INTRODUCTION It is estimated that by the year 2010, the American population will consist of 40.2 million people over the age of 65.1 This rise in the aging population has led to an increase in the number of cosmetic procedures performed each year. According to the American Society for Aesthetic Plastic Surgery (ASAPS) 2006 statistics report, nearly 11.5 million cosmetic procedures were performed in the USA in 2005.2 In addition, there was a reported increase in noninvasive procedures with 19% surgical and 81% nonsurgical procedures, being performed in 2005.2 As is evident from these recent statistics, cosmetic surgery has embarked on a new trend toward less invasive procedures.The aging population is looking for rejuvenation procedures that deliver achievable results, yet with reduced downtime and minimal risk profile. This movement in cosmetic medicine has been away from invasive and destructive processes and toward innovative technologies and techniques that spare tissue and promote growth. However, while these treatments have fewer sideeffects and decreased downtime, they often require multiple treatments for comparable results. Improving the appearance of the skin without injury to the epidermis is the hallmark of nonablative skin rejuvenation. This novel arena of rejuvenation monopolizes on the intrinsic energies of nonablative laser, radiofrequency, and optical devices to treat a wide array of skin afflictions, ranging from eliminating vascular and benign pigmented lesions of the skin to improving the appearance of photodamaged skin and rhytids. Nonablative technologies, which have been successful on the face and neck, are now being applied to the body in the hope of eradicating some of the more
displeasing physical changes characteristic of aging, such as striae distensae, cellulite, and fat, while having the added capacity of contouring flaccid skin. Up until recently, body rejuvenation therapy has been solely contingent on invasive procedures, such as liposuction, abdominoplasty, reconstructive surgeries, and ablative procedures as a means of returning the body’s appearance to a more aesthetically pleasing ideal. While achieving appreciable results, these procedures are not without adverse effects, well-described morbidities, significant downtime, and long-term sequelae (pigmentary changes and scarring). With the increasing amounts of clinical data and results from scientific studies, the techniques of nonablative body rejuvenation, producing safe and effective treatment for an ever-growing aging population, are being refined.This chapter summarizes the current data and the use of noninvasive technologies for body rejuvenation.
STRIAE DISTENSAE Striae distensae, known colloquially as stretchmarks, were described as a clinical entity hundreds of years ago, with the first histological description appearing in the medical literature in 1889.3 Striae are common cutaneous lesions that are cosmetically displeasing to many patients. They are characterized by wide linear bands of atrophic or wrinkled skin that occur in areas of dermal damage secondary to stretching.The distribution of striae is quite variable, but typically involves the abdomen, buttocks, breasts, and skin flexures. Extremities, including the arms, thighs, and bicepital areas, may also be involved. Women develop striae more commonly than men, with studies showing that
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70% of adolescent females and 40% of adolescent males develop these lesions.4 The etiology of striae is still controversial and is closely related to the variable clinical scenarios it accompanies.They usually occur during diverse physiological states, including pregnancy, adrenocortical excess (long-term steroid therapy and Cushing’s syndrome), changes in body habitus, obesity, and rapid weight gain.3,4 There is an association with sudden changes in glucocorticoid levels, which commonly occur during pregnancy or growth spurts of adolescence. Striae are seen in 90% of pregnant women due to a combination of hormonal factors along with increased lateral stress on connective tissue.5 A recent study of 161 women found that striae gravidum are most likely to develop early in gestation, with peak incidence occurring in the first and second trimesters.6 Several studies have shown the pathogenesis of striae to be related to changes among the dermal extracellular matrix components, including fibrillin, collagen, and elastin, during stretching of the skin.7 Different theories have been proposed with regard to what happens to these components during stretching, including dermal collagen rupture, elastolysis, and mast cell degranulation leading to elastic fiber changes and disrupture of crosslinked collagen.7–9 In one study, Lee et al10 found a possible genetic predisposition to striae. They found a decreased expression of collagen and fibronectin genes in striae distensae tissue. The development of striae distensae can further be seen as an evolution of both clinical and histological changes. Initially, striae rubra represent thin, red to pink, raised lesions that eventually enlarge in size and acquire a vivid purple appearance. These fresh striae show acute inflammatory changes, such as deep and superficial lymphocytic infiltration accompanied by dilated vasculature and edema of the upper dermis. Over time, bundles of collagen and elastic tissues in the reticular dermis disappear, leaving behind a much thinner epidermis with attenuation of the rete ridges. These striae are now more atrophic and scar-like, and turn to white striae alba.11 The treatment of striae distensae has been challenging, and various modalities have been studied. These include topical therapies such as topical tretinoin 0.1% alone or in combination with 20% glycolic acid, as
well as the combination of 20% glycolic acid with 10% acid.12,13 Microdermabrasion has also been added to these treatment regimens to enhance the penetration of the topical therapies. These therapies have yielded variable cosmetic results, working to productively decrease redness and size of striae rubra but having much less success in older, more atrophied striae alba.14 L-ascorbic
Pulsed dye laser The use of noninvasive laser devices to correct striae distensae has gained popularity due to their reliability. The pulsed dye laser was the first to be tried, based on its success in treating hypertrophic and keloidal scars.15–18 McDaniel et al19 showed that the 585 nm flashlamp-pumped pulsed dye laser can be used to treat striae. They treated 39 patients with striae using this laser at four different fluence treatment protocols. Results were evaluated using a combination of blinded objective grading and skin surface analysis with optical profilometry. Pulsed dye laser therapy was shown to improve the appearance of the striae. In addition, the optimal treatment fluence was determined to be 3 J/cm2 using a 10 mm spot size. Biopsies obtained during this study found an increase in dermal elastin content coinciding with the improvement of clinical appearance.Further biopsies taken 8–12 weeks after treatment showed a marked increase in elastin content in the papillary and reticular dermis. McDaniel et al19 concluded that laser therapy for striae may produce clinical improvement for up to 6–12 months post treatment. Another study looking at the treatment of mature striae with the pulsed dye laser confirmed the histological changes in elastin.20 Five patients were prospectively treated with the 585 nm pulsed dye laser at 2-month intervals for 1–2 years.The response of the striae was evaluated through sequential clinical, photographic, textural, and histological assessment. All five patients showed clinical improvement, and serial biopsies of the striae 8 weeks post treatment revealed an increase in dermal elastin that coincided with this clinical improvement. Alster and colleagues21 conducted a larger multicenter trial using the 585 nm flashlamppumped pulsed dye laser at low energy settings to treat striae. The patients were followed for 6 months
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Noninvasive body rejuvenation technologies prospectively to determine the results of multiple treatments and length of therapy.They concluded that striae responded best to lower energy densities at 3.0 J/cm2, and that there was continued improvement of appearance for as long as 6 months after a single treatment. They further postulated that the improvement may be due to the laser-induced effects on hemoglobin, elastin, collagen, or other undiscovered factors. Another study comparing the treatment of striae rubra and striae alba using the 585 nm pulsed dye laser on 29 patients for 12 weeks concluded that the pulsed laser had a moderate beneficial effect in reducing the degree of erythema in striae rubra; however, no effect of the laser on striae alba was found. It was further found that the total weight of collagen per gram of dry weight of sampled tissue increased in the striae rubra treated with the pulsed dye laser as compared with controls. A study using a copper bromide laser (577 nm), with a similar wavelength to the pulsed dye laser, treated 15 patients with striae and followed these patients for 2 years post treatment.22 These authors treated patients with skin types II–III with the copper bromide laser at 4 J/cm2, with five sessions 1 month apart, with clinical improvement. A follow-up at 2 years confirmed the stability of the results achieved. The use of the pulsed dye laser for the treatment of striae distensae has been recommended with caution or avoided in patients with skin types IV–VI. A study comparing the 585 nm pulsed dye laser and the short pulsed carbon dioxide (CO2) laser in the treatment of striae distensae in skin types IV and VI observed marked hyperpigmentation in darker skin types.23 It was concluded that this was secondary either to the inflammation created during the treatment or to the hemoglobin-competing chromophore melanin at the 585 nm wavelength.
Intense pulsed light Intense pulsed light (IPL) is another type of therapy currently being used to improve stretch marks. IPL is generated by a noncoherent filtered flashlamp with a very broad spectrum (515–1200 nm). It can provoke favorable microscopic effects via direct emission of a visible polychromatic pulsed light of high intensity. IPL has been proven to be effective for the treatment of
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telengiectasias, lentigines, vascular malformations, and leg veins and for photoepilation.24–27 It has also shown efficacy in the treatment of poikiloderma of Civatte and for facial photorejuvination.28,29 Based on these results, studies were conducted using IPL to treat striae. In a prospective study of 15 women with abdominal striae treated with five sessions of IPL once every 2 weeks, IPL was found to improve the clinical and histological appearance of the striae in all 15 patients.11 Post-treatment histology showed epidermal thickening, increases in dermal thickness, and improvement of the quality of collagen fibers, with reappearance of rete ridges due to the deposition of new fibers. However, postinflammatory hyperpigmentation occurred in 40% of patients, making this modality difficult to use in dark-skinned patients.
Ultraviolet While both the pulsed dye laser and IPL have been used with slight success in treating striae rubra, they have not been shown to be as effective for the treatment of leukoderma in striae alba.14,19,22 In cases of cutaneous hypopigmentation and depigmentation, phototherapy has been shown to be of value for disorders such as vitiligo, scars, and postresurfacing leukoderma.30–32 Recently, the narrowband 308 nm UVB excimer laser has been used to treat striae alba. One study treated 31 patients, who were randomized to a treatment arm with site-matched control areas.33 Treatments were initiated with a minimal erythema dose minus 50 mJ/cm2 to affected areas. Treatments were performed twice a week until 50–70% pigment correction (maximum 10 treatments). Pigment correction assessment was done by visual and colorimetric assessments compared with the untreated control lesions.The results showed a 68% increase in pigmentation by visual assessment and almost a 100% increase by colorimetric analysis after nine treatments. The authors further noted that these results declined over the 6-month follow-up, and recommended that maintenance treatment would be needed every 2–4 months to sustain the cosmetic benefit. Goldberg et al34 examined the histological and ultrastructual changes in UVB laser-induced repigmentation of striae alba.They showed histological evidence of an increase in melanin content, hypertrophy of melanocytes, and an increase
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in the number of dopa-positive melanocytes in all treated lesions. They concluded that targeted UVB phototherapy is a safe and effective temporary treatment for the leukoderma in striae distensae, but that retreatment may be required. The results obtained with the UVB pulsed excimer laser led to the use of a combined UVB (304–313 nm)/UVA1 (360–370 nm) narrowband light source (the MultiClear system) to treat striae alba in the hope of accelerating the repigmentation response by combining the UV wavelengths. In a study by Sadick et al,35 10 patients with striae alba were treated twice a week with a blend of UVB and UVA1 to the hypopigmented areas until repigmentation occurred (maximum 20 treatments). Repigmentation was assessed by baseline and post-therapy photography. The authors noted that repigmentation of striae alba occurred within one to six treatments and that
a
darker-skinned patients repigmented faster (Fig. 13.1). They concluded that combined UVB/ UVA1 high-intensity light enhances the restoration of pigment in the hypopigmented skin of striae alba.
Mid-infrared Nonablative lasers in the mid-infrared (Mid-IR) range have recently been examined for the treatment of striae distensae, secondary to their studied improvement in dermal remodeling and in the treatment of facial rejuvenation and atrophic acne scars.36–38 Tay et al39 treated 11 Asian patients with striae distensae with the nonablative 1450 diode laser. Patients were randomly assigned to receive 4, 8, or 12 J/cm2 with a 6 mm spot size and a dynamic cooling device for 40 ms to protect the epidermis. A total of three treatments were given at 3-week intervals and assessment
b
Fig. 13.1 (a) Striae alba before treatment. (b) After treatment with the MultiClear combined UVB (304–313 nm)/UVA1 (360–370 nm) narrowband and light source.
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Noninvasive body rejuvenation technologies was done using serial photographs.The results showed no significant improvement in any of the striae treated. In addition, significant postinflammatory hyperpigmentation was noted in 64% of the patients, leading to the conclusion that this modality is not useful for darker skin types. Recent new developments in nonablative laser technology have focused on fractional photothermolysis. This produces arrays of microscopic thermal wounds called microscopic treatment zones (MTZs) at specific depths in the skin without injuring surrounding tissue. There is controlled dermal heating without dermal damage. Wounding is not apparent, because the stratum corneum remains intact during treatment and acts as a natural bandage. Downtime is minimal and erythema is mild; however, multiple treatments are usually required. This new concept in skin rejuvenation has recently been used to treat melasma, acne scars, and photoaging.40,41 One recently published case report looked at the treatment of surgical scars and noted a 75% visual improvement 2 weeks after a single treatment with the 1550 nm Fraxel SR laser.42 An unpublished study presented at the 5th World Congress for Cosmetic Dermatology43 treated 10 patients with striae distensae in five sessions at weekly intervals with fractional photothermolysis. Digital photography and patient surveys showed significant improvement in the clinical appearance and texture of the striae. It is likely that optimal treatment parameters for striae are similar to those used to treat acne scars and fine rhytids. Striae are further likely to improve with multiple treatments or with a combination of other therapeutic modalities.We await further trials looking at the treatment of striae distensae with this new technology of fractional photothermolysis.
CELLULITE Cellulite affects 85–98% of postpubertal females of all races, but has a higher prevalence in Caucasians and Asians.44,45 Although nonpathological, the unaesthetic lipodystrophic changes that characterize cellulite have sparked the conception of a therapeutic market geared toward more noninvasive, patient-friendly techniques that eliminate these unsightly fat depositions. Cellulite
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describes an orange peel- or cottage cheese-type dimpling of the skin.46–48 The distribution of cellulite is localized to any area of the body containing subcutaneous adipose tissue.There are certain target areas that are more prone to developing cellulite, including the hips, upper outer and posterior thighs, and buttocks. In these areas, the local microcirculation has certain tendencies to deposit more fat and to retain more interstitial fluids. Cellulite can also be found on the breasts, the lower part of the abdomen, the upper arms, and the nape of the neck.49 Although cellulite may be found in any area where excess adipose tissue is deposited, obesity is not necessary for its presence.44 The dimpling of skin in cellulite is anatomically due to herniations of fat, known as papillae adiposae, that protrude from the subcutis through the inferior surface of a weakened dermis at the dermo–hypodermal interface.44 Various hypotheses as to how cellulite develops have been proposed, yet the lack of a definitive explanation only adds to the challenge of treatment. One leading hypotheses is based on genderrelated differences in the architecture of subcutaneous fat lobules and the connective tissue septae that divide them.44,47,50,51 Nurnberger and Muller44 found that women have of inherent vertical fascial bands that are easily stretched, leading to weakening of the connective tissue foundation and making herniations mechanistically more likely. In contrast, in males, the subcutis is organized by interlocking fascial bands, creating a stronger interface through which fat is rarely able to penetrate.49 In addition, Rosenblaum et al47 found women to have an irregular, discontinuous connective tissue pattern immediately below the dermis, but this same layer of connective tissue was both smooth and continuous in men. The hormonal and genetic differences in the nature of skin between genders make cellulite atypical in males who have normal levels of androgens, regardless of their weight.52 Another hypothesis centers on the vascular changes that accompany the formation of cellulite.50 Alterations to the precapillary arteriolar sphincters and deposition of hyperpolymerized glycosaminoglycans in the capillary walls of the dermis initiate vessel atrophy. The increased capillary pressure and hydrophilic tendency of glycosaminoglycans increase capillary permeability and cause edema. Surrounding tissues are deprived of
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an adequate supply of blood, and the resulting hypoxia increases lipolytic resistance. When combined with an increase in lipogenesis due to estrogen, prolactin, or high carbohydrate diets, the subcutaneous layer becomes overwhelmed by adipocyte hypertrophy.The enlarged fat cells, along with hypertrophy and hyperplasia of periadipocyte reticular fibers, form micronodules surrounded by clumps of proteins. With continued hypoxia, sclerosis of fibrose septae occurs, leading to dimpling of the skin.52 A recent study using MRI compared the water content of adipose tissue in women of different ages and found a higher content of water within the dermis of the older women. This greater amount of water is related to collagen degradation during the aging process leaves fewer interaction sites between water and macromolecules, and further promotes the formation of cellulite.53,54 Currently, there is no definitive treatment for cellulite, although a variety of treatments have been directed at these hypotheses of the pathophysiology of its development. These include topical, surgical, laser and mesotherapy.These treatments try to enhance the esthetic appearance of skin by improving tone and superficial tightening while promoting lymphatic drainage of fats. We will discuss the data on noninvasive lasers for the treatment for cellulite.
Velasmooth Two laser light devices at present have received approval from the US Food and Drug Administration (FDA) for the safe and effective treatment of cellulite. One system, Velasmooth (Syneron Medical Ltd) utilizes a unique integration of bipolar radiofrequency (RF), 700 nm wavelength IR, and negative tissue massage to noninvasively treat cellulite. Twice-weekly treatment for a total of 8–10 sessions has been recommended. A synergistic effect is employed between the two forms of energy when the various optical and bipolar RF parameters are set optimally.55 Additionally, lower energy levels can also be used to potentially reduce side-effects associated with either the IR or RF alone, making this treatment available to a variety of skin types. It has been proposed that improved microcirculation is effected by the vasodilatory effect and enhanced lymphatic drainage of the
mechanical massage, while neocollagenesis, collagen contraction, and controlled tissue inflammation are induced by heating of tissue by RF and IR.56 Shaoul57 conducted a study treating 15 female patients with cellulite with combined optical and IR energy sources and showed improved appearance of cellulite in all patients by an average of 65%. Additionally, hip parameters were reduced by an average of 3.2 cm, and all patients reported feeling skin contraction as a result of the treatment. No complications were noted either during or after the treatment, thereby showing the success of the VelaSmooth system in delivering a sufficient quantity of deep heat without any superficial damage. Another study, conducted by Alster et al,56 involved 20 patients of varying skin phototypes (I–V) who underwent eight 30-minute sessions of the VelaSmooth device delivered to the randomly selected upper anteromedial and posteolateral thigh and buttock twice a week over a 1-month period, using the contralateral side as a nontreated comparative control. Circumferential thigh measurements were reduced by 0.8 cm on the treatment side, with mean clinical improvement scores of 50%. Side-effects were limited to transient erythema, lasting less than an hour, in most patients upon initial treatment. In another twocenter study involving 35 females (mean age 43) with cellulite abnormalities of the thighs and/or buttocks, 8–16 VelaSmooth treatments were administered biweekly.58 The treatment had positive results, including a moderate improvement in skin smoothing and cellulite appearance and an overall mean decrease in thigh circumference of 0.8 inches (Fig. 13.2). Punch biopsies were taken at baseline, after two treatments, and after eight treatments of the lateral thighs in order to evaluate the histological changes at the molecular level. Histological assessment showed no evidence of morphological damage to any of the skin structures, either epithelial or mesenchymal. This analysis indicates that VelaSmooth, used at specified energy levels, does not result in any significant skin damage. Therefore, any clinically evident changes are probably associated with deeply located alterations, in either the subcutaneous tissue or the subfascial structures. In terms of safety, a few patients reported minimal discomfort and temporary swelling, while two patients reported crusting that resolved in less than 72 hours. These occurrences were attributed to improper
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Fig. 13.2 (a) Cellulite before treatment. (b) 8 weeks after treatment with the Velasmooth combined radiofrequency, infrared, and negative tissue massage device. vacuum contact and coupling of electrodes. These studies demonstrate that the VelaSmooth system can have beneficial effects on the appearance of cellulite, as the negative-pressure massage serves to improve circulation and loosen bands of connective tissue around the fat deposits that cause fat dimpling, while the RF and IR energies heat the skin, creating a controlled inflammatory response that renders fat more malleable to the rolling action of the massage unit. Lymphatic drainage is thus enhanced, thereby reducing tissue bulk and dimpling. The synergistic effects of RF, IR, and suction-based massage are safe and effective, and maintenance treatments may be used to extend the esthetic results obtained.52,56–58
and thighs, as well as clinical evidence of increased skin elasticity. Boyce et al60 conducted a study on 16 female patients with cellulite on the thighs or hips and an average starting body fat percentage of 22.18%. After 12 treatments, all subjects had reported some improvement in the appearance of cellulite, skin tone, and texture. Blinded investigators found an average improvement of 23% for the appearance of the cellulite upon evaluation of photographs. Additionally, no long-term adverse complications such as scarring, dyspigmentation, or cellulite worsening were reported during the use of the TriActive system.
TriActive
The most recent cellulite treatment uses unipolar RF energy and is known as the Accent RF System (Alma Lasers, Inc). The selective electrothermolysis produced by RF is highly effective in creating a thermal effect on tissues. Unlike optical energy, which depends on the chromophore concentration of the skin in order to achieve a selective thermal destruction of target tissue, RF depends on the electrical properties of the tissues.61 The Accent system consists of a base system that generates RF energy (at 40.68 MHz), which is delivered through one of two handpiece applicators to induce controlled volumetric tissue heating. The individual applicators provide a functional delivery of energy to different depths.The first handpiece delivers bipolar energy and has a penetration between 2 and 6 mm to stimulate dermal structural changes. This
The other FDA-approved system is the TriActive LaserDermology System (Cynosure, Inc.).This system works to eliminate the appearance of cellulite by combining three different modalities. An 810 nm diode laser promotes arterial, venous, and lymphatic drainage in conjunction with a localized cooling system that reduces edema. Lastly, a rhythmic massage works in various directions in order to reactivate the collagenic and elastic toning while stimulating lymphatic drainage. A study by Zerbinati et al59 employed the TriActive device on 10 patients with localized cellulite. The sessions lasted 30 minutes and were conducted three times a week. The results showed a marked reduction in circumference of the treated hips
Monopolar radiofrequency
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bipolar handpiece promotes local dermal heating and a subsequent contraction of collagen tissue. The second handpiece delivers unipolar energy with a penetration of 20 mm and is designed to reach subcutaneous adipose tissue.The unipolar device induces thermal injury and inflammation, which promotes collagen remodeling while simultaneously enhancing local microcirculation and fatty acid dissolution to the lymphatic system.62 Emilia del Pino et al54 conducted RF treatments on 26 women between the ages of 18 and 50 while using real-time scanning-image ultrasound with a multifrequency linear transducer to evaluate the thickness of subcutaneous tissue on the buttocks and thighs.The treatments were delivered in two sessions, 15 days apart, and the ultrasound evaluations were made at baseline and 15 days after the final treatment. Dermal thickness was measured as the average of the two distances between the dermal–epidermal union up to the limit of Camper’s fascia, superficial and deep. In the thigh, the shortening of this distance was over 70%, with an average reduction of 2.64 mm. In the buttocks, measurements of the thickness of the dermis to Camper’s fascia demonstrated a reduction of 64%, with an average shortening of 1.8 mm. Additionally, analysis of the echogenicity changes in Camper’s fascia between the first session and 45 days later showed a noticeable organization of the fibrous lines as well as an increase of fibrous tissue in 53% of cases, accompanied by an increase of thickness of the fibers in 57% of cases. Adverse effects were reported during the treatment, and included small blisters in two of the patients as well as ecchymosis on the thighs of three of the patients 24 hours post treatment. While this preliminary study seems promising, more clinical studies are needed to evaluate the use of unipolar RF for the treatment of cellulite. Currently, there is no perfect treatment of cellulite. Part of the problem is the lack of complete understanding of its etiology. There are many opportunities for further investigation into both the pathophysiology and the noninvasive treatment of cellulite.
LIPOLYSIS Similar to laser treatment for cellulite, several lasers have been developed to decrease adipose tissue.
Adipose tissue is a complex endocrine organ comprised primarily of fat cells surrounded by a framework of protein fibers and ground substance. Each adipocyte is composed of a plasma membrane containing a flat nucleus, a small amount of cytoplasm, and typically one large triglyceride droplet. The triglyceride molecule is hydrolyzed via lipolysis to glycerol and free fatty acids. The released fatty acids may undergo further breakdown, be re-esterified, or move into the blood to fuel other organs. Lipolysis is a complex process that is dependent on the hormonesensitive lipase, an enzyme that is tightly regulated by physical activity, age, pathological conditions, and dietary state. Chronic overfeeding, the most powerful cause of obesity, can stimulate adipocytes to differentiate into precursor cells and increase the size of fat cells at certain localized subcutaneous adipose tissue sites.63 Attempts to reduce localized adiposity by diet or exercise alone are often unsuccessful. Over the years, a variety of surgical and medical interventions have been used to remove subcutaneous fat in order to reduce downtime, operator effort, and bleeding, as well as to achieve tightening, fine sculpture, and treatment of fibrous, reoperative areas.64 The use of lasers in the removal of unwanted fat was introduced in 1992.65 Laser lipolysis offers excellent patient tolerance and rapid recovery, as well as the benefit of dermal tightening. It can be used alone for small focal areas or it potentially can be combined with liposuction as an adjunct to reduce operator effort and to enhance skin retraction. Laser lipolysis is associated with rapid recovery due to minimal mechanical disruption. It is a minimally invasive option for people who want to avoid more aggressive procedures such as necklifts. It may also be helpful in areas that are not suitable for liposuction or in focal areas that have already undergone liposuction and require additional sculpting.65 Laser lipolysis is a precise, delicate method that has the advantage of the thermal laser effect, which can be used for refinement in very small areas, including the face.66 The variety of nonablative techniques currently being employed, each of which manipulates different laser frequencies to mechanistically target fat, allows for an individualization of the treatment regimen according to the patient’s aesthetic wishes. The mechanism of action of laser lipolysis is selective photohyperthermia.67 In this process, laser light
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Noninvasive body rejuvenation technologies energy is converted into heat energy when absorbed by fat. Conducted by a flexible fiberoptic delivered through a cannula, the laser energy is transmitted to the adipocytes, which absorb it, expand, and rupture. A photoacoustic effect may also play a role in cellular lysis, due to the rapid absorption of laser light by the cell and the consequent heating.The action time of the laser varies according to the area to be treated and the tissue resistance. In areas of fibrosis or previously treated zones, the treatment time is typically longer. All subjects suitable for the traditional liposuction method can also be treated with laser lipolysis.67
Nd:YAG laser lipolysis Laser lipolysis with the pulsed neodymium : yttrium aluminum garnet (Nd:YAG) laser has shown very promising results. Badin et al66 performed Nd:YAG lipolysis using the higher-energy 1064 nm laser on 245 patients with focal areas of moderate flaccidity, after which aspiration of the liquid fat allowed for histological analysis. The area created with the laser received irreversible damage (cytoplasmic retraction and disruption of membranes) and a decrease in diameter of each adipocyte as seen histologically.66,68 The interaction of the laser with the collagenous and subdermal bands also showed histological evidence of melting and rupture – a process that liberated the retracted skin and remodeled the collagenous tissue. Along with the original theories proposed in 1992, the authors further concluded that the results showed that the laser– tissue interaction causes thermal damage the cellular membrane of the adipocyte through the liberation of heat and alteration of the sodium–potassium pump. This alteration of sodium–potassium cell homeostasis permits migration of water into the cells, forcing them to rupture.69–70 Clinically, the tissue interaction produced minimal swelling and yielded good contour results. Recently, Goldman67 studied 82 patients who underwent submental laser lipolysis for neck lipodystrophy using the Nd:YAG laser, with the main parameter of assessment being histological studies of tissues removed from the subjects immediately following the procedure and of biopsies taken approximately 40 days post treatment. Significant findings following the procedure included coagulation of small blood vessels in the fatty tissue, rupture of adipocytes, the appearance
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of small channels produced by laser action, reorganization of the reticular dermis, and coagulation of collagen in the fat tissue. These factors were thought to be responsible for the observed tissue retraction observed following the procedure. Ichikawa et al71 reported on the histological evaluation of subcutaneous tissue treated first with the pulsed Nd:YAG laser as an adjunct to lipoplasty. Scanning electron microscopy of the removed tissue showed a greater destruction of adipocytes than in the nontreated control tissue. In addition, degenerated cell membrane, vaporization, liquefaction, and thermally coagulated collagen fibers were observed. Kim and Geronemus65 conducted a study using the 1064 Nd:YAG laser to evaluate safety and efficacy in the treatment of small areas of unwanted fat.Thirty female subjects were randomly assigned to three treatment groups: 10 subjects underwent 1064 nm Nd:YAG laser lipolysis, 10 subjects underwent laser lipolysis followed by biweekly treatment with the TriActive diode laser with contact cooling and suction, and 10 subjects served as the control group. Assessment was done at baseline, 1 week, 1 month, and 3 months post procedure using clinical evaluation, weight, photographs, and subject questionnaires, as well as magnetic resonance imaging (MRI) evaluation for the laser lipolysis-only group. Selfassessment evaluations reported an average individual improvement of 37% at the 3-month follow-up.Those who underwent the TriActive treatments reported a higher subjective improvement of 47% compared with those who were treated with the 1064 nm Nd:YAG laser alone (33%), suggesting a beneficial role of the combined modality. MRI obtained pre procedure and 3 months post procedure of the 1064 nm Nd:YAGtreated group showed an average 17% reduction in fat volume of the treated areas, with the submentum having the greatest reduction compared with other larger treatment sites. This, in turn, may suggest a dosedependent relationship.
Ultrasound A novel device for noninvasive destruction of fat cells by focused ultrasound has been developed by UltraShape System Ltd (TelAviv, Israel) and is currently undergoing clinical trials. This technique produces selective fat lysis by breaking the adipocyte
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membranes, with no damage to neighboring structures such as skin, blood vessels, and peripheral nerves. It is proposed that triglycerides from the broken adipocytes are released into interstitial fluid, where they are transported by the lymphatics to the liver and metabolized.72,73 In multicenter clinical trials for CE approval in Europe, 165 patients were followed for 3 months following a single treatment to the abdomen, flanks, or external thighs.74 Blood analysis, weight, and circumference measurements were recorded. Circumference reduction following a single treatment averaged more than 2 cm, and all blood levels remained within the normal range. Another preliminary study involved 34 healthy volunteers who were treated with the UltraShape system to either the abdomen, external thighs, or flanks for up to 2 hours.72 Reduction in circumference of all three treated areas was observed in all patients, as well as a pronounced reduction in the average fat thickness, as measured by ultrasonic imaging. LipoSonix, Inc. have developed another variant on ultrasound technology that achieves targeted reduction of tissue volume by precisely concentrating highintensity focused ultrasound (HIFU) energy on adipose tissue.The ultrasound transducer is delivered across the skin surface at a relatively low intensity but brings this energy to a sharp focus in the subcutaneous fat. At the skin surface, the intensity of the ultrasound energy is low enough that no damage occurs. In a recent animal model, transcutaneous HIFU was administered at the sites of thermocouples anatomically placed at the epidermis, dermis, and subcutaneous adipose tissue of swine at depths of 10 and 15 mm, and within the intraabdominal cavity.75 Temperature data showed a steep temperature gradient between the HIFU-treated tissue and the adjacent tissue that was not within the HIFU treatment beam. The thermal and mechanical effects of the ultrasound within the targeted tissue were shown to induce cell death through focused thermal coagulation without damaging intervening or underlying structures. In a clinical trial, 24 patients underwent HIFU to their lower abdominal tissue followed by abdominoplasty.76 Eight-week histology revealed 75% resolution of the treated adipose tissue, with collapse of the surrounding fibrovascular stroma. This study provided a histopathological examination of the effect of HIFU on adipose tissue.
Low-level Laser Recently, low-level laser lipoplasty has been increasingly used as an effective lipolysis treatment for a broad range of conditions, showing results such as improved wound healing, reduced edema, and relief of pain. Neira et al77 stated that 99% of fat was released from adipocytes after 6 minutes of 635 nm, 10 mW diode laser exposures in a study involving patients treated with low-level laser-assisted lipoplasty. Total energy values of 1.2 J/cm2, 2.4 J/cm2, and 3.6 J/cm2 were applied to human adipose tissue taken from lipectomy samples of 12 healthy women. The samples were irradiated for 0, 2, 4, and 6 minutes and were analyzed using both scanning and transmission electron microscopy. Histological results showed that after just 4 minutes of laser exposure, 80% of the fat was released and collected in the interstitial space. The low-level laser works by opening a transitory pore in the cell membrane, allowing the fat content to seep out of the cell.77–79 Laser lipolysis is a relatively new technique, and is still under development and in need of further clinical trials.The main objectives are rapid recovery and skin tightening. Basic and clinical research is needed on the laser effect of catabolic activation, softening, and liquefying fat.
SKIN TIGHTENING Redundant body skin laxity is a major feature of aging. Rejuvenation of loose skin has become an increasingly popular practice as a result of the maturing ‘baby boomer’ population concomitant with a greater societal acceptance of cosmetic procedures. Although dramatic clinical improvement can be achieved with surgical lifting procedures, patients may be hesitant to pursue this treatment option because of the extensive postoperative recovery period and the inherent risks of the procedure. Nonablative modalities obviate the need for epidermal injury and promote both reorganization and increase of important dermal structures to potentially reverse aging of the skin.80,81 Aging skin manifests as rhytids, pigmentary changes, skin coarseness, and roughness with diminished elasticity. The skin displays characteristic alterations in dermal
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Noninvasive body rejuvenation technologies connective tissue, evidenced histologically by disorganized collagen fibrils and abnormal elastic material.82–85 Repeated sun exposure is accompanied by elevations in matrix metalloproteinases and collagen degradation, and may lead to persistent breakdown of dermal elements.These alterations in collagen organization contribute to the skin laxity and wrinkling seen in aging and photodamaged skin.82 Long-term studies examining the histological changes after CO2 and erbium laser resurfacing have been predominantly confined to the dermis, with extensive collagen and elastic fiber reorganization.86–88 The significance of these microscopic findings lies in their correlation with clinical improvement of rhytids, suggesting that dermal remodeling rather than epidermal ablation is largely responsible for wrinkle reduction and that epidermal removal may not be necessary.89 Only a deep penetrating method of heating the dermis and possibly the fibrous septae supporting the dermis and subcutaneous fat to the underlying fascia could possibly have the effect of tightening and contouring nonsurgically mild to moderate laxity of the skin.81 On the basis of these results, it is believed that promoting dermal collagen remodeling with nonablative laser treatments can improve the clinical manifestations of photoaging, including rhytids, texture, and tone.89 Although much remains to be elucidated about the precise mechanism of action of nonablative techniques, important factors have been extrapolated from existing studies. Spatially selective photocoagulation is a term used to refer to the process of epidermal sparing and selective thermal injury to the dermis, and most precisely describes nonablative laser techniques. Key components to nonablative rejuvenation are epidermal sparing and proper selection of laser irradiation wavelength and energy to evoke the desired thermal response in the papillary and upper reticular dermis.89 The depth of thermal injury should be limited to 100–400 µm below the epidermis – the area where solar elastosis is seen histologically.87,88 Epidermal protection can be accomplished by cryogen spray or contact cooling. By cooling the skin, thermal injury can be confined to the papillary and upper reticular dermis. One should avoid heating the epidermis to temperatures above 65ºC, as this is the threshold for epidermal denaturation.90 Heating the dermis causes
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collagen denaturation and fibroblast stimulation via an inflammatory cascade leading to neocollagenesis.91 Nonablative rejuvenation has great applicability in the treatment of darker skin types, making it an attractive option for individuals with atrophic scars or those who want to improve their skin texture and tone but are not candidates for skin resurfacing procedures due to the increased risk of pigmentary alterations. The ease and tolerability of the treatments, the lack of downtime, and the low risk of epidermal injury make nonablative treatments a mainstay of therapy for all skin types.89
Radiofrequency RF energy is electromagnetic radiation with frequencies ranging from 3 kHz to 300 GHz. Delivery of RF energy to living tissue is thought to induce dermal heating to the critical temperature of 65ºC, causing collagen to denature and allowing wound healing with subsequent contraction.89 As exemplified by the ThermaCool TC system, RF energy is distributed over a volume of tissue though a thin capacitive membrane, while a cryogen system simultaneously cools the epidermis for protection. Tissue heat is generated based on the tissue’s natural resistance to movement of ions within an RF field. This unique volumetric heating method allows large amounts of energy to be distributed over a three-dimensional volume of dermal tissue while protecting the epidermis.81 Unlike lasers, RF sources are not limited by the disadvantages of optical energy, in that they do not rely on the strong interdependence between treatment efficacy/safety and chromophore levels within the epidermis.92 The high efficiency of RF current for tissue heating makes it an attractive energy source for various dermatological applications, including skin tightening, hair and leg vein removal, treatment of acne scarring, skin rejuvenation, and wrinkle reduction. RF is similar to optical energy in that it interacts with the tissue to produce thermal changes. In contrast, however, RF energy is conducted electrically to tissues, and heat arises from a current of ions rather than absorption of photons.93 While a variety of studies have documented the efficacy of RF skin rejuvenation on periorbital rhytids, nasolabial folds, eyebrow elevation, and cheek laxity,93 there is a growing use of RF to treat skin laxity on the
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Fig. 13.3 (a) Before treatment. (b) After treatment with the Thermage radiofrequency device.
body (Fig. 13.3). A pilot study reported the histological and ultrastructural effects of various settings of RF on in vivo human skin using abdominal skin from two women undergoing abdominoplasty using RF treatment before excision.94 Electron microscopy results taken from the human skin showed a loss of distinct borders of collagen fibrils and an increase in size, with no change being observed in the control group. On Northern blot analysis, treated skin had higher levels of collagen messenger RNA on days 2 and 7 post treatment, which is highly suggestive of increased collagen gene expression. Kist et al95 investigated whether more advanced collagen changes would occur with multiple passes of the Thermacool device on the periauricular area of three subjects. Biopsies taken at 24 hours and at 6 months post treatment showed that RF treatment resulted in collagen contraction. The response to injury is the production of new collagen, which in turn decreases skin laxity. Electron microscopy revealed that collagen fibrils increased in diameter proportionally to the number of passes of RF conducted on the patient.Additionally, increases in the energy setting also increased the occurrence of irreversible collagen fibril damage; however, this was associated with increased pain. Alster et al96 studied 50 patients of varying skin phototypes with mild to
moderate cheek or neck laxity in a study employing nonablative RF treatment delivered in a single, nonoverlapping pass. Significant improvements in cheek and neck skin laxity were observed in the majority of patients, with patient satisfaction scores paralleling the clinical improvements observed. Sideeffects were mild and limited to transient erythema, edema, and rare dysesthesia, and no scarring or pigmentary alteration was seen. Applying the results of RF to improve facial laxity, studies are currently being conducted using it for body rejuvenation. Another device, the Polaris WR (Syneron Medical, Ltd) is a combination of RF and a 900 nm diode laser. It delivers optical energy to preheat the target and RF energy to heat it. The Polaris has shown efficacy and safety in the treatment of facial rhytids, skin laxity, and skin texture.97,98
Nd:YAG laser The 1320 nm Nd:YAG laser system was specifically designed for nonablative resurfacing as it has both a thermal sensing device and a built-in cryogen cooling system. This laser mechanistically injures the dermis while protecting the epidermis with its skin cooling
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Fig. 13.4 (a) Before treatment. (b) After treatment with the Titan infrared device. mechanism. By cooling the dermis, the epidermal chromophores are effectively shielded by the incident light.99 The long-pulse Nd:YAG laser emits energy in the IR region of the spectrum (at 1064 nm), with extended pulse durations. This wavelength achieves excellent penetration into the papillary and midreticular dermis, where it is nonspecifically absorbed by dermal water.99–101 The large scattering coefficient of the 1320 nm Nd:YAG laser causes the thermal energy to disperse laterally within the dermis, inducing a large volume of dermal injury relative to the beam size.102 Diffuse heating of dermal tissue at this wavelength penetrates to depths of 5–10 mm and permits slow heat diffusion with low energy absorption by melanin.89 Sadick et al102 conducted a study of seven subjects treated with the 1320 nm Nd:YAG laser to the posterior aspects of the hands.They had six laser treatments performed during a 1-month interval. Each treatment consisted of two consecutive passes of the laser beam, with each pass being delivered to the entire dorsal surface of the hand in uniform nonoverlapping pulses. Evaluation of improvement was based on increased smoothness of the skin. Improvement was measured by both objective and patient assessments. Significant improvement was reported by six of the seven patients at the 6-month visit. A study comparing the effectiveness of a single treatment of RF versus a single treatment of long-pulse Nd:YAG laser
for skin laxity of the face and neck found equal or moderately better results in the cohort receiving the long-pulse Nd:YAG laser treatment.103 A study comparing the long-pulse 532 nm potassium titanyl phosphate (KTP) laser with the 1064 nm Nd:YAG laser alone or in combination has been reported.104 A total of 150 patients with varying skin types were treated in three groups: 50 patients were treated with the 532 nm laser alone, 50 patients were treated with the 1064 nm laser alone, and 50 patients were treated with both lasers together. Clinical parameters of investigator, subject, and observer assessment were conducted after three and six treatments, and included redness, pigmentation, tone/tightening, texture, and rhytids. Although statistically significant improvements were found in all categories in all three groups, the KTP and Nd:YAG laser in combination yielded greater results than either used alone, and the KTP laser was found to be superior to the Nd:YAG laser alone. Serial skin biopsies taken from the inner upper arms of four random patients showed that the amounts of collagen and elastin more than doubled after six treatments with the KTP and Nd:YAG laser combined.The energy was shown histologically to be absorbed in different areas within the dermal papillae and dermis, with the KTP laser mainly targeting more superficial and smaller vessels and the Nd:YAG laser being absorbed in deeper layers.
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Fig. 13.5 (a,b) Before treatment. (c,d) After treatment with the ReFirme combined infrared and radiofrequency device.
Infrared IR light can also be used as an alternative source of energy for the purpose of skin tightening. A noncoherent, selectively filtered IR device, such as the Titan system, emits IR light in multisecond cycles and has been developed with the intention to provide dermal heating. Water, as the target chromophore, allows for uniform heating of the targeted reticular dermis. The epidermis is protected by contact cooling (Fig. 13.4).81 Another system, ReFirme, combines pulses of IR light (700–2000 nm) simultaneously with bipolar RF, which intersect to provide controlled thermal energy. The bipolar electrodes deliver an RF current inside the tissue along the route of lowest impedance between the electrodes.93 Sleightholm et al105 evaluated the ReFirme device on 31 patients with skin laxity of the face, neck, and abdomen. Skin laxity clearance rates were found to be highly correlated with patient
satisfaction levels.When compared to previous studies done on the 900 nm Polaris device, the ReFirme device was shown to provide similar outcomes, possibly due to the broader IR spectrum (Fig. 13.5).
CONCLUSIONS Noninvasive body rejuvenation is in its infancy. As the aging population continues to look for rejuvenation procedures that deliver achievable results yet with reduced downtime and minimal risk profile, this field will continue to emerge. Several systems have been shown to effect striae distensae, cellulite, lipolysis, and skin tightening. However, no system has emerged as being clearly superior. With increasing technological advances and increases in clinical data and scientific studies, the techniques of noninvasive body rejuvenation will continue to be a popular choice for patients seeking treatment.
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REFERENCES 1. Aging statistics. Available at www.agingstats.gov. 2. Cosmetic Surgery Statistics. Highlights of the ASAPS 2005 Statistics on Cosmetic Surgery. Available at www.surgery.org. 3. Garcia HL. Dematologic complications of obesity. Am J Clin Dermatol 2002;3:497–506. 4. Goldberg DJ, Marmur ES, Schmults C, Hussain M, Phelps R. Histologic and ultrastructural analysis of ultraviolet B laser and light source treatment of leukoderma in striae distensae. Dermatol Surg 2005;31: 385–7. 5. Lawley TJ,Yancey KB. Skin changes and diseases in pregnancy. In: Freedberg IM, Eisen AZ, Wolff K, et al, eds. Fˇitzpatrick’s Dermatology in General Medicine, 6th edn. New York: McGraw-Hill, 2003:1361–5. 6. Chang AL, Agredano YZ, Kimbell AB. Risk factors associated with striae gravidarum. J Am Acad of Dermatol 2004;51:881–5. 7. Watson RE, Parry EJ, Humphries JD, et al. Fibrillin mcrofibrils are reduced in skin exhibiting striae distensae. Br J Dermatol 1998;138:931–7. 8. Arem AJ, Kischer CW. Analysis of striae. Plast Reconstr Surg. 1980;65:22–9. 9. Sheu HM,Yu HS, Chang CH. Mast cell degranulation and elastolysis in the early stage of striae distensae. J Cutan Pathol 1991;18:4101–6. 10. Lee KS, Rho YJ, Jang SI, et al. Decreased expression of collagen and fibronectin genes in stria distensae tissue. Clin Exp Dermatol 1994;19:285–8. 11. Hernandez-Perez E, Colombo-Charier E, Valencia-I biett E. Intense pulsed light in the treatment of striae distensae. Dermatol Surg 2002;28:1124–30. 12. Elson ML. Treatment of striae distensae with topical tretinoin. J Dermatol Surg Oncal 1990;16:267–70. 13. Ash K, Lord J, Zukowski M, et al. Comparison of topical therapy for striae alba. Dermatol Surg 1998;24: 849–56. 14. Jimenez GP, Flores F, Berman B, Gunja-Smith Z. Treatment of striae rubra and striae alba with 585-nm pulsed-dye laser. Dermatol Surg 2003;29:362–5. 15. Alster TS, West TB. Treatment of scars. Ann Plast Surg 1997;39:418–32. 16. Alster TS, Williams CM. Improvement of keloid sternotomy scars with the 585 nm pulsed dye laser: a controlled study. Lancet 1995;345:1198–200. 17. Goldman MP, Fitzpatrick RE. Laser treatment of scars. Dermatol Surg 1995;21:685–7. 18. Alster TS. Improvement of erythematous and hypertrophic scars by the 585 nm flashlamp-pumped pulsed dye laser. Ann Plast Surg 1994;32:186–90.
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19. McDaniel DH, Ash K, Zukowski M. Treatment of stretch marks with the 585 nm flashlamp-pumped pulse dye laser. Dermatol Surg 1996;22:332–7. 20. Nehal KS, Lichtenstein DA, Kamino H, et al.Treatment of mature striae with the pulsed dye laser. J Cutan Laser Ther 1999;1:41–4. 21. Alster TS. Laser treatment of hypertrophic scars, keloids, and striae. Dermatol Clin 1997;15:419–29. 22. Longo L, Postiglione MG, Marangoni O, Melato M. Two-year follow-up results of copper bromide laser treatment of striae.. J Clin Laser Med Surg 2003;21:157–60 23. Nouri K, Romagosa R, Chartier T, et al. Comparison of the 585 nm pulse dye laser and the short pulsed CO2 laser in the treatment of striae distensae in skin types IV and VI. Dermatol Surg 1999;25:368–70. 24. Raulin C, Weiss RA, Schonermark MP. Treatment of essential telangiectasias with an intense pulsed light source (PhotoDerm VL). Dermatol Surg 1997;23:941–5. 25. Sadick NS,Weiss RA, Shea CR, et al. Long-term photoepilation using a broad-spectrum intense pulsed light source. Arch Dermatol 2000;136:1336–40. 26. Raulin C, Schroeter C, Weiss RA, et al. Treatment of port-wine stains with a noncoherent pulsed light source: a retrospective study. Arch Dermatol 1999;135:679–83. 27. Sadick NS. Laser and intense pulsed light therapy for the esthetic treatment of lower extremity veins. Am J Clin Dermatol 2003;4:545–54. 28. Weiss RA, Goldman MP,Weiss MA.Treatment of poikiloderma of Civatte with an intense pulsed light source. Dermatol Surg 2000;26:823–7. 29. Sadick NS, Weiss R, Kilmer S, Bitter P. Photorejuvenation with intense pulsed light: results of a multi-center study. J Drugs Dermatol 2004;3:41–9. 30. Scherschun L, Kim JJ, Lim HW. Narrow-band ultraviolet B is a useful and well-tolerated treatment for vitiligo. J Am Acad Dermatol 2001;44:999–1003. 31. Spencer JM, Nossa R, Ajmeri J. Treatment of vitiligo with the 308 nm excimer laser: a pilot study. J Am Acad Dermatol 2002;46:727–31 32. Friedman PM, Geronemus RG. Use of the 308 nm excimer laser for postresurfacing leukoderma. Arch Dermatol 2001;137:824–5. 33. Alexiades-Armenakas MR, Bernstein LJ, Friedman PM, Geronemus RG. The safety and efficacy of the 308-nm excimer laser for pigment correction of hypopigmented scars and striae alba. Arch Dermatol 2004; 140:955–60. 34. Goldberg, David J. 308-nm excimer laser treatment of mature hypopigmented striae. Dermatol Surg 2003; 29:596–9.
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35. Sadick NS, Friedman D, Harth Y. Successful treatment of localized leukoderma with the MulticlearTM. http:// www.curelight.com/_uploads/73 Neil Sadick article.pdf 36. Hardaway CA, Ross EV. Nonablative laser skin remodeling. Dermatol Clin 2002;20:97–111, ix. 37. 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 histologic study. Dermatol Surg 2004;30:152–7. 38. Chua SH, Ang P, Khoo LSW, Goh CL. Nonablative 1450-nm diode laser in the treatment of facial atrophic acne scars in type IV to V Asian skin: a prospective clinical study. Dermatol Surg 2004;30:1287–91. 39. Tay YK, Kwok C, Tan E. Non-ablative 1,450-nm diode laser treatment of striae distensae. Lasers Surg Med 2006;38:196–9. 40. Tannous ZS, Astner S. Utilizing fractional resurfacing in the treatment of therapy-resistant melasma. J Cosmet Laser Ther 2005;7:39–43. 41. Hasegawa T. Clinical trial of a laser device called fractional photothermolysis system for acne scars. J Dermatol 2006;33:623–7. 42. Behroozan DS, Goldberg LH, Dai T, Geronemus RG, Friedman PM. Fractional photothermolysis for the treatment of surgical scars: a case report. J Cosmet Laser Ther 2006;8:35–8. 43. Macedo O. Fractional photothermolysis for the treatment of striae distensae. Abstract presented at the 5th World Congress of the International Academy of Cosmetic Dermatology, 2006. 44. Nurnberger F, Muller G. So-called cellulite: a review. J Eur Acad Dermatol Venereol 2000;14:251–62. 45. Draelos ZD. In search of answers regarding cellulite. Cosmet Dermatol 2001;14:221–9. 46. Draelos Z, Marenus KD. Cellulite etiology and purported treatment. Dermatol Surg 1997;23:1177–81. 47. Rosenbaum M, Prieto V, Hellmer J, et al.An exploratory investigation of the morphology and biochemistry of cellulite. Plast Reconstr Surg 1998;101:1934–9. 48. Pierard GE, Nizet JL, Pierard-Franchimont C. Cellulite: from standing fat herniation to hypodermal stretch marks. Am J Dermatopathol 2000;22:34–7. 49. Avram MM. Cellulite: a review of its pathology and treatment. J Cosmet Laser Ther 2004;6:181–5. 50. Querleux B, Cornillon C, Jolivet O, Bittoun J. Anatomy and physiology of subcutaneous adipose tissue by in vivo magnetic resonance imaging and spectroscopy: relationships with sex and presence of cellulite. Skin Res Technol 2002;8:118–24. 51. Lucassen GW, van der Sluys WLN, van Herk JJ, et al.The effectiveness of massage treatment on cellulite as monitored by ultrasound imaging. Skin Res Technol 1997;3:154–60.
52. Alster TS,Tehrani M.Treatment of cellulite with optical devices: an overview with practical considerations. Lasers Surg Med 2006;28:727–30. 53. Chung JH, Seo JY, Choi HR, et al. Modulation of skin collagen metabolism in aged and photoaged human skin in vivo. J Invest Dermatol 2001;117:1218–24. 54. Emilia del Pino M, Rosado RH,Azuela A, et al. Effect of controlled volumetric tissue heating with radiofrequency on cellulite and subcutaneous tissue of the buttocks and thighs. J Drugs Dermatol 2006;5:714–22. 55. Sadick NS. Combination radiofrequency and light energies: electro-optical synergy technology in esthetic medicine. Dermatol Surg 2005;31:1211–17. 56. Alster TS, Tanzi EL. Cellulite treatment using a novel combination radiofrequency, infrared light, and mechanical tissue manipulation device. J Cosmet Laser Ther 2005;7:81–85. 57. Shaoul J. Cellulite breakthrough. Australian Cosmetic Surgery Magazine: 32–3. http://www.syneron.com/ assets/downloads/_pdf/eloscellulite.pdf 58. Sadick NS, Mulholland SR. A prospective clinical study to evaluate the efficacy and safety of cellulite treatment using the combination of optical and RF energies for subcutaneous tissue heating. J Cosmet Laser Ther 2004;6:187–90. 59. Zerbinati N,Vergani R, Beltrami B.The TriActive system: a simple and efficacious way of combating cellulite. http:// www.cynosure laser.co.uk/Triactive/White Paper.pdf. 60. Boyce S, Pabby A, Chuchaltkaren P, et al. Clinical evaluation of a device for the treatment of cellulite:TriActive. Am J Cosmet Surg 2005;22:233–7. 61. Sadick NS, Makino Y. Selective electro-thermolysis in esthetic medicine: a review. Lasers Surg Med 2004;34: 91–7. 62. Brown A, Olson de Almeida G. Novel radiofrequency (RF) device for celllulite & body reshaping therapy. http://www.almalasers.com.website. 63. Fodor PB, Smoller BR, Stecco KA, et al. Biochemical changes in adipocytes and lipid metabolism secondary to the use of high-intensity focused ultrasound for noninvasive body sculpting (abst). American Society for esthetic Plastic Surgery. http://www.liposonix.com/lipo0011_ handout.pdf 64. Ichikawa K, Miyasaka M, Tanaka R, et al. Histologic evaluation of the pulsed Nd:YAG laser for laser lipolysis. Lasers Surg Med 2005;36:43–6. 65. Kim KH, Geronemus RG. Laser lipolysis using a novel 1,064 nm Nd:YAG Laser. Dermatol Surg 2006;32: 241–8. 66. Badin AZD, Moraes LM, Gondek L, et al. Laser lipolysis: flaccidity under control. Aesthetic Plast Surg 2002; 25:335–9. 67. Goldman A. Submental Nd:YAG laser-assisted liposuction. Lasers Surg Med 2006;38:181–184.
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Noninvasive body rejuvenation technologies 68. Badin AZD, Luciana BE, Gondek MJG, et al. Analysis of laser lipolysis effects on human tissue samples obtained from liposuction. Aesthetic Plast Surg 2005;29:281–6. 69. Apfelberg DB, Rosenthal S, Hunstad JP. Progress report on multicenter study of laser-assisted liposuction. Aesthetic Plast Surg 1994;18:259. 70. Apfelberg DB, Results of multicenter study of laserassisted liposuction. Clin Plast Surgery 1996;23:713. 71. Ichikawa K, Miyasaka M, Tanaka R, et al. Histologic evaluation of the pulsed Nd:YAG laser for laser lipolysis. Lasers Surg Med 2005;36:43–6. 72. Otto J. Non invasive ultrasonic body contouring – initial experience. http://www.ultrashape.com/data/ uploads/InformationForPhysicians/Ultrashape% 20White%20Paper%20Initial%20Experience.pdf 73. Brown S. What happens to the fat after treatment with the UltraShapeTM device. http://www.rocol. com.co/ pdf/ultrashape/White_Character Paper_What_Happens_ to_the_Fat_Rev_C.pdf 74. Glicksman A, Eshel Y. Non-invasive body contouring by focused ultrasound. IMCAS, Paris, France, July 2006. 75. Fodor PB, Stecco K, Johnson J. The precision of highintensity focused ultrasound (HIFU) for non-invasive body sculpting: in situ thermocouple measurement of the HIFU treatment zone within adipose tissue (abst). Plastic Surgery, 2006. http://www.liposonix.com/ lipo0013 ASPSE 06.pdf. 76. Smoller BR, Garcia-Murray E, Rivas OA, et al. The histopathological changes from the use of high-intensity focused ultrasound (HIFU) in adipose tissue (Abst). American Academy of Dermatology, 2006. http://www. liposonix.com/lipo0008 AAD 06.pdf. 77. Neira R, Ortiz-Neira C. Low level laser assisted liposculpture: clinical report in 700 cases. Esthetic Surg J 2002;22:451. 78. Neira R, Arroyave J, Ramirez H, et al. Fat liquefaction: effect of low-level laser energy on adipose tissue. Plast Reconstr Surg 2002;110:912–22. 79. Solarte E, Gutierrez O, Neira R, et al. Laser-induced lipolysis on adipose cells. 5th Iberoamerican Meeting on Optics and 8th Latin American Meeting on Optics, Lasers, and Their Applications. Proc SPIE 2004;6522:5–10. 80. Alster TS,Tanzi E. Improvement of neck and cheek laxity with a nonablative radiofrequency device: a lifting experience. Dermatol Surg 2004;30:503–7. 81. Dierickx CC. The role of deep heating for noninvasive skin rejuvenation. Lasers Surg Med 2006;38:799–807. 82. Fischer GJ, Wang ZQ, Datta SC, et al. Pathophysiology of premature skin aging induced by ultraviolet light. N Engl J Med 1997;337:1419–28. 83. Smith JJ, Davidson E, Sams WJ, et al. Alterations in human dermal connective tissue with age and chronic sun damage. J Invest Dermatol 1962;39:347–50.
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84. Lavker RM. Cutaneous aging: chronologic versus photoaging, In: Gilchrest BA, ed. Photodamage. Cambridge, MA: Blackwell Science, 1995;3:123–35. 85. Bernstein EF, Chen YQ, 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. 86. Kuo T, Speyer MR, Reiss WR, et al. Collagen thermal damage and collagen synthesis after cutaneous laser resurfacing. Dermatol Clin 1997;15:459–67. 87. Kauvar AN, Geronemus RG. Histology of high-energy pulse CO2 laser resurfacing. Dermatol Clin 1997;15: 459–67. 88. Alster TS, Kauvar AN, Geronemus RG. Histology of high-energy pulsed CO2 laser resurfacing. Semin Cutan Med Surg 1996;15:189–93. 89. Kim KH, Geronemus RG. Nonablative laser and light therapies for skin rejuvenation. Arch Facial Plast Surg 2004;6:398–409. 90. Nelson JS, Majaron B, Kelly KM. Active skin cooling in conjunction with laser dermatologic surgery. Semin Cutan Med Surg 2000;19:253–66. 91. Nelson JS, Majaron B, Kelly KM. What is nonablative photorejuvenation of human skin? Semin Cutan Med Surg 2002;21:238–50. 92. Sadick N, MakinoY. Selective electro-thermolysis in esthetic medicine: a review. Lasers Surg Med 2004;34:91–7. 93. Sadick N, Sorhaindo L. The radiofrequency frontier: a review of radiofrequency and combined radiofrequency pulsed light technology in esthetic medicine. Facial Plast Surg 2005;21:131–8. 94. Zellickson BD, Kist D, Bernstein E, et al. Histologic and ultrastructual evaluation of the effects of a radiofrequency-based nonablative dermal remodeling device: a pilot study. Arch Dermatol 2004;140:204. 95. Kist D, Burn AJ, Sanner R, et al. Ultrastructural evaluation of multiple pass low energy versus single pass high energy radio-frequency treatment. Lasers Surg Med 2006;38:150–4. 96. Alster TS,Tanzi E. Improvement of neck and cheek laxity with nonablative radiofrequency device: a lifting experience. Dermatol Surg 2004;30:503–7. 97. Doshi SN, Alter TS. Combination radiofrequency and diode laser for treatment of facial rhytides and skin laxity. J Cosmet Laser Ther 2005;7:11–15. 98. Sadick NS,Trelles MA. Nonablative wrinkle treatment of the face and neck using a combined diode laser and radiofrequency technology. Dermatol Surg 2005;31:1695–9. 99. Levit E, Daly D, Scarborough DA, et al.The case for nonablative laser resurfacing. Cosmet Dermatol 2002; 15:39–44.
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100. Goldberg DJ. Full-face nonablative dermal remodeling with a 1320 nm Nd:YAG laser. Dermatol Surg 2000; 26:915–18. 101. Sadick NS. Update on non-ablative light therapy for rejuvenation: a review. Lasers Surg Med 2003;32: 120–8. 102. Sadick N, Schecter AK. Utilization of the 1320 nm Nd:YAG laser for the reduction of photoaging of the hands. Dermatol Surg 2004;30:1140–4. 103. Taylor MB. Split-face/neck comparison of a single treatment of radiofrequency versus a single treatment of
long-pulse Nd:YAG for skin laxity of the face and neck. Lasers Surg Med 2005;36 (Suppl 17):21–42 (abst). 104. Lee MW. Combination 532 nm and 1064 nm lasers for noninvasive skin rejuvenation and toning. Arch Dermatol 2003;139:1265–76. 105. Sleightholm R, Bartholomeusz, H. Skin tightening and treatment of facial rhytides with combined infrared light and bipolar radiofrequency technology. http://www. syneron.com/asserts/downloads/_pdf/ReFirme_White_ Paper.pdf
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14. Treatment of leg telangiectasia with laser and pulsed light* Mitchel P Goldman
INTRODUCTION Lasers and intense pulsed light (IPL) are used to treat leg telangiectasia for various reasons. First, both treatments have a futuristic appeal not only to the general public but also to physicians. By virtue of their advanced technology, they are perceived as ‘state-of-the-art’ treatment modalities and are sought by the general public because ‘high tech’ is thought of as safer and better than traditional sclerotherapy. Unfortunately, these perceptions have often resulted in unanticipated adverse sequelae (scarring and pain) at an increased cost to the patient (lasers costing considerably more to purchase and maintain than a needle, syringe, and sclerosing solution). Second, lasers may have theoretical advantages compared with sclerotherapy for treating leg telangiectasia. Sclerotherapy-induced pigmentation is caused by hemosiderin deposition through extravasated erythrocytes. Laser coagulation of vessels should not have this effect. Telangiectatic matting (TM) has also not been associated with laser treatment of any vascular condition and occurs in a significant percent of sclerotherapy-treated patients. Finally, allergenic reactions that may rarely occur from the sclerosing solution do not occur with laser treatment. Both lasers and IPL act in a different manner to effect vessel destruction. Effective lasers and IPL are pulsed so that they act within the thermal relaxation times of blood vessels to produce specific destruction of vessels of various diameters based on the pulse duration. Lasers of various wavelengths and
*
broadspectrum IPL are used to selectively treat blood vessels by taking advantage of the difference between the absorption of the components in a blood vessel (oxygenated, deoxygenated, and met-hemoglobin) and the overlying epidermis and surrounding dermis (as described below) to selectively thermocoagulate blood vessels. In addition, each wavelength requires a specific fluence to cause vessel destruction. Unlike the oxygenated blood of port wine stains (PWS) and hemangiomas, leg veins harbor deoxygenated hemoglobin, which gives the blue color of venous blood. Deoxyhemoglobin has distinct optical properties, with two absorption spectrum peaks at approximately 545 and 580 nm, and a broader peak at about 650 nm. The optical properties of blood are mainly determined by the absorption and scattering coefficients of its various oxyhemoglobin components. Figure 14.1 shows the oxyhemoglobin absorption and scattering coefficient for penetration into blood.1 The main feature to note in the curve is the strong absorption at wavelengths below 600 nm, with less absorption at longer wavelengths. However, a vessel 1 mm in diameter absorbs more than 67% of light even at wavelengths longer than 600 nm.This absorption is even more significant for blood vessels 2 mm in diameter.Therefore the use of a light source above 600 nm would result in deeper penetration of thermal energy without negating absorption by oxyhemoglobin in vessels greater than 1 mm in diameter.This is because the absorption coefficient in blood is higher than that of surrounding tissue
Portions of this chapter are excerpted from Goldman MP, Bergan JB, Guex JJ, eds. Sclerotherapy Treatment of Varicose and Telangiectatic Leg Veins, 4th edn. London: Elsevier, 2006.
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Clinical procedures in laser skin rejuvenation Diode Nd:YAG PDL 532 Nd:YAG
Absorption (log scale)
Melanin
Oxyhemoglobin
Water
300
500
700
1000
2000
Wavelength (nm)
Fig. 14.1 Oxygenated and deoxygenated hemoglobin.Water and melanin absorption curves as a function of wavelength. (Adapted from Boulnois JL. Lasers Med Sci 1986; and reproduced with permission from Sclerotherapy Treatment of Varicose and Telangiectatic Leg Veins, 4th edn. Goldman MP, Bergan JB, Guex JJ, eds. Elsevier, London, 2006.)
for wavelengths between 600 and 1064 nm. Ideally, a light source should have a pulse duration that would allow the light energy to build up in the target vessel so that its entire diameter is thermocoagulated. Optimal pulse durations have been calculated for blood vessels of various diameter (Table 14.1). During the process of delivering a sufficient amount of energy to thermocoagulate the target vessel, the overlying epidermis and perivascular tissue should be unharmed. This selective preservation of tissue requires some form of epidermal cooling. A number of different laser and IPL systems have been developed toward this end, and are discussed in subsequent sections.
Table 14.1 Thermal relaxation times of blood vessels Vessel diameter (mm) 0.1 0.2 0.4 0.8 2.0
Relaxation time (s) 0.01 0.04 0.16 0.6 4.0
Patients seek treatment for leg veins mostly for cosmetic reasons, and any treatment that is effective should be relatively free of adverse sequelae.2 Bernstein,3 for example, evaluated the clinical characteristics of 500 consecutive patients presenting for removal of
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Treatment of leg telangiectasia with laser and pulsed light lower extremity spider veins. Patients ranged in age from 20 to 70 years and had had noticeable spider veins for an average of 14 years; 28% had leg veins less than 0.5 mm in diameter and 39% veins less than 1.5 mm in diameter. Interestingly, regardless of exactly how sclerotherapy was performed, more than half (56%) of patients developed TM. Recent advances in laser and IPL treatments for treating telangiectatic vessels, if used appropriately, assure minimal (if any) adverse events. An understanding of the appropriate target vessel for each laser and/or IPL is important so that treatment is tailored to the appropriate target. As detailed in sclerotherapy textbooks and articles,4 most telangiectasias arise from reticular veins.Therefore the single most important concept to keep in mind is that feeding reticular veins must be treated completely before treating telangiectasia. This minimizes adverse sequelae and enhances therapeutic results. Failure to treat ‘feeding’ reticular veins and short follow-up periods after the use of lasers may give inflated estimates of the success of laser treatment.5 This chapter reviews and evaluates the use of these nonspecific and specific laser and light systems in the treatment of leg venules and telangiectasias (Table 14.2).
HISTOLOGY OF LEG TELANGIECTASIA The choice of proper wavelength(s), degree of energy fluence, and pulse duration of light exposure are all related to the type and size of target vessel treated. Deeper vessels necessitate a longer wavelength to allow penetration. Large-diameter vessels necessitate a longer pulse duration to effectively thermocoagulate the entire vessel wall, allowing sufficient time for thermal energy to diffuse evenly throughout the vessel lumen. The correct choice of treatment parameters is aided by an understanding of the histology of the target telangiectasia. Venules in the upper and middle dermis typically maintain a horizontal orientation.The diameter of the postcapillary venule ranges from 12 to 35 µm.6 Collecting venules range from 40 to 60 µm in the upper and middle dermis and enlarge to 100–400 µm in diameter in the deeper tissues. Histological
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examination of simple telangiectasia demonstrates dilated blood channels in a normal dermal stroma, with a single endothelial cell lining, limited muscularis, and adventitial layers.7,8 Most leg telangiectasias measure from 26 to 225 µm in diameter. Electron microscopic examination of ‘sunburst’ varicosities of the leg has demonstrated that these vessels are widened cutaneous veins.They are found 175–382 µm below the stratum granulosum. The thickened vessel walls are composed of endothelial cells covered with collagen, elastic, and muscle fibers. Unlike leg telangiectasias, the ectatic vessels of PWS are arranged in a loose fashion throughout the superficial and deep dermis. They are more superficial (0.46 mm) and much smaller than leg telangiectasias, usually measuring 10–40 µm in diameter. This may explain the lack of efficacy reported by many physicians who treat leg telangiectasias with the same laser and parameters as they do with PWS.
KTP AND FREQUENCY-DOUBLED Nd-YAG (532 nm) LASERS Modulated potassium titanyl phosphate (KTP) lasers have been reported to be effective at removing leg telangiectasia, using pulse durations between 1 and 50 ms. The 532 nm wavelength is one of the hemoglobin absorption peaks. Although this wavelength does not penetrate deeply into the dermis (about 0.75 mm), relatively specific damage (compared with argon laser) can occur in the vascular target by selection of an optimal pulse duration, enlargement of spot size, and addition of epidermal cooling. Effective results have been achieved by tracing vessels with a 1mm projected spot. Typically, the laser is moved between adjacent 1 mm spots, with vessels traced at 5–10 mm/s. Immediately after laser exposure, the epidermis is blanched. Lengthening of the pulse duration to match the diameter of the vessel is attempted to optimize treatment. We and others have found the long-pulse 532 nm laser (frequency-doubled neodymium : yttrium aluminum garnet (Nd:YAG)) to be effective in treating leg veins less than 1 mm in diameter that are not directly connected to a feeding reticular vein.9 When used with a 4°C chilled tip, a fluence of 12–15 J/cm2 is
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Table 14.2 Lasers and light sources for leg veins Wavelength (nm)
Energy (J)
Pulse duration (ms)
480, 515, 535, 550, 580–1200
Up to 90
Up to 500
1064
5–500
5–00
550–900
10–50
CuBr
578
55
300
1.5
None
Vbeam
PDL
595
25
0.45–40
5, 7, 10, 12
DCD
Cbeam
PDL
585
8–16
0.45
5, 7, 10
DCD
Gentle YAG
Nd:YAG
1064
Up to 600
0.25–300
CoolTouch
Varia
Nd:YAG
1064
Up to 500
300–500
3–10
Cutera
Vantage
Nd:YAG
1064
Up to 300
0.1–300
3, 5, 7, 10
XEO
IPL
600–850
5–20
?Automatic
PhotoGenicaV
PDL
585
20
0.45
3, 5, 7, 10
Cold air
PhotoGenica V-Star
PDL
585–595
40
0.5–40
5, 7, 10, 12
Cold air
SmartEpill II
Nd:YAG
1064
1–200
Up to 100
2, 5, 7, 10
Cold air
Acclaim 7000
Nd:YAG
1064
300
0.4–300
3, 5, 7, 10, 12
Cold air
PhotoLight
IPL
400–1200
3–30
5–50
46 × 18, 46 × 10
Cynergie
IPL/Nd:YAG
595/1064
20/160
0.5–40/
7
Supplier
Product name
Device typea
American BioCare
OmniLight FPL
Fluorescent IPL
Adept Medical
Ultrawave
Nd:YAG
Alderm
Prolite
IPL
AsclepionMeditech
Pro Yellow
Candela
Cynosure
Spot diameter (mm)
Coolingb External continuous
2, 4, 6, 8, 10, 12
None
10 × 20, 20 × 25
DCD DCD Copper contact None
None Cold air
0.3–300 DDD
Elipse
IPL
400–950
Up to 21
0.2–50
10 × 48
DermaMed USA
Quadra Q4
IPL
510–1200
10–20
60–200
33 × 15
None
Fotana
Dualis
Nd:YAG
1064
Up to 600
5–200
2–10
None
Iridex
Apex-800
Diode
800
5–60
5–100
7, 9, 11
Cooling handpiece
Laserscope
Lyra
Nd:YAG
1064
5–900
20–100
1–5 continuously adjustable
Cooling handpiece
Aura
KTP
532
1–240
1–50
1–5 continuously adjustable
Cooling handpiece
Gemini
KTP
532
Up to 100
1–100
1–5 continuously adjustable
Cooling handpiece
Nd:YAG
1064
Up to 990
10–100
1–5 continuously adjustable
Cooling handpiece (Continued)
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Treatment of leg telangiectasia with laser and pulsed light Table 14.2 (Continued) Spot diameter (mm)
Supplier
Device typea
Wavelength (nm)
Lumenis
Quantum
IPL
515–1200
Vasculite Elite
IPL
515–1200
3–90
1–75
35 × 8
1064
70–150
2–48
6
Cooled sapphire crystal
515–1200
10–40
3–100
15 × 35, 8 × 15
Cooled sapphire crystal
Nd:YAG
1064
10–225
2–20
2 × 4, 6, 9
Cooled sapphire
Quantel Viridis
Diode
532
Up to 110
15–150
ProliteII
IPL
550–900
10–50
OpusMed
F1
Diode
800
10–40
Orion Lasers
Harmony
Fluorescent IPL
540–950
Nd:YAG Nd:YAG
Nd:YAG
Lumenis One
Med-Surge
Palomar
IPL
Energy (J)
Pulse duration (ms)
Product name
Cooled sapphire crystal
10 × 20, 20 × 25
None
15–40
5, 7
None
5–20
10, 12, 15
40 × 16
None
1064
35–145
40–60
6
None
1064
35–450
10
2
None
470–1400 470–1400
Up to 45
10–100
12 × 12
None
Up to 45
10–100
16 × 46
None
550–670/870– 1400/1064
Up to 700
0.5–500 4
None
MediLux
IPL
EsteLux
IPL
StarLux
IPL/Nd:YAG
Quantel
Athos
Nd:YAG
1064
Up to 80
3.5
Sciton
Profile
Nd:YAG
1064
4–400
0.1–200
Profile BBL
IPL
400–1400
Up to 30
Up to 200
30 × 30, 13 × 15
Aurora SR
IPL/RF
580–980
10–30/ 2–25RF
Up to 200
12 × 25
Polaris
Diode/RF
900
Up to 50/up to 100RF
Galaxy
Diode
580–980
Up to 140/up to 100RF
Up to 200
Mydon
Nd:YAG
1064
10–450
5–90
Syneron
WaveLight
Coolingb
Contact Sapphire
Contact or cold air
a IPL, intense pulsed light; Nd:YAG, neodymium:yttrium aluminum garnet laser; CuBr, copper bromide (copper vapor) laser; PDL, pulsed dye laser; diode; diode laser; KTP, potassium titanyl phosphate laser; RF, radiofrequency. b DCD, dynamic cooling device. Modified from Goldman MP. Cutaneous and Cosmetic Laser Surgery. Philadelphia: Elsevier, 2006.
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delivered as a train of pulses in a 3–4 mm diameter spot size to trace the vessel until spasm or thrombosis occurs. Some overlying epidermal scabbing is noted, and hypopigmentation is not uncommon in darkskinned patients.Although individual physicians report considerable variation in results, usually more than one treatment is necessary for maximum vessel improvement, with only rare reports of 100% resolution of the leg vein. A comparative study of the 532 nm Nd:YAG laser at 20 J/cm2 delivered as a 50 ms pulse through a contact cooling and 5 mm diameter spot was made with a 595 nm pulsed dye laser (PDL) at 25 J/cm2, with a pulse duration of 40 ms, cryogen spray cooling, and a 3 mm × 10 mm spot.10 After one treatment with the 532 nm Nd:YAG laser, there was 50–75% improvement in 2 of 10 patients and more than 75% improvement in 3 of 10 patients.There was better improvement in the PDL-treated patients, with 6 of 10 having 50–75% improvement. Another study compared the 532 nm diode laser with a 1 mm diameter spot at fluences of 2–32 J/cm2 with the 1064 nm Nd:YAG laser at 1–20 ms pulses through a 3 mm diameter spot at 130–160 J/cm2 in the treatment of TM vessels less than 0.3 mm in diameter that did not respond to sclerotheraopy.11 Two to three passes were needed to close the vessels with each laser. Thirty-nine percent of the 532 nm-treated and 55% of the 1064 nm-treated vessels had better than 50% lightening. In short, the 532 nm, long-pulsed, cutaneous, chilled Nd:YAG laser is effective in treating leg telangiectasia. As summarized previously, efficacy is techniquedependent, with a potential for achieving excellent results. Patients need to be informed of the possibility of prolonged pigmentation at an incidence similar to sclerotherapy, as well as temporary blistering and hypopigmentation that is predominantly caused by epidermal damage in pigmented skin (type III or above, especially when tanned).
PULSED DYE LASER, 585 OR 595nm The PDL has been demonstrated to be highly effective in treating cutaneous vascular lesions consisting of very small vessels, including PWS, hemangiomas, and
facial telangiectasia. The depth of vascular damage is estimated to be 1.5 mm at 585 nm, and 15–20 µm deeper at 595 nm. Consequently, penetration to the typical depth of superficial leg telangiectasia may be achieved.12 However, telangiectasia over the lower extremities has not responded as well, with less lightening and more post-treatment hyperpigmentation. This may be due to the larger diameter of leg telangiectasia as compared with dermal vessels in PWS and larger diameter feeding reticular veins, as described previously. Vessels that should respond optimally to PDL treatment are predicted to be red telangiectasias less than 0.2 mm in diameter, particularly those vessels arising as a function of TM after sclerotherapy. This is based on the time of thermocoagulation produced by this relatively short-pulse laser system (Table 14.1). In an effort to thermocoagulate larger-diameter blood vessels, the pulse duration of the PDL has been lengthened to 1.5–40 ms and the wavelength increased to 595 nm. This theoretically permits more thorough heating of larger vessels. These longer pulse durations are created by using two separate lasers, each emitting a 2.4 ms pulse. Such LPDLs operate at 595 nm, with an adjustable pulse duration from 0.5 to 40 ms delivered through a 5, 7, or 10 mm diameter spot size or a 3 mm × 10 mm or 5 mm × 8 mm elliptical spot. Dynamic cooling with a cryogen spray is also available, with the cooling spray adjustable from 0 to 100 ms, given 10–40 ms after the laser pulse or as continuous 4°C air cooling at variable speed.A fluence of 10–25 J/cm2 can be delivered through a 3 mm × 10 mm or 5 mm × 8 mm spot. Polla13 evaluated the Candela LPDL on 40 patients with leg veins 0.05–1.5 mm in diameter. He used a 6 or 20 ms pulse with 7 or 10 mm diameter spot at 10–13 J/cm2 and 6–7 J/cm2, respectively, with a dynamic cooling device (DCD) setting of 30 ms and 10 ms delay. One to seven treatments were performed at 3-week intervals. Optimal results were obtained after two sessions, with 8% having total clearance and 67% having clearance above 40%.All patients had purpura for 7–10 days, 33% had pigmentation for less than 2 months, and 15% for over 2 months. Weiss and Weiss14 had similar results using the Cynosure LPDL on 20 patients with sclerotherapyresistant TM. They performed a single treatment with
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Treatment of leg telangiectasia with laser and pulsed light a 20 ms pulse and a 7 mm diameter spot at 7 J/cm2 for a total of three stacked pulses with simultaneous cold air cooling. Of 20 patients, 18 had at least 50% improvement at 3 months post treatment. Purpura only occurred in 25% of patients and lasted 10 days. A longer pulse duration of 40 ms was used on 10 patients with leg telangiectasia up to 1 mm in diameter at 595 nm with DCD cooling at 25 J/cm2.10 Six patients had 50–75% improvement and 2 of 10 had hyperpigmentation that lasted over 3 months. Our experience is similar to that reported above. We utilize the LPDL at pulse durations matching the thermal relaxation time of the leg veins. The energy fluence used is just enough to produce vessel purpura and/or spasm. Like Weiss and Weiss,14 we use stacked pulses to achieve this clinical endpoint. We have used both LPDL systems and have found them to be comparable. Because of the necessity for multiple treatments and the significant occurrence of long-lasting hyperpigmentation, we reserve the use of the LPDL for sclerotherapy-resistant, red, telangiectasia less than 0.2 mm in diameter.
DIODE LASERS Many diode-pumped lasers are now available, including a 532, 810, 915, and 940 nm devices (Table 14.2). Diode lasers generate coherent monochromatic light through excitation of small diodes. As a result, these devices are lightweight and portable, with a relatively small desktop footprint. Thirty-five patients with spider leg veins were treated with an 810 nm diode laser with a 12 mm diameter spot, 60 ms pulse duration, and 80–100 J/cm2, with a cooled hand-piece.15 Of these 35 patients,15 showed complete disappearance of the spider veins. Six months after the second laser treatment, 12 patients with partial or no response had dropped out of the study and 7 patients had a relapse in their leg veins, with an additional patient having a relapse at 1 year follow-up. Of the 35 patients, 2 had scarring. One hour of topical EMLA cream had to be applied to limit pain during treatment. A 940 nm diode laser has also been used in the treatment of blue leg telangiectasia less than 1 mm in diameter without Doppler evidence of refluxing feeding
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veins.16 Twenty-six patients were treated with 300–350 J/cm2 with a 40–70 ms pulse and 1 mm diameter spot, and this gave a clearance of greater than 50% in 20 patients and greater than 75% in 12 patients. Slight textural changes were seen in 5 patients and pigmentation took several months to resolve in 4 patients. No cooling was provided except for ice packs after treatment. In a follow-up of these patients 1 year later, 75% of patients had greater than 75% clearance.17 These outstanding long-term results were not seen in a separate study using the same laser but with a variety of pulse durations (10–100 ms) and fluences (200–1000 J/cm2) through a 0.5 mm diameter spot for vessels less than 0.4 mm in diameter, a 1 mm diameter spot for vessels 0.4–0.8 mm in diameter, and a 1.5 mm diameter spot for vessels 0.8–1.4 mm in diameter.18 Fluences were adapted to have complete vessel clearance without epidermal blanching . No cooling device was used and patients were evaluated at 1 year. The largest-diameter vessels had the highest clearance rates, with 13% of vessels less than 0.4 mm in diameter clearing by more than 75%, versus 88% of vessels 0.8–1.4 mm in diameter clearing by more than 75%. Laser therapy was more painful than sclerotherapy in 31 of 46 patients, with equal efficacy being noted by the patients who had had both forms of treatment. Finally, a combination diode laser at 915 nm with radiofrequency (RF) at levels up to 100 J/cm2 has been used to treat leg telangiectasia. Chess19 treated 25 patients with 35 leg veins 0.3–5 mm in diameter with 60–80 J/cm2 fluence and 100 J/cm2 RF energy through a 5 mm × 8 mm spot size with 5°C contact cooling in up to three sessions every 4–10 weeks. He found that 77% of treated sites exhibited greater than 75% improvement at 6 months.The average discomfort rating was 7 out of 10. Three sites on three different patients developed eschar formation without permanent scarring. Another study treated leg telangiectasia 1–4 mm in diameter with 60–80 J/cm2 fluence and 100 J/cm2 RF energy through a 5 mm × 8 mm spot size with 5°C contact cooling in three separate sessions at 2- to 4-week intervals.20 Seventy-five percent of vessels had greater than 50% improvement and 30% had greater than 75% improvement at 2-month follow-up. Almost no complications were noted to occur. In summary, diode lasers are limited by treatment pain and adverse effects. Of note, unless feeding reticular veins
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800 700 600 500 400 300 200 100 0
Oxy
1000
960
920
880
840
800
760
720
680
640
600
560
520
480
440
DeOxy
400
∆ T (°C)
Average temperature increase across a 0.2-mm deep, 0.05-mm diameter vessel vs wavelength
Wavelength (nm) Average temperature increase across a 2-mm deep, 1-mm diameter vessel vs wavelength 12
∆ T (°C)
10
Oxy
8
DeOxy
6 4 2 1000
960
920
880
840
800
760
720
680
640
600
560
520
480
440
400
0
Wavelength (nm)
Fig.14.2 Average temperature increase across a cutaneous vessel as a function of wavelength for two cases:a shallow capillary vessel (similar to those found in a port wine vascular malformation) and a deeper (2 mm) and larger (1 mm) vessel typical of a leg venule.The calculated curves are generated assuming that the main light-absorbing chromophore in the blood is either oxygenated or deoxygenated hemoglobin.The calculation is carried out for a 10 J/cm2 fluence and does not take into account cooling by heat conductivity.Note the dramatic shift in the optimal wavelength as a function of vessel depth and diameter.Also note the difference between oxygenated and deoxygenated hemoglobin.(Reproduced with permission from Sclerotherapy Treatment of Varicose and Telangiectatic Leg Veins,4th edn.Goldman MP,Bergan JB,Guex JJ,eds.Elsevier,London,2006.) are treated, the distal treated telangiectasias recur at 6–12 months post treatment. Some authors appear to be able to achieve better results than others using similar parameters.The addition of RF to the diode laser appears to offer little advantage over the laser alone.
INTENSE PULSED LIGHT IPL was developed as an alternative to lasers to maximize efficacy in treating leg veins (PhotoDerm VL, ESC/Sharplan, now Lumenis Santa Clara, CA). This device permits sequential rapid pulsing, longer-duration
pulses, and longer penetrating wavelengths than laser systems. Theoretically, a phototherapy device that produces noncoherent light as a continuous spectrum with wavelengths longer than 550 nm should have multiple advantages over a single-wavelength laser system. First, both oxygenated and deoxygenated hemoglobin absorb light at these wavelengths. Second, blood vessels located deeper in the dermis are affected.Third, thermal absorption by the exposed blood vessels should occur with less overlying epidermal absorption, since the longer wavelengths penetrate deeper and are absorbed less by the epidermis, including melanin (Fig. 14.2).
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Fig. 14.3 Before and after treatment of essential leg telangiectasia with intense pulsed light. (Reproduced with permission from Sclerotherapy Treatment ofVaricose and Telangiectatic LegVeins, 4th edn. Goldman MP, Bergan JB, Guex JJ, eds. Elsevier, London, 2006.)
With the theoretical considerations just mentioned, an IPL in the 515–1000 nm range was used at varying energy fluences (5–90 J/cm2) and various pulse durations (2–25 ms) to treat venectasia 0.4–2.0 mm in diameter. This IPL allows treatment through a quartz crystal of 8 mm × 35 mm or 8 mm × 15 mm (up to 2.8 cm2) that can be decreased in size to match the clinical area of treatment. Clinical trials using various parameters with the IPL, including multiple pulses of variable duration, demonstrated efficacy ranging from over 90% to total clearance in vessels less than 0.2 mm in diameter, 80% in vessels 0.2–0.5 mm in diameter, and 80% in vessels 0.5–1 mm in diameter.21 The incidence of adverse sequelae was minimal, with hypopigmentation occurring in 1–3% of patients, resolving within 4–6 months. Tanned or darkly pigmented Fitzpatrick type III patients were more likely to develop hypopigmentation and hyperpigmentation in addition to blistering and superficial erosions.These all cleared over a few months.Treatment parameters found to be most successful ranged from a single pulse of 22 J/cm2 in 3 ms for vessels less than 0.2 mm or a double pulse of 35–40 J/cm2 given in 2.4 and 4.0 ms with a 10 ms delay.
Vessels between 0.2 and 0.5 mm were treated with the same double-pulse parameters or with a 3.0–6.0 ms pulse at 35–45 J/cm2 with a 20 ms delay time. Vessels above 0.5 mm were treated with triple pulses of 3.5, 3.1, and 2.6 ms with pulse delays of 20 ms at a fluence of 50 J/cm2 or with triple pulses of 3, 4, and 6 ms with a pulse delay of 30 ms at a fluence of 55–60 J/cm2. The choice of a cutoff filter was based on skin color, with light-skinned patients using a 550 nm filter and darkerskinned patients a 570 or 590 nm filter. Treatment of essential telangiectasia, especially on the legs, is efficiently accomplished with the IPL (Fig. 14.3). A variety of parameters have been shown to be effective.We recommend testing a few different parameters during the first treatment session and using the most efficient and least painful parameter on subsequent treatments. The use of IPL to treat leg veins is encouraging but far from being easily reproduced. This technology requires significant experience and surgical ability to produce good results. Various parameters must be matched to the patient’s skin type as well as to the diameter, color, and depth of the leg vein. With older
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machines that do not have integrated cooling through sapphire crystals, a cold gel must be placed between the IPL crystal and the skin surface to provide optimal elimination of epidermal heat. Many have compared using the IPL to playing a violin. A 2- to 3-year-old playing a violin will make a squeaky noise, but, with practice, by the time the child is 7 or 8, he or she will make beautiful music. Regarding the IPL, it is the art of medicine that assumes an equal importance to its science. Fortunately, for those who do not play musical instruments, there are now dozens of IPLs available from many different manufacturers (Table 14.2).
Nd:YAG LASER, 1064 nm The Nd:YAG laser, 1064 nm, is probably the most effective laser available to treat leg telangiectasia. In an effort to deliver laser energy to the depths of leg veins (often 1–2 mm beneath the epidermis) with thermocoagulation of vessels 1–3 mm in diameter, 1064 nm lasers with pulse durations between 1 and 250 ms have been developed. However, because of the poor absorption of hemoglobin and oxyhemoglobin at 1064 nm wavelength, higher fluences must be used. Depending on the amount of energy delivered, the epidermis must be protected to minimize damage to pigment cells and keratinocytes. Three mechanisms are available to minimize epidermal damage through heat absorption. First, the longer the wavelength, the less energy will be absorbed by melanocytes or melanosomes. This will allow darker skin types to be treated with minimum risks to the epidermis due to a decrease in melanin interaction. Second, delivering the energy with a delay in pulses greater than the thermal relaxation time for the epidermis (1–2 ms) allows the epidermis to cool conductively between pulses. This cooling effect is enhanced by the application to the skin surface of cold gel that conducts away epidermal heat more efficiently than air. Finally, the epidermis can be cooled directly to allow the photons to pass through without generating sufficient heat to cause damaging effects. Epidermal cooling can be given in many different ways. The simplest method is continuous contact
cooling with chilled water, which can be circulated in glass, sapphire, or plastic housings.The laser impulse is given through the transparent housing, which should be constructed to ensure that the laser’s effective fluence is not diminished.This method is referred to continuous contact cooling.The benefit is its simplicity.The disadvantage is that the cooling effect continues throughout the time that the device–crystal is in contact on the skin. This results in a variable degree and depth of cooling, determined by the length of time the cold housing is in contact with the skin. This nonselective and variable depth and temperature of cooling may necessitate additional treatment energy so that the cooled vessel will heat up sufficiently to thermocoagulate. Another method of cooling is contact precooling. In this approach, the cooling device contacts the epidermis adjacent to the laser aperture. The epidermis is precooled and then treated as the handpiece glides along the treatment area. Because the cooling surface is not in the beam path, no optical window is required, and better thermal contact can be made between the cooling device and the epidermis. The drawback is the nonreproducibility of cooling levels and degrees, which are based on the speed and pressure at which the surgeon uses the contact cooling device. Yet another method for cooling the skin is to deliver to the skin a cold spray of refrigerant that is timed to precool the skin before laser penetration and also to postcool the skin to minimize thermal backscattering from the lasergenerated heat in the target vessel.We have termed this latter effect ‘thermal quenching’. This method reproducibly protects the epidermis and superficial nerve endings. In addition, it acts to decrease the perception of thermal laser epidermal pain by providing another sensation (cold) to the sensory nerves. Finally, it allows an efficient use of laser energy because of the relative selectivity of the cooling spray, which can be limited to the epidermis. The millisecond control of the cryogen spray prevents cooling of the deeper vascular targets and is given in varying amounts so that epidermal absorption of heat is counteracted by exposure to cryogen. Since the target vessel absorbs the 1064 nm wavelength poorly, a much higher fluence is necessary to cause thermocoagulation. Whereas a fluence of 10–20 J/cm2 is sufficient to thermocoagulate blood vessels when delivered at 532 or 585 nm, a fluence of
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Treatment of leg telangiectasia with laser and pulsed light 70–150 J/cm2 is required to generate sufficient heat absorption at 1064 nm.Various 1064 nm lasers are currently available that meet the criteria for selectively thermocoagulating blood vessels, including, among others, the Lumenis One and Vasculite (Lumenis, Santa Clara, CA), Varia (CoolTouch Corp., Roseville, CA), Lyra (Laserscope, San Jose, CA), GentleYAG (Candela, Wayland, MA), SmartEpil II (Cynosure, Chelmsford, MA), Harmony (Orion Lasers, FL), Profile (Sciton, Palo Alto, CA), Mydon (WaveLight, Erlsngen, Germany), and CoolGlide (Cutera, Burlingame, CA) (Table 14.2). The long-pulse 1064 nm Nd:YAG lasers are not all the same.There are variabilities in spot size, laser output both in fluence and in how the extended time of the laser pulse is generated), pulse duration, and epidermal cooling. In addition, although many claims are made by the laser manufacturers, few wellcontrolled peer-reviewed medical studies are available. Because of the vaariability between the 1064 nm Nd:YAG lasers, a review of the clinical studies with each system will be presented separately.
Vasculite The Vasculite was the first long-pulsed 1064 nm laser to be approved by the US Food and Drug Administration (FDA) for vascular treatment. The Nd:YAG 1064 nm laser is pulsed with IPL technology. Individual pulses up to 16 ms in length can be delivered as single, double, or triple synchronized pulses with a total maximum fluence of 150 J/cm2. The laser beam is generated in the handpiece and delivered through a sapphire crystal 6 mm, 9 mm, or 3 mm × 6 mm in size. Weiss and Weiss,22 Sadick,23 and Goldman24 have reported excellent results in treating leg telangiectasia from 0.1 to 3 mm in diameter. Application of a cool gel to the skin (without cooling of the crystal – which is not necessary with the most advanced version, Lumenis 1, which is thermokinetically cooled to 4°C) and synchronization of the pulses allow epidermal cooling and protection. In addition, synchronized timing between pulses can be tailored to the thermal relaxation times of blood vessels. Weiss and Weiss22 treated 30 patients who had been dissatisfied with previous leg vein treatments with either sclerotherapy or other laser light or IPL.A single
167
14–16 ms pulse at 110–130 J/cm2 was given to treat vessels 1–3 mm in diameter. A double pulse of 7 ms separated by 20–30 ms at a fluence of 90–120 J/cm2 was used to treat vessels 0.6–1 mm in diameter, and a triple synchronized pulse of 3–4 ms at a fluence of 80–110 J/cm2 was used to treat vessels 0.3–0.6 mm in diameter. Immediate contraction of the vessel was used as an endpoint of treatment, followed by urtication. Immediate bruising from vessel rupture occurred in 50% of vessels. At 3 months after treatment, the majority of sites improved by over 75% (Fig. 14.4). Hyperpigmentation was noted in 28% of patients at the 3-month follow-up. In short, this report demonstrated successful treatment of otherwise-difficult vessels, and mirrors our experience. Weiss and Weiss25 reported on 3-year results in the treatment of leg telangiectasia 0.3–3 mm in diameter at slightly higher fluences of 110–150 J/cm2. They found an average 75% improvement in 2.38 treatments. Sixteen percent of patients developed pigmentation which resolved at 6 months, and 4% developed TM. Sadick26 reported on 12-month follow-up in 25 patients with leg veins with a fluence of 120 J/cm2 given through a 6 mm diameter spot in a 7 ms double pulse to vessels 0.2–2 mm in diameter and as a single pulse of 14 ms and a fluence of 130 J/cm2 to vessels 2–4 mm in diameter. Using these parameters, 64% of patients could achieve 75% or greater clearance in three treatments. Two of the 25 treated patients who had less than 25% vessel clearance developed a recurrence of the veins within 6–12 months. Sixteen percent of patients developed pigmentation, which lasted 4 months, and 8% developed TM.
CoolTouch Varia The CoolTouch Varia combines a multiple train of pulses to generate a pulse width from 10 to 300 ms bursts. Fluences of up to 150 J/cm2 can be generated. A 3–10 mm diameter beam is delivered through a fiberoptic cable. Dynamic cooling is given with a cryogen spray that can be delivered before, during, and/or after the laser pulse. The cooling spray can be varied from 5 to 200 ms and can be given in 5–30 ms bursts in 5 ms intervals before and/or after the laser pulse. In this manner, in the treatment of larger or deeper
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a
b
Fig. 14.4 Treatment of leg telangiectasia with theVasculight at the parameters specified in the text. (a) Before treatment. (b) 60 days after treatment. (Courtesy of RobertWeiss MD and reproduced with permission from Sclerotherapy Treatment of Varicose and Telangiectatic LegVeins, 4th edn. Goldman MP, Bergan JB, Guex JJ, eds. Elsevier, London, 2006.)
vessels, the postcooling quenching cryogen spray can be given 20–30 ms after the laser pulse to coincide with conduction of heat absorbed by the vessel propagating back to the epidermis. More superficial and smaller vessels require a shorter delay in the postlaser cooling spray of 5 ms. We have found this laser to be therapeutically beneficial in treating leg telangiectasia 0.1–2 mm in diameter (Fig. 14.5). A comparative study of two long-pulsed 1064 nm Nd:YAG lasers was performed on 11 patients with leg telangiectasia without feeding (or with previously treated) feeding reticular veins.The CoolTouch Varia was used with a 6 mm diameter spot size at a fluence of 135 J/cm2 with a 25 ms pulse and precooling of 5 ms and postcooling of 15 ms. The CoolGlide laser was used with a 5 mm diameter spot, 25 ms pulse at 200 J/cm2 and contact cooling. Both lasers produced comparable clearing of 75% in all treated vessels. However, the CoolGlide laser was significantly more painful.27 Two papers were published on the same 23 of 30 leg vein patients (completing the study) treated with the CoolTouch Varia.28,29 Greater than 75% improvement was noted at 85% of treated sites.Transient pigmentation was noted in 6 of 23 patients, with TM in 1 of 23 patients. Fluences of 150 J/cm2 were used for alldiameter veins, with a 25 ms pulse duration on veins less than 1.5 mm in diameter and 50–100 ms on veins 1.5–3 mm in diameter. Patients received up to two treatments 4–6 weeks apart. One to three passes were
required to blanch the targeted vessels. Laser spot diameters and the time of pre and/or pulse cooling was not noted in either of the two papers. Patients who had previously had treatment with nonhypertonic saline sclerotherapy preferred sclerotherapy over laser because of the increased pain with the laser. A direct comparison of the CoolTouch Varia with sclerotherapy utilizing sodium tetradecyl sulfate (STS) was performed on 20 patients with size-matched superficial leg telangiectasia 0.5–1.5 mm in diameter.30 Laser treatments were given through a 5.5 mm diameter spot at 125–150 J/cm2 with a 25 ms pulse duration. Precooling ranged from 0 to 5 ms and postcooling from 20 to 50 ms with a delay of 5–20 ms.The endpoint of laser treatment was vessel contraction. Sclerotherapy with STS 0.25% was followed by 48 hours of 20–30 mmHg graduated compression stockings. Sclerotherapy-treated patients had a significantly better response in fewer treatments, with comparable adverse effects.
CoolGlide The CoolGlide can deliver fluences up to 100 J/cm2 through a 10 mm diameter spot. The pulse duration can be varied continuously from 10 to 100 ms. Unlike the other two systems, which can deliver each burst at a 1 Hz speed, the CoolGlide can deliver pulses at 2 Hz. Cooling is provided by a contact system that glides in
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a
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b
Fig. 14.5 (a) After sclerotherapy – an ulceration occurred that is covered with an occlusive dressing. (b) After treatment of a foot telangiectasia with the CoolTouchVaria at 150 J/cm2 with a 50 ms pulse and 5 ms of precooling 10 ms before the laser pulse, followed by a 10 ms cooling burst 10 ms after the laser pulse. Note the complete clearing 60 days after treatment. (Reproduced with permission from Sclerotherapy Treatment of Varicose and Telangiectatic Leg Veins, 4th edn. Goldman MP, Bergan JB, Guex JJ, eds. Elsevier, London, 2006.)
front of the laser beam so that 2 cm of skin is precooled before the laser aperture glides over the treatment site. We have also found this system to be effective in treating leg telangiectasia 0.1–3 mm in diameter.27 However, the lack of effective, reproducible cooling can lead to the production of epidermal scars more often than the other 1064 nm laser systems, as well as an increase in procedural pain. Fifteen women with 21 sites of leg telangiectasia 0.25–4 mm in diameter were treated twice at 6–8 weeks with the CoolGlide using a 7 mm spot, fluences of 90–160 J/cm2 and pulse durations of 10–50 ms.31 Significant improvement was seen in 71% of sites, but hyperpigmentation was present in 61% of sites at 3month follow-up. A second study on 20 patients with reticular veins 1–3 mm in diameter was performed using 100 J/cm2 and 50 ms pulse, without mention of the laser spot diameter.32 Although 66% of the vessels cleared more than 75% with one treatment at 3 months, pain was significant, especially without the use of EMLA cream applied for 1 hour. Unfortunately, longer follow-up was not reported.
0.5–5 mm in diameter with 100–200 J/cm2 at 50–100 ms with a 3–5 mm diameter spot and one to four treatments.33 Comparable telangiectasias on the same patient were treated with one treatment of STS 0.6%. No compression was used. Even at these parameters with excessive concentration of STS without compression, and four laser treatments versus one sclerotherapy treatment, adverse effects and treatment efficacy were not statistically different between the two treatment modalities. Patient surveys found that 35% preferred laser and 45% preferred sclerotherapy. Sadick34 also evaluated the Lyra with a 30–50 ms pulse duration, 1.5 mm diameter, 400–600 J/cm2 for red vessels and a 50–60 ms pulse, 1–3 mm diameter spot, and 250–370 J/cm2 for blue vessels through a 4°C cold window for three treatments. At 6 months, 80% of vessels had greater than 75% clearance. This was a limited study on 10 patients. Two of the 10 patients had pigmentation lasting up to 6 months, and TM occurred in 1 of the 10. Moderate discomfort was experienced by all patients.
Lyra
Quantel Medical Multipulse mode
The Lyra long-pulse 1064 nm Nd:YAG laser was used to treat 20 patients with leg telangiectasia
The most recent development in long-pulse 1064 nm Nd:YAG technology has been the production of a
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nonuniform pulse sequence mode device with contact cooling to 5°C.35 This device has a fluence of 300–360 J/cm2 through a 2 mm diameter spot. The rationale for multiple pulsing is to convert oxyhemoglobin to met-hemoglobin, which will be absorbed better at 1064 nm.The pulse duration consists of a series of three 3.5 ms pulses separated by 250 ms between each pulse; 60% of the energy is delivered in the first pulse, with 20% in each of the next two pulses. In an initial study on 11 patients with blue leg veins 1–2 mm in diameter, patients had up to three treatments at 6-week intervals. There was 98% clearance after three treatments, with moderate pain with each treatment. To summarize, we have found the 1064 nm longpulsed Nd:YAG lasers to be beneficial in the treatment of leg telangiectasia not responsive to sclerotherapy or other lasers. The benefit in using a 1064 nm laser is that its longer wavelength can penetrate more deeply, allowing effective thermosclerosis of vessels up to 3–4 mm in diameter. In addition, the 1064 nm wavelength permits treatment of patients of skin types I–VI with or without a tan, since melanin absorption is minimal. The 1064 nm long-pulse laser systems are not entirely without side-effects, however. Cutaneous burns with resulting ulcerations, pigmentation, and TM have been observed with each of these systems as parameters are being tested. The dynamically cooled 1064 nm Nd:YAG laser appears to produce the best clinical resolution, with less pain and fever adverse effects than other long-pulse 1064 nm lasers. However, sclerotherapy still provides better results with fewer treatments, less pain, and comparable adverse effects to lasers. Thus, the reader should evaluate the latest studies to ensure ideal results.
COMBINATION/SEQUENTIAL 595 nm PDL AND 1064 nm Nd:YAG – CYNERGY The latest device to enter the market uses a novel sequential 595 nm PDL pulse followed by a 1064 nm Nd:YAG laser pulse. This laser, Cynergy (Cynosure, Westford, MA), is presently undergoing clinical testing by our group, among others. The rationale for enhanced efficacy is that the 595 nm pulse generates met-hemoglobin, which absorbs more strongly at the
1064 nm wavelength. Thus, lower energies from both lasers can be used, with the possibility of less pigmentation and adverse sequelae. Preliminary experience is promising in treating bright red vessels less than 0.1 mm in diameter, which are the most difficult vessels to treat with sclerotherapy.
CONCLUSIONS Since sclerotherapy is relatively cost-effective compared with laser or IPL treatment, when is it appropriate to use this advanced therapy? Obviously, needle-phobic patients will tolerate the use of this technology, even though the pain from lasers and IPL is more intense than from sclerotherapy with all but hypertonic solutions. Patients who are prone to TM are also appropriate candidates. Vessels below the ankle are particularly appropriate to treat with light, since sclerotherapy has a relatively high incidence of ulceration in this area because of the higher distribution of arteriovenous anastomosis. Finally, patients who have vessels that are resistant to sclerotherapy are excellent candidates. An efficacy of 75% clearance with two to three IPL treatments occurred in sclerotherapy-resistant vessels.36 The optimal efficacy in treating common leg telangiectasia uses sclerotherapy to treat the feeding venous system and a laser or IPL to seal superficial vessels to prevent extravasation with resulting pigmentation, recanalization, and TM. So, is there a single laser that can adequately treat leg veins? The answer is both yes and no. Yes, because lasers are now available with pulse durations optimized to treat various sized blood vessels. One can select virtually any wavelength from 532 to 1064 nm, as well as a broad spectrum of IPL. It has been demonstrated that any wavelength can be used effectively, as long as the pulse duration matches the diameter of the vessel and the appropriate fluence is utilized. This also assumes that the epidermis will be protected from nonspecific thermal effects by a variety of cooling and pulsing scenarios. One can cool the skin directly with a contact probe before and after the laser pulse or through a sapphire window before, during, and after the laser pulse. Cooling can also be given dynamically
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Treatment of leg telangiectasia with laser and pulsed light with a cryogen spray before, during, or after the laser pulse. Most patients prefer dynamic cooling, as it provides the highest degree of pain control. Contact cooling has the unpredictability of adequately cooling the epidermis, so that, unless optimal technique is used, epidermal burns will occur. However, the answer is also no, as the lasers presently available still require skillful use for safe and effective treatment. The laser of the future was detailed in a September 2001 publication.37 This ideal laser will have a built-in thermal sensor to detect both epidermal and vascular heating. This will automatically regulate the fluence so that the vessel is completely thermocoagulated, as well as epidermal cooling so that the epidermis is kept below a damaging temperature threshold. Even better would be an infrared sensor that would determine the location of feeding dermal vessels so that they too can be treated along with the visible telangiectasia. One could imagine, in the future, the patient placing the leg into a laser machine that would map the visible veins to be thermocoagulated and automatically treat the entire superficial venous network. At present, the only barrier preventing the development of such a laser is money and the willingness of a company to produce a machine of this type.
REFERENCES 1. Anderson AR, Parrish JA. The optics of human skin. J Invest Dermatol 1981;77:13–19. 2. Weiss RA, Weiss MA. Resolution of pain associated with varicose and telangiectatic leg veins after compression sclerotherapy. J Dermatol Surg Oncol 1990;16:333–6. 3. Bernstein EF. Clinical characteristics of 500 consecutive patients presenting for removal of lower extremity spider veins. Dermatol Surg 2001;27:31–3. 4. Goldman MP, Bergan JB, Guex JJ, eds. Sclerotherapy Treatment of Varicose and Telangiectatic Leg Veins, 4th edn. London: Elsevier, 2006. 5. Goldman MP. Laser and sclerotherapy treatment of leg veins: my perspective on treatment outcomes. Dermatol Surg 2002;28:969. 6. Braverman IM. Ultrastructure and organization of the cutaneous microvasculature in normal and pathologic states. J Invest Dermatol 1989;93(Suppl):2S–9S. 7. Wokalek H, Varscheidt W, Martay K, Ledor O. Morphology and localization of sunburst varicosities: an
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electron microscopic and morphometric study. J Dermatol Surg Oncol 1989;15:149–54. Bodian EL. Sclerotherapy. J Dermatol Surg Oncol 1989;15:156–61. Adrian RM. Treatment of leg telangiectasias using a long-pulse frequency-doubled neodymium:YAG laser at 532 nm. Dermatol Surg 1998;24:19–23. Woo WK, Jasim ZF, Handley JM. 532-nm Nd:YAG and 595-nm pulsed dye laser treatment of leg telangiectasia using ultralong pulse duration. Dermatol Surg 2003;29:1176–80. Raskin B, Fany RR. Laser treatment for neovascular formation. Lasers Surg Med 2004;34:189–92. Garden JM, Tan OT, Kerschmann R, et al. Effect of dye laser pulse duration on selective cutaneous vascular injury. J Invest Dermatol 1986;87:653–7. Polla LL. Treatment of leg telangiectasia with a 595 nm LPDL. Lasers Surg Med 2002;14(Suppl):78. Weiss RA, Weiss MA. Long pulsed dye laser (LPDL) treatment of resistant telangiectatic matting of the legs. Lasers Surg Med 2002;14(Suppl):86. Wollina U, Konrad H, Schmidt W-D, et al. Response of spider leg veins to pulsed diode laser (810 nm): a clinical, histological and remission spectroscopy study. J Cosmet Laser Ther 2003;5:154–62. Kaudewitz P, Kloverkorn W, Rother W. Effective treatment of leg vein telangiectasia with a new 940 nm diode laser. Dermatol Surg 2001;27:101–6. Kaudewitz P, Kloverkorn W, Rother W. Treatment of leg vein telangiectasias: 1-year results with a new 940 nm diode laser. Dermatol Surg 2002;28:1031–4. Passeron T, Olivier V, Duteil L, et al. The new 940nanometet diode laser: an effective treatment for leg venulectasia. J Am Acad Dermatol 2003;48:768–74. Chess C. Prospective study on combination diode laser and radiofrequency energies (ELOSTM) for the treatment of leg veins. J Cosmet Laser Ther 2004;6:86–90. Sadick NS, Trelles MA. A clinical and histological, and computer-based assessment of the Polaris LV, combination diode, and radiofrequency system, for leg vein treatment. Lasers Surg Med 2005;36:98–104. Schroeter CA,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. 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. Sadick NS.The utilization of a new Nd:YAG pulsed laser (1064 nm) for the treatment of varicose veins. Lasers Med Surg 1999;11(Suppl):21. Goldman MP. Laser treatment of leg veins with 1064 nm long-pulsed lasers. Cosmet Dermatol 2000;13:27–30.
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25. Weiss MA, Weiss RA. Three year results with the long pulsed Nd:YAG 1064 laser for leg telangiectasia. Presented at the American Society for Dermatologic Surgery Annual Meeting, Dallas,TX, October, 2001. 26. Sadick NS. Long-term results with a multiple synchronized-pulse 1064 nm Nd:YAG laser for the treatment of leg venuelectasias and reticular veins. Dermatol Surg 2001;27:365–9. 27. Bowes LE, Goldman MP.Treatment of leg telangiectasias with a 1064 nm long pulse Nd:YAG laser using dynamic vs contact cooling: a comparative study. Lasers Surg Med 2002;14(Suppl):40. 28. Eremia S, Li CY. Treatment of leg and face veins with a cryogen spray variable pulse width 1064-nm Nd:YAG laser – a prospective study of 47 patients. J Cosmet Laser Ther 2001;3:147–53. 29. Li CY, Eremia S. Treatment of leg and face veins with a cryogen spray, variable pulse width 1064 nm Nd:YAG laser – a prospective study of 47 patients. Am J Cosmet Surg 2002;19:3–8. 30. Lupton JR, Alster TS, Romero P. Clinical comparison of sclerotherapy versus long-pulsed Nd:YAG laser treatment for lower extremity telangiectases. Dermatol Surg 2002;28:694–7. 31. Rogachefsky AS, Silapunt S, Goldberg DJ. Nd:YAG laser (1064 nm) irradiation for lower extremity telangiectasias
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and small reticular veins: efficacy as measured by vessel color and size. Dermatol Surg 2002;28:220–3. Omura NF, Dover JS, Arndt KA, Kauvar ANB.Treatment of reticular leg veins with a 1064 nm long-pulsed Nd:YAG laser. J Am Acad Dermatol 2003;48:76–81. Coles MC,Werner RS, Zelickson BD. Comparative pilot study evaluating the treatment of leg veins with a long pulse Nd:YAG laser and sclerotherapy. Lasers Surg Med 2002;30:154–9. Sadick NS. Laser treatment with a 1064-nm laser for lower extremity class I–III veins employing variable spots and pulse width parameters. Dermatol Surg 2003;29: 916–19. Mordon S, Brisot D, Fournier N. Using a ‘non uniform pulse sequence’ can improve selective coagulation with a Nd:YAG laser (1.064 µm) thanks to met-hemoglobin absorption: a clinical study on blue veins. Lasers Surg Med 2003;32:160–70. Weiss RA,Weiss MA. Photothermal sclerosis of resistant telangiectatic leg and facial veins using the PhotoDerm VL. Presented at the Annual Meeting of the Mexican Academy of Dermatology, Monterey, Mexico, April 24, 1996. Goldman MP. Are lasers or non-coherent light sources the treatment of choice for leg veins? A look into the future. Cosmet Dermatol 2001;14:58–9.
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15. Photodynamic therapy Papri Sarkar and Ranella Hirsch
HISTORY The use of light therapy began in 1400 BC when Hindus first applied naturally occurring plant psoralens to their skin followed by ambient sun exposure to treat vitiligo.1 Later, groups as diverse as the ancient Egyptians, Greeks, and Romans used photosensitizing agents plus light to treat a multitude of skin diseases. However, it was not until 1984 that Lahmann in Germany invented the first artificial light source to treat skin diseases.2 Since then, options to treat skin disease with an activating source and light have vastly multiplied. Most recently, the technique has been further honed with the advent of psoralen plus UVA treatment,3 extracorporeal photophoresis for cutaneous T-cell lymphoma,4 and high dose UVA-1 phototherapy for atopic dermatitis.5 In the year 1900 a German medical student, Oscar Raab, noted that acridine orange was lethal for paramecia only when combined with sunlight. Seven years later, Hermann von Tappeiner coined the term ‘photodynamic reaction’ to describe reactions that require a photosensitizing agent, oxygen, and light.6 These three components are the required ingredients of photodynamic therapy (PDT) to this day.
MECHANISM PDT is a two-step system that requires the presence of a photosensitizing agent, photoactive wavelengths of light, and oxygen. First, the photosensitizing agent is delivered orally, topically, or intravenously for uptake by the patient’s target cells. Second, a photon of light is absorbed by the photosensitizer, which leads to its
activation. Once activated, the photosensitizer transfers its energy to a singlet oxygen species, leading to destruction of the target cell.7 Early descriptions of PDT involved the use of eosin as a photosensitizing agent and light to treat skin cancer, lupus vulgaris, and condyloma lata.7,8 Since that time, porphyrins have become the photosensitizer of choice. Initial work focused on hematoporphyrin and hematoporphyrin derivatives. Unfortunately, these agents persisted in the body for many months, subjecting patients to undesirable prolonged phototoxicity. Dermatologists have since focused on photosensitizers such as δ-aminolevulinic acid (also known as 5aminolevulinic acid, ALA) and its more lipophilic methyl ester (MAL).9 These topical porphyrin precursors cause less phototoxicity and are more readily cleared by the body. Moreover, topical administration of the photosensitizer is a logical approach, since the skin is a readily accessible target.10 The most common topically applied photosensitizing agent in the USA is ALA, the first intermediate in the heme biosynthesis pathway. Topical application of ALA bypasses the rate-limiting step of heme biosynthesis11 (Fig. 15.1).When ALA enters cells, it is converted to the endogenous photosensitizer protoporphyrin IX (PpIX) and permits a buildup of the latter.10 Activation of PpIX by the appropriate visible wavelength of light results in the production of cytotoxic oxygen free radicals (singlet oxygen). Singlet oxygen is a highly reactive excited molecule that irreversibly oxidizes essential cellular components, causing tissue injury and necrosis.12 PDT also affects the microvasculature and immune system.Vascular effects include vasoconstriction of the arterioles within a tumor, reduction of erythrocyte flow in nearby venules, and thrombosis of tumor vessels leading to ischemia and vascular
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Glycine and succinyl CoA Heme ALA synthase (note-limiting step) Topical ALA or MAL
Ferrochelatase and Fe2+
ALA ALA dehydratase
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Porphobilinogen Protoporphyrinogen oxidase
Porphobilinogen deaminase
Protoporphyrinogen IX Hydroxymethylbilane Coproporphyrinogen III oxidase
Uroporphyrinogen III cosynthase
Coproporphyrinogen III
Uroporphyrinogen III Uroporphyrinogen III decarboxylase
Fig. 15.1 The heme biosynthesis pathway. Production of δ-aminolevulinic acid (ALA) is the rate-limiting step in this pathway. Exogenous ALA or methyl δ-aminolevulinate (MAL) bypasses this step and drives heme synthesis, producing the endogenous photosensitizer protoporphyrin IX (PpIX).
compromise. Direct cell killing and immunological effects, including the production of interleukin-1β (IL-1β), IL-2, tumor necrosis factor (TNF), and granulocyte colony-stimulating factor (G-CSF), also occur.7 Of note, singlet oxygen can also target and destroy the photosensitizer itself, limiting further effect. Because the ALA–PDT reaction is relatively shortlived, any photosensitivity resolves relatively rapidly. Resolution occurs within 24–48 hours after treatment. Depending upon the condition to be treated, the time of application of ALA varies. The goal of PDT is the selective destruction of diseased cells. Exogenously applied ALA preferentially accumulates in pilosebaceous units and abnormal keratinocytes, helping to target abnormal cells while preserving normal structures.13 In addition, targeting of specific lesional tissue is possible by selection of the
appropriate wavelength of light. PpIX has a maximum absorption peak at 410 nm and smaller ones at 510, 545, 585 and 635 nm14,15 (Fig. 15.2). In general, the longer the wavelength (up to 850 nm), the deeper is its penetration into tissue.11 With this dual selectivity, tissue damage to unaffected bystander tissue is greatly minimized. Concern regarding carcinogenesis arises with all new therapeutic modalities. Because most photosensitizers do not accumulate in cell nuclei, PDT generally has a low potential for causing DNA damage, mutations, and carcinogenesis.16
LASERS AND LIGHT SOURCES Both coherent and noncoherent light sources with suitable spectral characteristics and high output can be
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Absorption (arbitrary units)
2.5 2.0 1.5 1.0 0.5
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BLU-U Clearlight 417– 432 nm
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Fig. 15.2 Protoporphyrin IX absorption spectrum.There is a maximum absorption peak at 410 nm and smaller ones at 510, 545, 585, and 635 nm.
used in PDT. As noted in Fig. 15.3, the breadth of the PpIX absorption spectra allows a variety of light sources for PDT. Since longer wavelengths generally allow for deeper tissue penetration, one can selectively target different epithelial levels. For example, blue light in the 410 nm range is appropriate for superficial skin targets, whereas dermal targets require activation by longer-wavelength light sources (>600 nm).
CLINICAL APPLICATIONS A critical review of the cosmetic dermatology literature reveals a fundamental difficulty in assessing PDT data. Variations between studies are routinely noted because there are no set protocols for the majority of conditions evaluated. Differences between methods include the photosensitizer utilized, skin preparation, incubation times of photosensitizers, and light sources and their settings. Much of the data are anecdotal in nature. Thus, a critical flaw is the lack of meaningful statistical analysis proving scientific significance. In addition, almost all studies have limited follow-up intervals, making assessment of recurrence rates problematic. Recently, a number of controlled clinical trials with statistical analysis have been reported in which PDT has held up favorably.
Fig. 15.3 The wide range in the absorption spectrum of protoporphyrin IX allows a variety of light sources to be used for photodynamic therapy. KTP, potassium titanyl phosphate; PDL, pulsed dye laser; IPL, intense pulsed light. (Reproduced from Gold MH. 5-aminolevulinic acid in photodynamic therapy. An exciting future. US Dermatology Review 2006;1:81–8717 with permission.
PHOTOREJUVENATION The visible signs of photodamage are characterized by wrinkling, coarse skin texture, pigmentary alterations, telangiectases, and, in some cases, actinic keratosis (AK). Multiple investigators have reported the benefits of ALA–PDT on photodamage. Light sources described include multiple intense pulsed light sources with the delivery of filtered wavelengths of noncoherent light (IPL), combination IPL and radiofrequency (RF) devices, the pulsed dye laser (PDL), and the potassium titanyl phosphate (KTP) laser.11 In addition, various authors have reported on the benefits of ALA in combination with blue light, IPL, and PDL to treat actinic keratoses (AK) (Fig. 15.4). Ruiz-Rodriguez et al18 reported on 17 patients with varying degrees of photodamage and AK treated with two treatments of ALA–PDT using IPL as a light source. Patients were treated with a 615 nm cutoff filter and total fluence of 40 J/cm2 in a double-pulse mode of 4.0 ms with a 20 ms interpulse delay. Thirtythree of 38 AK disappeared with two treatments of ALA–PDT.Treatments were well tolerated. Erythema and crusting took 1 week to resolve. Although no
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a
b
Fig. 15.4 Photorejuvenation using δ-aminolevulinic acid (ALA) followed by intense pulsed light (IPL) and radiofrequency (RF).The patient received two treatment sessions.The ALA incubation time was 30 minutes, which was followed by IPL at 18 J/cm2 and RF at 18 J/cm2, each in a short pulse. (a) Before treatment. (b) After treatment. (Courtesy of Neil S Sadick.)
statistical analysis or coding of photoaging parameters was reported, cosmetic results were described as ‘excellent’ in all patients, with no resulting pigmentary alterations or scarring. Alster et al19 subsequently performed a comparative split-face study pairing IPL alone versus ALA–IPL.Ten patients with mild to moderate photodamage were recruited. The patients were treated with 60 minutes of ALA followed by IPL to one-half of the face and IPL alone on the contralateral side. Two treatments were delivered at 4-week intervals. Higher clinical improvement scores were noted on the combination ALA–IPLtreated areas. Mild edema, erythema, and desquamation were observed on the half of the face where ALA was applied. No scarring or unwanted pigmentary alteration was seen. The authors concluded that PDT with combination topical ALA–IPL is safe and more effective for facial rejuvenation than IPL treatment alone. In 2005, Dover et al20 published a prospective, randomized, controlled, split-face study with statistical analysis comparing ALA–IPL versus IPL alone.Twenty patients with at least a modest degree of photoaging were included. Patients were treated three times at 3-week intervals within a split-face protocol with ALA–IPL to one side and IPL alone to the contralateral
side (fluence 23–28 J/cm2, with cold contact epidermal cooling). Subsequently, all patients were treated two additional times at 3-week intervals with full-face IPL alone. Photodamage variables were assessed by an independent investigator before each treatment, as well as 4 weeks after the final treatment. Satisfaction with treatment was rated by both subjects and a blinded investigator. In addition, tolerability was assessed by unblinded investigators at every visit. The authors reported statistically significant improvements in global photoaging and mottled pigmentation with ALA–IPL versus IPL alone. In addition, both the blinded investigators and subjects preferred the benefits of the combined ALA–IPL treatment. Interestingly, adverse effects and tolerability did not differ significantly between the IPL-only treated areas and the areas treated with ALA–IPL. In June 2006, Gold et al21 published another splitface trial with ALA–IPL versus IPL alone, but did not include statistical analysis. Sixteen patients with mild to moderate photodamage were treated with ALA–IPL and IPL alone (34 J/cm2). Patients received treatments 1 month apart and were followed 1 month and 3 months after final treatment. Photographs and grading of photodamage were performed by a blinded investigator. For all photoaging parameters, greater
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Photodynamic therapy improvement was seen on the side of the face treated with ALA–IPL. For example, ALA–IPL showed 55% versus 29.5% improvement in crow’s feet and tactile skin roughness and 60% versus 37% in mottled hyperpigmentation. Adverse effects included erythema and edema, which resolved in all patients without sequelae. Butler et al22 compared ALA–IPL and ALA–KTP for photoaging with a split-face trial, but again, did not perform statistical analysis. Seventeen patients with prominent dyschromias and/or discrete telangiectases were enrolled and treated once on each side of the face. Subjects were evaluated and photographed 1 week and 1 month after treatment and photographs were reviewed by a panel of blinded observers. At 1 month, the average improvement for the ALA–IPL side was 38% for vascular lesions and 35% for pigmented lesions as scored by independent evaluators. The average improvements for the ALA–KTP side were 42% and 30%, respectively. Patients rated the two devices very similarly, with global improvement scores of 66% for ALA–IPL versus 61% for KTP. However, a majority of patients found the KTP to be slightly more painful and experienced greater postprocedure swelling. The authors concluded that both KTP and IPL provided marked improvement in vascular and pigmented dyschromias after one treatment. Marmur et al23 evaluated tissue samples in an attempt to correlate clinical improvement with histological changes in patients treated with PDT. Seven subjects with minimal photodamage were treated with ALA–IPL versus IPL alone in a split-face protocol. Pre- and post-treatment biopsies were analyzed for changes in collagen by electron microscopic ultrastructural analysis.An increase in type I collagen fibers was seen after treatment in both sides, but patients pretreated with ALA showed a greater increase in type I collagen formation.
SEBACEOUS GLAND HYPERPLASIA Sebaceous gland hyperplasia (SGH) is a common, benign proliferation of sebaceous glands, which occurs predominantly on the face. Sebaceous glands increase
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with age and are often of cosmetic concern to patients.24 Treatment with the PDL alone has shown promising results in two patients with SGH.25 In addition, studies have shown that PpIX accumulates in pilosebaceous units.20,26 Based on these findings, the effect of PDT on sebaceous hyperplasia and acne has recently been investigated. Light sources have included polychromatic light from a slide projector,27 red light,28 PDL,29 blue light alone,30 and blue light/IPL.31 Horio et al27 treated one patient with multiple lesions.They pretreated papules for 4 hours with ALA and then exposed the patient to the light of a slide projector through a red glass filter. This was repeated three times at 1-week intervals. The authors reported that small papules nearly disappeared and larger papules became smaller but did not completely resolve. One year after treatment, there was no recurrence of any lesions. Interestingly, prior to treating with the light source, the authors also excised one papule for fluorescence microscopy. This showed red fluorescence of topically applied ALA into the hyperplastic sebaceous gland. Alster et al29 reported on 10 patients with at least three prominent sebaceous hyperplasia papules who received ALA–PDL (595 nm) versus no treatment or PDL alone. Patients were evaluated at 1 and 3 months after the final treatment. No patients experienced adverse reactions with the topical ALA per the investigators. Unfortunately, results were not shown in table form and control lesions did not receive consistent treatment (some were treated with PDL while others were untreated).At 3-month follow-up, seven patients had cleared with one treatment, while three patients cleared with two. Richey et al30 treated 10 patients with SGH with ALA followed by blue light. They reported a 70% clearance, but a 20% recurrence of lesions at 3–4 months. Gold et al31 pretreated 12 patients with ALA and then randomized them into two groups. Patients were treated with either a 405–420 nm blue light or a 500–1200 nm IPL device monthly for 4 consecutive months. Eleven patients completed the study. The average reduction in SGH lesion count 3 months after the last treatment was 55% for both the blue light- and IPL-treated patients. Neither group had recurrence of lesions during this period. Adverse effects were
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experienced by three patients, and were limited to erythema and one bulla. Recently, Perrett et al28 investigated the treatment of sebaceous hyperplasia in an immunosuppressed patient. Organ transplant recipients are susceptible to SGH, particularly on the face. Perrett et al pretreated the forehead of a renal transplant recipient with MAL and then treated it with IPL (633 nm, 80 mW/cm2, and 75 J/cm2). This was repeated once 3 weeks later. One month after the last treatment, all of the lesions were either substantially reduced or decreased in size. Six months from the initial treatment, the improvement was sustained.
ACNE Propionibacterium acnes and sebum secretion have been shown to play major roles in acne production.As noted previously, PpIX accumulates in pilosebaceous units. In addition, it has been shown that exogenous ALA can cause a preferential accumulation of protoporphyrin in P. acnes.32 These observations were exploited by Hongcharu et al13 in their seminal study to investigate the effect of PDT on acne vulgaris. They treated 22 patients with mild to moderate acne of the back. Each subject was treated at four sites with (a) ALA and red light (500–700 nm at 150 J/cm2), (b) ALA alone, (c) red light alone and (d) no treatment.The subjects were randomized into two groups, with one half receiving one treatment while the other half received all four. The investigators measured changes in sebum excretion rate, autofluorescence from bacteria in follicles, protoporphyrin synthesis in pilosebaceous units, and histological changes associated with treatment. They discovered that after PDT treatment, porphyrin fluorescence was suppressed in the bacteria, sebaceous glands were damaged, and multiple PDT treatments were associated with reduced sebum excretion rates. In addition, they reported that inflammatory acne was cleared for 10 weeks after a single treatment and 20 weeks after multiple treatments. However, a significant side-effect profile ensued, with reports of acne-like folliculitis, prominent hyperpigmentation, exfoliation and crusting. None of the subjects developed permanent scarring.
Since then, multiple studies have investigated the role of PDT on acne vulgaris using pulsed excimer–dye lasers,32 halogen light (600–700 nm),34 IPL,35 blue light,36,37 or PDL.38 Results have shown that inflammatory acne vulgaris responds well to fullface PDT treatments. Recently, a number of blinded, randomized control trials with statistical analysis have been published on this subject. In 2006,Wiegell et al38 investigated the effect of MAL–PDT versus no treatment on moderate to severe acne vulgaris. Patients were incubated with 3 hours of MAL under occlusion and then with red light (37 J/cm2) on two occasions, 2 weeks apart. In their small trial, they found that 12 weeks after treatment the MAL–PDT group had a 68% reduction in lesions (p = 0.0023). However, all patients experienced pain, pustular lesions, and epithelial exfoliation. Recently, in an effort to decrease some of the phototoxicity that has long been associated with PDT, various investigators have experimented with the effects of decreasing the incubation time of topical photosensitizers (from 3–4 hours to 30 minutes or 1 hour). Many report significant clearing of acne lesions in these patients, with what does seem to be fewer adverse effects after treatment. However, long-term follow-up has been absent from many of these reports, and is a needed area for future study to confirm the sustainability of the reported outcomes.36–41
HAIR REMOVAL Multiple modalities are available for permanent laser hair reduction. Some light and laser options include ruby (694 nm), alexandrite (755 nm), diode (810 nm), and neodymium : yttrium aluminum garnet (Nd:YAG) (1064 nm) lasers, as well as IPL.42 However, PDT is currently the only form of permanent hair removal that functions independently of hair pigmentation. In a pilot study in 1995, 12 patients were treated with 630 nm light, 3 hours after incubation with ALA. An average of 40% hair loss was reported 6 months after this treatment. Although this may offer utility in the management of nonpigmented hair, further study is required.43
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Photodynamic therapy
SIDE-EFFECTS OF PDT The major side-effect seen with PDT is cutaneous photosensitivity after application of a topical photosensitizer – what has been termed the ‘PDT effect’. Protective clothing, barrier sunscreens, and rigorous sun avoidance are necessary for 72 hours after therapy to avoid sunburn. During the light delivery, patients may experience burning, stinging, pruritus, or pain at treatment sites. These sensations may represent direct nerve stimulation and/or damage by reactive singlet oxygen and released mediators. Discomfort is usually tolerable, but premedication with anxiolytics may be necessary in certain patients. For the majority, the discomfort can be managed with conservative measures, including the application of ice or the injection of a local anesthetic. The local discomfort is not prolonged. Localized edema, erythema, and a p’eau d’orange appearance typically last for 1 day after treatment, but may last for several days. Scarring is rare, but possible. Transient hyperpigmentation and hypopigmentation are the most common adverse effects.
THE FUTURE PDT has generated a great deal of interest in the dermatology community over the past several years. Short-contact, full-face ALA–PDT treatments with a variety of lasers and light sources have been shown to be a successful modality for photorejuvenation and the treatment of associated AK, as well as sebaceous gland disorders such as acne vulgaris. PDT is a proven modality for the treatment of superficial skin growths: AK, Bowen’s disease, and superficial basal cell carcinomas, as well as chronic inflammatory diseases such as psoriasis. The treatments are relatively efficacious and safe, but do have the downside of pain and photosensitivity, even in cooler climates. At present, it appears that PDT offers a safe and controlled modality for targeted therapies of specific skin conditions. A number of new applications are currently being investigated and we look forward to discovering new roles for this innovative dermatological therapy. Looking forward, we hope to see more
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double-blind randomized controlled trials to better establish the safety and efficacy of PDT.
REFERENCES 1. Fitzpatrick TB, Pathak MA. Historical aspects of methoxsalen and other furocouramins. J Invest Dermatol 1959;31:229–31. 2. Roelandts R. The history of phototherapy: Something new under the sun? J Am Acad Dermatol 2002; 46:926–30. 3. Parrish JA, Fitzpatrick TB, Tanenbaum L, Pathak MA. Photochemotherapy of psoriasis with oral methoxysalen and longwave ultraviolet light. N Engl J Med 1974; 291:1207–11. 4. Edelson R, Berger C, Gasparro F, et al.Treatment of cutaneous T-cell lymphoma by extracorpeal photochemotherapy. Preliminary results. N Engl J Med 1987;316:297–303. 5. Krutmann J, Schopf E. High-dose-UVA1 phototherapy: a novel and highly effective approach for the treatment of acute exacerbation of atopic dermatitis. Acta Derm Venereol Suppl (Stockh) 1992;176:120–2. 6. Babilas P, Karrer S, Sidoroff A, Landthaler M, Szeimies RM. Photodynamic therapy in dermatology – an update. Photodermatol Photoimmunol Photomed 2005;21:142–9. 7. Gold MH, Goldman MP. 5-Aminolevulinic acid photodynamic therapy: Where we have been and where we are going. Dermatol Surg 2004;30:1077–83. 8. Daniell MD, Hill JS. A history of photodynamic therapy. Aust NZ J Surg 1991;61:340–48. 9. Kennedy J, Pottier RH, Pross DC. Photodynamic therapy with endogenous protoporphyrin IX: Basic principles and present clinical experience. J Photochem Photobiol B Biol 1990;6:143–8. 10. Nestor MS, Gold MH, Kauvar AN, et al.The use of photodynamic therapy in dermatology: results of a consensus conference. J Drugs Dermatol 2006;5:140–54. 11. Fritsch C, Verwohlt B, Bolsen K, Ruzicka T, Goerz G. Influence of topical photodynamic therapy with 5aminolevulinic acid on porphyrin metabolism. Arch Dermatol Res 1996;288:517–21. 12. Bissonnette R, Lui H. Current status of photodynamic therapy in dermatology. Dermatol Clin 1997;15:507–19. 13. Hongcharu W, Taylor CR, Chang Y, et al. Topical ALA–photodynamic therapy for the treatment of acne vulgaris. J Invest Dermatol 2000;115:183–92. 14. Pottier RH, Chow YFA, LaPlante JP et al. Non-invasive technique for obtaining fluorescence excitation and emission spectra in vivo. Photochem Photobiol 1986;44: 679–87.
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15. Morton CA. Photodynamic therapy in skin cancer. In: Rigel DS, Friedman RJ, Dzubow LM, eds. Cancer of the Skin. Philadelphia: Elsevier Saunders, 2005:515–26. 16. Szeimies RM,Abels C, Fritsch C.Wavelength dependency of photodynamic effects after sensitization with 5aminolevulinic acid in vitro and in vivo. J Invest Dermatol 1995;105:672–7. 17. Gold MH. 5-aminolevulinic acid in photodynamic therapy. An exciting future. VS Dermatology Review 2006;7:81–7. 18. Ruiz-Rodriguez R, Sanz-Sanchez T, Cordoba S. Photodynamic photorejuvenation. Dermatol Surg 2002;28:742–4. 19. 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;4:35–8. 20. Dover JS, Bhatia AC, Stewart B, Arndt KA. Topical 5aminolevulinic acid combined with intense pulsed light in the treatment of photoaging. Arch Dermatol 2005; 141:1247–52. 21. Gold MH, Bradshaw VL, Boring MM, Bridges TM, Biron JA. Split-face comparison of photodynamic therapy with 5-aminolevulinic acid and intense pulsed light versus intense pulsed light alone for photodamage. Dermatol Surg 2006;32:795–803. 22. Butler EG , McClellan SD, Ross EV. Split treatment of photodamaged skin with KTP 532 nm laser with 10 mm handpiece versus IPL: a cheek-to-cheek comparison. Lasers Surg Med 2006;38:124–8. 23. Marmur ES, Phelps R, Goldberg DJ. Ultrastructural changes seen after ALA–IPL photorejuvenation: a pilot study. J Cosmet Laser Ther 2005;7:21–4. 24. Balin AK, Pratt LA. Physiologic consequences of human skin aging. Cutis 1989;43:431–6. 25. Schonermark MP, Schmidt C, Raulin C. Treatment of sebaceous gland hyperplasia with pulsed dye laser. Lasers Surg Med 1997;21:310–13. 26. 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 fluorescence. Am J Pathol 1990;136:891–7. 27. Horio T, Horio O, Miyauchi-Hashimoto H, Ohnuki M, Isei T. Photodynamic therapy of sebaceous hyperplasia with topical 5-aminolevulinic acid and a slide projector. Br J Dermatol 2003;148:1274–6. 28. Perrett CM, McGregor J, Barlow RJ, et al.Topical photodynamic therapy with methyl aminolevulinate to treat sebaceous hyperplasia in an organ transplant recipient. Arch Dermatol 2006;142:781–2. 29. Alster TS, Tanzi EL. Photodynamic therapy with topical aminolevulinic acid and pulsed dye laser irradiation for sebaceous hyperplasia. J Drugs Dermatol 2003;2:501–4.
30. Richey DF, Hopson B. Treatment of sebaceous hyperplasia by photodynamic therapy. Cosmet Dermatol 2004; 17:525–9. 31. Gold MH, Bradshaw VL, Boring MM, Bridges TM, Biron JA.Treatment of sebaceous gland hyperplasia by photodynamic therapy with 5-aminolevulinic acid and a blue light source or intense pulsed light source. J Drugs Dermatol 2004;3:S6–9. 32. Ramsted S, Futsaether CM, Johnsson A. Porphyrin sensitization and intracellular calcium changes in the prokaryote, Propionibacterium acnes. J Photochem Photobiol 1997;40:141–8. 33. Itoh Y, Ninomiya Y, Tajima S, Ishibashi A. Photodynamic therapy of acne vulgaris with topical 5-aminolevulinic acid. Arch Dermatol 2000;136:1093–5. 34. Itoh Y, Ninomiya Y, Tajima S, Ishibashi A. Photodynamic therapy of acne vulgaris with topical delta-aminolevulinic acid and incoherent light in Japanese patients. Br J Dermatol 2001;144:575–9. 35. Goldman MP, Boyce SM. A single center study of 5-aminolevulinic acid and 417 nm photodynamic therapy in the treatment of moderate to severe acne vulgaris. J Drugs Dermatol 2003;2:393–6. 36. Gold MH. A single-center open-label investigatory study of photodynamic therapy in the treatment of moderate to severe acne vulgaris with aminolevulinic acid topical solution 20% and visible blue light. Abstract presented at 61st Annual Meeting of the American Academy of Dermatology, San Francisco, 2003. 37. Gold MH, Bradshaw VL, Boring MM, et al. The use of a novel intense pulsed light and heat source and ALA–PDT in the treatment of moderate to severe inflammatory acne vulgaris. J Drugs Dermatol 2004;3:S14–18. 38. Alexiades-Armenakas M. Long-pulsed dye laser-mediated photodynamic therapy combined with topical therapy for mild to severe comedonal, inflammatory or cystic acne. J Drugs Dermatol 2006;5:45–55. 39. Wiegell SR, Wulf HC. Photodynamic therapy of acne vulgaris: a blinded, randomized, controlled trial. Br J Dermatol 2006;154:969–76. 40. Taub A. Photodynamic therapy for the treatment of acne: a pilot study. J Drugs Dermatol 2004;3:S10–14. 41. Santos MA, Belo VG, Santos G. Effectiveness of photodynamic therapy with topical 5-aminolevulinic acid and intense pulsed light versus intense pulsed light alone in the treatment of acne vulgaris: comparative study. Dermatol Surg 2005;31:910–15. 42. Wanner M. Laser hair removal. Dermatol Ther 2005;18: 209–16. 43. Dierickx CC, Grossman MC. Laser hair removal. In: Goldberg DJ, Rohrer TE, Dover JS, eds. Laser and Lights, Vol 2. Philadelphia: Elsevier Saunders, 2005:61–76.
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16. Adjunctive techniques I: the bioscience of the use of botulinum toxins and fillers for non-surgical facial rejuvenation Kristin Egan and Corey S Maas
INTRODUCTION The contemporary clinician is faced with both biological and alloplastic materials to use as soft tissue fillers. The clinician is eager to find an ideal implant, i.e., one that will maintain its shape and consistency without inciting an adverse host response. This ideal implant has not yet been developed. Therefore, the clinician must weigh the advantages and disadvantages of each product on the market in order to achieve the most harmonious result for a patient. Finally, the clinician should seek to match the advantages and limitations of each product with the desired result while becoming personally comfortable with the use of a product.
BOTULINUM NEUROMODULATORS In the 1980s, Allen Scott in San Francisco used botulinum neuromodulator in laboratory chick models for selective weakening of treated muscles, and soon thereafter it was used for the management of strabismus.1 Botulinum neuromodulator is found in nature in seven serotypes (A–G) defined by their specific biological action in cleaving particular proteins involved in the active transport of acetylcholine into the neurosynaptic cleft responsible for muscle contraction (and other autonomic functions).2,3 These naturally occurring proteins were originally described as toxins causing the illness botulism, which is associated with the ingestion of large amounts of foodstuffs contaminated with the bacterium Clostridium botulinum.They are better described, with respect to their now widespread medical use, as
neuromodulators. Their distinct beneficial action is selective weakening, relaxation, or paralysis of treated muscles or muscle groups. By selective weakening of certain hypertrophic muscle groups in the face and neck, unwanted lines and facial expressions can be suppressed or even eliminated. While the B-serotype neuromodulator (Myobloc, Solstice Neurosciences, San Francisco, CA) has demonstrated benefit in the treatment of hyperfunctional frown lines (HFL), its benefit under current formulations is limited by the shorter duration of effect of the product.4,5 Therefore, the A-serotype neuromodulator is most optimal for the aesthetic practitioner. The A serotype has demonstrated the longest duration of effect (90–120 days) and least discomfort with injection. The most commonly used of the available Aserotype neuromodulators is Botox (Allergan, Inc., Irvine, CA), which has a demonstrated safety and efficacy record of over 15 years. Reloxin (Medicis Inc., Scottsdale,AZ), known as Dysport in Europe, is in current phase III Food and Drug Administration (FDA) clinical trials in the USA, and shows promise, as does Purtox (Mentor Corp., Santa Barbara, CA), which is in its early-phase FDA trials. An understanding of how to use Botox relies on a clear understanding of the facial muscular anatomy. While many techniques and surface points of injection have proven effective, it is clear that optimal response with minimal effective dosages requires precise placement in the selected muscle or muscle group (Fig. 16.1). The use of Botox on the upper face has been demonstrated in controlled large-population anatomical studies.6 Interest in lower facial applications has reinforced
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Fig. 16.1 The glabellar complex as demonstrated before and after injection of botulinum toxin.
the need for a fundamental understanding of this muscular anatomy.7 It is clear, however, that, due to diffusion effects and the relative safety of Botox, the variability in points of injection and dosages has not significantly reduced the product’s overall satisfactory clinical results. In our opinion, required dosages for a given anatomical area can be reduced by precise localization and direct injection into the targeted muscle or muscle groups. It is imperative that one keep in mind not only the specific muscle locations when providing neuromodulator treatment, but also the functional interrelationships of the muscle action. Many of these act as antagonist– protagonists in the position of the brow. The use of Botox in general has evolved with experienced and thoughtful injectors from a simple wrinkle treatment to a means of reshaping, contouring, and softening the facial features associated with aging and the stigmata of the frowning, angry or worried facial form. Botox is frequently used to specifically target different muscular units. In the glabellar region, targeting of the procerus and corrugator muscles is used to eliminate furrowing along the radix and medial eyebrow region. The lateral orbital region, which is commonly referred to as the ‘crow’s feet’, is also a region in which Botox may be of use to target the orbicularis oculi muscle and reshape the upper face.The use of Botox in the forehead must be conservative in order to balance the risk of brow ptosis by targeting the only brow elevator, the frontalis muscle. Perioral lip lines have also been treated with sparing amounts of Botox to suppress the pursing effect of the orbicularis oris muscle. One must
be careful not to compromise oral competence as a result of this treatment. Botox injection into the depressor anguli oris muscle can target marionette lines, and its use for contraction of the mentalis muscle can alleviate complaints of a dimpled chin appearance, but one must be careful to avoid the lower lip depressors. Platysmal banding in the neck due to overactive platysmal muscle action can be treated using Botox. However, this works best for younger patients with good skin elasticity or postoperative residual bands.8 This facial characteristic may ultimately only be treated optimally with surgical intervention. The use of botulinum toxin type A and laser resurfacing has been studied recently due to the proliferation of nonsurgical treatments for the aging face and the desire to perform more than one treatment in one visit. It has been demonstrated that the use of Botox in conjunction with laser resurfacing results in improved outcomes in the periorbital region.9 Other areas of the face have also been studied and have been shown to have less rhytids after Botox and laser than those areas treated with laser alone, and these results were clinically most significant in the crow’s feet region.10 It has also been shown that the use of Botox as an adjunctive treatment will prolong the beneficial results of laser resurfacing and should therefore be offered as an option to patients wishing to have longer-lasting elimination of rhytids.11 It is safe to use laser resurfacing after treatment with Botox, as this will have no effect on the efficacy of the Botox injection or other apparent untoward effects.12
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HISTORICAL PERSPECTIVE The search for an ideal product to be used for soft tissue augmentation has been ongoing with varying degrees of success since the end of the 19th century. Autologous fat was first reported as a soft tissue filler by Neuber in 1893.13 Paraffin was later used, but with significant drawbacks.13,14 The ensuing years brought the use of vegetable oils, mineral oil, lanolin, and beeswax; all demonstrating the problems that continue to be associated with fillers in use today, namely chronic inflammation and migration.15–18 Purified bovine dermal collagen was first developed in an injectable form in 1977 by Knapp et al.19 In early trials, the most common complications seen were cellulitis, urticaria, and hyperpigmentation of the skin making it superior to its predecessors.19 Teflon, polytetrafluoroethylene paste, was initially thought to be a useful soft tissue filler. However, its consistency and injectability limit its main commercial use today to vocal cord augmentation procedures.20 It is reasonable to divide soft tissue fillers into the biologicals and the nonbiologicals.We will first discuss the biologicals, both tissue-derived and synthetic. Finally, we will discuss the nonbiologicals, i.e., fillers not based on animal tissue. Table 16.1 is offered as a reference to help guide clinicians in the selection of a soft tissue filler.
BIOLOGICAL MATERIALS USED AS INJECTABLE IMPLANTS The use of biological materials for injection is thought to be advantageous in that the inflammatory response should be less for a substance that is of nonimmunogenic biological origin. However, cross-reactivity has not been eliminated altogether, and although biological fillers do result in less fibrosis and contraction around the injection site, problems still exist. The most common side-effect seen with the use of soft tissue fillers is the localized reaction to the injection or implantation. Swelling, redness, and pain can all be treated with conservative measures. Allergies and delayed hypersensitivity responses are more serious complications, and indeed preclude the further use of the material.
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Table 16.1 Soft tissue fillers Biological filler materials Bovine collagen Recombinant human collagen Juvederm Hyaluronic acid Dermal matrices
Synthesized bioactive fillers
Synthetic non-resorbable polymers
Sculptra Reviderm intra
Artecoll Silicone
Radiesse
Ultrasoft Softform Advanta, Dermalive, Dermadeep
Collagen Collagen was the first material to be approved by the FDA for used as an injectable soft tissue filler, in 1981.15 Many derivatives are available today, including Zyderm I (35 mg/dl), Zyderm II (65 mg/dl), and Zyplast (Collagen Corp., Palo Alto, CA). Cosmoderm and Cosmoplast (Inamed Corp., Santa Barbara, CA) differ from Zyderm and Zyplast only in that they are injectable human collagen products derived from a single cell line source. Zyderm I was the first nonautologous agent to be approved for use as a soft tissue filler in the USA, in 1981.21 Zyderm II was soon developed as a more concentrated form.These substances work on the basis of low-grade focal inflammation and are of a forgiving nature.They are easy to inject, and precise injection technique is not very important. Zyderm is derived from bovine dermal collagen, with 95% type I and 5% type III collagen. The processing of Zyderm removes the telopeptide regions of the molecule without disrupting the natural helical structure. However, 3–3.5% of the population still demonstrate a hypersensitivity to the substance, and after one negative skin test, 1–5 % of patients will still show an allergic reaction when the material is placed in the face.22 Zyplast is crosslinked by the addition of glutaraldehyde, which lessens the immune response to it and also serves to increase resistance to bacterial collagenase. Zyderm injections will provide cosmetic results for 2–3 months, at which time repeat injections are needed. Zyplast provides longer results (on average 2–4 months) due to its crosslinking, but eventually
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repeat injections are also necessary. Zyderm and Zyplast have to be injected intradermally. Zyderm is infiltrated into the papillary dermis, whereas Zyplast is preferably placed into the midreticular or deep reticular dermis at the dermal–subcutaneous interface. Zyplast should not be injected into the superficial papillary dermis or in areas of thin skin, because it forms beads on placement.23
Hyaluronic acid Hyaluronic acid is a biopolymer of glycosaminoglycan chains, which coil on themselves resulting in an elastic and viscous matrix. It is found naturally in the dermis and has a high affinity for water, thereby serving to hydrate and plump the skin.24 The loss of hyaluronic acid with age leads to dermal dehydration and the formation of rhytids.25 Crosslinking can lengthen the half-life of hyaluronic acid, but cannot eliminate its degradation. Products clinically available include Hyalform, Hyalform Plus and Hyalform Fine Line (Biomatrix, Inc., Ridgefield, NJ), Restylane (Q-Med, Uppsala, Sweden), and Captique (Genzyme, Ridgefield, NJ), and other forms, such as Juvederm (Allergan, Irvine, CA), are under clinical trail in the USA. Q-Med is also responsible for Restylane Fine Line and Perlane. Perlane is designed for subcutaneous injection and is primarily used for volume replacement. It is a larger particle than that found in Restylane, and therefore has a longer duration. While Juvederm is a pure hyaluronic acid form that is rapidly absorbed, Hyalform is a crosslinked xenogenic variety derived from rooster combs, which was submitted for FDA approval as an equivalent product to Restylane.The latter is only partially crosslinked and is processed from a streptococcal fermentation.24 Neither material requires skin testing. Restylane, not being derived from an animal source, has a lower risk of immune reaction. Both forms are reabsorbed, albeit at a slower rated than the collagen products. It has been reported that effects last up to 6 months.26 Hylaform is less viscous, and this may decrease the duration of its effect to 2–4 months, although no side-by-side trials have been published. Hylaform is a modified form of hyaluronan, a naturally occurring substance found in human skin and throughout the body. Since Hylaform is based on
natural hyaluronan, the human body accepts it as its own. Hylaform also mimics the hydrating and lifting effect of hyaluronan, which keeps the skin hydrated and elastic. In side-by-side comparison with Restylane, Hyalform showed a higher incidence of skin reaction.26 Hyalform also behaves as a stronger hydrogel than Restylane and contains a lower amount of crosslinked hyaluronic acid. Restylane can contain up to four times as much protein, from bacterial fermentation, as Hyalform for the same volume. Finally, hyaluronan derived from rooster combs has been in use longer than that derived from streptococci, and has demonstrated its reliability and safety. A randomized study of 138 patients comparing Restylane and Zyplast for the correction of nasolabial folds demonstrated that a more durable aesthetic improvement was found with Restylane.27 Less injection volume was required with Restylane, which was also superior to Zyplast in retaining its shape. A comparison of Restylane with and without the addition of Botox demonstrated that glabellar rhytides responded better to the combination of Restylane and Botox.28 Those patients who present with deep vertical glabellar lines at rest may not be able to eliminate those lines with the use of Botox alone. Restylane can serve to fill the resting lines, and the addition of Botox prevents the deformation of the filler residing in the dermis, thereby performing a protective function. Restylane is also useful as a soft tissue filler for microchelia (Fig. 16.2). Captique is a filler that utilizes a recombinant form of hyaluronic acid that lowers the probability of immunological reactions. The profiles of this filler are much the same as those of Hyalform, with a duration of 2–4 months and a similar injection and viscosity profile. Materials that are resorbable by the body are less likely to provoke a longstanding immunological response, because of their transient nature. However, substances that are derived from nonautologous sources have the potential to evoke cross-reactivity. Restylane and Hylaform are newer materials that are beginning to undergo long-term studies, which are beginning to show side-effects. A study of 709 patients over 4 years showed positive skin tests in those who developed delayed skin reactions to these materials. The manufacturer does not recommend skin testing for these materials – but these reports may suggest
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Fig. 16.2 Restylane used as a soft tissue filler for lip augmentation.
otherwise.29 Case reports have also shown the potential for granuloma formation with the use of hyaluronic acid derivatives.30 Positive skin tests have demonstrated chronic inflammatory reactions at up to 11 months and serum immunoglobulin G (IgG) and IgE antibodies to hyaluronic acid.32 Of course, these aesthetic complications must be fully addressed with the patient before any procedure is performed.
Dermal matrices The search for soft tissue fillers free of antigenicity has led to the development of Alloderm and Cymetra (LifeCell Corp., Branchburg, NJ).Alloderm is processed from cadaveric skin, preserving the basement membrane and dermal collagen matrix. After the fibroblasts have been extracted, the material is cryoprotected, which enables it to be freeze-dried in a two-step procedure. Alloderm is screened and monitored for bacterial contamination before it is shipped to the physician. It is supplied in sheets of differing sizes and thicknesses, which must be rehydrated by the physician before use. The sizing of this material makes it ideal for repairing large tissue defects. Skin testing is not necessary, because it is an acellular graft. It is also less likely to
develop secondary infection. However, if infection does occur, it is not necessary to remove the implant, only to treat the infection.22 Alloderm does not appear to last as long or be as consistent as originally described, which, along with its high cost, has decreased its use and popularity.The requirement for a surgical procedure has also limited its use. Zyplast was studied in direct comparison with Alloderm with follow-up at 1 year, by Sclafani et al.32 Superior results were seen with Alloderm which stabilized in resorption at 6 months, while Zyplast was progressively absorbed. Cymetra is a micronized injection of Alloderm tissue. It is created by homogenizing an Alloderm sheet cut into strips. In a study of 44 patients involving the use of Cymetra and Zyplast to fill upper lip lines, there was a statistically significant improvement at 1 year in lip appearance among those randomized to receive Cymetra. Some reports suggest that Cymetra does not reabsorb as Zyplast is observed to do, and therefore repeated treatments provide an additive effect and are more effective.33 Cymetra carries an increased incidence of inflammatory reactions and has not been shown to last longer than Zyplast. It also requires mixing into a thick paste, usually with 1% or 2% lidocaine. This thick mixture can be difficult to inject. Due to the lack of
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long-term results and the increased cost, Cymetra is not used as frequently as other soft tissue fillers. Small-intestinal submucosa, marketed as Oasis, Surgisis, or Stratasis, is a sterile acellular graft material extracted from the small intestine of pigs. Its main uses continue to be for nasal reconstructive surgery, but increasing experience may broaden its applications. Isolagen (Isolagen Tech., Metuchen, NJ) is currently under FDA investigation. It consists of injectable fibroblasts derived from an autologous source and cultured for 4–6 weeks. Skin is harvested from the preauricular region in a 3 mm punch biopsy.34 Repeat injections, most commonly three, are required, spaced 2 weeks apart. A 6-month study by Watson et al35 showed increased thickness and density of the postauricular dermal collagen and no inflammatory reaction. Due to the viability of the fibroblasts, Isolagen must be shipped, processed, and injected within 24 hours. However, it theoretically has the advantage of low immunoreactivity, as with the other human derivatives. A significant drawback is that patients must also be willing to wait up to 18 months to see results, as the fibroblasts must first produce new collagen.
hydroxyapatite (similar to the composition of bone) microspheres ranging in size from 25 to 40 µm in a carboxymethylcellulose gel. The microspheres of Reviderm produced the greatest amount of granulation tissue, but were also disintegrated at 9 months. Radiesse microspheres were gone at 9 months, but they stimulated almost no foreign body reaction.36 Few macrophages were visualized surrounding the microspheres of Radiesse, suggesting that they are degraded by enzymatic processes rather than cellular one. Radiesse is not recommended for use in lip augmentation, as the microspheres will be compressed into strands during the act of mastication. Radiesse is a thick paste, which can be difficult to inject and must be injected only in deep dermis. It is used in the nasolabial folds, but we caution use in the lips, which is also the policy of the manufacturer. It has an increased incidence of nodule formation, which can only be dealt with by surgical excision.
SYNTHESIZED BIOACTIVE FILLERS
Materials that are foreign to the human body have also been used in the development of soft tissue fillers in both injectable and implantable forms.
The search for the ideal soft tissue fillers has led to the development of materials that do not mimic collagen but rather serve to increase volume for a longer period of time due to their preformed microsphere shapes. Sculptra (Biotech Industry, SA, Luxembourg) is a powder of poly-L-lactic acid microspheres ranging from 2 to 50 µm. Studies comparing the various soft tissue fillers have shown the microspheres of Sculptra to be histologically degraded at 9 months. Sculptra has only been FDA-approved for the treatment of HIV lipodystrophy, and provokes an intense inflammatory reaction leading to a fibroblastic response resulting in increased appearance of the tissue. The complications reported include draining granulomas, and (like other fillers) it must be injected subcutaneously. Reviderm intra (Medical International, Netherlands), available in Europe, is a suspension of 2.5% dextran microspheres of 40 µm in 2.0% hyaluronic acid. Radiesse (formerly Radiance FN) (Bioform Inc., Franksville, WI) is a suspension of 30% calcium
SYNTHETIC NONRESORBABLE POLYMERS
Injectable Artecoll (Artes Medical Inc., San Diego, CA) is a suspension of 20% microspheres 40 µm in diameter made of polymethylmethacrylate (PMMA) in 3.5% bovine collagen solution.Artecoll works by microgranuloma formation, which may not be controllable. This product produces immediate correction with collagen and also permanent replacement with new collagen produced as part of the inflammatory response.22 Artecoll, unlike the other microspheres, does not become reabsorbed, and histologically new collagen deposits are visible at 1 month.36 A minimal immunogenic response has been observed due to the fact that the telopeptides are removed from the collagen.As with other xenogenic injectables, skin testing is required before use. The smooth surface of the microsphere prevents a foreign body reaction, and the size prevents migration
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The bioscience of the use of botulinum toxins and fillers for non-surgical facial rejuvenation and phagocytosis.37 It should not be used in areas of fine skin, as the implants may be more visible, and should be avoided in those patients prone to keloids, as any foreign material may serve to increase the incidence of keloids. However, Artecoll demonstrates a much lower incidence of immunological response, 0.06%, as compared with Zyderm, which has an incidence of 3%.36 Migration has only been observed when the material is injected into the dermis in trials with guinea pigs, and has not been observed with correct placement of the material.38 Artes Medical may reformulate the product in a US version with hyaluronic acid to meet FDA requirements. All injectable filler materials may lead to overexpression of the host’s foreign body-type immunological reaction.This may, in rare cases, lead to the formation of a granuloma. The combination of materials is foreshadowed in the development of Dermalive and Dermadeep (Dermatech, Paris, France). In Europe, 30 or more synthetic polymers are available for use in general, although this may vary somewhat by country. Examples of such polymers include Dermalive, and Dermadeep, which are combinations of pure hyaluronic acid (40% and 60%, respectively) and an acrylic hydrogel. The hyaluronic acid is used as a carrier for the acrylic polymer.They have been developed in response to the need for repeat injections when using such materials as pure hyaluronic acid and collagen. The tolerance of Dermalive is excellent and it has been supplemented with injections of Juvederm or Restylane for fine line and superficial defects.39 A 3-year study of this combination therapy in 455 patients demonstrates an 88% patient satisfaction rate with minimal side effects.39 Silicone, much maligned due to its history in breast augmentation, is another synthetic injectable. Its use has been associated with the development of connective tissue ingrowth and granulomas from macrophages and foreign body cells (Fig. 16.3).40 This is more commonly seen in patients with very lax skin, which facilitates the migration of the silicone, and with the substitution of cheaper, non-medicalgrade silicone fluids used by nonprofessionals.36 When used as silicone fluid, the material is injected via the microdroplet technique. In the rare case of siliconoma development, the use of corticosteroids has proven helpful, but this is rarely a completely satisfactory treatment.41 Late-term granulomas are not
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Fig. 16.3 Granuloma and foreign body reaction after injection of silicone.
uncommon. As a result, we do not recommend this material.
Implantable Implantable expanded polytetrafluoroethylene (ePTFE) (WL Gore and Assoc., Flagstaff, AZ) has been used in the field of vascular surgery for over 30 years, demonstrating its safety and reliability.42 Tissue ingrowth is marginal into the material, but when it is shaped into a tube, longitudinal growth occurs. This serves to strengthen the filler and secure it to the site of implantation.43 Ultrasoft is a thinner, softer form of the tubular form of implantable expanded polytetrafluoroethylene (Fig. 16.4). The tubular form was originally marketed under the name SoftForm (Collagen Corp., Palo Alto, CA), and was used as soft tissue filler for lip augmentation. There still exists a risk of extrusion or exposure of the ends of the material at the entrance wound where the implant is delivered. Softform showed wall stiffening due to the abundance of ePTFE creating an accordion effect. The risk of extrusion at the insertion sites creates a potential source of infection. If complications do arise, the implant is always removable. Due to the higher content of ePTFE, Softform shortens and hardens with time. This can create an ‘accordion effect’. Ultrasoft, with its thinner walls, has addressed this issue, with early success being reported.
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Fig. 16.4 Ultrasoft used for lip augmentation. Advanta (Atrium Medical Corp., Hudson, NH) is a dual-porosity implant developed to provide softer palpability, less migration, and reduced shrinkage.The outer core measures 40 µm and the inner 100 µm, with the inner core being exposed to the surrounding tissue. A study comparing Softform with Advanta demonstrated neovascularization and cellular integration into the interstices of the Advanta implant, while the Softform implant demonstrated a cellular capsule, more inflammatory cells, and fewer vascular elements within the devices.44 Advanta is designed for use in the nasolabial folds and for lip augmentation.
area. Finally, the droplet technique is used in a manner similar to that in linear threading. However, instead of an even distribution of filler as the needle is withdrawn, microdroplets of filler are delivered into the tissue by gentle pumping on the syringe as the needle is withdrawn. The droplet technique has been advocated for use when injecting silicone. The depth of injection, however, is dependent on the injectable material being used. Most clinicians prefer the serial injection technique for use in fine lines and the lips.The other options include the microdroplet technique or surgical implantation in the subcutaneous plane.
TECHNIQUES
CONCLUSIONS
When considering injectables, there are basically three techniques used to deliver material to the deep dermis or subcutaneous level: linear threading, serial puncture, and droplet. Linear threading is a technique by which an agent is delivered in a uniform fashion while the needle is slowly withdrawn from the tissue. It is particularly effective when performing lip augmentation along the mucocutaneous border.The serial puncture technique is used to deliver small aliquots of filler at multiple spots to achieve even distribution over a two-dimensional
Many patients who present to their physicians with complaints of an aging face or cosmetic deformities are eager to avoid surgical intervention. As such, they are willing to use newly introduced minimally invasive options for their desired corrections. Today, there is a myriad of injectable and implantable soft tissue augmentation options at the experienced clinician’s disposal. A concern with the use of permanent filler is the potential for migration to other areas outside of the injection site, which can lead to potential deformities.The choice of
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The bioscience of the use of botulinum toxins and fillers for non-surgical facial rejuvenation which product to use can be based on a number of factors, including the desires of the patient, the cost to the patient, and the experience of the clinician. Caution must be exercised, however, when considering the use of soft tissue fillers that have been newly introduced to the market and have not yet undergone long-term observation and study.With more knowledge and experience, one will be better able to tailor the use of specific materials to the particular desires of each patient.
REFERENCES 1. Scott AB, Botulinum toxin injection into extraocular muscles as an alternative to strabismus surgery. J Pediatr Ophthalmol Strabismus 1990;17:21–5. 2. Schantz EJ, Johnson EA. Botulinum toxin: the story of its development for the treatment of human disease. Persp Biol Med 1997;40:317–27. 3. Schantz EJ, Johnson EA. Preparation and characterization of botulinum toxin type A for human treatment. In: Jankovic J, Hallet M, eds.Therapy with Botulinum Toxin, 4th edn. New York: Marcel Dekker, 1994. 4. Ramirez AL, Reeck J, Maas CS. Preliminary experience with botulinum toxin type B in hyperkinetic facial lines. Plast Reconstr Surg 2002;109:2154–5. 5. Ramirez AL, Reeck J, Maas CS. Botulinum toxin type B (Myobloc) in the management of hyperkinetic facial lines. Otolaryngol Head Neck Surg 2002;126:459–67. 6. MacDonald M, Spiegel J, Maas CS. Glabellar anatomy: the anatomic basis for BoTox therapy. Arch Otolaryngol Head Neck Surg 1998;124:1315–20. 7. Loos BM, Maas CS. Relevant anatomy for botulinum toxin facial rejuvenation. Facial Plast Surg Clin North Am 2003;11:439–43. 8. Carruthers J, Fagien S, Matarasso SL. Consensus recommendations on the use of botulinum toxin type A in facial aesthetics. Plast Reconstr Surg 2004;114 (6 suppl): 1–22. 9. Yamauchi PS, Lask G, Lowe NJ. Botulinum toxin type A gives adjunctive benefit to periorbital laser resurfacing. J Cosmet Laser Ther 2004;6:145–8. 10. Zimbler MS, Holds JB, Kokoska MS, et al. Effect of botulinum toxin pretreatment on laser resurfacing results: a prospective, randomized, blinded trial. Arch Facial Plast Surg 2001;3:165–9. 11. West TB, Alster TS. Effect of botulinum toxin type A on movement-associated rhytids following CO2 laser resurfacing. Dermatol Surg 1999;25:259–61. 12. Semchyshyn NL, Kilmer SL. Does laser inactivate botulinum toxin? Dermatol Surg 2005;31:399–404.
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13. Neuber F. Fat grafting. Cuir Kongr Verh Otsum Ges Chir 1893;20:66. 14. Ersek RA, Beisang AA 3rd. Bioplastique: a new biphasic polymer for minimally invasive injection implantation. Aesthetic Plast Surg 1992;16:59–65. 15. Bailin PL, Bailin MD. Collagen implantation: clinical applications and lesion selection. Dermatol Surg Oncol 1988;14 (suppl 1):49. 16. Castrow FF 2nd, Krull EA. Injectable collagen implant – update. J Am Acad Dermatol 1983;9:889–93. 17. Maas CS, Papel ID, Greene D, Stoker DA. Complications of injectable synthetic polymers in facial augmentation. Dermatol Surg 1997;23:871–7. 18. Newcomer VD, Graham JH, Schaffert RR, Kaplan L. Sclerosing lipogranuloma resulting from exogenous lipids. AMA Arch Dermatol 1956;73:361–72. 19. Knapp TR, Kaplan EN, Daniels JR. Injectable collagen for soft tissue augmentation. Plast Reconstr Surg 1977; 60:398–405. 20. Landman MD, Strahan RW,Ward PH. Chin augmentation with polytef paste injection. Arch Otolaryngol 1972;95: 72–5. 21. Cooperman LS, Mackinnon V, Bechler G, Pharriss BB. Injectable collagen: a six-year clinical investigation. Aesthetic Plast Surg 1985;9:145–51. 22. Ashinoff R. Overview: soft tissue augmentation. Clin Plast Surg 2000;27:479–487. 23. Skouge JW DR. Soft tissue augmentation with injectable collagen. In: Papel ID, ed. Facial Plastic and Reconstructive Surgery, 2nd edn. St Louis, MO: Mosby, 1992:208. 24. Krauss MC. Recent advances in soft tissue augmentation. Semin Cutan Med Surg 1999;18:119–28. 25. Duranti F, Salti G, Bovani B, Calandra M, Rosati ML. Injectable hyaluronic acid gel for soft tissue augmentation. A clinical and histological study. Dermatol Surg 1998; 24:1317–25. 26. Lowe NJ, Maxwell CA, Lowe P, Duick MG, Shah K. Hyaluronic acid skin fillers: adverse reactions and skin testing. J Am Acad Dermatol 2001;45:930–3. 27. Narins RS, Brandt F, Leyden J, et al. A randomized, double-blind, multicenter comparison of the efficacy and tolerability of Restylane versus Zyplast for the correction of nasolabial folds. Dermatol Surg 2003; 29:588–95. 28. Carruthers J, Carruthers A. A prospective, randomized, parallel group study analyzing the effect of BTX-A (Botox) and nonanimal sourced hyaluronic acid (NASHA, Restylane) in combination compared with NASHA (Restylane) alone in severe glabellar rhytides in adult female subjects: treatment of severe glabellar rhytides with a hyaluronic acid derivative compared with the derivative and BTX-A. Dermatol Surg 2003;29:802–9.
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29. Lemperle G, Morhenn V, Charrier U. Human histology and persistence of various injectable filler substances for soft tissue augmentation. Aesthetic Plast Surg 2003;27: 354–66; discussion 367. 30. Fernandez-Acenero MJ, Zamora E, Borbujo J. Granulomatous foreign body reaction against hyaluronic acid: report of a case after lip augmentation. Dermatol Surg 2003;29:1225–6. 31. Micheels P. Human anti-hyaluronic acid antibodies: Is it possible? Dermatol Surg 2001;27:185–91. 32. Sclafani AP, Romo T 3rd, Jacono AA. Rejuvenation of the aging lip with an injectable acellular dermal graft (Cymetra). Arch Facial Plast Surg 2002;4:252–7. 33. Sclafani AP, Romo T 3rd, Parker A, et al. Homologous collagen dispersion (dermalogen) as a dermal filler: persistence and histology compared with bovine collagen. Ann Plast Surg 2002;49:181–8. 34. West TB, Alster TS. Autologous human collagen and dermal fibroblasts for soft tissue augmentation. Dermatol Surg 1998;24:510–12. 35. Watson D, Keller GS, Lacombe V, et al. Autologous fibroblasts for treatment of facial rhytids and dermal depressions. A pilot study. Arch Facial Plast Surg 1999;1: 165–70. 36. Lemperle G, Kind P. Biocompatibility of Artecoll. Plast Reconstr Surg 1999;103:338–40. 37. Lemperle G, Hazan-Gauthier N, Lemperle M. PMMA microspheres (Artecoll) for skin and soft-tissue
38.
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augmentation. Part II: Clinical investigations. Plast Reconstr Surg 1995;96:627–34. McClelland M, Egbert B, Hanko V, Berg RA, DeLustro F. Evaluation of artecoll polymethylmethacrylate implant for soft-tissue augmentation: biocompatibility and chemical characterization. Plast Reconstr Surg 1997;100:1466–1474. Bergeret-Galley C, Latouche X, Illouz YG.The value of a new filler material in corrective and cosmetic surgery: DermaLive and DermaDeep. Aesthetic Plast Surg 2001; 25:249–55. Rapaport MJ, Vinnik C, Zarem H. Injectable silicone: cause of facial nodules, cellulitis, ulceration, and migration. Aesthetic Plast Surg 1996;20:267–76. Bigata X, Ribera M, Bielsa I, Ferrandiz C. Adverse granulomatous reaction after cosmetic dermal silicone injection. Dermatol Surg 2001;27:198–200. Costantino PD. Synthetic biomaterials for soft-tissue augmentation and replacement in the head and neck. Otolaryngol Clin North Am 1994;27:223–62. Ahn MS MN, Maas CS. Soft tissue augmentation. Facial Plast Surg Clin North Am 1999;7:35–41. Truswell WH. Dual-porosity expanded polytetrafluoroethylene soft tissue implant: a new implant for facial soft tissue augmentation. Arch Facial Plast Surg 2002;4:92–7.
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17. Adjunctive techniques II: clinical aspects of the combined use of botulinum toxins and fillers for non-surgical facial rejuvenation Stephen Bosniak, Marian Cantisano-Zilkha, Baljeet K Purewal, and Ioannis P Glavas
INTRODUCTION Constantly evolving technology has given cosmetic physicians and surgeons an ever-increasing armamentarium with which to deliver more effective treatments with minimal or no downtime. Combining a variety of therapeutic options can yield an enhanced effect that is more than the sum of its individual parts. Understanding the balance of facial musculature is essential for facial rejuvenation and facial reshaping utilizing botulinum toxin. The concept of facial muscle relaxation and balance is the foundation on which further rejuvenation with fillers can be built. The expanding menu of fillers gives us an enlarging palate of materials for facial filling, volumizing, and rhytid ablation (Fig. 17.1).
BOTULINUM TOXIN TYPE A DILUTION AND INJECTION TECHNIQUE Botulinum toxin type A (Botox and Botox Cosmetic) binds to the nerve endplate and blocks the release of acetylcholine, decreasing the strength of muscle contraction and reducing dynamic rhytidosis.1,2 This bond is permanent, and acetylcholine release begins again when the nerve sprouts a new endplate. One hundred units of Botox is packaged as a powder.This purified protein is
reconstituted in sterile saline, typically in 1, 2, or 4 ml to give the desired dose in 0.1ml aliquots.3 Different vials can be mixed for different strengths for different muscles (Figure 17.1). During the actual mixing of Botox, the vacuum seal must be broken with two needle punctures before instilling the saline to avoid an overexuberant mixing and frothing of the Botox, which can affect potency.The saline should be added slowly, angled against the side of the vial, avoiding frothing of the mixture. Although it is claimed that the use of preserved saline diminishes discomfort during injection (there is less of a burning sensation) and that it lengthens the time that reconstituted refrigerated Botox can last, we continue to use non-preserved saline for reconstituting Botox.We feel that it may retain its potency for a longer period of time.4 When storing reconstituted Botox, it should be refrigerated and not frozen. Adequate dosage for each muscle group is key.While an insufficient dose will yield an insufficient result, overtreating is also not a desired cosmetic result. Because the patient may not begin to notice the clinical effect for at least 3–5 days, and the full effect may not be evident for 7–10 days, we request a revisit for a dose adjustment in 1–2 weeks following the initial treatment session. After cleansing the injection sites with alcohol (there is some discussion about alcohol reducing the effect of botulinum toxin), we prefer to apply a topical lidocaine/tetracaine anesthetic cream, Photocaine (Universal Pharmacy, Salt Lake City, Utah), for 15–20 minutes. Further vasoconstriction is encouraged by
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a
b
Fig. 17.1 Facial asymmetries can be corrected with an intimate knowledge of the balance of facial musculature. Botulinum toxin can be used to weaken the overactive muscles, allowing opposing musculature to function normally, thereby creating a balance. (a) This patient had a hemifacial spasm following Bell’s palsy. (b) Facial symmetry was achieved by understanding the balance of the facial musculature and injecting the appropriate muscles with botulinum toxin. application of iced compresses; we have not noted any rebound effect after using this technique. In addition, to avoid bruising, patients are given Arnica Montana C5 pellets (Boison, Newton Square, PA) sublingually immediately preceding their injections and asked to continue taking them four times a day for 2–3 days. Injections are given subcutaneously and tangentially when possible. Because of the diffusion characteristics of botulinum toxin, it is not necessary to inject into the muscle plane. Avoiding deep injections will avoid hematoma formation with accompanying bruising (and patient perception that this is an invasive procedure). Following the injections, direct pressure is applied until there is no sign of oozing from the injection sites. We follow a general guideline of doses that we have found to work safely and effectively for the different anatomical areas of the face (Table 17.1).While dosing may vary slightly on an individual basis, this may be adjusted on subsequent follow-up visits.
Dysport is also a type A botulinum toxin, but has a more marked spreading effect; these diffusion characteristics may affect the clinical outcome and the duration of the effect, but the exact differences between Botox™ and Dysport has yet to be determined. It is currently being used in Europe and South America, and will be available in the USA probably in 2007 or 2008, under the name Reloxan. Approximately 3–5 units of Dysport (Reloxan) are equivalent to one unit of Botox. Like Botox, Dysport (Reloxan) has to be reconstituted with sterile saline.
OVERVIEW OF FILLERS AND INJECTION TECHNIQUE Due to the wide variety of injectable fillers available today, when choosing the appropriate product, it is important to match the product with the tissue.
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Clinical aspects of the combined use of botulinum toxins and fillers Table 17.1 Botox dosages Anatomical region Forehead Glabellar Crow’s feet and lateral brow depressors Lower eyelids (pretarsal) Upper lip Depressor angulii oris Platysmal bands
Dose (units) 10–15 20–60 15–20 2 1–2 2–5 20–50
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seen which product will yield the best possible clinical outcome. More than likely, the multitude of available products will eventually have their own specific goals for indication of use. Gel particle size is, however, relevant for comparison of Q-Med Sweden hyaluronic acid products (Table 17.3). The more viscous products have a larger particle size. This is important in considering the area and depth of implantation of the product. Juvederm is composed of blended random-sized particles, which may conceivably affect its flow characteristics.
INJECTION TECHNIQUES The evolution of safer, longer-lasting and more convenient, readily available materials for adding volume to facial structures and filling in static facial lines and furrows has added a new dimension to noninvasive facial rejuvenation. An ideal filler should meet a number of requirements. It has to be long-lasting, nontoxic, fully biocompatible, nonimmunogenic, nonmigratory, and inexpensive, with the ability to be stored, shaped, removed, and sterilized easily.5 While we have not yet achieved filler nirvana, the non-animal-derived stabilized hyaluronic acid products are the current state of the art, fulfilling many of our criteria.6 Fillers can be classified as nonpermanent or permanent; biodegradable versus nonbiodegradable; animalbased versus non-animal-based; and autologous versus nonautologous. While autologous fat is historically the oldest available filler, bovine collagen in the form of Zyderm I, Zyderm II, and Zyplast was the most frequently used substance until hyaluronic acid products were approved by the US Food and Drug Administration (FDA) in 2003.7 The hyaluronic acids can be derived from avian or bacterial sources; each product has its own specific characteristics8 (Table 17.2). Hyaluronic acid must be crosslinked through chemical alteration to stabilize the molecule. While more crosslinking may increase the longevity of the clinical effect, it is difficult to compare the clinical efficacy of different products based on the amount of crosslinking alone. Excessive crosslinking may impair the ability of the hyaluronic acid molecules to retain and attract water molecules and secondarily limit the ultimate clinical effect. So it remains to be
There are four different implantation techniques that are generally utilized: linear threading, serial puncture, fanning, and cross-hatching. It is important to remember that for each technique, the more slowly the infection is performed, the less discomfort is caused to the patient and bruising is reduced. Serial puncture is technically the easiest method, since the needle tip does not move during injection. The needle enters the skin to the desired depth, a small aliquot of filler is deposited, and the needle is withdrawn.9 The linear threading technique consists of holding the needle parallel to the length of the wrinkle or fold to be treated, piercing the skin, and advancing the needle and injecting in either a retrograde or anterograde fashion, making sure to stop injecting prior to needle withdrawal.9 The fanning and cross-hatching techniques are variations of the linear threading technique. These techniques can be implemented in areas where a larger volume of filler is needed or a multicontoured area is being filled. Even though theoretically the fanning technique should yield less bruising, we have found that this is not necessarily true. In our experience, applying the fanning technique via multiple puncture sites has produced less bruising. Regardless of the product to be used, each patient is prepped with alcohol and treated while sitting in the upright position. The patient is given three sublingual Arnica C5 pellets and asked to continue taking them four times daily for 3 days. We use topical anesthetic (Photocaine) on every patient and rarely use regional blocks.
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Table 17.2 Hyaluronic acid products Product
Sourcea
Approved indication in USA
FDA approval
Duration
Restylane
Bacterial fermentation NASHA technology
For the correction of moderate to severe facial wrinkles and folds
December 2003
6–8 months
30-gauge
Perlane
Bacterial fermentation NASHA technology
Not yet FDA-approved. Designed for shaping facial contours (e.g., in the cheeks and chin), correcting deep folds, and for lip augmentation
Not yet in the USA
9–12 months
27-gauge
Fine Lines (Touch)
Bacterial fermentation NASHA technology
Not yet FDA-approved. Designed for correcting thin superficial lines, forehead lines, and perioral rhytids
Not yet in the USA
4–6 months
32-gauge
Restylane SubQ
Bacterial fermentation NASHA technology
Not yet FDA-approved. Designed for deep subcutaneous or supraperiostal injections
Not yet in the USA
9–18 months
18-gauge cannula
Captique
Produced by bacterial fermentation
For the correction of moderate to severe facial wrinkles and folds
November 2004
4–6 months
Juvederm Ultra plus
Produced by bacterial fermentation
For the correction of moderate to severe facial wrinkles and folds
June 2006
9–12 months
27-gauge
Juvederm Ultra
Produced by bacterial fermentation
For the correction of moderate to severe facial wrinkles and folds
June 2006
6–8 months
30-gauge
Cosmoderm
Bioengineered human collagen
For superficial lines: perioral, periocular, glabellar
March 2003
3–5 months
30-gauge
Cosmoplast
Bioengineered human collagen crosslinked with glutaraldehyde
For improvement of deep folds and wrinkles: nasolabial, vermilion border, marionette lines
March 2003
3–5 months
30-gauge
Zyderm
Highly purified reconstituted bovine collagen
For fine lines: perioral, periocular, glabellar
1981
3–5 months
30-gauge
Zyplast
Highly purified reconstituted bovine collagen crosslinked with glutaraldehyde
For improvement of deep folds and wrinkles: nasolabial, vermilion border, marionette lines
1985
3–5 months
30-gauge
Sculptra
Poly-L-lactic acid
For the restoration and/or the correction of facial fat loss (lipoatrophy) in patients with HIV
August 2004
1–2 years
26-gauge
Radiesse
Calcium hydroxyapatite microspheres suspended in an aqueous gel
Long-lasting correction of moderate to severe facial wrinkles and folds such as nasolabial folds. Radiesse also received a second FDA approval for the long-lasting correction of lipoatrophy in patients with HIV
December 2006
1–2 years
27-gauge
a
NASHA, nonanimal stabilized hyaluronic acid.
Injection needle
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Clinical aspects of the combined use of botulinum toxins and fillers Table 17.3 Particle sizes of Q-Med Sweden hyaluronic acid products Product
Gel particle size (µm)
Restylane Perlane Fine Lines Restylane SubQ Restylane Touch
250 1000 150 Approx. 2000 100
Certain products require preparation beforehand. For example, Sculptra (poly-L-lactic acid) must be reconstituted the day before it is used and shaken very well before use. Each bottle contains 0.15 g of powder that has to be mixed thoroughly to create a suspension. Seven milliliters of diluent (5 ml sterile water and 2 ml lidocaine) provide a sufficiently liquid suspension for easy injection and decrease the incidence of granuloma formation.The sterile water should be added first, and one should wait at least 2 hours before shaking the bottle. Preferably, the suspension should sit overnight and then, prior to injection, 1–2 ml of lidocaine may be added. It is important to shake the suspension well before use to decrease the incidence of granuloma formation and to avoid frequent clogging of the needle. If the suspension is not used immediately after being shaken, it may clog the needle and require frequent needle changing. Sculptra, injected in a retrograde fashion, is useful for filling in broad areas of facial depression. Because the amount of correction improves with time, inciting a mild subcutaneous inflammatory response and secondary collagen production, a gradual filling in the contour defect is recommended, avoiding overcorrection.At each injection session, the appearance of the final result is approximated. The patient is informed of a period of disappointment over the following several weeks when the diluent is absorbed and before secondary filling is observed. Repeat injections are typically given at 6-week intervals. Injecting 0.1 ml aliquots deeply and then massaging the tissue well is essential to avoid papule formation and to achieve an excellent result. Because Sculptra is a suspension, the ‘feel’ while injecting it is different from the hyaluronic acid gels and the ‘paste’ of hydroxyapatite.
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Radiesse is composed of calcium hydroxyapatite microspheres in a water-based gel carrier, and has been used for many years in the treatment of vocal fold insufficiency and as a radiological tissue marker.6 As a soft tissue filler, it acts as a scaffold for stimulating collagen production. It should be injected in a retrograde fashion in the subdermal plane. Placement of this filler too superficially may result in a whitish skin discoloration and palpable irregularities. After placement, it is helpful to massage the area to position the filler in the desired location and to mold the material to the desired shape into the tissue. We most often inject hyaluronic acids in an anterograde fashion, except for the glabellar region, where vascular occlusion can be a devasting, vision-compromising complication (Fig. 17.2). If the material is injected too superficially, or the overlying skin is translucent, the Tyndall effect or a grayish discoloration in the region will be evident. Overcorrection is not recommended. After injection, gentle massage may be performed to achieve a smooth and continuous contour with the surrounding tissue. Repeat injection may be performed at 1-week intervals until the final correction is achieved.
THE FOREHEAD Treating the brow depressors with botulinum toxin to modify brow level and contour has become standard practice. Understanding this concept has encouraged injectors to also modify their treatment of forehead rhytids. Botulinum toxin injections across the forehead can effectively obliterate forehead rhytidosis, but lower the brow level and alter the eyebrow arch. This unwanted brow lowering and flattening is particularly evident in patients who utilize their frontalis muscle to compensate for their blepharoptosis or heavy, redundant upper eyelid folds. To allow for full frontalis muscle action, and brow elevation, forehead botulinum toxin injections should be limited to the central forehead and the upper third of the forehead. We prefer to use 2.5 units of Botox per injection site in this region. Residual lateral brow peaking, should it occur, can be treated (dose adjustment) after 1–2 weeks at a follow-up visit. The injections should be placed in the area where the
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a
b
Fig. 17.2 (a) It is important to realize that furrows present at rest will need fillers in addition to muscle relaxation with botulinum toxin. (b) The glabella furrows were treated with 40 units of botulinum toxin and 0.5 ml Perlane.
rhytid is formed by the frontalis, but never closer than 1 cm to the brow. Residual lateral dynamic rhytids are best treated with volumetric radiofrequency (RF) skin tightening (Thermage) and hyaluronic acid fillers. The choice of filler is dictated by the depth of the static component of the rhytid. Most often we prefer the mildly viscous hyaluronic acids (Restylane or Juvederm Ultra). But, for superficial rhytids, we prefer superficial filling with minimally crosslinked hyaluronic acids (Restylane Fine Lines, Restylane Touch, or Captique) or localized intradermal plumping with non-crosslinked hyaluronic acids (Restylane Vital or SurgiLift).
THE PERIORBITAL AREA The periorbital area lends itself very well to noninvasive therapeutic modalities that can improve skin texture and redundancy and camouflage irregular contours. Botulinum toxin is the first step in periorbital rejuvenation, reestablishing an appropriate eyebrow– eyelid relationship, correcting brow ptosis (20–40 units to depressor supercilli muscles at 5 units of Botox per injection site), and enhancing effective collagen remodeling with orbicularis muscle relaxation (15–20 units to lateral canthal and lower lid pretarsal orbicularis muscles at 2.5 units per injection site), or even compensating for mild blepharoptosis (2.5 units to lateral upper lid pretarsal orbicularis muscle).
Eyelid skin quality, texture, pigmentation, redundancy, and subcutaneous vascular pooling can then be addressed with biweekly intradermal and subcutaneous carbon dioxide eyelid insufflation (CO2 Cellulair) augmented with volumetric RF eyelid skin tightening (Thermage eye tip) (Fig. 17.3). Further enhancement of eyelid texture and pigmentation can be achieved with one to three treatments with a pixelated erbium laser (Alma Laser Pixel). Pretreatment with botulinum toxin is essential for maximal collagen remodeling. Residual contour irregularities (tear trough, infraorbital, or lateral orbital sulcus deformities) can be camouflaged with mildly crosslinked hyaluronic acid (Restylane or Juvederm) (Fig. 17.4). We prefer the limited puncture technique, implanting the injected hyaluronic acid in the suborbicularis supraperiosteal plane and massaging it into position10–12 (Fig. 17.5).
THE MIDFACE Approaching the midface with a combination of tightening and filling can effectively yield a very natural result. Pretreating the entire midface with volumetric RF dermal heating (Thermage) and reinforcing with submalar and preauricular vectors will elevate the malar eminences. Further malar augmentation can be accomplished with longer-lasting more-viscous
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Fig. 17.3 CO2 Cellulair insufflation presumably enhances subcutaneous and cutaneous perfusion. (a,b) These patients have mild pigment irregularities and shadows secondary to vascular pooling.They are good candidates for CO2 Cellulair™ treatment. (c, d) CO2 Cellulair insufflation has improved eyelid skin quality, texture, pigmentation, redundancy, and subcutaneous vascular pooling after four weekly treatments.
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Fig. 17.4 Periorbital contour deformities can be camouflaged with hyaluronic acids. (a) This patient assumed that she had lower lid cutaneous pigmentary abnormalities. In fact, the dark circles that she saw on her lower lids were shadows secondary to prolapsing orbital fat. She was not emotionally prepared for a lower lid blepharoplasty, but did consent to correction with Restylane. (b) This patient was treated with suborbicularis, supraperiosteal placement of Restylane to correct her tear trough deformities.
hyaluronic acid (Perlane, Juvederm Ultra plus, or Restylane SubQ) or poly-L-lactic acid (Sculptra) or Hydroxyapatite (Radiesse). Lipoatrophy of the midface with sunken cheeks and redundant nasolabial folds needs larger volumes of
deeper, longer-lasting filling material. In our experience, Sculptra and autogenous fat work best for this purpose. Supporting the malar and cheek areas, we fill out the face, support the midface, and redrape the nasolabial folds (Fig. 17.6).
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Fig. 17.5 (a–c) Two aliquots of 0.2 ml are placed above the periosteum along the medial aspect of the inferior orbital rim and massaged into place. (Reproduced from Bosniak S et al. The ‘Restylane push’ technique for the treatment of the nasojugal groove. Submitted for publication.10
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Fig. 17.6 (a) Because of this patient’s relatively deep nasolabial folds, thick skin, and mild midfacial ptosis, we injected Radiesse trancutaneously in the canine fossa to fill her nasolabial folds and to give her some midface-lifting effect. (b) She has achieved a reasonable midface lifting and filling of her nasolabial folds; in addition, her multicontoured melomental folds were filled with Sculptra. Midface lifting can also be enhanced with implantation of a more-viscous, longer-lasting material injected into the canine fossa.We have found Radiesse to be effective for this purpose, supporting the midface and softening
the nasolabial grooves. Using 0.5–1.0 ml of Radiesse can achieve significant midface lifting.The effect can be furthered with additional Radiesse implanted subcutaneously under the nasolabial grooves13 (Figs. 17.7 and 17.8).
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0.5 ml 27 gauge Radiesse
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Fig. 17.7 (a) Using a 27-gauge needle, 0.5 ml of Radiesse is injected into the canine fossa on each side just above the periosteum anterior to the maxilla. (b) A sectional view shows digital massage over the bolus. (c) Filling of nasolabial folds.
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Fig. 17.8 (a) Like the patient shown in Fig. 17.7, this patient had relatively deep nasolabial folds, thick skin, and mild midfacial ptosis, and again we injected Radiesse trancutaneously in the canine fossa to fill her nasolabial folds and to give her some midface-lifting effect. (b) She has achieved a significant mid-face lifting and filling of her nasolabial folds.
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Fig. 17.9 (a, b) Restylane and Perlane were used to correct these nasal deformities while the patient was contemplating corrective surgery.
In addition, the hyaluronic acids can be very useful in effectively recontouring nasal deformities (Figure 17.9).
THE PERIORAL AREA The most prominent area of the lower third of the face is the mouth. Full lips transmit youth and sensuality. Perioral rhytids and thin lips give the impression of age, detachment, and coldness. Rejuvenating the lips is not simply about size or the lips themselves. It necessitates a balance between the lips, mouth, and the entire lower third of the face. Thin lips create too large a space between the nose and the upper lip and the appearance of an elongated, unattractive upper lip. Lips can be augmented and recontoured effectively with a combination of hyaluronic acid products of different viscosities.The upper lip can be accentuated and vertical rhytids softened with less-viscous materials, whereas the body of the lip is more efficiently filled with more-viscous products. For the border of the lip, we prefer to use Restylane, Juvederm Ultra, Captique, or Cosmoplast. Cosmoplast may be useful for the border, since it is mixed with lidocaine, facilitating painless filling of the body of the lip. For the body of the lip, if an increased volume is necessary for augmentation, Perlane and Juvederm
Ultra plus work well. Restylane and Juvederm Ultra are also effective for this area (Figs 17.10 and 17.11). Melomental folds, also known as marionette lines, and the downturning corners of the mouth can be ameliorated with the combination of filling agents and neuromodulation of the depressor oris angulii (DAO). The DAO arises fom the border of the mandible and inserts on the lateral corners of the mouth. This muscle contributes to the depth of the melomental fold and to the downward displacement of the lateral corners of the mouth. Relaxing the DAO allows the zygomaticus major and minor to elevate the corner of the mouth without opposition, raising the lateral corners and facilitating filling of the oral commissures.4 Restylane or Perlane may then be injected into the corners of the mouth to create a buttress. Sculptra can then be injected, utilizing the fanning technique to fill the multicontoured areas of the oral commissures and melomental depressions. Vertical upper lip rhytids may be treated with a combination of fillers (Restylane, Restylane Fine Lines, and Captique) using delicate cross-hatching and Botox at a maximum of 4 units spaced equidistant from each other and at least 1 cm from the midline. It is important to avoid asymmetry and incompetence of the orbicularis oris. Patients should be warned about difficulty whistling, smoking, and sipping through a straw. Pixel-fractionated erbium : yttrium aluminum
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Fig. 17.10 (a) Although the lip volume was adequate, the border was ill-defined. (b) Restylane was used to accentuate the border of the upper lip.
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Fig. 17.11 (a) Lower facial laxity and a disappearing upper lip were this patient’s main complaints. (b) This patient was treated with a combination of Thermage to the pre-jowl sulcus and lower face, botulinum toxin to the depressor oris anguli, Perlane to the body of the lip and corners of the mouth, and micropigmentation to the lips.These treatments gave her a better balance of the lower one-third of her face and decreased the distance between the upper lip border and her nose.
garnet (Er:YAG) laser resurfacing can further enhance the final result.
THE NECK Neck rejuvenation has a balancing and complementary role in the whole approach to a youthful appearance of an individual. The elements that influence the
appearance of the neck are the quality and texture of the skin; the firmness of the subcutaneous fat; the strength, thickness, and form of the platysma muscle; subplatysmal fat; and the anatomy and prominence of submaxillary glands, thyroid cartilage, and the surrounding bones.14 Relaxing the muscles of the neck using chemodenervation agents can improve the appearance of the neck and at the same time prepare the overlying tissues
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Fig. 17.12 (a) Lower facial laxity is demonstrated here, accentuating the melomental folds, and this creates a multicontoured area that requires more than fillers alone for an optimal result. (b) This patient had botulinum toxin to the platysma and depressor oris anguli to raise the corners of her mouth;Thermage was used to tighten the skin over the melomental folds, and Sculptra to fill the melomental sulcus.
to be maximally rejuvenated with complementary treatments. Prominent platysmal bands and horizontal neck rhytid formation are due to hyperkinetic acitivity and loss of tone of the platysmal muscle.15 Botox can be injected into the platysmal bands and necklace lines. Results are better for platysmal bands than for necklace lines because the latter are often not directly related to platysma muscle activity. Necklace lines are notoriously difficult to treat, but we have found that a combination of CO2 Cellulair (CO2 gas insufflation) and intradermal injection of non-crosslinked hyaluronic acid (Restylane Vital or Surgilift – neither of which is available in the USA) works well following pretreatment of the platysma with botulinum toxin. We routinely inject botulinum toxin into the platysmal bands using 2.5 units per injection site along the length of the band before treating the skin of the neck and submental area with volumetric RF deep dermal heating (Thermage). Stacked pulses of Thermage in the submental area will enhance the lipolytic effect (Fig. 17.12).When treating submental fat, other complementary noninvasive techniques include injection of phosphatidylcholine and deoxycholate, and intradermal and subdermal CO2 Cellulair for the further improvement of submental contour and reduction of the submental fat pocket.
REFERENCES 1. Holds JS, Alderson, Fogg SG, et al. Terminal nerve and motor end plate changes in human orbicularis muscle following botulinum A exotoxin injection. Invest Ophthalmol Vis Sci 1990;31:178–81. 2. Coffield JA, Considine RV, Simpson LL. The site and mechanism of action of botulinum neurotoxin. In: Jankoric J, Hallet M, eds.Therapy with Botulinum Toxin, 4th edn. New York: Marcel Dekker, 1994:3–13. 3. Carruthers J, Fagien S, Matarasso SL. Botox Consensus Group: consensus recommendations on the use of botulinum toxin type A in facial aesthetics. Plast Reconstr Surg 2004;114:1S–22S. 4. Bosniak S. Neuromodulation and management of facial rhytidosis. In: Bosniak S, Cantisano-Zilkha M, eds. Minimally Invasive Techniques of Oculofacial Rejuvenation. New York:Thieme, 2005:32–42. 5. Ellis DA, Makdessian AS, Brown DJ. Survey of future injectables. Facial Plast Surg Clin North Am 2001;9:405–11. 6. Glavas IP. Filling agents. Ophthalmol Clin North Am 2005;18:249–57. 7. Gladstone HB,Wu P, Carruthers J. Background information on the use of esthetic fillers. In: Carruthers J, Carruthers A, eds. Soft Tissue Augmentation. Philadelphia: Elsevier,2005:1–9. 8. Rzany B, Zielke H. Overview of injectable fillers. In: de Maio M, Rzany B, eds. Injectable Fillers in Aesthetic Medicine. Berlin: Springer-Verlag, 2006:1–9.
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Clinical aspects of the combined use of botulinum toxins and fillers 9. Bowman PH, Narins RS. Hylans and soft tissue augmentation. In: Carruthers J, Carruthers A, eds. Soft Tissue Augmentation. Philadelphia: Elsevier, 2005:33–53. 10. Bosniak S, Sadick NS, Cantisano-Zilkha M, et al. The ‘Restylane Push’ technique for the treatment of the nasojugal groove. Submitted for publication. 11. Bosniak S, Sadick NS, Cantisano-Zilkha M, et al. Definition of the tear trough and the tear trough rating scale (TTRS). Arch Facial Plast Surg (in press). 12. Bosniak S, Cantisano-Zilkha M, Purewal BK, Rubin M, Remington BK. Defining the tear trough. Ophthalmol Plast Reconstr Surg (in press).
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13. Zdinak L, Bosniak S, Sadick NS, et al. Midface lift with Radiance FN: a minimal puncture technique. Submitted for publication. 14. Glavas IP, Bosniak S. Noninvasive neck rejuvenation. In: Bosniak S, Cantisano-Zilkha M, eds. Minimally Invasive Techniques of Oculofacial Rejuvenation. New York: Thieme, 2005:65–72. 15. Matarasso A, Matarasso SL. Botulinum A exotoxin for the management of platysma bands. Plast Reconstr Surg 2003;112(5 Suppl):138S–40S.
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18. Adjunctive techniques III: complementary fat grafting Robert A Glasgold, Mark J Glasgold, and Samuel M Lam
INTRODUCTION Volume loss has become increasingly recognized as an important, if not primary, process that occurs during the aging process. Accordingly, soft-tissue fillers and facial fat grafting have assumed a greater role in a global strategy for facial rejuvenation. In the past, traditional surgical modalities were focused heavily on lifting redundant, prolapsed, and descended tissues. The new paradigm today is to view the face like a grape that, over time, deflates and shrivels into a raisin. Volume replacement will restore the raisin to a grape, while cutting away the excess skin will turn it into a tiny pea.The analogy to the aging face is overly simplistic, but contemporary facial rejuvenation must include some degree of volume restoration if it is to appear natural. In our opinion, a complementary approach that incorporates facial fat grafting for volume restoration along with facial lifting procedures and dermatological therapies will often provide the greatest improvement for a particular individual. The new paradigm of the aging face that views the primary mechanism of aging as volume contraction focuses on issues that are remarkably different from those that are important in lifting procedures. The volume and shape of the face takes centerstage. The youthful face is viewed as triangular or heart-shaped, but over time becomes more rectangular in appearance due to loss of midface volume and accumulation of fullness in the jowls.Volume restoration is aimed at returning the face to a more heart-shaped configuration by targeting the midface/cheek region and the chin/prejowl area in order to simulate the highlights of youth. Autologous fat transfer is often combined with a traditional cervicofacial rhytidectomy along
with microliposuction of the jowl to narrow and taper the lower face (Fig. 18.1). Another important objective of facial fat grafting is to restore the youthful frame of the eye. In the same manner as a picture, the beauty of the eye is accentuated by a flattering frame and diminished when not adequately framed. Periorbital fullness is the hallmark of a youthful framed eye. Traditional blepharoplasty is contingent upon removing the frame of the eye rather than restoring it primarily through aggressive removal of orbital fat. The result is a skeletonized and aged appearance. Complementary fat grafting advocates conservative removal of redundant upper eyelid skin and reduction of lower eyelid pseudoherniated fat, combined with periorbital fat, grafting to achieve a natural and youthful result (Fig. 18.2). We perform far fewer browlifts today, as this operation accentuates the unattractive long rectangular shape of the aging face and further skeletonizes the orbital rim. The new aesthetic favors the naturally appearing lower and fuller brow compared with a more superiorly situated and sculpted ‘done’ brow. A useful guideline to determine what is suitable for a particular patient is to review his or her old photographs to evaluate precisely how full or how high the eyelids and brow were at a young age. In this way, we can strive to help an individual look more like himself or herself at a younger age rather than an arbitrary and often inaccurate definition of what would look aesthetically pleasing. Unfortunately, too often, men and women look different after traditional surgery and less like they did when they were younger. Facial fat grafting, at times combined with traditional surgery, offers the ability to more closely approximate an individual’s younger self.
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Fig. 18.1 Preoperative (a) and postoperative (b) photographs of a patient who underwent a deep plane facelift, lower lid transconjunctival blepharoplasty, and upper lid blepharoplasty, combined with fat transfer to superior and inferior orbital rim, midface, and prejowl sulcus. a
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Fig. 18.2 (a) This patient has a prominent-appearing eye following an aggressive isolated lower lid transconjunctival blepharoplasty. (b) An attractively framed eye following periobital and midface fat transfer. Reprinted with permission from Lam SM, Glasgold MJ, Glasgold RA.:Complementary Fat Grafting. Philadelphia: LippincottWilliams & Wilkins; 2007.
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Fig. 18.3 A youthful face with an attractive periorbital frame.This young woman (who has not had surgery) demonstrates a full upper eyelid with only several millimeters of lid skin visible and a lower eyelid that transitions seamlessly into a full cheek. Reprinted with permission from Lam SM, Glasgold MJ, Glasgold RA.: Complementary Fat Grafting. Philadelphia: LippincottWilliams & Wilkins; 2007.
PREOPERATIVE CONSIDERATIONS Anatomy Periorbital volume restoration is of primary importance in creating an appropriately full frame around the eye. The most important component of the ‘frame’ is the inferior orbital rim. Reviewing photographs of models allows us to understand this aesthetic ideal.Variations in the upper periorbital frame exist, with the most common appearance being a full brow with a few millimeters of the upper lid skin visible (Fig. 18.3). Some very attractive individuals have relatively sculpted and hollowed brow/upper eyelid complexes, but uniformly every young beautiful face has a full lower eyelid that blends seamlessly with a full cheek. Again, review of an individual’s old photographs will help determine what is a natural appearance for the specific patient. As already mentioned, significant pseudoherniation of lower orbital fat will benefit from selective reduction via a transconjunctival blepharoplasty combined with concurrent filling of the inferior orbital rim by autologous fat transfer. Similarly, a truly deflated and hanging upper eyelid would be best approached with conservative removal of redundant skin, with some degree of fat transfer into the brow (Fig. 18.4).
The cheek is an extension of the lower frame of the eye and is a vital component of a youthul heartshaped face. The cheek can be divided into anterior and lateral components. With advancing age, the anterior cheek, which develops the most significant volume loss along the malar septum, is a primary target for fat transfer. The lateral cheek, when restored, should reveal the lustrous highlight that is associated with a convex youthful shape (Fig. 18.5). Often, the buccal region must be volume-enhanced, as it becomes relatively hollow after augmentation of the malar region. However, care must be taken to avoid overfilling this area if the patient desires the more sculpted look that manifests in one’s 30s as opposed to the fuller oval shape of someone in their early 20s. Placement of fat into the precanine fossa and nasolabial fold is not so much intended to efface the linear depression but rather to provide an improved contour from the newly augmented cheek to the upper lip.We believe that any one of a number of available dermal fillers is more useful for elimination of the nasolabial and labiomandibular folds. Similarly, lip augmentation with fat grafting only yields subtle results after considerable and protracted postoperative edema.
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Fig. 18.4 Preoperative (a) and postoperative (b) photographs of a patient who underwent upper lid skin-only blepharoplasty, lower lid transconjunctival blepharoplasty, and periorbital and midface fat transfer.
Facial fat grafting of the lower face is centered on finishing the lower point of the triangle of a youthful countenance.Therefore, the focus of fat grafting along the lower face is concentrated in the prejowl sulcus, anterior chin, labiomental sulcus, and labiomandibular depression. Augmentation of the lateral mandible cannot be undertaken concurrently with a facelift due to undermining of the skin in this portion of the face. Patients with mild jowling or prejowl volume loss can achieve a very good restoration of the jawline with fat grafting alone. In contrast, we have found that it is difficult to truly attain a straightened jawline with facial fat grafting alone in patients who have a heavy jowl and that, for optimal patient and surgeon satisfaction, a facelift should be incorporated for these patients. However, augmentation of the prejowl with fat grafting can enhance the result of any facelift, and is incorporated into most of our rhytidectomies (Fig. 18.6).
Consultation As with any cosmetic consultation, the ultimate goal is to establish aesthetic objectives for surgical and/or nonsurgical intervention mutually agreed between the surgeon and the prospective patient. Besides the standard psychological, emotional, and aesthetic considerations that are part of every initial patient encounter, the surgeon must establish aesthetic goals, realistic expectations, and an understanding of the potential recovery period that relate specifically to fat grafting. These unique considerations will be elaborated in this section, and can be incorporated into the framework of a standard consultation. Often during the consultation, the patient must be refocused on what truly gives them an aging appearance. Women, in particular, focus on fine lines that typically achieve disproportionate importance when
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Fig. 18.6 (a) Patient following a facelift, with the appearance of persistent jowling. (b) Volume augmentation of the prejowl sulcus creates a straight jawline. Reprinted with permission from Lam SM, Glasgold MJ, Glasgold RA.:Complementary Fat Grafting. Philadelphia: LippincottWilliams & Wilkins; 2007.
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viewed with a magnifying mirror and bright illumination during makeup application. The consultation aims to recalibrate their thinking to evaluate their face the way other people see them from conversational distances. Additionally, we point out that they primarily see themselves only in frontal view in a mirror, whereas in the real world they are usually seen at an oblique angle.To help the patient appreciate this, we will often take digital images of the patient and review these with them. Volume and shape are emphasized over fine wrinkles and minor cutaneous blemishes, which, to reiterate, are not truly ameliorated with facial fat grafting. Digital imaging of possible results plays a very limited role in the discussion of facial fat grafting. It is almost impossible to demonstrate the benefits of fat grafting with digital morphing analysis, since the technology is two-dimensional and the operative intervention is three-dimensional. Instead, use of a catalog of before-and-after photographs of patients whom the surgeon has taken care of is perhaps the most effective way of demonstrating to the patient the benefits of fat grafting. Showing patients how they may look at 1 week, 2 weeks, 1 month, etc. after surgery provides the most useful information about potential recovery time. Most often, when an individual views other patients during this early recovery period, he or she may not perceive that they look very swollen, just better. However, it is important to emphasize that most of these patients were uncomfortable with the way they looked during the first 2–3 weeks following surgery. These psychological details are helpful to discuss with each patient in the preoperative setting. Use of old photographs can also be very enlightening both for the patient and for the surgeon.The patient should readily grasp the volume changes associated with aging, and the surgeon can better discuss with the patient what aesthetic changes will be most beneficial toward reestablishing a youthful appearance.As already stated, many women do not like the fullness, often referred to as ‘baby fat’, that is prevalent in their teens and early 20s, but prefer the relative sculpted (but not yet hollow) appearance of themselves in their late 20s to early 30s.
OPERATIVE TECHNIQUE Donor harvesting For very thin individuals, it may be advisable to evaluate potential donor sites during a preoperative visit. Generally speaking, most patients will be able to inform the surgeon where they have abundant fat. For instance, men are predominately truncal-dominant, whereas women can either be truncal (abdomen/ waist) or extremity (inner or outer thigh) dominant. For very thin individuals or those who have undergone extensive prior body liposuctioning, the lower back and triceps may be ideal reserves that remain for harvesting. Most commonly, the lower abdomen and inner thigh serve as excellent donor sites for fat harvesting if intraoperative patient repositioning is problematic. Before lower abdomen harvesting is undertaken, it is imperative to inquire what abdominal procedures the patient has had in the past and to evaluate the distribution of abdominal scars. In order to ensure that the patient does not have an occult ventral or umbilical hernia, the surgeon should ask the patient to Valsalva in a supine position with his or her head elevated for optimal evaluation. Obviously, a hernia in the field of harvesting would preclude harvesting in that area. Many aesthetic surgeons who are uncomfortable with body harvesting express trepidation about unintentional violation of the visceral cavity during harvesting. This outcome is very unlikely, especially under conscious sedation, given the thickness of the muscular fascia as well as the exquisite discomfort elicited when the fascia is even abraded with the harvesting cannula. For the inner thigh, the surgeon must ensure that the cannula passes through a superficial fascial layer before fat harvesting can commence. Superficial passage of the cannula is evident by the visibility of the cannula through the skin, which should be immediately corrected to avoid a potential contour deformity in the donor area. Although fat grafting can be undertaken with any level of anesthesia, we have found that intravenous sedation provides excellent pain control and patient compliance. After the patient is adequately sedated,
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Complementary fat grafting the donor area is infiltrated with 0.25% lidocaine with 1:400 000 epinephrine using a 20 cm3 syringe outfitted with a 22-gauge spinal needle. (The mixture is attained by combining 5 cm3 of 1% lidocaine and 1:100 000 epinephrine with 15 cm3 of normal saline.) If the patient is under oral sedation, then a higher percentage of lidocaine (0.5% lidocaine with 1:200 000 epinephrine) should be used to improve patient comfort. (The mixture is attained by combining 10 cm3 of 1% lidocaine and 1:100 000 epinephrine with 10 cm3 of normal saline.) When allocating the 20 cm3 of local anesthesia, the surgeon should aim to place 10 cm3 in the deep aspect of the fat pad (immediately above the muscle/fascia) and 10 cm3 into the immediate subcutaneous plane, leaving the bulk of the fat pad untouched with anesthetic. After the patient has been sterilely prepped and draped, a 16-gauge Nokor needle (or No.11 Bard–Parker blade) is used to make a stab incision for entry of the harvesting cannula. For lower abdominal harvesting, the incision can be made inside the lower aspect of the umbilicus or suprapubically, and for the inner thigh, it can be made along the inguinal crease. Many different types of harvesting cannulas can be used.We prefer a 3 mm bullet-tipped cannula for harvesting (Fig. 18.7). All harvesting is undertaken with a 10 cm3 syringe manually, i.e., without machine assistance, using only 1–2 cm3 of negative pressure on the plunger. A few technical pearls that can help the novice surgeon undertake harvesting easily and effectively should be enumerated. First, the surgeon should attempt to remain within the middle substance of the fat pad. Rippling of the skin with passage of the cannula indicates that the cannula is too superficial.The surgeon should always be cognizant of where the cannula tip resides, as the tip is the active end where fat enters. If the cannula tip abrades the deep fascia or goes beyond the anesthetized area, the patient can experience undue and unnecessary discomfort. As the surgeon continues harvesting, the cannula should be retracted almost back to the entry site before redirecting to the adjacent site. If the cannula tip is not withdrawn prior to directing it to an adjacent site to continue harvesting, the surgeon will effectively be harvesting in the same passage site, not in a new area.While harvesting, the nondominant
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hand should stabilize the fat pad, not squeeze or deform the donor area, to prevent uneven harvesting and potential donor-site contour deformity.When harvesting, the surgeon should recall that usable fat will be about one half the harvest volume, e.g., each 10 cm3 syringe will yield approximately 5 cm3 of viable fat.
Processing the fat The next step is processing the fat.The 10 cm3 syringes are placed in the centrifuge and spun for approximately 2–3 minutes at 2000 to 3000 rpm.This will sufficiently separate the unwanted blood, lidocaine, and lysed fat cells from viable fat cells. Before centrifugation, each 10 cm3 syringe must be outfitted with customized caps and plugs to ensure that the contents do not spill out during the centrifugation process. It is imperative not to use the prepackaged plastic caps that fit onto the LuerLok side, as they will invariably become detached during centrifugation. It should also be emphasized that the centrifuge should be able to accommodate either sterile individual sleeves that hold each syringe or, alternatively, an entire central rotary element that holds all of the syringes, which can be removed and sterilized. After the fat has been centrifuged, the supranatant (from the plunger side), consisting of lysed fat cells, is poured off. Only after removing the supranatant is the Luer-Lok cap removed and the infranatant drained. A noncut 4 × 4 gauze (or cotton neuropaddy) is placed into the plunger side, making contact with the column of fat in order to wick the remaining supranatant away. After 5–10 minutes, the column of fat is then poured from the open plunger side of the 10 cm3 syringes into the open plunger side of a 20 cm3 Luer-Lok syringe. The 20 cm3 syringe should not be filled beyond the 15 cm3 mark. When pouring the fat into the 20 cm3 syringe, the surgeon should attempt to keep any residual bloody infranatant in the original 10 cm3 syringe.A Luer-Lok transfer hub allows transfer of fat from the 20 cm3 syringe into 1 cm3 Luer-Lok syringes used for fat injection. The plunger on the 1 cm3 syringe should be drawn all the way until it is actually removed from the syringe while filling the syringe with fat, so as to eliminate the air bubble that typically resides between
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Clinical procedures in laser skin rejuvenation resulting in less bruising and swelling.While injecting fat, the nondominant hand is used to palpate the underlying bony landmarks (to be discussed below) in order to guide the passage of the cannula in the correct depth and location. Finally, as the cannula tip cannot be visualized, the surgeon must mentally envision the depth of the tip during the procedure. We have divided the injection planes into three basic levels, which will be referred to throughout this section on infiltration technique, as deep (corresponding to the supraperiosteal level), medium (the musculofascial or deep subcutaneous level), and superficial (the superficial subcutaneous depth).
Fig. 18.7 The Glasgold Fat Transfer Set (Tulip Medical Inc.): 0.9 mm × 4 cm blunt spoon-tip infiltration cannula; 1.2 mm × 6 cm blunt spoon-tip infiltration cannula; 2 mm × 12 cm multiport harvesting cannula; 3 mm × 15 cm bullet-tip harvesting cannula. Reprinted with permission from Lam SM, Glasgold MJ, Glasgold RA.: Complementary Fat Grafting. Philadelphia: Lippincott Williams & Wilkins; 2007.
the plunger and the end of the fat column.The plunger is then returned to the 1.0 cm3 mark to maintain accurate volume counts.
Recipient site anesthesia The three skin entry sites (A: midcheek; B: lateral canthal; and C: posterior to the prejowl sulcus) are infiltrated with 1% lidocaine with 1:100 000 epinephrine (Fig. 18.8).Then, appropriate facial regional blocks are performed, usually including the infraorbital, zygomaticotemporal, zygomaticofacial, and supraorbital nerves. An 18-gauge needle is used to create the three entry sites on each side of the face. The same infiltration cannula intended for fat infiltration is used to inject local anesthesia (1% lidocaine with 1:100 000 epinephrine) into the planned recipient sites in order to minimize tissue trauma.
Fat infiltration The following general principles of technique will help to optimize results and minimize problems. The primary principle behind safe fat grafting, particularly when learning the technique, is to ‘hit doubles’ rather than strive for a ‘home run’. Placing too much fat into any area, especially in the periorbital region, is very difficult to correct, whereas placement of additional fat can be easily and quickly undertaken in a second session (see ‘Management of complications’ below). Placement of fat is done only in small parcels (0.03–0.05 cm3 per pass for sensitive areas and 0.1 cm3 per pass in more forgiving zones) in order to attain optimal fat cell survival by allowing maximal contact of each particle with the surrounding tissue and neighboring blood supply.The use of blunt cannulas (Fig. 18.7) (Tulip Medical Inc., San Diego, CA; Byron Medical Inc., Tucson, AZ; Miller Medical Inc., Mesa, AZ) allows for less traumatic insertion of fat,
Inferior orbital rim The inferior orbital rim is the area that requires special attention in terms of both total volume placed and technique. Fat grafting to the inferior orbital rim is done through an entry site on the cheek, which allows the fat to be deposited perpendicular to the bony orbital rim. In our experience, a lateral-based entry point in which the cannula is passed parallel to the orbital rim contributes to an unacceptably high incidence of fibrotic fat bulges. Generally speaking, for the beginning surgeon, we advocate placement of 1 cm3 of fat along the medial inferior orbital rim and 1 into the lateral inferior orbital rim.The fat is injected into the deep (supraperiosteal) plane.The nondominant index finger is used to palpate the rim to confirm the appropriate cannula depth and to guard against injury to the globe (Figure 18.9). As the cannula tip is passed perpendicularly across the inferior orbital rim (about 1 mm in either direction), 0.05 cm3 of fat is layered per pass of the cannula. Additional fat
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convexity. Filling a markedly hollow upper eyelid sulcus is an advanced technique, lying beyond the scope of this chapter. Placement of fat along the superior orbital rim can be undertaken easily from a lateral entry point and rapidly filled using 0.1 cm3 per pass without difficulty or significant risk of contour deformity.The passage of the cannula should follow the plane of least resistance.The appearance of this area being overfilled may arise toward the end of augmentation – this should give rise to alarm, as it will settle over time. Generally, 2 cm3 of fat begins to restore the deflated lateral-brow convexity.
Fig. 18.8 The three red marks correspond to the planned entry sites for fat injections: midcheek (A), lateral canthus (B), and posterior to the prejowl sulcus (C).The black marks indicate the areas for planned fat injections. Reprinted with permission from Lam SM, Glasgold MJ, Glasgold RA.: Complementary Fat Grafting. Philadelphia: Lippincott Williams & Wilkins; 2007.
can be placed for more volume-depleted patients at a medium depth. Fat infiltration superficial to the orbicularis oculi muscle is not recommended.The supramuscular plane in this region has no added advantage, and has significant potential for contour irregularity.We recommend being conservative with volumes in this area until the surgeon is comfortable with the technique. Even for the more experienced fat injector, we caution against exceeding 4 cm3 in the infraorbital rim at one setting in order to minimize problems. Superior orbital rim/brow The primary objective in filling the superior orbital rim is to re-establish a youthful appearing lateral brow
Nasojugal groove The nasojugal groove is the triangular depression outlined superiorly by the medial inferior orbital rim and medially by the nasal sidewall. For the purposes of fat transfer, we make a distinction between the nasojugal groove and the tear trough. The latter is distinguished as the visible depression in the region of the medial orbital rim, which, depending on a patient’s particular anatomy, may or may not directly correlate with the bony nasojugal groove.The nasojugal groove is generally filled with 1 cm3 of fat, which can be placed quickly with 0.1 cm3 per pass of the cannula. Anterior cheek The area of greatest volume loss in the anterior cheek is usually along a linear depression running from superomedial to inferolateral, corresponding to the malar septum. The anterior cheek is infiltrated from the lateral canthal entry point. As the cannula passes through the anterior cheek, it is common to feel resistance from the malar septum.The primary areas of fat deposition in the anterior cheek are along the malar septum and anteromedial to it. Caution should be taken to not overfill this region in men, as this may feminize the face. In general, 3 cm3 of fat are injected, with 0.1 cm3 per pass.The surgeon should try to visualize the passage of the cannula from a deeper to a progressively more superficial plane to distribute the fat cells more widely and thereby enhance the potential for adipocyte survival. The volumes used can be increased as needed for more volume-depleted patients. Anterior cheek volumes should be more conservative in males, where a fuller anterior cheek will tend to feminize the face.
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a
b
Fig. 18.9 Fat injection of the inferior orbital rim. (a) Demonstration of how placement of the index finger of the nondominant hand is used to protect the globe and give tactile feedback as to the cannula position. (b) Intraoperative demonstration of the vector for approaching the inferior orbital rim in a perpendicular orientation from the midcheek entry site. Reprinted with permission from Lam SM, Glasgold MJ, Glasgold RA.: Complementary Fat Grafting. Philadelphia: LippincottWilliams & Wilkins; 2007. Lateral cheek The lateral cheek highlight is a very important youthful landmark to restore. Approached from the midcheek
entry point, the area overlying the lateral zygoma is augmented with 2–3 cm3 of fat. The injection can be tapered into the submalar region as needed. The technique of gradual progression from a deep to a superficial plane and placement of 0.1 cm3 per pass is the same as that described for anterior cheek augmentation. Buccal Many women find the slight hollow of the buccal region that arises in their early 30s to be attractive by creating a more sculpted appearance. Progressive buccal volume loss will lend the appearance of poor health, and in women can also be masculinizing. During a fat augmentation procedure, the addition of volume to the cheeks may create a relative buccal hollowing, which should be addressed. The buccal area can be approached from multiple entry sites, including the midcheek or lateral canthal entry sites; alternatively, a separate lateral commissure entry site can be made for buccal access. Filling can progress rapidly as above, with 0.1 cm3 per pass in every tissue plane.The buccal area can sustain significant volume enhancement without deformity, e.g., 3–8 cm3 per side. Precanine fossa/nasolabial fold As mentioned above, the objective of filling the precanine fossa (the bony triangular depression deep to the superior limit of the nasolabial fold and adjacent to the nasal ala) and the nasolabial fold is not to eliminate the fold but to provide improved transition from the augmented cheek to the augmented upper lip.The patient should be cognizant of this limitation so that realistic expectations are established preoperatively. The precanine fossa is infiltrated in the deep supraperiosteal plane with approximately 2 cm3 of fat. The nasolabial fold can be augmented with 2–3 cm3 of fat along multiple levels using 0.1 cm3 per pass without significant risk of deformity.These areas are addressed from the midcheek entry point so the cannula will pass perpendicular to the nasolabial fold. Prejowl sulcus/anterior chin/labiomental sulcus/labiomandibular fold The prejowl sulcus is perhaps the most important area in the lower face to address with autologous fat transfer. Placement of fat along the prejowl sulcus will not
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Complementary fat grafting completely straighten a jawline that exhibits moderate to marked jowling, but will significantly enhance any facelift result.The prejowl sulcus should be thought of as a three-dimensional cylinder that runs along the anterior and inferior borders of the mandible. Generally, 3 cm3 of fat are placed using 0.1 cm3 per pass from an entry site just posterior to the prejowl sulcus, typically about midway along the mandibular body.The first 1 cm3 is placed deeply along the anterior madibular border.The second 1 cm3 is placed deeply along the inferior mandibular border, and the third 1 cm3 is placed at a medium-depth to transition between the two. In patients with a deeper sulcus, larger volumes will be needed to obtain the desired result. Additional fat can be feathered into the anterior chin, labiomental sulcus, and labiomandibular fold as needed. It is important to emphasize that the degree of variable resorption of fat in the anterior chin leads to less predictable results in terms of chin projection than can be achieved with an implant. Therefore, when the primary goal is anterior chin projection, an alloplastic chin implant is our preferred treatment option. Nevertheless, fat transfer to the anterior chin/mental sulcus region can accentuate the beauty of a youthful face by restoring the inferior apex of the ideal heart shape previously discussed.
POSTOPERATIVE CONSIDERATIONS Postoperative care At the end of the procedure, the patient does not require any dressings, bandages, drains, or suture closures for the body or for the face. Icing of all recipient sites will help mitigate postoperative edema. After the first 48–72 hours, the patient may ice the recipient areas as they would like. Sleeping with the head elevated for the first several days may also aid in reduction of edema. Reducing dietary for the first several weeks after surgery may also lessen edema.The patient should refrain from strenuous activity so as not to exacerbate and prolong edema unnecessarily. The patient can return to a modified exercise regimen after the first week and should slowly progress toward a full, standard program, verifying all the while that edema does not worsen with that activity.There are no
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restrictions on activity for harvested areas, except for not submerging the incisions for a week. Postoperatively, patients often complain of a dull ache and soreness in the donor areas that exceeds any discomfort felt in their face. However, there may be some degree of tenderness and tightness in the face, particularly in the malar region. Occasionally, patients can feel a flush sensation in the malar area during the first postoperative week, which can be ameliorated with icing. Ecchymosis and edema are most pronounced over the first two postoperative weeks. During the first week, the patient may appear grossly disfigured, which will be proportionate to the amount of fat transferred and the number and extent of concurrent rejuvenation procedures. Ongoing changes will be evident postoperatively for several months, and it should be emphasized to the patient that what he or she is seeing is normal and expected due to the dissipation of edema. Educating patients preoperatively and reviewing the expected changes postoperatively are helpful for the patient to have the appropriate understanding of the changes they are seeing as swelling subsides.
Management of complications The area most susceptible to complications is the periorbital region.The conservative policy of fat enhancement (‘hitting doubles’) previously outlined should be followed so as to minimize the occurrence of problems. In order to correct a complication, the surgeon must correctly identify the problem. This section will outline the unique types of problems that occur with fat grafting and how to treat each specific entity. The types of complications can be classified as follows: lumps, bulges, overcorrection, and undercorrection. Lumps A lump is a soft discrete contour deformity that arises when too much fat is transplanted to a specific locus or placed in an imprecise fashion. Although steroid injections have been attempted to manage this problem, they are generally not very effective. An incision with direct removal of the offending lump often must be undertaken. Although uncommon, visible lumps are most apt to occur along the inferior orbital rim. If a lump from the region of the lower lid is to be
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d
Fig. 18.10 (a) Preoperative photograph. (b) Following upper lid blepharoplasty and periorbital fat transfer, the patient presented with visible lumps in the inferior orbital rim. (c) Direct excision of transferred fat to correct contour. (d) Postoperative photograph showing correction of the complication.Reprinted with permission from Lam SM, Glasgold MJ, Glasgold RA.: Complementary Fat Grafting. Philadelphia: LippincottWilliams & Wilkins; 2007.
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Complementary fat grafting removed, an incision in the tear trough, following along the inferior orbital rim, heals very well and also allows for removal of excess skin (Fig. 18.10). Bulges A bulge represents a more oval-shaped contour deformity that is associated with fibrotic tissue, which can be palpated when pushing against the bony inferior orbital rim. It will most likely occur in the central to lateral portion of the inferior orbital rim. The exact cause of this is not known, but we have only encountered it when the inferior orbital rim was injected from a lateral canthal entry point. Dilute concentrations of triamcinolone acetonide (5–10 mg/cm3) can be used in most circumstances to correct this condition. Higher concentrations can be used progressively at monthly intervals as needed, taking into consideration the potential for creating a depression. Having changed technique so that the fat is always layered perpendicular to the inferior orbital rim, this problem has virtually been eliminated. Overcorrection Overcorrection should be avoided if the conservative policy of ‘hitting doubles’ is followed. Early in the postoperative period, patients may not uncommonly feel they are overcorrected. Due to the degree of and prolonged nature of swelling, we recommend waiting at least 6 months before deciding that there is too much volume and attempting to reduce it. Although rare, this is most likely to happen in the inferior orbital and malar regions, and will tend to be exaggerated when the patient smiles. An 18-gauge Klein–Capistrano microliposuction cannula (HK Surgical, Inc., San Clemente, CA) can be used to reduce the excessive volume.
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Undercorrection Undercorrection is the most favorable complication to encounter, as it can be easily corrected with an additional touch-up session. As autologous fat transfer involves a free graft, there will be variable resorption of the fat. The patient should be counseled preoperatively about the possibility of a touch-up procedure, so that they are prepared for it. Areas that required large initial volumes due to significant volume deficiency are more likely to need additional fat added at a second procedure. Generally, the surgeon should resist returning to the operating room for intervention earlier than 6 months, in order to provide ample time for edema to settle and any graft resorption to occur. At the 6-month juncture, the amount of volume loss (if any) can easily guide the surgeon on how much to infiltrate so as to provide appropriate correction.
CONCLUSIONS Autologous fat transfer is predicated on a new aesthetic paradigm that envisions a major component of the aging process as volume loss.The strategy outlined above advocates a conservative policy of volume enhancement that can easily be combined concurrently with other types of rejuvenative procedures, e.g., blepharoplasty, facelift, skin resurfacing, etc. Unlike some proponents of fat grafting, we do not strictly adhere to the philosophy that this is the only correct method of facial rejuvenation. A judicious combination of therapies can often provide the most satisfying aesthetic outcomes.
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Index Note: Page references in bold refer to Figures and Tables
abdominoplasty 139 ablative resurfacing in dermatoheliosis 118 vs nonablative skin resurfacing 51–2 Accent RF system in cellulite 145 Accreditation Association of Ambulatory Healthcare (AAAHC) 2, 3 acne excoriée 95 acne scarring 17, 18, 24, 89–100 age of scars and active acne 90–1 cytotoxic therapies 91–2 definition and classification 89–90, 89 fillers 97–8, 97–8 fractional thermolysis in 54 hypertrophic 99 hypopigmented cheek scars 95 incisional surgery 91–2, 96–7 keloidal 99 management 91 nonablative therapy 91–2, 94–5 partially ablative therapy 95 pathogenesis 91 resurfacing 91, 92–4 acne vulgaris 22, 31, 69–85 d-aminolevulinic acid (ALA) 78 and blue light 79 and IPL 79 and PDL 79–80 and polychromatic visible light 79 and red light 78–9 and red light diode laser 79 clinical experience 71 incidence 69 indocyanine green 80–1 infrared lasers 80, 81–4, 81 1450 nm 81–2 1450 nm laser in combination 82–4 1540 nm 84 CoolTouch 1320 nm 84 isotretinoin use in 81 KTP laser 75–6 laser 75–7 laser choice 71 lesion types 69 pathogenesis 69–71, 70 pathophysiological features 69 patient encounter 71 patient screening 71 photodynamic therapy 78–81, 177–8, 179, 181 photoinactivation with visible light 72–5 blue light 73 combination blue and red light 73–4
intense pulsed light 74 pulsed light and heat 74–5 UVA/UVB 72–3 yellow light 74 pilosebaceous units, targeting 78–85 porphyrins in 71–2, 72 pulsed dye laser 76–7 585 nm 76–7 595 nm 77 radiofrequency 84–5 SmoothBeam and Thermage 84 ThermaCool device 84 targeting 77 see also acne scarring actinic cheilitis 17 actinic keratosis 17, 42 actinic lentigines 42, 112–17, 113–14 actinic purpura 122 activation of laser, inadvertent 7 acyclovir 42 aesthetic skin rejuvenation (ASR) 31–44 age spots 42, 112–17, 113–14 ageless beauty 13 aging face 11–16 age specific features 12 analysis 12–13 chin position 15–16 chronological aging 11, 11 definition 11 features 11–12, 12 morphological aging 11–12, 11 non-age-specific features 12 perioral region 16 periorbital region 16 skin in 14 volume loss 14–15, 15 airborne contaminants, laser-generated 5–6 Alloderm 185 alpha-hydroxy acids, topical 19 American Association for Accreditation of Ambulatory Surgery Facilities (AAAASF) 3 American National Standards Institute (ANSI) 2, 3, 4, 7 d-aminolevulinic acid (5–aminolevulinic acid; ALA) 59, 59, 60, 173 in acne 78–80 anesthesia, safety recommendations 7 angiofibromas 17 antibiotics, prophylactic systemic 20 antioxidants, topical 19 Aquaphor 27 argon lasers, hazards 5
Arnica Montana C5 192 Artecoll 186–7 arteriovenous malformations 126, 131 Aura KTP laser 76 Baker–Gordon peel 93 basal cell carcinomas 17, 40 Bell’s palsy 192 beta-hydroxy acids, topical 19 biological hazards 4–5 biophotonics 33–4, 34, 35, 38 biopsy punch in acne scarring 97 birthmarks, vascular 125 bleomycin 129 blink reflex 4 Blu-U 73 Botox 181–2, 184, 192, 195, 196, 202 dosages 193 botulinum neuromodulators 181–3 botulinum toxin 20, 181–6 biological materials as injectable implants 183–6 collagen 183–4 dermal matrices 185–6 historical perspective 183 hyaluronic acid 184–5 type A dilution and injection technique 191–2 see also botulinum toxin/filler combined use botulinum toxin/filler combined use 191–202 forehead 195–6, 196 injection techniques 193–5 midface 196–200, 198–200 neck 201–2, 202 perioral area 200–1, 201 periorbital area 196, 197–8 Bowen’s disease, photodynamic therapy in 179 BURANE XL Er:YAG laser 38 burns 5, 8 Candela longer pulsed dye laser in leg telangiectasia 162 Candida infections 20 candidiasis, vaginal 18, 20 capillary vascular malformations 126 treatment 129–30 capillary angioma 126 Captique 97, 184, 196, 200 carbon dioxide laser, hazards of 4–5 carbon dioxide laser resurfacing 17–28 in acne 92, 93 complications 21–2, 22 indications 17–18 infections 22, 22
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laser development 17 laser surfacing 20–1 patient selection 18, 19 pigmentary abnormalities 23–6, 23 postoperative care 21 preoperative care 19–20 procedure 19–21 special considerations 26–8 cavernous hemangioma 126 Cellulair 202 cellulite 143–6 formation 143–4 monopolar radiofrequency 145–6 TriActive 145 Velasmooth 144–5, 145 cervicofacial rhytidectomy 103 cheilitis, actinic 17 chemical peel 23, 26, 31, 103 in acne scarring 93 chickenpox 31 chin position 15–16 chromophones, cutaneous 47 classification of hazards 2–4 of lasers 1–2 ClearLight 73 ClearTouch system 74, 75, 75 Coherent UltraFine Er:YAG laser 36, 36 collagen 183–4 induction therapy in acne scarring 95 complementary fat grafting 205–17, 206 anatomy 207–8, 207–9 complications 215–17 bulges 217 lumps 215–17 overcorrection 217 undercorrection 217 consultation 208–10 donor harvesting 210–11 fat infiltration 212–15 anterior cheek 213 buccal 214 inferior orbital rim 212–13 lateral cheek 214 nasojugal groove 213 precanine fossa/nasolabial fold 214 prejowl sulcus/anterior chin/labiomental sulcus/labiomandibular fold 214–15 superior orbital rim/brow 213 fat processing 211–12 operative technique 210–15 postoperative care 215 postoperative considerations 215–17 preoperative considerations 207–10 recipient site anesthesia 212 complications, lasers and light sources 45–50 causes 46 failure to anticipate, recognize and treat postoperative complications 48–9 failure to recognize the presenting clinical condition 48 failure to refer 49 failure to screen and inform patients 49 incorrect choice of laser or light source 47, 48 lack of operator knowledge and experience 46–7 computerized pattern generator (CPG) scanning devices 17
ConBio CB Erbium/2.94 36 condyloma lata 173 CoolGlide laser 167, 168–9 CoolScan 27 CoolTouch II 61 CoolTouch Varia 167–8 cornea, injury to 4 corneal protectors 5 Cosmoderm 97 Cosmoplast 97, 200 crow’s feet 182 cryotherapy in solar lentigines 114 Cushing’s syndrome 140 cutaneous injury 5 cutaneous T-cell lymphoma 173 Cyanosure CO3 laser 38O.K. or Cynosure Cymetra 185 Cyngery 170 Cynosure longer pulsed dye laser in leg telangiectasia 162–3 cystic hygromas 126 depigmentation 23–4, 23 dermabrasion 31 in acne scarring 93 Dermadeep 187 DermaK Er:YAG laser (Sharplan) 37 Dermalive 187 dermatitis atopic 173 contact 22, 24 dermatoheliosis 17, 18, 117–19 diazepam20 dyschromia, laser hair removal and 138, 138 Dysport (Rexolan) 181, 192 ectropion, postoperative 42 electrical hazards 5 electromagnetic interference 6 electro-optical synergy (ELOS) 61–2, 61 EMLA 20 environment of care 8–9 Er:YAG lasers 17 in ablative resurfacing for acne scarring 92–3 short-pulse Er:YAG systems 35–6, 36 dual-mode Er:YAG system 36–7 dual-mode, different laser type 36–7 same laser type, variable pulse duration 37 variable-pulse Er:YAG systems 38 erbium 33, 33 erbium laser aesthetic skin rejuvenation 31–44 avoidance and treatment of complications 41–2 clinical aesthetic applications 39–41 clinical dermatological applications 38–9, 38 commercially available lasers 34–8 erbium laser light—tissue interaction 33–4, 35 laser evolution 32 laser radiation safety 41 patient selection and perioperative management 41–3 physical properties 32–3, 34 techniques 41 cutaneous ablative surgery 41 deep LASR 41 dry erbium 41 medium LASR 41 superficial LASR 41 see also Er:YAG lasers
erbium:yttrium alumium garnet lasers see Er:YAG lasers excimer lasers, hazards 4 famciclovir 20, 42 fat as autologous filler for acne scarring 98 see also complementary fat grafting fillers in acne scarring 97–8, 97–8 classification 193 cross-hatching techniques 193 fanning technique 193 fat 98 injectable 192–3 linear threading technique 193 serial puncture technique 193 soft tissue 183, 183 see also botulinum toxin/filler combined use; complementary fat grafting fire extinguishers 8 fire hazard 6–7 fire, preparation for 8 fire triangle 6–7 Fitzpatrick skin types 14 flashlamp-pumped dye laser (FLPDL) 25 fluconazole 20 5–fluorouracil 25, 26 footprinting 23 fractional carbon dioxide resurfacing 27–8 fractional photothermolysis (FP) 51–2 fractional resurfacing 27–8 in acne scarring 95 in dermatoheliosis 118–19 in solar lentigines 116 fractional thermolysis 27 Fraxel laser 116–17, 117, 118–19 GentleYAG laser 167 Glasgold Fat Transfer Set 212 Glogau wrinkle scale 14 glucocorticosteroids, intralesional 25 hair removal, unwanted 135–8 candidate selection 135 complications 137–8, 138 consultation 135–6 future 138 photodynamic therapy 178 preoperative procedure 136 procedure 136–7, 137 Harmony laser 167 hazards biological 4–5 classification 2–4 electrical 5 fire 6–7 non-beam-related 5–6 training 9 Hebra 31 hemangiomas 125–6, 157 cavernous 126 congenital 125 infantile 125, 127–9, 127, 128 treatment 127–9 heme biosynthesis pathway 173, 174 herpes simplex virus (HSV) 18, 20, 42 post carbon dioxide laser resurfacing 46
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Index high-intensity focused ultrasound (HIFU) in lipolysis 148 Ho:YAG lasers, hazards 5 Hyalform 184 Hyalform Fine Line 184 Hyalform Plus 184 hyaluronic acids 184–5, 193, 194 hydroquinone, pretreatment with 19 Hylaform 97 Hylaform plus 97 hyperpigmentation 18, 19, 26 hypertrophic scarring 24, 26 in acne vulgaris 99 after carbon dioxide laser burn 47 formation 41 after long-pulse YAG laser treatment 47 hypopigmentation 18, 23, 24 in acne scarring 95, 97 imiquimod 129 indocyanine green in acne 80–1 infections 22 causative agents 22 informed consent 49 insurance 3–4 intense pulsed light (IPL) systems 23 in acne scarring 94 in acne vulgaris 79 in dermatoheliosis 119 in photorejuvenation 57, 60 in solar lentigines 114 in striae distensae 140–1 interferon therapy 129 Isolagen 186 isotretinon 41–2 Jessner’s peel 23, 26 in acne scarring 93 Joint Commission (Joint Commission on Accreditation of Healthcare Organizations; JCAHO) 2, 3 Juvederm 97, 184, 187, 196, 197, 200 keloid scarring 41, 99, 187 Kenalog 25 keratosis actinic 17, 42 seborrheic 17, 39, 40, 42 ketorolac 20 krypton laser in solar lentigines 114 KTP lasers 76 hazards 5 in acne scarring 94 in acne vularis 75–6 in leg telangiectasia 159–62 in poikiloderma of civatte 120 in skin tighening 151 laser-assisted skin rejuvenation (LASR) 32, 41 laser-generated electromagnetic interference 5 laser history 45 laser plume 5–6 laser smoke evacuator 6 lichen planus 18 lidocaine 20
lipolysis 146–8 low-level laser 148 Nd:YAG laser 147 ultrasound 147–8 liposuction 107, 139 liver spots 42, 112–17, 113–14 Lumenis One laser 167 lung, shock 8 lupus vulgaris 173 LuxVO (Palomar) 74 lymphatic malformations 126, 131 Lyra laser 167, 169 maximal permissible exposure (MPE) 5 Medlite laser system 113 melasma 53 MEND (microscopic epidermal necrotic debris) formation 116, 116, 121 Menderma gel 25 meperidine 20 mequinol 112 methicillin-resistant Stapylococcus aureus (MRSA) 20 microablative skin resurfacing 51–2 microdermabrasion in acne scarring 94 in striae distensae 140 microlaser peels 116 microscopic treatment zones (MTZs) 143 microthermal zones (MTZs) 52 midazolam 20 milia formation 22 monopolar radiofrequency skin tightening 104–7, 105 background 104 clinical effects 105–6 newer applications and additional uses 106–7 side-effects and limitations 106 treatment parameters 104–5, 105 MultiClear system 142, 142 mupricin, nasal 20 Mydon laser 167 Nd:YAG lasers hazards 5 in leg telangiectasia 159–62, 166–7, 170 in lipolysis 147 Q-switched, in solar lentigines 112–13 in skin tightening 150–1 near-infrared skin tightening 107–9 background 107–8 clinical effects 108–9 future directions 109 side-effects and limitations 109 treatment parameters 108 neck resurfacing 26–7 Nexgen pixel 36 Nlite System pulsed dye laser 61, 76 nominal hazard zone (NHZ) 5 nonablative skin resurfacing 51 vs ablative skin resurfacing 51–2 in acne scarring 91–2, 94–5 long-wavelength lasers and light sources for collagen stimulation 59–62 for photorejuvenation 52–62 skin tightening 62–5, 63, 64, 65 see also photodynamic therapy
non-beam-related hazards 5–6 nonerythematosus scars 26 nonsurgical tightening 103–9 monopolar radiofrequency 104–7, 105 near-infrared skin tightening 107–9 NSAIDS 22 Oasis 186 Occupational Safety and Health Administration (OSHA) 2 optical radiation hazard 4 pacemakers 6 PASS mnemonic 8 pathophysiology of aging 12 Pearl fractional laser 27 perifollicular hypopigmentation of acne scars 97 perioral region in aging face 16 periorbital region in aging face 16 Perlane 184, 197, 200, 200, 201 phenol 31 phenol peel 93 photoaging 17, 18, 111–22 photochemotherapy 24 photodynamic therapy 173–9 acne 78–81, 177–8, 179, 181 clinical applications 175 future 179 hair removal 178 lasers and light sources 174–5 mechanism 173–4 photorejuvenation 59, 59, 60, 175–7, 176 sebaceous gland hyperplasia 177–8 side-effects 179 photofacial technique 23 photohyperthermia selective 146–7 photorejuvenation 52–62 intense pulsed light 53–5, 55, 57, 60 laser or visible light technology 52–3 photomodulation 56–8 potassium titanyl phosphate 55–6, 58 pulsed dye laser 53, 55 photoprotection, preoperative 19 photothermolysis, selective 135 pigmentary abnormalities 23–6 plasma resurfacing in acne scarring 94 poikiloderma of civatte 119–21, 121 Polaris WR, skin tightening and 150 polycarbonate safety glasses5 portwine stains 128, 130, 157 potassium titanyl phosphate (KTP) lasers see KTP lasers pregnancy, striae distensae in 140 Profile laser 167 Propionibacterium acnes 69, 71–7 see also acne scarring; acne vulgaris Pseudomonas aeruginosa 22 psoriasis 18 pulsed-dye laser in acne scarring 94 in acne vulgaris 76–7 in leg telangiectasia 140–1 in photorejuvenation 53–5, 55, 57, 60 in poikiloderma of civatte 120, 121 Putrtox 181
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Index
Q-switched alexandrite laser in solar lentigines 113–14 Q-switched lasers in acne scarring 95 in solar lentigines 112–14 Q-switched Nd:YAG laser (QSNd:YAG laser) in solar lentigines 112–13 Q-switched ruby laser (QSRL) in solar lentigines 112–13 Quantel Medical Multipulse mode 169–70 Radiesse 97, 186, 195, 197, 198, 198, 199 ReFirme in skin tightening 152, 152 regulations 2 Reloxin 181 repigmentation 24 Restylane 97, 184, 185, 187, 197, 198, 200, 200, 201 Restylane Fine Lines 184, 196, 200 Restylane Touch 196 Restylane Vital 196, 202 resurfacing cosmetic units 26 retinal hazard region 4 retinoic acid 111, 112 retinoid, topical, preoperative 19 Reviderm intra 186 rhytids 18, 18, 20, 21 rosacea 125, 131–2 safety, laser 1–9 scar resurfacing 26 scarring, following laser surgery 24–6 Sciton Contour 37, 37 Sciton laser 21 scleroderma 18 sclerotherapy 130–1 leg telangiectasia 157, 168, 169, 169, 170 Sculptra 186, 195, 197 sebaceous gland hyperplasia, photodynamic therapy 177–8 seborrheic keratosis 17, 39, 40, 42 shock lung 8 silicone 187, 187 as filler for acne scarring 97–8 skin cancer 173 skin rejuvenation, modalities 31–2 skin rolling or needling in acne scarring 95 skin tightening 148–52 infrared light-based 65, 65, 151, 152 Nd:YAG laser 150–1 nonablative rejuvenation 62–5, 63, 149 radiofrequency-based 62–5, 63, 64, 149–50, 150
smallpox 31 SmartEpilII laser 167 SmoothBeam 61 soft tissue fillers droplet technique 188 linear threading 188 serial puncture technique 188 techniques 188 see also botulinum toxin SoftForm 187, 188 solar elastosis 51, 117, 118 solar lentigines 42, 112–17, 113–14 squamous-cell carcinoma 17 steroid-induced atrophy 24 Stratasis 186 strawberry angioma 126 stretchmarks 139–43 striae alba 140, 141, 142 striae distensae (stretchmarks) 139–43 intensed pulsed light 141 mid-infrared 142–3 pulsed dye laser 140–1 ultraviolet 141–2 striae rubra 140 Sturge–Weber syndrome 129 subcision in acne scarring 96–7, 96 sunspots 42, 112–17, 113–14 sunscreen use, preoperative 19 surgical masks 6 SurgiLift 196, 202 Surgisis 186 synthesized bioactive fillers 186 synthetic nonresorbable polymers 186–8 implantable 187–8 injectable 186–7 syringomas 17 system lupus erythematosis 18 telangiectasia 24 facial 131–2, 132 PDL in 120 see also telangiectasia, leg telangiectasia, leg 157–71 combination/sequential 595 nm PDL and 1064 nm Nd:YAG 170 CoolGlide 168–9 CoolTouch Varia 167–8 diode lasers 163–4 histology 159 intense pulsed light 164–6, 164, 165 KTP and frequency-doubled Nd-YAG lasers 159–62
lasers and light sources 160–1 Lyra 169 Nd:YAG laser 166–7 pathogenesis 157–9 pulsed dye laser 162–3 Quantel Medical Multipulse mode 169–70 Vasculite 167 telangiectatic matting ™ 157 ThermaCool TC 64, 103, 104–7 skin tightening and 149–50 Thermage 196, 201, 202 Titan (Cutera) 103, 107–8, 109 tobacco smoking 19–20 training in safety 9 tretinoin, topical, preoperative 19 TriActive laser in cellulite 145 in lipolysis 147 trichoepitheliomas 17 trypsin epidermal grafting in acne scarring 97 Tummy by Thermage treatment 107 UltraPulse carbon dioxide laser 17, 20 UltraShape System Ltd in lipolysis 147 Ultrasoft 187, 188 V Beam 25 valacyclovir 20, 42 varicella scars 24 vascular malformations 126, 128 VascuLight 25 Vasculite laser 167 Vbeam 61 Velasmooth 144–5, 145 venous malformations 126, 130–2 venular vascular malformations 126, 129–30, 130 Verapulse long-pulse (VLP) Nd:YAG laser in solar lentigines 113 Verapulse Q-switched (VQS) Nd:YAG laser in solar lentigines 113 vitiligo 18, 24, 141, 173 volume loss, facial 14–15 waste disposal 5 wrinkles 17 ystrium aluminum garnet (YAG) 32–3, 33 Zeno 85 Zyderm I and II 183 Zyplast 183–4, 185
