Clinical Procedures in Laser Skin Rejuvenation

Transcription

Prelims Carniol-8028.qxd
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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
8/23/2007
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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
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Within Continental USA
Tel: 1 (800) 272 7737; Fax: 1 (800) 374 3401
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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
vii
x
11 Management of vascular lesions
Marcelo Hochman and Paul J Carniol
125
1
12 Laser treatment for unwanted hair
Marc R Avram
135
11
17
14 Treatment of leg telangiectasia with
laser and pulsed light
Mitchel P Goldman
157
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
173
181
51
69
8 Treatment of acne scarring
Murad Alam and Greg Goodman
89
10 Laser treatment of pigmentation
associated with photoaging
David H Ciocon and Cameron K Rokhsar
139
31
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
103
111
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
191
205
219
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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
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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Ioannis P Glavas MD
Oculoplastic Surgery
Manhattan Eye, Ear and Throat
New York, NY
USA
Kavita Mariwalla MD
Yale School of Medicine
New Haven, CT
USA
Mitchel P Goldman MD
LaJolla Spa
LaJolla, CA
USA
Philip J Miller MD FACS
New York University School of Medicine and
The NatraLook ProcessTM and East Side Care
New York, NY
USA
Greg Goodman MD
Minash University
Melbourne
Australia
Monica Halem MD
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
UCSF
and
The Maas Clinic
San Francisco, CA
USA
Keyvan Nouri MD
University of Miami
Miami, FL
USA
Rita Patel MD
University of Miami
Miami, FL
USA
Baljeet K Purewal MD
Department of Opthalmology
Lutheran Medical Center
Brooklyn, NY
USA
Thomas E Rohrer MD
Boston University School of Medicine
and
Skin Care Physicians of Chestnut Hill
Chestnut Hill, MA
USA
Cameron K Rokhsar MD FAAD FAACS
Albert Einstein College of Medicine
New York, NY
USA
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Neil S Sadick MD
Sadick Aesthetic Surgery and Dermatology
New York, NY
USA
Papri Sarkar MD
Harvard Medical School
Boston, MA
USA
ix
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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Clinical procedures in laser skin rejuvenation
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
5
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
7
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.
9
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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Evaluation of the aging face
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
13
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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Evaluation of the aging face
a
15
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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Carbon dioxide laser resurfacing, fractionated resurfacing and YSGG resurfacing
19
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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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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23
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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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
29
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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minimal thermal effects (nonablative lasers and
light sources).
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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Erbium laser aesthetic skin rejuvenation
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
33
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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35
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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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
37
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
39
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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a
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b
c
d
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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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
41
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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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
43
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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47
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
49
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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Nonablative technology for treatment of aging skin
a
53
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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55
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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57
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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a
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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a
61
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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65
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.
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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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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
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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.
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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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.
78. Narins D, Narins R. Non-surgical radiofrequency facelift.
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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Hair shaft
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.
71
CLINICAL EXPERIENCE AND
CONSIDERATIONS
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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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
73
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 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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b
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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b
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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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.
79
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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a
81
b
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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a
83
b
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.
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37. Papageorgiou P, Katsambas A, Chu A. Phototherapy with
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38. Edwards C, Hill S, Anstey A. A safe and effective yellow
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39. Gupta A. Efficacy and safety of intense pulsed light therapy using wavelengths of 400–700 nm and 870–1200 nm
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40. Elman M, Lebzelter J. Evaluating pulsed light and heat
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41. Herd RM, Dover JS, Arndt KA. Basic laser principles.
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44. Gregory AN,Thornfeldt CR, Leibowitz KR et al. A study
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45. Baugh, WP and Kucaba WD. Nonablative phototherapy
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46. Bowes LE, Manstein D, Anderson RR. Effects of 532 nm
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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
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52. Ortiz A, Van Vilet M, Lask GP,Yamauchi PS. A review of
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53. Ashkenazi H, Malik Z, Harth Y et al. Eradication of
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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
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55. Hongcharu W, Taylor CR, Change Y et al. Topical ALAphotodynamic therapy for the treatment of acne vulgaris.
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57. Itoh Y, Ninomiya Y, Tajima S et al. Photodynamic therapy
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58. Goldman MP. Using 5-aminolevulinic acid to treat acne
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60. Pollock B,Turner D, Stringer MR et al.Topical amenolevulinic acid-photodynamic therapy for the treatment of
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61. Kimura M, Itoh Y, Tokuoka Y et al. Delta-aminolevulinic
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62. Hwang EJ and Seo K. Topical photodynamic therapy for
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63. Alexiades-Armenakas, M. Long-pulsed dye laser-mediated
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65. Tuchin VV, Genina EA, Bashkatov AN, et al. A pilot study
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66. Genina EA, Bashkatov AN, Simonenko GV, et al. Lowintensity indocyanine-green laser phototherapy of acne
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67. Lloyd JR and Mirko M. Selective photothermolysis of the
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68. Paithankar DY, Ross EV, Saleh BA, et al. Acne treatment
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69. Mazer JM.Treatment of facial acne with a 1450 nm diode
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70. Mazer JM and Fayard V. Eighteen months results after
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71. Santhanam A, Shah A and Kumar P. The 1450-nm diode
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72. Jih MH, Friedman PM, Goldberg LH et al.The 1450-nm
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73. Bernstein EF. Lower-energy double-pass 1450 nm laser
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74. Friedman PM, Jih MH, Kimyai-Asadi A, et al.Treatment of
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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
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77. Wang SQ, Counter JT, Flor Me and Zelickson BD.
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diode laser alone versus microdermabrasion pluse the
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78. Lupton JR,William CM,Alster TS. Nonablative laser skin
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79. Fournier N,Dahan S, Barneon G, et al. Nonablative
remodeling: clinical, histologic, ultrasound imaging, and
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80. Boineau D, Angel S, Nicole A, et al. Treatment of active
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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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Treatment of acne scarring
91
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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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
93
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.
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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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.
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
95
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
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
99
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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3. Kadunc BV,Trindade de Almeida AR. Surgical treatment
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4. Jacob CI, Dover JS, Kaminer MS. Acne scarring: a classification system and review of treatment options. J Am
Acad Dermatol 2001;45:109–17.
5. Goodman GJ, Baron JA. Post-acne scarring: a qualitative global scarring grading system. Dermatol Surg
2006;32:1458–66.
6. Taub AF. Treatment of rosacea with intense pulsed light.
7. Iyer S, Fitzpatrick RE. Long-pulsed dye laser treatment
for facial telangiectasias and erythema: evaluation of a single purpuric pass versus multiple subpurpuric passes.
8. Holland DB, Jeremy AH, Roberts SG, et al. Inflammation
in acne scarring: a comparison of the responses in lesions
from patients prone and not prone to scar. Br J Dermatol
2004;150:72–81.
9. Batra RS, Jacob CI, Hobbs L, Arndt KA, Dover JS. A
prospective survey of patient experiences after laser skin
resurfacing: results from 2½ years of follow-up. Arch
Dermatol 2003;139:1295–9.
10. Roxo RF, Sarmento DF, Kawalek AZ, Spencer JM.
Successful treatment of a hypochromic scar with manual
dermabrasion: case report. Dermatol Surg. 2003;29:
189–91.
11. Camirand A, Doucet J. Needle dermabrasion. Aesthet
Plast Surg 1997;21:48–51.
12. Yug A, Lane JE, Howard MS, Kent DE. Histologic study of
depressed acne scars treated with serial high-concentration
(95%) trichloroacetic acid. Dermatol Surg 2006;32:
985–90.
13. Lipper GM, Perez M. Nonablative acne scar reduction
after a series of treatments with a short-pulsed 1,064-nm
neodymium:YAG laser. Dermatol Surg 2006;32:
998–1006.
14. Bhatia AC, Dover JS, Arndt KA, Steward B, Alam M.
Patient satisfaction and reported long-term therapeutic
efficacy associated with 1,320 nm ND:YAG laser
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.
20. Abraham MT, Ross EV. Current concepts in nonablative
radiofrequency rejuvenation of the lower face and neck.
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.
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.
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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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.
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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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Nonsurgical tightening
105
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
107
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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a
109
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.
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.
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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Laser treatment of pigmentation associated with photoaging
a
113
b
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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a
115
b
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.)
a
b
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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a
117
b
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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a
b
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.
a
b
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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a
119
b
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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a
121
b
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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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.
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.
123
17. Goldberg DJ. New collagen formation after dermal
remodeling with an intense pulsed light source.
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.
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.
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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Management of vascular lesions
127
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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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
129
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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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.
131
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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a
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
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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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
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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Laser treatment for unwanted hair
137
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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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.
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 (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
141
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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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
143
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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a
145
b
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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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
147
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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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
149
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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a
b
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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a
151
b
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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a
b
c
d
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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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.
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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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.
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
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
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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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
159
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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161
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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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
163
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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165
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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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
169
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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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.
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
8.
9.
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11.
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16.
17.
18.
19.
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24.
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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
32.
33.
34.
35.
36.
37.
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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NEGATIVE FEED BACK
Glycine and
succinyl CoA
Heme
ALA synthase
(note-limiting step)
Topical
ALA or
MAL
Ferrochelatase
and Fe2+
ALA
ALA dehydratase
Pp
Porphobilinogen
Protoporphyrinogen
oxidase
Porphobilinogen
deaminase
Protoporphyrinogen IX
Hydroxymethylbilane
Coproporphyrinogen III
oxidase
Uroporphyrinogen III
cosynthase
Coproporphyrinogen 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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175
2.5
Absorption (arbitrary units)
Absorption (arbitrary units)
2.5
2.0
1.5
1.0
0.5
300
350
400
450
500
550
600
650
700
KTP laser
532 nm IPL 560–1200 nm
1.5
1.0
0.5
0
300
0
PDL 585–595 nm
2.0
BLU-U
Clearlight
417– 432 nm
350
400
450
500
550
600
650
700
Wavelength (nm)
Wavelength (nm)
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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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
177
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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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
179
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.
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.
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
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.
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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The bioscience of the use of botulinum toxins and fillers for non-surgical facial rejuvenation
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.
183
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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185
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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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
187
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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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.
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2. Schantz EJ, Johnson EA. Botulinum toxin: the story of its
development for the treatment of human disease. Persp
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3. Schantz EJ, Johnson EA. Preparation and characterization
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4. Ramirez AL, Reeck J, Maas CS. Preliminary experience
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6. MacDonald M, Spiegel J, Maas CS. Glabellar anatomy:
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13. Neuber F. Fat grafting. Cuir Kongr Verh Otsum Ges Chir
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15. Bailin PL, Bailin MD. Collagen implantation: clinical
applications and lesion selection. Dermatol Surg Oncol
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16. Castrow FF 2nd, Krull EA. Injectable collagen implant –
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17. Maas CS, Papel ID, Greene D, Stoker DA. Complications
of injectable synthetic polymers in facial augmentation.
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
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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.
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
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(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
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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
193
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
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
for deep subcutaneous
or supraperiostal injections
Not yet in
the USA
9–18
months
18-gauge
cannula
Captique
Produced by
bacterial fermentation
November
2004
4–6
months
Juvederm
Ultra plus
Produced by
June 2006
9–12
months
27-gauge
Juvederm
Ultra
Produced by
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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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.
195
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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a
b
c
d
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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.
a
b
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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c
b
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
a
b
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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a
b
c
0.5 ml
27 gauge
Radiesse
Digital massage
Nasolabial fold fills-in
microlift
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.
a
b
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.
199
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a
b
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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b
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.
a
b
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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a
b
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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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).
203
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:
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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a
b
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
b
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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Complementary fat grafting
207
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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a
b
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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a
209
b
Fig. 18.5 Preoperative (a) and postoperative (b) photographs of a patient who underwent transconjunctival lower lid
blepharoplasty and periorbital and midface fat transfer. Reprinted with permission from Lam SM, Glasgold MJ, Glasgold RA.:
Complementary Fat Grafting. Philadelphia: LippincottWilliams & Wilkins; 2007.
a
b
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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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
211
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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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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213
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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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
215
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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a
c
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b
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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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.
217
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 Carniol-8028.qxd
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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
220
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Index
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;
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 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 photorejuvenation 53–5, 55, 57, 60
in poikiloderma of civatte 120, 121
Putrtox 181
221
222
8/23/2007
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Index
Q-switched alexandrite laser
in solar lentigines 113–14
Q-switched lasers
in acne scarring 95
Q-switched Nd:YAG laser (QSNd:YAG laser)
Q-switched ruby laser (QSRL)
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
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
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

Clinical Procedures in Laser Skin Rejuvenation

Transcription

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