Ablative and Non AblativeF Acial Skin Rejuvenation

ABLATIVE AND NON-ABLATIVE FACIAL SKIN REJUVENATION
ABLATIVE AND NON-ABLATIVE FACIAL

SKIN REJUVENATION
DAVID J GOLDBERG MD
Clinical Professor of Dermatology
Director, Laser Research and Mohs Surgery
Mount Sinai School of Medicine, New York
Director, Skin Laser & Surgery Specialists of New York and New
Jersey
Hackensack, NJ
USA
With a contribution by R Stephen Mulholland MD, Toronto,

Ontario, Canada
LONDON AND NEW YORK

© 2003 Martin Dunitz, a member of the Taylor & Francis Group plc
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CONTENTS
Preface vi
1 Biology of collagen 1
2 Cutaneous wound healing 7
3 Carbon dioxide laser resurfacing 18
4 Erbium:YAG laser resurfacing 66
5 Combined Erbium:YAG/CO2 laser and variable pulsed Erbium:YAG laser 107
6 Electrosurgical skin resurfacing 143
7 Non-ablative dermal remodeling 161
8 Complications 197
9 Marketing facial skin rejuvenation 215
R Stephen Mulholland
Index 230
This book is dedicated to my dermatologic surgical fellows, Drs. Arlene
Rogachefsky, Sirunya Silapunt, Dale Sarradet, Luisa Garcia and
Mussarat Hussain. Without their commitment and assistance this book
would not have been possible.
PREFACE
Historically, chemical peeling of the skin has been used in the treatment of actinic damage,
pigmentary dyschromias and facial rhytides. This particular method can be very cost
effective, but results vary greatly due to the inconsistent level of injury. Classic dermabrasion
can also be a very effective method of treating wrinkled skin. However, this technique holds
the greatest risk of transmission of infectious diseases. Newer ablative and non-ablative facial
rejuvenation techniques offer a precise method for improving photoaged skin. This book will
review the various lasers, light sources and radiofrequency devices used for facial
rejuvenation. The first chapter of the book begins with a discussion of collagen biology. The
next chapter reviews the biology of wound healing. Subsequent chapters evaluate the use of
both ablative and non-ablative techniques, including carbon dioxide, Erbium:YAG and
electrosurgical resurfacing, as well as non-ablative dermal remodeling. Each chapter will
review currently available technologies and discuss the author's approach to using each
system. Finally, the last two chapters are dedicated to complications and the business
aspects of a facial rejuvenation practice.
David J Goldberg MD
1
BIOLOGY OF COLLAGEN
KEY POINTS
(1) Collagen fibers comprise more than 70% of the dry weight of the dermis
(2) Type I collagen represents approximately 80% of the total collagen in the adult
human dermis
(3) The varied thermal effects of heated collagen depend on the degree of temperature
elevation
(4) Slight temperature elevation dissociates the intermolecular cross-links that stabilize
the collagen triple-helix, resulting in collagen shrinkage
(5) Ablative and most non-ablative techniques will lead to an increase in Type I collagen
STRUCTURE
Collagen represents the main fibrillar component of connective tissue. Collagen also
represents the major extracellular protein of the human body. The physiologic role of collagen
fibers in the skin is to provide for the framework and mechanical strength of skin. This allows
skin to serve as a protective organ against external trauma. Collagen fibers comprise more
than 70% of the dry weight of the dermis. These fibers are composed of fibrils and microfibrils.
Under electron microscopy, collagen fibers demonstrate a pattern of cross-striations
appearing with a repeating periodicity approximately 70 nm apart. This regular banding
pattern results from collagen molecules aligned in a quarter-stagger arrangement. Collagen
molecules are composed of three polypeptides, known as chains, that are coiled around each
other in a right-handed triple-helix. Each polypeptide chain has glycine distributed in a
repeating Gly–X–Y sequence. The X position is often occupied by proline and the Y position is
mostly occupied by hydroxyproline. The relatively high contents of these amino acids, and the
repetitive positioning of glycine are necessary for the unique triple-helical conformation of the
collagen molecule. The intermolecular cross-links unite the collagen molecule into a
continuous polymeric network. This cross-linking is mediated by the copper-dependent
enzyme lysyl oxidase and is inhibited by heat and photonic energy. Intermolecular cross-links
give collagen unique properties of high tensile strength and elasticity.1
COLLAGEN TYPES
Collagen comprises a family of closely related yet genetically distinct proteins. The genetically
distinct collagens can be divided into different classes based on the fiber architecture in
tissues (Figure 1.1):
2 ABLATIVE AND NON-ABLATIVE FACIAL SKIN REJUVENATION
Figure 1.1. Location of various major collagen fibers in mature human skin
(1) Fibril-forming collagens, characterized by relatively large fibrils: collagen types I, II, III, V,
XI.
(2) Interlacing network collagen: collagen type IV.
(3) Microfibril-forming collagen: collagen types VI, VII.
(4) Fibril-associated collagens with interrupted triple helices (FACIT): collagen types IX, XII,
XIV.2
Type I collagen represents approximately 80% of the total collagen in the adult human dermis.
Major fractions of type I collagen contains two identical a chains, α1(I) and a third chain, α2(I)
which is different in amino acid composition. The chain composition of type I collagen is [α1
(I)]2α2(I). Collagen molecules containing three identical α1(1) chains represent a minor
fraction of collagen type I, called α1(I)3. Type I collagen is the most widely distributed and
most extensively characterized form of collagen. It is responsible for the tensile strength of
the human dermis. It represents the bulk of newly formed fully evolved collagen seen after
treatment with ablative and most non-ablative dermal remodeling.
Type III collagen accounts for approximately 10% of the total collagen of adult human
dermis. It predominates in human skin during embryonic life and is initially called fetal
collagen. However, the ratio of type I to type III collagen in adult human skin is ~6:1 due to the
accelerated synthesis of type I collagen during the early postnatal period.
Type IV collagen is predominantly present within the lamina densa of the dermal–epidermal
junction. The presence of non-collagenous interruptions within the triple-helical domain of
type IV collagen provides flexibility to the collagen molecule. In the lamina densa, type IV
collagen forms a lattice pattern rather than the fibers characteristic of collagen types I–III.
There are various a chains of type IV collagen identified as α1(IV), α2(IV), α3(IV), α4(IV), α5
(IV), and α6(IV).3 However, in human skin, collagen type IV is predominantly seen as the
heterotrimer, [α1(IV)]2α2(IV).
Type V collagen represents less than 5% of the total collagen in human skin. However,
migrating epidermal cells seen at the edge of an ablative resurfaced wound may produce type
V collagen.4 In human skin, the predominant chain composition of type V collagen is [α1(V)]
2α2(V).
Type VI collagen consists of three distinct chains, α1(VI), α2(VI), and α3(VI), folded into a
triple-helical domain of about 100 nm in length, with globular domains at both ends of the
molecule.5 Type VI collagen forms a microfibrillar network rather than the broad fiber
BIOLOGY OF COLLAGEN 3
characteristic of types I and III collagens. The microfibrillar network of type VI collagen
stabilizes the assembly of broad collagen fibers and basement membranes.
Type VII collagen is a major component of the anchoring fibrils that extend from the dermal–
epidermal junction to the papillary dermis. The type VII collagen molecule has an unusually
long triple-helical domain containing interchain disulfide bonds and a pepsin-sensitive, non-
helical site close to the center of the molecule.6,7 It contains only one type of α chain, thus the
chain composition of type VII collagen is [α1(VII)]3.
Type XII collagen contains more than one triple-helical domain separated by non-
collagenous segments. Type XII collagen is in the group of FACIT collagens which form fibers
in association with type I collagen.
Type XIV collagen, like other FACIT collagens, may also be oriented parallel to the surface
of large collagen fibers.
Collagen Synthesis
Collagen genes, like most eukaryotic genes, are composed of exon and intron genes. Intron
genes are non-coding DNA sequences of unknown function. The entire gene is transcribed
into a precursor mRNA which undergoes post-transcriptional modifications, such as capping
and polyadenylation. The mature mRNA undergoes a translation process in the cytoplasm of
cells. The translation of collagen polypeptides occurs on the ribosomes of fibroblasts and
related cells. The product of translation is called a prepro-α chain. This chain represents a
precursor polypeptide of procollagen. Precursor polypeptides are then released into the
cisternae of the rough endoplasmic reticulum. During this transmembrane transportation,
the signal sequence of prepro-α chains is enzymatically cleaved, resulting in polypeptides
called pro-α chains. Finally, these pro-α chains undergo post-translational modifications.
Synthesis of Hydroxyproline
Hydroxyproline represents about 10% of the amino acids in type I collagen. The presence of
hydroxyproline is required for the final collagen triple-helical formation. This triple-helical
conformation is the structure required for the normal secretion of procollagen molecules into
the extracellular space. The formation of hydroxyproline is catalyzed by two separate enzymes,
prolyl-4-hydroxylase and prolyl-3-hydroxylase. There are two isomeric forms of
hydroxyproline in pro-α chains; trans-4-hydroxy-L-proline and trans-3-hydroxy-L-proline.8
The hydroxylation of procollagen polypeptides is initiated while the polypeptides are growing
on the ribosomes and occurs only with prolyl residues residing in polypeptide pro-α chains.
Hydroxyproline formation does not occur once the collagen substrate is in a final triple-
helical conformation. Molecular oxygen, ferrous iron, α-ketoglutarate and a reducing agent
are required as cofactors for hydroxyproline formation. Because reducing agents such as
ascorbate and oxygen are required for the formation of hydroxyl groups in hydroxyproline,
ascorbic acid deficiency and relative anoxia lead to poor wound healing and decreased tensile
strength of the connetive tissue.9 The relative effect of ascorbic acid deficiency on post-laser
collagen formation is unclear.
Synthesis of Hydroxylysine
Lysyl residues in pro-α chains are hydroxylated to hydroxylysine. An enzyme, lysyl
hydroxylase, which requires molecular oxygen, ferrous iron, α-ketoglutarate, and ascorbate
as cosubstrates, catalyzes hydroxylysine formation. As with hydroxylation of prolyl residues,
only lysyl residues in peptide linkages are hydroxylated to hydroxylysine. Hydroxylysine
formation begins while the polypeptide chains are growing on ribosomes and continues for
some time after the release of polypeptides from the ribosomes. However, as is the situation
with hydroxyproline, lysyl hydroxylase does not hydroxylate a collagen substrate that is in the
triple-helical conformation. Thus, the rate of triple-helical formation of collagen can regulate
the amount of synthesized hydroxylysine in collagen molecules. Hydroxylysyl residues in
collagen molecules are required for the formation of collagen cross-links, and as an
attachment site for glycosylated sugar residues.10,11
Glycosylation
Sugar residues are added to pro-α chains by a reaction called glycosylation. The sugar
residues are linked to collagen polypeptides through the hydroxyl group of hydroxylysine.
There are two glycosylation reactions, which attach galactosyl and glucogalactosyl residues to
the collagen molecule. Collagen galactosyl-transferase and collagen glucosyl-transferase
enzymes separately catalyze those two glycosylation reactions. These two enzymes of
glycosylation require Mn2+ as a cofactor.10,11 The glycosylation reactions of pro-α chains begin
after the synthesis of hydroxylysyl residues and terminate if the collagen substrate is in a
triple-helical conformation.
After glycosylation, the three pro-α chains become associated. The association of the
extensions of the individual pro-α chains facilitates folding of the collagenous portion of the
polypeptides into a triple-helix. Interchain disulfide bonds are formed through the cysteine
residues on the extension portion of the pro-α chain to link three pro-α chains together. The
formation of the interchain disulfide bonds may have a role in the triple-helix formation of
procollagen molecules. The rate of triple-helix formation of procollagen molecules varies
between the genetically different types of procollagen. The rate of triple-helix formation limits
some of the posttranslational modification reactions through the relative number of
hydroxylysine and sugar residues in genetically distinct types of collagen. Hydroxylation,
glycosylation and triple-helical formation occur within cisterna of the rough endoplasmic
reticulum. Pro-α chains of collagen assembled on the membrane-bound ribosomes are
translocated into this cellular compartment with microtubule involvement. After procollagen
polypeptides are folded into a triple-helical conformation, procollagen molecules are then
secreted in golgi vacuoles and transported into the extracellular space.10 Microtubule-
disrupting agents such as colchicine delay the secretion of procollagen molecules in the
extracellular space. The triple-helical conformation is required for the secretion of procollagen
molecules. Newly synthesized but defective pro-α chains are degraded intracellularly before
secretion. Genetically different types of procollagen molecules differ in their rate of secretion.
In the extracellular space, procollagen molecules are converted to collagen by procollagen N-
proteinase and procollagen C-proteinase. These two enzymes remove extension peptides on
the collagen molecules. C-proteinase and N-proteinase are required for removal of the
carboxy-terminal and amino-terminal extensions, respectively.11,12 The conversion of
procollagen to collagen leads to subsequent collagen fiber formation. Failure to remove
extension peptides, either the amino-terminal or carboxyterminal extensions, results in
impaired tensile strength of collagen fibers in the skin. The collagen molecules spontaneously
form collagen fibers after the removal of the extension peptides. The collagen molecules then
undergo cross-linking to provide the tensile strength of collagen fibers. There are several
forms of cross-links in collagen. The common forms are derived from lysyl or hydroxylysyl
residues. These two residues undergo oxidative deamination, the first step in the cross-
linking of collagen, catalyzed by lysyl oxidase. The enzymatic synthesis of aldehyde derivatives
requires copper as a cofactor. Two synthesized aldehyde derivatives may form cross-links
together or an aldehyde may form cross-links with an 8-amino group presented in unmodified
lysine or hydroxylysine. This latter type of reaction is called a Shiff base-type of covalent
cross-link. The collagen cross-links can be either intramolecular, occurring between two
BIOLOGY OF COLLAGEN 5
adjacent α-chains in the same collagen molecule, or intermolecular, linking with neighboring
collagen molecules.
Thus the complicated process of collagen production is controlled at many different levels of
synthesis and degradation. These levels include the: transcription and post-transcription
level; translation and post-translation level; and degradation level. Any interference with
collagen production would impact on the healing after any dermal remodeling technique.
Heat–Collagen Interaction
The varied thermal effects of heated collagen depend on the degree of temperature elevation.
Slight temperature elevation dissociates the intermolecular cross-links that stabilize the
collagen triple-helix, resulting in collagen shrinkage. However, the cross-links between
collagen molecules remain intact. The heated polypeptide chains of collagen have a
considerable but incomplete capacity to resume the original intrachain characteristics at a
specific range of temperature elevation.13 Disruption of interpeptide bonds results in
immediate shortening of collagen fibers to about one-third of their initial length. The
shrinkage of collagen occurs along the long axis of collagen fibers and at a very specific
temperature. The mechanism of collagen shrinkage is a transition between the triple-helical
conformation and a random configuration. Newly synthesized collagen is less heat stable than
mature collagen because collagen continues forming more cross-links with time. Younger,
newer collagen contracts at lower temperature than mature collagen. Collagen with higher
amino acid content is more heat stable than collagen with lower amino acid content.
However, there is a very narrow zone of temperature at which collagen will shrink without
destroying collagen fibrils. As the temperature is raised, but within this narrow range, the
percentage of collagen shrinkage increases. The thermal properties of collagen vary with both
age and environmental conditions.14–16 Mammalian collagen, including human skin tissue,
shrinks at 61°C to 63°C. The degree of collagen shrinkage also depends on the mechanical
properties of the surrounding tissue. The tensile strength of ‘shrinkage’ collagen is lowered
and shows ‘rubber-like elasticity’. As the temperature keeps rising, more cross-links are
disrupted. If the temperatures exceeds the threshold for denaturation, collagen denaturation
will occur. Thermal coagulation, the visible thermal-induced collagen changes seen on light
microscopy, primarily results from thermal denaturation of structural proteins.
At temperatures greater than 58°C, the thermally coagulated collagen reveals histologic
evidence of hyalinization. This hyalinization of collagen indicates the merger of unraveled
swollen collagen fibrils. Partial loss or complete loss of native birefringence of thermally
coagulated collagen may result from intramolecular and intermolecular bond disruption.
Changes in birefringence of collagen have been consistently reportedly to occur at between 70°
C and 75°C.17 It is this damage to dermal collagen that leads to a wound-healing reaction.
This reaction, seen after many of the techniques discussed in this book, leads to removal of
damaged elastotic material and an increase in new collagen formation. The result is younger,
healthier appearing skin.
REFERENCES
1 Elomaa O, Kangas M, Sahlberg C, Tuukkanen J, et al. Cloning of a novel bacteria-
binding receptor structurally related to scavenger receptors and expressed in a subset of
macrophages. Cell 1995;80:603–9.
2 Shaw LM, Olsen BR. FACIT collagens: diverse molecular bridges in extracellular
matrices. Trends Biochem Sci 1991;16:191–4.
3 Lohi J, Korhonene M, Leivo I, Kangas L, et al. Expression of type IV collagen α1(IV)–α6
(IV) polypeptides in normal and developing human kidney and in renal cell carcinomas
and oncocytomas. Int J Cancer 1997;72:43–9.
4 Stenn KS, Madri JA, Roll FJ, et al. Migrating epidermis produces AB2 collagen and
requires continual collagen synthesis for movement. Nature 1979;277:229–32.
5 Chu M-L, Mann K, Dentzmann R, et al. Characterization of three constituent chains of
collagen type VI by peptide sequences and cDNA clones. Eur J Biochem 1987;168:
309–17.
6 Burgeson RE. Type VII collagen, anchoring fibrils, and epidermolysis bullosa. J Invest
Dermatol 1993;101:252–5.
7 Christiano AM, Greenspan DA, Lee S, et al. Cloning of human type VII collagen: complete
primary sequence of the α1(VII) chain and identification of intragenic polymorphism. J
Biol Chem 1994;269:20256–62.
8 Berg RA. Determination of 3- and 4-hydroxyproline. Methods Enzymol 1982;82:372–98.
9 Barnes MJ, Kodicek E. Biological hydroxylation and ascorbic acid with special regard to
collagen metabolism. Vitam Horm 1972;30:1–43.
10 Olsen BR, Prockop DJ. Ferritin conjugated antibodies used for labeling organelles
involved in the cellular synthesis and transport of procollagen. Proc Natl Acad Sci USA
1974;71:2033–7.
11 Prockop DJ, Tuderman L. Post-translational enzymes in the biosynthesis of collagen:
extracellular enzymes. Methods Enzymol 1982;82:305–25.
12 Colige A, Li SW, Sieron AL, et al. cDNA cloning and expression of bovine procollagen I N-
proteinase: a new member of the superfamily of zinc-metalloproteinase with binding sites
for cells and other matrix components. Proc Natl Acad Sci USA 1997;94:2374–9.
13 Mosler E, Foldhard W, Knorzer W, et al. Stress-induced molecular arrangement in tendon
collagen. J Mol Biol 1985;182:589–96.
14 Allain JC, Le Lous M, Cohen-Solal L, et al. Isometric tensions developed during the
hydrothermal swelling of rat skin. Connect Tissue Res 1980;7:127–33.
15 Verzar F, Nagy IZ. Electronmicroscopic analysis of thermal collagen denaturation in rat
tail tendons. Gerontologia 1970;16:77–82.
16 Shaw EL, Gasset AR. Thermokeratoplasty (TKP) temperature profile. Invest Ophthalmol
1974;13:181–6.
17 Thomsen S. Pathologic analysis of photo thermal and photomechanical effects of laser
tissue interactions. Photochem Photobiol 1991;53:825–35.
2
CUTANEOUS WOUND HEALING
KEY POINTS
(1) M and extracellular Matrix deposition lead to fibroplasia, the cellular aspects of new
collagen formation
(2) Type III collagen deposited at the beginning of wound healing is replaced by Type I
collagen which leads to increased tensile strength
(3) The stages of wound healing, seen with the various types of ablative and non-
ablative resurfacing, include fibroplasia with new collagen formation, matrix
formation, neovasculariztion, re-epithelialization, and wound contraction
(4) A moist laser resurfaced wound will tend to heal more quickly than a dry wound
BACKGROUND
The process of cutaneous wound healing is an integration of dynamic interactive phenomena
that begin with tissue injury. Recent advances in cellular and molecular biology have greatly
expanded our understanding of the biologic processes involved in wound healing. Tissue
response to injury has been divided into three overlapping phases: an inflammatory phase, a
proliferative phase, and a maturation phase. These responses occur in the healing of any
wound, including those seen after ablative and non-ablative resurfacing. (Figures 2.1–2.3).
INFLAMMATORY PHASE
The inflammatory phase of wound healing is composed of both a vascular and an
inflammatory response. The characteristic inflammatory response lasts between three and
ten days.1 Tissue injury usually causes blood vessel disruption with an initial period of
vasoconstriction followed by vasodilatation. Disruption of vessel walls exposes fibrillar
collagen. This injury leads to platelet aggregation and induction of the blood coagulation
cascade with resultant clot formation.1 In addition to hemostasis, bradykinin generated from
the intrinsic coagulation pathway via Hageman factor, triggers both classical and alternative
complement cascades. Complement-derived anaphylatoxins, C3a and C5a, increase
vasopermeability directly and indirectly via the release of numerous vasoactive mediators,
such as histamine and leukotriene C4 and D4, from mast cells. Inflammatory leukocytes are
also recruited to the injured site and stimulate the release of granule constituents and
biologically active oxygen products.2 Activated platelets not only facilitate the formation of a
hemostatic plug but also secrete various cytokines which promote new tissue formation and
inflammatory cell migration. Despite this, in the absence of hemorrhage, platelets are not
essential to wound healing.
Figure 2.1. Normal human skin
Figure 2.2. Skin after wounding
Figure 2.3. Healed skin
Leukocytes begin to migrate through vessel walls after tissue injury. Chemotactic factors
upregulate the expression of leukocyte surface complexes which facilitate diapedesis between
adjacent endothelial cells. Neutrophils infiltrate the injured area in the first three days after
wounding. During this phase, they phagocytize bacteria and other foreign bodies. If a
resurfaced wound becomes infected, bacterial proteins, other substances and/or other foreign
bodies continuously activate the alternative complement pathway which recruits additional
neutrophils to the site of injury. Neutrophil migration to the wound site ceases when the
wound is clean. In case of wound contamination, continuing neutrophil infiltration with an
associated persistent acute inflammatory phase will interfere with the subsequent phases of
wound healing.
Monocytes enter the wound site at the same time as neutrophils but exceed the population
of neutrophils by the third to fifth day after wounding. Monocytes undergo metamorphosis
into inflammatory or reparative macrophages by their interaction with extracellular matrix
proteins.2 Macrophages are armed for phagocytosis and digestion of pathogenic organisms
and scavenge tissue debris including effete neutrophils. In addition, macrophages play an
essential role in the transition between wound inflammation and wound repair. Macrophages
CUTANEOUS WOUND HEALING 9
secrete various kinds of growth factors, cytokines, vasoactive mediators and enzymes. These
products facilitate the recruitment of additional inflammatory cells and aid the macrophage in
tissue debridement and decontamination. These growth factors, and chemotactic factors,
enhance macrophage survival and are chemoattractive for, and mitogenic to, fibroblasts.
These wound macrophages, with their secreted multiple cytokines and growth factors such as
platelet-derived growth factor (PDGF) and vascular endothelial growth factor, are necessary
for the initiation and propagation of new tissue formation. Macrophage-depleted animals have
defective wound repair mechanisms.3 Thus, macrophages appear to play a pivotal role in the
transition between wound inflammation and granulation tissue formation. These processes
all take place in resurfaced wounds. However, a greater degree of wounding (as seen with
ablative procedures) will lead to a greater degree of inflammatory cell infiltration. Less
inflammatory cell infiltration would be expected in non-ablative procedures where there is a
lesser degree of wounding.
PROLIFERATIVE PHASE
This stage of wound healing is composed of fibroplasia, matrix formation, neovascularization,
re-epithelialization, and wound contraction.
Re-epithelialization, seen after ablative procedures, begins within 24 hours after tissue
injury. Re-epithelialization is an important part of the wound healing process which decreases
morbidity and mortality from skin injury. Undamaged epidermal cells, from the free edge of
adjacent skin, as well as the epithelium of hair follicles and other adnexal structures within
the wound, migrate over the denuded surface. Before migration, marked phenotypic alteration
of epidermal cells occurs. This allows for cell mobility. This epidermal cell metamorphosis
includes retraction of intracellular tonofilaments, formation of peripheral cytoplasmic actin
filaments, and dissolution of intercellular desmosomes and hemidesmosomes.4 This
phenotypic change provides the cell mobility and motor apparatus necessary for motility. The
epidermal cells at the wound edge lose their apical-basal polarity and extend pseudopodia
from their free basolateral side into the wound. The exact pattern of migration is unknown.
Possibilities include: single-cell migration across the wound surface; a leapfrog fashion
whereby cells above and behind the leading cell stream over the latter to attach to the wound
bed; or a tractor tread model in which integrin receptors are synthesized on the epithelial cell
surface and bind to fibronectin in the wound bed.5–7 The expression of integrin receptors on
epidermal cells allows them to interact with a variety of extracellular-matrix proteins. The
path of epidermal migration appears to be determined by the array of integrins that the
migrating epidermal cells express on their cell membranes.8–10 After migration begins, cell
proliferation at the original wound margin occurs in order to provide the additional cells for
migration. Epidermal proliferation is maximal at 24 to 72 hours after wounding. Multiple
inter-related stimuli are responsible for epidermal migration, proliferation, and
differentiation. Epidermal growth factor, transforming growth factor, and keratinocyte growth
factor are possible leading stimuli.11 The local release of epidermal growth factor (EGF) serves
as a mitogen for epithelium and stimulates other aspects of cutaneous wound repair. The
‘free edge effect’ caused by the absence of neighboring cells at the damaged wound margin
and contact inhibition between neighboring cells signals an epidermal cell phenotypic change
that in turn induces epidermal migration and proliferation.
The wound bed also participates in re-epithelialization. The epidermal cells glide over a
provisional matrix consisting of fibrin, fibronectin and type V collagen. Wound keratinocytes,
in contrast with normal epidermal cells, express functionally active integrin receptors for
fibronectin.12 Thus, wound keratinocytes may pave the wound surface with a fibronectin-rich
matrix and express fibronectin cell surface receptors which facilitate their lateral movement.13
Epidermal movement through tissue depends on epidermal production of collagenase and
plasminogen activator, which enzymatically activates the collagenase as well as plasmin, a

protease of broad specificity.14 These enzymes allow the migrating epidermal cells to dissect
between viable and non-viable tissue. Reformation of a laser resurfaced damaged epidermal
basement membrane occurs in stages. Basement membrane zone component, also
synthesized by epidermal cells, blocks the contact between epithelial cells and matrix
components and may provide part of the signal that induces keratinocytes to cease migration
and proliferation. With this, differentiation begins again.
The deposition of two basement membrane proteins, laminin and type IV collagen, begins at
the original wound margin and progresses inward in a zipper-like fashion that interlocks the
new epidermis to the neodermis. Once re-epithelialization is complete, epidermal cells revert
to their normal phenotype, firmly attaching to the basement membrane through
hemidesmosomes. The plane, and speed, of epidermal migration is determined in part by the
water content of the wound bed. Thus a moist laser wound will tend to heal more quickly
than a dry wound.
Granulation tissue begins to form two to four days after injury and is maintained until re-
epithelialization has occurred. Numerous newly formed capillaries endow the new stroma with
its granular appearance. The granulation tissue consists of macrophages, fibroblasts,
inflammatory cells and neovasculature embedded in a loose matrix of glycoprotein,
glycosaminoglycans, collagen and fibronectin. Continual generation of growth factors from
epidermal cells, fibroblasts, endothelial cells and macrophages stimulate fibroplasia,
angiogenesis and extracellular matrix formation. Macrophage-derived and platelet-derived
factors stimulate fibroblasts to proliferate, express appropriate integrin receptors, migrate
into the wound space, and deposit a connective tissue matrix. Fibroblasts are the most
important cells in the formation of granulation tissue. Fibroblasts generate additional
cytokines and produce collagen, elastin, fibronectin, glycosaminoglycans, and proteases such
as collagenase. The connective tissue matrix formed by the fibroblasts provides a substrate on
which macrophages, new blood vessels, and fibroblasts themselves can migrate. Connective
tissue matrix provides fibronectin and collagen as a scaffold for contact guidance and
hyaluronic acid for mobility in a low impedance setting.15 Fibronectin functions not only as a
chemoattractant but also, when cross-linked to fibrin, as an adhesive scaffolding for
fibroblast migration and collagen deposition. The fibroblasts are responsible for the synthesis,
deposition and remodeling of the extracellular matrix. This extracellular matrix can have a
positive or negative effect on the ability of fibroblasts to synthesize, deposit, remodel, and
generally interact with the extracellular matrix.16,17 A variety of fibroblast-derived enzymes
such as plasminogen activator, collagenase, gelatinase A, and stromelysin are important in cell
migration, tissue debridement and remodeling. This extracellular matrix, produced by
fibroblasts, is gradually replaced with a collagenous matrix,17,18 perhaps through the action
of transforming growth factor β1.17 These and other cytokines, including an oxygen
dependent macrophage angiogenesis factor, and fibronectin stimulate capillary bud formation
from nearby vessels.19 Blood vessels carry nutrients and oxygen to maintain cell metabolism.
Glycosaminoglycans help maintain wound hydration and promote cellular migration and
proliferation.
Fibroblastic proliferation and extracellular matrix deposition lead to fibroplasia, the cellular
aspect of new collagen formation. These processes are seen with both ablative and non-
ablative techniques. Numerous growth and chemotactic factors stimulate wound granulation
tissue. During granulation tissue formation, fibroblasts undergo a series of morphological
changes to assume a myofibroblast phenotype. The appearance of myofibroblasts corresponds
to the commencement of connective-tissue compaction and wound contraction. These cells
become increasingly spindle shaped and form large intracytoplasmic actin bundles to allow
contractile and migratory capabilities. As fibroblasts migrate into the wound space they
deposit a loose extracellular matrix initially composed of great quantities of fibronectin.20
Collagen fibers, produced by fibroblasts, are laid down on a frame-work of fibronectin. Once a
collagen-rich matrix is deposited, fibroblasts cease collagen production and the fibroblast-rich
granulation tissue is replaced by a relatively acellular scar. Cells in the wound undergo
apoptosis21 triggered by unknown signals. Transforming growth factor-β increases type I and
III collagen production by fibroblasts cultured in a collagen-poor environment.22,23
Transforming growth factor-β can both stimulate fibroblasts to deposit fibronectin matrix23
and upregulate the integrin receptors that bind fibronectin.24 Fibroblasts can use fibronectin
matrix for movement through the wound because fibronectin has the capacity to bind
connective tissue cells and other extracellular matrix material. These cells can also rapidly
adhere to and detach from fibronectin.25 Early granulation tissue is composed largely of type
III collagen, whereas collagen type I predominates in a mature scar or normal skin.
Fibroblasts link to the extracellular fibronectin matrix, through the integrin fibronectin
receptor, and to each other through direct cell–cell connections. It has been hypothesized that
the force of wound contraction is probably generated by actin bundles in the fibroblasts.
These actin bundles transmit contractile forces throughout the connective tissue matrix
through cell–cell and cell–stroma links. Cross-links between the individual collagen bundles
also adds linkage to the forces of traction. These forces can account for a 39–62% (mean 45%)
reduction in the wound surface area of a cutaneous defect.26 Fibronexus, colinear assemblage
of intracytoplasmic 5-nm microfilaments, and extracellular fibroblastic matrix fibrils have all
been postulated to be involved in fibroblast contraction during wound healing. It is this
contraction that may explain the tightening reported after CO2 laser resurfacing. Fibronectin
and types I and II procollagen are localized to the extracellular fibers of the fibronexus.27 Most
of the extracellular fibronectin fibrils are associated with intracellular actin microfilaments.
Fibronexus may, in fact, be a major cohesive complex that transmits the collective forces
generated by the contraction of actin microfilaments and thereby affects wound contraction.28
PDGF may provide the signal for wound contraction,29,30 whereas gamma-interferon may
provide both anti-proliferative and anti-synthetic factors.31,32
The formation of new blood vessels is essential in order to supply oxygen and nutrients to
the healing wound. Angiogenesis is a complex process that relies on alteration of endothelial
phenotype, migration, and mitogenic stimulation of endothelial cells. In addition, an
appropriate extracellular matrix is required for movement and for capillary stabilization. After
vascular disruption, endothelial cells migrate into the perivascular space by projecting
pseudopodia through a disrupted basement membrane. Migrating endothelial cells form new
blood vessels whereas endothelial cells remaining in the parent vessel begin to proliferate to
provide additional cells for migration into the wound space. Low oxygen tension,
elevated lactic acid, and multiple angiogenesis-related factors are involved in angiogenesis.
Hypoxic conditions stimulate: (i) macrophages to produce acidic and basic fibroblast growth
factor; and (ii) endothelial cells to release vascular endothelial cell growth factor. Activated
epidermal cells of the wound also secrete large quantities of vascular endothelial cell growth
factors.33 Basic fibroblast growth factor may set the stage for angiogenesis during the first
three days of wound repair, whereas vascular endothelial cell growth factor is critical for
angiogenesis during the formation of granulation tissue on days four through seven.34
Macrophage angiogenesis factors stimulate endothelial cells to release plasminogen activator
and procollagenase, leading to subsequent plasmin and collagenase production. These
proteases digest vascular basement membrane, allowing endothelial cell migration. There is
an increase in fibronectin surrounding the new vasculature of the healing wound.
Proliferating microvascular endothelial cells adjacent to and within wounds transiently
deposit increased amounts of fibronectin within the vessel wall.35 This perivascular
fibronectin may act as a contact guidance system for movement of endothelial cells into the
wound. The expression of fibronectin receptors by endothelial cells is also required for this
movement. With the now increasing oxygen tension, secretion of angiogenesis factors is now
downregulated, neoangiogenesis begins to cease and the new blood vessels disintegrate as a
result of apoptosis. This programmed cell death controls the population size of wound cells. If
this neoangiogenesis does not cease and the new blood vessels persist, hypertrophic scarring
may be seen after resurfacing procedures. The same mechanism could apply to non-ablative
procedures.
MATURATION PHASE
Wound remodeling begins at the onset of granulation tissue formation and continues over
many months. This explains why patients often do not see clinical improvement for months
after both ablative and non-ablative procedures. The extracellular matrix is deposited first at
the wound margin, concurrent with granulation tissue development, and then deposited more
centrally later on. At any given time, the more mature extracellular matrix at the wound margin
of an open laser wound will have different characteristics from those of the extracellular
matrix initially situated centrally. This maturation phase is characterized clinically by
gradual increases in the tensile strength of the scar, decreases in scar bulk and subsequent
paling of the scar. The tensile strength of a mature scar will be approximately 70% of that of
normal skin. The composition and structure of the extracellular matrix gradually and
continuously changes.
Fibronectin gradually disappears as mature collagen is laid down. As mentioned earlier,
Type III collagen deposited at the beginning of wound healing is replaced by Type I collagen
which leads to increased tensile strength. Hyaluronic acid is replaced by more resilient
proteoglycans. In addition to progressive intermolecular cross-linking of collagen, which
provides much of the increase in wound strength, there is progressive digestion of old and
abnormal collagen fibers while preserving those that are healthy. A balance of collagen
deposition and degradation regulated under the influence of growth factors, cytokines, and
proteolytic enzymes continues in a steady state. The matrix metalloproteinases, enzymes
secreted by macrophages, epidermal cells, endothelial cells, and fibroblasts control the
degradation of collagen. The combinations of matrix metalloproteinases and tissue inhibitors
of metalloproteinases are central in the wound healing process. With continued maturation,
neovasculature begins to regress, leaving a final scar that is relatively more avascular. As the
scar matures further, the concentration of proteoglycans declines and water is reabsorbed.1
Water resorption ultimately contributes to the observed histologic compaction of collagen
fibers.
FACTORS AFFECTING WOUND HEALING

The wound environment, whether because of substances contained within the actual wound
tissue or through more distant systemic factors, affects the normal progression of healing.
Local Factors
Micro-organisms
The presence of clinical signs of inflammation, a change in the color of the wound, or a newly
noted increase in pain are all possible points of evidence for a clinical wound infection. In
addition to local evidence of wound infection, fever and an elevation of white blood cell count
with predominance of neutrophils are systemic signs of infection. Bacterial wound infection is
the most common local cause for prolonged healing. Following ablative laser resurfacing,
Staphylococcus aureus and group A streptococci are the most common observed pathogens;36
gram-negative organisms and other less common gram-positive organisms may also
occasionally be encountered. The presence of pruritus and satellite pustules around the
wound should suggest an infection caused by Candida albicans. Such infections may also
impair wound healing. Infections impede wound healing by activation of the alternate
complement pathway. This prolongs the inflammatory phase of wound healing, delaying re-
epithelialization and granulation tissue formation. Infectious agents compete for the oxygen
and nutrients within the wound with resultant lactic acid production in this hypoxic
environment. Reduction in pH of the wound environment stimulates the release of damaging
proteolytic enzymes from inflammatory cells.37 A variety of infections, whether bacterial, yeast
or viral, may lead to scarring after laser resurfacing. Bacterial and yeast infections have yet to
be reported following treatment with epidermal sparing non-ablative approaches.
Hematoma
Hematoma formation within any wound serves as a nidus for infection. At the same time,
hematomas mechanically disrupt the wound healing. Expanding hematomas can increase
wound edge tension leading to tissue ischemia and dehiscence. This is not a common event
following ablative or non-ablative resurfacing.
Foreign Body Reaction

Foreign bodies provide a surface for alternate complement pathway activation and the
generation of prolonged inflammation and tissue destruction. Similar to the situation seen
with infection, oxygen tension and pH is lower than that seen in normal tissue. This condition
instigates cell lysis and prevents normal wound healing. This problem has not been reported
following either ablative or non-ablative procedures.
Tissue Ischemia and Eschar Formation—The Dry Wound

Dry wounds impede wound healing both mechanically and physiologically. An eschar or crust
blocks the contact between epithelial cell and the extracellular matrix, which impedes
epithelial migration. Water content of the wound bed influences cell migration; a moist wound
heals more quickly. As mentioned earlier, ablative resurfaced wounds must be kept moist for
appropriate healing. However, large amounts of moist necrotic tissue in a macerated wound
may also impair wound healing.
Oxygen Tension
Oxygen is important for wound healing. Many local and systemic factors that limit tissue
blood perfusion result in inadequate oxygenation. Each phase of wound healing requires
various levels of oxygenation. Oxygen tension increases along with the progression of wound
healing. Conversely, bacterial infections and foreign particles impede the healing process
partly by prolonging the hypoxic phase.
Cigarette Smoking
Cigarette smoking delays wound healing by impairing both perfusion and oxygenation.38
Carboxyhemoglobin, formed by carbon monoxide in the gas phase of cigarette smoke,
increases the affinity of the remaining hemoglobin for oxygen. Thus, carried oxygen is not
released effectively to tissue.39 Nicotine itself is a potent vasoconstric tor leading to
microvascular occlusion and tissue ischemia. Cigarette smoking has been associated with
poor healing after surgery.38–40 One might expect this to be a bigger issue with ablative
compared with non-ablative procedures. However, no study has definitively documented a

negative laser healing effect from cigarette smoking.
Systemic Factors
Vascular Insufficiency and Impaired Oxygenation

Arterial insufficiency is seen in the setting of atherosclerosis, chronic pulmonary disease,
congestive heart failure, diabetes and as a sequela to vasculitis. Tissue ischemia in the region
of arterial insufficiency impairs wound healing. Tissue oxygen tension depends on both blood
perfusion and hemoglobin content in the blood. Respiratory disease in itself may not impair
wound healing if the tissue is well vascularized. Anemia will not inhibit wound healing as long
as there is no persistent hypovolemia.36 Vascular insufficiency does not appear to be a
significant problem in the healing process following laser resurfacing.
Aging
Aging diminishes all phases of wound healing. With aging, cell proliferation and metabolic
activities are slowed. Physical barriers to injury are reduced due to dry and brittle skin.
Macrophage function declines and the number of Langerhans cells, keratinocytes and
melanocytes decrease with aging. Repair of older skin is characterized by decreased immune
responsiveness, slow epithelialization, reduced collagen synthesis, and degradation and
delayed angiogenesis compared with that of younger skin. Wound dehiscence is three times
more frequent in patients more than 60 years old. The relatively greater vascular supply on
the face may reduce these problems when older individuals undergo laser resurfacing.
Coagulation Disorders
Deficiencies of clotting factors predispose to hematoma formation and produce a faulty clot
associated with structurally poor or delayed fibrin matrix formation. Platelet deficiency or
functional alteration results in delayed inflammatory and proliferative phases because
platelets are involved in the formation of the fibrin matrix and the release of chemotactic and
growth factors. Although ablative thermal lasers may lead to less post-laser bleeding than
shorter pulsed Erbium:YAG lasers, there still may be associated healing problems with these
two lasers during the inflammatory and proliferative phases in patients with coagulative
disorders.
Immunodeficiency
The immunologic response is required during wound healing, especially during the
inflammatory phase. Conditions that impair immunologic response include old
age, malnutrition, diabetes, connective tissue disorders and primary immunologic deficiency
states. Complement or immunoglobulin deficiency may also result in altered inflammatory
response and opsonization. Opsonization is a process that aids in the recognition and
ingestion of bacteria and foreign particles by leukocytes and macrophages. Disorders of
phagocytosis impair the ability to eliminate intracellular bacterial colonization, necrotic debris
and foreign material. Deficient leukocyte chemotaxis will cause problems during the early
inflammatory phases of healing and may also increase the rate of infection following ablative
laser resurfacing.
Systemic Medications
Systemic corticosteroids directly suppress many aspects of wound healing. They suppress
inflammatory cell migration and phagocytosis, resulting in inflammatory response reduction.
An anti-mitotic effect on keratinocytes and fibroblasts inhibits re-epithelialization and
neodermis formation. They also decrease protein and collagen synthesis and promotes
collagen catabolism. Nutrients and oxygen supplementation are also reduced due to
corticosteroid-induced vasoconstriction. A bleeding wound may provide an excellent culture
medium for micro-organisms. Aspirin and salicylates induce an irreversible inhibition of
platelets lasting up to ten days. Warfarin impairs fibrin hemostasis by reducing the activity of
vitamin K-dependent clotting factors and anticoagulant proteins C and S. Heparin also
interferes with hemostasis by inactivation of thrombin and factors IX, X and XI. Alcohol
interferes with platelet function and decreases platelet survival.
The administration of systemic isotretinoin within six months before dermabrasion has
been associated with abnormal scar formation.41 The spontaneous appearance of exuberant
granulation tissue at acne sites has been reported during systemic isotretinoin therapy.
Retinoid-induced inhibition of collagenase may be responsible for these effects.36 Retinoids
may also impair the bacterial killing ability of neutrophils.36 Penicillamine decreases levels of
copper and zinc which are important cofactors for healing. Phenytoin reduces collagenase
formation which may modify dermal remodeling. Before either ablative or non-ablative
procedures, it is important to determine what medications are being taken by prospective
patients.
Endocrine Abnormalities
Diabetics have impaired wound healing. Atheroslerosis and diabetic angiopathy increase the
risk of injury from pressure and trauma.42,43 Chronic hyperglycemia reduces the ability to
resist infection by impairing leukocyte chemotaxis and phagocytosis. The reduction or
absence of insulin impairs fibroblast growth factor by suppressing collagen synthesis and
deposition.44 Diabetics have a five times increased risk of infection in a clean incisional
wound than non-diabetics.45 However, diabetics appear to have no problems with re-
epithelializatiion following laser resurfacing. Parathyroid hormone and calcitonin may have an
effect on keratinocyte proliferation and differentiation by regulating plasma calcium levels.
Patients with hypothyroid-induced myxedema may have impaired wound healing.46 Because
patients with acromegaly have an increased incidence of keloid formation, growth hormone
may also play a role in wound healing.
The wound healing process is complicated and multifaceted. Any interference with the
cascade of wound healing processes may affect the response to, and healing after, ablative
and non-ablative resurfacing.
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2 Clark RAF. Basics of cutaneous wound repair. J Dermatol Surg Oncol 1993;19:693–706.
3 Leibovich SJ, Ross R. The role of the macrophage in wound repair. Am J Pathol 1975;78:
71–100.
4 Gabbiani G, Chaponnier C, Huttner I. Cytoplasmic filaments and gap junctions in
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5 Kanzler MH, Gorsulowsky DC, Swanson NA. Basic mechanisms in the healing cutaneous
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fibronectin receptor function in vitro. J Invest Dermatol 1985;85:304–8.
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8 King LE. What does epidermal growth factor do and how does it do it? J Invest Dermatol
1985;84:165–7.
9 Fourtanier AY, Courty J, Muller E, et al. Eye-derived growth factor isolated from bovine
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10 Brown GL, Curtsinger L 3rd, Brightwell JR, et al. Enhancement of epidermal regeneration
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11 Werner S, Smola H, Liao X, et al. The function of KGF in morphogenesis of epithelium
and re-epithelialization of wounds. Science 1994;266:819–22.
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and their expression during cell culture. J Cell Biol 1987;105:3097–104.
13 Clark RAF. Fibronectin matrix deposition and fibronectin receptor expression in healing
and normal skin. J Invest Dermatol 1990;94:128S-34S.
14 Grondahl-Hansen J, Lund LR, Ralfkiaer E, Ottevanger V, Dano K. Urokinase-and
tissuetype plasminogen activators in keratinocytes during wound re-epithelialization in
vivo. J Invest Dermatol 1988;90:790–5.
15 Nathan C, Sporn M. Cytokines in context. J Cell Biol 1991;113:981–6.
16 Xu J, Clark RAF. Extracellular matrix alters PDGF regulation of fibroblast integrins. J
Cell Biol 1996;132:239–49.
17 Clark RAF, Nielsen LD, Welch MP, McPherson JM. Collagen matrices attenuate the
collagen-synthetic response of cultured fibroblasts to TGF-β. J Cell Sci 1995;108:
1251–61.
18 Welch MP, Odland GF, Clark RAF. Temporal relationships of F-actin bundle formation,
collagen and fibronectin matrix assembly, and fibronectin receptor expression to wound
contraction. J Cell Biol 1990;110:133–45.
19 Folkman J, Klagsbrun M. Angiogenetic factors. Science 1987;235:442–7.
20 Grinnell F, Billingham RE, Burgess L. Distribution of fibronectin during wound healing in
vivo. J Invest Dermatol 1981;76:181–9.
21 Desmouliere A, Redard M, Dardy I, Gabbiani G. Apoptosis mediates the decrease in
cellularity during the transition between granulation tissue and scar. Am J Pathol 1995;
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22 Roberts AB, Sporn MB, Assoian RK, et al. Transforming growth factor type β:Rapid
induction of fibrosis and angiogenesis in vivo and stimulation of collagen formation in
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23 Ignotz RA, Massague J. Transforming growth factor-β stimulates the expression of
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Chem 1986;261:4337–45.
24 Heino J, Ignotz RA, Hemler ME, et al. Regulation of cell adhesion receptors by transform
ing growth factor-β. J Biol Chem 1989;264:380–8.
25 Hsieh P, Chen LB. Behavior of cells seeded in isolated fibronectin matrices. J Cell Biol
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26 Lawrence CM, Comaish JS, Dahl MGC. Excision of skin tumours without wound closure.
Br J Dermatol 1986;115:563–71.
27 Singer II. The fibronexus: A transmembrane association of fibronectin-containing fibers
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28 Singer II, Kawka DW, Kazazis DM, Clark RAF. In vivo codistribution of fibronectin and
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29 Clark RAF, Folkvord JM, Hart CE, et al. Platelet isoforms of platelet-derived growth factor
stimulate fibroblasts to contract collagen matrices. J Clin Invest 1989;84:1036–40.
30 Rappolee DA, Mark D, Banda MJ, Werb Z. Wound macrophages express TGF-α and other
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monokine responsible for inhibition of fibroblast collagen production and late but not
early fibroblast proliferation. J Exp Med 1985;162:516–27.
32 Granstein RD, Murphy GF, Margolis RJ, et al. Gamma-interferon inhibits collagen
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33 Brown LF, Yeo KT, Berse B, et al. Expression of vascular permeability factor (vascular
endothelial growth factor) by epidermal keratinocytes during wound healing. J Exp Med
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34 Nissen NN, Polverini PJ, Koch AE, et al. Vascular endothelial growth factor mediates
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39 Riefkohl R, Wolfe JA, Cox EB, et al. Association between cutaneous occlusive vascular
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26:885–902.
3
CARBON DIOXIDE LASER RESURFACING
KEY POINTS
(1) Newer carbon dioxide lasers, by combining high fluences and short pulse durations,
are capable of precise tissue vaporization with minimal residual thermal damage
(2) Periorbital rhytides respond most dramatically after laser resurfacing
(3) When the carbon dioxide laser interacts with skin, its laser induced heat dissociates
collagen’s interpeptide bonds and collagen contraction occurs
(4) An ablation plateau occurs at 200–250 μm
(5) Residual thermal damage is increased by longer pulse durations, higher enerpes,
and number of laser passes
(6) Long-term biopsies (up to 4 years) show thickened dermal collagen and improvement
of solar elastosis
BACKGROUND
Carbon dioxide (CO2) lasers produce laser irradiation at 10,600 nm, in the far infrared portion
of the electromagnetic spectrum. These lasers destroy tissue by rapidly heating and
vaporizing tissue water (Figure 3.1). The CO2 laser has been used extensively in dermatologic
surgery over the past 30 years because of its ability to efficiently vaporize and cut tissue.
Early models of the CO2 laser were available only in the continuous, non-pulsed, mode;
clinical results were unpredictable. These older lasers produced a zone of thermal necrosis
measuring 0.2 to 1 mm in thickness, resulting from tissue temperatures reaching 120° to
200°C or more during ablation, with subsequent char formation. Non-specific heat diffusion
into surrounding skin resulted in unwanted thermal necrosis and unacceptable rates of
scarring and pigmentary change.
In order to achieve well-controlled tissue vaporization, it was necessary to develop lasers
with both high peak powers to maximize tissue vaporization, and short pulse durations to
minimize thermal injury (Figure 3.2). Investigators responded by developing pulsed CO2
lasers.1–7 The first significant modification of older continuous wave CO2 lasers involved
electronically shuttering a continuous beam of laser irradiation to produce ‘pulses’ of 0.1–1
seconds in duration, with consistent power.8
The next generation of CO2 lasers brought the development of ‘superpulsed’ carbon dioxide
systems, which could attain peak powers between two and ten times higher, and pulse
durations 10–100 times shorter, than conventional continuous wave models. Rapid pulse
repetition rates of 200–1000 pulses per second were used to achieve average powers
comparable to continuous wave lasers. Although the zone of thermally damaged tissue in
treated animal models was limited, there were still significant rates of scarring.9–12
CARBON DIOXIDE LASER RESURFACING 19
Figure 3.1. Water absorption curve of 10,600 nm carbon dioxide laser
Figure 3.2. Ablative and thermal effect of carbon dioxide laser
In the mid-1990s, in response to the theory of selective photothermolysis, technical

advances brought about two major different competing technologies. Both provided a CO2
wavelength (10,600 nm) absorbed by the targeted water chromophore, emitted sufficient
energy (vaporization threshold of 5 J/cm2) to damage the targeted tissue, and delivered this
energy at a rate faster than the thermal relaxation time of tissue (under 1 ms). Both
technologies shared the theoretical ideals of providing precise tissue vaporization with
minimal residual thermal damage. One technology, of which the Ultrapulse 5000 laser is the
prototype, represents high energy pulsed technology using single pulses with peak energies
up to 500 mJ, delivered within pulse durations of 600 μs to 1 ms. When used with a
collimated stand-alone 3 mm spot size, energy fluences of 5–7 J/cm2 can be achieved. A
computerized pattern generator (CPG), attached to the laser delivery system, can rapidly and
precisely place 2.25-mm spots in any of several patterns while maintaining appropriate
ablation parameters. Newer versions of this model now deliver similar energies through an
even smaller spot size. A competing second type of technology uses a flashscanner that is
used in conjunction with a lower power CO2 laser in the continuous mode. An example of this
technology, the SilkTouch/FeatherTouch laser system, achieves high peak powers by focusing
the laser beam to a small spot size, and rapidly scans the focused beam over a predetermined
geometric pattern, exposing the individual tissue sites for less than 1 ms.
Cutaneous CO2 laser resurfacing, as currently performed, has been shown to be highly
effective in the treatment of photodamaged skin. In addition to superficial ablation, there is a
‘tissue tightening’ effect following use of these lasers. This effect is thought to be related to
heat-induced collagen shrinkage which occurs maximally at 63°C.
CLINICAL STUDIES
Both pulsed and scanning CO2 laser systems overcome the limitations seen with older
continuous mode systems by limiting the laser-tissue interaction time; thermal damage is
reduced. By combining high fluences (energy/unit area) and short laser-tissue times
(UltraPulse laser) or by scanning a highly focused continuous mode beam (SilkTouch or
FeatherTouch laser), these systems are capable of precise tissue vaporization with minimal
residual thermal damage (approximately 150 μm after two to three passes).8 The clinical
studies summarized below evaluate the efficacy of these pulsed laser systems in treating
rhytides and scars. Other concepts, such as optimally treated anatomic sites, the role of
collagen contraction, end-points for CO2 laser resurfacing, and recommended pre-operative
treatments, are also presented.
Fitzpatrick et al.13
This study was among the first to evaluate clinical improvement in mild, moderate, and
severe perioral and periorbital wrinkles seen after pulsed carbon dioxide laser resurfacing.
In this study, multiple passes of confluent single pulses using a pulsed carbon dioxide laser
(UltraPulse 5000) were utilized with 10% overlap and a 3-mm collimated beam. Pulse energies
of 450 mJ were used for the first pass and subsequent passes were delivered at 450 mJ
(perioral) and 350 mJ (periorbital). Tissue was cleansed and debrided with normal saline
between passes.
Patients (73 females with perioral wrinkles, 38 females with periorbital wrinkles) were
evaluated post-operatively for up to 12 months (average follow-up of 89 days for perioral
wrinkles and 74 days for subjects with periorbital wrinkles).
Mild, moderate, and severe rhytides responded equally well, demonstrating an average
wrinkle reduction of 45–50% for both treatment areas. The authors noted the unexpected
finding of tightening of loose and folded skin and attributed it to heat-induced collagen
shrinkage.
Although this study did not include a multi-year follow-up period, the authors
demonstrated significant improvement in wrinkles in the perioral and periorbital regions of
the face after pulsed carbon dioxide laser resurfacing.
Lowe et al.14
Lowe et al. reported clinical observations for up to 6 months after skin resurfacing with the
UltraPulse carbon dioxide laser. Their study varied from the previous one in that they only
treated moderately or severely damaged skin, examined periorbital, perioral, forehead, and
cheek sites, and laser delivery took place with either the 3-mm collimated beam or in some
cases with the newly-introduced 2.25-mm spot size attached to a computerized scanner
(CPG).
A total of 100 subjects were treated with two to four passes (mean 2.7 passes). Initial
passes were 350–500 mJ; subsequent passes were 350–400 mJ. When the CPG was used, the
delivered energy was 150–300 mJ using a 2.25-mm spot size. Between each pass, the skin
was wiped firmly with a saline-soaked gauze. Color change and skin retraction were closely
observed during laser treatment.
Patients were subjectively evaluated for up to 6 months post-laser treatment. The authors
noted that some patients observed a relatively small response at the end of 1 month;
however, at 2, 3, and 6 months, significant improvement was noted. At 1 month post-laser
treatment, 68 patients were reported to have moderate improvement, five patients achieved
marked improvement, and the remaining 27 patients showed minimal improvement. By 2
months post-laser treatment, 20 of the 27 patients who at 1 month showed only minimal
improvement revealed moderate to marked improvement from baseline.
Lowe et al. concluded that this pulsed carbon dioxide laser was highly effective in the
treatment of photodamaged skin and rhytides. They also found the CPG scanner to be very
helpful in speedily treating large areas. They recommended pretreating all patients with broad
spectrum antibiotics and antiviral therapy. It should be noted that use of pre-treatment
antiviral agents, before extensive ablative facial laser resurfacing, is now considered standard
procedure. Use of pre-treatment antibiotics has been questioned by some, while advocated by
others.
Waldorf et al.4
This retrospective review evaluated the clinical results in 47 patients with fine to deep
glabellar, perioral, and periorbital rhytides after treatment with the SilkTouch laser.
The continuous wave low power SilkTouch laser was used with a mechanical scanner. The
scanner leads to rapid movement of the beam over the tissue by way of rotating mirrors. The
resultant delivered spiral scans ensure a less than 1-ms exposure duration, adhering to the
principles of selective photothermolysis and thermal relaxation time. One to three passes were
provided with a 3-mm spot size (energy 7.5 W, pulse duration 0.2 s) or a 6-mm spot size (18–
20 W). Between passes, the vaporized skin was removed with water-soaked gauze. The
clinical end-point for a given treated area was the disappearance of the wrinkle or the
appearance of a yellow hue representing the observed upper reticular dermis.
The authors graded improvement based on a 0–4 scale and demonstrated a mean
improvement score of 3.4 for periorbital wrinkles (85% improvement), 3.2 for perioral wrinkles
(80% improvement), and 2.7 for glabellar wrinkles (60% improvement). They concluded that
the greatest improvement was seen in the periorbital area and the least improvement was
seen in the glabellar area.
Lask et al.15
Lask et al. also conducted a clinical evaluation of facial rhytides after laser skin resurfacing
with the SilkTouch laser and scanning device. They used slightly lesser powers than reported
by Waldorf et al.4, treated variable facial cosmetic units including isolated nasolabial folds
with a mean number of 2.6 laser passes, and wiped with saline gauze between passes.
Clinical follow-up at 2 months revealed that the treatment of isolated nasolabial folds
showed insignificant improvement. Treated regional cosmetic units responded best. The
authors concluded that it takes more laser passes (three to four) to get significant
improvement of the perioral wrinkles, compared to the periorbital wrinkles (two passes).
Shim et al.16
Shim et al. also evaluated the SilkTouch laser. They studied scars due to acne, trauma,
varicella, and surgery in addition to periorbital, perioral, and glabellar rhytides for up to 1
year following treatment.
Twenty-three patients (12 evaluated for scars, 11 evaluated for rhytides) were treated with
one to three passes (6–8 W, 4-mm spot size or 16–18 W, 6-mm spot size) and the areas were
wiped with saline-soaked gauze between passes.
They found that patients with scars had a mean clinical improvement of 53% (mean follow-
up 3.3 months). Patients with rhytides demonstrated a mean clinical improvement of 70%
(mean follow-up 4.6 months). The authors concluded that although both scars and rhytides
demonstrated clinical improvement, rhytides demonstrated greater improvement than scars.
Skin biopsies were taken from nine of the patients with rhytides. The results of this portion
of the study are summarized later in this chapter.
Ross et al.17
In this study, a total of 28 patients with facial rhytides were treated with either of two different
laser systems. In five additional patients, in a direct comparison of the two lasers,
contralateral cosmetic units were treated with each representative system. All patients were
examined immediately after surgery, at 1,4, and 8 weeks and at 6 and 12 months after
surgery.
The following two lasers were utilized: (i) The UltraPulse 5000 with its 3-mm spot diameter
and collimated beam and a pulse duration of 800 us; and (ii) the SilkTouch continuous wave
laser coupled to a mechanical flashscanner with a 3mm scan size and a dwell time of
approximately 1 ms. For the first pass, the UltraPulse laser was set to 500 mj per pulse (7 J/
cm2) and the SilkTouch laser power was set at 7 W (18J/cm2). For the second and third
passes, the UltraPulse laser pulse energies were reduced by 50–100 mJ and the SilkTouch
laser power was decreased to 5 W although maintaining the same scan size. For periorbital
sites, settings were reduced to 350 mJ for the first UltraPulse laser pass and 250 mJ for the
second and third passes; reduced settings for the SilkTouch laser were 6 W for the first pass
and 5 W for the second and third passes. Overlap of laser pulses was avoided with both
systems. After each pass, the surface was wiped with saline-soaked gauze for debris removal
and then immediately patted with dry gauze. After treatment, the open areas were covered
with petrolatum.
Both lasers achieved significant wrinkle reduction at 2 months and 1 year, compared to pre-
treatment. There was a lack of significant clinical difference between the two laser systems.
Ross et al. concluded that both lasers cosmetically improved wrinkles for at least 1 year.
Alster18
This study compared the UltraPulse laser with a lesser used CO2 laser system, the Surgipulse
in the treatment of periorbital rhytides. Ten patients with moderate to severe periorbital
rhytides were treated with similar laser parameters. One side was treated with the Surgipulse
laser at 400 mJ and 10 W using a 3-mm spot delivery system. The other side was treated with
the Ultrapulse laser at 400–500 mJ and 5 W using a 3-mm spot delivered through a
collimated handpiece. After each laser pass, the thermally coagulated skin was removed with
saline-soaked gauze. Laser passes were delivered until relative effacement of rhytides was
achieved.
Four months post-treatment, a 63% average clinical improvement was seen after Surgipulse
laser treatment and an 82% mean clinical improvement was observed after Ultrapulse laser
treatment. The average number of delivered passes were 3.9 with the Surgipulse laser and 1.6
for the UltraPulse laser.
Silicone rubber skin surface impressions (profilometry) were taken prior to and at 4 months
following laser treatment in five patients. Computer analysis of skin surface impressions
correlated with clinical observations—a more substantial improvement was noted after
UltraPulse laser treatment, compared to Surgipulse treatment.
This study, in agreement with the previous studies, demonstrated the efficacy of pulsed
carbon dioxide lasers in reducing periorbital wrinkles, both clinically and texturally. The
UltraPulse laser provided superior results when compared to the Surgipulse laser. In addition,
fewer laser passes were required to achieve those results.
Gardner et al.19
These authors noted tissue contraction visible to the naked eye following a pulsed CO2 laser
impact. This was most evident after the first and second dermal passes, once the epidermis
had been removed. Subtracting the small amount of tissue contraction due to tissue volume
loss, the remainder was thought to result from collagen contraction.
This study compared 305 treated human tissue samples with matched controls and found a
positive linear correlation between the number of passes and the degree of skin shrinkage. A
linear regression model showed a 6% size reduction per pass with the SilkTouch laser and a
5% reduction per pass with the Ultrapulse laser. Rehydrating the tissue between passes
resulted in only slight correction of the shrinkage.
Weinstein20
In reporting a long-term follow-up in 2,123 patients after carbon dioxide laser resurfacing,
Weinstein noted that clinical improvement obtained from laser resurfacing was evident at 6
months and tended to last for a long term period; up to or longer than a 5-year period.
She concluded that the wrinkles that responded best to resurfacing were nondynamic lines,
those caused by actinic damage, and those located in the following regions of the face:
periocular, perioral and cheeks.
Weinstein suggested that if the vaporized tissue was not wiped between passes, a barrier
was left on the surface that prevented deeper vaporization or coagulation and/or led to
irregular and unpredictable dermal thermal necrosis. Therefore, she recommended gentle
wiping (with a wet gauze) between passes.
She also commented on the three macroscopic indicators of resurfacing depth: color, pore
size, and surface topography. Using color as an indicator of depth, she noted that once the
vaporized epidermis was removed, the underlying papillary dermis had a pinkish hue, which
indicated an intact papillary dermal plexus and minimal or no coagulation of the papillary
dermis. After a second pass was made, the dermis appeared tanner, corresponding to the
deeper papillary dermis. With subsequent passes, the underlying tissue becomes increasingly
yellow indicating the presence of the upper reticular dermis and associated significant
coagulation necrosis. She advised laser surgeons, upon encountering this yellowish color, to
stop the procedure to prevent further coagulation and potential scarring. Regarding pore size,
Weinstein found that the greater the resurfacing depth, the wider the sebaceous pores, and
the greater the probability of seeing sebaceous material emanate from the glandular apparatus.
Finally, she found that surface topography could be an indicator of resurfacing depth (with
the aid of loupes). As the operator resurfaces from the papillary to the reticular dermis, she
noted the surface becomes coarser, corresponding to the irregular arrangement of collagen
bundles.
Weinstein concluded that any of these three end-points could be used as helpful guides
during laser resurfacing. Thus, one should look for the appearance of yellow color,
roughening of collagen bundles, or disappearance of the wrinkle.
West and Alster21

Although there is general consensus regarding the need for prophylactic oral antiviral agents,
there is wide divergence of opinion regarding other pre-treatment regimens for laser
resurfacing.
West and Alster conducted a controlled study of 100 patients in whom pre-operative topical
tretinoin, hydroquinone, and/or glycolic acid was used. They found no significant effect on
the incidence of post-treatment hyperpigmentation. They concluded that pre-treatment with
tretinoin, hydroquinone and/or glycolic acid was unnecessary. The authors have also
questioned the use of pre-treatment antibiotic therapy.
HISTOLOGIC STUDIES
Multiple studies have evaluated the unique interaction between the carbon dioxide laser and
the collagen molecule. Histologic studies have evaluated various different pulsed CO2 laser
systems. Because of these studies, important concepts such as ablation threshold, residual
thermal damage and the changes induced in the grenz zone became understandable. An
evaluation of these histologic studies provides assistance with understanding pertinent topics
such as the optimal settings for the CPG, the effects of manual wiping between laser passes
and the long-term effects of collagen contraction.
Goldman and Fitzpatrick22

These authors noted that when the carbon dioxide laser interacts with skin, three distinct
zones of tissue alteration correlate with the degree of tissue heating. The zone of direct impact
results in vaporization of intracellular water and tissue ablation (>100°C). Underlying this is a
zone of irreversible thermal damage and denaturation resulting in tissue necrosis (70–100°C).
Below this layer, is a zone of reversible, non-lethal thermal damage in which collagen
shrinkage occurs (61–63°C). It is this zone that accounts for the visible tissue tightening
observable as the CO2 laser interacts with the dermis. Mammalian collagen, including human
scleral and skin tissue, has been found to shrink at 61–63°C, whereas in humans, the cornea
shrinks at a lower temperature, 55–58°C.23 Irreversible alterations of post-laser treated
collagen are seen on light microscopy. When temperatures of 70–75°C are created, the effects
of thermal coagulation ensue.24 Therefore, the goal of laser resurfacing is to heat a tissue
layer of collagen in the range of 61–70°C. These temperatures achieve the desired shrinkage
of collagen without completely denaturing collagen.
The characteristic collagen response to heat is a hydrothermal shrinkage of collagen fibers.
The proposed mechanism of this thermal contraction is thought to be a molecular structure
transition between the triple collagen helix and a random coil. Temperature elevation
ruptures the ultrastructural cross-links that stabilize the collagen helix. The fibers immediately
contract to about one-third their original length. Although heat application dissociates the
interpeptide bonds, the cross-linkage between molecules remains intact. The contraction of
these linked molecules leads to shortening of the collagen fiber.25 Ultrastructurally, the
collagen fiber diameter becomes wider, there is a loss of banding, and the periodicity is
reduced from 64 nm to 48 nm.26
Ratner et al.27 and Other Studies28–32

Ratner et al. summarized the carbon dioxide laser induced histopathologic features of human
skin from 24 hours to 1 year after resurfacing. At 24 hours, extensive epidermal coagulation
necrosis and coagulative thermal necrosis in the superficial papillary dermis are evident. A
moderately dense perivascular and interstitial dermal infiltrate is present, consisting of
predominantly mononuclear cells. A band of neutrophils line the wound base in a ‘picket
fence’ fashion. By day 3, partial or complete epithelialization may be seen.27–28
The temporal wound contraction profile is biphasic for post-CO2 laser resurfaced wounds.
Immediate heat-induced contraction is followed by a period of expansion until 7–10 days.
Then, the second slow onset of contraction occurs.
At fifteen days, the epidermis is fully regenerated, the keratinocytes are separated by
intercellular spaces, and cytologic atypia is absent. The dermis is infiltrated with fibroblasts,
dermal dendrocytes, and lymphocytes. At day 21, a rich supply of dermal blood vessels are
apparent and dermal collagen is haphazardly arranged.29–30
By 90 days, the epidermis is indistinguishable from that of younger, normal skin. A dense
repair zone is filled with collagen fibers aligned in parallel array. Fine parallel-aligned elastic
fibers are present in varying depths (50–300 μm) into the dermis depending on the laser
system used. This region is bordered by residual thicker elastotic tissue below. Persistent
neocollagenesis is seen at 6 months31 and 1 year after resurfacing.32
Long-term biopsies (up to 4 years post-operatively) have shown reversal of epidermal
dysplasia, with maintenance and continued thickening of the grenz zone. There is marked
improvement in the layer of solar elastosis underlying the grenz zone, with reduction in its
overall depth. The new collagen tends to be of a more fibrillar character.22
Walsh et al.6
This study, performed on guinea pig skin, showed that a pulse width of 50 ms, typical of
shuttered, continuous wave CO2 lasers, produced thermal damage of 750 µm while the use of
a much shorter 2 µs pulse reduced this damaged zone to as little as 50 μm.
This histologic study was particularly instructive because it confirmed that minimal thermal
damage can be achieved by using pulse widths shorter than the thermal relaxation of skin.
In another informative histologic study, Fitzpatrick et al. compared the depth of thermal
necrosis from the carbon dioxide laser in the conventional continuous wave mode to that from
the quasi-continuous wave chopped superpulsed mode.
Thirty-two human skin specimens were examined for depth of thermal damage after one
impact with a non-pulsed continuous wave CO2 laser and another impact with a superpulsed
delivery system. As would be expected, the average depth of coagulation necrosis was 0.1 mm
for the superpulsed mode compared to the deeper 0.2-mm depth seen following continuous
wave settings.
The authors concluded that the superpulsed mode resulted in a decreased depth of thermal
burn by a factor of two.
It should be noted that superpulsed CO2 lasers are not currently in popular use for ablative
laser resurfacing.
Yang et al.30
Yang et al. performed an early histologic animal study using the UltraPulse CO2 laser. They
investigated the microscopic appearance of rabbit skin immediately after and up to 1 month
after one—pass CO2 laser resurfacing.
The UltraPulse CO2 laser delivered 250 mj of energy per pulse, with a corresponding fluence
of 3.5 J/cm2. The 3-mm spot size collimated handpiece, and a pulse duration less than 950 us,
was used. One pass was delivered to four separate areas on each of the bilateral
paravertebral skin regions of two adult New Zealand white rabbits. Two sites (one from each
rabbit) were selected for histologic light microscopy evaluation.
Microscopic investigation of the single-pulse impaction demonstrated a layer of thermal
necrosis measuring 70±10 μm. Four weeks after laser treatment, the thickened epidermal
layer appeared normal and the repaired papillary dermal collagen showed a relatively
compact configuration with greater cellularity.
The authors saw a histologic advantage in that this laser delivered short, sharp bursts of
higher energy which rapidly and precisely heated targeted tissue with less resulting damage
to adjacent tissue. They concluded that quicker wound healing resulted (approximately 1
month duration) after one pass delivery of UltraPulse short duration, high energy laser pulses
to rabbit skin.
This study investigated the concepts of ablation depth and residual thermal damage, and
noted how these factors change as one progresses from single pulse treatment to the use of
multiple non-overlapping unstacked pulse passes. In addition, the effects of multiple
overlapping stacked pulses were evaluated.
An UltraPulse 5000C laser with a 3-mm collimated handpiece was used for all specimens.
Pulse energies of 250 and 500 mJ with the 3-mm spot size were chosen for the study. These
parameters were chosen because: (i) they correspond to the fluences used to achieve the
ablation threshold of skin (3.5 J/cm2) and (ii) they are the fluences most commonly used in
clinical practice (7.0 J/cm2). The CPG scanning device was not used. Skin excised for
rhytidectomy was treated with up to 10 passes, wiping with saline between passes. Single
pulse and multiple pulse impacts were utilized. Depth of ablation and residual thermal
damage were examined from 70 biopsies.
Non-overlapping, non-stacked, treatment sites were irradiated with minimal overlap. Each
pass (one to ten) was separated by several seconds to allow complete cooling of the tissue. For
stacking passes, a repetition rate of 10 Hz was selected and either two or three laser impacts
were provided at each spot site.
The authors found that with single pulse vaporization (with either 250 or 500 mj pulses), an
ablation plateau occurred at approximately 200–250 μm. With 250 mJ pulses, they found a
regular rate of vaporization equal to 30–50 μm per pass for passes one to three. With more
than three passes, the rate fell to an average of 10 μm per pass. At 500 mJ, they found a regular
rate of vaporization of nearly 75 μm per pass for the first three passes. Again, an ablation
plateau occurred with the fourth pass at approximately 10 μm per pass.
With rapid pulse stacking, a similar curve was generated showing that an ablation plateau
was reached after three or four passes at 225 to 250 μm in the dermis. An unanticipated
finding was that overall, there was a reduced depth of ablation with extensive pulse stacking.
The purported explanation for this ablation threshold is that vaporization does not progress
once the tissue targeted water chromophore diminishes with the procedure progression. In
the first pass, the laser interacts with intracellular water. Once the epidermis is stripped
away, the laser is interacting with the extracellular water in the dermis. Additionally, the
water content in the epidermis is closer to 80% whereas the dermal water content is
approximately 60%. The dermis, because it consists of primarily collagen fibrils and elastic
tissue, has a much higher threshold of vaporization than seen with the epidermis. Therefore,
the amount of tissue vaporized with each pass becomes diminished with each subsequent
pass.
The study showed a linear relationship between residual thermal damage and both pulse
energy and number of passes. With single-pulse vaporization, there was maximal thermal
damage at pass #7 (100 μm). Surprisingly, even after 10 pulses, cumulative thermal damage
never exceeded 100 μm. In contrast, pulse stacking had a marked impact on thermal injury per
pass; rapid double pulses added significantly more thermal injury per pass. Triple pulses
provided even greater damage (approximately 30 μm additional damage). Pulse stacking,
which may occur unintentionally by moving the handpiece too slowly or by excessive overlap
of pulses (40–60% overlap), may be a critical factor in causing delayed wound healing,
hypopigmentation, or scarring. This effect occurs because when several pulses are delivered
to tissue in rapid succession, the target tissue has insufficient time to cool; thermal effects
become additive.
In summary, with stacking pulses, the zone of thermal necrosis increases to a much greater
degree than with single pulse vaporization (even with multiple passes). However, either the
stacking of pulses or single pulsing with the CO2 laser will result in an ablation plateau of
200–250 μm after three or four passes. The controlled degree of vaporization and the now
well-defined ablation plateau allow for excellent control over depth of injury with the pulsed
CO2 laser.
Fitzpatrick et al. also compared and contrasted the porcine skin effect of a pulsed CO2 laser,
35% trichloroacetic acid (TCA), Baker-Gordon phenol (50%), and dermabrasion. The
UltraPulse laser was used with energies of 150, 250, 350, or 450 mj per pulse. One to three
laser passes were delivered with removal of tissue debris between the passes by saline-soaked
gauze.
Re-epithelialization was complete in laser-irradiated skin, as well as in the 35% TCA- and
dermabrasion-treated skin, at 1 week. The Baker-Gordon phenol-treated skin required 3
weeks to heal. The TCA-treated skin showed clinical and histologic changes comparable to
skin that had been irradiated with one to two CO2 laser treated passes using pulse energies
of 150–250 mJ, whereas the dermabraded skin was comparable to skin which was treated
with two to three passes at 250–450 mJ per pulse. The findings in phenol-treated skin did
not correlate with any combination of either laser pulse energies or number of passes
undertaken in the study. The phenol treated skin also showed the slowest healing response.
The authors also noted that the depth of residual thermal damage after one laser pass,
utilizing varying energies, was minimal (< 40 μm), but after two to three passes at increasing
pulse energies, the residual thermal damage ranged from 53–106 μm. These findings were
consistent with the thermal damage concepts previously reported by Fitzpatrick et al.34
The authors concluded that superficial resurfacing of the epidermis and papillary dermis
could be achieved with a pulsed CO2 laser at 150–250 mJ per pulse or with a 35% TCA peel.
Medium depth resurfacing into the upper reticular dermis could be achieved by using either
higher laser energies (> 350 mj per pulse) or by dermabrasion. Deep resurfacing into the mid-
reticular dermis was achieved only through a Baker-Gordon phenol peel.
Kauvar et al.8
Kauvar et al. used 14 post-treatment biopsies from in vivo human skin to compare three
pulsed CO2 lasers with a continuous wave CO2 laser. The purpose of this investigation was to
determine the depth of ablation and the depth of residual thermal injury produced with each
laser system.
The same laser pulse parameters could not be utilized for all three systems because of the
variable technologies. Therefore, ‘clinically optimal parameters’ determined by the authors
were employed.
The first utilized laser was the previously described UltraPulse 5000 system with a 3.0-mm
collimated handpiece capable of delivering up to 500 mj of energy per pulse within 950 us. The
second pulsed CO2 laser system was the SurgiPulse 150 XJ. This system also utilized a 3-mm
collimated handpiece to produce closely spaced pulse pairs that sum to 400 mj and provide
fluences of 5 J/cm.2 The third pulsed system, the SilkTouch laser, used a computer-
controlled flashscanner with a continuous mode CO2 laser to focus the laser beam to a 0.2-
mm focal spot as it rapidly scanned a specified area of tissue. The beam uniformly exposed
each spot on the spiral scan area for less than 1 ms. The SilkTouch system was operated at
18 W, with 0.2 second exposure times, and a 6-mm diameter spot size. As a control, the
Surgicenter 40 non-pulsed continuous mode laser was used at 10 W power with 0.2 second
exposures.
The depth of ablation was found to be greater for the the SilkTouch flashscanner laser (30–
50 μm) and the SurgiPulse XL laser (30–50 μm) than for the UltraPulse laser (20–30 μm).
With all three systems, the zone of residual thermal damage increased with subsequent
passes, consistent with previous studies.34 After one, two and three passes, the depth of
residual thermal damage measured 30, 80 and 150 μm, respectively, with the SilkTouch
laser; 30, 100 and 150 μm with the SurgiPulse laser; and 20, 50 and 70 μm with the
UltraPulse laser. The continuous wave CO2 laser, with its greater thermal damage capacity, left
a 400-μm layer of thermal necrosis.
Experimental studies suggest that thermal coagulation zones of less than 150 μm pose
minimal risk for impaired wound healing or scarring. Therefore, the authors concluded that
although there was more thermal damage with each pass of the SilkTouch flashscanner and
SurgiPulse 150 XJ lasers, compared with the UltraPulse laser, the ensuing thermal damage
of all three laser systems were in a safe and desirable range of 30–150 μm.
Weinstein20
Weinstein compared the histologic effect of two different modes of the SilkTouch laser; the
SilkTouch and FeatherTouch modes. In the SilkTouch mode, the pattern was scanned twice.
All utilized parameters are more aggressive in this mode than in the FeatherTouch mode. The
delivered fluence was higher (28 J/cm2), the exposure time on tissue was longer, and the
thermal injury was greater. For the first pass, there was epidermal vaporization and dermal
thermal coagulation necrosis of 70 μm; after the second pass, there was epidermal
vaporization and dermal coagulation of 100 μm. The depth of vaporization into the dermis
was not reported.
In the FeatherTouch mode, the delivered fluence was lower at 10 J/cm2. The first pass
resulted in epidermal vaporization and dermal coagulation necrosis of 10 μm; the second
pass resulted in epidermal vaporization and dermal coagulation necrosis of 30 μm; and the
third pass resulted in epidermal vaporization and dermal coagulation necrosis of 50 μm.
Again, the depth of vaporization into the dermis was not reported.
In comparing the SilkTouch mode (increased fluence; more thermal damage) and the
FeatherTouch mode (less fluence; less thermal damage (even with three rather than two
passes)), Weinstein demonstrated that increasing time on tissue by scanning twice with the
SilkTouch mode increases depth of coagulation necrosis in a non-linear fashion.
Cotton et al.28
Cotton et al. were the first to report the histologic presence of the dermal collagen ‘repair zone’
after pulsed CO2 laser resurfacing. They documented these grenz zone morphologic changes
in human skin 90 days after treatment.
Four human subjects, each with two pre- and two post-auricular designated sites, were
treated with a high energy, short-pulsed, CO2 laser (SurgiPulse XJ-150) with a 3-mm
collimated laser beam. For the four designated sites per patient, each of the following
parameters was used: (i) 250 mJ—one pulse, (ii) 300 mJ—one pulse; (iii) 400 mJ—one pulse;
and (iv) 400 mJ—two pulses (no wiping between pulses). Biopsy specimens were obtained up
to 90 days after laser vaporization and stained with hematoxylin-eosin and acid orcein-
Geimsa.
At day 90, most specimens, at all chosen parameters, demonstrated a well demarcated
papillary dermal ‘repair zone’ composed of dense compact collagen bundles in parallel
alignment with the epidermal surface. They also observed alterations in the elastic fibers in
the most superficial papillary dermis (thinner, parallel orientation) and upper reticular dermis
(thicker, haphazardly arranged).
This study proved that pulsed CO2 laser resurfacing can create a histologic subepidermal
grenz zone of fibrosis with alterations in collagen and elastic fibers.
Stuzin et al.36
This study evaluated the histopathologic laser induced effects between 15 days and 6 months
following laser resurfacing. Ten photodamaged patients, aged 51–85 years, underwent laser
resurfacing of the pre-auricular skin. Two laser passes utilizing the UltraPulse CO2 laser with
a 3-mm spot size at 500 mJ were delivered. Specimens were microscopically analyzed to
compare the effect of laser resurfaced skin compared to the adjacent control area of non-
lasered photodamaged skin.
The laser-treated sites were clinically re-epithelialized within 7–10 days in all patients. Post-
treatment erythema followed for a period of 2–3 months.
Biopsies at 15 days demonstrated a regenerated epidermis with large and uniform
keratinocytes. Biopsies at 3 months showed that the epidermal atypia still seen in adjacent
controlled areas was eliminated. Cellular polarity was restored. There were also fewer and
more evenly distributed melanin granules. The histologic findings correlated with the
clinically evident improvement of dyspigmentation. At 3 months, the treated epidermis was
indistinguishable from younger normal skin.
In the dermis, a new wide band of normal collagen was noted in the form of compact
parallel bundles oriented horizontally to the surface. This replaced the solar elastosis in the
upper to mid-dermis. New finer elastic fibers were interspersed among collagen bundles.
There was an overall increase in dermal collagen and decrease in glycosaminoglycans,
accounting for palpable firmness and less laxity. At 6-month biopsies, an essentially normal
dermis was noted.
The authors also compared the histologic dermal changes seen after CO2 laser resurfacing
to those of phenol peeling. In contrast to other investigators, they found indistinguishable
differences.35 They suggested that the permanent clinical hypopigmentation that is usually
seen after phenol peeling is due to the cessation of melanin synthesis, and not the destruction
of epidermal melanocytes. The process may be similar to that seen with laser induced delayed
hypopigmentation (See Complications, Chapter 8). In this short-term follow-up study,
melanocyte structure and function appeared intact after healing. Repigmentation returned to
the original level at 3 months, even in the three treated African–American patients.
Shim et al.16
This study supported the finding of a post-laser induced grenz zone of new collagen formation
as reported by both Cotton et al.28 and Stuzin et al.36
The authors evaluated nine patients, with rhytides, treated with one to three passes of the
SilkTouch CO2 laser. Biopsies were obtained both pre- and posttreatment. Specimens were
stained with hematoxylin and eosin and Verhoff’s elastin stain and were analyzed for collagen
deposition and elastin quantity and quality.
Biopsies demonstrated new collagen formation (grenz zone) in all post-operative specimens
(mean follow-up of 15 weeks). The mean increased thickness of the collagen layer at the post-
operative biopsy was 158%. There was less collagen deposition at the seven perioral sites
(average increase of 150%) than at the two periorbital sites (average increase of 190%). These
findings were consistent with the findings reported by Waldorf et al.4 The authors noted that
periorbital sites had greater increases in collagen thickness compared to perioral sites.
Ross et al.17
Ross et al. also evaluated the histopathologic findings after CO2 laser resurfacing. A total of
28 patients, with facial rhytides, were treated with either the UltraPulse or SilkTouch laser
systems. Biopsies of 2 mm were taken before, immediately after, and 1 year after treatment
from seven representative patients.
The following two lasers were utilized: the UltraPulse 5000C laser with a 3-mm spot
diameter collimated beam and a pulse duration of 800 us; and the SilkTouch 40 W continuous
wave laser coupled to a mechanical flashscanner with a 3-mm scan size and a dwell time of
approximately 1 ms. For the first facial pass, the UltraPulse laser was set at 500 mj per pulse
(7 J/cm2) and the SilkTouch laser power was set at 7 W (18 J/cm2). For the second and third
passes, the UltraPulse pulse energies were reduced by 50–100 mJ and the SilkTouch laser
power was decreased to 5 W while maintaining the same scan size. For periorbital sites, the
UltraPulse settings were reduced to 350 mJ for the first pass and 250 mJ for the second and
third passes; reduced settings for the SilkTouch laser were 6 W for the first pass and 5 W for
the second and third passes. Overlap was avoided with both systems.
The SilkTouch histological findings, showing greater immediate thermal damage, were
consistent with those previously described by Kauvar et al.8 Mean thermal damage for the
SilkTouch laser was 130 μm (range 90–180), while mean thermal damage for the UltraPulse
laser was less, at 90 μm (range 70–130).
It can be assumed that the increase in residual thermal damage, seen after the SilkTouch
laser treatment, can be attributed to cumulative heating from the concentric spirals seen with
this laser’s delivery system.
One year post-operative histopathologic specimens showed papillary dermal changes
consistent with new collagen deposition and reduction of pre-treatment solar elastosis. Pre-
treatment grenz zones of varying thickness were noted (mean of 25 μm and range of 10–40 μm
for both laser systems) between the zone of solar elastosis and the epidermis. Biopsy
specimens performed 1 year after treatment revealed a zone of widened fibroplasia measuring
80–300 μm, with a mean zone of fibroplasia of 220 μm (range of 80–300) for the SilkTouch
laser and a mean zone of fibroplasia of 150 μm (range of 60–200) for the UltraPulse laser.
Ross et al. concluded that 1-year post-treatment biopsies with both lasers demonstrated
new collagen formation and reduction of solar elastosis. Although the SilkTouch laser
produced more immediate thermal damage and a larger zone of fibroplasia than that seen
with the UltraPulse laser, there were no significant differences in clinical efficacy between the
two lasers.
In summary, the histologic evidence of Cotton et al.,28 Shim et al.,16 Stuzin et al.36 and Ross
et al.17 all demonstrate that carbon dioxide laser resurfacing induces long-term collagen
formation accompanied by decreased solar elastosis. These studies suggest that clinical
improvement of rhytides and scars induced by CO2 laser resurfacing may be attributed to the
changes seen in dermal collagen and elastic tissue fibers.
Rubach et al.37
The CPG scanner was developed for use with the UltraPulse CO2 laser technology to decrease
surgical operating time and to increase uniformity, accuracy, and reproducibility of tissue
ablation. The CPG is a computerized scanning device that most commonly uses a 2.25-mm
collimated beam to ablate tissue. The result is a constant beam diameter at any treatment
distance, alleviating the need for the surgeon to maintain a specific focal distance from the
treatment site. With the collimated beam, the energy is applied in a gaussian distribution,
with more energy and deeper penetration in the center of the beam and slightly less energy
and more superficial ablation at the margins of the beam. The clinician has the ablility to vary
the degree of overlap of the collimated beam generated by the CPG by using different density
settings (ranging from 1 to 9).
The authors attempted to determine the ideal treatment parameters using the CPG. They
treated five pre-auricular specimens, from patients undergoing rhytidectomy, with the
UltraPulse 5000C at 300 mj with density settings varying from 1 to 9.
Histologic evaluation, after one laser pass, revealed that a density setting of 3, 4, or 5,
resulted in uniform ablation of the epidermis with minimal thermal injury to the underlying
dermis. At density settings of 1 and 2, irregular ablation of the tissue occurred, while at
density settings of 6 through 9, increasing degrees of thermal injury and tissue necrosis
occurred.
At a density setting of 5, the mean depth of ablation was 78 μm (range 65–90) and the
mean thermal effect was 28 μm (range 0–45 μm). Complete reepithelialization occurred at an
average of 7 days following use of these treatment parameters.
The authors concluded that the ideal treatment parameters with the CPG are achieved at a
density setting of 3, 4, or 5. At these settings, tissue is uniformly ablated with minimal
coagulative thermal changes to the underlying dermis.
Ross et al.38
Ross et al. investigated the effects of wiping after single and multiple-pass high energy pulsed
CO2 laser surfacing in a pig model. The UltraPulse laser was used with pulse energy of 300
mj and a density setting of 5 using the CPG (fluence of 7J/cm2). Four different approaches
were utilized: (i) one pass, no wipe; (ii) one pass, wipe after pass; (iii) three passes, no wiping
between passes; and (iv) three passes, wiping after all passes. Wiping consisted of using wet
gauze moistened with normal saline and rubbing vigorously until all surface debris was
grossly removed. Biopsies were performed immediately following laser treatment and on post-
operative days 1 and 21.
With a one-pass wound, wiping was associated with increased inflammation and slightly
prolonged healing. In contrast, not wiping between and after multiple pass wounds
significantly increased the depth and variability of residual thermal damage and necrosis,
resulting in prolonged healing.
This study supports the notion that no post-treatment wiping is required when one is
performing single-pass laser treatment. In contrast, wiping is appropriate for multiple-pass
laser treatments. Possible explanations for the increased inflammation seen after one laser
pass wiping include the loss of damaged epidermis as a potential biologic dressing, and the
mechanical skin irritating process of wiping.
Ross et al.’s study validated the now widely accepted clinical benefits of wiping with wet
gauze between CO2 laser passes. They suggested that wiping between passes leaves behind a
uniformly hydrated layer at the base of the wound. This base facilitates further water
vaporization, which results in lower peak surface temperatures and minimal thermal damage.
Conversely, without wiping between laser passes, the ratio of tissue thermal injury to ablation
increases, which in turn decreases ablation efficiency.
This nine-patient study evaluated the immediate clinical and histologic tissue tightening
effects seen with carbon dioxide laser-induced collagen contraction. The authors compared
CO2 laser induced contraction with that seen following Erbium:YAG laser induced contraction
(see Chapter 4).
The amount of collagen tightening induced by the CO2 laser was found to be greatest
during the first three passes. There was no increased tightening with a fourth pass. Collagen
tightening was noted to be dependent on fluence and epidermal thickness.
In the vertical plane, the UltraPulse CO2 laser induced an average of 43% tightening
intraoperatively, which gradually diminished to an average of 34% at 6 months. Wound
contracture following short-pulsed Erbium:YAG laser resurfacing was not seen until 1 month
post-operatively, at which time 42% tightening was seen, gradually diminishing to 36% at 6
months. In the horizontal plane, the CO2 laser led to a 31% intraoperative tightening,
decreasing to 19% at 6 months. Shortpulsed Erbium:YAG laser induced wound contracture
was 12% at 1 month, which remained stable and unchanged.
Biopsies (five out of nine) taken at 6 months after treatment supported these differences
seen between the CO2 and Erbium:YAG laser procedures. On CO2 laser treated sites,
papillary dermal collagen was noted to be finer and more fibrillar. On the erbium treated sites,
a more tightly packed, clumped collagen was noted with an arrangement parallel to the skin
surface, resembling a scar.
The authors concluded that the two laser processes used to achieve tissue tightening are very
different. Although both procedures achieve tissue tightening, the unique CO2 laser induced
collagen contraction effect may be longer lasting and may account for the superior clinical
improvement seen with CO2 laser resurfacing, compared to that seen with the short-pulsed
Erbium:YAG laser.
MY APPROACH
I have found CO2 lasers to be highly effective when used for the treatment of Class I–III
rhytides and some acne scars. (Figures 3.3–3.62) These more aggressive ablative lasers can
be used successfully in the treatment of Fitzpatrick skin types I–IV. However, it should be
expected that almost all Fitzpatrick IV individuals will show some evidence of post-
inflammatory hyperpigmentation.40 I have not noted any method of pre-treatment that will
consistently stop this. However, as a general rule the hyperpigmentation is self-limited. It
appears to be most profound in those individuals with a history of melasma. Prior to
treatment, I start all patients on oral antiviral agents and antibiotics.
The treatment technique consists of pre-operative cleaning of the skin with a non-
flammable cleansing agent. This precludes the possibility of a fire resulting from the laser
irradiation’s heating of a flammable agent. Local anesthesia can be used when treating partial
or full-face areas. Generally, we do not treat localized anatomic areas if there will be a high
risk of visible zones of demarcation. This is particularly true in patients with greater evidence
of photodamage. Although fullface procedures can be performed with appropriate local
anesthetic nerve blocks, it is generally our preference to carry out such procedures under light
sedation. This provides greater comfort for the patient and allows the procedure to be
completed in a more efficient manner.
Once the patient is anesthetized, all adjacent areas of skin are covered with wet towels.
Generally I will treat the affected areas with one to three passes of the chosen laser. I have
found that, as a general rule, one pass with the SilkTouch laser, at standard parameters,
leads to a greater thermal effect than one similar pass with the UltraPulse laser. More than
three passes appears to provide more thermal damage, but not much in the way of any further
ablative benefit. This is because the water absorbing chromophore is now absent. Wiping
away of debris between passes is suggested. There appears to be nothing gained by doing this
after the final laser pass.
It is important to note that a decision to use very low fluences, in a somewhat counter-
intuitive manner, is not necessarily safer. Very low fluences from any pulsed CO2 laser will
tend to destroy tissue thermally rather than lead to tissue ablation. This will lead to a greater
potential for scarring. The ideal treatment parameters must be individualized for each
patient, based on clinical experience and professional judgment. Whatever energies are
chosen, tapering along the mandible and the preauricular areas should be performed at
lesser fluences. Although some have suggested that CO2 lasers be used on the neck, we have
shied away from such an aggressive approach in that area. It should be attempted only when
the surgeon is very experienced with laser resurfacing. I prefer to use either short-pulsed
Erbium:YAG lasers, or non-ablative devices, in this anatomic region (see Chapters 4 and 7).
In addition to proper technique and avoidance of infection, appropriate wound care is
mandatory. CO2 laser treated sites share much in common with second degree burns. There
are physician advocates for post-laser open dressings and physician advocates for closed
dressings. We have used them both. What is important is that the wound be kept moist until
complete re-epithelialization has occurred. This usually occurs within 7–10 days. Use of
antiviral agents is mandatory during this entire period. Full re-epithelialization after 7–14
days is to be expected. Clinical improvement can be expected to last for several years.
After re-epithelaization, intense erythema followed by mild erythema will be seen. This
usually tends to be generalized in the treatment area and can last up to 6 months or longer.
Localized hardened or erythema that lasts more than 6 months, is suggestive of the onset of
hypertrophic scars. This should be managed aggressively (see Chapter 8).
There are more accumulated data about the CO2 laser’s efficacy than of any other device
described in this text. This laser provides both ablative and thermal benefits. Although CO2
laser treatment has been joined by other ablative and non-ablative techniques, it remains the
‘gold standard’ with which all other methods are compared.
Figure 3.3. Before CO2 laser resurfacing
Figure 3.4. Immediately after CO2 laser resurfacing (whitish skin hue represents thermally denatured tissue)
Figure 3.5. Four days after CO2 laser resurfacing. Exudative wound is seen
Figure 3.6. Two months after CO2 laser resurfacing. Post-treatment erythema is still present
Figure 3.7. Typical immediate post-CO2 laser appearance. Note minimal char from pulsed CO2 laser
Figure 3.8. Before CO2 laser resurfacing of the periorbital area

Figure 3.9. Immediately after CO2 laser resurfacing
Figure 3.10. Six months after CO2 laser resurfacing

Figure 3.11. Before CO2 laser resurfacing of the perioral area
Figure 3.12. Five days after CO2 laser resurfacing

Figure 3.13. Before CO2 laser resurfacing of the full face

Figure 3.16. Three days after CO2 laser resurfacing

Figure 3.17. One year after CO2 laser resurfacing

Figure 3.19. Four days after CO2 laser resurfacing. One side of upper lip treated with UltraPulse CO2 laser. Other
side of lip treated with SilkTouch flashscanned CO2 laser. Note similar appearance
Figure 3.20. Nine months after CO2 laser resurfacing




Figure 3.28. Two years after CO2 laser resurfacing




Figure 3.35. Three months after CO2 laser resurfacing. Erythema persists

Figure 3.37. Four days after CO2 laser resurfacing

Figure 3.39. Two months after CO2 laser resurfacing

Figure 3.42. Three months after CO2 laser resurfacing

Figure 3.44. Immediately after CO2 laser resurfacing

Figure 3.46. Two months after CO2 laser resurfacing




Figure 3.54. Before CO2 laser resurfacing for acne scars

Figure 3.55. One week after CO2 laser resurfacing
Figure 3.56. Before CO2 laser resurfacing of forehead

Figure 3.57. Two weeks after CO2 laser resurfacing



REFERENCES
1 Hobbs ER, Bailin PL, Wheeland RG, Ratz JL. Superpulsed lasers: Minimizing thermal
damage with short pulse duration, high irradiance pulses. J Dermatol Surg Oncol 1987;
13:955–64.
2 Fitzpatrick RE, Ruiz-Espara J, Goldman MP. The depth of thermal necrosis using the
CO2 laser: a comparison of the superpulsed mode and conventional modes. J Dermatol
Surg Oncol 1991;17:340–4.
3 Zweigh AD, Meierhofer B, Muller OM, et al. Lateral thermal damage along pulsed laser
incisions. Lasers Surg Med 1990;10:262–74.
4 Waldorf HA, Kauvar ANB, Geronemus RG. Skin resurfacing of fine to deep rhytides using
a char-free carbon dioxide laser in 47 patients. Dermatol Surg 1995;21:940–6.
5 Flemming MG, Brody N. A new technique for laser treatment of cutaneous tumors. J
Dermatol Surg Oncol 1986;12:1170–5.
6 Walsh JT, Flotte TJ, Anderson RR, et al. Pulsed CO2 laser tissue ablation: Effect of tissue
type and pulse duration on thermal damage. Lasers Surg Med 1988;8:109–18.
7 Walsh JT, Deutsh TF. Pulsed CO2 laser ablation: Measurement of the ablation rate.
Lasers Surg Med 1988;8:264–75.
8 Kauvar ANB, Waldorf HA, Geronemus RG. A histopathological comparison of ‘char-free’
carbon dioxide lasers. Dermatol Surg 1996;22:343–8.
9 McKenzie AL. How far does thermal damage extend beneath the surface of the CO2
incisions? Phys Med Biol 1983;28:905–12.
10 Lanzafame RJ, Nairn JO, Rogert DW, et al. Comparisons of continuous-wave, chop-wave,
and super-pulse laser wounds. Lasers Surg Med 1988;8:119–24.
11 Fitzpatrick RE, Goldman MP, Ruiz-Espara J. Clinical advantage of the CO2 laser
superpulsed mode: Treatment of verruca vulgaris, seborrheic keratoses, lentigines, and
actinic cheilitis. J Dermatol Surg Oncol 1994;20:449–56.
12 Olbreicht SM. Use of the carbon dioxide laser in dermatologic surgery: A clinically
relevant update. J Dermatol Surg 1993;19:364–9.
13 Fitzpatrick RE, Goldman MP, Satur NM, et al. Pulsed carbon dioxide laser resurfacing of
photoaged facial skin. Arch Dermatol 1996;132:395–402.
14 Lowe NJ, Lask G, Griffin ME, et al. Skin resurfacing with the Ultrapulse carbon dioxide
laser: Observations on 100 patients. Dermatol Surg 1995;21:1025–9.
15 Lask G, Keller G, Lowe N, et al. Laser skin resurfacing with the SilkTouch flashscanner
for facial rhytides. Dermatol Surg 1995;21:1021–4.
16 Shim E, Tse Y, Velazquez E, et al. Short-pulse carbon dioxide laser resurfacing in the
treatment of rhytides and scars: A clinical and histopathological study. Dermatol Surg
1998;24:113–17.
17 Ross EV, Grossman MC, Duke D, et al. Long-term results after CO2 laser skin
resurfacing: a comparison of scanned and pulsed system. J Am Acad Dermatol 1997;37:
709–18.
18 Alster T. Comparison of two high-energy, pulsed carbon dioxide lasers in the treatment of
periorbital rhytides. Dermatol Surg 1996;22:541–5.
19 Gardner ES, Reinisch L, Stricklin GP, et al. In vitro changes in non-facial human skin
following CO2 laser resurfacing: A comparison study. Lasers Surg Med 1996;19:379–87.
20 Weinstein C. Carbon dioxide laser resurfacing: Long-term follow-up in 2123 patients. Clin
Plast Surg 1998;25:109–30.
21 West TB, Alster TS. Effect of pretreatment of the incidence of hyperpigmentation following
continuous CO2 resurfacing. Dermatol Surg 1999;25:15–17.
22 Fitzpatrick RE, Goldman, MP. Skin resurfacing with carbon dioxide and erbium lasers. In:
Goldman MP, Fitzpatrick RE eds. Cutaneous Laser Resurfacing. Second edn. St. Louis:
Mosby;1999.
23 Gassett AR, Shaw EL, Kaufman HE, et al. Thermokeratoplasty. Trans Acad Opthalmol
Otol 1973;77:441–54.
24 McCally RL, Bargeron CB, Green WR, et al. Stromal damage in rat corneas exposed to
CO2 laser radiation. Exp Eye Res 1983;37:543.
25 Stryer L. The stability of the collagen helix depends on cooperative interactions. In:
Biochemistry. Second edn. New York: Freeman; 1981.
26 Zelickson, B. Presented at the annual meeting, American Society of Lasers Surgery and
Medicine, New Orleans, 4/01.
27 Ratner D, Tse Y, Marchell N, et al. Cutaneous laser resurfacing. J Am Acad Dermatol
1999;41:365–89.
28 Cotton J, Hood AF, Gonin R, et al. Histologic evaluation of preauricular and
postauricular human skin after high-energy, short-pulse carbon dioxide laser. Arch
Dermatol 1996; 132: 425–8.
29 Trelles MA, David LM, Rigau J. Penetration depth of Ultrapulse carbon dioxide laser in
human skin. Dermatol Surg 1996;22:863–5.
30 Yang CC, Chai CY. Animal study of skin resurfacing using the Ultrapulse carbon dioxide
laser. Ann Plast Surg 1995;35:154–8.
31 Rosenberg GJ. The long-term histologic effects of the CO2 laser on collagen and elastin in
twenty-two patients. Lasers Surg Med 1998;22:54–5.
32 Fitzpatrick RE, Bernstein E. Histological findings associated with Ultrapulse CO2 laser
resurfacing. Lasers Surg Med 1996; 18 (suppl 8):34.
33 Fitzpatrick RE, Ruiz-Espara J, Goldman MP. The depth of thermal necrosis using CO2
laser: A comparison of the superpulsed mode and conventional mode. J Dermatol Surg
Oncol 1991;17:340–4.
34 Fitzpatrick RE, Smith SR, Sriprachya-anunt S. Depth of vaporization and the effect of
pulse stacking with a high-energy, pulsed carbon dioxide laser. J Am Acad Dermatol
1999;40:615–22.
35 Fitzpatrick RE, Tope WD, Goldman MP, et al. Pulsed carbon dioxide laser, trichloroacetic
acid, Baker-Gordon phenol, and dermabrasion: A comparative clinical and histologic
study of cutaneous resurfacing in a porcine model. Arch Dermatol 1996; 132:469–71.
36 Stuzin JM, Baker TJ, Baker TM, et al. Histologic effects of the high-energy pulsed CO2
laser on photoaged facial skin. Plast Reconstr Surg 1997;99:2036–50.
37 Rubach BW, Schoenrock LD. Histological and clinical evaluation of facial resurfacing
using a carbon dioxide laser with the computer pattern generator. Arch Otolaryngol Head
Neck Surg 1997;123:929–34.
38 Ross EV, Mowlavi A, Barnette D, et al. The effect of wiping on skin resurfacing in a pig
model using a high energy pulsed CO2 laser system. Dermatol Surg 1999;25:81–8.
39 Fitzpatrick RE, Rostan EF, Marchell N, et al. Collagen tightening induced by carbon
dioxide laser versus erbium:YAG laser. Lasers Surg Med 2000;27;395–403.
40 Sripachaya-anunt S, Marchell N, Fitzpatrick RE, et al. Facial resurfacing in patients with
Fitzpatrick skin type IV. Lasers Surg Med 2002; 30:86–92.
4
ERBIUM:YAG LASER RESURFACING
KEY POINTS
(1) The Erbium:YAG (Er:YAG) laser, with its 2940-nm wavelength, has ten times
greater affinity for water than the carbon dioxide laser
(2) With its higher affinity for water, the short-pulsed Er:YAG laser causes almost pure
ablation
(3) The ablation threshold of the Er:YAG laser, the energy density required to ablate, is
1.6J/cm2
(4) Total depth of injury following use of a short-pulsed Er:YAG laser is directly
proportional to the total fluence delivered
(5) Repetition rate rather than fluence can significantly increase thermal damage
(6) Fine lines, and mild photodamage, are ideally treated with Er:YAG laser resurfacing
(7) Deeper rhytides show a greater response to CO2 laser resurfacing, multiple sessions
of short-pulsed Er:YAG laser treatment, or a modulated Er:YAG laser system (See
Chapters 3 and 5)
BACKGROUND
Laser resurfacing of facial rhytides is a treatment option for many patients with wrinkles,
photoaging, and acne scarring. The search for alternative methods of skin resurfacing to
minimize the associated morbidity and side effects of the carbon dioxide laser has led to the
popularity of the short-pulsed Erbium:YAG (Er:YAG) laser.
At a wavelength of 2940 nm, the Er:YAG laser has ten times greater affinity for water than
does the 10,600-nm CO2 laser (Figures 4.1 and 4.2). With its higher affinity for water, the
250–400-μs short-pulsed Er:YAG laser is absorbed more superficially in the skin and causes
almost pure ablation. Ablation depth of the short-pulsed Er:YAG laser is directly proportional
to the total fluence delivered to the skin.1,2 The human adult epidermis is usually at least 60
μm in thickness. Generally 4 μm of tissue is ablated with each 1 J/cm2. Thus, fluences of at
least 15 J/cm2 are required to completely ablate the epidermis.3 At typical fluences (5 J/cm2),
only a shallow zone of thermal damage (5–20 μm) is left behind.1,3 The thermal damage zone,
in contrast to that seen with CO2 lasers, is fixed and very small (Figure 4.3). This thermal
damage is so shallow that it is insufficient to coagulate dermal capillaries. This explains why
Er;YAG lasered skin bleeds.
Because the Er:YAG laser ablates more efficiently than the CO2 laser, one might
hypothesize that lesser total fluences are required with the Er:YAG laser compared to the CO2
laser; this is not the case. Fleming has shown that to achieve equal depth of injury, the
Er:YAG laser must ablate deeper than the CO2 laser because there is minimal Er:YAG laser
induced thermal damage.1
ERBIUM:YAG LASER RESURFACING 67
Figure 4.1. Water absorption of Er:YAG laser
Figure 4.2. Comparison between water absorption of Er:YAG and CO2 lasers
End-points for Er:YAG laser resurfacing are well defined.2 Resurfacing within the epidermis
produces a yellow-brown keratinized surface. At the epidermal–dermal junction, the pinkish
appearance of the upper papillary dermis can be appreciated. The level of the lower papillary
dermis demonstrates pin-point bleeding and transudate; splotchy bleeding and profuse
transudate are recognized at the reticular dermis.
The most significant advantage of Er:YAG resurfacing is the precise removal of skin,
providing safety and reliability. The minimal associated thermal damage is another great
advantage, which may account for the rapid healing and decreased untoward effects.
The greatest limitation of Er:YAG resurfacing is the need for multiple passes to obtain
improvement (especially for deeper wrinkles and acne scars), making the procedure
potentially slower than CO2 resurfacing. Other limitations include dermal bleeding with
Figure 4.3. Differences between ablative and thermal effects of Er:YAG and CO2 lasers
deeper resurfacing, the associated noise level, and the large amount of plume produced. The
lack of thermal damage may also be considered a disadvantage when treating severe wrinkles
because studies suggest that CO2 thermal damage is responsible for the associated
improvement.4
CLINICAL STUDIES
Teikemeier and Goldberg5

Teikemeier and Goldberg were among the first to evaluate the role of the Er:YAG laser for the
treatment of superficial rhytides. Twenty patients with mild periorbital, perioral, or forehead
rhytides were treated with a 350-μs pulse duration Er:YAG laser. Pulses of energy varying
from 400 mJ to 800 mJ and spot sizes of 2.5 and 5 mm were chosen. The end-point of
treatment was the disappearance of clinical rhytides. Patients were evaluated at 2 days, 1
month, and 2 months for degree of improvement, time of healing, and resolution of erythema.
At 2 months, all 20 patients were found to have improvement of their wrinkles. Re-
epithelialization occurred between 4 and 10 days. Post-operative erythema resolved in less
than 2 weeks.
This early study demonstrated that the Er:YAG laser was efficacious in improving
superficial rhytides. The quicker re-epithelialization and resolution of erythema were
attributed to the minimal thermal damage resulting from Er:YAG laser resurfacing.
Perez et al.6
Perez et al. studied the effect of the Er:YAG laser on a variety of rhytides. They defined Class I
rhytides as fine line wrinkles, Class II rhytides as generalized deep lines with moderate
textural changes, and Class III rhytides as sharply defined deep lines with dermal elastosis
and skin folds.
Fifteen patients were treated with a short-pulsed Er:YAG laser. Five patients underwent
full-face resurfacing (five to seven passes), five had the perioral region treated (four to six
passes), and five had the periorbital region treated (two to three passes). Fluences ranged from
4 to 5 J/cm2 at 5 pulses/second. All patients applied topical tretinoin daily for at least 2
weeks prior to surgery.
Patients were followed daily for the first week after treatment, weekly for 2 months, and
then up to 6 months. Two blinded observers determined the degree of clinical improvement.
All patients showed some degree of wrinkle improvement. Marked improvement was seen in
eight out of 15 patients (all with Class I–II rhytides), moderate improvement was seen in six
out of 15 (all had Class III rhytides), and mild improvement was seen in one out of 15 (had
Class III rhytides).
Re-epithelialization occurred between 3 and 8 days. All erythema resolved between 3 and 6
weeks.
This study broadened the role of the Er:YAG laser to treat both superficial (Class I) and
medium depth wrinkles (Class II). The study also suggested that the Er:YAG laser may play a
role in the treatment of severe (Class III) rhytides.
Goldberg and Cutler7

Goldberg et al. expanded the previous study by evaluating the Er:YAG laser for the treatment
of Class III rhytides. Class III rhytides were defined as generalized deep lines (greater than four)
with distinctive textural changes of dermal elastosis.
Twenty subjects were treated with four 250-μs Er:YAG laser passes at 5 J/cm2, spot size of
7 mm and a repetition rate 10 Hz. Three months after the initial treatment, a second
treatment with similar parameters was performed. Six months after the initial treatment, a
third treatment with identical parameters was performed. Sites included periorbital, perioral,
and cheek regions. No pre-treatment medications such as retinoids or alpha-hydroxyacids
were applied.
Although no improvement was seen after the final laser session, mild to excellent
improvement was noted at 6 months after the initial treatment. Fourteen subjects had mild
improvement, four subjects had moderate improvement, and two subjects had excellent
improvement.
The authors concluded that with multiple sessions, the Er:YAG laser can successfully treat
Class III rhytides.
Weinstein3
In a series of 625 patients treated with Er:YAG laser resurfacing, Weinstein noted that long
term (>6 months) improvement in wrinkles and acne scars could be achieved. Total fluences
were quite high. Periocular wrinkles required the least total fluences (20–40 J/cm2), perioral
rhytides required the greatest total fluences (40–80 J/cm2), and the forehead required
intermediate fluences (30–60 J/cm2).
Weinstein concluded that although the Er:YAG laser can successfully remove both
superficial and deeper wrinkles with great accuracy, there was often significant bleeding
associated with deeper Er:YAG laser resurfacing. She suggested that deeper wrinkles were
best treated with either a modulated Er:YAG laser or a CO2 laser (See Chapter 5).
Weinstein8
Scanners, some similar to those used with CO2 lasers, are designed to maximize the evenness
of Er:YAG laser ablation.
Weinstein studied 141 patients with a variety of skin conditions (pigmentation, wrinkles,
acne scars, other scars) using a computerized scanning Er:YAG laser. The majority of
periocular and perioral wrinkles showed good to excellent improvement. The majority of acne
scars showed good improvement (at 3–12 months follow-up period). The time to re-
epithelialization was reported as 5–10 days. This length of time compared favorably with the
CO2 laser resurfacing healing time of 7–14 days. Side effects, including erythema,
hyperpigmentation, infection, acne, and ectropion, were quite rare. Hypertrophic scarring
developed in one patient. There were no cases of hypopigmentation.
Weinstein found that scanning Er:YAG laser systems were fast, precise, and lead to
cosmetically pleasing results with minimal post-operative morbidity and a low incidence of
side effects.
Goldberg and Meine,9 and Goldman et al.10

Laser resurfacing of neck skin is particularly challenging because of its relatively thinner
epidermis and decrease in vascularity and adnexal structures. The inferior half of the neck is
particularly prone to scarring. Because of the increased risk of scarring after neck
resurfacing, the goals should be modest: to improve pigmentary mottling coupled with slight
wrinkle improvement. The following two studies achieved cosmetic benefits while avoiding
permanent sequelae.
Goldberg and Meine used the short-pulsed Er:YAG laser to resurface the necks of ten
patients. They resurfaced necks with four laser passes and fluences of less than 5 J/cm2. All
patients showed fair to excellent results with no scarring or pigmentary changes at the 6-
month follow-up. They had a minimum of 25% improvement in their wrinkles and 50%
improvement in their mottled pigmentation. All patients were completely healed within 10
days and resolution of erythema occurred at 7–20 days.
Goldman et al.10 used two passes with higher fluences and achieved similar results (follow-
up at 3 months). Overall, there was a 51% satisfaction rating among patients. Skin texture
improved by an average of 39%. Skin color improved by an average of 37%. Rates of healing
and erythema resolution were comparable to those reported by Goldberg and Meine except for
one case of post-treatment infection which led to delayed resolution of erythema.
Koch and Cheng11

Koch and Cheng evaluated 25 patients undergoing full-face CO2 laser resurfacing compared
to 25 patients undergoing full-face Er:YAG resurfacing. They compared re-epithelialization at
1 week, erythema at 1 month, and improvement in elasticity and rhytide resolution at 6
months.
Results with a CO2 laser in the superpulse mode (at 6 W, 730 µs pulse duration, and a
fluence of 4.7 J/cm2) were compared with those of an Er:YAG laser (at 14 W, 350 us pulse
duration, and a fluence of 4.7 J/cm2). It should be noted that parameters were selected to
provide identical fluences between the laser systems compared in this study.
Visual grading at 1 week found 100% re-epithelialization in patients treated with Er:YAG
laser versus 70% re-epithialization in those treated with CO2 laser (mean time for re-
epithelialization was 8 days). At one month, 0% of the patients treated with the Er:YAG laser
and 60% of the patients treated with CO2 laser still had erythema.
The CO2 laser group had the most dramatic improvement in rhytide resolution and
improved elasticity (measured at 6 months by a cutometer at 18.2% mean increase in skin
elasticity). Visual assessment found an 80% improvement in the CO2 laser cohort and 45%
improvement with the Er:YAG laser treated group.
The authors concluded that the short-pulsed Er:YAG laser has the quickest recovery period
but the most limited long-term benefits. At the other end of the spectrum, CO2 laser
treatment had the longest recovery period but the most dramatic long-term results.
Adrian4
Adrian also compared pulsed CO2 and short-pulsed Er:YAG laser resurfacing. He performed a
bilateral study (20 patients) where half the patient’s face was treated with a CO2 laser and the
other half was treated with an Er:YAG laser (at 5 J/cm2). He noted similar bilateral results for
superficial rhytides. However, better results were achieved with the CO2 laser for deeper
rhytides.
He concluded that CO2 laser induced thermal damage was responsible for the improvement
seen with severe rhytides.
Hughes,12 and Fitzpatrick et al.13

Hughes attempted to quantify skin contraction following short-pulsed Er:YAG laser
resurfacing. Using lentigines as skin markers, five square areas on the volar forearm on each
of two human volunteers were ablated with the Er:YAG laser. The goal of this study was to
achieve epidermal and upper papillary dermal ablation. Two to three passes were delivered
using the 5-mm handpiece at 2.1–4.6 J/cm2. There was no post-operative bleeding. The
distance between skin markers was measured before, immediately after, at 3 days, and then
weekly for 16 weeks.
The results were an immediate 4% linear tightening of skin, which persisted at 3 days,
increased to 8% at 1 week, was 11% at 2 and 4 weeks, 13% at 6 weeks, and 14% at 16
weeks.
This small, yet appreciable, tissue contraction may reflect the small amount of thermal
damage associated with even short-pulsed Er:YAG laser resurfacing. This effect most likely
contributes to the small amount of clinical tightening seen following short-pulsed Er:YAG
laser resurfacing.
Fitzpatrick et al. have documented a much higher intraoperative collagen tightening (43%
intraoperatively in the vertical plane, 31% intraoperatively in the horizontal plane), associated
with CO2 laser resurfacing. This tissue contraction phenomenon tends to diminish in time.
Nevertheless, they have also observed a delayed onset increase in ‘tissue tightening’
associated with Er:YAG laser resurfacing. Fitzpatrick et al. suggest that this Er:YAG laser
related process is not true tissue contraction, but rather wound contracture.
HISTOLOGIC STUDIES
Histologic studies have helped explain the tissue effects of short-pulsed Er:YAG laser
resurfacing. Studies have evaluated the depth and uniformity of ablation, as well as the
associated thermal damage zone. Human and animal in vivo models have helped in
evaluating the effects of this laser on physiologic normal living skin. A series of studies are
presented below that summarize the most pertinent histologic findings. The microscopic
findings of CO2 resurfacing have been summarized in Chapter 3.14,15 The microscopic and
clinical effects of short-pulsed Er:YAG laser resurfacing differ from those seen after CO2 laser
treatment in the following ways: (i) during or immediately after the short-pulsed Er:YAG laser
treatment, there is only a fine band of histologic thermally denatured collagen, little clinical
immediate wound contracture, and imperfect hemostasis; (ii) one day after surgery, there is
an irregular band of PMNs extending from the wound surface with associated fibrin and an
abundance of eosinophils; (iii) there is usually rapid clinical epithelialization (3–5 days); (iv)
wound contracture typically begins only 2–4 days after surgery; (v) there is no biphasic
contraction pattern as seen following a CO2 laser treated wound; and (vi) histologic findings
60 days after Er:YAG laser wounding demonstrate less tightly packed collagen fibers with a
less horizontal orientation of elastic fibers than seen following CO2 wounds.16
Hohenleutner et al.17 and Majaron et al.18

These two studies evaluated human skin (in vitro and in vivo)17 and rat skin (in vivo)18 to
examine post Er:YAG laser depths of ablation and thermal damage in addition to the effects
of varying fluences and pulse stackings. Both studies showed that fluence was the most
crucial determinant of ablation. Repetition rate rather than fluence can significantly increase
thermal damage. The ablation threshold, the energy density required to ablate, was found to
be 1.6 J/cm2. Previous authors have reported that a single pass with the short-pulsed Er:YAG
laser at typical settings (3–10 J/cm2) ablates at between 10–40 μm with 5–30 μm of thermal
damage.2,8
Hohenleutner et al.17 used an Er:YAG laser with a maximum pulse energy of 500 mj, 250
us pulse duration, 3–4-mm spot size and fluence of 4–7 J/cm2. Sixty human skin specimens
were histologically evaluated.
The ablation threshold was found to be 1.6 J/cm2 (corresponds to 200 mj per pulse with a
4-mm spot size). The ablation threshold efficacy was between approximately 2.5 and 4.0 μm
per pulse per J/cm2. As expected, the highest pulse energy (500 mJ) and the largest spot size
(4 mm), led to the most effective ablation. At low repetition rates, ablation rates increased
linearly with fluence. With increasing pulse stacking, the ablation per pulse decreased
significantly.
The zone of thermal damage only minimally increased with increasing fluences. However,
the amount of thermal damage clearly increased with high repetition rates (around 25 μm
with < 10 consecutive impacts, up to 100 μm with 40 consecutive impacts).
Majaron et al.18 performed an in vivo animal study to further evaluate the potential for deep
thermal damage by stacking repetitive Er:YAG laser pulses (pulse stacking).
Ten sites on the back of a rat were irradiated with one to ten laser pulses at a repetition
rate of 10 or 33 Hz. The chosen Er:YAG laser delivered 0.8–1.4 J/cm2 with a 4-mm handpiece
and scanner. Punch biopsies were taken 1 hour after laser exposure. Two blinded examiners
used an optical micrometer to determine the depth of thermal injury (measured from the
dermal–epidermal junction).
For single pulse exposure, an overall 12 μm of residual thermal damage was observed. The
depth of thermal damage increased dramatically when three to ten low-fluence Er:YAG laser
pulses were stacked at a repetition rate of 10 or 33 Hz. By pulse stacking at frequencies of 10
and 33 Hz, thermal damage greater than 200 μm below the dermal–epidermal junction was
achieved. However, there were no significant differences in thermal damage when the
repetition rates were varied from 10 to 33 Hz. It should be noted that this saturation of
thermal damage, achieved by pulse stacking, has also been shown by Fitzpatrick et al. with
the CO2 laser.19
Majaron et al. also demonstrated that coagulation of dermal collagen, deeper than 200 μm
below the dermal–epidermal junction, was possible by pulse stacking with the Er:YAG laser.
This is in contrast to single pulse traditional Er:YAG laser irradiation, where coagulation
depths beyond 30–50 μm are not possible.
Alster20
In this double blinded, prospective study, six commercially available Er:YAG laser systems
were compared both clinically and histologically.
The facial halves of twelve patients with mild photodamage and/or atrophic scars were
randomly resurfaced with one of six laser systems. Identical laser technique (three passes)
was performed by a single laser operator with equivalent parameters (5 J/cm2). Adjacent
spots or scans were placed with approximately 30% overlap. Partially dessicated tissue was
removed with saline-soaked gauze after each pass. Punch biopsies were obtained from pre-
auricular skin at baseline and immediately after surgery for all six laser systems. Clinical
assessments were performed at multiple intervals and up to 1 year.
Equivalent clinical and histological results were seen with all six studied shortpulsed
Er:YAG lasers. A mean clinical improvement of 50% (25–75%) was observed, with mild
photodamage showing greater improvement than acne scars. Length of time for complete re-
epithelialization (typically 0.5 weeks) and severity and duration of erythema (1–2 weeks) did
not vary from system to system.
Histopathologic results revealed equivalent depths of tissue ablation and lack of residual
dermal thermal damage in all six studied Er:YAG laser systems. This study confirmed that
depth of ablation, following Er: YAG laser resurfacing, is determined by fluence. This report
also demonstrated that with identical fluences, similar Er:YAG systems ablate to similar
depths. Three laser passes with all systems ablated the epidermis to the level of the dermal–
epidermal junction. This minimal depth of ablation, coupled with the lack of thermal damage,
presumably accounts for the only mild improvement (50% overall) in superficial rhytides and
acne scars.
Alster noted that further clinical improvement and delayed hypopigmentation were not
present 1 year after short-pulsed Er:YAG laser resurfacing. This contrasts with the findings
that may occur following CO2 laser resurfacing.21 She and others16 attributed the
photothermal effect of CO2 laser resurfacing to the immediate collagen shrinkage, continued
collagen deposition, and potentially greater morbidity associated with CO2 laser resurfacing.
Alster suggested that the Er:YAG laser may be used for mild photodamage and atrophic
scars. The CO2 laser was to be considered for moderate to severe cutaneous involvement.
Khatri et al.22
Khatri et al. also performed a comparative clinical and histological study following Er:YAG
and CO2 laser resurfacing of facial rhytides. Their findings were similar to those of Alster et
al.20 They suggested that the short-pulsed Er:YAG laser was suitable for mild photodamage.
In this study, participants were followed for 6 months and clinically evaluated by a blinded
panel of experts. Twenty-one subjects with perioral and periorbital rhytides were treated.
Twelve subjects had class II rhytides, eight had class III rhytides, and one had class I
rhytides. All patients applied 0.05% tretinoin cream to the treatment area daily for 3 weeks
before treatment. One side of the face was treated with a CO2 laser and the contralateral side
was treated with an Er:YAG laser.
The two systems utilized were: (i) a pulsed CO2 laser producing a 3-mm spot, pulse
duration of 800 us, fluences of 3.5–6.5 J/cm2; and (ii) an Er:YAG laser producing a 5-mm
spot, pulse duration of 300 us, and fluences of 5–8 J/cm2. No scanners were used on either
side. The number of Er:YAG laser passes was determined by the operator in order to create a
symmetric intraoperative appearance.
The CO2 laser side demonstrated statistically significantly greater wrinkle improvement
when evaluating all subjects. However, in patients receiving more than five passes of Er:YAG
laser treatment, improvement scores were not significantly different from those of CO2 laser
resurfacing. Post-treatment erythema resolved faster on the Er:YAG laser sides than on the
CO2 laser sides at 2 and 8 weeks. Hypopigmentation was significantly decreased on the
Er:YAG laser-treated sides (5%), compared to the CO2 laser-treated sides (43%).
Histologic evaluation showed residual thermal damage of up to 50 μm on the Er:YAG
treated side and up to 200 μm on the CO2 laser treated side.
This informative study demonstrated that a short-pulsed Er:YAG laser treatment, at similar
fluence and number of passes as used with a CO2 laser, produced more superficial ablation
and promoted faster healing, but was somewhat less effective. By increasing the number of
short-pulsed Er:YAG laser passes (to greater than five), the depth of injury can be increased
to mimic that seen with standard CO2 laser resurfacing. However, such a multi-pass Er:YAG
laser procedure is time consuming and is associated with poor hemostasis.
Khatri et al. concluded that the Er:YAG laser should be used for mild photodamage or in
patients in whom the CO2 laser induced reversible side effects of erythema or
hyperpigmentation would not be well tolerated.
Utley et al.23 and Greene et al.24

Utley et al. and Greene et al. published further studies comparing the in vivo histologic effects
of the CO2 and Er:YAG lasers. Histologic analysis was performed at 1 hour and 7 days after
treatment in the Ultey et al. study and 4–6 months after treatment in Greene et al. study.
In the study conducted by Utley et al.,23 ten patients, with Fitzpatrick skin types II or III,
underwent laser treatment to left pre-auricular sites as follows: CO2 laser alone (four passes),
Er:YAG laser alone (eight passes), and various combinations of these modalities. The right
pre-auricular area was identically treated 1 hour prior to rhytidectomy. Laser-treated skin
was excised during rhytidectomy and evaluated histopathologically with an optical
micrometer in a blinded manner.
The two utilized lasers were a superpulsed CO2 laser used at a fluence of 4.7 J/cm2 and a
short-pulsed Er:YAG laser used at an identical fluence of 4.7 J/cm2.
All specimens were clinically re-epithelialized at 7 days. New collagen was seen with
histologic examination in all groups after 7 days. There was no statistical differences between
groups. There was also no statistically significant difference in the amount of inflammation
detectable between the groups after 7 days. Epidermal thickness after 7 days was greater in
all treated subjects; epidermal thickness was greater in the Er:YAG laser group and less in
the CO2 laser group. Papillary dermal thickness after 7 days also increased in all treated
subjects.
Specimens treated 1 hour prior to excision were graded for level of thermal collagen injury
and depth of ablation. There was less evidence of thermal collagen injury and thermal
necrosis in the solely Er:YAG laser-treated group compared to the solely CO2 laser-treated
group.
Depth of ablation was measured in both the CO2 and Er:YAG laser-treated groups. Using a
fluence of 4.7 J/cm2 in the CO2 laser treated group, four passes resulted in a mean ablation
of 250±540 μm (mean 62.5 μm per pass). In the Er:YAG laser group, eight passes resulted in
a mean ablation of 160 ± 528 μm (mean 20 μm per pass).
This short-term (1–7 days) histologic study showed that at 7 days, re-epithelialization is
complete and new collagen formation was observed equally in patients treated with the
Er:YAG and the CO2 lasers. The Er;YAG laser specimens had the least amount of collagen
injury and thermal necrosis. At 7 days, both epidermal and papillary dermal thickness were
greater in the Er:YAG laser group than in the CO2 laser group. The authors concluded that
the short-pulsed Er:YAG laser’s lessened thermal injury may allow for more exuberant re-
epithelialization and dermal regeneration.
Greene et al.24 designed a similar study using the same two lasers and identical parameters.
The purpose of their study was to examine the histologic changes resulting from patients’
healing response to laser treatment on a long-term follow-up of 4–6 months.
Nine patients with actinic damage were treated. The pre-auricular area was treated with
either CO2 laser alone (four passes) or short-pulsed Er:YAG laser alone (eight passes). Each
patient was clinically evaluated daily for 1 week and then weekly over a 4–6 month period. At
4–6 months, five patients underwent rhytidectomy, and their laser-treated skin was evaluated
histologically.
Histologic studies showed that CO2 laser treatment produced the greatest thickness of
neocollagen, the highest neocollagen density, and the greatest decrease in elastosis. However,
CO2 laser-treated sites also took the longest time for healing and resolution of erythema and
inflammation (up to 6 months). Those sites solely treated with the short-pulsed Er:YAG laser
produced the least collagen density, the thinnest band of neocollagen and a smaller decrease
in elastosis than seen with CO2 laser-treated sites. However, Er:YAG laser-treated sites
showed the most rapid resolution of erythema and inflammation (within 10 days).
Greene concluded that collagenesis was greatest with the CO2 laser and least with the
short-pulsed Er:YAG laser. Elastosis decreased to the greatest degree following CO2 laser
treatment, less with short-pulsed Er:YAG laser treatment.
MY APPROACH
I have found short-pulsed Er:YAG lasers to be highly effective when used for the treatment of
Class I and early Class II rhytides (Figures 4.4–4.59). These less aggressive ablative lasers can
be used successfully in the treatment of Fitzpatrick skin types I–IV. However, it should be
expected that even with these lasers darker skin types will show some evidence of post-
inflammatory hyperpigmentation. I have not noted any method of pre-treatment that will
consistently stop this. However, as a general rule the hyperpigmentation is self-limited. It
appears to be most profound in those individuals with a history of melasma. Prior to
treatment, I start all patients on oral antiviral agents and antibiotics.
of photodamage. Although full-face procedures can be performed with appropriate local
Generally I will treat the affected areas with sufficient fluence and number of passes to
achieve a depth of ablation of 100–200 μm. It should be noted that with CO2 lasers, more
than three passes appears to provide more thermal damage, but not much in the way of any
further ablative damage. This contrasts with short-pulsed, purely ablative Er:YAG lasers.
With these systems each pass leads to further ablation. Thus the advantage of these lasers
can also be their weakness. Precise control of ablation can be used for those with early
photodamage. Conversely, a very aggressive ablative approach with short-pulsed Er:YAG
lasers can penetrate more deeply into the dermis than is seen with thermal CO2 lasers.
Wiping away of debris between passes is not required with short-pulsed Er:YAG lasers.
The ideal treatment parameters must be individualized for each patient, based on clinical
experience and professional judgment. Whatever energies are chosen, tapering along the
mandible and the pre-auricular areas should be carried out at lesser fluences. Although we
and others have used short-pulsed Er:YAG lasers on the necks, it should not be the first
anatomic site treated by the novice laser surgeon.
mandatory. There are physician advocates for post-laser open dressings and physician
advocates for closed dressings. We have used them both. What is important is that the wound
be kept moist until complete re-epithelialization has occurred. This usually occurs within 5–7
days. Use of antiviral agents is mandatory during this entire period. Full re-epithelialization
after 7 days is to be expected.
After re-epithelialization, mild to moderate erythema will be seen. This usually tends to be
generalized in the treatment area and can last up to 3 months or longer. Localized hardened
erythema, or erythema that lasts more than 6 months, is suggestive of the onset of
hypertrophic scars. This should be managed aggressively (See Chapter 8).
There are now significant accumulated data about the short-pulsed Er:YAG laser. This
laser provides a predominantly ablative effect. It is ideal for resurfacing those with early
photodamage.
Figure 4.4. Before Er:YAG laser resurfacing
Figure 4.5. One day after Er:YAG laser resurfacing

Figure 4.6. One week after Er:YAG laser resurfacing
Figure 4.7. Three months after Er:YAG laser resurfacing

ERBIUM:YAG LASER RESURFACIN 79
Figure 4.9. Immediately after Er:YAG laser resurfacing



Figure 4.14. Five days after Er:YAG laser resurfacing
Figure 4.15. Four weeks after Er:YAG laser resurfacing


Figure 4.19. Six months after Er:YAG laser resurfacing


Figure 4.22. Four days after Er:YAG laser resurfacing
Figure 4.23. One month after Er:YAG laser resurfacing




Figure 4.30. Two weeks after Er:YAG laser resurfacing
Figure 4.31. One month after Er:YAG laser resurfacing



Figure 4.37. Two months after Er:YAG laser resurfacing


Figure 4.41. Five days after Er:YAG laser resurfacing





Figure 4.51. Two months after Er:YAG laser resurfacing

Figure 4.52. Twelve months after Er:YAG laser resurfacing


Figure 4.56. 12 months after Er:YAG laser resurfacing
Figure 4.57. Before Er:YAG neck laser resurfacing

Figure 4.58. Immediately after Er:YAG neck laser resurfacing
Figure 4.59. Six months after Er:YAG neck laser resurfacing

REFERENCES
1 Fleming D. Controversies in skin resurfacing: The role of the Erbium:YAG Laser. J Cutan
Laser Ther 1999;1:15–21.
2 Kaufman R, Hibst R. Pulsed Erbium:YAG laser ablation in cutaneous surgery. Lasers
Surg Med 1996; 19:324–30.
3 Weinstein C. Erbium laser resurfacing: Current concepts. Plast Reconstr Surg 1999;103:
602–16.
4 Adrian RM. The Erbium:YAG laser: Facts and fiction. Dermatol Surg 1998;24:296.
5 Teikemeier G, Goldberg DJ. Skin resurfacing with the Erbium:YAG laser. Dermatol Surg
1997;23:685–7.
6 Perez MI, Bank DE, Silvers D. Skin resurfacing of the face with the Erbium:YAG laser.
Dermatol Surg 1998;24:653–9.
7 Goldberg DJ, Cutler KB. The use of the Erbium:YAG laser for the treatment of class III
rhytides. Dermatol Surg 1999;25:713–15.
8 Weinstein C. Computerized scanning Erbium:YAG laser for skin resurfacing. Dermatol
Surg 1998;24:83–9.
9 Goldberg DJ, Meine J. Treatment of photoaged neck skin with the pulsed Erbium:YAG
laser. Dermatol Surg 1998;24:619–21.
10 Goldman MP, Fitzpatrick RE, Manuskiattti W. Laser resurfacing of the neck with the
Erbium:YAG laser. Dermatol Surg 1999;25; 164–8.
11 Koch RJ, Cheng E. Quantification of skin elasticity changes associated with laser skin
resurfacing. Arch Facial Plast Surg 1999;1:159–64.
12 Hughes PSH. Skin contraction following Erbium:YAG laser resurfacing. Dermatol Surg
1998;24:109–11.
13 Fitzpatrick RE, Rostan EF, Marchell N, et al. Collagen tightening induced by carbon
dioxide laser versus Erbium:YAG laser. Lasers Surg Med 2000;27;395–403.
14 Zelickson, B, Ross EV. Presented at the Annual Meeting, American Society of Lasers
Surgery and Medicine, New Orleans, 4/01.
15 Ratner D, Tse Y, Marchell N, et al. Cutaneous laser resurfacing. J Am Acad Dermatol
1999;41:365–89.
16 Ross EV, Naseef GS, McKinlay JR, et al. Comparison of carbon dioxide laser, Erbium:YAG
laser, dermabrasion, and dermatome. Dermatol Surg 2000;42:92–105.
17 Hohenleutner U, Hohenleutner S, Baumier W, et al. Fast and effective skin ablation with
an Er:YAG laser: Determination of ablation rates and thermal damage zones. Lasers Surg
Med 1997;20:242–7.
18 Majaron B, Srinivas SM, Huang HL, et al. Deep coagulation of dermal collagen with
repetitive Er:YAG laser irradiation. Lasers Surg Med 2000;26:215–22.
19 Fitzpatrick RE, Ruiz-Espara J, Goldman MP. The depth of thermal necrosis using CO2
laser: A comparison of the superpulsed mode and conventional mode. J Dermatol Surg
Oncol 1991; 17:340–4.
20 Alster T. Clinical and histologic evaluation of six Erbium:YAG lasers for cutaneous
resurfacing. Lasers Surg Med 1999;24:87–92.
21 Alster T. Cutaneous resurfacing with CO2 and Erbium:YAG lasers: Plast. Reconstr Surg
1999;103:1–13.
22 Khatri KA, Ross V, Grevelink JM, et al. Comparison of Erbium:YAG and carbon dioxide
lasers in resurfacing of facial rhytides. Arch Dermatol 1999;135;391–7.
23 Utley DS, Koch RJ, Egbert BM. Histologic analysis of the thermal effect on epidermal and
dermal structures following treatment with the superpulsed CO2 laser and the
Erbium:YAG laser: An in vivo study. Lasers Surg Med 1999;24:93–102.
24 Greene D, Egbert BM, Utley DS, et al. In vivo model of histologic changes after treatment
with the superpulsed CO2 laser, Erbium:YAG laser, and blended lasers: A 4–to 6–month
prospective histologic and clinical study. Lasers Surg Med 2000;27:362–72.
5
COMBINED ERBIUM:YAG/CO2 LASER AND VARIABLE
PULSED ERBIUM:YAG LASER
KEY POINTS
(1) Laser resurfacing with either sequential CO2 and Er:YAG lasers; a combined
Erbhtm:YAG/CO2 laser; or a variable pulsed Erbium:YAG laser can achieve clinical
and histologic results equivalent to that seen with CO2 laser resurfacing
(2) Laser resurfacing with either sequential CO2 and Er:YAG lasers; a combined
Erbium:YAG/CO2 laser; or a variable pulsed Erbium:YAG laser may lead to a
decreased amount and greater control of thermal injury
(3) Clinical studies using either sequential CO2 and Er:YAG lasers; a combined
Erbium:YAG/CO2 laser; or a variable pulsed Erbium:YAG laser demonstrate
decreased post-treatment time to complete re-epithelialization, compared to CO2
laser treatment
(4) Clinical studies with a combined Erbium:YAG/CO2 laser demonstrate decreased time
to complete resolution of post-operative erythema
(5) Clinical studies with a combined Erbium:YAG/CO2 laser demonstrate decreased
occurrence of clinically significant or permanent post-operative hyperpigmentation
and hypopigmentation
BACKGROUND
Previous studies with CO2 lasers demonstrate that this modality ablates approximately 100
μm of skin, leaving an additional 50–300 μm of collateral thermal damage.1–3 This thermal
damage promotes collagen contraction and remodeling.4–6 However, it can also lead to
prolonged recovery time and complications.7–9
Studies with short-pulsed Erbium:YAG (Er:YAG) lasers, with their higher water absorption
rate and shorter pulse duration than CO2 lasers, demonstrate tissue ablation of 20 to 40 μm
with each pass, and collateral thermal damage of 5 to 30 μm (see Chapter 4).10,11 This amount
of tissue ablation and thermal damage is typically much less than that seen with CO2 laser
resurfacing.
In theory, combining the deep tissue penetration of a CO2 laser with the fine depth control
of an Er:YAG laser may improve clinical outcome, and decrease both recovery time and
associated complications. The use of combinations of CO2 lasers and Er:YAG lasers prompted
the development of alternative laser resurfacing technology. One such system, the DermaK
laser, is a combined CO2/Er:YAG laser. This system combines simultaneous low fluence CO2
laser and short-pulsed Er:YAG laser delivery.12,13 Such a laser delivers the combined deep
thermal damage and associated collagen remodeling of a CO2 laser with the more precise
ablative capacity of an Er:YAG laser.14 Another new approach to laser resurfacing are the CO3
and Contour variable pulsed Er;YAG lasers. The CO3 laser is a single variable pulse width
Er:YAG laser. The Contour laser, is in fact, two separate Er:YAG lasers that fire almost
simultaneously. One of these lasers is a short-pulsed Er:YAG laser. The other laser emits a
longer variable pulse width Er:YAG laser pulse.15 The variability seen with both of these
lasers allows the user to choose various levels of tissue ablation and/or coagulation. These
choices can provide a unique degree of control in resurfacing that is not provided by either
standard short-pulsed Er:YAG or CO2 lasers.
CLINICAL STUDIES
Manuskiatti et al.16
Manuskiatti et al. performed one of the earliest clinical evaluations of sequential CO2 and
Er:YAG laser treatment. In this study, 30 patients were treated with full-face CO2 laser
resurfacing. Some were then treated with a short-pulsed Er:YAG laser in an attempt to
remove a portion of the CO2 laser induced residual thermal damage. Post-operative follow-up
varied with each patient.
According to the authors, all deep rhytides and all deep acne scars responded better to
sequential CO2/Er:YAG laser treatment compared to CO2 laser treatment alone. Healing times
were on average 2–3 days shorter with sequential treatment.
Cho and Kim17

Cho and Kim further evaluated the effect of sequential CO2 and Er:YAG laser resurfacing.17 A
total of 158 Korean patients with atrophic scars were treated with the UltraPulse short-
pulsed, high energy CO2 laser. This treatment was immediately followed by short-pulsed
Er:YAG laser ablation. Average follow-up periods were 10.6 months.
Most patients showed full re-epithelialization in 6–7 days. The clinical results were as
follows: 32 patients showed > 90% improvement, 65 patients showed 80–89% improvement,
56 patients showed 70–79% improvement, and five patients showed < 69% improvement.
Post-operative erythema was present in 100% of patients and lasted an average of 84 days.
All patients also developed edema and pruritis that resolved in 2 weeks. A sensation of
tightness, noted in many, resolved in 4 weeks. Twenty-two patients developed post-
inflammatory hyperpigmentation. The majority of subjects with post-inflammatory
hyperpigmentation showed resolution within 2 months.
McDaniel et al.18
McDaniel et al. also investigated the laser resurfacing effects of sequential CO2 and Er:YAG
laser treatment. Twenty patients were treated on both sides of the upper lip with two non-
overlapping passes using the CO2 laser (300 mJ, spot size 2.25 mm). One side of the lip was
then treated with an additional three 10% overlapping passes of the Er:YAG laser (2J, 7-mm
spot size). The lateral borders of all treated areas were feathered with two passes of the Er:
YAG laser for maximum cosmetic results. All patients kept a daily diary of side effects. Serial
photographs were taken pre-operatively, immediately post-operatively, at 3, 6 and 10 days,
and 1, 2, and 4 months.
Patient diary data revealed less crusting on the side treated with both CO2 and Er:YAG
lasers. There was a 17% reduction in the average time to re-epithelialization on the side
treated with both CO2 and Er:YAG lasers, compared to the CO2-alone laser-treated sites.
Clinical evidence of erythema, as well as improvement of perioral rhytides, was the same in
both treatment groups. There were no reported long-term adverse effects.
COMBINED ERBIUM:YAG/CO2 LASER AND VARIABLE PULSED LASER 109
Goldman and Marchell13

Goldman and Marchell were among the first to evaluate the effect of a combined CO2/Er:YAG
laser. In their study, eleven patients were treated with two passes of the combined CO2/
Er:YAG laser (CO2 laser; 5 W and 50 ms pulse), Er:YAG laser; (1.7 J and 4-mm spot size) on
the neck, and four passes of the CO2/Er:YAG laser (same settings) on the face. The patients
were monitored for 2 weeks postoperatively and then re-evaluated at 3–6 months.
Physician evaluation demonstrated moderate improvement (~50%) in skin color and marked
improvement (~75%) in skin texture and wrinkling. Most of the patients felt that they had a
75–100% improvement in their skin texture. The overall patient satisfaction rating was 75–
100% in 10 out of 11 patients, with one patient giving a rating of 50–74%. There was no
hypopigmentation or scarring demonstrated in this study.
Weinstein19
Weinstein investigated the use of the same combined CO2/Er:YAG laser for the treatment of
acne scars. In this study, 78 patients with acne scarring were evaluated. A total of 63
subjects were treated with the Er:YAG laser alone; 15 patients were treated with two passes
of the combined CO2/Er:YAG laser (CO2 laser: 2–3 W, 50ms pulse; and Er:YAG laser: 18J/cm2).
The shoulders of all deep scars were further treated with another Er:YAG laser pass (7 J/
cm2). No patients were pretreated with topical bleaching agents or tretinoin. All results were
graded by each patient, in addition to two independent nurses and a dermatologist at 6
weeks, 3, 6, and 12 months.
This study showed that all patients achieved between fair (50–70% correction) and good (70–
90%) correction. All patients were satisfied with their results. The mean time to re-
epithelialization was 7.3 days for Er:YAG laser treatment alone, versus 9.6 days when the
combined CO2/Er:YAG laser was used. Erythema lasted longer following treatment with the
combined CO2/Er:YAG laser system—an average of 7.3 weeks. There was no difference in the
incidence of post-inflammatory hyperpigmentation between the Er:YAG laser-alone treated
side versus the combined CO2/Er:YAG laser treated side. All post-inflammitory
hyperpigmentation responded to treatment with bleaching preparations. A total of six patients
had mild hypopigmentation. There was no difference in the incidence of hypopigmentation
between both treatment groups. No patient had cosmetically significant hypopigmentation at
the 6- and 12-month evaluations.
Weinstein and Scheflan14

Weinstein and Scheflan reported on the use of the combined CO2/Er:YAG laser (varied
parameters) in over 500 patients. The authors reported that the average time for re-
epithelialization was 11.3 days. They found that post-operative erythema lasted an average of
8.3 weeks. The authors noted temporary hyperpigmentation in 4.4% of patients, induration of
the upper lip in 2.2% of patients, hypertrophic scarring in 0.7% of patients, acne flare in 2.9%
of patients, cosmetically insignificant hypopigmentation in 6.6% of patients, and cosmetically
significant hypopigmentation in 1.5% of patients. Most of these side effects resolved with
time, with the exception of hypopigmentation.
Newman et al.20
Newman et al. investigated the effects of the CO3 variable pulsed Er;YAG laser (CO3 laser) on
perioral rhytides, and compared these results with CO2 laser treatment. In this study, 21
patients had CO2 laser treatment (95 W, 300 mJ) on one side of the upper lip and variable
pulsed Er:YAG laser treatment (variety of parameters) on the other side. Photographs were
taken immediately after treatment and at post-operative days 3, 7, and 14, and at 1 and 2
months. All evaluations were undertaken in a blinded manner by physicians as well as a team
of trained research assistants.
This study demonstrated that crusting resolved in an average of 3.5 days following variable
pulsed Er:YAG laser treatment, versus 7.8 days following CO2 laser treatment. There was no
statistical difference in post-operative erythema between the two treatments. Overall rhytide
improvement was 54% with variable pulsed Er:YAG laser treatment, versus 63% with CO2
laser treatment. There were no permanent adverse effects at the 2-month follow-up period.
HISTOLOGIC STUDIES
Millman and Manner21

Millman and Mannor were the first to publish both clinical and histologic results in a series
of 23 patients whose eyelid skin was treated with a combination of Er:YAG and CO2 lasers.
Patients were first treated with two passes of the short-pulsed Er:YAG laser (1 J and a 3-mm
spot size) followed by a single pass of a pulsed CO2 laser (300 mj). Patients were evaluated
daily for 2 weeks, until the occurrence of complete skin re-epithelialization, and then monthly
for 6 months. These patients were compared to a historical control group of 25 patients
whose eyelid skin had been treated with two passes of the same CO2 laser at the same
settings. Biopsies were obtained after re-epithelialization on post-operative days 8–10 from all
patients.
This study demonstrated re-epithelialization occurring in 7 days in the combined treatment
group vs. 12 days in the CO2 laser-alone control group. The study also demonstrated that
post-operative erythema persisted for 2.5 weeks in the combined treatment group, compared
to 7 weeks in the control group. Biopsy specimens revealed minimal superficial papillary
thermal necrosis in the combined treatment group. The dermis in the control CO2 laser-alone
treated group demonstrated extensive thermal coagulative necrosis into the deep reticular
dermis. There were no permanent complications in any treated patients. Cosmetic outcome
was similar in both groups.
Goldman and Manuskiatti22

Goldman and Manuskiatti also evaluated the facial resurfacing effect of sequential CO2 and
Er:YAG laser treatment. In this study, 10 patients received three passes with the 950 us
pulsed UltraPulse CO2 laser (300 mJ) to one half of the face, and two passes of the same
pulsed CO2 laser followed by two passes with a short-pulsed Er:YAG laser (1.7 J and 4-mm
spot size) to the other side of the face. Clinical photographs and histologic specimens were
taken before resurfacing, immediately after resurfacing, 2–3 days post-operatively, 1 week
post-operatively, and 4–8 weeks post-operatively. All specimens and photographs were
evaluated in a blinded manner.
The average extent of histologic thermal damage immediately after resurfacing was 80 μm
for skin treated with the CO2 laser alone vs. 20 μm for skin treated with a combination of CO2
and Er:YAG lasers. There was less inflammation at 2–3 days in the combined group. Re-
epithelialization occurred 1–2 days faster in the CO2/Er:YAG laser treated group. Erythema
resolved within 2–3 weeks in skin treated with the combination of CO2 and Er;YAG lasers.
Erythema persisted at the 8-week follow-up in all skin treated with CO2 laser alone. There
was no difference in the improvement rating between the two treatment groups.
Goldman et al.13
Goldman et al. further evaluated the safety, efficacy and histologic impact of the combined
CO2/Er:YAG laser for facial resurfacing. Ten patients were treated with four passes of the
combined CO2/Er:YAG laser (CO2 laser: 5 W, 50-ms pulse and Er:YAG laser: 1.7 J and a 4-
mm spot size). Patients with Type III skin or a history of post-inflammatory
hyperpigmentation were also pre-treated with 4% hydroquinone. Patients were evaluated with
before and after photographs. Histologic specimens were taken before, immediately after the
procedure, and at 3 months post-operatively. All treated patients showed clinical improvement.
There was no incidence of hypopigmentation, hyperpigmentation, or scarring.
The average depth of thermal damage in treated skin was 20 μm immediately after
treatment. All treatments led to a histologic increase in new collagen thickness.
Trelles et al.23
Trelles et al. further investigated the histologic effect of the combined CO2/Er:YAG laser in
their study on philtrum remodeling. In this study, 32 patients were treated for wrinkles of the
upper lip using the combined CO2/Er:YAG laser. The first pass was carried out in the
combined mode (CO2 laser: 5 W, 50 ms pulse and Er:YAG laser: 29 J/cm2, 3-mm spot size). A
second pass was then carried out using only the Er:YAG laser (1.4 J/cm2, 3-mm spot size).
Several further passes were then undertaken to areas of deep wrinkles, with a focus on the
philtrum area. Post-treatment biopsies were undertaken.
The authors reported excellent cosmetic results in all 32 patients, with post-operative
erythema resolving in approximately 2 months. The authors reported no scarring in any of
the treated patients. Histologic evaluation revealed thermal damage in the deep dermal
collagen and indirect stretching of the muscle fibers of the lip.
Utley et al.24
Utley et al. compared the histologic effect of treatment with CO2 laser alone, CO2 laser
followed by short-pulsed Er:YAG laser, short-pulsed Er:YAG laser alone, or short-pulsed
Er:YAG laser followed by CO2 laser treatment. Each of ten patients underwent treatment to
one side of the pre-auricular face, in four separate treatment areas. Treatment areas received
the following: (i) four passes of the CO2 laser alone; (ii) two passes of the CO2 laser followed by
four passes of the Er:YAG laser; (iii) eight passes of the Er:YAG laser alone; and (iv) four
passes of the Er:YAG laser followed by two passes of the CO2 laser. Sequential biopsies were
undertaken up to 1 week after laser treatment.
At 1 hour after treatment, specimens treated with the CO2 laser followed by the Er:YAG
laser, or those treated with the Er:YAG laser alone had the least amount of thermal injury to
collagen. Treatment with the CO2 laser followed by the Er:YAG laser resulted in tissue
ablation of 260 μm and thermal necrosis of 56 μm. This compared to 250 μm of tissue
ablation and 89 μm thermal necrosis for the CO2 laser alone, and 160 μm of tissue ablation
and 43 μm of thermal necrosis for the Er:YAG laser alone. At 7 days after treatment, all
groups had clinically reepithelialized. At 7 days, treatment with the CO2 laser followed by the
Er:YAG laser, or the Er:YAG laser alone, showed the least collagen injury and the greatest
resultant epidermal thickness.
Green et al.25
Green et al. investigated nine patients for long-term post-laser histologic effects after various
treatment modalities. In this study, the nine patients were treated in the pre-auricular face
area with: (i) four passes of the CO2 laser alone; (ii) two passes of the CO2 laser followed by
four passes of the Er:YAG laser; (iii) eight passes of the Er:YAG laser alone; and (iv) five
passes with a combined CO2/Er:YAG laser. The laser parameters used were as follows: (i) CO2
laser—6 W, 730-μs pulse duration; (ii) Er:YAG laser—14 W, 6-mm spot size, 350-μs pulse
duration; (iii) CO2/Er:YAG laser—CO2 laser—3 W, 50-ms pulse, Er:YAG laser—14 W, 6-
mm spot size, 350-μs pulse duration. Patients were followed both clinically and histologically
for 6 months.
This study demonstrated that combined CO2/Er:YAG laser treatment resulted in a mean
collagen thickness, at 6 months after treatment, of 0.21 mm, compared to 0.27 mm with CO2
laser alone and 0.20 mm with CO2 laser followed by Er:YAG laser treatment. Combined CO2/
Er:YAG laser treatment resulted in a new collagen thickness of 2.7 (on a relative scale of 1–5),
compared to 3.4 with CO2 laser alone and 3.6 with CO2 laser followed by Er:YAG laser
treatment. There was a 14% decrease in elastosis with combined CO2/Er:YAG laser
treatment, compared to 27% with CO2 laser alone and 4% with CO2 laser followed by Er:YAG
laser treatment. Treatment with combined CO2/Er:YAG laser resulted in resolution of
erythema at 1 month. In the CO2 laser alone treatment sites, full resolution of erythema was
not seen until 4 months after treatment. Of note, the sites treated with CO2 laser alone were
clinically most improved. The authors also reported clinical results on 100 patients treated
with either CO2 laser alone, Er:YAG laser alone, CO2 laser followed by Er:YAG laser
treatment, or combined CO2/Er:YAG laser treatment (25 patients in each group). The authors
reported complete re-epithelialization in 7 days in 90% of patients treated with a combined
CO2/Er:YAG laser, compared to 70% of patients treated with CO2 laser alone and 100% of
patients treated with CO2 laser followed by Er:YAG laser treatment.
Pozner and Goldberg26

Pozner and Goldberg investigated the biopsy-proven histologic effect of a variable pulsed
Er:YAG laser (Contour) and compared those with the parameters noted on the actual laser
machine. Various depths of ablation and/or coagulation (thermal effect) were utilized on
abdominal skin. Tissue was excised post-operatively and evaluated histologically.
This study demonstrated that the laser panel settings of the variable pulsed Er:YAG laser
did correlate with the amount of both tissue ablation and thermal necrosis seen on histologic
evaluation. The authors also noted that this machine was able to achieve a histologic thermal
effect equivalent to that produced by CO2 laser treatment.
Conclusion
Previous studies suggest that the use of combined individual CO2 and Er:YAG lasers can give
an equivalent clinical outcome to the use of a CO2 laser alone. The more recent development
of the combined CO2/Er:YAG laser has enabled further study on the use of these lasers
together. These most recent studies demonstrate excellent clinical outcomes with decreased
side effects and decreased recovery time. These improvements are associated with more
precise tissue ablation and a more consistent level of thermal damage. Similarly, variable
pulsed Er:YAG lasers have now also been shown to produce both a clinical and histologic
result similar to that seen with CO2 lasers.
MY APPROACH
I have found combined CO2/Er:YAG lasers and variable pulsed Er:YAG lasers to be highly
effective when used for the treatment of Class I–III rhytides and acne scars (Figures 5.1–5.54).
By varying parameters, these ablative lasers can be used successfully in the treatment of
Fitzpatrick skin types I–V. However, it should be expected that almost all Fitzpatrick IV–V
individuals will show some evidence of post-inflammatory hyperpigmentation. I have not
noted any method of pretreatment that will consistently stop this. However, as a general rule
the hyperpigmentation is self-limited. It appears to be most profound in those individuals
with a history of melasma. Prior to treatment, I start all patients on oral antiviral agents and
antibiotics.
of photodamage. Although fullface procedures can be performed with appropriate local
Once the patient is anesthetized all adjacent areas of skin are covered with wet towels.
Generally I will treat the affected areas with one to three passes to achieve a depth of
abalation of 100–200 μm. It should be noted that with standard CO2 laser treatment, more
than three passes appears to provide more thermal damage, but not much in the way of any
further ablative damage. This contrasts sharply with short-pulsed, purely ablative Er:YAG
lasers. With these systems each pass leads to further ablation. Thus the strength of these
lasers can also be their weakness. Precise control of ablation can be used for those with early
photodamage. Conversely, a very aggressive ablative approach with short-pulsed Er:YAG
lasers can penetrate more deeply into the dermis than the thermal CO2 lasers. By varying the
thermal and ablative properties of a combined CO2/Er:YAG laser or a variable pulsed Er:YAG
laser, one can choose and vary the degree of ablation and thermal damage. Wiping away of
debris between passes is suggested only when the thermal effects of these lasers are utilized.
There appears to be nothing gained by doing this after the final laser pass.
The ideal treatment parameters must be individualized for each patient, based on clinical
experience and professional judgment. Whatever energies are chosen, tapering along the
mandible and the pre-auricular areas should be done at lesser fluences.
mandatory. There are physician advocates for post-laser open dressings and physician
advocates for closed dressings. We have used them both. What is important is that the wound
be kept moist until complete re-epithelialization has occurred. This usually occurs within 5–
10 days. Use of antiviral agents is mandatory during this entire period.
After re-epithelialization, mild to moderate erythema will be seen. This usually tends to be
generalized in the treatment area and can last up to 3 months or longer. Localized hardened
erythema or erythema, that lasts more than 6 months, is suggestive of the onset of
hypertrophic scars. This should be managed aggressively. (See Chapter 8).
There are now increasing accumulated data about both the combined CO2/Er:YAG lasers
and variable pulsed Er:YAG lasers. Their effect and healing response appear to be a nice
compromise between the more aggressive, yet highly effective CO2 lasers and the less
aggressive, albeit not as effective short-pulsed Er:YAG lasers.
Figure 5.1. Before variable pulsed Er:YAG laser resurfacing
Figure 5.2. Three days after variable pulsed Er:YAG laser resurfacing
Figure 5.3. One month after variable pulsed E:YAG laser resurfacing
Figure 5.4. Three months after variable pulsed Er:YAG laser resurfacing
Figure 5.6. Immediately after variable pulsed Er:YAG laser resurfacing

Figure 5.7. One week after variable pulsed Er:YAG laser resurfacing
Figure 5.8. One month after variable pulsed Er:YAG laser resurfacing
Figure 5.9. Before variable pulsed Er:YAG full-face laser resurfacing
Figure 5.10. Three months after variable pulsed Er:YAG full-face laser resurfacing
Figure 5.12. Five days after variable pulsed Er:YAG laser resurfacing

Figure 5.15. Immediately after variable pulsed Er:YAG laser resurfacing
Figure 5.16. One week after variable pulsed Er:YAG laser resurfacing
Figure 5.17. Two months after variable pulsed Er:YAG laser resurfacing
Figure 5.18. Before variable pulsed Er:YAG perioral laser resurfacing

Figure 5.19. Immediately after variable pulsed Er:YAG perioral laser resurfacing
Figure 5.20. Before variable pulsed Er:YAG acne scar laser resurfacing
Figure 5.21. Immediately after variable pulsed Er:YAG acne scar laser resurfacing
Figure 5.23. Before combined CO2/Er:YAG laser resurfacing
Figure 5.24. Immediately after combined CO2/Er:YAG laser resurfacing

Figure 5.25. One week after combined CO2/Er:YAG laser resurfacing
Figure 5.26. One month after combined CO2/Er:YAG laser resurfacing

Figure 5.27. Before combined CO2/En:YAG laser resurfacing


Figure 5.31. Three months after combined CO2/Er:YAG laser resurfacing
Figure 5.32. Twelve months after combined CO2/Er:YAG laser resurfacing


Figure 5.35. Four days after combined CO2/Er:YAG laser resurfacing
Figure 5.37. Immediately after variable pulsed Er:YAG acne scar laser resurfacing
Figure 5.39. Before variable pulsed Er:YAG scar laser resurfacing
Figure 5.41. One week after variable pulsed Er:YAG acne scar laser resurfacing
Figure 5.42. One week after variable pulsed Er:YAG acne scar laser resurfacing
Figure 5.43. Two weeks after variable pulsed Er:YAG acne scar laser resurfacing
Figure 5.44. Three weeks after variable pulsed Er:YAG acne scar laser resurfacing
Figure 5.45. Three weeks after variable pulsed Er:YAG acne scar laser resurfacing
Figure 5.46. Seven weeks after variable pulsed Er:YAG acne scar laser resurfacing
Figure 5.47. Three months after variable pulsed Er:YAG acne scar laser resurfacing
Figure 5.48. Three months after variable pulsed Er:YAG acne scar laser resurfacing


Figure 5.53. Three days after combined CO2/Er:YAG laser resurfacing

REFERENCES
1 Hruza GJ. Laser skin resurfacing. Arch Dermatol 1996; 132:451–5.
2 Cotton J, Hood AF, Gonin R, Beesen WH, Hanke CW. Histologic evaluation of
preauricular and post-auricular human skin after high-energy, short-pulse carbon
dioxide laser. Arch Dermatol 1996; 132:425–8.
3 Stuzin JM, Baker TJ, Baker TM, Kligman AM. Histologic effects of the high-energy pulsed
CO2 laser on photoaged facial skin. Plast Reconstr Surg 1997;99:2036–50.
4 Gardner ES, Reinish L, Strickland GP. In vitro changes in non-facial human skin
following CO2 laser resurfacing: a comparison study. Lasers Surg Med 1996; 19:379–87.
5 Fulton JE, Barnes T. Collagen shrinkage (selective dermaplasty) with high-energy pulsed
carbon dioxide laser. Dermatol Surg 1998;24:37–41.
6 Trelles MA, Rigau J, Mellor TK. A clinical and histological comparison of flashscanning
versus pulsed technology in carbon dioxide laser facial skin resurfacing. Dermatol Surg
1998;24:43–9.
7 Bernstein LJ, Kauvar ANB, Grossman MC, Geronemus RG. The short- and long-term
side effects of carbon dioxide laser resurfacing. Dermatol Surg 1997;23:519–25.
8 Nanni CA, Alster TS. Complications of carbon dioxide laser resurfacing: An evaluation of
500 patients. Dermatol Surg 1998;24:315–20.
9 Ross EV, Grossman MC, Duke D, Grevelink JM. Long-term results after CO2 laser skin
resurfacing: A comparison of scanned and pulsed systems. J Am Acad Dermatol 1997;
37:709–18.
10 Goldman MP. Techniques for Erbium:YAG laser skin resurfacing: initial pearls from 100
patients. Dermatol Surg 1997;23:1219–21.
11 Kauvar ANB, Grossman MC, Bernstein LJ, Kovacs SO, Quintana AT, Geronemus RG.
Erbium: YAG laser resurfacing: a clinical histopathologic evaluation. Lasers Surg Med
1998;suppl 10:33.
12 Goldman RP, Marchell NL. Laser resurfacing of the neck with combined CO2/Er:YAG
laser. Dermatol Surg 1999;25:923–5.
13 Goldman MP, Marchell N, Fitzpatrick RE. Laser skin resurfacing of the face with
combined CO2/Er:YAG laser. Dermatol Surg 2000;26:102–4.
14 Weinstein C, Scheflan M. Simultaneously combined Er:YAG and carbon dioxide laser
(Derma K) for skin resurfacing. Clin Plast Surg 2000;27:273–85.
15 Pozner JN, Roberts TL. Variable-pulse width Er:YAG laser resurfacing. Clin Plast Surg
2000;27:263–71.
16 Manuskiatti W, Fitzpatrick RE, Goldman MP. Treatment of facial skin using
combinations of CO2, Q-switched alexandrite, flashlamp-pumped pulsed dye, and Er:YAG
lasers in the same treatment session. Dermatol Surg 2000;26:114–20.
17 Cho SI, Kim YC. Treatment of atrophic facial scars with combined use of high-energy
pulsed CO2 laser and Er:YAG laser: A practical guide of the laser techniques for the
Er;YAG laser. Dermatol Surg 1999;25:959–64.
18 McDaniel DH, Lord J, Ash K, Newman J. Combined CO2/Erbium:YAG laser resurfacing of
peri-oral rhytides and side-by-side comparison with carbon dioxide laser alone. Dermatol
Surg 1999;25:289–93.
19 Weinstein C. Modulated dual mode Erbium/CO2 lasers for the treatment of acne scars. J
Cutan. Laser Surg 1999; 1:203–8.
20 Newman JB, Lord JL, Ash K, McDaniel DH. Variable pulse Erbium:YAG laser skin
resurfacing of perioral rhytides and side-by-side comparison with carbon dioxide laser.
21 Millman AL, Mannor GE. Histologic and clinical evaluation of combined eyelid
Erbium:YAG and CO2 laser resurfacing. Am J Opthalmol 1999;127:614–16.
22 Goldman MP, Manuskiatti W. Combined laser resurfacing with the 950-μsec pulsed CO2+
Er:YAG lasers. Dermatol Surg 1999;25:160–3.
23 Trelles MA, Garcia-Solana L, Rigau J. The filtrum remodelling with combined Er:YAG
CO2 laser resurfacing. J Cutan Laser Ther 1999; 1:225–8.
24 Utley DS, Koch RJ, Egbert BM. Histologic analysis of the thermal effect on epidermal and
dermal structures following treatment with the superpulsed CO2 laser and the
Erbium:YAG laser: An in vivo study. Lasers Surg Med 1999;24:93–102.
25 Greene D, Egbert BM, Utley DS, Koch RJ. In vivo model of histologic changes after
treatment with the superpulsed CO2 laser, the Erbium:YAG laser, and blended lasers: A
4–to 6-month prospective histologic and clinical study. Lasers Surg Med 2000;27:
362–72.
26 Pozner JM, Goldberg DJ. Histologic effect of a variable pulsed Er:YAG laser. Dermatol
Surg 2000;26:733–6.
6
ELECTROSURGICAL SKIN RESURFACING
KEY POINTS
(1) Radiofrequency electrosurgical resurfacing involves the skin application of low

voltage energy through multiple current delivery electrodes
(2) The delivered energy, in combination with saline conduction media, generates an
ionized vapor (or plasma) layer that disassociates the treated skin
(3) The thickness of the residual thermal collagen damage zone varies consistendy with
increasing number of passes
(4) The thickness of the residual thermal collagen damage zone may not vary
consistently with increasing voltage
(5) The overall depth of injury seen with electrosurgical resurfacing can be similar to
that seen with CO2 laser resurfacing
(6) Electrosurgical resurfacing causes localized tissue ablation and has been used to
treat post-operative surgical scars, as well as perioral and periorbital rhytides
BACKGROUND
Previous chapters have discussed CO2, Er:YAG, combined CO2/Er:YAG and variable pulsed
Er:YAG lasers. Each of these modalities is associated with both advantages and
disadvantages.
Historically, chemical peeling of the skin has been used in the treatment of actinic damage,
pigmentary dyschromias and facial rhytides. This particular method can be very cost
effective, but results vary greatly due to the inconsistent level of injury. Such inconsistencies
have been thought to be secondary to such variables as skin preparation methods, chemical
agents used and application technique.1–4 Classic dermabrasion can also be a very cost-
effective method of treating small areas, but holds the greatest risk of transmission of
infectious diseases.5 Laser resurfacing offers great marketability, due to high popular demand
and decreased variability of results secondary to operator technique. However, laser
approaches can be costly and have associated post-procedure morbidity.6–11 Due to their
mechanism of action, lasers also pose a risk of ocular damage to both the patient and the
physician, thus requiring the use of protective eye wear.
The most recent addition to the facial resurfacing arsenal is electrosurgery. One recently
popularized electrosurgical device is the Visage electrosurgical device. This device utilizes an
electrosurgical instrument with a bipolar, multi-electrode configuration that generates
radiofrequency energy to achieve tissue ablation. This technology has been referred to as
coblation, radiofrequency resurfacing, or electrosurgical resurfacing, all of which refer to one
aspect of the mechanism behind this method of resurfacing. Electrosurgical resurfacing
appears to be a more appropriate designation for this technique.
Electrosurgical resurfacing was originally designed for resurfacing articular cartilage in

arthroscopic surgery.12 For cutaneous resurfacing, the device is utilized with a handpiece
containing a probe that has both current delivery and dispersive electrodes. The Visage
system utilizes normal saline as a conductive medium between the device probe and the skin.
This can be supplied by constant drip or by application of saline gel. Electrical energy is
transferred from the current delivery electrodes through the conduction medium (i.e. saline)
to the dispersive electrode. It has been postulated that the delivery of high frequency, low
voltage energy through multiple current delivery electrodes, in combination with the saline
conduction media, generates an ionized vapor (or plasma) layer that is then in direct contact
with the skin.13 This leads to localized tissue ablation, secondary to heat transfer and
molecular dissociation of tissue. The tissue disassociation is localized to the area covered by
the plasma layer. Tissue ablation is accomplished at temperatures much lower than that seen
with traditional high voltage, single electrode electrosurgical units. Another possible
mechanism of action may be dielectric breakdown of tissue, in which the strong electrical field
generated at the probe electrodes causes direct physical disruption of biomolecules.14
CLINICAL STUDIES
Grekin et al.15
Grekin et al. in a prospective multi-center study, evaluated the efficacy and safety of
electrosurgical resurfacing for the treatment of facial wrinkles. The Visage electrosurgical
device was utilized. A total of 95 patients with Fitzpatrick Class I–III perioral and/or
periorbital rhytides were treated with one to three passes of the electrosurgical probe. Each
pass was performed at a rate of approximately 1.0 to 1.5cm/s.
Normal saline was used in a drip fashion to provide continuous wetting of the skin
specimens during the treatments. Devitalized tissue was debrided with saline soaked gauze
after each pass. The investigators demonstrated statistically significant improvement in the
treatment of both perioral and periorbital areas in subjects with Fitzpatrick type II and III
photodamage. Grekin et al. noted that increased improvement was associated with an
increased number of passes. In contrast to other studies, the authors also noted increased
improvement with increased voltage settings. Post-operative recovery was rapid, with minimal
physical discomfort and almost total resolution of erythema by the end of the second month.
The investigators noted that there was rare bleeding associated with the treatment. The post-
operative morbidity was less than that seen with CO2 or Er:YAG laser resurfacing.
HISTOLOGIC STUDIES
Tope16
One of the first published studies of electrosurgical resurfacing was undertaken by Tope, who
utilized the Visage system. Tope compared 86-, 108- and 139-V power settings with one, two,
or three passes on fresh specimens of ex-vivo human arm or breast skin. The device probe
was drawn with light pressure over skin specimens under taut traction. Normal saline was
used in a drip fashion to provide continuous wetting of the skin specimens during the
treatments. This study revealed no epidermal ablation but increased residual thermal
collagen damage with one, two or three passes, respectively. The mean thickness of the
residual thermal collagen damage zone was 80–97 μm after three passes. Tope suggested that
these findings correlated with the depth of injury seen after high energy, pulsed CO2 laser
resurfacing. Of note, the thickness of the residual thermal collagen damage zone did not vary
consistently with increasing voltage.
ELECTROSURGICAL SKIN RESURFACING 145
Burns et al.17
Burns et al. evaluated both efficacy and safety of electrosurgical resurfacing. They used the
Visage system on six post-operative surgical scars. The investigators also evaluated the depth
of injury achieved with electrosurgical resurfacing performed on in vivo/ex vivo human facial
skin. Treatment consisted of up to 25 passes over a designated area until desired skin
changes were achieved. Normal saline was used in a drip fashion to provide continuous
wetting of the skin specimens during the treatments. All six skin specimens demonstrated
improvement that was, in the opinion of the investigators, similar to that seen with manual
dermabrasion. Increased depth of injury, with an increased number of passes, was noted.
Minimal differences were noted using increased power levels. The authors felt that the overall
depth of injury was similar to that seen with CO2 laser resurfacing.
MY APPROACH
I have found electrosurgical resurfacing to be highly effective when used for the treatment of
Class I–II rhytides. (Figures 6.1 to 6.27). This non-laser device can be used successfully in the
treatment of Fitzpatrick skin types I–IV. However, it should be expected that almost all
Fitzpatrick IV individuals will show some evidence of post-inflammatory hyperpigmentation. I
have not noted any method of pre-treatment that will consistently stop this. However, as a
general rule the hyperpigmentation is self-limited. It appears to be most profound in those
individuals with a history of melasma. Prior to treatment, I start all patients on oral antiviral
agents and antibiotics.
flammable cleansing agent. This precludes the possibility of a fire resulting from the
electrosurgical device’s heating of a flammable agent. Local anesthesia can be used when
treating partial or full-face areas. Generally, we do not treat localized anatomic areas if there
will be a high risk of visible zones of demarcation. This is particularly true in patients with
greater evidence of photodamage. Although full-face procedures can be performed with
appropriate local anesthetic nerve blocks, it is our preference to carry out such procedures
under light sedation. This provides greater comfort for the patient and allows the procedure to
be completed in a more efficient manner.
Generally I will treat the affected areas with one to three passes of the electrosurgical device.
More than three passes, in my experience, tends to lead to greater thermal damage, without
significantly greater clinical improvement.
mandatory. There are physician advocates for post-electrosurgical resurfacing open dressings
and physician advocates for closed dressings. We have used them both. What is important is
that the wound be kept moist until complete reepithelialization has occurred. This usually
occurs within 4–6 days. Use of antiviral agents is mandatory during this entire period. Full re-
epithelialization after 7 days is to be expected.
After re-epithelialization, mild erythema followed by minimal erythema will be seen. This
usually tends to be generalized in the treatment area and can last up to 3 months or longer.
Localized hardened erythema, or erythema that lasts more than 6 months, is suggestive of the
onset of hypertrophic scars. This should be managed aggressively (see Chapter 8).
There are minimal accumulated data about the use of electrosurgical resurfacing devices. It
would appear that there are several benefits associated with the use of this technology. These
include the usual complete hemostasis during the procedure, lack of a smoke
plume, no need for eye protection, and compact solid state technology.15,18 Electrosurgical
resurfacing may also have a decreased morbidity and shorter recovery time when compared to
CO2 or Er:YAG laser resurfacing. Because there are few reported studies, further clinical
Figure 6.1. Before electrosurgical resurfacing
Figure 6.2. Immediately after electrosurgical resurfacing

Figure 6.3. One week after electrosurgical resurfacing
Figure 6.4. One month after electrosurgical resurfacing

Figure 6.5. Six months after electrosurgical resurfacing


Figure 6.10. During electrosurgical resurfacing




Figure 6.17. Immediately after electrosurgical resurfacing
Figure 6.18. Three days after electrosurgical resurfacing


Figure 6.22. One year after electrosurgical resurfacing

Figure 6.23. Histologic evidence of epidermal ablation, dermal damage and thermal effects immediately after
electrosurgical resurfacing


studies looking at electrosurgical resurfacing and comparing electrosurgical resurfacing to

other modalities will be necessary to determine its true efficacy and utility.
REFERENCES
1 Duffy DM. Alphahydroxy acids/trichloroacetic acids risk/benefit strategies: a
photographic review. Dermatol Surg 1998;24:181–9.
2 Glogau RG, Matarasso SL. Chemical peels. Trichloroacteic acid and phenol. Dermatol
Clin 1995;13:263–76.
3 Matarasso SL, Glogau RG. Chemical face peels. Dermatol Clin 1991;9:131–50.
4 Brody HJ. Complications of chemical peeling. J Dermatol Surg Oncol 1989;15:1010–19.
5 Wentzell JM, Robinson JK, Wentzell JM Jr, Schwartz DE, Carlson SE. Physical properties
of aerosols produced by dermabrasion. Arch Dermatol 1989;125:1637–43.
6 Nanni CA, Alster TS. Complications of carbon dioxide laser resurfacing: an evaluation of
500 patients. Dermatol, Surg 1998;24:315–20.
7 Bernstein LJ, Kauvar AN, Grossman MC, Geronemus RG. The short- and long-term side
effects of carbon dioxide laser resurfacing. Dermatol Surg 1997;23:519–25.
8 Fulton JE Jr. Complications of laser resurfacing: methods of prevention and
management. Dermatol Surg 1997;24:91–9.
9 Alster TS. Manual of Cutaneous Laser Techniquies. Philadelphia: Lippencott-Raven,
1997.
10 Lowe NJ, Lask G, Griffen ME, Maxwell A, Lowe P, Quilada F. Skin resurfacing with the
Ultrapulse carbon dioxide laser. Observations on 100 patients. Dermatol Surg 1995;21:
10,025–9.
11 Sriprachya-Anunt S, Fitzpatrick RE, Goldman MP, Smith SR. Infections complicating
pulsed carbon dioxide laser resurfacing for photoaged facial skin. Dermatol Surg 1997;23:
527–36.
12 Rasor JS, Antounian F, Click JM. Multi- and single electrode electrosurgery for partial
meniscectomy: comparison of depth of injury and ablation rate. In: Research Outcomes
in Arthroscopic Surgery. Sunnyvale, CA: ArthoCare Corporation, 1995; 1:1–9.
13 Eggers PE, Thapliyal HV. System and method for electrosurgical cutting and ablation.
United States Patent 5,697,882. December 16, 1997.
14 Cross FW, Dyer PE, Al-Dahir RA, MacRobert AJ, Brown SG. Evidence from photoacoustic
spectroscopy for a photoablative process in the UV laser ablation of vascular tissue.
Lasers Surg Med 1987;7:80.
15 Grekin RC, Tope WD, Yarborough JM, et al. Electrosurgical facial resurfacing. Arch
Dermatol 2000; 136:1309–16.
16 Tope WD. Multi-electrode radio frequency resurfacing of ex vivo human skin. Dermatol
Surg 1999;25:348–52.
17 Burns RL, Carruthers A, Langtry JA, Trotter MJ. Electrosurgical skin resurfacing: a new
bipolar instrument. Dermatol Surg 1999;25:582–6.
18 Alster TA. Electrosurgical ablation. A new mode of cutaneous resurfacing. Plast Recontsr
Surg 2001; 107:1890–4.
7
NON-ABLATIVE DERMAL REMODELING
KEY POINTS
(1) Non-ablative techniques provide a cosmetically elegant method to improve the

quality, tone and texture of skin
(2) All chosen techniques lead to an increase in upper papillary dermal collagen
formation
(3) Some techniques also lessen solar lentigines and telangiectases
(4) Multiple treatments are required. Periodic re-treatments are to be expected
(5) Degree of improvement is generally less than that seen with ablative techniques
BACKGROUND
Pulsed char-free carbon dioxide (CO2) laser skin resurfacing has provided a method of
removing thin layers of skin with minimal thermal damage. As described in previous
chapters, this laser improves mild, moderate and severe rhytides, as well as photoaged skin.
Laser energy is delivered at the ‘ablation threshold' of skin, without the side effects seen with
older non-pulsed, continuous wave carbon dioxide lasers.1
Despite the clinical improvement seen after CO2 and variable pulsed Er:YAG laser
treatment, the prolonged healing and significant erythema that is commonly seen following
laser treatment have tempered the enthusiasm for these systems. Although this erythema
may resolve in 1 month, it commonly lasts for several months. Novice laser physicians have
not found such ablative laser systems to be user friendly. With this significant learning curve,
some physicians have shied away from laser resurfacing.
The Er;YAG laser, with its 2940-nm wavelength, emits laser energy in the midinfrared
invisible light spectrum. This wavelength has 10–15 times the affinity for water absorption
compared to the CO2 (10,600 nm) wavelength. As discussed, it is this fact that leads to the
difference in clinical response seen after treatment with CO2 and short-pulsed Er:YAG
lasers.2,3
Both CO2 and Er:YAG laser technology, although promising in their benefits, are sometimes
accompanied by untoward side effects and complications. The most common of these, as
mentioned above, is post-operative erythema, a side effect experienced by virtually all patients
treated with these modalities. Other potential risks induced by ablative, dermal wounding
modalities, are delayed healing, postoperative pigmentary changes, and scarring.
If a dermal wound and new collagen formation are the primary mechanisms behind the
improvement seen after laser resurfacing, techniques that induce a dermal wound without
epidermal ablation should theoretically lead to cosmetic improvement of dermal
photodamage. The primary mechanism responsible for the effect of non-ablative treatments is
thermal denaturation of collagen associated with unwinding of the triple helical structure of
Figure 7.1. Dermal water absorption of near-infrared wavelengths
the collagen molecule.4 This is thought to occur either through dermal water absorption
(1064–1540 nm) (Figure 7.1) or through a direct effect on dermal vasculature with resultant
leakage of vessels and wound formation (Figures 7.2–7.4). This arena of non-ablative dermal
remodeling is a very new area of technology.
CLINICAL AND HISTOLOGIC STUDIES
Goldberg and Whitworth5

In one of the first studies evaluating a non-ablative approach to dermal remodeling, a 1064-
nm Q-switched Nd:YAG laser was used in an attempt to improve rhytides.5 (Figure 7.5).
Eleven subjects with perioral or periorbital rhytides were
Figure 7.2. Blood vessel hemoglobin absorption of 585-nm wavelength
evaluated using a Q-switched Nd:YAG laser at 5.5 J/cm2 and a 3-mm spot size. All subjects
were of skin phenotypes I and II; all had Class I or II rhytides. The authors sought a non-
specific clinical end-point of pinpoint bleeding. Subjects were treated only once and were
evaluated 7, 30, 60 and 90 days after treatment. At follow-up, each subject was evaluated for
improvement of rhytides, healing, pigmentary
NON-ABLATIVE DERMAL REMODELING 163
Figure 7.3. Blood vessel hemoglobin absorption of 595-nm wavelength
Figure 7.4. Blood vessel absorption from broad spectrum intense pulsed light source
Figure 7.5. Water absorption of 1064-nm

changes and erythema. In three patients (two perioral, one periorbital), the authors noted
improvement thought to be comparable to that following ablative laser resurfacing. In six
patients (three perioral, three periorbital), clinical improvement was noted, but was not
thought to be as significant as that seen with an ablative laser system. In two patients (one
perioral, one periorbital), no clinical improvement was noted. In those subjects where clinical
improvement was noted, the clinical changes were consistent the full 90 days of the study. No
pigmentary changes or scarring were noted in any of the treated subjects. At one month,
three of 11 subjects showed persistent erythema at the treated sites. At 3 months, all
erythema was resolved.
Dermal remodeling was thought to occur through increased collagen type I deposition with
collagen reorganization into parallel arrays of compact fibrils. Such an effect, the authors
suggested, might occur with non-ablative as well as ablative laser systems. Of note, the
greatest improvement occurred in those individuals who had the most persistent erythema.
This suggested that the degree of improvement following any dermal wounding approach
might be directly related to the degree of induced wound.
Goldberg and Metzler6

The aforementioned study was expanded when the non-ablative, dermal remodeling effect of a
Q-switched Nd:YAG laser were potentiated by the use of a topical carbon assisted solution.6 A
total of 242 solar damaged anatomic sites on 61 human subjects were treated with three
1064-nm Q-switched Nd:YAG laser treatments. Parameters of treatment included a fluence of
2.5 J/cm2, pulse duration of 6–20 nanoseconds, and a spot size of 7 mm. The treatment sites
were evaluated at baseline, 4, 8, 14, 20 and 32 weeks after the final treatment for skin
texture, skin elasticity, and rhytide reduction. All sites were treated at a baseline visit, and
later at 4 and 8 weeks. Adverse events were recorded throughout the study.
In this study, a low fluence Q-switched Nd:YAG laser was utilized for treating mildly solar-
damaged skin. Unlike the previous study, there was no epidermal disruption when the lower
fluences were used. The Q-switched Nd:YAG laser energy is not well absorbed by tissue water
(see Figure 7.5); it is non-selectively placed within the dermis. The 1064-nm wavelength
results in relatively deep penetration into the skin, which is indicative of minimal laser/tissue
interaction. As a result: (i) cellular damage is localized to the tissue immediately adjacent to
the carbon; (ii) non-targeted tissue is minimally affected; and (iii) less than 10% of the typical
energy output from CO2 lasers is required for the treatment. At 8 months, the investigators
reported improvement in skin texture and skin elasticity, as well as rhytide reduction
compared to baseline. The majority of adverse events were limited to mild, brief erythema.
Cisneros et al.7
In this study 22 subjects with facial rhytides showed improvement after two Qswitched
Nd:YAG laser treatments. The investigators used the following parameters: 3-mm spot size
and 6–7 J/cm2. They also noted improvement in post-acne scarring.7
Goldberg and Silapunt8

In a recent study the efficacy and safety of multiple Q-switched Nd: YAG laser treatments in
the non-ablative treatment of facial rhytides was evaluated.8 Eight female subjects ranging in
age from 40 to 63 years (average 51.6 years) were enrolled in this study. Five subjects had
Fitzpatrick skin type II; two subjects had skin type IV; one subject had skin type III. The
periorbital area was treated in five out of eight subjects; the perioral area was treated in the
remaining three subjects. Two subjects were noted to have Class I rhytides; three subjects
had Class II rhytides; three subjects had Class III rhytides. Treatments were undertaken with
a Q-switched Nd:YAG laser at fluences of 7 J/cm2 and a 3-mm spot size. Two laser passes
were used in all subjects in an attempt to promote petechiae as the typical visible endpoints.
All subjects used bacitracin ointment for post-treatment care. All subjects received three
treatments, once a month, over a consecutive 3-month period. Photographs were taken before
treatment and 3 months after the third treatment. Subjects filled out a questionnaire at 24
hours and 7 days after each treatment. Subjects quantified and recorded the level of
discomfort they felt as a result of the laser treatment as: (1) no pain at all; (2) mild pain, not
requiring any pain medication; (3) moderate pain, requiring non-prescription pain medicine;
(4) severe pain, requiring prescription pain medication; or (5) extreme pain, requiring a
physician call. At the end of the study, each subject assessed their satisfaction with the laser
treatment as follows: (1) unsatisfactory results, not worth the time and effort; (2) fair results,
but wishing the results were better; (3) good results, satisfied with the procedure; and (4)
excellent results, very satisfied. The investigators also evaluated improvement based on a
percentile scale of 0–25% (poor), 26–50% (fair), 51–75% (good), and 76–100% (excellent).
Independent investigator assessment showed six out of eight subjects having at least fair
clinical improvement in rhytides. Two out of eight subjects showed a poor outcome. In
contrast, subject assessment was fair in five out of eight subjects; two subjects reported an
unsatisfactory outcome; one subject reported a good overall outcome.
At 24 hours after each treatment, 80% of subjects reported no pain at all. There was mild
pain, not requiring pain medication in 20% of subjects. Only one subject reported pain at 7
days after each treatment.
Petechiae were observed in 75% of subjects immediately after each treatment. 33% of
subjects had pinpoint bleeding immediately after each treatment. No erythema, edema,
purpura, pigmentary changes, or scarring was observed at 1 month after each treatment and
3 months following the last treatment.
In a further study evaluating the histologic changes seen after Q-switched Nd:YAG laser
non-ablative treatment, six female subjects ranging in age from 48 to 63 years received laser
treatment.9 Subjects had Fitzpatrick skin types II–IV. Subjects were precluded from using any
topical collagen promoting agents for 1 month prior to the study and during the entire course
of the study. Sun damaged 4×4–cm areas of infra-auricular skin were exposed to a 1064-nm
Q-switched Nd:YAG laser at fluences of 7 J/cm2 and a 3-mm. spot size. Two laser passes,
with a 10–20% overlap, were used in all subjects in an attempt to promote petechiae as the
visible end-point. Petrolatum dressings were applied for 1 week after treatment. Punch
biopsies of 3 mm were taken from each subject before treatment; photographs were taken of
the biopsy sites. At 3 months after the last treatment, another biopsy was taken from a
different previously treated area. Histologic specimens were evaluated blindly by a board
certified dermatopathologist.
Four out of six skin biopsy specimens obtained 3 months after laser treatment showed mild
fibrosis with histologic improvement in pre-treatment solar elastosis. There was a mildly
thickened upper papillary dermal collagen zone, with an improvement in the organization of
collagen fibrils. The remaining two specimens showed no changes.
Friedman et al.10
Friedman et al. recognized the inherent limitations of photographic and clinical evaluation of
improvement after non-ablative treatment.10 They looked at the results in two subjects after
five treatments with a low fluence Q-switched Nd:YAG laser. Clinical results were analyzed
using a 30-mm, three-dimensional microtopography imaging system (PRIMOS, GFM, Teltow,
Germany). Six-month results, as measured by this 3 dimensional method, showed a decrease
in skin roughness of 26%. Such methods provide a more precise measurement of clinical
improvement than is seen with clinical and/or photographic evaluation.
Goldberg and Samady11

Further studies were performed with a non-Q-switched millisecond Nd:YAG laser at fluences
of 100–130 J/cm2, pulse durations of 3–8 ms and up to five treatments over an 8-week
period.11 Ten subjects with Fitzpatrick types II–III skin were followed for 6 months after their
final treatment. Side effects were minimal with only one subject showing post-treatment
blistering. This healed without scarring. Most patients showed some degree of clinical
improvement.
Goldberg12 and Lee13

Goldberg, in a small study of 10 subjects,12 and Lee, in a larger study of 150 subjects,13
found that the clinical improvement following treatment with both a millisecond Nd:YAG laser
and a millisecond KTP laser was greater than when either the Nd:YAG or KTP laser was used
alone.
Zelickson et al.14
Other non-ablative lasers, such as the pulsed dye laser, have been shown to improve dermal
collagen. Histopathologic examination of 585-nm pulsed dye laser treated scars revealed
improvement in dermal collagen. This may result from a 585-nm primary effect on dermal
vasculature (see Figure 7.2). There is also an increase in the number of regional mast cells in
pulsed dye laser irradiated scars. Because mast cells elaborate a variety of cytokines, their
presence following irradiation and accompanying tissue revascularization may provide an
explanation for therapeutic improvement following laser treatment. Using this concept,
Zelickson et al. evaluated the use of a pulsed dye laser in the treatment of rhytides.14 In this
study, the authors treated 10 subjects with a 585-nm, 450-μs pulsed dye laser. Laser
treatment was undertaken at 3.0–6.5 J/cm2 using a 7–10-mm spot size. Nine out of 10
subjects with mild to moderate rhytides showed 50% or more improvement with three out of
10 showing 75% or greater improvement. Four out of ten subjects, with moderate to severe
rhytides improved. All subjects maintained their level of improvement for 6 months as did five
out of six subjects evaluated at 12 months after treatment. Of note, though, were the results
seen in subjects with moderate to severe rhytides. At 12 weeks, only three out often subjects
had clinically observable improvement. At 14 months after treatment, only four subjects
treated in the study still showed clinically observable improvement. The study results were
tempered by cosmetically unacceptable post-treatment purpura and swelling. This lasted 1–2
weeks. Two subjects were also noted to have postinflammatory hyperpigmentation. Histologic
examination of biopsies taken 6–12 weeks after treatment showed evidence of both a
thickened epidermis and a thickened layer of superficial dermal collagen. This manifested as
more organized elastin and collagen fibers replacing the pre-treatment solar elastic tissue.
There was also an increase in mucin deposition in the superficial dermis. In a subsequent
study, Zelickson and Kist noted that the pulsed dye laser, when used for dermal remodeling,
could increase up to 86% the levels of Type I and III collagen, as well as elastin.15
Most recently, Zelickson and Coles evaluated a 595-nm pulsed dye laser. In this study, the
investigators treated 20 subjects with three treatments at 3-week intervals16 (see Figure 7.3).
The subjects ranged in age from 44 to 68 years, with a mean age of 59 years. All had mild to
moderate photodamage. All were treated with either a 595-nm pulsed dye laser at 4.5–6 J/cm2
with a 20-ms pulse, or an identical laser with 5–7 J/cm2 and a 30-ms pulse. Treatment
parameters were chosen so as not to produce purpura. All subjects felt they had improved.
Results were slightly better with the shorter pulse durations.
Bjerring et al.17
Bjerring et al. have shown increased levels of collagen precursors following treatment with a
350-μs pulsed dye laser.17 In their study, ten subjects, with an average age of 38 years, had
350-μs pulsed dye laser treatment on their arm. Laser treatment was undertaken at 2.4 J/cm2
with a 5-mm spot size. Suction blisters, taken after laser treatment, revealed increased pro-
collagen III levels. In addition to the suction blister study, the authors also evaluated the
clinical response to this laser. Thirty subjects, with Class I–III rhytides, and an average age of
46 years, were treated with the same laser parameters as the first group. Only the periorbital
area was treated. Subjects were evaluated immediately after treatment and at 7, 30, 90 and
180 days. There was no significant post-treatment pain or noted purpura. There was no
reported incidence of any pigmentary or textural changes. Clinical improvement was noted in
all skin types.
Fournier et al.18
Another near-infrarred laser is the 1540-nm Er:Glass laser (Figure 7.6). Fournier et al.
evaluated this laser in 60 subjects.18 Subjects were Fitzpatrick skin types I–IV
and were treated four times at 6 week intervals. Clinical improvement was noted by
photography and through profilometry and ultrasound methods. A 40% reduction in wrinkles
was noted by profilometry at 6 weeks after the fourth treatment. Ultrasound imaging
demonstrated a 17% increase in dermal thickness. Histologic evidence of new collagen
formation was also noted. There were no significant adverse effects.
Goldberg and Cutler19

In a study evaluating the effect of intense pulsed light (IPL) in the treatment of rhytides, 30
female subjects, aged 35–65 years, Fitzpatrick Type I–II and Class I–II skin phenotypes were
treated (see Figure 7.4).19 Treatment areas included the periorbital, perioral, and forehead
regions. Between one and four treatments were provided over 10 weeks. Non-coherent IPL
was delivered to the skin using a 645-nm cut-off filter. This led to emission of light with
wavelengths between 645 nm and 1100 nm. Light was delivered through a bracketed cooling
device, in triple 7-ms pulses, with a 50-ms interpulse delay. Delivered fluences were 40–50J/
cm2. The authors evaluated the degree of improvement 6 months after the last treatment.
Complications were also evaluated at this time. Clinical improvement was divided into four
quartiles: (i) no improvement; (ii) some improvement; (iii) substantial improvement; and (iv)
total improvement.
Six months after the final treatment, five subjects were noted to have no improvement.
Similarly, no subjects were noted to have total improvement. Sixteen subjects showed some
improvement, while nine subjects showed substantial improvement. All subjects were
evaluated for pigmentary changes, post-treatment blistering, erythema and scarring. Three of
the 30 subjects were noted to have blistering immediately after treatment. All 30 subjects had
post-treatment erythema. Six months after treatment, no pigmentary changes, erythema or
scarring was noted. The authors concluded that IPL could improve some rhytides. New
collagen formation and improvement of age-related vascular and pigmented lesions can also
follow treatment with this non-laser technology.20–21 However, the dermal changes appear to
be more subtle than those seen with ablative techniques.
Weiss et al.
In a recent study, Weiss et al. evaluated the observed clinical results 4 years after IPL
treatment (personal communication, 2002). A total of 8 subjects with skin types I–IV were
treated over the course of 2 years. Four years after treatment, 83% of subjects were still noted
to have skin textural improvement. Telangiectases were improved in 82% of subjects, while
pigmentatation remained improved in 79%.
Bjerring and Troilius

In another recent study, Bjerring and Troilius evaluated the use of an IPL for the purpose of
photorejuvenation (personal communication, 2002). Nineteen women between the ages of 32
and 68 years with skin types I–III were treated with an IPL different from that used by
Goldberg and Cutler,19 and Weiss et al. (see above). Most subjects reported some stinging and
burning sensations during the treatments. Some subjects showed a transient post-treatment
erythema. No scarring was noted. More than 50% reduction in unwanted pigment was
observed in 80% of treated subjects. More than 50% reduction in telangiectases was observed
in 68% of subjects. Overall improvement in skin texture was reported in 53% of individuals.
What was significant about this study was the reported clearance seen after only after two
treatments.
Nelson et al.22
The first specifically non-ablative laser to be solely marketed to the physician community is a
1320-nm Nd:YAG laser.22 The goal of this system, similar to that of the previously described
systems, is improvement of rhytides without the creation of a wound. The 1320-nm
wavelength is advantageous in its high scattering coefficient. Thus, the laser irradiation
scatters throughout the treated dermis after nonspecific absorption by dermal water
(Figure 7.7).
In the Nelson et al. study, one or more passes of a 1320-nm Nd:YAG laser were used on
photoaged skin. The waveform consisted of three 200-μs laser pulses at a 100Hz repetition
rate. Laser energy was delivered through a 5-mm spot size with fluences up to 10 J/cm2. A
dynamic cryogen cooling technique was applied immediately prior to laser treatment in order
to produce selective subsurface skin heating without epidermal damage. Immediately after
treatment, mild edema and erythema appeared in the treated skin. These side effects resolved
within 2 days. At 2 months after treatment, facial rhytides were noted to be improved. No
persistent erythema or pigmentary changes were noted. The currently available model of this
1320-nm Nd:YAG laser is accompanied by a unique handpiece with three portals. One portal
contains the cryogen spray that cools the epidermis prior to and during treatment, one portal
emits the 1320-nm Nd:YAG laser irradiation; and one portal contains a thermal sensor.
Patients are usually treated at 2–4 week intervals and can be expected to show the degree of
improvement expected from a non-ablative approach.23–26 Consistent with the noted clinical
improvement is the histologic replacement of the irregular collagen bands with organized new
collagen fibrils. Because this laser produces new collagen formation, it has also been used as
part of a full-face anti-aging approach.27
Goldberg et al.28
A recent study evaluated a 1450-nm mid-infrared diode laser in an attempt to: (i) determine
its efficacy in promoting non-ablative dermal remodeling; and
(ii) determine if the laser induced injury was selective or whether a cryogen injury alone could
produce the same effect as the laser with cryogen.28 The laser emitted a pulse width of 160–
260 ms and spot size was 4 mm. The 1450-nm wavelength is well absorbed by dermal water
(Figure 7.8).
Twenty subjects, nineteen women and one man, skin types I–IV, age range 42–70 years
were enrolled in the study. Class I and II rhytides were treated in 12 subjects with periorbital
rhytides and eight subjects with perioral rhytides. One side was treated with the laser and
cryogen while the contralateral side was treated with cryogen alone. Pre-, intermediate, and
post-laser cryogen cooling ranging from 40–80 ms in total was provided. Choice of treated
sides was randomized. Two to four laser treatment sessions were performed, separated by
monthly intervals. Evaluated acute clinical reactions included erythema, blistering and
edematous skin changes.
Evaluated 6-month post-treated complications included hyperpigmentation,
hypopigmentation, erythema, and scarring. Clinical improvement of rhytides was designated
as none, mild (same number of rhytides, but reduced in depth), moderate (decreased number
of rhytides) or significant (no rhytides after treatment). Optical profilometry moldings were
undertaken before and 6 months after the final treatment.
Immediate erythema was seen in 19 out of 20 treated subjects. It was always subjectively
evaluated as either mild or moderate and was noted on both the laser/cryogen treated site as
well as the cryogen-only treated site. No immediate post-treatment blisters were noted; post-
treatment edema, usually seen as small edematous papules, seen at various times in six of 20
laser/cryogen treated subjects. Their duration was anywhere between 1 and 7 days. Six
month post-treatment post-inflammatory hyperpigmentation was noted in only one subject
and only at the laser/cryogen site. No hypopigmentation, erythema or scarring was noted 6
months after final treatment.
Of the 20 laser/cryogen treated sites, seven showed no obvious clinical improvement, 10
showed mild improvement and three sites were noted to have moderate improvement. None of
the cryogen alone treated sites were noted to show any improvement 6 months following the
final treatment. Clinical improvement was consistent with optical profilometry findings. The
number of treatments did not appear to correlate with degree of improvement. No perioral
sites were noted to have more than mild improvement.
MY APPROACH
I have found non-ablative techniques to be most helpful with Class I rhytide individuals or
those with deeper rhytides who are willing to accept less clinical improvement than seen with
ablative techniques, but desire minimal to no wound (Figures 7.9–7.53). Those systems
emitting near-infrared irradiation (1064–1540 nm) are generally utilized for new dermal
collagen formation. Lasers and light sources emitting visible light may also improve superficial
cutaneous pigmentation and vascularity. Whether such systems lead to as much new
collagen formation as is seen following treatment with near-infrared systems has yet to be
determined. No pre-treatment is required. Patients with a history of herpes simplex infections
are given oral antiviral agents. Procedures generally take less than 30 minutes; re-treatments
are to be expected. Ideally non-ablative treatments are combined with other modalities such
as microdermabrasion, botulinum toxin injections and filler agents.
Non-ablative dermal remodeling represents the newest approach to improve photodamaged
skin.29,30 Because the degree of collagen remodeling is not expected to be as great as that
seen with other more destructive, ablative approaches, the non-ablative techniques are meant
for those individuals who do not wish to take time away from their daily activities in order to
laser-improve the quality of their sun damaged skin. The technique is also not meant for
those with extensive solar induced epidermal pigmentary changes. Those individuals are best
treated with either an ablative laser or a specific pigmented lesion laser. Newer non-ablative
radiofrequency devices may also significantly improve solar damaged skin (Figures 7.54 and
Figure 7.9. Before non-ablative treatment otf periorbital rhytides with a high fluence Q-switched Nd:YAG laser
Figure 7.10. Petechiae seen after non-ablative treatment with a high fluence Q-switched Nd:YAG laser
Figure 7.11. Improvement in rhytides after high fluence Q-switched Nd:YAG laser
Figure 7.12. Before non-ablative treatment with a high fluence Q-switched Nd:YAG laser
Figure 7.13. Improvement in rhytides after high fluence Q-switched Nd:YAG laser
Figure 7.14. Carbon application before treatment with a carbon assisted, low fluence Q-switched Nd:YAG laser
Figure 7.15. Periorbital rhytides before treatment with a carbon assisted, low fluence Q-switched Nd:YAG laser
Figure 7.16. Improvement in rhytides after treatment with a carbon assisted, low fluence Q-switched Nd:YAG
laser
laser
laser
laser
Figure 7.23. New upper papillary dermal collagen formation after treatment with a carbon assisted, low fluence Q-
switched Nd:YAG laser
Figure 7.24. Perioral rhytides before treatment with a millisecond Nd:YAG laser
Figure 7.25. Improvement in quality of skin after treatment with a millisecond Nd:YAG laser
Figure 7.26. Periorbital rhytides before treatment with an IPL source

Figure 7.27. Improvement in rhytides after treatment with an IPL source
Figure 7.28. Photodamaged skin before treatment with an IPL source

Figure 7.29. Improvement in quality of skin after treatment with an IPL source
Figure 7.30. Periorbital rhytides before treatment with an IPL source

Figure 7.31. Improvement in rhytides after treatment with an IPL source
Figure 7.32. Photodamaged skin before treatment with an IPL source (photograph by courtesy of Agneta Troilius
MD, PhD)
Figure 7.34. Photodamaged skin before

Figure 7.33. Improvement in quality of skin after treatment with an I IPL source (photograph by
treatment with an I PL source (photograph by courtesy of Agneta Troilius MD, PhD)
courtesy of Agneta Troilius MD, PhD)
Figure 7.35. Improvement in

quality of skin after treatment with
an IPL source (photograph by
courtesy of Agneta Troilius MD,
PhD)
Figure 7.36. Periorbital rhytides before treatment with a 1320-nm Nd:YAG laser
Figure 7.37. Improvement in rhytides after treatment with a 1320-nm Nd:YAG laser
Figure 7.38. Periorbital rhytides before treatment with a 1320-nm Nd:YAG laser
Figure 7.39. Improvement in rhytides after treatment with a 1320-nm Nd:YAG laser
Figure 7.40. Deep saucerized acne scars before treatment with a 1320-nm Nd:YAG laser
Figure 7.41. Improvement in scars after treatment with a 1320-nm Nd:YAG laser
Figure 7.42. Histologic findings consistent with solar elastosis

Figure 7.43. Histologic findings 6 months after four treatments with a 1320-nm Nd:YAG laser. Note upper
papillary dermal fibrosis
Figure 7.44. Periorbital rhytides before treatment with a 1450-nm diode laser
Figure 7.45. Improvement in rhytides after treatment with a 1450-nm diode laser
Figure 7.49. Improvement in rhytides after treatment with a 1450-nm diode laser. Skin quality was improved
Figure 7.52. Perioral rhytides before treatment with a 1450-nm diode laser
Figure 7.54. Before treatment with a nonablative radiofrequency device

Figure 7.55. After

treatment with a non
ablative radiofrequency
device
7.55). In the future, lasers, light sources or radiofrequency devices may be created that can
result in the same degree of improvement as that seen with ablative systems—without the
potential complications and downtime of such systems.
REFERENCES
1 Hruza GJ. Laser skin resurfacing. Arch Dermatol 1996; 132:451–5.
2 Teikameyer G, Goldberg D. Skin resurfacing with the Er:YAG laser. Dermatol Surg 1997;
23:685–7.
3 Goldberg DJ. EYAGr; laser resurfacing: What is its role? Aes Surg J 1998;18:255–60.
4 Hayashi K, Peters DM, Mabit G 3rd, et al. The mechanism of joint capsule thermal
modification in an in-vitro sheep model. Clin Orthop 2000;370:236–49.
5 Goldberg DJ, Whitworth J. Laser skin resurfacing with the Q-switched Nd:YAG laser.
6 Goldberg DJ, Metzler C. Skin resurfacing utilizing a low-fluence Nd:YAG laser. J Cutan
Laser Ther 1999;1:23–7.
7 Cisneros JL, Del Rio R, Palou M. The Q-switched Neodymium (Nd):YAG laser with
quadruple frequency. Dermatol Surg 1998;23:345–50.
8 Goldberg DJ, Silapunt S. Q-switched Nd:YAG laser: rhytide improvement by non-ablative
dermal remodeling. J Cutan Laser Ther 2000;2:157–60.
9 Goldberg DJ, Silapunt S. Histologic evaluation of a Q-switched Nd:YAG laser in the non-
ablative treatment of wrinkles. Dermatol Surg 2001;27:744–6.
10 Friedman PM, Sklover GR, Payonk G, et al. 3D in-vivo optical imaging for topographical
quantitative assessment of non-ablative laser technology. Dermatol Surg 2002;28:
199–204.
11 Goldberg DJ, Samady J. Comparison of intense pulsed light and Nd:YAG laser for non-
ablative treatment of facial rhytides. Lasers Surg Med 2001;28:141–4.
12 Goldberg DJ. Non-ablative dermal remodeling: comparing 3 different wavelengths: does it
make a difference? Lasers Surg Med 2002;30:31.
13 Lee MC. Combination aura 532 nm and lyra 1064 nm lasers for non-invasive skin
rejuvenation and toning. Lasers Surg Med 2002;30:32.
14 Zelickson BD, Kilmer SL, Bernstein E, et al. Pulsed dye laser for sun damaged skin.
15 Zelickson B, Kist D. Effect of pulsed dye laser and intense pulsed light source on the
dermal extracellular matrix remodeling. Lasers Surg Med 2000;12:17.
16 Zelickson B, Coles C. Treatment of photodamaged skin using long pulsed dye (595 nm).
Lasers Surg Med 2002;30:29.
17 Bjerring P, Clement M, Heickendorff L, et al. Selective non-ablative wrinkle reduction by
laser. J Cutan Laser Ther 2000;2:9–15.
18 Fournier N, Dahan S, Barneon G, et al. Nonablative remodeling: clinical, histologic,
ultrasound imaging, and profilometric evaluation of a 1540 nm Er:Glass laser. Dermatol
Surg 2001;27:799–806.
19 Goldberg DJ, Cutler KB. Nonablative treatment of rhytides with intense pulsed light.
20 Goldberg DJ. Histologic changes after treatment with an intense pulsed light. J Cutan
Laser Ther 2000;2:53–6.
21 Bitter PJ. Noninvasive rejuvenation of photoaged skin using serial, full-face intense
pulsed light treatments. Dermatol Surg 2000;26:835–43.
22 Nelson JS, Millner TE, Dave D, et al. Clinical study of non-ablative laser treatment of
facial rhytides. Lasers Surg Med 1998;17:150.
23 Goldberg DJ. Non-ablative subsurface remodeling: Clinical and histologic evaluation of a
1320-nm Nd: YAG laser. J Cutan Laser Ther 1999;1:153–7.
24 Goldberg DJ. Subdermal resurfacing. Oper Tech in Oculoplst, Orbital, and Reconstruct
Surg 1999;2:188–93.
25 Goldberg DJ. Nonablative resurfacing. Clin Plas Surg 2000;27:287–92.
26 Trelles MA, Allones I, Luna R. Facial rejuvenation with a nonablative 1320 nm Nd:YAG
laser: A preliminary clinical and histologic evlauation. Dermatol Surg 2001;27:111–16.
27 Goldberg DJ. Full-face nonablative dermal remodeling with a 1320 nm Nd:YAG laser.
28 Goldberg DJ, Rogachefsky AS, Silapunt S. Non-ablative treatment of facial rhytides: A
comparison of 1450 nm diode laser treatment with dynamic cooling as opposed to
treatment with dynamic cooling alone. Lasers Surg Med 2002;30:79–81.
29 . Leffell DJ. Clinical efficacy of devices for nonablative photorejuvenation. Arch Dermatol
2002;138:1503–8.
30. Pozner JN, Goldberg DJ. Nonablative laser resurfacing: state of the art 2002. Aes Surg J
2202;22:427–34.
31. Goldberg DJ. Nonablative dermal remodeling. Does it really work? Arch Dermatol 2002;
138:1366–38.
8
COMPLICATIONS
KEY POINTS
(1) Both ablative and non-ablative facial rejuvenation techniques can lead to scarring
(2) The most common causes of scarring from ablative techniques are poor technique,
inappropriate wound care and infection
(3) Infections after ablative laser resurfacing can present in an atypical fashion
(4) Both scarring and pigmentary changes can occur after non-ablative facial
rejuvenation
Laser skin resurfacing has become increasingly popular as a technique for improving
photoaged skin. With this popularity has come the recognition that complications can and do
occur.1–6 The use of scanning or pulsed carbon dioxide lasers has led to control of thermally
induced damage. The potentially damaging thermal nature of CO2 lasers, although clearly of
beneficial nature in deeper rhytides, has led to the development of the Er:YAG lasers. The
Er:YAG lasers with their higher water absorption allow potentially greater precision,
producing less tissue ablation and minimal thermal injury. Re-epithelialization with short-
pulsed Er:YAG lasers is faster when minimal ablation is the goal. Superficial Er:YAG laser
ablation, in expert hands, can also be used on the neck and hands. Less damaging non-
ablative systems stimulate new papillary dermal collagen formation with a resultant
improvement in photoaged skin.
With any technique there is the possibility of complications. The risk of such complications
can be minimized with experience and correct surgical technique. Proper technique requires a
good understanding of laser–tissue interaction, collagen biology and wound healing. Patient
selection is also important. For proper patient selection, one must consider recent oral
isotretinoin intake, a history of hypertrophic scars, keloids, some systemic diseases, as well
as other previous skin treatments that may interfere with appropriate healing after laser
resurfacing. Finally, appropriate wound care after ablative techniques is mandatory to
promote wound healing. Even in the ideal situation, complications can occur. Early
recognition of complications may lead to an improved final result. Post-ablative resurfacing
side effects are to be expected. These include oozing, crusting and swelling. Post-operative
erythema occurs following all ablative procedures and is often proportional to the depth of
ablation. Other short-term or permanent complications include prolonged erythema,
hyperpigmentation, hypopigmentation, contact dermatitis, milia and excoriated acne,
infectious processes, scarring, ectropion or lagophthalmus, excoriations and/or vascular
proliferations.2 Contact dermatitis, when it occurs, usually develops in the first month after
ablative treatments. This occurs most commonly due to patient sensitivity to some topically
applied product. It must be emphasized that although all the aforementioned complications
Figure 8.1. Erythema 6 months after CO2 laser resurfacing
Figure 8.2. Erythema 1 month after short-pulsed Er:YAG laser resurfacing

COMPLICATIONS 199
Figure 8.3. Erythema 3 months after variable pulsed Er:YAG laser resurfacing
can occur after ablative techniques, some, such as scarring and pigmentary changes, can
also be seen after non-ablative treatments.
ERYTHEMA
Edema, pain, tightening and erythema are to be expected in the post-operative healing period
after ablative resurfacing (Figures 8.1–8.3). Erythema should not be considered a true

Figure 8.5. Post-inflammatory hyperpigmentation 2 months after CO2 laser resurfacing
Figure 8.6. Post-inflammatory hyperpigmentation 2 months after short-pulsed Er:YAG laser resurfacing
COMPLICATIONS 201
Figure 8.7. Post-inflammatory hyperpigmentation 1 month after non-ablative 1450-nm diode laser treatment
Figure 8.8. Post-inflammatory hyperpigmentation 1 month after non-ablative 1450-nm diode laser treatment
Figure 8.9. Post-inflammatory hyperpigmentation 1 month after non-ablative 1320-nm Nd:YAG laser treatment
complication unless it lasts more than 6 months. Most commonly, the intensity and duration
of erythema depend on the depth of skin ablation and the delivered laser energy. Erythema
may be more evident when only partial anatomic regions are treated. Erythema can also be
minimized by the use of nonirritating topical agents once full re-epithelialization has occurred.
Non-irritating cosmetics and sunscreens will help to camouflage erythema.
HYPERPIGMENTATION
The most common complications seen after laser resurfacing are pigmentary in nature
(Figures 8.4–8.9). Post-treatment hyperpigmentation is seen in 20–30% of skin phenotypes III
and is almost 100% in type IV.1–3 The incidence is extraordinarily high in those with melasma.
Hyperpigmentation, when it occurs, usually occurs after the first month of post-resurfacing
healing. It is thought to occur as the result of activation of melanocytes during the post-
operative inflammatory laserremodeling period. When isolated areas such as the periorbital or
perioral areas are treated, post-inflammatory hyperpigmentation is usually more evident.
Figure 8.10. Delayed hypopigmentation 1 year after CO2 laser resurfacing

COMPLICATIONS 203
Figure 8.11. Hypopigmentation 4 months after CO2 laser resurfacing of the neck
Figure 8.12. Hypopigmentation 6 months after CO2 laser resurfacing of the neck
Figure 8.13. Hypopigmentation and erythema 2 months after Er:YAG laser resurfacing of the neck
Figure 8.14. Hypopigmentation following intense pulsed light (IPL) non-ablative treatment
COMPLICATIONS 205
The early and aggressive use of both bleaching creams and appropriate sunblocking agents,
especially in the higher phototypes, can decrease the incidence of this complication. Typically
treatment consists of a daily 2–4% topical hydroquinone cream or solution. In addition, or as
an alternative, topical glycolic, retinoic, azelaic and/or kojic acids can be used.7
HYPOPIGMENTATION
Permanent hypopigmentation is rare following facial resurfacing. When it occurs, it is usually
delayed, appearing some 6–12 months after laser treatment (Figures 8.10–8.14).4 When
occurring this late, it generally tends to be permanent. It may also occur more commonly in
patients with prior aggressive dermabrasion and/or deep chemical peels. Recent data suggest
that topical psoralens (8–MOP) in combination with sunlight or artificial UVA light source
treatment can improve this laser induced delayed hypopigmentation.6 A similar result may
ensue following treatment with the 308-nm excimer laser.
CONTACT DERMATITIS
The reported incidence of post-laser resurfacing contact dermatitis has been up to 65%
(Figures 8.15–8.17).1–4 It would appear that topical agents, which in a normal situation would
not be expected to cause significant contact irritation, are difficult to use when there is a post-
laser treated decrease in barrier function. Topical sensitization to bacitracin appears to be a
common problem. Petrolatum emollients are usually well-tolerated. If contact dermatitis does
occur, it is ideally treated with a bland emollient and topical corticosteroid ointments. When
severe pruritis becomes an issue, oral antihistamines may be required.
Figure 8.15. Contact dermatitis following CO2 laser resurfacing

Figure 8.16. Contact dermatitis following Er:YAG laser resurfacing
Figure 8.17. Contact dermatitis following Er:YAG laser resurfacing

COMPLICATIONS 207
Figure 8.18. Acne following CO2 laser resurfacing
Figure 8.19. Acne following variable pulsed Er:YAG laser resurfacing

MILIA AND ACNE

During the process of re-epithelialization the use of emollients and occlusive dressings can
cause follicular inflammation. This may lead to milia and exacerbation of acne (Figures 8.18
and 8.19).1–4 Milia, reported in up to 14% of post-ablative laser patients, usually resolves
spontaneously. In patients with numerous milia, comedonal extraction may be required.
Because of the potential for acne flares, patients who seek ablative laser resurfacing for acne
scars, require control of their underlying acne. Post-laser inflammatory acne, if it is to occur,
is usually seen several weeks after resurfacing. In such patients, one must consider the use
of oral antibiotics both prior to and after laser treatment.
INFECTIONS
Any procedure that ablates the epidermis and superficial dermis, may predispose
patients toinfection (Figures 8.20–8.24). 1–4 Herpes simplex virus (HSV) infection
Figure 8.20. Monilial infection following CO2 laser resurfacing
has been reported in up to 2–7% of laser-resurfaced patients. This traditionally represents

activation of latent virus during the re-epithelialization phase; usually occurring 7–10 days
after laser resurfacing. When it occurs, infection usually presents in the perioral region. Early
diagnosis may be difficult because the lesions can have an atypical herpetic manifestation.
Typical presentations usually manifest as abundant crusting or punctated lesions. Most
experts recommend oral antiviral prophylaxis, even in patients without a previous history of
HSV. It should be noted that herpes zoster reactivation has also been reported in post-laser
treatment. Either of these two viral infections can lead to scarring. Other reported infections
include staphylococcal and streptococcal impetiginizations, as well as Pseudomonas and
candidal infections. The last two are rare and usually only occur in prolonged occluded post-
COMPLICATIONS 209
Figure 8.21. Culture positive herpetic infection following non-ablative IPL treatment
Figure 8.22. Culture positive herpetic infection following short-pulsed Er:YAG laser resurfacing
Figure 8.23. Bacterial infection after laser resurfacing
Figure 8.24. Bacterial infection after laser resurfacing

COMPLICATIONS 211
laser wounds. These infections tend to occur within the first 2 weeks after laser treatment. If
not treated appropriately, scarring or even worse, toxic shock syndrome, may occur. In most
situations, these infections are caused by skin and/or oropharyngeal colonization, which is
then permitted to seed the skin after laser treatment. Early detection is the best treatment. In
addition, regular dressing changes and skin inspection during the re-epithialization phase is
helpful. There is some controversy as to the efficacy of pre-treatment antibiotics.
HYPERTROPHIC SCARRING
A 1% incidence of hypertrophic scarring has been reported after ablative laser resurfacing
(Figures 8.25–8.28).1–4 Adequate laser experience and technique are important factors in
decreasing the incidence of scarring. Periorbital, perioral, chin and malar areas have a greater
predisposition towards the development of hypertrophic scars.
Prior deep chemical peels, dermabrasion, recent use of oral isotretinoin and keloid tendency
all predispose towards the development of hypertrophic scars. In addition to proper technique,
close patient follow-up and good wound care is essential to lessen complications. When
hypertrophic scarring occurs, treatment consists of intralesional corticosteroids and pulsed
dye laser treatment.
ECTROPION AND LAGOPHTHALMUS

Ectropion and lagophthalmus, although quite rare, occur most commonly, when laser skin
resurfacing is combined with a prior blepharoplasty (Figures 8.29 and 8.30).1–3 The upper and
lower eyelid skin is very thin and the number of passes and laser fluence must be carefully
tailored for the anatomic area. Ectropion and lagophthalmus can be improved with surgical
intervention.
Figure 8.25. Before laser resurfacing

Figure 8.26. Hypertrophic scarring after laser resurfacing
Figure 8.27. Hypertrophic scarring after laser resurfacing on the neck

COMPLICATIONS 213
Figure 8.28. Hypertrophic scarring after laser resurfacing on the back
Figure 8.29. Ectropion following CO2 laser resurfacing (photograph courtesy of Brian Biesman, MD)
Figure 8.30. Ectropion following CO2 laser resurfacing (photograph courtesy of Brian Biesman, MD)
REFERENCES
1. Fulton JE. Complications of laser resurfacing. Methods of prevention and management.
2. Redon-Pellerano MI, Lentini J, Eaglstein WE, Kirsner RS, et al. Laser resurfacing: usual
and unusual complications. Dermatol Surg 1999;25:360–7.
3. Nanni CA, Alster TA. Complications of cutaneous laser surgery. Dermatol Surg 1998;24:
209–19.
4. Bernstein LJ, Kauvar AB, Grossman MC, Geronemus RG. The short- and long-term
effects of carbon dioxide laser resurfacing. Dermatol Surg 1997;23:519–25.
5. Trelles MA, Pardo L, Velez M, Garcia-Solana L, Rigau J. The search for a youthful upper
lip via laser resurfacing. Plast Reconstr Surg 2000;105:1162–9.
6. Grimes PE, 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.
7. Goldman MP. The use of hydroquinone with facial laser resurfacing. J Cutan Laser Ther
2000;2:73–7.
9
MARKETING FACIAL SKIN REJUVENATION
R Stephen Mulholland
KEY POINTS
(1) Laser and non-laser facial rejuvenation procedures represent the core of any
cosmetic medical practice
(2) Marketing starts with ‘high-quality therapy’ in a patient friendly environment:
presentation of services is important
(3) Promotion varies enormously in cost, depending on method, and should be
rigorously assessed in terms of its success in attracting patients
INTRODUCTION
As one reflects on the marketing of facial skin rejuvenation, two striking observations become
self-evident. First, laser services are no longer ancillary in any cosmetic practice. The revenue
streams from a full service cosmetic surgery practice and an esthetic ablative and non-
ablative skin rejuvenation clinic can be equal. Because in many locations non-ablative
treatment is a delegable act, this has been a tremendous addition to many practices. It
expands the revenue base without the physician having to perform the services him or
herself. Anytime one can develop such ‘multipliers’ in a business, there is a powerful
opportunity to maximize revenue or free oneself to do other things.
The ablative and non-ablative skin rejuvenation techniques are fundamentally different, not
only in their physics and clinical effects, but, most importantly, in how they should be
intelligently and successfully marketed within an esthetic practice.
One of the most important methods of achieving a successful esthetic practice is the
management of patients’ expectations. One must understand a patient’s concerns,
expectations and goals and then be able to select only those patients who will be happy with
the likely outcome of the suggested therapy. Nonablative facial skin rejuvenation techniques,
performed well, can deliver more attractive skin, often with improved tone, color, texture, pore
size and minimal to modest wrinkle enhancements. The success of non-ablative techniques is
very dependent upon creating realistic expectations in the potential patient. Nonablative
techniques are not the same as ablative resurfacing approaches. It is imperative that the
patients fully understand the pros and cons of each technique.
An excellent physician, armed with a desirable esthetic service and the right technology and
product, is not always the formula to a successful esthetic laser or cosmetic surgery practice.
In today’s competitive climate, it is often vital to the success of an esthetic medical practice
that these services and products be marketed effectively. It is critical to let potential clients
know who you are and what you offer.
Today, the revenue streams from laser resurfacing, delegated esthetic laser skin care and
non-ablative skin rejuvenation therapies may exceed the revenue from the remaining parts of
a successful full service cosmetic surgery practice. No longer is laser skin care a ‘poor sister’.
This is especially encouraging in that some laser services are delegated to other health care
professionals in many jurisdictions. In those jurisdictions, photo-rejuvenation, laser hair
removal, laser leg vein and laser skin care treatments are delegable acts. Ablative techniques,
on the other hand, do not have this passive revenue potential and generally need to be
performed by a physician. The delegable nature of many of these procedures can be a
tremendous addition to any medical business, as it expands a physicians revenue base
without the doctor having to perform the actual services. Delegable act health care personnel,
under the supervision of a physician, have much more economical hourly labor costs
associated with their time than a physician. Further, delegation of laser skin care services,
such as non-ablative treatments, allows the proprietor physician to pursue traditional
managed care or private medical revenue streams. It may also allow the physician to create
more leisure, family or expanded interest time while the delegated services are generating
additional revenue. Any method by which one can develop such ‘multipliers’ in a business
offers a powerful opportunity to maximize revenue or free oneself to do these ‘other things’.
At the same time as the largest, most affluent population purchasing group, the ‘baby
boomers’, enters into its prime spending years, all of medicine and allied health services have
witnessed an increase in managed care and a major contraction in third party payer
reimbursements. In the United States, it is now estimated that somebody is turning 50 years
old every eight seconds! The combination of the baby boomer-fueled demand for esthetic
procedures, which help maintain the appearance of youth and vitality, with the explosion in
new, minimally invasive cosmetic surgery techniques, laser skin care, and esthetic service
technology, has created an attractive market and source of additional revenue for all medical
practitioners.
The marketing principles outlined in this chapter are general enough to benefit any
practitioner who wants to begin a laser skin rejuvenation practice. They are also specific
enough for anyone who has purchased a laser, intense pulsed light source or radiofrequency
device to benefit immediately from its pearls.
WHAT IS MARKETING?
Most physicians starting a cosmetic laser practice equate marketing with advertising. Most
doctors are very good at spending money on advertising to make the phone ring but are very
poor at marketing. Anyone can spend money to make the phone ring. That’s not marketing;
that’s the easy part. Marketing is a summation of all the activities and procedures that a
physician, as the provider of a product (your esthetic services), must perform/implement to
deliver the product into the hands of the consumer. Advertising may only represent a very
small or non-existent component of a practice’s marketing plan. There are many yardsticks
by which to measure a successful marketing plan, but profitability and Return On Investment
(ROI) are the most important for practitioners of esthetic laser services. Concepts of medical
marketing can be condensed into the following 10 Ps of Medical Marketing.
10 Ps of Esthetic Medical Marketing
1. Physician 6. Price
2. Product 7. Precision
3. Plan 8. Predictability
4. People 9. Profitability
5. Place 10. Pleasure
MARKETING FACIAL SKIN REJUVENATION 217
PHYSICIAN
In medicine, unlike some businesses, promotion can be not substituted for quality. The most
important aspect of a profitable practice and marketing that practice, is a quality physician.
As doctors, our product is not a disposable plastic toy, where quality can be variable; ours
must only be measured in excellent patient outcomes. We have an ethical and moral
obligation to our patients, as physicians, to deliver quality esthetic health care and above all
else ‘do no harm’. Most businesses and their products are not bound by such intimate and
ethical standards. We, as physicians delivering an esthetic service, can never compromise the
well being of our clients with our products. Of course ‘do no harm’ is important, but in
esthetic laser skin care services, this time-honored principle is not enough, one must actually
‘do some good’. To be successful, it is critical that your non-ablative and ablative skin
rejuvenation services must actually provide for a noticeable enhancement in the cutaneous
appearance of the patient’s face or body. Providing significant noticeable skin enhancements
that are pleasing to the patient can be a real concern to nonablative skin rejuvenation
patients and highlights the importance of creating realistic expectations.
Part of our role, as physicians delivering skin rejuvenation services is to know the product
and potential outcomes well. We must learn the basics of laser medicine, laser safety, wound
healing and hair biology. We must also keep up to date on the latest developments by going to
meetings, reading journals and maintaining our continuing medical education. We never must
lose sight of our role as a physician. If we do, then all the other Ps of practitioner marketing
are worthless.
PRODUCT
Once one becomes a high quality laser physician, the next step is the delivery of a quality
product to the photoaged, wrinkled and/or anti-aging client. Deciding upon the right
technology can be a very difficult decision. There are many difficult questions such as
optimum fluence, pulse duration, wavelength(s), and skin cooling. Laser resurfacing and non-
ablative dermal remodeling are two entirely different techniques and as such must be
marketed differently. It is inevitable that there will continue to be technological advances in
optimizing the removal of unwanted hair. Features of laser or intense pulsed light systems
that are important include:
(1) Speed: the faster the system (Hertz and spot size dependent) the more afford able your
skin rejuvenation product will be for your clients and the more profitable it may be for the
physician. This is especially so when considering the large surface areas involved in non-
ablative skin rejuvenation photorejuvenation techniques and Photo-body treatments. Of
course, speed itself is not enough if there are no results. Systems that are somewhat slow,
may be just as successful if they can deliver the same non-ablative or ablative outcomes
with fewer treatments.
(2) Service and Support: you will want to choose a laser or intense pulse light company that
will still be doing business in a year, provide excellent service in the field and whose
technology has an excellent track record. Remember, if (when) you get busy enough, all
systems will need some downtime for repair and maintenance.
(3) Upgradable: most importantly, you want a technology that will not be out of date within a
few months, or years of your purchase. Avoid planned obsolescence. Planned obsolescence
is a laser manufacturer’s policy of improving a laser system’s performance to the extent
that your laser purchase becomes less effective in delivering the intended treatments and
you, as the holder of the lease, are not able to upgrade. You do not want to be left with a
technology that cannot be reasonably upgraded via a platform to their original system. The
cost of these upgrades is often written down by attending workshops and preceptorships.
Hence, the avoidance of ‘planned obsolescence’.
PLAN
An excellent physician with a good laser ablative or non-ablative system needs a plan. If one
‘fails to plan—then one plans to fail’. Short of an actual business performa, there are three
simple questions one must answer as part of a plan to implement skin rejuvenation into a
practice.
Market Analysis
If you are a physician with 10,000–20,000 patients in your roster or practice database, then
you are in an enviable position to implement skin rejuvenation techniques. Your initial market
is your own large patient roster. Similarly, you may be a physician with a busy laser skin care
practice already, and implementing ablative and non-ablative techniques by cross-marketing
the service will be greatly facilitated.
If you have the type of practice where you will need to recruit potential patients for these
techniques, then you should conduct a quick (and easy) marketing analy-sis to determine the
viability of your enterprise in your present locale. You will be required to go out and ‘recruit’
patients by promoting your services.
Any time you consider implementing and marketing a clinical service, or product, it is
critically important to understand who will be accessing this service. The more closely you
can define the demographic, pyschographic and behavioral characteristics of your potential
clients, then the more effective marketing decisions you can make regarding the various
advertising and promotional media you will be paying to target this market. Precise
identification and characterization of the clients who will be accessing your laser services is
called ‘Market Segmentation’. Who are these ‘baby boomers’ that are turning 50 years old at
the rate of one every eight seconds? What pyschographic, retail-specific behavioral
characteristics do they share? The group of women entering their fifth decade tend to be very
confident, well adjusted, self-actualizers. This is a generation that created the cult of vitality
and youth. These patients want to look good as well as feel good. Baby boomers who are now
turning 50 years old are in senior positions in their professional, personal and economic lives.
When a self-actualizer looks in the mirror and sees someone looking back that does not look
as young or as vital as they might feel, a conflict, duality or disharmony arises. This duality of
feeling younger than appearance would suggest propels many baby boomers to seek
procedures that help them restore the balance between the ‘internal vitality’ and the ‘external
appearance’. The goal of any procedure will be to ‘look as good as they feel’. If the procedure
(s) offer significant enhancement, are minimally invasive and lead to no downtime, such as
the nonablative procedures, then such techniques will be extremely popular.
The ablative and non-ablative rejuvenation target market includes women between 20 and
65 years old (the majority are 30–65 year olds), with a household income over $40,000 per
year. There are many other segmentation characteristics that can be used to further
subdivide your potential clients, including psychological and behavioral characteristics, such
as those women who tend to be college or university trained, take one or more vacations a
year when they must travel, and spend freely on cosmetics and clothing more than once per
month. However, such specific segmentation data do not always help you decide advertising
and promotional opportunities or the associated lead costs any more than simply looking for
market reach for women 20–65 years old, with households incomes over $40,000.
To find out the size of this targeted cohort of potential women living within one hour of your
practice location, simply contact any medium in which you might be interested in advertising
(radio, newspapers or magazines) and they will gladly send you their market breakdown and
market reach for your area (as they have already paid for this marketing analysis
themselves). Your potential advertisers, in effect, can provide you with all the CMA (central
marketing area) data that you will need to identify how many photo-rejuvenation market
segment cohorts actually live in your region. When the advertising media send you the data,
you will be able to quickly take the four to five year age block breakdowns sub-classified by
sex and income and combine them into the global target cohort in the your immediate area.
The following is an example of the simple analysis you will require.
(1) City population: 2 million.

(2) Demographic matches (target market): Women, 20–65 years, making over $30,000, say
for example 680,000.
(3) ‘2.5% Rule’: this is an advertising assumption, which states that, of a susceptible target
market for a product, only 1/40 (2.5%) might respond to advertising for this product.
(4) 680,000÷40=17,000 potential clients; however, there will be other clinics, possibly 30,
performing laser skin rejuvenation in you locale.
(5) 17,000÷30=567 clients=market share: the number of potential clients in your region that
can be obtained from your advertisements. This does not include potential patients that
may come from other laser skin rejuvenation clinics.
If the potential market share is 300 people or greater, then the region is not saturated. A
profitable skin rejuvenation practice should result.
Financial Modeling
If there are 500 clients in the clinic’s market share, the average skin rejuvenation client
spends approximately $500.00 per visit. The average patient returns four times: 500 clients×
$500.00×4 treatments=$1,000,000. Thus, if you are converting maximally all potential
patients into treatments, re-treatments and word of mouth referrals, then a $1 million dollar
per year skin rejuventation practice should result. However, because physicians never
convert anywhere near maximally (100%), most physicians will earn between $50,000 and
$100,000 after expenses.
Marketing Plan
All the Ps in this chapter must be implemented for a successful marketing plan. A good
marketing plan will keep you profitable.
PEOPLE
The first step is to become a well-trained, knowledgeable laser practitioner. Then one needs a
quality, fast, reliable ablative or non-ablative system. This is followed by a planning and
marketing analysis that indicates there is a viable opportunity to generate additional revenue
in the local skin rejuventation market. Only then is it time to consider the people who will be
delivering the product. The people a physician hires to represent the esthetic laser service are
the next most important critical resource, after the doctor and the product, in delivery of
cosmetic skin rejuvenation. Remember, these are the people who will present, represent, and
promote your skin rejuvenation product on the phone, in your office and in the community.
This highly sales oriented position requires an outgoing, friendly and persuasive individual.
How does one hire these motivated outgoing types? They are in high demand. Obviously
careful interviewing, references, and experience are necessary. Some have even hired human
resource consultants to uncover the required sales traits and skills. In the final analysis, after
the usual due diligence, interviewing and reference checks, one often hires such individuals
on gut instinct. A certain amount of luck is always required!
After hiring staff, the members of the staff must be empowered by teaching them about skin
rejuvenation. This will allow them to sell the procedure. Give them phone scripts for new
callers. Offer staff complimentary treatments. They will become the most enthusiastic
supporters of the services. They will sell ablative and non-ablative treatments with a
tremendous sense of conviction that clients can sense.
Finally, remuneration is critical. Giving staff a feeling that they share in the success always
helps. Front desk staff (client service representatives), office managers and laser technicians
should always be paid a healthy base salary, commensurate with expertise and/or experience.
One could advocate leaving room for bonus incentives based upon the staff’s ability to convert
contacts to treatments. For the receptionist, it will be the number of calls (leads) to
consultations; for the laser nurse it will be converting treatments to re-treatments, and for the
office manager, who oversees the whole process, it will be a bonus on the percentage of
incremental increase in sales. These monthly bonuses must always be an acceptable
percentage of the increasing bottom line. Some form of bonus remuneration will lead to
welltrained, happy, motivated staff.
PLACE
The clinic will need a place for staff and technology. The clinic should always reflect the image
of the provider (the physician), and the product. Remember people are paying out of their
pockets for a non-insured service and they will expect a quality outcome that is also delivered
in pleasant surroundings. There is competition for their cosmetic dollar. That does not mean
you must have museum quality paintings hanging on the walls. However, it is important to
pay careful attention to the ‘look’ and ‘feel’ of the clinic setting so as to maximize the positive
impact upon your potential skin rejuventation patients.
After providing for a careful, tasteful, appropriate and coordinated approach to interior
decorating, one must carefully plan all contact points with skin rejuventation patients and
create a positive image.
The Waiting Room

Keep this a relatively small private area, with no more than one or two patients waiting at a
time. Private patients hate to feel ‘herded’ and do not like to wait. His or her time is as
valuable as that of anyone else. Schedule clients so they have five minutes to settle into the
atmosphere of the clinic. During this ‘absorption phase’, they should be exposed (through
brochures, videos, posters, prompts, guides, and product displays) to some of the other
wonderful cosmetic aspects of the office. Ablative and non-ablative patients will go onto other
cosmetic laser procedures up to 20% of the time.
As the clients arrive, greet them by name. Act as if you know them. Don’t be afraid to offer a
refreshment or snack (examples would include mineral or spring water, tea, coffee, or a light
snack).
The Consultation
The consultation or treatment, whether offered by a nurse or physician, should be part sales
and part informed consent. The positive side of skin rejuventation should always be
emphasized first. Once clients know about the procedure, benefits and costs, the informed
consent should include alternative treatments, advantages, disadvantages, and risks. The
patient should have an opportunity to fully read the consent, have any questions answered to
their satisfaction, and should then sign each page of the consent document (indicating that it
was read and understood).
A well-executed consultation and consent for ablative or non-ablative techniques should
leave the client excited and hopeful about the potential results, well informed, understanding
of the risks and enthusiastic about going on to treatment.
The Treatment Room

A 3×4m room is ideal. Provide room for changing and reapplication of makeup after non-
ablative techniques. Never miss an opportunity to cross-market other cosmetic services
during treatments. Posters, videos and motivated laser nurses can assist laser patients assess
other available esthetic services. If ablative techniques are performed under sedation, then
basic life support systems must be readily available. Family or friends must be ready to
escort such a patient away from the office.
PRICE
The fees charged for skin rejuventation services will vary according to the anatomic zone, type
of practice, who delivers the service, laser speed, laser type and competitive prices (the price-
point) in the local skin rejuventation market.
This last factor, price-point in the market will probably be the most important influence in
setting fees. In most markets there will be a fairly narrow range of prices charged for both
ablative and non-ablative laser techniques. It is important to find out what other clinics are
charging. This is called ‘Mystery Shopping’. Ask friends or employees to call all the
competitors, find out what they charge per treatment or groups of treatments, who performs
it, what system they use, and how long it takes. Ask for informational mailings. Send mystery
shoppers in for consultation and treatment to see what is said and done.
Non-ablative treatments can vary in price between $300 and $1500, depending on the size
of the area being treated. Full-face ablative resurfacing can cost up to $10,000. Single or
multiple treatment non-ablative packages may be sold.
In general, for the new skin rejuventation clinic, prices should be in the low to middle range.
The best possible service must be provided.
Do not make it difficult for clients to pay. Take cash, checks, money orders, and credit
cards. Also, do not have clients reconcile accounts over a counter in the waiting area. Create
a small, private billing office where the skin rejuvenation patient can settle their accounts in a
confidential atmosphere. They will always appreciate this.
Presentation
The presentation of the laser center’s product will be critical to the success of the clinic’s
profitability. Presentation links physician, staff, place, price and even promotion into one
harmonious symphony that is known as internal marketing or ‘invertising’. Invertising is the
summation of all the experiences of the laser client’s, from the time they respond to a
promotion to the last time that they come for treatment. From the time of the first phone call,
every single client contact point should be broken down into all the possible events. Physician
and staff must script, practice and orchestrate in such a manner that the experiences or
‘through-put’ of the client, as they flow through the clinic, creates a positive experience and
converts them on to the next phase. The summation of all these small coordinated bursts of
activity is the quality performance of a team that can beat the competition.
The standard contact phases that must be orchestrated in the ‘through-put’ are as follows:
Promotion → Inquiry → Consultation → Treatment → Word of Mouth → Re-treatment →
New procedure
The obvious goal is maximizing the client conversion from one phase onto the next.
Conversion rates will determine the success and profitability of the clinic. Excellent promotion
will generate a large number of leads and consultations. This, through excellent ‘invertising’
will result in increased treatments. The quality of the product and treatment delivery will
maximize word-of-mouth referrals, re-treatments and conversions to new procedures.
Inquiry (Lead Stage)

Promotion (advertising), although technically the first stage of the process, will be covered
later. Making the ‘phone ring’ is usually the easy part. Anyone can utilize funds for adverts
that lead to a ringing phone. Where most physicians fail is in maximizing the conversion of
phone calls to treatments and re-treatments. Unless one prepares for this, a maximum return
on advertising or promotional investments will never be achieved.
Each promotional advertising that leads to a call into a skin rejuvenation practice will likely
cost between $75 and $250 per call, depending upon the advert, the medium and the market.
Each time the phone rings, the clinic will either convert that $75–$250 call into potential
revenue or lost money.
For maximum lead conversion careful telemarketing scripts must be created. These scripts
are the exact responses a physician wants the staff to provide during an introductory phone
call. It is this interaction that leads to consultations being booked. Keep these scripts short,
answering common questions, but always playing up the benefits of the skin rejuventation
product. Staff must be focused on the ‘closure to consult’ where ‘everything will be explained
fully’. The script should focus on the unique and positive selling points of the clinic and the
various available ablative and non-ablative treatments, including competitive prices and
extraordinary service. Avoid giving too much information over the phone. Unfortunately, the
risk of providing too much information over the phone will increase, as staff become more
knowledgeable. Surprisingly, the increased knowledge only increases the risk of staff saying
something inaccurate. This can dissuade prospective leads before they can experience the
laser center’s wonderful services.
The topic of telemarketing can be a book in itself. There are many books and one-day
courses on this very topic. Success will be documented by measuring conversion rates.
Scripts, price or presentations may occasionally have to be changed. Once the laser clinic is
up and running, one should not settle for anything less than a 50% conversion rate of all
calls to consultations. In the beginning, the lead conversions will probably be at 20–25%.
However, pay attention to the details of the 10 Ps; individualize the approach to maximize
profits.
Active leads are the calls that book consultations. Passive leads are the leads that everyone
forgets about. These are the callers that did not book a consultation, but may have only
requested information. Unfortunately, the clinic has already paid for the passive lead phone
call ($75–$250). These callers must become part of a pool the laser clinic continues to access.
Part of the telemarketing database will gather necessary demographic data. Consider the
mailing of a complimentary information package. The information package is sent to active
(consultation booked) and passive (information only requested) leads. It describes the
procedure of interest, the physician, the facility and other services offered. Active lead
management is simple; these clients are led into the consultation phase. Passive lead
management involves a succession of triggered mailings over the first month designed to keep
the passive lead (prospective client) interested in the facility. If no consultation is booked after
1 month, the passive lead receives a quarterly newsletter for 2 years. If the passive lead has
spent no money in the clinic after 2 years, the prospective client is dropped from the mailing
list.
Clearly this kind of lead management or ‘contact management’ requires the help of a
computer software program. These ‘contact managers’ are abundant. Goldmine™ and ACT™
are two of the popular general business contact manager’s programs. Several programs are
adapted to the medical practice, such as Nextech 99™ and Inform and Enhance™. No one
program is perfect, but they should offer contact management, triggered mailouts, full
reporting, scheduling, and some limited charting. It is difficult to be maximally efficient
without one.
Consultation Phase
As mentioned, the skin rejuvenation consultation is part sales and part informed consent.
The informed consent must be implemented fully, accurately, and ethically. This is even more
important in those jurisdictions where the non-ablative laser services (including consultation)
may be delegated to a nurse or technician. The consultation must be broken down into its
sales components. A typical skin rejuventation consultation is scheduled for 1 hour. This
includes the waiting room 5 minute cross-marketing absorption phase, 30 minutes for the
consultation and consent signing, 10 minutes for a possible test spot with a non-ablative
system and finally 15 minutes for patient clean-up, make-over, re-booking, account payments
and departure. A staff member who is goal oriented, and has a great smile should assist the
client with all phases.
The consultation is broken into the following elements:
(1) Be positive. The goal at the end of a 30–minute consultation is to pique the patients
interest to the point where they will purchase the product on the spot. During these
concentrated consultation periods, the delegated consultation team (usually the
receptionist, physician or nurse and office manager) must present a positive attitude.
Remember, much has been spent on: (i) the purchase of the lead (promotion); (ii) the
conversion of that lead into a consultation (telemarketing); and (iii) the creation of the
right ambience, atmosphere, marketing literature and flow through your clinic
(presentation). Consultation conversion rates are another stage the clinic will have to live
by. It is mandatory that the skin rejuvenation clinic projects an organized, confident, well-
groomed image.
(2) Demonstrate your interest in the patient. For the first 10 minutes of every interview,
find out about the patient. It needn’t be the physician who does this. Ask about their
families, what they enjoy about their work, etc. Try to make a connection that allows that
patient to know that you know how interesting they are.
(3) Find out what the patient really wants. Ask the patient directly what it is they really
wish to achieve from laser resurfacing. By clearly getting the client to state their goals, the
clinic will better be able to service their needs.
(4) Reassure the patient that you can deliver what they want. Make sure that ablative
and/or non-ablative techniques can satisfy the specific expectations of the client. Be
certain the client understand the advantages and disadvantages of each procedure. The
client may have to modify their expectations if they are unrealistic (the usual unrealistic
patient is one who expects 100% clearance of wrinkles).
(5) Assume the sale. Carefully word all discussions with the client to include the assumption
of purchase of the product. ‘Mrs X, when you are undergoing your skin rejuvenation you will
find…’. Assuming the sale reinforces the urge/impulse of the client to purchase the
product. This will translate into a patient undergoing treatment.
(6) Prevent ‘buyer’s remorse’ (future pacing). The patients mind must be put at ease over
the expense of their purchase. This is required to prevent the inevitable remorse
experienced by many consumers after a sizable purchase. Patients should be told of the
direct benefits of the treatment. As an example, one might ask ‘do you have any upcoming
social events where your skin will look so much more youthful?’
(7) The ‘closer’: The ‘closer’ should always be someone other than the physician—usually the
office manager. This removes the doctor or nurse from discussing finances and squarely
keeps them in the role of esthetic health service delivery. The closer is often an individual
with sales experience who will be able to convert a higher percentage of consultations to
treatments. The closer will also discuss payment terms and options.
Similar to the lead conversion rate, the percentage of consultations leading to ablative or non-
ablative techniques should be no less than 50%. In practices with a high percentage of word-
of-mouth referrals (clients who come from other happy clients), the closure rate can approach
80–90%. These successful practices are servicing ‘buyers’. Buyers are those clients who call
and come knowing they will have treatment. This type of ‘buyers’ practice is the ideal practice
profile, but is usually achieved by ‘purchasing’ enough ‘shoppers’ (through promotion) and
converting a high percentage of them to happy patients. With attention to the 10 Ps of
cosmetic medical marketing, one can achieve this type of practice much sooner. Such a
clinic’s ‘through-put’ and service will be superior to its competitors.
For the new skin rejuvenation clinic, where an exclusive ‘buyers practice’ does not exist,
most clients are simply ‘shoppers’. These are patients who were purchased through
promotion. ‘Shopper practices’ need to work very hard with lead and consultation conversion
to achieve maximum profitability. Most shoppers’ practices that attend to service and the 10
Ps should convert at least 50% of consultations to treatment.
Treatment
Like the other stages of contact and conversions, careful consideration must be given to what
occurs during the treatment. First and foremost is the obvious—treatments must be safe and
effective. If the non-ablative treatment is delegated to a laser nurse, ensure that they have
been well trained. They must know all clinical parameters necessary to safely, autonomously
and effectively deliver the treatment. Create a written ‘Delegable Laser Skin Rejuvenation
Document’ that clearly outlines the training, continuing education, treatment parameter and
adverse outcome protocol. This document should be kept on file in the clinic, be posted in the
laser rooms and constantly reviewed and updated. Only when safety and efficacy are
addressed can one focus on presentation, comfort and promotion. Have the laser treatment
room nicely decorated, clean, well ventilated, and cooled. Have a comfortable clinic gown,
room, slippers, towel(s) and treatment bed. Educate the laser nurse(s) on the other
procedures, services and products provided by the cosmetic clinic. Give them the cross-
marketing scripts, skills and bonus remuneration to allow and motivate them into selling the
available services. Ensure that posters, wall-prompts, brochures and continuously running
videos on the other clinic services and products are placed, exposed or provided to clients
during treatment. Finally, provide a private available clinic space for the client to re-apply
make-up and freshen-up after nonablative treatments before leaving the clinic.
Word of Mouth, Re-treatment, and New Procedure

With a well delivered skin rejuvenation product, the majority (over 80%) of nonablative
patients should return for their mandatory second treatment and over 60–70% should come
back multiple times for re-treatments over several years. Retreatment conversion is not only
built on the excellent experiences at earlier contact phases, but also depends heavily on the
comfortable delivery of the product and its success. Remember, if the patient expects ‘some’
degree of improvement and ongoing, intermittent maintenance treatments at affordable prices,
most clients will be happy repeat customers. A successful skin rejuvenation clinic should
keep growing; the client base should keep expanding. They will choose other new procedures
as well.
One contented client can generate an average of four word-of-mouth referrals (and the clinic
only paid for the first lead). Send cosmetic laser clients birthday notices and holiday greetings
acknowledging your appreciation for the business and perhaps a time limited discount
coupon that can be applied towards clinic services, for each known referral they send.
Actively solicit word-of-mouth referrals with mailings to clients and gifts or bonuses (in the
form of treatments) if they refer a client.
Conversion is the key to a successful practice. Attention to the 10 Ps will maximize the
ability to measure, improve and control conversion.
Promotion
Thus far, this chapter has focused on the details of the ‘through-put’ and the internal
marketing details. The surest way to waste money is to promote a practice and product before
working out the intricate details of its delivery. If one does not take time with the first few Ps,
then one is likely to waste tens of thousands of dollars on advertising with unacceptably low
conversion rates.
Promotion can be divided into internal and external promotion. Promotion can be an
isolated campaign, usually 6–12 weeks in duration, with one or more media (e.g. radio,
newspaper, and direct mail). The advantage of one focused, time-limited promotional
campaign is that it saturates the target market for a brief period of time.
Consistent promotion or advert placement is often used on a weekly or bimonthly basis to
maintain leads using the best performing medium. Adverts may be strongly ‘image oriented’
or ‘call to action’ or a combination of ‘imaging’ and ‘call to action’. Image advertising is easily
recognized as the most common form seen on television, radio and magazines. Image adverts
are often run by large companies with a large advertising budget. These are directed to the
creation and implementation of advert slicks with an ‘image’ oriented design. Such an
approach allows the consumer to identify with the image; the image becomes brand
recognition. Image marketing is not designed for, nor does it require of the consumer, any
immediate action. An advert designed to prompt the consumer to pick-up the phone and
impulsively/decisively call a number is called ‘call to action’ advertising.
Cosmetic laser surgery adverts are often examples of a combined ‘image’ and ‘call to action’
advert. Because laser esthetic services are a very visual product, imagery evokes strong
emotion and consumer impulses. A laser resurfacing advert showing before and after images
of a consenting patient’s healthier, more youthful appearing skin would be such an example.
However, most medical practices cannot afford to place image adverts with the hope that
patients will call for a consultation. Medical practices are not usually large corporations. A
medical practice must produce immediate leads and business with its advertising dollars. A
medical practice may entice the patient with image marketing. This must be followed by a
strong ‘call to action’ such as ‘call now for a free consultation’ or ‘upper lip hair removal at a
$99 discount, for the first 100 callers’. In medical advertising, combinations of strong imagery,
bold print, before and afters, strong call to actions, and the word ‘free’ usually generate an
adequate number of leads with low lead costs.
‘Lead cost’ is the amount it costs to acquire each phone call (lead) assigned to a specific
advert. The calculation is very easy; it is an automatic component of most contact
management reports. It is the cost of the specific advert divided by the number of leads
attributed to that advert. For example, if an advert costs $3000 to implement and generates
30 calls over the next 3–4 weeks, the lead cost is $3000/30 =$100 lead cost. As a rule, in non-
ablative treatments where the product price per treatment may average only $500, the lead
cost cannot exceed more than $100 per call.
Internal Marketing ‘Invertising’
Direct Mail
For practices with large existing patient bases, direct mail is where promotion should begin.
Dermatologists and plastic surgeons often have large rosters of long-term repeat patients.
These patients already know and trust their physicians. These physicians have brand
recognition. The lead conversion rates should approach 80% (converting leads to
consultations). The lead costs should be around $20–50/lead. Here the cost is a simple direct
mail campaign to existing patients. The ideal target group is female patients 20–65 years of
age. A mass mailing to your existing patients, describing your new skin rejuventation services,
should cost $2000 for 5000 mailouts. You should generate 40–50 calls (leads) from this
simple campaign ($50 lead cost).
This routine can give the physician and staff a trial run of both the presentation and
‘through-put’ the clinic has developed with the simplest group of clients. This simple example
can improve the telemarketing, consultation and treatment skills on existing happy patients.
This should always be the first trial before the clinic goes out and buys ‘shoppers’ through
more expensive promotion activities.
Cross Marketing
Provide clients who come to the office with all the clinic awareness materials (customized
brochures, video exposure, posters) regarding all available services. Remember to track the
cost of these materials and the percentages of clients who come from these activities. These
lead to an assessment of efficacy and possibly alterations to the approach.
External Marketing
This comprises promotional activities outside the current existing practice.
Public Relations
Make an effort to speak at various medical societies, women’s groups, and home shows that
match the target market. Given the expense of a physician’s time, the lead cost of these
activities will be very high. However, this is a good way to generate awareness during the
start-up phase of an ablative and non-ablative laser clinic.
Public Relations Consultant

If laser activities and services are the only offered services, then the lead costs of $200–500
for a consultant will be too expensive. However, a good public relations consultant can be
indispensable to a large, multi-service practice over the long run, especially if other cosmetic
surgical procedures are offered. A good public relations consultant will generate awareness
and media stories about the physician, the clinic and its services. It doesn’t take long to
become known as a laser esthetic expert.
Internet
One-time start-up costs of $1000–20,000 and maintenance of $500–1000/year are quite
high. Initial lead costs, due to the one-time start-up expense, may prohibit this. However, lead
costs decrease with time (due to the one-time only expense). A web site also serves as an
information center, somewhat akin to the yellow pages for the digital set. Unfortunately,
much of the target market of women aged 20–65 years old, do not, as of yet, use the Internet.
However, it is estimated that the percentage of female Internet users will increase by at least
100% per year for the next 10 years. So it is wise to consider going ‘on line’. However, do not
expect that a web site will keep the clinic busy in the beginning.
Radio
Aggressive 30- and 60-second skin rejuventation adverts on the radio usually cannot be
achieved with lead costs of less than $150. In large cities, fees of up to $10,000 per week
usually makes this medium too expensive.
Television
Lead costs of $175–250 are again too expensive for skin rejuvenation (remember, the average
treatment cost is $500).
Direct Mail
Such lists are purchased from a variety of companies. These are similar to direct cold calls,
with lead costs of $200 or more. The response rate is often less than 1–2%. Thus, success
rates are not high.
Telephone Directories
Telephone directory (‘yellow page’) advertisements are indispensable. They generate leads
themselves—as well as support leads generated from other promotional activities. When
measured by themselves, yellow page skin rejuventation lead costs of $150–200 can be
expected. However, because leads generated from other promotional media such as
newspapers, radio, etc. often look for the clinic yellow page number, their supportive and
integrated value cannot be ignored. Do not purchase full-page, four-color adverts in multiple
telephone books! Unless the laser clinic has other more expensive cosmetic services to offer,
the fees of up to $10,000/month in yellow pages adverts are not worthwhile.
Magazines
Line rates are more expensive than similar rates in newspapers. However, adverts are sexier
and shelf life is longer. Conversely, the market reach is usually smaller with magazine
adverts. In general, lead costs of $150 can be achieved with magazine generated laser
adverts.
Newspapers
As a general rule, the newspaper generates the lowest lead costs for laser treatment. If there
is more than one daily newspaper in the target area, research which news-paper reaches the
greatest percentage of the your target market (women 20–65 years old and earning over $40,
000). A large launch advert with a subsequent weekly presence preceding and during peak
times (fall, winter, spring) should result in lead costs of $75–125. These adverts should be a
combination of image advertising, with a little story about the product, and a strong ‘call to
action’.
Use these lead cost figures as a guide. Utilize the advertising departments of newspapers
and magazines or employ the services of an advertising agency ($2000–3000 per advert). Try
different media, but above all measure! If an advert does not work, and enough calls are not
generated, lead costs will be too high. Anything above $150 is too high. By measuring lead
costs, promotions can be adjusted. If the advert does not work, than the wrong medium may
have been chosen (try another) or the message may be poorly designed (change it). Do not be
satisfied until lead costs are $125/lead or lower.
PRECISION AND PREDICTABILITY

Conversion rates will determine clinic success and profitability. Implementing the 10 Ps will
help maximize conversions. Measurements of conversions must always be made.
Measurements lead to adjustments, re-engineering and alterations of the process at each
contact stage. Remember:
Advert → Lead → Consultation → Treatment → Re-treatment → Word-of-mouth
By measuring the conversion rates and the associated rates, one can know the precise
conversion rates for each stage. If at any time the conversion rate falls below optimum
standards, adjustments become mandatory. If the clinic is already converting at 50%, do not
accept this; strive for 75% or 90%.
Measure conversions weekly. Staff bonuses should be based on optimal rates. By
conducting weekly staff meetings where conversion rates are discussed, sudden drops in
otherwise optimal rates will often reveal a cause. There might be an inadvertent change in
protocol or a staff interpersonal and/or family crisis. Measurement will be the key to
micromanagement of a successful laser practice. Measurement will give one the power to
control practice flow and profitability.
The following, then, are the measurements that must be tracked.
(1) Referral source cost (advertising cost)

(2) Lead cost=cost of advert/no. of leads (calls)
— keep less than $125, aim for $75

— measures success of the advert (or promotion)
(3) Lead conversion rate=no. of leads/no, of consultations
— percentage of leads converted to consultations

— measures telemarketing success
— keep over 50%, aim for > 75%
(4) Consultation conversion rate=no. of treatments/no. of consultations
— measures success of consultation phase

— keep over 50%, aim for 75%
(5) Re-treatment conversion=no. of re-treatments/no. of treatments
— percentage of clients who come back for re-treatment

— measures success of the treatment phase
— keep over 75% between non-ablative treatment one and two and 50% there-after
(6) Word-of-mouth referral rate=no. of word-of-mouth referrals/no. of treatments
— percentage of patients who refer other patients

— aim for 25%
(7) Return on investment (ROI)=revenue in sales from an advert/cost of the advert
— return on investment for each advertising dollar

— minimal acceptable ROI should be 3:1; that is $3 in revenue for each dollar in
advertising
— aim for 10:1 to 15:1, with re-treatment and word-or-mouth referrals augmenting the
profitability from the initial lead costs
PROFITABILITY AND PLEASURE

By using the 10 Ps as a template to construct an ablative and/or non-ablative laser practice,
happy patients will follow. These clients, in turn, generate word-of-mouth referrals, which
makes for a profitable program. With this profitability, and selfdetermination, comes
pleasure. It is this pleasure that leads to enjoyment. A laser skin rejuvenation practice can be
lucrative, stimulating and pleasurable.
INDEX
ablation thresholds SurgiPulse lasers 29

CO2 lasers 34, 35 UltraPulse lasers 26–7, 28–9
Er:YAG lasers 85 histologic studies 31–41
acne (post-laser) 228–30 ablation threshold 34, 35
advertising collagen contraction 31–2, 41
2.5% rule 242 comparison with Er:YAG lasers 86–6
advert design 251 comparison with other resurfacing methods 35, 38
direct mail 251–2, 253 CPG treatment parameters 40
internet 252–3 effects over time 32, 37–8
media 253–4 effects of wiping 40–1
return on investment 255 laser mode and thermal damage 33–5
age, effects on wound healing 18 laser systems compared 36–7, 39
angiogenesis in wound healing 14–15 new collagen formation 37, 38, 39, 89
antibiotic prophylaxis 27 pulse stacking effects 34–5
antiviral prophylaxis 232 pulse width and thermal damage 32–3
ascorbic acid deficiency 4 in sequence with ER:YAG lasers 125–6, 127, 128
aspirin 19 zones of thermal damage 31
recommended approach 42, 73
baby boomer demands 238, 241–2 wound care 42, 73
bacterial wound infections 16–17, 232 see also combined CO2/Er:YAG laser resurfacing;
Baker–Gordon phenol resurfacing 35, 38 complications of laser resurfacing
‘buyer’ 249 chemical peeling of skin 35, 38, 161, 223
cigarette smoking, effects on wound healing 17–18
calcitonin 19–20 CO2 lasers see carbon dioxide (CO2) lasers
Candida albicans infections 16 CO3 lasers 122, 125
carbon assisted Q-switched Nd:YAG laser treatments coagulation disorders, effects on wound healing 18
182–5, 194–199 coblation see electrosurgical skin resurfacing
carbon dioxide (CO2) lasers collagen 1–8
ablative effects 25, 79 contraction with CO2 lasers 26, 29–30, 31–2, 41
absorption by water 24, 78 formation after laser treatment 37, 38, 39, 89, 128,
technical development 23–5 199
thermal effects 25, 79 genes 3–4
carbon dioxide laser resurfacing 23–75 production
clinical photographs 43–72 cross-link formation 6
clinical studies 26–31 glycosylation 5
collagen contraction 26, 29–30 collagen (cont.)
comparison with Er:YAG lasers 83–4, 125 hydroxylysine synthesis 4–5
end-points 30 hydroxyproline synthesis 4
pre-treatment regimens 27, 31 prepro-α/pro-α chains 4
in sequence with ER:YAG lasers 122–3 procollagen conversion to collagen 5
SilkTouch lasers 27–9 triple helix formation 5
230
INDEX 231
structure 1–2 histologic studies

thermal effects 6–7, 312–2 depth of injury 161–2
types 2–3 thermal damage 161
in wound healing 13, 14, 15–16 mechanism of action 160
collagen galactosyl-transferase 5 recommended approach 162, 176
collagen glucosyl-transferase 5 Visage system 160
combined CO2/Er:YAG laser resurfacing endocrine abnormalities, effects on wound healing 19–
clinical photographs 141–7, 153–5 20
clinical studies 123–4 epithelial renewal in wound healing 11–13
DermaK lasers 122 Erbium:
histologic studies 126–7, 127–8 Glass (Er:Glass) lasers 186–7
recommended approach 129, 157 Erbium:
complement, in wound healing 10 YAG (Er:YAG) lasers:ablative effects 78; 79
complications of laser resurfacing 217–37 absorption by water 77–8
acne flares 228–30 thermal effects 79, 80
contact dermatitis 226–7 Erbium:YAG laser resurfacing 77–119
ectropion 232, 235 clinical photographs 90–117
erythema 218–20 clinical studies 80–4
hyperpigmentation 219–23 comparison with CO2 lasers 83–4, 125
hypertrophic scarring 232, 233–4 evaluation 80–2
hypopigmentation 223–6 neck skin resurfacing 82–3, 118
infections 229–32 scanning laser systems 82
lagophthalmus 232 in sequence with CO2 lasers 122–3
milia 229 skin contraction 84
minimization of risks 217 endpoints 80
computer programs, contact management 247 histologic studies 84–9
computerized pattern generators (CPGs) 25, 40 ablation threshold 85
consultations collagen contraction 41
conversion to treatment 249, 255 comparison with CO2 lasers 84–5, 86–9
informed consent 245, 248 laser systems compared 86–7
sales technique 245, 248–9 new collagen formation 88, 89
contact dermatitis 226–7 pulse stacking effects 86
contact managers 247 in sequence with CO2 lasers 125–6, 127, 128
Contour lasers 122, 128 thermal damage 85–6
corticosteroid suppression of wound healing 19 limitations 80
CPGs (computerized pattern generators) 25, 40 recommended approach 89, 118
cryogen injury 190, 191 variable pulsed lasers see variable pulsed Er:YAG
cutaneous wound healing see wound healing laser resurfacing
wound care 118
delegation of laser treatments 238, 249 see also combined CO2/Er:YAG laser resurfacing;
dermabrasion 35, 159–60, 223 complications of laser resurfacing
DermaK lasers 122 erythema 218–19
diabetes, effects on wound healing 19 external marketing 252–4
diode laser evaluation 191–3, 211–16 extracellular matrix 13, 14, 15
direct mail 251–2, 253
dry wounds, healing of 17 facial rejuvenation practices
choice of technology 240–1
ectropion 232, 235 delegation of care 238, 249
electrosurgical skin resurfacing 159–77 patients’ expectations 238
clinical photographs 163–76 payment 246
clinical study 160–1 physician quality 239–40
232 INDEX
price setting 245 conversion to consultations 247, 255

staff 243–4 costs of 246–50, 251, 252, 253, 254
treatment rooms 245, 249–50 passive 247
waiting rooms 244 lysyl hydroxylase 4
see also marketing lysyl oxidase 2, 6
FeatherTouch lasers 25, 26, 36–7
fibril-associated collagens with interrupted triple helices macrophages, in wound healing 11
(FACIT) 2, 3 magazine advertisements 253
fibril-forming collagens 2–3 market segmentation 241–2
fibroblasts, in wound healing 13–14 marketing 237–55
fibronectin 13, 14, 15 advertising see advertising
fibroplasia 13–14 defined 239
financial modeling 243 external
fluence 26 media 252–4
public relations 252
glycolic acid 31 internal
glycosylation of collagen 5 lead stage 246–7
granulation tissue 13 consultation phase 245, 248–9
growth hormone in wound healing 20 treatment phase 249–50
re-treatments 250
heat, effects on collagen 6–7, 31–2 cross marketing 252
hematomas, effects on wound healing 17 direct mail 251–2
hemoglobin, absorption of laser wavelengths 181 word-of-mouth referrals 250
heparin 19 market analysis 241–2
herpes simplex virus (HSV) infections 229, 230, 232 measurement of conversion rates 254–5
herpes zoster infections 232 Ps of medical marketing 239
hydroquinone 31 people 243–4
hydroxylysine synthesis 4–5 physician 239–40
hydroxyproline synthesis 4 place 244–5
hyperpigmentation 219–23 plan 241–2
hypertrophic scarring 232, 233–4 pleasure 255
hypopigmentation 223 precision/predictability 254–5
price 245–48
immunodeficiency, effects on wound healing 18–19 product 240–1
infections 16–17, 229–32 profitability 255
informed consent 245, 248 telemarketing scripts 249
inquiries see leads mast cells 185
intense pulsed light (IPL) treatment 187–88, 200–5 matrix metalloproteinases 16
interlacing network collagen (type IV) 2, 3 medications, effects on wound healing 19
internal marketing see marketing: microbiological wound infections 16–17, 229–32
internal microfibril-forming collagen 2, 3
internet advertisements 252–3 micro topography imaging system 185
introns 3 milia 229
invertising see marketing: millisecond Nd:YAG lasers185, 199–200
internal monilial wound infections 229
isotretinoin 19 monocytes 11
myofibroblasts 13–14
lagophthalmus 232
laser systems, important features 240–1 neck skin resurfacing 82–3, 118
leads neodymium (Nd:YAG) lasers
active 247 1320nm 189–90, 205–8
INDEX 233
neodymium (Nd:YAG) lasers (cont.) retinoids 19

millisecond 185, 199–200
Q-switched 180–5, 192–199 scars
neutrophils 11 hypertrophic 232, 231–2
newspaper advertisements 254 maturation of 15, 16
non-ablative dermal remodeling 179–216 ‘shoppers’ 248
clinical and histologic studies 180–91 SilkTouch lasers 25, 26, 27–9, 36–7, 39
3D microtopograpical evaluation 185 staff of facial rejuvenation practices 243–4
diode lasers 189–1 SurgiPulse lasers 29, 36
Er:Glass lasers 186–7
intense pulsed light 187–88 telemarketing 247
millisecond Nd:YAG lasers 185 telephone directory advertisements 253
Nd:YAG laser (1320nm) 188–9 television advertisements 253
pulsed dye lasers 185–6 temperature, effects on collagen 6–7, 31–2
Q-switched Nd:YAG lasers 180–5 tissue tightening
clinical photographs Er:YAG lasers 41, 84
diode lasers 209–14 see also collagen:
intense pulsed light 200–5 contraction with CO2 lasers
millisecond Nd:YAG lasers 199–200 transforming growth factor- 14
Nd:YAG laser (1320nm) 205–8 treatment rooms 249, 249–0
Q-switched Nd:YAG lasers 192–199 tretinoin 31, 81
radiofrequency devices 214–15 trichloracetic acid (TCA) resurfacing 35
mechanism 180, 181
recommended approach 191 Ultrapulse 5000 lasers 25, 26–7, 28–9, 36, 39
see also complications of laser resurfacing
variable pulsed Er:YAG laser resurfacing
opsonization 19 clinical photographs 128–38, 146–52
oxygen, in wound healing 17, 18 CO3 lasers 122, 125
Contour lasers 122, 128
parathyroid hormone 19–20 recommended approach 129, 156
patients’ expectations 238 vascular insufficiency, effects on wound healing 18
penicillamine 19 Visage electrosurgical device 160
phenol resurfacing 35, 38
phenytoin 19 waiting rooms 244
planned obsolescence 241 warfarin 19
platelets water, absorption of laser wavelengths 179, 180, 182,
effects of alcohol on 19 187, 189
in wound healing 10–11, 18 word-of-mouth referrals 250, 255
prepro-α chains 4 wound contraction 14
pro-α chains 4, 5 wound healing 9–22
procollagen proteinases 5 factors
procollagens 4, 5 local 16–18
public relations 252 systemic 18–20
pulsed CO2 laser development 24–5 inflammatory phase 9–11
pulsed dye lasers 185–6 maturation phase 15–16
proliferative phase
Q-switched Nd:YAG laser treatments 180–5, 192–199 angiogenesis 14–15
fibroplasia 13–14
radio advertisements 253 matrix formation 13
radiofrequency resurfacing see electrosurgical skin re-epithelialization 11–13
resurfacing wound contraction 14
234 INDEX
wound infections 16–17, 229–32
yellow page advertisements 253

Ablative and Non AblativeF Acial Skin Rejuvenation

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Ablative and Non AblativeF Acial Skin Rejuvenation

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ABLATIVE AND NON-ABLATIVE FACIAL SKIN REJUVENATION

ABLATIVE AND NON-ABLATIVE FACIAL

With a contribution by R Stephen Mulholland MD, Toronto,

LONDON AND NEW YORK

ISBN 0-203-00874-X Master e-book ISBN

ISBN 1-84184-175-7 (Print Edition)

Distributed in the USA by

Figure 2.1. Normal human skin

Figure 2.2. Skin after wounding

Figure 2.3. Healed skin

plasminogen activator, which enzymatically activates the collagenase as well as plasmin, a

FACTORS AFFECTING WOUND HEALING

Foreign Body Reaction

Tissue Ischemia and Eschar Formation—The Dry Wound

compared with non-ablative procedures. However, no study has definitively documented a

Vascular Insufficiency and Impaired Oxygenation

6 Takashima A, Grinnell F. Fibronectin-mediated keratinocyte migration and initiation of

Figure 3.1. Water absorption curve of 10,600 nm carbon dioxide laser

Figure 3.2. Ablative and thermal effect of carbon dioxide laser

In the mid-1990s, in response to the theory of selective photothermolysis, technical

West and Alster21

Goldman and Fitzpatrick22

Ratner et al.27 and Other Studies28–32

Figure 3.3. Before CO2 laser resurfacing

Figure 3.8. Before CO2 laser resurfacing of the periorbital area

Figure 3.9. Immediately after CO2 laser resurfacing

Figure 3.10. Six months after CO2 laser resurfacing

Figure 3.11. Before CO2 laser resurfacing of the perioral area

Figure 3.12. Five days after CO2 laser resurfacing

Figure 3.13. Before CO2 laser resurfacing of the full face

Figure 3.14. Six months after CO2 laser resurfacing

Figure 3.15. Before CO2 laser resurfacing

Figure 3.16. Three days after CO2 laser resurfacing

Figure 3.17. One year after CO2 laser resurfacing

Figure 3.18. Before CO2 laser resurfacing

Figure 3.20. Nine months after CO2 laser resurfacing

Figure 3.21. Before CO2 laser resurfacing

Figure 3.22. One year after CO2 laser resurfacing

Figure 3.23. Before CO2 laser resurfacing

Figure 3.24. One year after CO2 laser resurfacing

Figure 3.25. Before CO2 laser resurfacing

Figure 3.26. One year after CO2 laser resurfacing

Figure 3.27. Before CO2 laser resurfacing

Figure 3.28. Two years after CO2 laser resurfacing

Figure 3.29. Before CO2 laser resurfacing

Figure 3.30. Three days after CO2 laser resurfacing

Figure 3.31. Six months after CO2 laser resurfacing

Figure 3.32. Before CO2 laser resurfacing

Figure 3.33. One year after CO2 laser resurfacing

Figure 3.34. Before CO2 laser resurfacing

Figure 3.36. Before CO2 laser resurfacing of the perioral area

Figure 3.37. Four days after CO2 laser resurfacing

Figure 3.38. Before CO2 laser resurfacing of the perioral area

Figure 3.39. Two months after CO2 laser resurfacing

Figure 3.40. Before CO2 laser resurfacing of the perioral area

Figure 3.41. Four days after CO2 laser resurfacing

Figure 3.42. Three months after CO2 laser resurfacing

Figure 3.43. Before CO2 laser resurfacing

Figure 3.44. Immediately after CO2 laser resurfacing

Figure 3.45. Four days after CO2 laser resurfacing

Figure 3.46. Two months after CO2 laser resurfacing

Figure 3.47. One year after CO2 laser resurfacing

Figure 3.48. Before CO2 laser resurfacing

Figure 3.49. Three days after CO2 laser resurfacing