Laser Scar Revision: A Review

Transcription

Laser Scar Revision: A Review
REVIEW ARTICLE
Laser Scar Revision: A Review
TINA ALSTER, MD,
AND
LARISSA ZAULYANOV-SCANLON, MDy
Tina Alster, MD, and Larissa Zaulyanov-Scanlon, MD, have indicated no significant interest with
commercial supporters.
C
utaneous injuries causing scar tissue formation
are relatively common and lead patients to seek
treatment for cosmetic or functional improvement.
Laser technology has evolved over the past few
decades to become the treatment of choice for
many types of scars, but determining the appropriate
use of this technology comes with experience.
This review will provide practical guidelines for
the dermatologic surgeon interested in performing
laser scar revision.
Scar Formation: Background
Integumental injury sets the cascade of wound healing events into motion. The stages of wound healing
include inflammation, proliferation, and maturation.1 There is a complex interplay between various
cells, growth factors, cytokines, and components of
the extracellular matrix during the wound healing
process. Tissue blanching is the first visible clinical
change and is the manifestation of vasoconstriction,
a key element in hemostasis. Vasoconstriction gives
way to vasodilation, manifested as erythema, which
signals inflammation and increased capillary permeability. The first inflammatory cells to arrive at
the wound site are neutrophils.2 Subsequently, a
variety of growth factors and cytokines are produced
by macrophages that create an environment suited
for granulation tissue formation, which includes the
migration and proliferation of fibroblasts, collagen
production, and angiogenesis. Neocollagenesis begins approximately 3 to 5 days after initial wounding
and is induced by cytokines that are initially produced by macrophages, such as fibroblast growth
factor-2, transforming growth factor-b, and insulinlike growth factor.2 Similar to fetal skin, the composition of early wounds is approximately 80% Type
III collagen and 20% Type I collagen. In contradistinction, mature scars and unwounded skin have
approximately 80% Type I collagen and only 20%
Type III collagen.3 Scars result from a deviation in
the orderly pattern of healing. An overzealous healing response can create a raised nodule of fibrotic
tissue, whereas ‘‘pitted’’ and atrophic scars may result from inadequate replacement of deleted collagen
fibers. Although vascular and pigment alterations
associated with wound healing are typically transient, the textural changes caused by collagen disruption are often permanent. Histologically, what makes
scars unique is the relative absence of skin appendages and elastic fibersFconstituents of normal skin
that may account for the loss of flexibility seen in
scar tissue.3
Laser Scar Revision: Preoperative
Considerations
A patient’s candidacy for laser scar revision is based
on several factors, including certain patient variables
and pertinent characteristics of the scar4 (Table 1).
Washington Institute of Dermatologic Laser Surgery, Washington, DC; yDepartment of Dermatology and Cutaneous,
University of Miami, Miami, FL
& 2007 by the American Society for Dermatologic Surgery, Inc. Published by Blackwell Publishing ISSN: 1076-0512 Dermatol Surg 2007;33:131–140 DOI: 10.1111/j.1524-4725.2006.33030.x
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TABLE 1. Patient Characteristics for Optimal Laser Efficacy
Skin phototype
Concurrent infection/Inflammation
Medication use
Prior treatment
Expectations and compliance
Scar qualities such as color, texture, location, and
previous treatments affect the choice of laser system,
the laser parameters, and the number of treatment
sessions needed for revision4 (Table 2). Only after
the patient and the scar have been fully evaluated
can an appropriate laser system and treatment protocol be outlined.
Patient Selection
Skin Phototype
Ethnic background is important when contemplating
laser outcomes. For instance, the presence of increased epidermal pigment in patients with darker
skin tones (skin phototypes III or higher) interferes
with the targeted hemoglobin’s absorption of vascular-specific laser energy. As a result, reduced laser
energy is delivered to dermal scar tissue, limiting the
effect of treatment. In addition, the risk of undesirable melanin destruction is increased, leading to
postoperative skin dyspigmentation. While darker-
Darker skin tones require lower energy densities
Avoid laser treatment to affected area
Discontinue anticoagulants (for PDL)
Note presence of background dyspigmentation
Assess whether realistic and agreeable to treatment
skinned patients may be treated safely with lasers for
scar revision, intraoperative energy densities are
typically lowered to avoid postoperative sequelae.4
Consequently, the clinical response to laser treatment
may be reduced and additional treatment sessions
may be necessary to treat patients with darker skin
tones than those with light skin.5 Likewise, patients
who have recently tanned or been exposed to sun
should be warned of potential pigment changes and
avoid laser treatment to the involved skin areas until
the excess pigment has resolved.
Presence of Infection or Inflammation
Patients with acute or chronic skin infections or inflammatory processes should be given careful attention before proceeding with laser surgery. While
disseminated skin infections, such as herpes simplex
or impetigo, are most often seen after ablative laser
procedures, patients undergoing any type of laser
surgery should have a thorough history and
physical as concurrent infections (e.g., verruca
TABLE 2. Scar Types and Appropriate Laser Treatment
Scar type
Scar characteristics
Appropriate laser
Hypertrophic
Raised, erythematous
Confined to wound border
Often symptomatic
Firm, raised, reddish-purple
Growth beyond original wound
Rapid proliferation
Often symptomatic
Characteristic histology
Indented
Early: erythematous, Late: pale
PDL
Keloid
Atrophic
Prescar
Pink
Occur in scar-prone skin
PDL
CO2/Er:YAG
1,064/1,320 Nd:YAG, 1,450 nm diode
Fraxel
PDL
PDL, pulsed dye laser; CO2, carbon dioxide; Er:YAG, erbium:yttrium-aluminum-garnet; Nd:YAG, neodymium:yttrium-aluminum-garnet.
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A L S T E R A N D Z A U LYA N O V- S C A N L O N
or molluscum), inflammatory skin disorders (e.g.,
psoriasis and eczema), or autoimmune diseases (e.g.,
vitiligo, lupus) may be exacerbated or disseminated
by laser treatment.6 In addition, dermal inflammation may interfere with postoperative healing and
ultimate clinical effect.7
Medication Use and History of Prior Treatments
History of medications and prior treatments for
scarring should also be explored with patients. Isotretinoin use, commonly encountered in acne patients presenting for laser scar therapy, can foster the
development of hypertrophic scars after dermal resurfacing procedures due to the effect of isotretinoin
on collagen metabolism and wound repair.8
Although it has been customary for patients to
postpone ablative laser skin resurfacing for at least
6 months after completion of a course of isotretinoin, recent studies have not demonstrated an
increased risk of side effects when isotretinoin has
been used concomitantly with other laser treatments,9 leading to a more lax approach with this
medication in skin resurfacing procedures. If possible, patients should discontinue anticoagulant or
antiplatelet medications at least 1 week before
laser treatment, because use of these medications
may increase the severity and duration of postoperative purpura. Prior phenol chemical peels or
dermabrasion may have resulted in tissue fibrosis,
which potentially limits laser-tissue vaporization,
necessitating the use of higher energy densities.
Likewise, these treatments may have produced
skin hypopigmentation, which could potentially
appear worse once the overlying skin has been
vaporized by laser irradiation.4 Finally, prior injections with silicone or other nonabsorbable fillers
may preclude laser surgery due to the possibility
of granuloma formation and/or reduced tissue
healing.
Patient Expectations and Compliance
Patients should have realistic expectations before
undergoing laser scar revision. Although it is likely
that laser therapy will improve scar quality (color
and texture), it should be made clear to patients that
it is not possible to achieve complete scar eradication.4,10 Likewise, it is important for patients to
understand that strict posttreatment regimen
compliance is necessary to achieve optimal clinical
results. A patient who has a history of noncompliance is a poor treatment candidate. The role of
postoperative skin care must be fully described and
understood. Thorough review of instructions in
both written and oral form is a necessary component
of the treatment process. Careful documentation
of treatment progress, including sequential photographs, is the best way to determine scar response.
Scar Classification
Hypertrophic Scars
Hypertrophic scars are erythematous, raised, firm
nodular growths that occur more commonly in areas
subject to increased pressure or movement or in
body sites that exhibit slow wound healing. The
growth of these scars is limited to the site of original
tissue injury and represents unrestrained proliferation of collagen during the wound remodeling
phase. These abnormal tissue proliferations typically
occur within 1 month of injury and may regress over
time. Patients with hypertrophic scars may complain
of pruritus or dysesthesia. The fibrotic collagen seen
on histologic examination of hypertrophic scars
is often indistinguishable from any other type of
dermal scar.10
Keloids
Keloids present as deep reddish-purple papules and
nodules. In contrast to hypertrophic scars, keloids
proliferate beyond the boundaries of the initial
wound and often continue to grow without regression. They may develop weeks or even years after the
inciting trauma or even arise spontaneously without
a history of preceding integument injury. Keloids are
often cosmetically disfiguring and frequently occur
on the earlobes, anterior chest, shoulders, and upper
back. They are more common in darker-skinned
persons and, like hypertrophic scars, may be pruritic
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or dysesthetic. Histologically, keloids are distinguished by their thickened bundles of hyalinized
acellular collagen haphazardly arranged in whorls
and nodules with an increased amount of
hyaluronidase.10
Atrophic Scars
Atrophic scars are dermal depressions that result
from an acute inflammatory process affecting the
skin, such as cystic acne or varicella. Surgery or other
forms of skin trauma may also result in atrophic
scars. The inflammation associated with these conditions leads to collagen destruction with dermal
atrophy. Atrophic scars are initially erythematous
and become increasingly hypopigmented and fibrotic
over time.
Prescars
Prescars are early wounds in scar-prone skin.
Prophylactic or early laser treatment of traumatized
skin concomitant with or shortly after cutaneous
wounding has been shown to reduce or even
prevent scar formation in patients at high risk for
scarring.11–13 Laser therapy may improve the
appearance of wounded skin by promoting better
collagen organization in healing wounds.14
Laser Treatment Protocol
Hypertrophic Scars and Keloids
The current laser of choice in treating hypertrophic
scars and keloids is the vascular-specific 585-nm
pulsed dye laser (PDL).10 There is no consensus on
precisely how the PDL achieves its effect on these
scars. A recent study demonstrated that the PDL
induces reduction in transforming growth factor-b
expression, fibroblast proliferation, and collagen
Type III deposition.15 Other plausible explanations
include selective photothermolysis of vasculature,16
released mast cell constituents (such as histamine
and interleukins) that could affect collagen metabolism,17 and the heating of collagen fibers and
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breaking of disulfide bonds with subsequent collagen
realignment.18
Scar revision with the PDL is typically performed on
an outpatient basis without anesthesia. If topical
anesthesia is desired, a lidocaine-containing cream
or gel can be applied to the areas to be treated 30 to
60 minutes before laser irradiation. To avoid interference with laser penetration, the skin should be
cleansed with soap and water to remove residual
makeup, powder, or creams. Flammable solutions,
such as alcohol, should be avoided in preparing the
skin. Wet gauze may be used to protect hair-bearing
areas during treatment and to avoid unnecessary
thermal injury to nontargeted skin. The patient and
other individuals present in the treatment room must
wear protective eyewear capable of filtering 585-nm
light to avoid retinal damage.
The entire surface of the scar should be treated with
adjacent, nonoverlapping laser pulses. The fluences
chosen are determined by the skin phototype of the
patient, the type of scar, and previous treatments
applied to the area. In general, hypertrophic scars
and keloids are treated with low energy densities
ranging from 6.0 to 7.5 J/cm2 when using a spot size
of 5 or 7 mm and 4.5 to 5.5 J/cm2 when using a spot
size of 10 mm.4 Pulse durations ranging from 0.45 to
1.5 ms are commonly used. Energy densities should
be lowered by at least 0.5 J/cm2 in patients with
darker skin and for scars in more delicate or thin
body locations (such as the chest or neck).4,5 It is
prudent to begin treatments with the lowest effective
energy densities, using increased energies on subsequent visits only when the response to the previous
treatment is suboptimal. Laser treatments are typically repeated at 6- to 8-week time intervals. Any
concern regarding patient response to treatment
should prompt a test spot or patch in a small area
before irradiation of the entire lesion. If postoperative oozing, crusting, or vesiculation is observed, then the fluence used on subsequent visits
must be decreased and retreatment postponed until
the skin has completely healed. If scar proliferation
continues despite laser irradiation, the use of
A L S T E R A N D Z A U LYA N O V- S C A N L O N
Figure 1. Hypertrophic facial scars before (A) and after PDL treatment (B).
concomitant intralesional corticosteroids or 5-fluorouracil has been shown to provide additional benefit.19,20 Otherwise, PDL treatment alone has been
shown to be sufficient.19 Intralesional injections of
corticosteroids (20 mg/mL triamcinolone) are more
easily delivered immediately after (rather than before) PDL irradiation because the laser-irradiated
scar becomes edematous (making needle penetration
easier). An additional consideration is that when
steroid injection is performed before laser irradiation,
the skin blanches, rendering the skin a potentially less
amenable target for vascular-specific irradiation.
The most common side effect of treatment with the
PDL is postoperative purpura, which often persists
for several (7–10) days. Edema of treated skin may
also occur, but it usually subsides within 48 hours. A
topical healing ointment under a nonstick bandage
can be applied for the first few postoperative days to
protect the skin. Treated areas should be gently
cleansed daily with water and mild soap. Strict sun
avoidance and photoprotection should be advocated
between treatment sessions to reduce the risk of
pigment alteration. If hyperpigmentation develops,
treatment should be suspended until the pigment
change resolves to reduce the further risk of epidermal melanin interference with laser energy penetration. Topical bleaching agents (such as hydroquinone
or kojic acid) may be used to hasten pigment
resolution.
Most hypertrophic scars will improve by at least
50% after two treatments with the PDL using the
aforementioned laser parameters (Figures 1
Figure 2. Hypertrophic abdominal scar before (A) and after PDL treatment (B).
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Figure 3. Keloid on the neck before (A) and after PDL treatment (B).
and 2). Keloids often require more treatment sessions to achieve significant improvement, but some
may prove unresponsive altogether (Figures 3 and 4).
Although no studies regarding the use of 532-nm
potassium titanyl phosphate (KTP) lasers have been
published, some practitioners advocate their use for
erythematous scars due to their ability to reduce erythema. Similarly, intense pulsed light systems have
been demonstrated to improve scar erythema.21 The
carbon dioxide (CO2) laser has also been used to
vaporize keloids, particularly on the earlobes and
posterior neck, but scar recurrences are often seen.22
Atrophic Scars
Successful recontouring of atrophic scars has been
achieved with CO2 or erbium:yttrium-aluminumgarnet (Er:YAG or erbium) laser vaporization23–27
(Figure 5). Although other treatments such as
dermabrasion and injection of various filler materials can also be used for atrophic scars, their operator-dependent efficacy and side effect profile, as
well as temporary clinical effect (in the case of filler
injections), limit their usefulness and widespread
acceptance for the long-term. What popularized laser skin resurfacing treatment for atrophic scar revision was its ability to selectively and reproducibly
vaporize skin, with improved operator control and
clinical efficacy.28–32 Comparisons with dermabrasion and chemical peels showed that a predictable
amount of skin vaporization and residual thermal
damage could only be achieved through lasers,
thereby demonstrating the superiority of laser treatment for skin resurfacing.33 The photothermal effect
of these ablative lasers on the skin accounted for
shrinkage of collagen, with noticeable clinical skin
tightening, as well as neocollagenesis and collagen
Figure 4. Keloid on the scapula before (A) and after PDL treatment (B).
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A L S T E R A N D Z A U LYA N O V- S C A N L O N
Figure 5. Atrophic acne scars before (A) and after ablative laser treatment (B).
remodeling, with marked reduction of skin textural
irregularities.34
Laser treatment of atrophic scars is aimed at reducing the depths of the scar borders and stimulating
neocollagenesis to fill in the depressions. Although
spot (or local) vaporization of isolated scars is a viable treatment option, extended treatment (at least
an entire cosmetic unit) is recommended for more
widely distributed defects to avoid obvious lines of
demarcation between treated and untreated site. In
addition, treatment of a larger surface area increases
the overall collagen tightening effect, thereby improving clinical response by making scars appear
more shallow. The CO2 laser is generally used at
fluences of 250 to 350 mJ to ablate the epidermis in a
single pass. Short-pulsed Er:YAG lasers that are operated at 5 to 15 J/cm2 often require several passes to
result in a similar depth of penetration as CO2,
whereas longer-pulsed Er:YAG systems can be operated at higher fluences (22.5 J/cm2) to achieve
comparable results in a single pass. Because of their
depth and fibrotic nature, most atrophic scars will
require at least two laser passes regardless of the
laser system chosen for treatment. It is important
that any partially desiccated tissue be removed with
saline- or water-soaked gauze between laser passes
for char formation to be avoided. The development
of char indicates excessive thermal damage, which
can lead to unwanted tissue fibrosis and/or scarring.
Ablative laser skin resurfacing is typically performed
on an outpatient basis and requires a thoughtful
approach by both doctor and patient, including
thorough preoperative counseling related to the
postoperative recovery period. Various anesthetic
options can be employed, including topical, intralesional, intravenous, and general anesthesia. Generally, larger treatment areas (e.g., full face) require the
use of intravenous or general anesthesia for maximal
patient comfort. The requisite protective eyewear
and other safety precautions (e.g., smoke evacuator
to capture laser plume) should be used.
The vaporized skin appears erythematous and edematous immediately after treatment, with copious
serous discharge and generalized worsening of the
skin’s appearance over the first few days. It is imperative that patients be monitored closely for appropriate healing responses and potential
complications, such as dermatitis or infection, during the 7- to 10-day reepithelialization process.6,7,35
Full-face procedures or large treatment areas often
necessitate the use of prophylactic antibiotics and/or
antiviral medications to reduce the risk of infection.36–38 The use of topical antibiotics is avoided
due to the potential development of contact dermatitis.39 Application of topical ointments, semiocclusive dressings, and/or cooling masks promote healing
and reduce swelling.7 Postoperative erythema typically lasts several (4–6) weeks after Er:YAG laser
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Figure 6. Atrophic acne scars before (A) and after Fraxel laser treatment (B).
treatment and even longer (3–4 months) after CO2
laser ablation due to their relative degree of tissue
necrosis. Hyperpigmentation is transient and generally appears 3 to 4 weeks after treatment. Its resolution can be hastened with the use of topical
bleaching agents. Although hyperpigmentation is
relatively common (particularly in patients with
darker skin tones), hypopigmentation is rare. The
most severe complications of ablative skin resurfacing include hypertrophic scarring and ectropion
formation, both related to overly aggressive laser
techniques and/or undiagnosed/untreated suprainfections. Hypertrophic burn scars can be effectively
treated with the PDL as previously described,18
whereas ectropion typically requires surgical reconstruction. Retreatment after ablative laser skin resurfacing should be postponed for at least 1 year to
accurately gauge clinical improvement and permit
full tissue recovery.26
As a consequence of side effects and prolonged
postoperative recovery associated with ablative laser
treatment, nonablative lasers were subsequently developed to provide a noninvasive option for atrophic
scar revision.24 The most popular and widely used of
these nonablative systems include the 1,320-nm
neodymium:yttrium-aluminum-garnet (Nd:YAG)
and the 1,450-nm diode lasers, as well as the
1,064-nm Nd:YAG system.40–42 These devices deliver concomitant epidermal surface cooling with
deeply penetrating infrared wavelengths that target
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tissue water and stimulate collagen production
through dermal heating without disruption of the
epidermis.43 A series of three to five treatments are
typically performed on a monthly basis with optimal
clinical efficacy appreciated several (3–6) months
after the final laser treatment session. Sustained
clinical improvement of scars by 40% to 50% has
been observed after the series of treatments. The low
side effect profile of these nonablative systems
(limited to local erythema and edema and, rarely,
vesiculation or herpes simplex reactivation) compensates for their reduced clinical efficacy (relative
to ablative lasers).
The recent introduction of fractional laser skin resurfacing (Fraxel, Reliant Technologies, Mountain
View, CA) involving a novel 1,550-nm erbiumdoped fiber laser has been another promising
noninvasive laser treatment for atrophic
scarring.44,45 This system combines both ablative
and nonablative principles to effect optimal skin
recontouring (Figure 6).
Prescars
Treatment of potential scars with lasers is a relatively
new concept that is gaining in popularity. Two different approaches for scar prevention within prescars
have been outlined. Wound edges can be vaporized
with either a CO2 or an Er:YAG laser before primary
surgical closure to enhance ultimate cosmesis.45
Alternatively, a 585-nm PDL system can be used to
A L S T E R A N D Z A U LYA N O V- S C A N L O N
Figure 7. Prescars on the neck before (A) and after PDL treatment (B).
treat surgical sites, traumatic wounds, or ulcerations
to improve the quality of scarring and prevent excessive scar formation11–13 (Figure 7).
3. Monaco JL, Lawrence WT. Acute wound healing: an overview.
Clin Plast Surg 2003;30:1–12.
Conclusion
5. Macedo O, Alster TS. Laser treatment of darker skin tones: a
practical approach. Dermatol Ther 2000;13:114–26.
There are several laser systems available that permit
successful treatment of various types of scars. The
585-nm PDL remains the gold standard for laser
treatment of hypertrophic scars and keloids. Although atrophic scars may best be treated with ablative CO2 and Er:YAG lasers, the intense interest in
procedures with reduced morbidity profiles have
increased the popularity of nonablative laser
procedures. Laser scar revision is optimized when
individual patient and scar characteristics are
thoroughly evaluated to determine the best course
of treatment and, more importantly, to determine
whether the patient and physician share realistic
expectations and treatment goals. As lasers evolve
and the mechanics of wound healing continue to be
elucidated, new uses for the technology will be
identified, resulting in improved management of a
wide range of wounds and scars.
6. Nanni CA, Alster TS. Complications of CO2 laser resurfacing: an
evaluation of 500 patients. Dermatol Surg 1998;24:315–20.
References
1. Baum CL, Arpey CJ. Normal cutaneous wound healing: clinical
correlation with cellular and molecular events. Dermatol Surg
2005;31:674–86.
2. Lawrence WT. Physiology of the acute wound. Clin Plast Surg
1998;25:321–40.
4. Alster TS. Laser treatment of scars and striae. In: Alster TS,
Manual of cutaneous laser techniques. Philadelphia:LippincottRaven; 2000:p. 89–107.
7. Horton S, Alster TS. Preoperative and postoperative considerations for cutaneous laser resurfacing. Cutis 1999;64:
399–406.
8. Zachariae H. Delayed wound healing and keloid formation following argon laser treatment or dermabrasion during irotretinoin
treatment. Br J Dermatol 1988;118:703–6.
9. Khatri KA. Diode laser hair removal in patients undergoing isotretinoin therapy. Dermatol Surg 2004;30:1205–7.
10. Alster TS, Tanzi EL. Hypertrophic scars and keloids: etiology and
management. Am J Clin Dermatol 2003;4:235–43.
11. McCraw JB, McCraw JA, McMellin A, Bettancourt N. Prevention
of unfavorable scars using early pulsed dye laser treatments: a
preliminary report. Ann Plast Surg 1999;42:7–14.
12. Bowes LE, Alster TS. Treatment of facial scarring and ulceration
resulting from acne excoriée with 585-nm pulsed dye laser
irradiation and cognitive psychotherapy. Dermatol Surg
2004;30:934–8.
13. Nouri K, Jimenez GP, Harrison-Balestra C, Elgart GW. 585-nm
pulsed dye laser in the treatment of surgical scars starting on the
suture removal day. Dermatol Surg 2003;29:65–73.
14. Pinheiro AL, Pozza DH, Oliveira MG, et al. Polarized light
(400–2000 nm) and non-ablative laser (685 nm): a description of
the wound healing process using immunohistochemistry analysis.
Photomed Laser Surg 2005;23:485–92.
15. Kuo YR, Jeng SF, Wang FS, et al. Flashlamp pulsed dye laser
(PDL) suppression of keloid proliferation through down-regulation of TGF-beta1 expression and extracellular matrix expression.
Lasers Surg Med 2004;34:104–8.
3 3 : 2 : F E B R U A RY 2 0 0 7
139
LASER SCAR REVISION
16. Reiken SR, Wolfort SF, Berthiamume F, et al. Control of hypertrophic scar growth using selective photothermolysis. Lasers Surg
Med 1997;21:7–12.
17. Alster TS, Williams CM. Improvement of keloid sternotomy scars
by the 585 nm pulsed dye laser: a controlled study. Lancet
1995;345:1198–200.
18. Alster TS, Nanni CA. Pulsed dye laser treatment of hypertrophic
burn scars. Plast Reconstr Surg 1998;102:2190–5.
19. Alster TS. Laser scar revision: comparison of pulsed dye laser with
and without intralesional corticosteroids. Dermatol Surg
2002;29:25–9.
20. Manuskiatti W, Fitzpatrick RE. Treatment response of keloidal
and hypertrophic sternotomy scars: comparison among intralesional corticosteroid, 5-fluorouracil, and 585-nm flashlamppumped pulsed-dye laser treatments. Arch Dermatol
2002;138:1149–55.
21. Bellew SG, Weiss MA, Weiss RA. Comparison of intense pulsed
light to 585-nm long-pulsed pulsed dye laser for treatment of
hypertrophic surgical scars: a pilot study. J Drugs Dermatol
2005;4:448–52.
34. Fitzpatrick RE, Rostan EF, Marchell N. Collagen tightening induced by carbon dioxide laser versus erbium: YAG laser. Lasers
Surg Med 2000;27:395–403.
35. Alster TS, Lupton JR. Prevention and treatment of side effects and
complications of cutaneous laser resurfacing. Plast Reconstr Surg
2002;109:308–16.
36. Walia S, Alster TS. Cutaneous CO2 laser resurfacing infection rate
with and without prophylactic antibiotics. Dermatol Surg
1999;25:857–61.
37. Alster TS, Nanni CA. Famciclovir prophylaxis of herpes simplex
virus reactivation after cutaneous laser resurfacing. Dermatol Surg
1997;25:242–6.
38. Beeson WH, Rachel JD. Valacyclovir prophylaxis for herpes
simplex virus infection or infection recurrence following laser skin
resurfacing. Dermatol Surg 2002;28:331–6.
22. Apfelberg DB, Maser MR, White DN, Lash H. Failure of carbon
dioxide laser excision of keloids. Lasers Surg Med 1989;9:
382–88.
39. Fisher AA. Lasers and allergic contact dermatitis to topical antibiotics, with particular reference to bacitracin. Cutis
1996;58:252–4.
23. Alster TS. Cutaneous resurfacing with CO2 and erbium: YAG
laser: preoperative, intraoperative, and postoperative considerations. Plast Reconstr Surg 1999;103:619–32.
40. Tanzi EL, Alster TS. Comparison of a 1450 nm diode laser and a
1320 nm Nd:YAG laser in the treatment of atrophic facial scars: a
prospective clinical and histological study. Dermatol Surg
2004;30:152–7.
24. Alster TS, Tanzi EL. Laser skin resurfacing: ablative and nonablative. In: Robinson J, Sengelman R, Siegel DM, Hanke CM,
editors. Surgery of the skin. Philadelphia:Elsevier, 2005.
p. 611–24.
41. Rogachefsky AS, Hussain M, Goldberg DJ. Atrophic and mixed
pattern of acne scars with a 1320 nm Nd:YAG laser. Dermatol
Surg 2003;29:904–8.
25. Alster TS, West TB. Resurfacing atrophic facial scars with a highenergy, pulsed carbon dioxide laser. Dermatol Surg 1996;22:
151–5.
42. Friedman PM, Jih MH, Skover GR, et al. Treatment of atrophic
facial acne scars with the 1064-nm Q-switched Nd:YAG laser.
Arch Dermatol 2004;140:1337–41.
26. Walia S, Alster TS. Prolonged clinical and histological effects from
CO2 laser resurfacing of atrophic scars. Dermatol Surg
1999;25:926–30.
43. Friedman PM, Skover GR, Payonik G, et al. 3D in-vivo
optical skin imaging for topographical quantitative
assessment of non-ablative laser technology. Dermatol Surg
2002;28:199–204.
27. Tanzi EL, Alster TS. Treatment of atrophic facial acne scars with a
dual-mode Er: YAG laser. Dermatol Surg 2002;28:551–5.
28. Alster TS, Nanni CA, Williams CM. Comparison of four carbon
dioxide resurfacing lasers: a clinical and histopathologic evaluation. Dermatol Surg 1999;25:153–9.
29. Alster TS, Kauvar AN, Geronemus RG. Histology of high-energy
pulsed CO2 laser resurfacing. Semin Cutan Med Surg
1996;15:189–93.
30. 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.
31. Green D, Egbert BM, Utley DS, Koch RJ. In vivo model of histologic changes after treatment with the superpulsed CO2 laser,
erbium: YAG laser, and blended lasers: a 4- to 6-month prospective histologic and clinical study. Lasers Surg Med 2000;27:
362–72.
32. Alster TS. Clinical and histological evaluation of six erbium:
YAG lasers for cutaneous resurfacing. Laser Surg Med 1999;
24:87–92.
140
33. Fitzpatrick RE, Tope WD, Goldman MP, Satur NM. Pulsed carbon dioxide laser 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.
D E R M AT O L O G I C S U R G E RY
44. Manstein D, Herron GS, Sink RK, et al. Fractional photothermoloysis: a new concept for cutaneous remodeling using
microscopic patterns of thermal injury. Lasers Surg Med
2004;34:426–38.
45. Alster TS, Tanzi EL, Lazarus M. The use of fractional laser
photothermolysis for the treatment of atrophic scars. Dermatol
Surg 2007;33 (in press).
46. Greenbaum SS, Rubin MG. Surgical pearl: the high-energy pulsed
carbon dioxide laser for immediate scar resurfacing. J Am Acad
Dermatol 1999;40:998–1000.
Address correspondence and reprint requests to: Tina S.
Alster, MD, Washington Institute of Dermatologic Laser
Surgery, 1430 K Street, NW, Suite 200, Washington, DC
20005, or e-mail: [email protected].