laser scar revision: a review

10
REVIEW ARTICLE Laser Scar Revision: A Review TINA ALSTER, MD, AND LARISSA ZAULYANOV -SCANLON, MD y 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 heal- ing events into motion. The stages of wound healing include inflammation, proliferation, and matur- ation. 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 per- meability. 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 be- gins approximately 3 to 5 days after initial wounding and is induced by cytokines that are initially pro- duced by macrophages, such as fibroblast growth factor-2, transforming growth factor-b, and insulin- like growth factor. 2 Similar to fetal skin, the com- position of early wounds is approximately 80% Type III collagen and 20% Type I collagen. In contradis- tinction, 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 heal- ing response can create a raised nodule of fibrotic tissue, whereas ‘‘pitted’’ and atrophic scars may re- sult from inadequate replacement of deleted collagen fibers. Although vascular and pigment alterations associated with wound healing are typically transi- ent, the textural changes caused by collagen disrup- tion are often permanent. Histologically, what makes scars unique is the relative absence of skin append- ages 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 scar 4 (Table 1). & 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 131 Washington Institute of Dermatologic Laser Surgery, Washington, DC; y Department of Dermatology and Cutaneous, University of Miami, Miami, FL

Upload: hathuy

Post on 14-Feb-2017

232 views

Category:

Documents


0 download

TRANSCRIPT

Page 1: 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 withcommercial supporters.

Cutaneous 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 heal-

ing events into motion. The stages of wound healing

include inflammation, proliferation, and matur-

ation.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 per-

meability. 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 be-

gins approximately 3 to 5 days after initial wounding

and is induced by cytokines that are initially pro-

duced by macrophages, such as fibroblast growth

factor-2, transforming growth factor-b, and insulin-

like growth factor.2 Similar to fetal skin, the com-

position of early wounds is approximately 80% Type

III collagen and 20% Type I collagen. In contradis-

tinction, 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 heal-

ing response can create a raised nodule of fibrotic

tissue, whereas ‘‘pitted’’ and atrophic scars may re-

sult from inadequate replacement of deleted collagen

fibers. Although vascular and pigment alterations

associated with wound healing are typically transi-

ent, the textural changes caused by collagen disrup-

tion are often permanent. Histologically, what makes

scars unique is the relative absence of skin append-

ages 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).

& 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

1 3 1

�Washington Institute of Dermatologic Laser Surgery, Washington, DC; yDepartment of Dermatology and Cutaneous,University of Miami, Miami, FL

Page 2: Laser Scar Revision: A Review

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 pro-

tocol be outlined.

Patient Selection

Skin Phototype

Ethnic background is important when contemplating

laser outcomes. For instance, the presence of in-

creased epidermal pigment in patients with darker

skin tones (skin phototypes III or higher) interferes

with the targeted hemoglobin’s absorption of vas-

cular-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 undesir-

able melanin destruction is increased, leading to

postoperative skin dyspigmentation. While darker-

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 in-

flammatory processes should be given careful atten-

tion 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 1. Patient Characteristics for Optimal Laser Efficacy

Skin phototype Darker skin tones require lower energy densities

Concurrent infection/Inflammation Avoid laser treatment to affected area

Medication use Discontinue anticoagulants (for PDL)

Prior treatment Note presence of background dyspigmentation

Expectations and compliance Assess whether realistic and agreeable to treatment

TABLE 2. Scar Types and Appropriate Laser Treatment

Scar type Scar characteristics Appropriate laser

Hypertrophic Raised, erythematous

Confined to wound border

Often symptomatic

PDL

Keloid Firm, raised, reddish-purple

Growth beyond original wound

Rapid proliferation

Often symptomatic

Characteristic histology

PDL

Atrophic Indented

Early: erythematous, Late: pale

CO2/Er:YAG

1,064/1,320 Nd:YAG, 1,450 nm diode

Fraxel

Prescar Pink

Occur in scar-prone skin

PDL

PDL, pulsed dye laser; CO2, carbon dioxide; Er:YAG, erbium:yttrium-aluminum-garnet; Nd:YAG, neodymium:yttrium-aluminum-garnet.

D E R M AT O L O G I C S U R G E RY1 3 2

L A S E R S C A R R E V I S I O N

Page 3: Laser Scar Revision: A Review

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 inflamma-

tion 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. Iso-

tretinoin use, commonly encountered in acne pa-

tients presenting for laser scar therapy, can foster the

development of hypertrophic scars after dermal re-

surfacing 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 isotreti-

noin, recent studies have not demonstrated an

increased risk of side effects when isotretinoin has

been used concomitantly with other laser treat-

ments,9 leading to a more lax approach with this

medication in skin resurfacing procedures. If possi-

ble, 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 post-

operative 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 injec-

tions 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 eradi-

cation.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 noncompli-

ance 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 photo-

graphs, 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 prolifera-

tion 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 regres-

sion. 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

3 3 : 2 : F E B R U A RY 2 0 0 7 1 3 3

A L S T E R A N D Z A U LYA N O V- S C A N L O N

Page 4: Laser Scar Revision: A Review

or dysesthetic. Histologically, keloids are distin-

guished 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 con-

ditions 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-bexpression, 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 metab-

olism,17 and the heating of collagen fibers and

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 inter-

ference 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 subse-

quent visits only when the response to the previous

treatment is suboptimal. Laser treatments are typic-

ally 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 post-

operative oozing, crusting, or vesiculation is ob-

served, 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

D E R M AT O L O G I C S U R G E RY1 3 4

L A S E R S C A R R E V I S I O N

Page 5: Laser Scar Revision: A Review

concomitant intralesional corticosteroids or 5-fluor-

ouracil has been shown to provide additional bene-

fit.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 be-

fore) 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 epider-

mal melanin interference with laser energy penetra-

tion. 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 1. Hypertrophic facial scars before (A) and after PDL treatment (B).

Figure 2. Hypertrophic abdominal scar before (A) and after PDL treatment (B).

3 3 : 2 : F E B R U A RY 2 0 0 7 1 3 5

A L S T E R A N D Z A U LYA N O V- S C A N L O N

Page 6: Laser Scar Revision: A Review

and 2). Keloids often require more treatment ses-

sions 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 er-

ythema. 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-aluminum-

garnet (Er:YAG or erbium) laser vaporization23–27

(Figure 5). Although other treatments such as

dermabrasion and injection of various filler materi-

als can also be used for atrophic scars, their oper-

ator-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 la-

ser skin resurfacing treatment for atrophic scar re-

vision was its ability to selectively and reproducibly

vaporize skin, with improved operator control and

clinical efficacy.28–32 Comparisons with dermabra-

sion 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 treat-

ment 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 3. Keloid on the neck before (A) and after PDL treatment (B).

Figure 4. Keloid on the scapula before (A) and after PDL treatment (B).

D E R M AT O L O G I C S U R G E RY1 3 6

L A S E R S C A R R E V I S I O N

Page 7: Laser Scar Revision: A Review

remodeling, with marked reduction of skin textural

irregularities.34

Laser treatment of atrophic scars is aimed at redu-

cing the depths of the scar borders and stimulating

neocollagenesis to fill in the depressions. Although

spot (or local) vaporization of isolated scars is a vi-

able 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 im-

proving 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 op-

erated 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 op-

erated 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, intrale-

sional, intravenous, and general anesthesia. Gener-

ally, 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 ede-

matous immediately after treatment, with copious

serous discharge and generalized worsening of the

skin’s appearance over the first few days. It is im-

perative that patients be monitored closely for ap-

propriate healing responses and potential

complications, such as dermatitis or infection, dur-

ing 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 infec-

tion.36–38 The use of topical antibiotics is avoided

due to the potential development of contact derma-

titis.39 Application of topical ointments, semiocclu-

sive dressings, and/or cooling masks promote healing

and reduce swelling.7 Postoperative erythema typic-

ally lasts several (4–6) weeks after Er:YAG laser

Figure 5. Atrophic acne scars before (A) and after ablative laser treatment (B).

3 3 : 2 : F E B R U A RY 2 0 0 7 1 3 7

A L S T E R A N D Z A U LYA N O V- S C A N L O N

Page 8: Laser Scar Revision: A Review

treatment and even longer (3–4 months) after CO2

laser ablation due to their relative degree of tissue

necrosis. Hyperpigmentation is transient and gener-

ally appears 3 to 4 weeks after treatment. Its reso-

lution 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 resur-

facing include hypertrophic scarring and ectropion

formation, both related to overly aggressive laser

techniques and/or undiagnosed/untreated suprain-

fections. Hypertrophic burn scars can be effectively

treated with the PDL as previously described,18

whereas ectropion typically requires surgical recon-

struction. Retreatment after ablative laser skin re-

surfacing 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 de-

veloped 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 de-

liver concomitant epidermal surface cooling with

deeply penetrating infrared wavelengths that target

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) com-

pensates for their reduced clinical efficacy (relative

to ablative lasers).

The recent introduction of fractional laser skin re-

surfacing (Fraxel, Reliant Technologies, Mountain

View, CA) involving a novel 1,550-nm erbium-

doped 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 dif-

ferent 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

Figure 6. Atrophic acne scars before (A) and after Fraxel laser treatment (B).

D E R M AT O L O G I C S U R G E RY1 3 8

L A S E R S C A R R E V I S I O N

Page 9: Laser Scar Revision: A Review

treat surgical sites, traumatic wounds, or ulcerations

to improve the quality of scarring and prevent ex-

cessive scar formation11–13 (Figure 7).

Conclusion

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. Al-

though atrophic scars may best be treated with ab-

lative 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.

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.

3. Monaco JL, Lawrence WT. Acute wound healing: an overview.

Clin Plast Surg 2003;30:1–12.

4. Alster TS. Laser treatment of scars and striae. In: Alster TS,

Manual of cutaneous laser techniques. Philadelphia:Lippincott-

Raven; 2000:p. 89–107.

5. Macedo O, Alster TS. Laser treatment of darker skin tones: a

practical approach. Dermatol Ther 2000;13:114–26.

6. Nanni CA, Alster TS. Complications of CO2 laser resurfacing: an

evaluation of 500 patients. Dermatol Surg 1998;24:315–20.

7. Horton S, Alster TS. Preoperative and postoperative con-

siderations for cutaneous laser resurfacing. Cutis 1999;64:

399–406.

8. Zachariae H. Delayed wound healing and keloid formation fol-

lowing 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 iso-

tretinoin 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 excoriee 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-regula-

tion of TGF-beta1 expression and extracellular matrix expression.

Lasers Surg Med 2004;34:104–8.

Figure 7. Prescars on the neck before (A) and after PDL treatment (B).

3 3 : 2 : F E B R U A RY 2 0 0 7 1 3 9

A L S T E R A N D Z A U LYA N O V- S C A N L O N

Page 10: Laser Scar Revision: A Review

16. Reiken SR, Wolfort SF, Berthiamume F, et al. Control of hyper-

trophic 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 intrale-

sional corticosteroid, 5-fluorouracil, and 585-nm flashlamp-

pumped 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.

22. Apfelberg DB, Maser MR, White DN, Lash H. Failure of carbon

dioxide laser excision of keloids. Lasers Surg Med 1989;9:

382–88.

23. Alster TS. Cutaneous resurfacing with CO2 and erbium: YAG

laser: preoperative, intraoperative, and postoperative consider-

ations. Plast Reconstr Surg 1999;103:619–32.

24. Alster TS, Tanzi EL. Laser skin resurfacing: ablative and nonab-

lative. In: Robinson J, Sengelman R, Siegel DM, Hanke CM,

editors. Surgery of the skin. Philadelphia:Elsevier, 2005.

p. 611–24.

25. Alster TS, West TB. Resurfacing atrophic facial scars with a high-

energy, pulsed carbon dioxide laser. Dermatol Surg 1996;22:

151–5.

26. Walia S, Alster TS. Prolonged clinical and histological effects from

CO2 laser resurfacing of atrophic scars. Dermatol Surg

1999;25:926–30.

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 evalu-

ation. 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 re-

sults 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 his-

tologic changes after treatment with the superpulsed CO2 laser,

erbium: YAG laser, and blended lasers: a 4- to 6-month prospec-

tive 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.

33. Fitzpatrick RE, Tope WD, Goldman MP, Satur NM. Pulsed car-

bon dioxide laser laser, trichloroacetic acid, Baker-Gordon phe-

nol, and dermabrasion: a comparative clinical and histologic

study of cutaneous resurfacing in a porcine model. Arch Dermatol

1996;132:469–71.

34. Fitzpatrick RE, Rostan EF, Marchell N. Collagen tightening in-

duced 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.

39. Fisher AA. Lasers and allergic contact dermatitis to topical an-

tibiotics, with particular reference to bacitracin. Cutis

1996;58:252–4.

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.

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.

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.

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.

44. Manstein D, Herron GS, Sink RK, et al. Fractional photother-

moloysis: 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 LaserSurgery, 1430 K Street, NW, Suite 200, Washington, DC20005, or e-mail: [email protected].

D E R M AT O L O G I C S U R G E RY1 4 0

L A S E R S C A R R E V I S I O N