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 131 LASER SCAR REVISION 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. 132 D E R M AT O L O G I C S U R G E RY 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 3 3 : 2 : F E B R U A RY 2 0 0 7 133 LASER SCAR REVISION 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 134 D E R M AT O L O G I C S U R G E RY 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). 3 3 : 2 : F E B R U A RY 2 0 0 7 135 LASER SCAR REVISION 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). 136 D E R M AT O L O G I C S U R G E RY 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 3 3 : 2 : F E B R U A RY 2 0 0 7 137 LASER SCAR REVISION 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 138 D E R M AT O L O G I C S U R G E RY 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 excorie´e 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].
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