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1 Anderson RR, Parrish JA Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation Science 1983;220:524 2 Uebelhoer NS, Bogle MA, Stewart B, et al A split-face comparison study of pulsed 532-nm KTP laser and 595-nm pulsed dye laser in the treatment of facial telangiectasias and diffuse telangiectatic facial erythema Dermatol Surg 2007;33: 441 3 Taylor CR, Gange RW, Dover JS, et al Treatment of tattoos by Q-switched ruby laser A dose-response study Arch Dermatol 1990;126:893 4 Alster TS Q-switched alexandrite laser treatment (755 nm) of professional and amateur tattoos J Am Acad Dermatol 1995;33:69 5 Fitzpatrick RE, Goldman MP Tattoo removal using the alexandrite laser Arch Dermatol 1994;130:1508 6 Bernstein EF Laser treatment of tattoos Clin Dermatol 2006;24:43 7 Alajlan A, Shapiro J, Rivers JK, et al Paradoxical hypertrichosis after laser epilation J Am Acad Dermatol 2005;53:85
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SUMMARY 220
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Since their introduction in 1960, lasers have continued to expand in popularity
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8 Rao J, Goldman MP Prospective, comparative evaluation of three laser systems used individually and in combination for axillary hair removal Dermatol Surg 2005;31:1671 9 Amin SP, Goldberg, DJ Clinical comparison of four hair removal lasers and light sources J Cosmet Laser Ther 2006;8:65 10 Hantash BM, Bedi VP, Chan KF, et al Ex vivo histological characterization of a novel ablative fractional resurfacing device Lasers Surg Med 2007;39:87 11 Manstein D, Herron GS, Sink RK, et al Fractional photothermolysis: a new concept for cutaneous remodeling using microscopic patterns of thermal injury Lasers Surg Med 2004;34:426 12 Goldman MP, Weiss RA, Weiss MA Intense pulsed light as a nonablative approach to photoaging Dermatol Surg 2005;31:1179 13 Negishi K, Tezuka Y, Kushikata N, et al Photorejuvenation for Asian skin by intense pulsed light Dermatol Surg 2001; 27:627 14 Kawada A, Shiraishi H, Asai M, et al Clinical improvement of solar lentigines and ephelides with an intense pulsed light source Dermatol Surg 2002;28:504 15 Bitter PH Noninvasive rejuvenation of photodamaged skin using serial, full-face intense pulsed light treatments Dermatol Surg 2000;26:835 16 Whelan HT, Buchmann EV, Dhokalia A, et al Effect of NASA light-emitting diode irradiation on molecular changes for wound healing in diabetic mice J Clin Laser Med Surg 2003;21:67 17 Baxter GD Therapeutic Lasers: Theory and Practice Oxford, UK: Churchill Livingstone; 1994 18 Enwemeka CS, Parker JC, Dowdy DS, et al The efficacy of low-power lasers in tissue repair and pain control: a metaanalysis study Photomed Laser Surg 2004; 22:323 19 Takezaki S, Omi T, Sato S, et al Lightemitting diode phototherapy at 630 / 3 nm increases local levels of skin-homing T-cells in human subjects J Nippon Med Sch 2006;73:75 20 Rigau J, Trelles MA, Calderhead RG, et al Changes in fibroblast proliferation and metabolism following in vitro heliumneon laser irradiation Laser Therapy 1991; 3:25 21 Kennedy JC, Pottier RH, Pross DC Photodynamic therapy with endogenous protoporphyrin IX: basic principles and present clinical experience J Photochem Photobiol B 1990;6:143 22 Dover JS, Bhatia AC, Stewart B, et al Topical 5-aminolevulinic acid combined with intense pulsed light in the treatment of photoaging Arch Dermatol 2005;141: 1247 23 Alster TS, Tanzi EL Photodynamic therapy with topical aminolevulinic acid and pulsed dye laser irradiation for sebaceous hyperplasia J Drugs Dermatol 2003;2:501 24 Alster TS, Tanzi EL, Welsh E Photorejuvenation of facial skin with topical 20% 5-aminolevulinic acid and intense pulsed light treatment: a split-face comparison study J Drugs Dermatol 2005;4:35 25 Marmur ES, Phelps R, Goldberg DJ Ultrastructural changes seen after ALAIPL photorejuvenation: a pilot study J Cosmet Laser Surg 2005;7:21
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COSMETIC DERMATOLOGY: PRINCIPLES AND PRACTICE
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CHAPTER 25 Sclerotherapy
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In addition to the face, neck, chest, and hands, the aesthetic appearance of the legs is a significant area of concern to patients In 2005, according to statistics gathered by the American Society for Aesthetic Plastic Surgery, sclerotherapy ranked as the sixth most common nonsurgical cosmetic procedure1 In order to maximize the successful treatment of leg veins with sclerotherapy, a thorough understanding of venous pathology, specifically venous hypertension and chronic venous insufficiency, is crucial for practitioners The aim of this chapter is to familiarize the reader with the underlying pathology, the diagnosis, and the treatment of venous hypertension, and to help the reader differentiate between the medical and the cosmetic sclerotherapy patient In keeping with the theme of this textbook, the treatment section of this chapter will focus on sclerotherapy as it pertains to the cosmetic patient, specifically regarding the treatment of leg telangiectasias, venulectasias, and reticular veins Treatment options for patients with clinically relevant venous disease will be briefly mentioned culation The contractile action of the skeletal muscles, primarily the calf muscles, helps to transport blood upward reflux Varicose veins impede proper circulation by permitting blood to flow away from the heart, decreasing the efficiency of the entire venous system, and leading to venous hypertension The severity of venous hypertension is directly related to the skin changes seen in chronic venous insufficiency The progression to chronic venous insufficiency follows the leaking of fluids out of the veins into the perivascular tissue, engendering symptoms of leg swelling, aching, and eventually dermatologic manifestations such as increased vascular markings, skin discoloration (hyperor hypopigmentation and hemosiderin deposition), dermatitis, fibrosis, and ulceration The etiology of varicose vein formation is multifactorial There is a familial tendency to develop varicose veins, usually in patients who present with this disease early in life Its relation to gender appears to be a more significant factor, as it is seen in approximately 26% of women versus 5% of men In addition, advancing age appears to be involved, as those older than age 35 almost triple their risk compared to those aged 24 to 35 years2 Physical states that increase the pressure on the venous system by physically compromising venous return, such as pregnancy, obesity, decreased mobility, and frequent constipation, are also associated with an increased risk of varicose vein formation2 4 Other factors, such as the presence of estrogen, have been shown to have an impact on the vascular system While estrogen appears to protect against the formation of venous ulcers of the lower limbs,5 it has been implicated in raising telangiectatic matting (the appearance of tiny vessels less than 02 mm in diameter), which occurs in women after undergoing sclerotherapy for the treatment of leg veins6 Current research on the etiology and pathology of varicose veins and chronic venous insufficiency suggests that the underlying pathologic mechanism is an inflammatory response that is hypothesized to be initiated by an increase in shear stress on the venous endothelium Several studies suggest that an increase in venous pressure induces leukocyte accumulation and subsequent free radical production that leads to degradation of valve leaflets by metalloproteinases,7 9 which are enzymes that degrade collagen, elastin, and other components of the extracellular matrix Based on this free radical-driven model of venous
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