Atlas Phẫu Thuật Thẩm Mỹ (Tập 2) – Atlas of Cosmetic Surgery

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Chapter 8    Cosmetic surgery procedures and techniques
kinase, c-jun N-terminal protein kinase, and p38), which
amass in cell nuclei, forming cFos/cJun complexes of tran­
scription factor activator protein 1, and triggering the ma­
trix metalloproteinases collagenase, 92 kDa gelatinase, and
­stromelysin that attack collagen and other connective tissue
of the skin.99,100
Understood with more certainty, though, are the direct ef­
fects of free radicals on the aging process and skin aging. Kang
et al. recently demonstrated that free radical activation of the
MAP kinase pathways stimulates production of collagenase,
which results in the breakdown of collagen.101 Using antioxi­
dants to inhibit these pathways is believed to impede photo­
aging by preventing collagenase production and its subsequent
deleterious effects on collagen. Using human skin, Kang et al.
demonstrated that the UV induction of the cJun-driven
­enzyme collagenase was inhibited in skin pretreated with the
antioxidants genistein and N-acetyl cysteine.
Numerous antioxidants are used as ingredients in topical
skin care products, including green tea, vitamins C and E,
ferulic acid, coenzyme Q10, pycnogenol, silymarin, and ide­
benone. In the future, we can reasonably expect the potential
of growth factors, cytokines, and telomerase to be harnessed
through technological advances in tissue engineering and
gene therapy.102 In the meantime, avoiding exposure to the
sun, using sunscreen when avoiding the sun is impossible,
avoiding cigarette smoke and pollution, taking oral antioxi­
dant supplements or topical antioxidant formulations, and
eating a diet high in fruits and vegetables can help reduce or
prevent extrinsic skin aging. Unwanted wrinkles can also be
prevented or treated through the regular use of prescription
retinoids.
COMBINATIONS OF TYPES
The various permutations of the four skin parameters yield
16 different skin types (Table 8-1). Using the BSTS can help
consumers identify their particular skin problem areas and act
accordingly. For example, a person with an oily, sensitive, non­
pigmented, wrinkled (OSNW) skin type would be advised to
use products with retinoids and antioxidants but one with a
DSNT profile should use products with barrier repair
­ingredients. While this typing system has the potential to offer
significant assistance, it is important to note that an individu­
al’s skin type can change, particularly during stressful periods
and when changing environments, and this must be taken into
account in the overall skin-type assessment. Also, there are
certain tendencies worth noting when considering the BSTI
skin typing system. In other words, some skin problems are
typically associated with particular skin types. Pigmented,
wrinkled skin (PW) is more often observed in a person with
a significant history of sun exposure, as manifested by wrin­
kles and solar lentigos. Dark skin is more common among PT
types whereas light skin is more typical among NW types. Fur­
ther, OSNW types with lighter skin have a greater proclivity
toward developing rosacea than those with other skin types.
People with DS skin tend to experience eczema more often
than individuals with other skin types. Acne is most common
among people with OS skin.
CONCLUSION
There are four basic parameters by which the nature of
human skin is currently understood and described. With the
intention of identifying the most suitable topical treatments for
individuals’ skin, the dermatologic establishment has come to
view skin types as either: dry or oily; sensitive or resistant; pig­
mented or nonpigmented; and wrinkled or unwrinkled. These
parameters have helped practitioners differentiate between
various skin types and represent an advance over earlier clas­
sifications, but they do not provide a complete characteriza­
tion of the skin when used alone, as they typically are, because
these skin dichotomies are not mutually exclusive. The BSTS
is based on this understanding that skin types can be more
accurately identified and distinguished when considering the
various permutations yielded when one end of the spectrum
of each parameter is identified in a patient. Sixteen possible
skin types emerge from this classification system, which has
the potential to assist physicians in treating numerous skin
conditions and could also help patients select for themselves
the most appropriate OTC topical skin care products (Tables
8-2, 8-3). There are numerous topical skin care products avail­
able to meet the needs of most of the 16 skin types.
Table 8-1  The Baumann Skin Typing System (BSTS)
Oily
Dry
Pigmented
Nonpigmented
Pigmented
Nonpigmented
Wrinkled
OSPW
OSNW
DSPW
DSNW
Sensitive
Tight
OSPT
OSNT
DSPT
DSNT
Sensitive
Wrinkled
ORPW
ORNW
DRPW
DRNW
Resistant
Tight
ORPT
ORNT
DRPT
DRNT
Resistant
The 16 skin types are a result of the combination of 4 skin type issues that should be considered when ascertaining skin care needs. The skin types are determined
by a questionnaire that takes into account historical data, genetic history, and skin concerns.

103
Topical skin care  •  Chapter 8
REFERENCES
  1. Tsao A. The changing face of skin care. Business Week online, Nov. 30,
2004.
nf20041130_0962_db035.htm (accessed 10/26/05).
  2. Baumann L. The skin type solution. New York: Bantam Dell; 2006.
  3. Chernosky ME. Clinical aspects of dry skin. J Soc Cosmet Chem
1976; 27:365–376.
  4. Rawlings A, Hope J, Rogers J, et al. Skin dryness – what is it? J Invest
Dermatol 1993; 100:510.
  5. Elias PM. Stratum corneum defensive functions: an integrated view.
J Invest Dermatol 2005; 125(2):183–200.
  6. Wildnauer RH, Bothwell JW, Douglass AB. Stratum corneum
biomechanical properties. I. Influence of relative humidity on normal
and extracted human stratum corneum. J Invest Dermatol 1971;
56(1):72–78.
  7. Orth D, Appa Y, Glycerine. A natural ingredient for moisturizing
skin. In: Loden M, Maibach H, eds. Dry skin and moisturizers. Boca
Raton: CRC Press; 2000:214.
  8. Ekholm IE, Brattsand M, Egelrud T. Stratum corneum tryptic enzyme
in normal epidermis: a missing link in the desquamation process?
J Invest Dermatol 2000; 114(1):56–63.
  9. Elias PM. The epidermal permeability barrier: from the early days at
Harvard to emerging concepts. J Invest Dermatol 2004; 122(2):xxxvi–
xxxix.
10. Scott IR, Harding CR. Filaggrin breakdown to water binding
compounds during development of the rat stratum corneum is
controlled by the water activity of the environment. Dev Biol 1986;
115(1):84–92.
11. Sato J, Denda M, Chang S, et al. Abrupt decreases in environmental
humidity induce abnormalities in permeability barrier homeostasis.
J Invest Dermatol 2002; 119(4):900–904.
12. Wang F, Feng XC, Li YM, et al. Aquaporins as potential drug targets.
Acta Pharmacol Sin 2006; 27(4):395–401.
13. Sougrat R, Morand M, Gondran C, et al. Functional expression
of AQP3 in human skin epidermis and reconstructed epidermis.
J Invest Dermatol 2002; 118(4):678–685.
14. Takenouchi M, Suzuki H, Tagami H. Hydration characteristics
of pathologic stratum corneum – evaluation of bound water.
J Invest Dermatol 1986; 87(5):574–576.
15. Warner RR, Bush RD, Ruebusch NA. Corneocytes undergo
systematic changes in element concentrations across the human inner
stratum corneum. J Invest Dermatol 1995; 104(4):530–536.
16. Warner RR, Myers MC, Taylor DA. Electron probe analysis of
human skin: element concentration profiles. J Invest Dermatol 1988;
90(1):78–85.
17. Warner RR, Myers MC, Taylor DA. Electron probe analysis
of human skin: determination of the water concentration profile.
J Invest Dermatol 1988; 90(2):218–224.
18. Ma T, Hara M, Sougrat R, et-al. Impaired stratum corneum hydration
in mice lacking epidermal water channel aquaporin-3. J Biol Chem
2002 1 0;277(19):17147–17153.
19. Yang B, Verkman AS. Water and glycerol permeabilities of
aquaporins 1–5 and MIP determined quantitatively by expression
of epitope-tagged constructs in Xenopus oocytes. J Biol Chem 1997;
272(26):16140–16146.
20. Dumas M, Gondran C, Barre P, et al. Effect of an Ajuga turkestanica
extract on aquaporin 3 expression, water flux, differentiation and
barrier parameters of the human epidermis. Eur J Dermatol 2002;
12(6):xxv–xxvi.
21. Thiboutot D. Regulation of human sebaceous glands. J Invest
Dermatol 2004; 123(1):1–12.
22. Clarys P, Barel A. Quantitative evaluation of skin surface lipids.
Clin Dermatol 1995; 13(4):307–321.
23. Thody AJ, Shuster S. Control and function of sebaceous glands.
Physiol Rev 1989; 69(2):383–416.
24. Elias PM, Fritsch PO, Lampe M, et al. Retinoid effects on epidermal
structure, differentiation, and permeability. Lab Invest 1981;
44(6):531–540.
25. Gomez EC. Differential effect of 13-cis-retinoic acid and an aromatic
retinoid (Ro 10-9359) on the sebaceous glands of the hamster flank
organ. J Invest Dermatol 1981; 76(1):68–69.
26. Geiger JM. Retinoids and sebaceous gland activity. Dermatology 1995;
191(4):305–310.
27. Mathers WD, Lane JA. Meibomian gland lipids, evaporation, and tear
film stability. Adv Exp Med Biol 1998; 438:349–360.
28. Tiffany JM. The role of meibomian secretion in the tears. Trans
Ophthalmol Soc UK 1985; 104(Pt 4):396–401.
29. Fluhr JW, Mao-Qiang M, Brown BE, et al. Glycerol regulates stratum
corneum hydration in sebaceous gland deficient (asebia) mice. J Invest
Dermatol 2003; 120(5):728–737.
Table 8-2  How to treat dry skin
Preserve and replace skin lipids
Avoiding
  Detergents
  Prolonged water immersion, especially in chlorine
and hard water
  Vigorously foaming cleansers
  Surfactants
Using
  Moisturizers containing fatty acids, ceramides
and ­cholesterol
  For dry, resistant (DR) skin: Look for moisturizers
containing occlusives and humectants
Prevent loss of NMF
Avoid detergents
Avoid UV exposure
Increase function of Aquaporin-3
Look for ingredients such as Ajuga turkestanica
Table 8-3  How to prevent wrinkles
Daily broad-spectrum sunscreen
Sun avoidance
Cigarette avoidance
Retinoids
Antioxidants – oral and topical
  Green tea
  Vitamin C
  Vitamin E
  Lycopene
  Lutein
  Coenzyme Q10
  Idebenone
  Silymarin
  Polypodium Leucotomos
  Pycogenol
  Feverfew
  Ferulic acid

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Chapter 8    Cosmetic surgery procedures and techniques
30. Fluhr JW, Gloor M, Lehmann L, et al. Glycerol accelerates recovery
of barrier function in vivo. Acta Derm Venereol 1999; 79(6):418–421.
31. Pochi PE, Strauss JS, Downing DT. Age-related changes in sebaceous
gland activity. J Invest Dermatol 1979; 73(1):108–111.
32. Walton S, Wyatt EH, Cunliffe WJ. Genetic control of sebum excretion
and acne – a twin study. Br J Dermatol. 1988; 118(3):393–396.
33. De Pedrini P, Rapisarda R, Spano G. The effect of ketoconazole on
sebum secretion in patients suffering from acne and seborrhoea. Int
J Tissue React 1988; 10(2):111–113.
34. Goldstein JA, Socha-Szott A, Thomsen RJ, et al. Comparative effect
of isotretinoin and etretinate on acne and sebaceous gland secretion.
J Am Acad Dermatol 1982; 6(4 Pt 2 Suppl):760–765.
35. Vogel CA, Balkrishnan R, Fleischer AB, et al. Over-the-counter
topical skin care products – a common component of skin disease
management. Cutis 2004; 74(1):55–67.
36. Morrison D. Petrolatum. In: Loden M, Maibach H, eds. Dry skin and
moisturizers. Boca Raton: CRC Press; 2000:251.
37. Spruit D. The interference of some substances with the water vapour
loss of human skin. Dermatologica 1971; 142(2):89–92.
38. Draelos Z. Moisturizers. In: Draelos Z Atlas of cosmetic dermatology.
New York: Churchill Livingstone; 2000:83.
39. Kraft JN, Lynde CW. Moisturizers: what they are and a practical
approach to product selection. Skin Therapy Lett 2005; 10(5):1–8.
40. Kligman AM. The myth of lanolin allergy. Contact Dermatitis 1998;
39:103.
41. Hannuksela M. Glycols. In: Loden M, Maibach H, eds. Dry skin and
moisturizers. Boca Raton: CRC Press; 2000:413–415.
42. Wehr RF, Krochmal L. Considerations in selecting a moisturizer. Cutis
1987; 39(6):512–515.
43. Idson B. Dry skin: moisturizing and emolliency. Cosmet Toiletr 1992;
107:69.
44. Del Rosso JQ. Cosmeceutical moisturizers. In: Draelos ZD, ed.
Procedures in cosmetic dermatology series: Cosmeceuticals. 1st edn.
Philadelphia: Elsevier; 2005:97–102.
45. Mitsui T, ed. New cosmetic science, New York; Elsevier; 1997:134.
46. Orth D, Appa Y. Glycerine: a natural ingredient for moisturizing
skin. In: Loden M, Maibach H, eds. Dry skin and moisturizers, Boca
Raton: CRC Press, 2000:217.
47. Orth D, Appa Y, Contard E, et-al. Effect of high glycerin therapeutic
moisturizers on the ultrastructure of the stratum corneum. Poster
presentation at the 53rd annual meeting of the American Academy of
Dermatology, February 1995.
48. Kligman AM. Dermatologic uses of urea. Acta Derm Venereol 1957;
37:155.
49. Harding C, Bartolone J, Rawlings A. Effects of natural moisturizing
factor and lactic acid isomers on skin function. In: Loden M, Maibach
H, eds. Dry skin and moisturizers. Boca Raton: CRC Press; 2000:217.
50. Wohlrab W. The influence of urea on the penetration kinetics of
topically applied corticosteroids. Acta Derm Venereol 1984; 64:233.
51. Wohlrab W. Effect of urea on the penetration kinetics of vitamin A
acid in human skin. Z Hautkr 1990; 65:803.
52. The Cosmetic Ingredient Review (CIR) Expert Panel. Final report of
the safety assessment of urea. Int J Toxicol 2005; 24(Suppl 3):1–56.
53. Serup J. A double-blind comparison of two creams containing urea as
the active ingredient. Assessment of efficacy and side-effects by non-
invasive techniques and a clinical scoring scheme. Acta Derm Venereol
Suppl (Stockh) 1992; 177:34.
54. Van Scott EJ, Yu RJ. Control of keratinization with alpha hydroxy
acids and related compounds. I. Topical treatment of ichthyotic
disorders. Arch Dermatol 1974; 110:586.
55. Perricone NV, Dinardo JC. Photoprotective and antiinflammatory
effects of topical glycolic acid. Dermatol Surg 1996; 22:435.
56. Draelos ZD. Rediscovering the cutaneous benefits of salicylic acid.
Cosm Derm Supp 1997; (10)4.
57. Van Scott EJ, Yu R. Hyperkeratinization, corneocyte cohesion, and
alpha hydroxy acids. J Am Acad Dermatol 1984; 11:867.
58. Berardesca E, Distante F, Vignoli GP, et al. Alpha hydroxyl acids
modulate stratum corneum barrier function. Br J Dermatol 1997;
137:934.
59. Stern E. Topical application of lactic acid in the treatment and
prevention of certain disorders of the skin. Urol Cutaneous Rev 1943;
50:106.
60. Rawlings AV, Davies V, Carlomusto M, et al. Effect of lactic acid
isomers on keratinocyte ceramide synthesis, stratum corneum lipid
levels and stratum corneum barrier function. Arch Dermatol Res 1996;
288:383.
61. Harding C, Bartolone J, Rawlings A. Effects of natural moisturizing
factor and lactic acid isomers on skin function. In: Loden M,
Maibach H, eds. Dry skin and moisturizers. Boca Raton: CRC Press;
2000:236.
62. Stiller MJ, Bartolone J, Stern R, et al. Topical 8% glycolic acid and
8% L-lactic acid creams for the treatment of photodamaged skin.
A double-blind vehicle-controlled clinical trial. Arch Dermatol 1996;
132:631.
63. Draelos Z. Moisturizers. In: Draelos Z. Atlas of cosmetic dermatology.
New York: Churchill Livingstone; 2000:85.
64. Gonzalo MA, de Argila D, Garcia JM, et al. Allergic contact dermatitis
to propylene glycol. Allergy 1999; 54:82.
65. Baumann LS, Spencer J. The effects of topical vitamin E on the
cosmetic appearance of scars. Dermatol Surg 1999; 25:311.
66. Jackson EM. The science of cosmetics. Am J Contact Dermat 1993;
4:108.
67. White GM. Recent findings in the epidemiologic evidence,
classification, and subtypes of acne vulgaris. J Am Acad Dermatol
1998; 39(2 Pt 3):S34–S37.
68. Mitsui T, ed. Cosmetics and skin. In: New cosmetic science.
Philadelphia: Elsevier; 1993:28.
69. Rothenberg ME, Hogan SP. The eosinophil. Annu Rev Immunol
2006; 24:147–174.
70. Shakoory B, Fitzgerald SM, Lee SA, et al. The role of human mast
cell-derived cytokines in eosinophil biology. J Interferon Cytokine Res
2004; 24(5):271–281.
71. Brown DJ, Dattner AM. Phytotherapeutic approaches to common
dermatologic conditions. Arch Dermatol 1998; 134(11):1401–1404.
72. Basketter DA, Griffiths HA. A study of the relationship between
susceptibility to skin stinging and skin irritation. Contact Dermatitis
1993; 29(4):185–188.
73. Lonne-Rahm SB, Fischer T, Berg M. Stinging and rosacea. Acta
Derm Venereol 1999; 79(6):460–461.
74. Orton DI, Wilkinson JD. Cosmetic allergy: incidence, diagnosis, and
management. Am J Clin Dermatol 2004; 5(5):327–337.
75. Mehta SS, Reddy BS. Cosmetic dermatitis – current perspectives. Int
J Dermatol 2003; 42(7):533–542.
76. Jovanovic M, Poljacki M, Duran V, et al. Contact allergy to Compositae
plants in patients with atopic dermatitis. Med Pregl 2004; 57(5-6):
209–218.
77. Hermanns JF, Petit L, Martalo O, et al. Unraveling the patterns of
subclinical pheomelanin-enriched facial hyperpigmentation: effect
of depigmenting agents. Dermatology 2000; 201(2):118–122.
78. Freedberg IM, Eisen AZ, Wolff K, et al., eds. Fitzpatrick’s dermatology
in general medicine, 5th edn. New York: McGraw-Hill; 1999:996.
79. Wakamatsu K, Kavanagh R, Kadekaro AL, et al. Diversity of
pigmentation in cultured human melanocytes is due to differences
in the type as well as quantity of melanin. Pigment Cell Res 2006;
19(2):154–162.
80. Szabo G, Gerald AB, Pathak MA, et al. Racial differences in the fate
of melanosomes in human epidermis. Nature 1969; 222(198):1081–
1082.
81. Jimbow K, Sugiyama S. Melanosomal translocation and
transfer. In: Nordlund JJ, et al., eds. The pigmentary system.
Physiology and pathophysiology. New York: Oxford University
Press; 1998.
82. Paine C, Sharlow E, Liebel F, et al. An alternative approach to
depigmentation by soybean extracts via inhibition of the PAR-2
pathway. J Invest Dermatol 2001; 116(4):587–595.
83. Seiberg M, Paine C, Sharlow E, et al. Inhibition of melanosome
transfer results in skin lightening. J Invest Dermatol 2000; 115(2):
162–167.

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84. Hakozaki T, Minwalla L, Zhuang J, et al. The effect of niacinamide
on reducing cutaneous pigmentation and suppression of melanosome
transfer. Br J Dermatol 2002; 147(1):20–31.
85. Boukamp P. Ageing mechanisms: the role of telomere loss. Clin Exp
Dermatol 2001; 26(7):562–565.
86. Boukamp P. Skin aging: a role for telomerase and telomere dynamics?
Curr Mol Med 2005; 5(2):171–177.
87. Uitto J. Understanding premature skin aging. N Engl J Med 1997;
337(20):1463–1465.
88. Kosmadaki MG, Gilchrest BA. The role of telomeres in skin aging/
photoaging. Micron 2004; 35(3):155–159.
89. Kappes UP, Luo D, Potter M, et al. Short- and long-wave UV light
(UVB and UVA) induce similar mutations in human skin cells. J Invest
Dermatol 2006; 126(3):667–675.
90. Marrot L, Belaïdi JP, Meunier JR. Importance of UVA
photoprotection as shown by genotoxic related endpoints: DNA
damage and p53 status. Mutat Res 2005; 571(1–2):175–184.
91. Baumann L. How to prevent photoaging? J Invest Dermatol 2005;
125(4):xii–xiii.
92. Varani J, Warner RL, Gharaee-Kermani M, et al. Vitamin A
antagonizes decreased cell growth and elevated collagen-degrading
matrix metalloproteinases and stimulates collagen accumulation in
naturally aged human skin. J Invest Dermatol 2000; 114(3):480–486.
93. Nusgens BV, Humbert P, Rougier A, et al. Topically applied vitamin C
enhances the mRNA level of collagens I and III, their processing enzymes
and tissue inhibitor of matrix metalloproteinase 1 in the human dermis.
J Invest Dermatol 2001; 116(6):853–859.
94. Kockaert M, Neumann M. Systemic and topical drugs for aging skin.
J Drugs Dermatol 2003; 2(4):435–441.
95. Margelin D, Medaisko C, Lombard D, et al. Hyaluronic acid and
dermatan sulfate are selectively stimulated by retinoic acid in irradiated
and nonirradiated hairless mouse skin. J Invest Dermatol 1996;
106(3):505–509.
96. Tajima S, Hayashi A, Suzuki T. Elastin expression is up-regulated
by retinoic acid but not by retinol in chick embryonic skin fibroblasts.
J Dermatol Sci 1997; 15(3):166–172.
97. Matheson AJ, Perry CM. Glucosamine: a review of its use in the
management of osteoarthritis. Drugs Aging 2003; 20(14):1041–1060.
98. Fitzpatrick RE. Endogenous growth factors as cosmeceuticals.
Dermatol Surg 2005; 31(7 Pt 2):827–831; discussion 831.
99. Fisher GJ, Voorhees JJ. Molecular mechanisms of photoaging and
its prevention by retinoic acid: ultraviolet irradiation induces MAP
kinase signal transduction cascades that induce Ap-1-regulated
matrix metalloproteinases that degrade human skin in vivo. J Investig
Dermatol Symp Proc 1998; 3(1):61–68.
100. Kang S, Chung JH, Lee JH, et al. Topical N-acetyl cysteine and
genistein prevent ultraviolet-light-induced signaling that leads to
photoaging in human skin in vivo. J Invest Dermatol 2003; 120(5):
835–841.
101. Kang S, Chung JH, Lee JH, JJ. Topical N-acetyl cysteine and genistein
prevent ultraviolet-light-induced signaling that leads to photoaging in
human skin in vivo. J Invest Dermatol 2003; 120(5):835–841.
102. Ostler EL, Wallis CV, Aboalchamat B, et al. Telomerase and the
cellular lifespan: implications of the aging process. J Pediatr Endocrinol
Metab 2000; 13(Suppl 6):1467–1476.

HISTORY AND SCIENCE
Corrective camoufl age is the process of masking physical fl aws
with makeup, prostheses, and artifi cial hair. Skin camoufl age
is the process of correcting cutaneous fl aws with specialized
makeup preparations and techniques. It acts as a cosmetic
prosthesis, providing customized, immediate appearance
normalization for a variety of macular skin conditions.
Skin camoufl aage is useful for patients with chronic macu-
lar conditions, such as vitiligo ( Fig. 9-1 ), melasma ( Fig. 9-2 ),
rosacea ( Fig. 9-3 ), and port-wine stains. It is a valuable ad-
junct following ablative and nonablative procedures with very
Skin Camoufl age
Diedre A. Steinman and
Howard K. Steinman
C H A P T E R
9
P A R T 2
KEY POINTS
■ Skin camoufl age (SC) is very useful for medical and
surgical patients and is particularly well suited for
cosmetic surgery.
■ It immediately normalizes the appearance of chronic
skin conditions and postoperative discoloration,
reduces the ‘downtime’ from ablative procedures,
and ameliorates dissatisfaction from unintentional
bruising and wounding.
■ It has high degrees of both patient and physician
satisfaction. SC patients experience signifi cantly
improved senses of well-being and quality of life.
Physicians experience decreased anxiety from
unintentional discoloration.
■ SC has negligible risk and requires minimal offi ce
and storage space.
■ It is easy to provide in an offi ce setting.
■ Training is readily available.
high degrees of patient satisfaction. SC permits patients to re-
turn to public activities days sooner after surgical procedures,
and quickly restores the appearance of patients unintention-
ally and unexpectedly injured by nonablative treatments
( Figs 9-4 , 9-5 ).
Dedicated postsurgical camoufl age makeups (CMs) are
highly specialized, and waterproof preparations that can be
safely applied to healing skin as soon as it has epithelialized.
They mask postsurgical incisions, erythema, bruising, and
pigmentation. In recent years, easier to apply mineral make-
ups (also called mineral cosmetics,) are often being used to
minimize the impact of medical macular changes and post-
surgical skin conditions, when the epidermis has not been
injured.
Patients seek cosmetic surgery and often desire dermatol-
ogy care for appearance improvement. The singular benefi t
of SC is that it improves appearance immediately. The physi-
cian’s goal is to improve conditions prudently, safely, and effec-
tively over time. Regardless of the cause, duration, symptoms,
or prognosis, patients want appearance improvement as soon
as possible, with minimal ‘downtime.’ ‘Downtime’ can be de-
fi ned as time away from work and out of the public eye caused
by visibly healing skin. Camoufl age makeup provides this
immediately upon application, early in the treatment course.
There is a signifi cant trend in cosmetic surgery toward non-
ablative procedures to avoid downtime. Even when ablative
procedures would be more effective, patients and physicians
often prefer less rapidly effective, nonablative procedures to
avoid ‘downtime.’ Incorporating SC permits cosmetic sur-
geons to recommend and perform surgically invasive and
ablative procedures, because it allows patients to reduce and
more accurately schedule their expected downtime ( Fig. 9-6 ).
SC is also very valuable for many other patient concerns
( Table 9-1 ).
The incorporation of SC is very valuable for treating post-
treatment discoloration, for use between surgical revisions,
after traumatic injuries, and for chronic macular conditions.
This chapter will discuss the types of CMs, their use for sur-
gical and medical patients, and how to incorporate makeup
services into a cosmetic surgical practice.

108
Chapter 9
Cosmetic surgery procedures and techniques
A
B
Fig. 9-1  Vitiligo treated with paste camouflage makeup.
A
B
Fig. 9-3  Rosacea treated with crushed mineral camouflage makeup.
A
B
Fig. 9-2  Melasma treated with cream ­mineral
concealer and crushed mineral camouflage
makeup.

109
Skin camouflage  •  Chapter 9
A
B
Fig. 9-4  Unintentional pulse dye laser-induced purpura treated with paste camouflage makeup.
A
B
Fig. 9-5  Persistent generalized erythema,
3 weeks after ablative facial laser surgery.
Treated with paste camouflage makeup.
A
B
Fig. 9-6  Ecchymoses from blepharoplasty corrected with paste camouflage makeup as a scheduled treatment 7 days after surgery.

110
Chapter 9
Cosmetic surgery procedures and techniques
Background and history
Camouflage makeups were developed in the early twentieth
century when movie makeups were modified to mask the
severely disfiguring scars of war victims. Max Factor ­developed
the first movie foundations to allow flawless, natural-looking
complexions under intense studio lighting. He is credited with
coining the term ‘makeup’ and developed the ‘color harmony
principle’ of tailoring makeup colors to the wearer’s natural
skin, eye, and hair colors. He worked with plastic surgeons
to create makeups to camouflage the scars of movie actors
injured in the war and other war victims.
Lydia O’Leary, born with a facial port-wine stain, devel-
oped Covermark in 1928. This helped SC gain legitimacy as
a medical treatment, especially in Great Britain.
During World War II, Harold Gillies and Archibald
McIndoe, pioneering British plastic surgeons, helped develop
treatments for the horrific burn injuries, suffered particularly by
fighter pilots. Dr. McIndoe encouraged recovering, ­hospitalized
patients to wear normal clothing and venture out in public
­during their long convalescences. He appreciated that effective
SC would greatly help patients’ reintegration into society.
Eve Gardiner, of Max Factor’s London Salon, pioneered
many SC techniques for Dr. Gillies’s patients and later
helped found the SC programs of the British Red Cross.
Gillies enlisted Thomas Blake to formulate colored camou-
flage creams, still widely prescribed as Veil Cover Cream.
In the United States, Elizabeth Arden created ‘scar cream’
during World War II and actively toured hospitals after
the war promoting her CM line. Since then, Keromask,
Dermacolor, and Dermablend have also become widely
used CM lines.1
In Great Britain and other countries, SC therapy by
­hundreds of formally trained therapists is an integral part of
inpatient and outpatient medical care. The British Red Cross
currently has 16 formal trainers and more than 280 ­volunteers
delivering SC therapy in hospital dermatology departments
and other outpatient settings.2 Founded in 1985, the British
Association of Skin Camouflage has offered compr­ehensive
basic courses in SC and has provided an active professional
setting for continuing education.1 The British National
Health Service currently offers Covermark, Veil, Keromask,
Dermacolor, and Dermablend by physician prescription.
In the United States and Canada, there are no national
­organizations for SC therapists and no systematic integration
of SC into the practice of medicine. Only very few medical
institutions and physician practices integrate SC into their care.
Several makeup manufacturers offer training specific to their
line. A small number of makeup artists have offered compre-
hensive training in SC therapy. These thought leaders, including
Lee Graff, Christine Heathman, Nancy Ogden-West, Victoria
Raynor, Maurice Stein, and Marvin Westmore, have organized
formal courses and published in peer-reviewed medical journals.
Like Max Factor, Westmore is a movie and television makeup
artist whose school routinely teaches formal courses in SC.
Basic science clinical studies
A limited number of studies have confirmed that disfig-
ured patients receiving CM therapy experience significantly
improved senses of well-being and quality of life. Well known
since Dr. McIndoe’s efforts to mainstream his recovering
patients, it has been said (by Christine Heathman) that CM
‘acts first on the patient’s skin, then on the patient’s psyche,
then on the attitude of others towards the patient.’ We would
add that it then acts on the attitude of the patient and others
towards the procedure and surgeon.
Aydogdu et al.3 studied rhinoplasty and blepharoplasty
­patients, half receiving camouflage therapy and half not.
Using the State-Trait Anxiety Inventory Test, results showed
the group receiving makeup training experienced significant
psychological benefit.
Holmes et al.4 reported a multicenter quality of life study
of patients before and 1 month after their first visits to CM
clinics. Using the Dermatology Life Quality Index, they
found significant improvements in quality of life indices with
­treatment
Aside from psychological benefits, there is only very limited
evidence that CMs impart beneficial effects to diseased or heal-
ing skin. Some newer CMs contain live yeast cell ­derivatives
that may improve oxygen absorption, thereby increasing the
rate of wound healing.5
Table 9-1  Uses of camouflage makeup
Ablative procedures
  Chemical peels
  Laser resurfacing
  Brow lifts
  Blepharoplasty
  Rhytidectomy
  Neck lifts
  Fat transfer
  Face and neck liposuction
Accidental discoloration after nonablative procedures
  Laser and light treatments
  Injection procedures: fillers and botulinum toxin
  Epidermal and superficial chemical peels
After excisional and reconstructive surgery
Between surgical revisions
Fixed scars from surgery or trauma
Acute and chronic macular dyspigmentation
  Scars
  Birthmarks (vascular and melanocytic)
  Melasma and postinflammatory hyperpigmentation
  Vitiligo and hypopigmentation
  Rosacea

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Skin camouflage  •  Chapter 9
Types of camouflage makeup
The characteristics of the ideal CM are listed in Table 9-2.
Dedicated postsurgical camouflage preparations are de-
signed for application to newly epithelialized skin. They are
oil- or cream-based with a pigment content of up to 45–50%.
By comparison, conventional liquid makeup contains no more
than 10–15% pigment. Mineral makeups are made from natu-
rally occurring earth minerals. Some are primarily composed
of crushed minerals mixed with other inorganic pigments
to create specific colors. Others contain crushed minerals
in combination with zinc oxide, titanium dioxide, bismuth
­oxychloride, iron oxides, and others ingredients.
Paste makeup
The first makeups used for camouflaging disfigurements were
in paste form, derived from heavy theatrical makeups. These
formulations adhere to newly epithelialized skin, as well as
acrylic, silicone, and rubber prostheses. They can also act
as a filler substance to fill in small indentations. The current
formulations are nonirritating, with no known contraindica-
tions for patients being treated with concurrent oral or topical
medications.
The extreme opacity of paste formulations make them well
suited to correct a variety of conditions. They are ­especially
useful for camouflaging abnormal tones contrasting sharply
with adjacent normal skin (e.g. bruises, vitiligo, and port-
wine stains) (see Fig. 9-1.) Because their color pigments are
highly concentrated, excellent normalization of tones and
good ­preservation of natural skin textures (such as pores) can
be preserved with very light applications.
The paste formulations, applied correctly, can be water-
proof and can be applied to all parts of the body. Off the
face, they can be ‘set,’ for long duration of use, by applying a
fixing spray (Fig. 9-7).
Mineral makeup
The availability of high-quality mineral makeups has greatly
enhanced the practice of SC therapy. They are significantly
easier to apply and are often very effective. Their ­development
has changed SC in a way analogous to how nonablative treat-
ments have revolutionized cosmetic surgery.
Mineral makeups are crushed inert minerals in powder
form. They are non-comedogenic, hypoallergenic, and ­water
resistant. They may be unsuitable early in the ­postoperative
course of ablative procedures, because the skin must be
­completely epithelialized, dry to the touch, and no longer
­requiring healing ointments.
Mineral makeups are much easier to apply than paste
­postsurgical makeups, making them much more ‘user friendly’
for patients and less-trained office personnel. They provide
complete coverage and are currently the makeup of choice
for erythema following chemical peels and laser resurfacing
(once epithelialized), acne erythema, acne rosacea, melasma,
facial lentigines, and postinflammatory hyperpigmentation
(see Fig. 9-2).
Mineral makeup can be applied with a brush for a light,
natural finish and a sponge for heavier concentrations. It
can also be mixed with water to make a highly concen-
trated concealer, useful, for example, for under-eye dark cir-
cles. They may be mixed with sunscreens to make a tinted
sunscreen.
Liquid makeup
Liquid makeups, because their formulations lack opacity,
are not commonly used for SC. Until recently, postsurgical
patients were often cautioned to avoid liquid makeup for up
to 3 weeks post-treatment, because some formulations con-
tained alcohol-based preservatives that might cause irritation
and raise the risk of infection.
Liquid makeups sold in retail settings lack staying power.
They cannot conceal all day, because they do not contain
­sufficient amounts of pigment and are usually water-based.
One silica gel-based liquid foundation that uses live yeast
cell derivatives (also used in postsurgical and burn prepara-
tions) may help to heal postoperative skin while camouflaging
erythema and light bruising. The authors have found it useful
for application immediately after unintended ­erythema and
bruising from light source and injection ­treatments.
Discussion
Indications
Camouflage makeups normalize macular changes, as summa-
rized in Table 9-1. They are used after planned incisional and
ablative procedures and after accidental, unexpected discol-
oration from trauma and procedures.
Benefits
Offering makeup services is associated with negligible risk,
minimal cost, minimal office space, no physician time, and
high patient satisfaction. It imparts instant appearance
improvement and decreased patient, doctor, and staff anxiety
and permits the use of more ablative procedures with contin-
ued patient satisfaction.
Table 9-2  Characteristics of the ideal camouflage makeup
Easy to apply and remove
Adheres to smooth, pore-less areas
Can fill in small contour changes
Long lasting
Heat and muscle-movement resistant
Waterproof and sweat proof
Non-comedogenic
UV protection

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Cosmetic surgery procedures and techniques
Limitations
Camouflage makeups cannot mask three-dimensional condi-
tions such as focal edema, keloids, acne scars, and deep fur-
rows (see Fig. 9-7). They are also incompletely effective for dark
bruising, smooth texture changes, and scars with an absence of
hair and pores. Their use requires a specially trained provider
while providing no direct or significant economic benefit.
Importance of makeup
Many (primarily male) physicians do not appreciate the impor-
tance of makeup to their patients. For many patients, makeup
is an integral and essential part of their daily grooming, and
its application often requires a significant time commitment.
For them, the opposite of not wearing makeup is not ‘looking
natural.’ For them, not wearing makeup means they are incom-
pletely groomed and dressed.
Many physicians ask patients to present to the office with-
out makeup or to remove it before examination and treat-
ment. When these patients arrive or must leave the office not
wearing their makeup, they feel incompletely groomed and
uncomfortable about their appearance. (Imagine the feeling
of arriving at a formal-dress affair mistakenly wearing casual
attire.) Consider how these patients feel having to return to
public activities still bruised, red, or hyperpigmented. Further,
consider how they feel when they are accidentally and unex-
pectedly discolored from a procedure and must immediately
return to public activities (see Figs 9-4, 9-5).
Most patients have limited training in makeup application,
having learned techniques from relatives, friends, sales personnel,
magazine articles, and television programs. They have no experi-
ence and no makeup to mask their injured or discolored skin.
Physicians and patients also often have very different mind-
sets during postoperative visits. Physicians see expected swell-
ing, erythema, bruising, oozing, crusting, sutures, and the
patients’ anxiety as ‘normal.’ Despite meticulous preoperative
counseling and postoperative reassurance, patients do not feel
‘normal’ and are often ill-equipped, emotionally or physically,
to deal with their appearance. Their anxiety is often exacer-
bated by the fact that physicians usually only show completely
healed ‘after’ pictures during consultations, presentations, in
brochures and advertising, and on their web sites. Interim
pictures showing the expected swelling and discoloration are
seldom, if ever, presented.
Many surgeons recommend that healing patients purchase
a green-tinted concealer or camouflage product at a cosmetic
retailer. Green-tinted concealers correct reds to tans that rarely
match the patients’ normal skin; their discoloration is altered
but incompletely corrected or camouflaged. Patients already
anxious about their appearance are very uncomfortable going
to the very public cosmetic counter, where the bright lights ac-
centuate their skin discoloration. Once there, the perfectly made
up sales personnel are usually poorly trained and disinclined to
apply makeup to the patients’ visibly damaged skin. SC requires
careful instruction and support in a much more private, sup-
portive setting than at a retail cosmetics ­counter. This is why
effective camouflage services are best when office/clinic based.
The paramedical camouflage makeup
­therapist
Camouflage makeup therapists (CMTs) are highly skilled
makeup artists or estheticians, trained to understand the
unique psyche of disfigured patients, surgical procedures, skin
A
B
Fig. 9-7  Fifteen-year-old girl with scarring after emergency abdominal surgery treated with paste CM.

113
Skin camouflage  •  Chapter 9
conditions, skin care, and proper postoperative care. When
working in a doctor’s office, CMTs have greater credibil-
ity, demonstrate their surgeon’s concern, receive important
patient history (especially concerning the patient’s psycho-
logical state and compliance with postoperative care), and can
recommend additional services.
They are an asset in patient relations, spending consider-
able time with the postoperative patient. CMTs reassure the
uncertain, red, peeling, crusted, bruised, or still wrinkled
­patients that their healing process is normal and that they
can expect a good result.
Procedures and Techniques
Pretreatment considerations
Matching and counseling
In preparation for procedures that will discolor and cause
downtime, it is beneficial for patients to consult with the
CMT preoperatively to match the correct shade of CM to
their native skin tones. After full-face procedures, normal skin
will not be present for matching. In some cases, the correct
makeup color will not be on site and must be ordered. Patients
are instructed to bring their own makeup (lipstick, blush, eye
shadow) to their postoperative makeup appointment to better
normalize their looks.
The CMT preoperatively assesses the patients’ knowledge
and preconceptions about makeup and their regular use of
makeup. Patients who do not use makeup require greater
preparation to ensure they have reasonable expectations about
their postsurgical SC appearance.
The consultation permits the patient to view the CMT’s
portfolio of before and after SC pictures of patients who have
undergone similar procedures. The CMT’s ‘before’ pictures
show the appearance of patients 1 week postoperatively. They
are the emotive ‘after’ pictures, seldom shown in surgeons’
portfolios, brochures and web sites. The CMT’s ‘after’ pic-
tures show the immediate benefits of SC. Thus, the CMT
helps psychologically prepare the patient for their appearance
while healing. The CMT reassures patients that the CMT
will be there to normalize the patients’ appearance at the post­
surgical makeup session.
Photography
It is important to obtain pre- and post-SC photographs.
Patients commonly forget how they appeared before the CM
application and may not be accepting of their ­appearance
wearing CM. Their before and after pictures provide strong
positive reinforcement of SC’s benefits. The CMT’s portfolio is
also very useful with patients who are accidentally ­discolored.
They are usually anxious and upset, and may not otherwise
appreciate and accept the SC being offered to them.
Postoperative consultation and makeup
application
The goal of the postoperative consultation is to teach patients
how to apply their new and often very different makeup at
home. The CMT must also teach the patient how to vary the
CM application over time as the ­unnatural colors ­lighten.
Patients must, and usually do, leave the ­ session pleased
with their appearance and confident that they will be able
to ­reapply their new makeup. Detailed written instructions
and the availability of the CMT to answer questions are
essential.
The postoperative makeup session is scheduled for when
complete epithelialization is expected, usually 7–10 days post-
treatment. CM is not suitable for crusted and denuded skin
and can only be applied when the skin has completely epi-
thelialized and sutures have been removed. Patients, anxious
to return to public activities, may pressure their surgeon and
CMT to provide makeup while oozing and crusting are still
present, but results of SC under these circumstances are usu-
ally suboptimal. When applied after epithelialization, many
patients, especially those healing after chemical peels or la-
ser resurfacing, report that the highly pigmented camouflage
creams and powders make their skin feel better with less burn-
ing and/or itching.
The postoperative session is when the CMT’s knowledge
of psychology and postoperative healing is vital. Because
the patient and CMT have met previously, there is an estab-
lished rapport, and the CMT has greater credibility. Despite
even meticulous preoperative preparation, including the
CMT’s graphic pictures, many patients are surprised and
upset by their appearance. They are often more likely to
express their true concerns to the CMT than to the ­surgeon.
As they ­ apply the makeup and teach its proper use, the
CMT encourages and reassures anxious patients, and as-
sesses whether they are complying with their postoperative­
care regimen.
The CMT’s psychology and makeup skills are of even
greater importance, and more challenged, when treating
­patients accidentally discolored from nonablative procedures.
Although they often affect a tolerant, forgiving demeanor to
the physician, patients are usually extremely concerned about
their appearance and about how they are going to cope with
their normal public activities. The CMT’s interpersonal,
teaching, and makeup skills very often correct the visible flaws,
relieve, and reassure the patient, while preserving a positive
doctor–patient relationship.
It should now be evident that SC is best offered in a medical
setting as an integrated part of routine surgical and patient care.
The specialized skills of the CMTs and their CM can hardly be
duplicated by cosmetic sales personnel in a public, retail setting.

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Cosmetic surgery procedures and techniques
Techniques
There are three basic techniques for camouflaging skin defects:
concealing, color correcting, and contouring. ­ Concealing is
­hiding blemishes and bruises by completely ­ covering them
with makeup. Color correcting is neutralizing red, blue, or
­yellow tones to more natural tones of ­complimentary colors
(e.g. using green to correct red tones.) Contouring is creating
the ­ illusion of highlights and shadows to disguise ­ swelling.
­Contouring ­creates dimension using light and shadow (lighter
areas appear to come forward, while darker areas recede).
Initial steps for all forms of camouflage
• Determine if the skin has completely epithelialized and
gently cleanse. Apply a sunscreen-containing moisturizer to
hydrate the skin.
• Evaluate the skin’s texture (oily, dry, and sensitive) and the
entire face for its color values and light/dark values. Next,
examine the areas to be corrected and determine their
color and light values. These will determine which form of
makeup (e.g. paste, liquid, mineral) is most suitable as well as
the proper application technique.
• Color matching: Match the correct CM color using normal skin
closest (preferably adjacent) to the area to be camouflaged.
The makeup color that ‘disappears’ into the adjacent normal
skin color is the correct selection.
Applying paste-type camouflage makeup
The basic steps for applying paste-type makeup are summa-
rized in Table 9-3. Some makeup brands offer a very wide
variety of shades that match virtually any skin tone. Others
offer fewer choices, requiring the CMT to custom-blend two
or more tones or use a stippling of one color over another to
best match the patient’s skin.
Crushed mineral foundations
The basic steps for crushed mineral foundations are summa-
rized in Table 9-4. When using crushed mineral foundations,
it is important to ensure that the skin is dry to the touch
before the makeup is applied. If not, a light dusting of rice
powder or finely milled loose facial powder will prepare the
skin.
Table 9-3  Paste-type makeup application techniques
Warm a small amount of the paste on the back of the hand, thinning it and allowing a more measured amount to be applied.
Apply the makeup in a thin layer using a finger, makeup sponge, or foundation brush.
Excess makeup can be blended and thinned with a clean sponge dampened with an oil-free moisturizer or sunscreen.
The edges of the field are blended with a dry sponge using a dabbing motion.
A stipple sponge (with various pore sizes) can also be used to replicate sun damage, beard shadows, and other skin variations.
Shading for beards, moustaches, and eyebrows is applied using darker colors of makeup or makeup pencils.
When the right color match, application, and blending have been achieved, a liberal amount of fixing powder is applied using
a clean powder puff.
Allow 10–15 minutes for the makeup to set, to ensure that the product will be waterproof and rub resistant.
Then gently dust off the excess powder with a large, soft powder brush using downward strokes.
A light ‘mist’ of mineral water will make the finish look less matte and offers an additional step in setting the foundation.
Table 9-4  Mineral makeup application techniques
Dip a soft kabuki-type makeup brush into the crushed minerals and lightly tap off the excess.
Use a swirling motion to apply the crushed minerals, as this delivers a light coverage.
Determine which areas need more coverage and use a dry makeup sponge or soft foundation brush to apply another layer of the
minerals.
When the color and coverage is satisfactory, ‘buff’ the face with small amount of foundation using the kabuki brush. This will
remove excess minerals, bring out their natural glow, and leave a more natural-looking finish.
If desired, a light dusting of either rice powder or finely milled loose facial powder will finish the look and make it last longer. This is
especially beneficial for patients with oily skin.

115
Skin camouflage  •  Chapter 9
Additional benefit of offering makeup
services
In addition to procedural therapy, cosmetic surgery ­practices
commonly offer cosmeceutical and skin care products. They
offer a range of cleansers, toners, general and specialty mois-
turizers, fading creams, cosmeceutical ‘rejuvenation’ products,
and sometimes prescription products. Remarkably, very few
also offer makeup, the only remaining product their patients
may require to complete their facial grooming. After SC and
CMTs are incorporated into a cosmetic ­ surgery practice,
very little additional effort is needed to incorporate standard
makeup­ into the practice. The office CMT and other staff
(especially estheticians) can then completely coordinate a
patient’s entire facial skin care regimen. This is especially help-
ful when the cosmetic surgeon is also caring for the patient’s
facial dermatology concerns.
REFERENCES
1. [Anonymous]. A ‘potted’ history of skin camouflage. Available: http://

2. [Anonymous]. Skin camouflage service – a brief history. Available:

3. Aydogdu E, et al. Postoperative camouflage therapy in facial aesthetic
surgery. Aesthetic Plast Surg 2005; 29(3):190–194.
4. Holme SA, Beattie PE, Fleming CJ. Cosmetic camouflage advice
improves quality of life. Br J Dermatol 2002; 147(5):946–949.
5. Bentley JP, et al. Peptides from live yeast cell derivative stimulate wound
healing. Arch Surg 1990; 125:641–646.

HISTORY AND SCIENCE
Cutaneous basic science, anatomy,
and physiology
In order to understand the beneficial effects of topical treat­
ments on photoaged skin, we must first gain an understand­
ing of the alterations that occur as a result of chronic sun
Chemical Peels
Eric F. Bernstein
C h a p t e r
10
p a r t 2
Key Points
n History: The development of various peeling agents
is discussed and the research that led to using
topicals to alter the dermis.
n Science: In order to understand how we can remodel
the dermis to improve photodamaged or scarred
skin, we must first understand the composition of
normal skin. Once we understand the composition
of normal skin, an understanding of the alterations
that take place due to chronic photodamage is a
fundamental requirement prior to undertaking a
treatment to restore a normal epidermis and dermis.
n Studies: A body of literature exits which leads to
our understanding of the way that remodeling takes
place following a chemical peel.
n Discussion: How best to incorporate peeling agents
into a regimen for skin rejuvenation requires a basic
understanding of skin anatomy and physiology,
the effect of photoaging and dermal remodeling in
response to inflammation such as acne, and the
wound healing response to various peeling agents.
exposure. Most of the changes we attribute to chronological
aging actually result from long-term sun exposure. To illus­
trate this fact, one can compare the pigmentary alterations,
sallow color, fine lines, and wrinkles of sun-exposed skin to
the smooth, supple, sun-protected skin on the same individual.
Our skin attempts to protect itself from the effects of chronic
sun exposure via a number of mechanisms. These include our
baseline melanin content that responds with an increase in
synthesis and deposition of melanin in response to sun expo­
sure, as well as our endogenous means of preventing oxidative
damage. As much as half or more of the photodamage that
occurs may result from oxidative mechanisms. Our natural
defenses against oxidative damage include superoxide dis­
mutase, glutathione-based systems, and the antioxidant vita­
mins C and E. As we age chronologically and gain cumulative
damage from repeated sun exposure, these systems begin to
fail. As a result of the decline in our defenses and repeated
assaults on our cellular DNA from the sun, both the epidermis
and dermis start to show signs of chronic photoaging.
The epidermis
Clinically, the epidermis in sun-damaged skin may demon­
strate irregularities in pigmentation including ephelides and
solar lentigines. In addition, damage to keratinocytes leads to
actinic keratoses. The viable epidermal layer in photoaged skin
becomes hypertrophic compared with similar sites in the same
individual. However, with severe photodamage, the ­epidermis
will eventually become extremely atrophic. Although epider­
mal alterations resulting from chronic photodamage may be
quite apparent due to the pigmentary changes that occur and
their superficial location, the most striking alterations result­
ing from chronic sun damage occur in the dermis.
The dermis
The dermis is composed of a number of extracellular matrix
molecules that supply the stroma for the resident cells of the der­
mis and the dermal vasculature. The viable and nonviable com­
ponents of the dermis interact extensively to maintain a healthy

118
Chapter 10
Cosmetic surgery procedures and techniques
environment in the skin. The extracellular matrix includes col­
lagen that provides strength to skin, elastic fibers that impart
extensibility and resilience to skin, and the glycosaminoglycans
(GAGs) and proteoglycans that serve a number of functions
including maintaining the integrity of basement membrane
zones and maintaining dermal hydration.
Collagen
The principal structural component of skin is collagen.
­Collagen composes approximately 80% of the dry weight of
non-sun-­damaged skin.1,2 The triple helix configuration is
characteristic of the collagen molecule and forms as a result
of the amino acid sequence of the collagen chains. This
sequence is the Gly-X-Y sequence where Gly represents the
amino acid, glycine, and the X and Y positions are frequently
the amino acids proline and hydroxyproline.1,2 Together with
vitamin C, hydroxyproline stabilizes the triple helical portion
of the collagen molecule.3,4
The various collagens are named with roman numerals in
order of their discovery. The most abundant type of colla­
gen in adult skin is, by far, type I collagen. Type I collagen
is the main structural protein in the entire body. The three-
­polypeptide chains that form the triple helix for collagen
fibrils are two identical α1(I) chains and a third distinct α2(I)
chain. Collagen is deposited by the dermal fibroblasts, which
are constantly breaking down and regenerating collagen,
the steady state of which is the phenotype for skin. External
­factors such as wounding or sun exposure can alter the steady
state amount and arrangement of collagen fibers.2,5
Collagen formation involves a number of steps. The first
steps occur within the fibroblasts, with further refinement of
the collagen molecule occurring in the extracellular space.
Initially, transcription factors bind to the promoter region of
the collagen DNA. A mirror of the collagen DNA template
is formed, resulting in collagen messenger RNA (mRNA).
Following transcription, post-transcriptional modification of
collagen mRNA takes place where introns are removed. Fol­
lowing this, procollagen molecules are synthesized and form
the triple helix due to their Gly-X-Y structure. The procolla­
gen molecules are then released from the cell to the extracel­
lular space. These molecules contain nonhelical N-terminal
and C-terminal domains. These domains are then cleaved
from the procollagen molecule, resulting in the formation of
more mature type I collagen. The fibrillar structure of a col­
lagen molecule is quite characteristic when viewed by elec­
tron microscopy as a banding pattern that has a periodicity of
68  nm.1–3,5 Lysyl oxidase then provides further strength to the
collagen molecule by deamination of lysyl- and hydroxylysyl-
residues.6,7 Immunoperoxidase staining for the N-terminal
and C-terminal domains of procollagen are often used as an
indicator of new collagen production. Since the dermis is
composed of 80% collagen, identifying new mature ­collagen
can be difficult. Thus, these components of the procolla­
gen precursor molecule are often used as indicators of new
­collagen formation.
Type III collagen is the second most abundant type of col­
lagen found in adult skin. Because it is present in large quanti­
ties in fetal skin, type III collagen is also known as fetal collagen.8
Although abundant in fetal skin, it comprises only one-seventh
of the total collagen in adult skin. Type III collagen is com­
posed of three identical chains referred to as α1(III) chains.
As is typical for all collagen molecules, these chains arrange
themselves in the prototypical triple helix configuration. Type
III collagen is highly abundant in extensible tissues including
the gastrointestinal tract, arteries, and skin.2,5,9 Type III col­
lagen fibers associate with type I collagen fibers and may play
a role in the formation of the latter. Also possibly indicative of
its role in assisting mature collagen fiber formation is its pres­
ence in early healing of wounds.10 Type III collagen is the first
type of collagen to appear in a healing wound.
In addition to serving as a structural protein in the der­
mis, collagen fibers also serve as components of the basement
membrane zone separating the epidermis and dermis. Type IV
collagen helps form the complex barrier that facilitates trans­
portation of nutrients and waste products through the dermal–
epidermal junction. Type IV collagen has interruptions in the
triple helical domain that are thought to confer flexibility on the
type IV collagen molecule. In addition, type IV collagen forms
a scaffold for the incorporation of other extracellular matrix
components.11 Type VII collagen is also a major component
of the basement membrane zone. Type VII collagen forms the
anchoring fibers that help attach the epidermis to the underly­
ing dermis.12–14 The role of these fibers is well illustrated by the
hereditary disorder dystrophic epidermolysis bullosa.14 In this
disorder blisters form deep in the basement membrane zone in
persons with mutations of type VII collagen. Other collagens
such as type VI collagen and the FACIT (Fibril-Associated
Collagen with Interrupted Triple helices) may help form type I
collagen fibers as well.15–17 Decorin, a small chondroitin sulfate
proteoglycan, is found in association with collagen fibers.18,19
It is thought that decorin may contribute to the final arrange­
ment of collagen fibers within skin.
Elastic fibers
Elastic fibers confer the ability to stretch and recoil to skin
and other organs (Fig. 10-1). Despite their prominent role as
a structural component of skin, they compose only 1–2% of
the dry weight of non-sun-damaged skin.20,21 Elastic fibers
are complex and are formed by a number of components,
only one of which is the protein elastin. Elastic fibers can be
compared to a bungee cord, which has a stretchy inner core
and a more rigid outer string wrapping. The inner core may
be compared to the protein elastin, while the outer wrapping
is analogous to the protein fibrillin. The fibrillins comprise a
family of highly insoluble proteins that are a component of
elastic fibers.22 In addition, the oxytalan fibers, which extend
from the superficial dermis vertically to the dermal–­epidermal
junction, are composed solely of fibrillin.
Just as decorin is associated with collagen fibers, the proteo-
glycan versican is associated with elastic fibers.23–25 However,

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Chemical peels  •  Chapter 10
in contrast to the small size of decorin, versican is a very large
chondroitin sulfate proteoglycan. Versican may play a role in
elastic fiber formation and arrangement within the dermis.
Glycosaminoglycans, proteoglycans,
and fibronectin
Although GAGs comprise only a small portion of the dry
weight of skin, they are critical to its proper functioning. They
are widely distributed throughout skin as well as other ­tissues.
Because GAGs bind a large amount of water, they help to
regulate skin hydration and enable cell mobility within
skin.10,26,27 Hyaluronic acid may be found free in the dermis
unattached to a protein, or associated with a protein by the
terminal reducing sugar residue, thus forming a proteoglycan.
Proteoglycans serve a number of functions, which include
maintaining the integrity of basement membrane zones, regu­
lating cell mobility and communication, and helping to form
collagen and elastic fibers.
Decorin is a very small chondroitin sulfate proteoglycan
that is distributed throughout the dermis in association with
collagen fibers.18,19 Decorin is composed of a core protein
with only one attached chondroitin sulfate chain. Studies
have demonstrated that decorin binds to specific areas on the
collagen fibers, possibly helping to form the normal arrange­
ment of collagen fibrils and thus determining collagen fiber
diameter.19 Decorin has also been found to bind transforming
growth factor-β, and thus may regulate dermal remodeling
during normal conditions, as well as during wound healing.28
In contrast to the small size of decorin, versican is a very large
chondroitin sulfate proteoglycan with many attached chon­
droitin sulfate chains. Versican is present diffusely throughout
the superficial dermis as well as being found in association
with elastic fibers throughout the dermis. Because versican
has been found in association with elastic fibers, it is postulat­
ed that it may play a role in regulating elastic fiber formation
in a manner similar to decorin.25,28 Fibronectin is a glycopro­
tein that has an amino acid sequence, arg-gly-asp-ser (RGDS),
that is known to serve as a binding site for cells. Fibronectin,
therefore, aids in cell migration and thus may play a critical
role in skin remodeling and wound healing.29–31
Resident cells of the dermis
The cellular component of the dermis creates and maintains
the dermal extracellular matrix. When wounding occurs, these
cells respond with a healing response restoring dermal integ­
rity. Fibroblasts are connective tissue cells that are responsible
for the production of the majority of the extracellular matrix.
They help maintain the dermis by constantly remodeling the
dermal extracellular matrix. These cells respond with other
blood-borne cells to the site of an injury and help restore the
injured extracellular matrix.2,10 A healing response may be
stimulated without a break in the integrity of the skin by a
variety of agents including alpha-hydroxy acids (AHAs), retin­
oids, and laser treatment.
Mast cells are bone marrow-derived cells residing in the
dermis. These cells are capable of releasing vasoactive
cytokines that can stimulate the production of dermal extra­
cellular matrix. Mast cells are often clustered around blood
vessels and thus respond quite rapidly to blood-borne stimuli.
They are thus important participants in the wound-healing
response.32,33 Macrophages are also bone marrow-derived cells
that develop from circulating monocytes. They function as
phagocytes and produce large amounts of lysosomal enzymes.
Thus, they can help remove injured tissue and dead cells from
the site of a wound and help with the normal remodeling of
skin that occurs on an ongoing basis.30,32,34
Clinical studies
Dermal photoaging
Although most of us attribute an aged appearance to the pas­
sage of time, the majority of changes we commonly associate
with aging are due to sun damage. Severely photodamaged skin
has pigmentary alterations, wrinkles, a sallow color, and thick
Fig. 10-1  Laser scanning confocal microscopy of
­immunoperoxidase-stained skin demonstrates the close association
of a dermal collagen fiber (red) with elastic fibers (green).

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Chapter 10
Cosmetic surgery procedures and techniques
leathery appearance. Chronologically aged, sun-protected
sites show few of the changes present in photodamaged skin.
In addition, when compared under histopathologic examina­
tion, photoaged skin differs dramatically from chronologically
aged skin taken from the same individual. In contrast, chrono­
logically aged skin taken from sun-protected sites shows only
minor changes when compared with skin taken from sun-
­protected sites of much younger individuals: the dermis taken
from sun-­protected aged skin has fewer cells, blood vessels,
and elastic fibers. The reduction in the number of elastic
­fibers may be responsible for the fine wrinkling seen in sun-
protected sites.9,35–39
The microscopic changes resulting from chronic photoag­
ing are quite profound in comparison with the subtle ­changes
in sun-protected sites. Sun-damaged skin demonstrates a
massive accumulation of abnormally arranged elastic ­tissue,
termed solar elastosis (Fig. 10-2).40–42 Although the solar
­elastotic material is composed of the same constituents as
normal elastic fibers, including elastin, fibrillin, versican, and
hyaluronic acid, these constituents are arranged in a very dis­
ordered and haphazard manner.25,40–44 The elastic fibers that
normally extend vertically from the superficial dermis to the
epidermis are partially destroyed or missing in severely sun-
damaged skin. The fine elastic meshwork embedded in a rich
dermal collagen matrix is replaced by large clumps of solar
elastotic material. This elastotic material is intermixed with
a decreased number of poorly organized collagen ­ fibers.44
Although abundant, the elastic tissue affected by solar ­elastosis
is nonfunctional, and as a result sun-damaged skin loses its
elasticity and resilience.
The zone of normal-appearing collagen that separates
the solar elastotic material from the epidermis is referred
to as a ‘grenz,’ or border zone. This border zone is ­critical
to the maintenance of a healthy epidermis. Because the
epidermis lacks its own vascular supply, it must depend on
the underlying dermis for nutrients. Thus, it is quite likely
that the epidermal keratinocytes themselves secrete growth
factors that maintain the underlying grenz zone. Many of
the agents used to improve photodamaged skin exert their
effects in this superficial grenz zone of normal-appearing
collagen.
Dermal wound healing
After either an injury or a treatment that is able to stimulate
the healing response in the absence of an injury such as AHA
or retinoid treatment, the skin repairs itself with a distinct set
of interrelated events. When a wound is created in the skin,
one of the first events is formation of a fibrin clot. ­Following
this, there is an influx of circulating cells to the site of injury. In
addition, circulating fibronectin accumulates at the wound site
and provides a provisional matrix for cell migration and pro­
liferation.30,45,46 The first matrix to be formed by ­fibroblasts
attracted to the wound site is rich in hyaluronic acid.26 This
matrix of hyaluronic acid allows cell migration to further
occur, leading to the formation of granulation tissue and the
first migration of keratinocytes to cover the wound surface.
Granulation tissue is rich in blood vessels with their associated
basement membrane zones and thus contains large amounts
of chondroitin sulfate. Keratinocytes continue to migrate over
the wound surface. The first type of collagen to be seen in
a healing wound is type III collagen.30 Following this, type I
collagen is formed. Type I collagen continues to evolve and
mature, giving the wound additional strength over the ensuing
months. Although they are a component of normal skin, elas­
tic fibers may not appear until very late in the healing cycle.30
Agents used to treat photodamaged skin can stimulate this
A
B
Fig. 10-2  (A) Laser scanning confocal microscopy of immunoperoxidase-stained sun-protected skin reveals a dense collagen framework in
red with a more intense red staining of the collagen just below the dermal–epidermal junction. The epidermis is to the upper right of this panel
and is dark (unstained). The elastic fiber network is evident as green fibers forming a meshwork within the dense collagen network. (B) Sun-
damaged skin taken from the same individual reveals a dramatically altered morphology with a paucity of collagen fibers (red) intermixed with
large clumps of abnormal elastic material (green). A faint red band of collagen is evident beneath the unstained epidermis in the upper right
portion of this micrograph.

121
Chemical peels  •  Chapter 10
orderly sequence of extracellular matrix deposition even in
the absence of an open wound.
Chemical peels as a treatment
for ­cutaneous photoaging
Many patients are interested in obtaining a more youthful appear­
ance to their skin, but they are not interested in the prospect of
time away from work or looking unnatural. Since all patients
will age in unique, subtle, but meaningfully different ways, it is
useful to have a treatment option that can be custom fit to each
individual patient. Chemical peels are just such an option.
With the ability to peel the skin to differing depths, physi­
cians can choose peeling agents that take into account patient
­preference and risk tolerance, depth of cutaneous ­photoaging,
amount of photoinjury to the epidermis, dermis, and dermal
architecture, and the physician’s skill with different techniques.
It is possible to use chemical peels to treat from the most super­
ficial aspect of the skin all the way to the deepest portion of
the reticular dermis. The skill in chemical peeling comes not
only from being able to master individual techniques but from
learning how to custom fit the differing depths of ­chemical
peels to the needs of the patient.
PROCEDURES AND Techniques
Preoperative clinical considerations
Pretreatment evaluation is an important determinant of post-
treatment results when utilizing chemical peels to rejuvenate
photodamaged skin. Medical history must be obtained, with an
emphasis on history of abnormal or keloid scarring, ­perioral
herpes simplex virus (HSV) infection, past 13-cis-retinoic acid
(Accutane) therapy, prior laser skin resurfacing, as well as
medications that may photosensitize the patient. In addition,
the patient’s Fitzpatrick skin type must be assessed to help
the physician determine the potential risks of ­postoperative
­pigment alteration.
Patients with a history of perioral HSV infection can be
treated prophylactically with an oral antiviral medication,
usually beginning 1–2 days prior to the procedure and con­
tinuing for 10–14 days after. Many physicians do not routinely
use HSV prophylaxis for superficial chemical peels. Prior use
of Accutane is not a contraindication to chemical peeling, but
many physicians wait a minimum of 6 months after the last
Accutane dose before performing a chemical peel. Although
clinically unproven, the risk of abnormal scarring appears
to increase in the post-treatment period with Accutane, and
therefore a delay in injuring the skin is advisable.
Pigment alteration is a significant risk when one is using
chemical peeling agents for skin rejuvenation. Patients with
Fitzpatrick skin types I and II are unlikely to develop long-
term pigment alteration from chemical peels, but patients with
skin types III and IV often develop limited and transient (last­
ing less than 3 months) hyperpigmentation, particularly with
deeper or more aggressive chemical peels (Table 10-1). Deci­
sions to use a chemical peel for patients with Fitzpatrick skin
types V and VI should be approached with great caution, as
the risk of permanent pigment alteration is quite significant.
Superficial chemical peels can be of significant value in these
patients, but the risk of pigment alteration should be discussed
with the patient in detail prior to proceeding with treatment.
Key Points
n Preoperative Considerations: First, an evaluation of
the condition to be treated such as photodamage or
acne scarring must be undertaken. The degree of
epidermal and dermal alteration must be assessed,
and the amount of risk a given patient is willing to
take to achieve a suitable reward. Patients with very
minimal photodamage, for example, may be unwill­
ing to accept even a small amount of permanent
hypopigmentation, while a severely photodamaged
patient may be willing to live with some hypopig­
mentation in exchange for a dramatic decrease in
severe rhytides, for example. Pigmentary changes,
for example, are easier to disguise with makeup
than severe rhytides. Establishing realistic expecta­
tions requires multiple levels of repetition including
verbal discussion, consent forms with expectations
highlighted, and reminders during follow-up. Careful
patient selection to rule out those who should not
be treated, such as patients with active cold sores or
those on isotretinoin, for example, is critical.
n Techniques: Careful planning including uniform
preparation of the skin each and every time,
uniform application, and watching for signs of the
intensity of depth of peeling are critical to achieving
uniform results.
n Postoperative Considerations: Both oral and written
instructions to the patient regarding postoperative
care and signs and symptoms of problems are key.
The patient needs to know that she or he is criti­
cal to the end results of a peel. The author tells the
patients that often 50% of the results depend upon
what the physician does, while 50% depends upon
the patient following a proper postpeel care
regimen.

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Chapter 10
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Choosing the proper chemical peeling agent
There are three basic types of chemical peels: superficial,
medium, and deep. This classification system is based on
the achievable depth of penetration and clinical effect of
the peeling agent used. Glycolic and salicylic acid peels are
considered superficial, as are Jessner’s-only peels. Trichloro­
acetic acid (TCA) peels are medium-depth peels, and phenol
is used for deep peels. In general, superficial peels penetrate
down through the epidermis and may reach as far as the pap­
illary dermis. Medium-depth peels extend deeper, reaching
the deep papillary dermis and often the superficial reticular
dermis. Deep chemical peels are used to penetrate into the
mid-reticular dermis.
With this classification system in mind, the physician must
assess the depth of photoaging and wrinkles the patient is
interested in treating. Once the depth of photoaging has been
determined, the physician can help the patient choose the
proper peeling agent. As an example, it would be unwise to
perform a deep phenol peel on a patient with limited super­
ficial photodamage. The significant risks associated with the
deeper peel would not justify its use in this instance. However,
patients with significant deep photodamage may benefit most
from a deeper peel. Yet some patients may be unwilling to
accept the risks or morbidity associated with a deeper peel
and may elect to have a more superficial peel, knowing that
the benefit may be less significant. In general, it is acceptable
to perform a peel that is more superficial than the depth of
photoaging as the physician factors in patient preferences, but
it is unwise to perform a peel that penetrates deeper than the
level of photodamage. The simple premise is that the deeper
the peel the greater the risks and morbidity, and the physician
should choose the peeling agent that most closely matches the
patient’s depth of photodamage.
Procedural techniques
Alpha-hydroxy acids and glycolic acid
­chemical peels
The objective of AHA treatment and glycolic acid peels is to
stimulate a healing response without ablating the epidermis
or superficial dermis. The first report of a beneficial effect of
AHAs applied to the skin was published over a quarter cen­
tury ago.47 Despite this initial report, AHAs have only recently
been developed for widespread use. They have been used to
treat a number of conditions including disorders of keratini­
zation, xerosis, photoaging, acne, and pigmentary disorders,
and to augment other topical preparations (Fig. 10-3). For
example, AHAs have been shown to counteract the atropho­
genic effects of topical corticosteroids on both the epidermis
and the dermis.48 They act by increasing viable epidermal
thickness as well as by thickening the dermal compartment of
skin.48–50 Since both hyaluronic acid and chondroitin sulfate
are among the first extracellular matrix components depos­
ited in a healing wound, these may also be the first to be meas­
ured following AHA treatment. Indeed, application of AHAs
increases not only epidermal thickness but also epidermal gly­
cosaminoglycan deposition.48–50 Specifically, hyaluronic acid
has been shown to be increased in the epidermis of treated
skin.49 In addition, both hyaluronic acid and chondroitin sul­
fate have been shown to be increased in the dermis of AHA-
treated skin.49 Indirect evidence for the deposition of dermal
collagen following AHA treatment has been demonstrated in
human skin. Collagen mRNA expression has been shown to
be increased in glycolic acid-treated skin.51 In addition, in vitro
data suggest that collagen production may be stimulated by
application of glycolic acid.52 This suggests that mature colla­
gen may be measured after long treatment times with AHAs.
Demonstrating increases in mature type I collagen is techni­
cally difficult, since the skin is normally composed largely of
collagen. Since AHAs are applied topically, it is likely that they
exert the majority of their effects superficially. The subepi­
dermal grenz zone in sun-damaged skin is where the effect of
AHAs and agents that rejuvenate skin is often demonstrated.
This grenz zone has been shown to increase in thickness fol­
lowing deep chemical peels,53 and ablative laser resurfacing,54
treatments that rejuvenate photodamaged skin. The increase
in thickness of the subepidermal grenz zone following deep
chemical peels and laser resurfacing may indeed account for
the clinical improvement that is seen following these treat­
ments. It is quite probable that the epidermal keratinocytes
play a significant role in the extracellular matrix formation
following application of AHAs. These cells experience the
highest concentrations of AHAs and may actively secrete
growth factors to stimulate extracellular matrix production in
the underlying grenz zone.
A number of AHAs have demonstrated the ability to
increase both epidermal and dermal GAGs. Although GAGs
make up only about 0.1–0.3% of the dry weight of normal
skin, their ability to bind many times their weight in water
increases their importance in maintaining skin hydration.
As a result, small increases in the amount of epidermal and
dermal GAGs may result in relatively large increases in epi­
dermal and dermal hydration. This increase in dermal hydra­
tion may account for the increase in skin thickness measured
after relatively short treatment periods with AHAs.49,50 Skin
treated with retinoids responds in a fashion nearly identical
Table 10-1  Fitzpatrick skin types
Skin type
Tanning response
I
Always burns, never tans
II
Usually burns, tans with difficulty
III
Sometimes mild burn, tans average
IV
Rarely burns, tans with ease
V
Very rarely burns, tans very easily
VI
No burn, tans very easily

123
Chemical peels  •  Chapter 10
to AHA-treated skin. An increase in epidermal thickness and
hyaluronic acid staining, nearly identical to that measured fol­
lowing AHA treatment, has been demonstrated after retinoic
acid treatment.55 In addition, dermal GAG staining is also
increased following retinoid treatment.56 The deposition of
epidermal and dermal GAGs may in turn affect collagen and
elastic fiber formation. Thus, the early events associated with
GAG deposition may lead to collagen formation that occurs
much later. Indeed, procollagen formation has been demon­
strated following 9 months of tretinoin treatment.57 Just as
altering one extracellular matrix component may affect many
others subsequently, changes in epidermal thickness, stratum
corneum morphology, and epidermal GAG content will have
an effect on skin barrier function. Alterations in skin barrier
function may, through a cascade of interrelated steps, affect
the overall architecture of the dermal extracellular matrix.
These changes in turn are capable of changing the structure,
function, and appearance of skin.
Topical glycolic acid preparations in low concentrations
have been shown to improve photodamaged skin.58–60 Further
improvement may be achieved by using high-concentration,
short-duration applications of glycolic acid. Glycolic acid
treatments, more commonly referred to as peels, are usually
performed at weekly to monthly intervals. Improvement in
skin texture, fine wrinkling, and actinic keratoses and light­
ening of solar keratoses have been demonstrated following
glycolic acid peels with 50% glycolic acid.61 Histopathologic
examination of treated skin in these patients demonstrated
increases in epidermal thickness and an increase in the thick­
ness of the collagen layer of the dermis in some patients.61
Recently, a new short-contact peel has been described ­utiliz-
ing glycolic acid with 5-fluorouracil for the treatment of
­actinic keratoses and other signs of cutaneous photodamage.62
One study of these combination peels recorded the effect
on actinic keratoses following eight weekly applications. The
combination peel reduced more than 90% of actinic keratoses
6 months following cessation of the peels, as compared with
less than 20% clearing using glycolic acid alone. This clear­
ing occurred without the usual erythema and irritation associ­
ated with the daily use of 5-fluorouracil alone. In addition,
patients showed improvement in the cosmetic appearance of
their skin that typically results from glycolic acid treatments.62
Thus, patients utilizing this combination approach were able
to derive the cosmetic benefits of an improvement in the
A
B
C
Fig. 10-3  (A) An individual with lamellar ichthyosis has been treated on the right portion of his back with a combination of AHAs, while the left
portion remains untreated. (B) Histopathologic examination of a skin biopsy taken from untreated skin reveals a massively thickened stratum
corneum, that is absent in treated skin (C).

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Chapter 10
Cosmetic surgery procedures and techniques
­appearance of photodamaged skin, while also ­ dramatically
reducing the number of actinic keratoses (Fig. 10-4).
Glycolic acid peels are also well suited for improving pig­
mentary alterations of the epidermis. They have been shown
to increase epidermal cell turnover63 and thus may hasten
a return to normal pigmentation in hyperpigmented areas.
Studies have demonstrated the efficacy of glycolic acid peels
for improving postinflammatory hyperpigmentation in ­dark-
complexioned individuals.64–66 Melasma is one of the most
common pigmentary abnormalities occurring in women.
­Glycolic acid products accompanied by glycolic acid peels can
produce dramatic improvements in patients with ­melasma.65,67
In addition, if corticosteroids are used as lightening agents, the
ability of AHAs to negate the atrophogenic effect of ­topical
corticosteroid preparations may permit them to be used for
longer time intervals, even on the face.
Most of the claims regarding the ability of AHAs to improve
acne focus only on improving postinflammatory hyperpigmen­
tation, erythema, or scarring that arise secondary to acne.
However, glycolic acid and glycolic acid peels are extensively
used to improve acne quite successfully.68 All types of acne
have been shown to respond to glycolic acid peels. Comedonal
acne improves most rapidly, followed by papulo-pustular acne,
with nodular-cystic acne requiring the most treatments prior to
significant improvement.69 Glycolic acid peels are an ­effective
treatment for the range of acne types and have the added
­benefit of improving acne-induced postinflammatory hyper­
pigmentation and erythema, as well as improving the depressed
scars that often accompany severe acne. Daily application of
topical glycolic acid preparations combined with glycolic acid
peels is also quite effective for treating pseudofolliculitis barbae.
In addition to improving the inflammatory papules associated
with pseudofolliculitis barbae, glycolic acid peels may also help
control the associated hyperpigmentation.70 Although con­
trary to the popular opinion that glycolic acid treatment will
aggravate rosacea, many individuals with rosacea respond quite
well to glycolic acid treatment. Glycolic acid not only reduces
the papular and pustular component of rosacea but may also
decrease the associated erythema in many patients, despite fears
that glycolic acid will increase associated erythema (Fig. 10-5).
A
B
C
D
Fig. 10-4  (A) Multiple actinic keratoses and other signs of sun damage are evident before glycolic acid/5-fluorouracil. (B) Close-up of the area
shown in (A). (C) Improvement of actinic keratoses and other signs of sun damage after pulse-peels. (D) Close-up of the treated area shown in
(B). (Courtesy Dr. Bruce Katz.)

125
Chemical peels  •  Chapter 10
Complications from lower-strength glycolic acid peels are
predominantly limited to dryness and mild irritation. Irrita­
tion may also occur from application of products containing
glycolic acid or tretinoin too soon following a glycolic peel.
Transient hyperpigmentation may occur even following
­lower-strength peels in some darker-skinned or tanned indi­
viduals. This appears to be particularly true in Asian patients.
Although glycolic acid is a weak peeling agent, 70% glycolic
acid peel solutions may have a pH as low as 0.1.71 The epider­
mis is normally left intact, in contrast to deeper peeling agents
highlighted below, but significant epidermal damage evident
as crusting can occur following a glycolic peel. Complications
occasionally seen following medium-to-deep peels or laser
resurfacing such as herpes simplex activation, bacterial infec­
tion, or scarring are rare following a glycolic acid peel; how­
ever, these complications can occur after significant epidermal
damage from any therapy.
Glycolic acid treatment: technique
Common pitfalls in the administration of AHA peels include
treating patients with active herpes simplex, or those on or
recently on oral or topical retinoids. The prepeel evaluation
should go over the patient’s medical history, paying particular
attention to a history of perioral herpes virus infection (cold
sores) or unusual tendency to scar; medication list, paying
particular attention to current or previous 13-cis-retinoic acid
(Accutane) therapy; medication allergies; and any sensitivity to
AHAs or retinoids. Patients taking 13-cis-retinoic acid should
not receive glycolic acid peels, and physicians may wish to
delay starting glycolic acid peels until 6 months following a
course of 13-cis-retinoic acid treatment. In addition, use of
tretinoin cream may enhance penetration of a glycolic peel,
and thus the person performing the peel should be aware of
its use. The time a peel can be left on the skin without ­crusting
or the risk of hyperpigmentation will shorten considerably if a
patient begins using tretinoin during a course of glycolic peels.
Concomitant administration of photosensitizing oral medica-
tions should also be noted and appropriate sun protection
always used. It is also advisable to have the patient use a ­glycolic
acid lotion for approximately 2 weeks prior to administering
a glycolic acid peel. This helps create a more uniform ­stratum
corneum barrier, ensuring a more uniform peel. In addition,
it will identify patients who are sensitive to glycolic acid and
who therefore may not be candidates for higher-strength
A
B
Fig. 10-5  The erythema associated with mild rosacea (A) is decreased following use of a 10% glycolic acid lotion for 6 weeks (B).

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Chapter 10
Cosmetic surgery procedures and techniques
glycolic acid peels. Asian patients are often found to be more
sensitive to glycolic acid peels, and thus a lower concentration
than is typically used should be administered. The use of a
lower-strength glycolic acid preparation decreases the risk of
inadvertent overtreatment.
Although glycolic acid treatments are referred to as glycolic
acid peels, this moniker often gives patients the impression they
are going to be peeling for a number of days. Thus, it is more
appropriate to refer to peels as glycolic acid treatments. Glycolic
acid treatments not only help reverse the signs of cutaneous
photodamage but also improve acne scarring, as well as dra­
matically improving acne itself. However, glycolic treatments
for acne need to be administered at monthly intervals or the
acne may recur. Thus, to control even severe acne in patients
who may not tolerate 13-cis-retinoic acid, monthly glycolic
peels are a viable alternative. Peels for photodamage may be
administered at monthly intervals for 3 or more months and
then spaced out less frequently according to the individual
patient’s skin response and lifestyle. As the skin responds to
the glycolic treatments, the treatment time necessary to reach
the desired end point of uniform erythema usually increases
from session to session. This will not happen if the patient uses
tretinoin for the first time during a course of glycolic treat­
ments. Tretinoin use dramatically shortens the time to reach
the desired end points. This effect may be exploited in patients
whose treatment times exceed 5 minutes. Adding tretinoin
will often shorten the treatment time significantly and allow
continued clinical improvement without excessive treatment
times. Administering peels at intervals less than 1 month will
also result in a decrease in the treatment time, possibly because
the epidermis and the stratum corneum have not had enough
time to respond to the peel. In addition, during the drier win­
ter months, treatments times may decrease, and a clinician
should be aware of this potential in order to end a peel before
skin whitening or epidermolysis takes place. Epidermolysis, or
superficial whitening of the skin, is probably the clinical sign
that low pH glycolic acid solution has reached the keratinoc­
ytes and is denaturing protein. This will result in superficial
crusting of a small percentage of the whitened area.
Prior to performing a glycolic treatment, cleanse the skin
with a nonirritating cleanser, followed by a mild degreasing
agent (Fig. 10-6). A degreasing agent such as acetone that
strips a considerable amount, perhaps too much, oil from the
skin may result in an uneven glycolic treatment. Areas where
glycolic acid can accumulate and cause irritation, such as the
nasal ala, lips, and lateral canthal folds should be treated with
petrolatum to prevent accumulation of glycolic acid and pos­
sible dryness or crusting. Once the skin is prepared, the gly­
colic acid is then applied. Low-strength peel solutions typically
contain 20–35% glycolic acid, while higher-strength peels uti­
lize 50–70% glycolic acid solutions. Especially when using a
high concentration of glycolic acid, administer the solution
evenly and rapidly. Rapid administration may be more easily
accomplished using a cotton ball as opposed to a brush. The
extra time it takes to cover the entire face using a brush may
result in one portion of the face receiving an uneven peel rela­
tive to the other. At the sign of a diffuse erythematous glow,
increased sensation or pain as reported by the patient, or
immediately upon any evidence of epidermolysis (skin whit­
ening), the peel should be neutralized. Often during a patient’s
first peel clinicians will neutralize the peel after a period of
2 minutes in the absence of any of these findings. A basic neu­
tralizing solution containing sodium bicarbonate is preferable
to water alone, especially when using a high-strength glycolic
acid solution. Rapid neutralization often prevents progression
of the peel during the neutralization phase, thus avoiding epi­
dermolysis and subsequent crusting. Following a glycolic treat­
ment, a bland emollient is administered to soothe the skin.
In acne-prone individuals, this step should be avoided, since
even noncomedogenic topicals can lead to the development
of acne in such patients. A pearl for treating patients with
acne is to administer the peels at regular monthly intervals.
If this interval is extended, acne will likely recur. In addition,
AHA peels are not only excellent for reducing acne, but also
for improving the postinflammatory hyperpigmentation asso­
ciated with acne.
Salicylic acid chemical peels
Salicylic acid has been used as a component of a number of
peeling agents including Jessner’s solution. In addition, it is
a common component of numerous over-the-counter acne
treatments. Recently, salicylic acid has been used in higher
concentrations as a peeling agent, predominantly for the treat­
ment of acne. A recent study investigated the effect of salicylic
acid peels for treating acne, enlarged pores and oily skin, and
pigmentary alterations in dark-skinned patients. Moderate to
significant improvement was seen in 88% of patients. Side
effects were minimal, occurring in only 16% of patients, and
were limited to crusting and hypopigmentation, dryness, and
hyperpigmentation.72 Salicylic acid peels have been intro­
duced relatively recently and may increasingly be used for the
treatment of acne. Pitfalls common to AHA peels apply to
salicylic acid peels, including the need to reduce peel times
in patients on topical retinoids, and the need to avoid peeling
patients with active herpes simplex or those on or recently on
oral retinoids.
Salicylic acid treatment: technique
Patients wash their skin before application of a pretreatment
cleanser. Common solutions contain alcohol and witch hazel
to remove surface oil and debris. Patients with very oily skin
may be treated twice with the pretreatment solution, which
is prepackaged on treated pads with one popular peel for­
mulation. The salicylic acid peel is applied with a sponge,
commonly using 20–30% concentrations of salicylic acid.
Stinging and burning may be felt during the first minute,
during which the skin begins to appear white. Mild discom­
fort may peak 2–3 minutes following application of the peel.
Whitening of the skin is complete 4–5 minutes after applica­
tion, when discomfort should be virtually gone. At this point

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Chemical peels  •  Chapter 10
A
B
C
D
E
F
Fig. 10-6  (A) Prior to performing a peel, the skin is cleansed and treated with a degreasing agent that gently removes surface oil. (B) The
­lateral canthi, nasolabial folds, and lips are treated with petrolatum to prevent pooling of the peel solution and subsequent irritation. (C) The
peel solution is applied rapidly and evenly to ensure that the entire skin surface receives virtually the same contact time with the peel solution.
(D) The peel solution is neutralized to end the peel. The bubbles present on the lip are carbon dioxide bubbles, and cessation of bubbling
signifies complete neutralization of the glycolic acid solution. Care should be taken to lift the cap to ensure no solution is left unneutralized. The
neutralizing solution is patted dry (E), and an emollient postpeel cream is applied (F). The latter step may be avoided in acne-prone individuals.

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Chapter 10
Cosmetic surgery procedures and techniques
the peel is finished without the need for neutralization. The
skin is often washed again following treatment, and a mild
lotion is applied to soothe the skin.
Trichloroacetic acid chemical peels
Trichloroacetic acid (TCA) has been widely used as a peeling
agent for a quarter century. It has been used in concentrations
ranging from 10% to 70%, most frequently as a light peel in
concentrations of 15%, 20%, 25%, and 35%. TCA peels may
be readministered after a period of weeks to months to enhance
improvement or improve skin that has been continuously
exposed to ultraviolet radiation. TCA peels have been found
to be effective at treating a number of hyperkeratotic lesions
including actinic keratoses, solar lentigines, and the signs of
photoaging.73,74 In addition to improvement in epidermal and
dermal signs of photoaging, tightening of lax photodamaged
skin, as is often seen following laser resurfacing,75 also occurs
following surface wounding with TCA.76 As is the case fol­
lowing laser resurfacing, it is unclear if skin tightening results
from normal skin contraction during wound healing or the
action of TCA on the partially damaged dermal collagen fib­
ers that are not removed during the peel procedure. Attempts
have been made to standardize the procedure of administer­
ing TCA peels to produce consistent results between patients,
as well as to minimize potential side effects. As with glycolic
peels, skin preparation is used to remove surface oil from the
skin to allow even penetration of a TCA peel.77 Because TCA
may penetrate quite deeply if used in higher concentrations,
skin preparation may be even more important than when
administering a glycolic acid peel.
A number of agents have been combined with TCA peels
to enhance penetration, ensure a more even peel, or promote
faster healing following treatment. The addition of retinoic
acid pretreatment to a TCA peel regimen may result in more
rapid healing following the peel.78 Jessner’s solution consisting
of resorcinol, salicylic acid, and lactic acid in ethanol has been
used in combination with TCA to enhance the effectiveness
of the peel while preserving its safety.74,79,80 Jessner’s solution
is commonly combined with 35% TCA. Signs of photoaging
as well as actinic keratoses have been successfully treated with
this combination.81 TCA has been combined with glycolic
acid and used as a peeling agent for nonfacial skin. One group
utilized glycolic acid gel augmented with TCA and neutralized
the peel with sodium bicarbonate solution. Care was taken to
prevent excessive skin damage by using a neutralizing solution.
The combination improved both epidermal and dermal signs
of cutaneous photoaging, with minimal complications.82
Because results may depend upon skin preparation, the
TCA itself, and other characteristics of the patient and proce­
dure, attempts have been made to standardize TCA peeling by
providing indicators of peel depth. One of the more popular
systems used is the Obagi TCA peel.83,84 TCA is mixed with
a solution containing glycerin, saponins, and a nonionic blue
color base. This mixture is thought to slow penetration of the
acid, resulting in a peel that is more easily controlled due to
the extra time allowed to reach the desired depth of damage
in the skin. The blue color base enables visualization of areas
that have been adequately covered with the TCA solution, as
opposed to using a colorless TCA solution where missed areas
may not be visible. Areas receiving more TCA than others will
appear darker blue in color. These investigators standardize
the procedure of administering TCA peels to yield more con­
sistently reproducible results. A specific concentration of TCA
is used, 15% and 20%, and a standardized volume is adminis­
tered to the skin with multiple coatings. Clinical signs of frost
quality, even blue coloration, a background pink color, and
excessive skin wrinkling when the skin is pinched are used to
estimate the depth of the peel. These signs have been shown
to correlate with healing time, and thus are presumed to cor­
relate with the depth of the peel. The peel may be repeated
two or three times 6 to 8 weeks apart.83 TCA peeling of non­
facial skin may also improve signs of photodamage, although
greater care must be taken to avoid scarring.82,85
TCA peels were introduced as a more superficial peeling
agent than the long-popular phenol peel discussed below.
Although more superficial than phenol peels as they are both
most commonly used, TCA peels still are capable of produc­
ing necrosis of the superficial dermis.86 When peeled to this
level, herpes simplex virus activation, bacterial infection, pig­
mentary abnormalities, and even scarring due to poor wound
healing are all possible. Hyperpigmentation when treating
dark-skinned or tan patients is a greater risk with TCA than
with glycolic acid (Fig. 10-7).
Trichloroacetic acid peels: technique
The skin is first thoroughly degreased with either an ace­
tone scrub or hexachlorophene with alcohol (Septisol). For
medium-depth peeling, Jessner’s solution (Table 10-2) is first
applied with either cotton-tipped applicators or 4 × 4 inch
gauze. One coat is usually sufficient to produce a light, even
frost. Some practitioners choose to use additional coats of
Jessner’s solution to increase the depth of penetration. The
Jessner’s frost is less intense than that produced with TCA
and does not cause discomfort for most patients. A pitfall
to be avoided is uneven preparation of the skin prior to a
peel. Much care must be ­taken to prepare the skin evenly.
Uneven preparation is as ­likely as or more likely to result in
an uneven result than uneven application of the peel. Oily
areas will resist ­penetration of a peel as compared to properly
degreased areas.
TCA 35% is then applied with either cotton-tipped appli­
cators or 4 × 4 inch gauze, depending on the surgeon’s pref­
erence. Even-handed application of the TCA is essential to
produce a uniform and consistent depth of peel. The color
and quality of the frost is the surgeon’s guide to peel depth
and uniformity. If inconsistencies are noted in the quality of
the frost, as can be seen with numerous actinic keratoses, addi­
tional TCA application can be carefully performed to pro­
duce the desired end point. Experience and skill ultimately

129
Chemical peels  •  Chapter 10
determine the end point of the procedure. Subtle color differ­
ences in the quality of the frost can be important clues to the
surgeon, and careful inspection, as well as a detailed preopera­
tive plan for peel depth, are imperative. Careful visualization
and good lighting throughout a peel are clinical pearls to con­
trolling the depth of a TCA peel. Treatment times during one
session may not be applicable to another one, and one should
err on the side of caution, choosing the shortest time interval
based on past experience or the clinical effect, choosing the
shortest one in each instant. One can always re-apply a peel
at a later date, but actually turning back the clock once a peel
has been left on too long is unfortunately not possible.
Iced saline compresses are applied immediately after com­
pletion of the procedure to provide comfort to the patient.
Although iced saline does not neutralize the TCA, it is an
important part of the procedure to soothe the patient’s skin.
Since TCA is not neutralized by water or saline, meticulous
application of TCA is essential to prevent overtreatment,
which can result in excessive peel depth and significant com­
plications. Application of too much TCA or Jessner’s solution
A
B
C
D
Fig. 10-7  A patient with mild-to-moderate
photodamage prior to a trichloroacetic acid
peel (A), during the peel (B), 1 day following
(C), and 1 month following the peel (D). Her
final result demonstrates improvements of the
signs of photodamage including pigmentary
­alterations, rhytides and enlarged pores.
(Photos courtesy of Alan Brackup, M.D.)

130
Chapter 10
Cosmetic surgery procedures and techniques
can be major causes of morbidity from medium-depth chemi­
cal peeling. An emollient such as Aquaphor (Biersdorf) can be
applied prior to discharge of the patient.
Erythema and edema are prominent for the first 48–72
hours after the procedure, as is the potential for discomfort.
Crusting of the skin begins as the edema resolves, and con­
tinuous application of emollients is encouraged. Crust and
exudate begin to separate from the skin with gentle ­washing
4–7 days after the procedure, and skin renewal is usually
­complete by postoperative day 10–14.
Phenol chemical peels
Phenol is one of the longest-used agents for medium-to-deep
peels. It has been in use for over a century, and in widespread
use for approximately a quarter century. Both epidermal and
dermal signs of cutaneous photoaging have been treated with
great success. In addition, phenol peels have been used to treat
facial scarring, most commonly scars resulting from acne.
Phenol has been used alone as a peeling agent, or in com­
bination with other agents. Phenol is commonly combined
with croton seed oil for peeling. Phenol alone in concentra­
tions of less than 50% fails to produce significant peeling in
the absence of occlusion.87 The addition of croton oil of up
to a maximum of 1% appears to result in the optimal clini­
cal response. Greater concentrations can result in pigmentary
alterations and other unwanted side effects.87 The most popu­
lar formula is the Baker-Gordon phenol peel, in which phenol
is combined with croton oil.87–92
Histopathologic examination of skin excised from phenol
peel patients during face lift surgery was performed 1.5–20
years following their phenol peels. Treated and untreated skin
was compared in the same specimens of excised skin. Exami­
nation of these specimens revealed a new band of collagen
2–3  mm thick beneath the epidermis, but above the abnormal
solar elastotic tissue that characterizes the dermis of photo­
aged skin.53 This border or grenz zone of normal collagen is
often present beneath the epidermis of sun-damaged skin. An
expansion of this zone results from regeneration of normal-
appearing dermis, in this case due to the administration of
a phenol peel. The presence of normal elastic fibers, often
absent in healed wounds, attests to the normal architecture of
this regenerated dermal extracellular matrix.53 Similar changes
are often demonstrated following other destructive treatments
such as carbon dioxide laser resurfacing.93 Because of their
abilities to superficially damage surface skin, deep chemi­
cal peels and laser resurfacing both improve epidermal and
­dermal signs of chronic sun exposure, including skin laxity.
Since phenol peels are most commonly used as medium-
to-deep peels, side effects are more common than with
the previously mentioned more superficial peeling agents.
Hyperpigmentation, or more frequently permanent hypopig­
mentation, are among the most commonly encountered com­
plications associated with phenol peeling (Fig. 10-8).94 Since
phenol is most commonly used as a medium-to-deep peel,
herpes simplex activation,95 bacterial infection,96 and scar­
ring96 are seen following peels. In addition, postpeel erythema
can persist for many weeks;97,98 this phenomenon is commonly
seen following carbon dioxide laser resurfacing. Phenol is
­absorbed systemically and associated with a significant risk of
cardiac toxicity. This risk can be reduced by peeling portions
of the face at a time interval of 20 minutes, to reduce the total
surface area exposed to phenol at any one time.99,100
Postoperative clinical considerations
Patients are instructed to maintain a moist environment on
their skin to facilitate and enhance wound healing following
chemical peels. The use of a bland petrolatum-based emol­
lient is usually sufficient. Patients who have had superficial
chemical peels may be able to use a medium to thick mois­
turizer in place of an emollient, but frequent application is
essential to prevent drying of the skin. The duration of use
for skin moisturizers depends on several factors, including the
rate at which a given patient heals as well as the depth of the
peel itself. In general, the deeper the peel, the longer the need
for postoperative moisturizer use.
Crusting, if present, should be carefully removed by the
patient or an assistant with gentle technique, including the use
of cotton swabs soaked in warm water. Frequent application
of moisturizers often helps to prevent crust formation. Once
reepithelialization is complete, the use of a sunscreen is rec­
ommended as part of the moisturizing routine. Prior to com­
plete reepithelialization, sun avoidance is essential. Although
superficial peels can produce a small amount of crusting and
Table 10-2  Jessner’s solution
Resorcinol
14 g
Salicylic acid
14 g
Lactic acid
14 g
Ethanol
95% to total volume 100 mL
Fig. 10-8  This patient developed permanent hypopigmentation
following a deep phenol peel. This may also occur following laser
resurfacing and may be a late complication following laser treatment.

131
Chemical peels  •  Chapter 10
epidermal loss, this is more an issue with medium and deep
chemical peels.
Erythema can persist for days to weeks depending on the
depth of the peel and the patient’s skin type. Treatment of post­
operative erythema is not necessary, but the physician should
monitor carefully, as in some cases persistent erythema follow­
ing deeper peels can be a sign of early hypertrophic scarring.
If scarring is suspected, the physician should consider the use
of a potent topical corticosteroid cream or ointment, as well as
intralesional steroid injection if the scar begins to mature.
Postinflammatory hyperpigmentation is usually a transient
element of healing following chemical peels but can be quite
troubling to the patient. Early intervention with twice daily use
of bleaching agents such as hydroquinone at a concentration of
3–4% is usually sufficient therapy. In some patients, the use of a
product containing hydroquinone and glycolic acid may be of
additional benefit. Topical agents such as tretinoin, sunscreens,
and topical steroids can also be added to the regimen. How­
ever, the most important element of treating postinflammatory
hyperpigmentation is avoiding it in the first place. Patients with
Fitzpatrick skin types IV to VI are most at risk for developing
pigment changes, and deeper peels are more likely to produce
long-term pigment alteration. Carefully matching skin type
with peel depth is an important determinant of post-treatment
complications such as long-term hyperpigmentation.
Future advances in facial resurfacing
and rejuvenation
The development of the short-pulsed and scanned carbon
dioxide lasers and the pulsed erbium:YAG lasers has revo­
lutionized facial resurfacing.75,101–105 These lasers remove
superficial layers of the epidermis or dermis while leav­
ing behind very small amounts of residual thermal dam­
age.93,106,107 The treatment effect is quite reproducible from
patient to patient, resulting in consistency and predictability
of outcomes (Fig. 10-9). Peeling agents are often used in com­
bination with laser resurfacing to diminish lines demarcating
the site of laser treatment. Superficial peeling agents such as
glycolic acid or topical tretinoin are often used prior to laser
resurfacing in an attempt to reduce complications such as
hyperpigmentation and possibly reduce healing time.
The recent popularity of nonablative resurfacing has added­
yet another modality of treatment for the signs of photoaging
and superficial acne scarring.108–111 This treatment exploits
the ability of lasers or light sources commonly used to treat
unwanted blood vessels to stimulate extracellular matrix dep­
osition without ablation of the epidermis. These lasers are fre­
quently combined with topical AHAs and glycolic­ acid peels
or tretinoin. As our understanding of the effects of peeling
agents increases, and the armamentarium of lasers for facial
rejuvenation grows, the ability to combine these modalities
should result in greater benefits for our patients.
REFERENCES
  1. Uitto J. Collagen biosynthesis in human skin: a review with emphasis
on scleroderma. Ann Clin Res 1971; 3:250–258.
  2. Uitto J, Olsen DR, Fazio MJ. Extracellular matrix of the skin: 50 years
of progress. J Invest Dermatol 1989; 92:61S–77S.
  3. Uitto J. A method for studying collagen biosynthesis in human skin
biopsies in vitro. Biochim Biophys Acta 1970; 201:438–445.
  4. Booth BA, Uitto J. Collagen biosynthesis by human skin fibroblasts,
III: the effects of ascorbic acid on procollagen production and prolyl
hydroxylase activity. Biochim Biophys Acta 1981; 675:117–122.
  5. Uitto J, Booth BA, Polak KL. Collagen biosynthesis by human skin
fibroblasts, II: isolation and further characterization of type I and
type III procollagens synthesized in culture. Biochim Biophys Acta
1980; 624:545–561.
  6. Majamaa K, Sasaki T, Uitto J. Inhibition of prolyl hydroxylation
during collagen biosynthesis in human skin fibroblast cultures by ethyl
3,4-dihydroxybenzoate. J Invest Dermatol 1987; 89:405–409.
  7. Uitto J, Lichtenstein JR. Defects in the biochemistry of collagen in
diseases of connective tissue. J Invest Dermatol 1976; 66:59–79.
  8. Epstein EH Jr. (Alpha1(3))3 human skin collagen: release by pepsin
digestion and preponderance in fetal life. J Biol Chem 1974; 249:
3225–3231.
A
B
Fig. 10-9  (A) Histopathologic examination of severely sun damaged skin demonstrates a thin band of collagen (pink) above massive clumps
of abnormal solar elastotic material (black) that characterizes sun-damaged skin. (B) Examination of a biopsy sample, taken from the same
patient after carbon dioxide laser resurfacing, reveals an expanded zone of collagen beneath the epidermis (pink) due to laser treatment.

132
Chapter 10
Cosmetic surgery procedures and techniques
  9. Uitto J, Fazio MJ, Olsen DR. Molecular mechanisms of cutaneous
aging: age-associated connective tissue alterations in the dermis. J Am
Acad Dermatol 1989; 21:614–622.
10. Clark RA. Biology of dermal wound repair. Dermatol Clin 1993;
11:647–666.
11. Timpl R. Structure and biological activity of basement membrane
proteins. Eur J Biochem 1989; 180:487–502.
12. Ryynanen M, Knowlton RG, Parente MG, et al. Human type VII
collagen: genetic linkage of the gene (COL7A1) on chromosome 3 to
dominant dystrophic epidermolysis bullosa. Am J Hum Genet 1991;
49:797–803.
13. Ryynanen J, Sollberg S, Parente MG, et al. Type VII collagen gene
expression by cultured human cells and in fetal skin: abundant mRNA
and protein levels in epidermal keratinocytes. J Clin Invest 1992;
89:163–168.
14. Uitto J, Chung-Honet LC, Christiano AM. Molecular biology and
pathology of type VII collagen. Exp Dermatol 1992; 1:2–11.
15. Castagnola P, Tavella S, Gerecke DR, et al. Tissue-specific expression
of type XIV collagen – a member of the FACIT class of collagens. Eur
J Cell Biol 1992; 59:340–347.
16. Yoshioka H, Zhang H, Ramirez F, et al. Synteny between the loci for a
novel FACIT-like collagen locus (D6S228E) and alpha 1 (IX) collagen
(COL9A1) on 6q12-q14 in humans. Genomics 1992; 13:884–886.
17. Shaw LM, Olsen BR. FACIT collagens: diverse molecular bridges in
extracellular matrices. Trends Biochem Sci 1991; 16:191–194.
18. Bianco P, Fisher LW, Young MF, et al. Expression and localization of
the two small proteoglycans biglycan and decorin in developing human
skeletal and non-skeletal tissues. J Histochem Cytochem 1990; 38:
1549–1563.
19. Fleischmajer R, Fisher LW, MacDonald ED, et al. Decorin interacts
with fibrillar collagen of embryonic and adult human skin. J Struct Biol
1991; 106:82–90.
20. Pasquali-Ronchetti I, Baccarani-Contri M. Elastic fiber during
development and aging. Microsc Res Tech 1997; 38:428–435.
21. Frances C, Robert L. Elastin and elastic fibers in normal and
pathologic skin. Int J Dermatol 1984; 23:166–179.
22. Dahlback K, Ljungquist A, Lofberg H, et al. Fibrillin immunoreactive
fibers constitute a unique network in the human dermis: immunohis­
tochemical comparison of the distributions of fibrillin, vitronectin,
amyloid P component, and orcein stainable structures in normal skin
and elastosis. J Invest Dermatol 1990; 94:284–291.
23. Tan EM, Hoffren J, Rouda S, et al. Decorin, versican, and biglycan
gene expression by keloid and normal dermal fibroblasts: differential
regulation by basic fibroblast growth factor. Exp Cell Res 1993; 209:
200–207.
24. Zimmermann DR, Dours-Zimmermann MT, Schubert M, et al.
Versican is expressed in the proliferating zone in the epidermis and in
association with the elastic network of the dermis. J Cell Biol 1994;
124:817–825.
25. Bernstein EF, Fisher LW, Li K, et al. Differential expression of the
versican and decorin genes in photoaged and sun-protected skin:
comparison by immunohistochemical and northern analyses. Lab
Invest 1995; 72:662–669.
26. Burd DA, Greco RM, Regauer S, et al. Hyaluronan and wound
healing: a new perspective. Br J Plast Surg 1991; 44:579–584.
27. Carrino DA, Sorrell JM, Caplan AI. Age-related changes in the
proteoglycans of human skin. Arch Biochem Biophys 2000; 373:
91–101.
28. Scott PG, Dodd CM, Tredget EE, et al. Immunohistochemical
localization of the proteoglycans decorin, biglycan and versican and
transforming growth factor-beta in human post-burn hypertrophic and
mature scars. Histopathology 1995; 26:423–431.
29. Clark RA. Fibronectin in the skin. J Invest Dermatol 1983; 81:475–479.
30. Clark RA. Cutaneous tissue repair: basic biologic considerations: I.
J Am Acad Dermatol 1985; 13:701–725.
31. Kubo M, Kan M, Isemura M, et al. Effects of extracellular matrices
on human keratinocyte adhesion and growth and on its secretion and
deposition of fibronectin in culture. J Invest Dermatol 1987; 88:
594–601.
32. Sueki H, Whitaker D, Buchsbaum M, et al. Novel interactions between
dermal dendrocytes and mast cells in human skin: implications for
hemostasis and matrix repair [see comments]. Lab Invest 1993; 69:
160–172.
33. Trabucchi E, Radaelli E, Marazzi M, et al. The role of mast cells in
wound healing. Int J Tissue React 1988; 10:367–372.
34. Schultz G, Rotatori DS, Clark W. EGF and TGF-alpha in wound
healing and repair. J Cell Biochem 1991; 45:346–352.
35. Daly CH, Odland GF. Age-related changes in the mechanical
properties of human skin. J Invest Dermatol 1979; 73:84–87.
36. Lavker RM, Kwong F, Kligman AM. Changes in skin surface patterns
with age. J Gerontol 1980; 35:348–354.
37. Lavker RM, Zheng PS, Dong G. Aged skin: a study by light,
transmission electron, and scanning electron microscopy. J Invest
Dermatol 1987; 88:44s–51s.
38. Escoffier C, de Rigal J, Rochefort A, et al. Age-related mechanical
properties of human skin: an in vivo study. J Invest Dermatol 1989;
93:353–357.
39. Lavker RM, Zheng PS, Dong G. Morphology of aged skin. Clin
Geriatr Med 1989; 5:53–67.
40. Kligman AM, Zheng P, Lavker RM. The anatomy and pathogenesis
of wrinkles. Br J Dermatol 1985; 113:37–42.
41. Oikarinen A, Karvonen J, Uitto J, et al. Connective tissue
alterations in skin exposed to natural and therapeutic UV radiation.
Photodermatology 1985; 2:15–26.
42. Bernstein EF, Uitto J. The effect of photodamage on dermal
extracellular matrix. Clin Dermatol 1996; 14:143–151.
43. Bernstein EF, Underhill CB, Hahn PJ, et al. Chronic sun exposure
alters both the content and distribution of dermal glycosaminoglycans.
Br J Dermatol 1996; 135:255–262.
44. Bernstein EF, Chen YQ, Kopp JB, et al. Long-term sun exposure alters
the collagen of the papillary dermis: comparison of sun-protected and
photoaged skin by northern analysis, immunohistochemical staining,
and confocal laser scanning microscopy. J Am Acad Dermatol 1996;
34:209–218.
45. Repesh LA, Fitzgerald TJ, Furcht LT. Fibronectin involvement
in granulation tissue and wound healing in rabbits. J Histochem
Cytochem 1982; 30:351–358.
46. Woodley DT, O’Keefe EJ, Prunieras M. Cutaneous wound healing: a
model for cell–matrix interactions. J Am Acad Dermatol 1985; 12:
420–433.
47. Van Scott EJ, Yu RJ. Control of keratinization with alpha-hydroxy
acids and related compounds, I: topical treatment of ichthyotic
disorders. Arch Dermatol 1974; 110:586–590.
48. Lavker RM, Kaidbey K, Leyden JJ. Effects of topical ammonium
lactate on cutaneous atrophy from a potent topical corticosteroid. J Am
Acad Dermatol 1992; 26:535–544.
49. Bernstein EF, Underhill CB, Lakkakorpi J, et al. Citric acid increases
viable epidermal thickness and glycosaminoglycan content of
sun-damaged skin. Dermatol Surg 1997; 23:689–694.
50. Ditre CM, Griffin TD, Murphy GF, et al. Effects of alpha-hydroxy
acids on photoaged skin: a pilot clinical, histologic, and ultrastructural
study [see comments]. J Am Acad Dermatol 1996; 34:187–195.
51. Bernstein EF, Lee J, Brown D, et al. Glycolic acid treatment increases
type I collagen mRNA and hyaluronic acid content of human skin.
Dermatol Surg 2001; 27:429–433.
52. Kim SJ, Won YH. The effect of glycolic acid on cultured human skin
fibroblasts: cell proliferative effect and increased collagen synthesis.
J Dermatol 1998; 25:85–89.
53. Kligman AM, Baker TJ, Gordon HL. Long-term histologic follow-up
of phenol face peels. Plast Reconstr Surg 1985; 75:652–659.
54. Rubach BW, Schoenrock LD. Histological and clinical evaluation
of facial resurfacing using a carbon dioxide laser with the computer
pattern generator. Arch Otolaryngol Head Neck Surg 1997; 123:
929–934.
55. Lundin A, Berne B, Michaelsson G. Topical retinoic acid treatment
of photoaged skin: its effects on hyaluronan distribution in epidermis
and on hyaluronan and retinoic acid in suction blister fluid. Acta Derm
Venereol 1992; 72:423–427.

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56. Kligman AM, Dogadkina D, Lavker RM. Effects of topical tretinoin
on non-sun-exposed protected skin of the elderly. J Am Acad Dermatol
1993; 29:25–33.
57. Griffiths CE, Russman AN, Majmudar G, et al. Restoration of
collagen formation in photodamaged human skin by tretinoin
(retinoic acid) [see comments]. N Engl J Med 1993; 329:530–535.
58. Stiller MJ, Bartolone J, Stern R, et al. Topical 8% glycolic acid and 8%
L-lactic acid creams for the treatment of photodamaged skin:
a double-blind vehicle-controlled clinical trial. Arch Dermatol 1996;
132:631–636.
59. Van Scott EJ, Ditre CM, Yu RJ. Alpha-hydroxyacids in the treatment
of signs of photoaging. Clin Dermatol 1996; 14:217–226.
60. Bergfeld W, Tung R, Vidimos A, et al. Improving the cosmetic
appearance of photoaged skin with glycolic acid. J Am Acad Dermatol
1997; 36:1011–1013.
61. Newman N, Newman A, Moy LS, et al. Clinical improvement
of photoaged skin with 50% glycolic acid: a double-blind
vehicle-controlled study. Dermatol Surg 1996; 22:455–460.
62. Marrero GM, Katz BE. The new fluor-hydroxy pulse peel:
a combination of 5-fluorouracil and glycolic acid. Dermatol Surg
1998; 24:973–978.
63. Effendy I, Kwangsukstith C, Lee JY, et al. Functional changes in
human stratum corneum induced by topical glycolic acid: comparison
with all-trans retinoic acid. Acta Derm Venereol 1995; 75:455–458.
64. Burns RL, Prevost-Blank PL, Lawry MA, et al. Glycolic acid peels for
postinflammatory hyperpigmentation in black patients: a comparative
study. Dermatol Surg 1997; 23:171–174; discussion 175.
65. Lim JT, Tham SN. Glycolic acid peels in the treatment of melasma
among Asian women. Dermatol Surg 1997; 23:177–179.
66. Tsai TF, Paul BH, Jee SH, et al. Effects of glycolic acid on light-induced
skin pigmentation in Asian and Caucasian subjects. J Am Acad Dermatol
2000; 43:238–243.
67. Garcia A, Fulton JE Jr. The combination of glycolic acid and
hydroquinone or kojic acid for the treatment of melasma and related
conditions. Dermatol Surg 1996; 22:443–447.
68. Kim SW, Moon SE, Kim JA, et al. Glycolic acid versus Jessner’s
solution: which is better for facial acne patients? A randomized
prospective clinical trial of split-face model therapy. Dermatol Surg
1999; 25:270–273.
69. Atzori L, Brundu MA, Orru A, et al. Glycolic acid peeling in the
treatment of acne. J Eur Acad Dermatol Venereol 1999; 12:119–122.
70. Perricone NV. Treatment of pseudofolliculitis barbae with topical
glycolic acid: a report of two studies. Cutis 1993; 52:232–235.
71. Becker FF, Langford FP, Rubin MG, et al. A histological comparison
of 50% and 70% glycolic acid peels using solutions with various pHs.
Dermatol Surg 1996; 22:463–465.
72. Grimes PE. The safety and efficacy of salicylic acid chemical peels in
darker racial-ethnic groups. Dermatol Surg 1999; 25:18–22.
73. Brodland DG, Roenigk RK. Trichloroacetic acid chemexfoliation
(chemical peel) for extensive premalignant actinic damage of the
face and scalp [published erratum appears in Mayo Clin Proc 1988;
63:1122]. Mayo Clin Proc 1988; 63:887–896.
74. Lawrence N, Cox SE, Cockerell CJ, et al. A comparison of the efficacy
and safety of Jessner’s solution and 35% trichloroacetic acid vs 5%
fluorouracil in the treatment of widespread facial actinic keratoses.
Arch Dermatol 1995; 131:176–181.
75. Alster TS, Kauvar AN, Geronemus RG. Histology of high-energy
pulsed CO2 laser resurfacing. Semin Cutan Med Surg 1996; 15:189–193.
76. Morrow DM. Chemical peeling of eyelids and periorbital area.
J Dermatol Surg Oncol 1992; 18:102–110.
77. Peikert JM, Krywonis NA, Rest EB, et al. The efficacy of various
degreasing agents used in trichloroacetic acid peels. J Dermatol Surg
Oncol 1994; 20:724–728.
78. Hevia O, Nemeth AJ, Taylor JR. Tretinoin accelerates healing after
trichloroacetic acid chemical peel. Arch Dermatol 1991; 127:678–682.
79. Monheit GD. The Jessner’s-trichloroacetic acid peel: an enhanced
medium-depth chemical peel. Dermatol Clin 1995; 13:277–283.
80. Monheit GD. The Jessner’s + TCA peel: a medium-depth chemical
peel. J Dermatol Surg Oncol 1989; 15:945–950.
81. Witheiler DD, Lawrence N, Cox SE, et al. Long-term efficacy and
safety of Jessner’s solution and 35% trichloroacetic acid vs 5%
fluorouracil in the treatment of widespread facial actinic keratoses.
Dermatol Surg 1997; 23:191–196.
82. Cook KK, Cook WR. Chemical peel of nonfacial skin using glycolic
acid gel augmented with TCA and neutralized based on visual staging.
Dermatol Surg 2000; 26:994–999.
83. Obagi ZE, Obagi S, Alaiti S, et al. TCA-based blue peel: a standardized
procedure with depth control. Dermatol Surg 1999; 25:773–780.
84. Johnson JB, Ichinose H, Obagi ZE, et al. Obagi’s modified
trichloroacetic acid (TCA)-controlled variable-depth peel: a study of
clinical signs correlating with histological findings [see comments]. Ann
Plast Surg 1996; 36:225–237.
85. Fulton JE, Rahimi AD, Helton P, et al. Neck rejuvenation by
combining Jessner/TCA peel, dermasanding, and CO2 laser
resurfacing [see comments]. Dermatol Surg 1999; 25:745–750.
86. Dailey RA, Gray JF, Rubin MG, et al. Histopathologic changes of the
eyelid skin following trichloroacetic acid chemical peel. Ophthal Plast
Reconstr Surg 1998; 14:9–12.
87. Hetter GP. An examination of the phenol-croton oil peel, part IV: face
peel results with different concentrations of phenol and croton oil. Plast
Reconstr Surg 2000; 105:1061–1083. discussion 1084–1087.
88. Alt TH. Occluded Baker-Gordon chemical peel: review and update
[see comments]. J Dermatol Surg Oncol 1989; 15:980–993.
89. Asken S. Unoccluded Baker-Gordon phenol peels – review and update.
J Dermatol Surg Oncol 1989; 15:998–1008.
90. Hetter GP. An examination of the phenol-croton oil peel, part I:
dissecting the formula. Plast Reconstr Surg 2000; 105:227–239.
discussion 249–251.
91. Hetter GP. An examination of the phenol-croton oil peel, part II: the
lay peelers and their croton oil formulas [published erratum appears
in Plast Reconstr Surg 2000; 105:1083]. Plast Reconstr Surg 2000;
105:240–248; discussion 249–251.
92. Hetter GP. An examination of the phenol-croton oil peel, part III: the
plastic surgeons’ role. Plast Reconstr Surg 2000; 105:752–763.
93. Ross EV, Grossman MC, Duke D, et al. Long-term results after CO2
laser skin resurfacing: a comparison of scanned and pulsed systems.
J Am Acad Dermatol 1997; 37:709–718.
94. Litton C, Trinidad G. Complications of chemical face peeling as
evaluated by a questionnaire. Plast Reconstr Surg 1981; 67:738–744.
95. Perkins SW, Sklarew EC. Prevention of facial herpetic infections
after chemical peel and dermabrasion: new treatment strategies in the
prophylaxis of patients undergoing procedures of the perioral area.
Plast Reconstr Surg 1996; 98:427–433. discussion 434–435.
96. Korcok M. Untoward effect of a face peel: toxic shock syndrome
[news]. JAMA 1982; 248:23.
97. Maloney BP, Millman B, Monheit G, et al. The etiology of prolonged
erythema after chemical peel [see comments]. Dermatol Surg 1998;
24:337–341.
98. Rapaport MJ, Rapaport V. Prolonged erythema after facial laser
resurfacing or phenol peel secondary to corticosteroid addiction.
Dermatol Surg 1999; 25:781–784; discussion 785.
99. Gross BG. Cardiac arrhythmias during phenol face peeling. Plast
Reconstr Surg 1984; 73:590–594.
100. Sorkin MJ. Cardiac arrhythmias during phenol face peel [letter].
J Dermatol Surg Oncol 1988; 14:477.
101. Fitzpatrick RE, Goldman MP, Satur NM, et al. Pulsed carbon dioxide
laser resurfacing of photo-aged facial skin [see comments]. Arch
Dermatol 1996; 132:395–402.
102. Fitzpatrick RE, Rostan EF, Marchell N. Collagen tightening induced
by carbon dioxide laser versus erbium:YAG laser. Lasers Surg Med
2000; 27:395–403.
103. Fitzpatrick RE, Smith SR, Sriprachya-Anunt S. Depth of vaporization
and the effect of pulse stacking with a high-energy, pulsed carbon
dioxide laser. J Am Acad Dermatol 1999; 40:615–622.
104. Alster TS. Cutaneous resurfacing with CO2 and erbium:YAG lasers:
preoperative, intraoperative, and postoperative considerations. Plast
Reconstr Surg 1999; 103:619–632; discussion 633–634.

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Cosmetic surgery procedures and techniques
105. Alster TS, Garg S. Treatment of facial rhytides with a high-energy
pulsed carbon dioxide laser. Plast Reconstr Surg 1996; 98:791–794.
106. Bernstein EF, Brown DB, Kenkel J, et al. Residual thermal damage
resulting from pulsed and scanned resurfacing lasers. Dermatol Surg
1999; 25:739–744.
107. Ross EV, Domankevitz Y, Skrobal M, et al. Effects of CO2 laser pulse
duration in ablation and residual thermal damage: implications for skin
resurfacing. Lasers Surg Med 1996; 19:123–129.
108. Goldberg DJ. Nonablative resurfacing. Clin Plast Surg 2000; 27:
287–292, xi.
109. Kelly KM, Nelson JS, Lask GP, et al. Cryogen spray cooling in
combination with nonablative laser treatment of facial rhytides. Arch
Dermatol 1999; 135:691–694.
110. Menaker GM, Wrone DA, Williams RM, et al. Treatment of facial
rhytides with a nonablative laser: a clinical and histologic study.
Dermatol Surg 1999; 25:440–444.
111. Zelickson BD, Kilmer SL, Bernstein E, et al. Pulsed dye laser
therapy for sun damaged skin. Lasers Surg Med 1999; 25:
229–236.

History and Science
Background and history
Classification of vascular lesions
Treating vascular lesions is one of the most common and
­effective uses of laser surgery. Correct diagnosis is needed
to decide when laser surgery is indicated and to select appro­
priate equipment and parameters. Most vascular lesions
­amenable to laser surgery can be classified into three categories
(Table 11-1): malformations, benign tumors, and dilatations
of pre-existing vessels.1
Vascular malformations are present at birth and never
­spontaneously regress. They do not exhibit cellular prolif­
eration but generally expand as patients grow and as ves­
sels ­ become more ectatic. Malformations are categorized
­according to ­predominant vessel type: venous, venular, capil­
lary, lymphatic, arterial, or arteriovenous.2,3 Port-wine stains
(PWS) are vascular malformations comprised of ectatic
venules in the superficial dermis (Fig. 11-1). Normal cutane­
ous blood vessels range in diameter from 10 to 50 μm.4 In
contrast, PWS vessel ­diameter ranges from 10 to 300 μm.5,6
As patients age, vessel number, mean vessel depth and vessel
diameter increase slightly.7
Benign vascular tumors are associated with endothelial cell
­proliferation. Hemangiomas are the most common benign
­vascular tumor in pediatric patients. They may appear any­
where on the skin but affect the head and neck most commonly.8
Cutaneous hemangiomas may be superficial (capillary), deep
(cavernous) or combined.8 Superficial ­ hemangiomas usually
Lasers in the Treatment
of Vascular Lesions
Jeffrey A. Vallee,
Kristen M. Kelly,
Thomas E. Rohrer,
Kenneth A. Arndt, and
Jeffrey S. Dover
C h a p t e r
11
P A R T 2
Key Points
n Lasers can effectively treat a wide range
of congenital and acquired vascular lesions.
n Correct diagnosis is needed to decide when laser
surgery is indicated and to select appropriate
equipment and parameters.
n Safety and effectiveness of vascular lesion laser
treatment is maximized when treatment adheres
to the principles of selective photothermolysis,
­delivering sufficient energy at a wavelength
that is well absorbed by the target, within a time
period less than or equal to the target thermal
relaxation time.
n Wavelengths targeting oxyhemoglobin or its
­derivatives are utilized for vascular lesion
treatment.
n Shorter pulse durations (e.g. <3 ms) often produce
purpura and are used to treat difficult to destroy
port-wine stain (PWS) vessels; longer pulse
durations (e.g., >6 ms) are often selected to
treat erythema or telangiectases with minimal
purpura for a more cosmetically acceptable
treatment course.
n Epidermal cooling protects the epidermis,
­improving treatment safety, mitigating pain,
and ­allowing treatment of dark skin types.

136
Chapter 11
Cosmetic surgery procedures and techniques
­exhibit a bright red color while deep lesions typically appear as
subcutaneous nodules with normal or blue-tinted overlying skin.
These lesions may be present at birth or may arise within
the first several weeks of life and are reported to occur in 2–3%
of all neonates and in 10% of infants by 1 year of age.9 Most
grow rapidly during an early proliferative phase which lasts un­
til about 6 months of age and then spontaneously involute. The
involution phase proceeds slowly with fibrous tissue replacing
vascular parenchyma with maximal involution at 5 years of
age in 50% and at 9 years of age in 90% of hemangiomas.9
Other examples of benign vascular tumors include cherry
angiomas (Fig. 11-2), kaposiform hemangioendotheliomas,
and glomus tumors.
Vascular dilatations are ectatic vessels with normal
­endothelial turnover. One of the most common examples is
telangiectases which are permanent dilatations of end vessels,
primarily venules. Telangiectases are associated with numerous
conditions including rosacea, collagen vascular diseases, and
cutaneous mastocytosis, or may occur as a result of trauma,
Table 11-1  Classification of vascular lesions
Category
Examples
Onset
Spontaneous involution
Malformations
Port-wine stains, venous,
­arterial, and lymphatic
­malformations
Always present at birth
Never
Benign tumors
Dilatations
Hemangiomas
Telangiectases, venous lakes,
spider angiomas
At birth or first few weeks
of life Variable; often arise
in ­adulthood
Often
Occasionally
Fig. 11-1  Typical facial port wine stain.
­radiation therapy, sun damage, endocrine factors, or high ve­
nous pressure. Venous lakes, spider angiomas, angiokeratomas,
and lymphangiectases are other examples of vascular dilata­
tions.
Early therapeutic lasers
The concept of light amplification by stimulated emission of
radiation (LASER) was developed by Albert Einstein nearly a
century ago.10 In the 1960s, dermatologist Leon Goldman first
applied lasers for treatment of cutaneous lesions. In the 1970s,
a commercially available argon laser allowed reliable treatment
of cutaneous vascular lesions. These early lasers were associ­
ated with frequent adverse effects as the result of non-specific
damage.11,12 Several factors contributed to these early adverse
effects. First, there is significant melanin absorption at the short
blue-green wavelengths (488, 514  nm) utilized for the argon
­laser. As light passes through the epidermis to targeted dermal
PWS blood vessels, it must pass through melanin in the epider­
mal basal layer. Absorption of light by melanin can result in
excessive epidermal heating and ­subsequent ­injury, including
scarring and dyspigmentation. Second, early argon laser de­
vices had relatively long pulse durations (0.5  s), which resulted
in excessive perivascular heating and collagen damage.
Science
The theory of selective photothermolysis
As our understanding of how lasers interact with the skin has
become more sophisticated, laser surgery has become more ef­
fective and safe. In 1983, Anderson and Parrish published the
theory of selective photothermolysis, which described how a
laser could be used to induce selective injury to a skin structure,
Fig. 11-2  Multiple
cherry angiomas
on the trunk of a
45-year-old man.

137
Lasers in the treatment of vascular lesions  •  Chapter 11
whilst minimizing damage to surrounding normal tissue.13
According to their theory, treatment efficacy could be maxi­
mized and scarring minimized through assiduous ­attention to
three parameters: wavelength, pulse duration, and fluence.
Wavelength
Injury of a cutaneous lesion can be achieved when a colored
target (chromophore) absorbs light radiation and this energy is
converted to heat. For selective injury, the wavelength utilized
should be preferentially absorbed by the targeted ­chromophore
and minimally absorbed by non-targeted chromophores.
In the case of vascular lesions, oxyhemoglobin (HbO2),
­deoxyhemoglobin and, in some instances, methemoglobin are
the chromophore targets (Fig. 11-3). Each of these absorbs light
over a range of wavelengths and has more than one absorption
peak (e.g. HbO2 absorbs at 418, 542, and 577 nm).13 Vascular
targeting lasers have a wavelength at or near one of the HbO2
absorption peaks. Since melanin absorption steadily decreases
over this range, peaks at longer wavelengths are generally uti­
lized to minimize epidermal melanin absorption (see Fig. 11-3).
Wavelength also determines depth of penetration (Fig. 11-4).
Generally, longer wavelengths scatter less and therefore pen­
etrate deeper into the skin (up to 1200 nm, above which the
energy is preferentially absorbed superficially by water).13 To
300 500 700 1000 2000
Wavelength
Oxyhemoglobin Melanin Water
Absorption
KTP
Alexandrite
Nd: YAG
PDL
DIODE
Fig. 11-3  Absorption spectra of common cutaneous chromo­
phores. KTP (potassium titanyl phosphate); PDL (pulsed dye laser);
Nd:YAG (neodymium:yttrium-aluminum-garnet).
KTP (532 nm)
PDL (595 nm)
Alexandrite
(755 nm)
Diode (800 nm)
Nd: YAG
(1064 nm)
Fig. 11-4  Relative depth of penetration of select lasers used to
treat vascular lesions. KTP (potassium titanyl phosphate); PDL
(pulsed dye laser); Nd:YAG (neodymium:yttrium-aluminum-garnet).
treat vascular lesions, laser light must penetrate at least into
the papillary dermis and preferably through the deep dermis
to reach targeted vessels. Although a laser that emits at 418 nm
would have the strongest and most efficient oxyhemoglobin
absorption, it would not penetrate through the epidermis
and therefore would be ineffective at treating dermal vascular
anomalies. As such, most lasers that are used to treat vascu­
lar lesions use wavelengths of at least 532 nm; wavelengths in
the near infrared (up to 1064 nm) can be used to treat deeper
­vessels. Sometimes it is necessary to use lasers of different
wavelengths over several treatments to treat both superficial
and deep aspects of a single vascular lesion.
Pulse duration
Laser pulse duration (also called the pulse width) should
­approximate the thermal relaxation time of the targeted
­vessel to minimize heat diffusion and concomitant damage
to surrounding tissue. The thermal relaxation time is the
time required for the target to cool to 50% of the maximum
temperature induced by the laser.13 Thermal relaxation time
is ­related to the size of the vessel, being proportional to the
square of its diameter. Pulse durations significantly shorter
than the thermal relaxation time of a vessel might not achieve
adequate heating of the vessel wall, resulting in insufficient
photocoagulation. High energies delivered over short pulse
durations also often result in vessel rupture and extravasa­
tion of red blood cells (i.e. purpura). Pulse durations signifi­
cantly longer than the thermal relaxation time result in heat

138
Chapter 11
Cosmetic surgery procedures and techniques
diffusion from the target to the surrounding tissue which can
result in scarring or permanent dyspigmentation. Loss of
­energy to the surrounding tissue may also result in insufficient
­photocoagulation of the target vessel.
As an example, blood vessels within a PWS range from
10 to 300 μm in diameter.14 Thermal relaxation time for these
vessels ranges from 1 to 10 ms.13,15 Shorter pulse durations
(e.g. <3 ms) usually produce purpura and are used to treat
difficult to destroy PWS vessels. Longer pulse durations
(e.g. >6 ms) with higher energies are often selected to treat
­erythema or telangiectases with minimal purpura for a more
cosmetically acceptable treatment course.
Fluence
Fluence (i.e. laser energy measured as watts × seconds/cm2)
must be sufficient to damage targeted blood vessels. Irreversible
vessel destruction occurs when blood is heated to approxi­
mately 70°C.13 Too much energy, even when delivered at the
desired wavelength and pulse duration, may produce residual
heat, injuring surrounding structures. Too little energy will
not achieve desired vessel destruction.
In summary, the theory of selective photothermolysis
described how selective thermal damage to a target can be
achieved if sufficient energy is delivered at a wavelength that
is well absorbed by the target and that is within a time period
less than or equal to the thermal relaxation time of the tar­
get.13 This theory forms the central basis for laser parameter
selection for treatment of vascular lesions and other chromo­
phore targets in the skin. However, there are additional
­considerations.
Spot size
Spot size is the diameter of the laser beam. Fluence is related
to spot size, being inversely proportional to the square of the
radius of the spot size. Spot size also affects the depth of laser
light penetration. With larger spot sizes, the beam is scattered
less and light penetrates deeper. As a result, the ratio of der­
mal to epidermal damage is increased as spot size increases.
Smaller spot sizes require relatively higher fluences to achieve
the desired effect in the dermis and these higher fluences inflict
greater epidermal damage. Therefore, using larger spot sizes
increases effectiveness at equal fluences and increases safety.
Epidermal cooling
Selective photothermolysis improved laser treatment ­outcome,
but significant issues remained. One of the most important
was competition for absorption of laser light by epidermal
melanin (see Fig. 11-3). Light absorption by epidermal mel­
anin increases treatment pain and may result in epidermal
injury manifested as blistering, hyperpigmentation, hypopig­
mentation, and scarring. In the 1990s, sophisticated epider­
mal cooling methods became widely available, decreasing
treatment pain, permitting safe use of higher fluences, and
allowing treatment of patients with darker skin types. Three
methods of epidermal cooling are commonly utilized: contact
(conductive) cooling, evaporative (cryogen spray) cooling, and
convective or air cooling (Table 11-2).
In contact cooling, a cold object is directly applied to
the skin surface, and the laser pulse is delivered through the
­cooling medium. This method provides cooling before, dur­
ing, and after the laser pulse. Ice or refrigerated aqueous gels
are simple methods which provide some degree of contact
cooling and act as a heat sink. However, they warm rapidly
and are messy. More sophisticated methods utilize a glass or
sapphire window through which chilled water (about 4°C) cir­
culates in a closed loop with an electrostatic chiller. Sapphire’s
high thermal conductivity provides more rapid surface heat
extraction than glass. Contact cooling methods also provide
improved index matching, optimizing laser light entry into
the skin and reducing backscatter.16 Contact cooling may,
however, cause inadvertent cooling of targeted blood vessels
if application is prolonged. This may be especially problem­
atic during treatment of small superficial vessels, for example,
those in PWS.
In evaporative cooling (also known as cryogen spray cool­
ing), a millisecond pulse of cryogen is sprayed onto the skin.
Evaporative cooling is intrinsically more efficient than conduc­
tive cooling, creating larger gradients between the epidermis
and dermis and minimizing inadvertent cooling of dermal tar­
gets.16,17 Commercially, the most commonly utilized cryogen
is 1, 1, 1 ,2-tetrafluoroethane, which is a nontoxic, nonflam­
mable Freon substitute (boiling point: −26.2°C). The duration
of the cryogen spurt (10–100 ms) and the time delay between
the spurt and the laser pulse (10–100 ms) is programmed by the
operator. For PWS treatment, it has been shown that ­cryogen
Table 11-2  Active epidermal cooling methods
Advantages
Disadvantages
Contact (conductive) cooling: Chilled
glass or sapphire plate
Cooling before, during, and after
laser pulse;
Provides index matching
Higher risk of dermal cooling
Evaporative cooling: Cryogen spray
­cooling
Intrinsically efficient cooling with large
temperature gradients;
Low risk of dermal cooling
Cryogen cost
Convective cooling: Chilled air
No interference with laser light;
No disposable costs
Air is a poor thermal conductor;
Bulky cooling devices

139
Lasers in the treatment of vascular lesions  •  Chapter 11
spray cooling permits safe use of higher fluences, leading to
improved clearance.18 One disadvantage of evaporative cool­
ing is the cost of the disposable cryogen.
Convective cooling utilizes a continuous flow of chilled air
directed at the skin during treatment. Different rates of airflow
may be selected. Studies have shown that chilled air is an ef­
fective epidermal protection method but has a relatively poor
thermal capacity and is inferior to a chilled sapphire window.19
Cold air has been demonstrated to reduce pain during 585 nm
pulsed dye laser treatment of telangiectases.20,21
Clinical studies: vascula lesion lasers
Over the last 45 years a wide range of lasers and light
sources have been utilized for treatment of vascular lesions
(Table 11-3). Current therapy most commonly relies on pulsed
lasers which provide greater adherence to the concept of
­selective photothermolysis and improved treatment response
with a low incidence of scarring and dyspigmentation.
Pulsed dye lasers
The flashlamp-pumped pulsed dye laser (PDL) has a long his­
tory of safe and effective use for treatment of vascular lesions
and is frequently used as a reference for comparison in discus­
sions of vascular lesion treatment.
PDLs produce yellow light by using a flashlamp to pump
rhodamine dye as the active medium. They have proven to be
both effective and safe in treating cutaneous vascular lesions
with atrophic scarring in less than 0.1% of patients.22 Original
PDLs were designed with a wavelength of 577 nm and pulse
width less than 1 ms in accordance with the principle of selec­
tive photothermolysis.13 These lasers achieved good results for
PWS treatment with minimal risk of scarring.23,24 However,
it was subsequently discovered that wavelengths in the
585–600 nm range penetrated deeper without sacrificing
­vascular selectivity, improving efficacy.25
Whereas the traditional 585 nm PDL had a pulse width of
450 μs, newer 585 and 595 nm PDLs deliver pulse widths
of 1.5–40 ms, allowing treatment of vessels with variable
diameter. Longer pulse durations can be achieved by group­
ing trains of shorter pulses, and can achieve vascular injury
without vessel wall rupture. Longer pulse duration signifi­
cantly reduces post-treatment purpura and is generally fa­
vored by patients undergoing cosmetic procedures.
The PDL utilizes a fiberoptic cable to deliver round spots
between 3 and 12 mm in diameter or 2 × 7 mm or 3 × 10 mm
elliptical spots designed to treat individual blood vessels.
Epidermal cooling is available on most devices and, as dis­
cussed previously, increases the threshold for epidermal dam­
age and decreases patient discomfort during treatment. As
a result, higher fluences can be used with excellent clinical
­response and minimal risk to the epidermis.26,27
The PDL is considered the treatment of choice for most
PWS and some hemangiomas. It is also an excellent treatment
modality for facial telangiectases, poikiloderma of Civatte,
spider angiomas, cherry angiomas, and some leg veins, as well
as a variety of nonvascular conditions.
Q-switched 532 nm potassium titanyl
­phosphate (KTP) lasers
When light from the neodynium:yttrium-aluminum-­­garnet
(Nd:YAG) laser is passed through a frequency-doubling po­
tassium titanyl phosphate (KTP) crystal, the wavelength
is halved to 532 nm (green light), which is near the 542 nm
absorption peak of oxyhemoglobin. In the Q-switched
mode, the 532 nm Nd:YAG laser delivers pulses of 5–15 ns
at high peak powers. Although this pulse duration is far
shorter than the thermal relaxation time of blood vessels,
it has been shown that the Q-switched 532 nm Nd:YAG la­
ser can effectively treat small vascular lesions. Unlike the
PDL, which causes intravascular coagulation of erythro­
cytes, the Q-switched 532 nm Nd:YAG laser causes acute
rupture of the vessel wall. In a study of 10 patients with te­
langiectases or angiomas treated at a fluence of 3–4 J/cm2,
excellent results were seen in 70%, good results in 20%, and
fair results in 10%.28 Results were not as good when lower
fluences (1–2 J/cm2) were used. While post-­­treatment pur­
pura was rarely observed at lower fluences, moderate purpura
was seen immediately after treatment in all patients treated
at higher energies, followed by hyperpigmentation in 20% of
subjects at 30 days and 10% at 60 days follow-up.
Millisecond-pulsed 532 nm KTP lasers
Pulsed 532 nm lasers deliver pulse widths of 1–50 ms, either
by grouping trains of Q-switched pulses or delivering true
­millisecond pulses. Millisecond domain pulses approximate
the thermal relaxation time of small cutaneous vessels such as
telangiectasia. A distinct advantage of longer pulse widths is
slower heating of blood vessels, reducing mechanical stresses
on the vessel wall, and causing coagulation of vessels without
rupture or purpura.29,30 The combination of selective absorp­
tion by oxyhemoglobin and pulse widths in the millisecond
range makes these lasers ideally suited for treatment of super­
ficial telangiectases, particularly those located on the face.31,32
Chowdhury et al. demonstrated that the 532 nm also has
­utility in treating PDL-­­resistant PWS, with 70% of patients
having at least 25% blanching.33
The pulsed 532 nm laser has several disadvantages. Its short
wavelength does not penetrate deeply (see Fig. 11-4) thereby
limiting its application to superficial vessels. Furthermore, the
532 nm wavelength has strong absorption by melanin, which
raises the risk of epidermal damage in patients with darker
skin. Adjuvant epidermal cooling can be used to address this
issue to some extent.
Alexandrite lasers
Millisecond-pulse alexandrite lasers emitting at a 755 nm
(near infrared) wavelength have achieved widespread use in
laser hair removal. Based on a small hemoglobin absorption
peak in the near-infrared range, alexandrite lasers have also

140
Chapter 11
Cosmetic surgery procedures and techniques
Table 11-3  Some lasers and pulsed light devices available for vascular lesion treatment
Device type product
name (supplier)
Wavelength (nm)
Pulse duration
Comments
Pulsed dye lasers
V-beam (Candela)
595
0.45–40 ms
Cryogen spray cooling
C-beam (Candela)
585
0.45 ms
Cryogen spray cooling
V Star (Cynosure)
585, 595
0.5–40 ms
Air cooling
Potassium titanyl phosphate (KTP) lasers
UltraLight 532
(Adept Medical Concepts)
532
0.3–1.5 ms
Compact, portable
Aura i/Gemini (Laserscope)
532
1–50 ms
Contact cooling; 10 mm spot
Alexandrite lasers
UltraWave (Adept Medical
­Concepts)
755
5–50 ms
GentleLASE (Candela)
755
3 ms
Cryogen spray cooling
Diode lasers
LightSheer XC (Lumenis)
800
5–400 ms
Sapphire contact cooling
Varilite (IRIDEX)
940
5–100 ms
MedilasD (Dornier MedTech)
940
10–1000+ ms
Contact cooling available
Nedoymium:yttrium-aluminum-garnet (Nd:YAG) lasers
UltraWave (Adept Medical
­Concepts)
1064
5–100 ms
Gentle:YAG (Candela)
1064
0.25–300 ms
Cryogen spray cooling
VARIA (CoolTouch)
1064
0.3–500 ms
Cryogen spray cooling
CoolGlide Vantage (Cutera)
1064
0.1–300 ms
Contact cooling
Acclaim 7000 (Cynosure)
1064
0.4–300 ms
Cold air cooling
Fidelis (Fotona)
1064
5–50 ms
Cryogen spray cooling
FriendlyLight (FriendlyLight)
1064
0.5–1.5 ms
Portable
Lyra i/Gemini (Laserscope)
1064
20–100 ms
Contact cooling
Lumenis One (Lumenis)
1064
2–20 ms
Contact cooling
Profile 1064 (Sciton)
1064
0.1–200 ms
Contact cooling
Combined wavelength lasers
Dualis VP (Fotona)
532 / 1064
5–200 ms
Cryogen spray cooling;
2 wavelengths fire
­simultaneously
Cynergy (Cynosure)
595 /1064
0.5–40 /0.3–300 ms
Air cooling; 2 wavelengths fire
consecutively
Intense pulsed light devices
Med-Flash (Alderm)
590–1000
0–40 ms
Harmony (Alma Lasers)
540–950
10, 12, 15 ms
Spot 40 × 16 mm
Omnilight
(American Medical Biocare)
480–1200
2500 ms
Spot 10 × 20 mm / 30 ×
30 mm / 20 × 50 mm
Ellipse I2PL (Candela)
400–950
1.5–100 ms
Spot 10 × 48 mm
Solera Opus (Cutera)
500–635
Variable

141
Lasers in the treatment of vascular lesions  •  Chapter 11
been utilized to target moderately deep, larger-caliber spider
and feeding reticular veins, thick port-wine stains, and heman­
giomas. An advantage of the 755 nm wavelength is deeper
penetration of light as well as absorption by ­ deoxygenated
­hemoglobin. One study demonstrated significant improve­
ment in bulky PWS using the 755 nm alexandrite laser.34
Other studies have shown that medium- and large-diameter
leg veins (0.4–3 mm diameter) respond well, while smaller
diameter vessels (0.4 mm diameter) respond less impressively
to these devices.35,36 Given the higher energy needed to treat
vascular lesions with alexandrite lasers as compared to PDL
and KTP devices, treatment is significantly more painful.
Diode lasers
High-powered diode lasers emitting from 800 to 980 nm (near
infrared) have also been used to treat vascular lesions. The
800 nm wavelength is moderately absorbed by hemoglobin,
and penetrates relatively deeply into the dermis. Some reports
have shown encouraging results in the treatment of medium-
sized leg veins (0.4–1 mm diameter).37,38
The 940 nm diode laser penetrates even deeper and has
increased hemoglobin absorption as compared to 800 nm.
The device has been shown to be effective in the treatment
of leg veins and facial telangiectases resistant to therapy with
a 532 nm PDL.39
Both the 810 and 940 nm lasers can be introduced percuta­
neously into leg veins via an optical fiber and used intravascu­
larly to treat leg veins. This will be further addressed in other
chapters.
Nd:YAG lasers
The 1064 nm Nd:YAG laser can deliver high-powered, milli­
second pulses to treat vascular lesions. Some systems allow de­
livery of multiple synchronized sequential pulses. Incomplete
absorption at 1064 nm by hemoglobin allows for penetration
of laser light into the entire vessel, including the posterior
wall. However, lower absorption of the 1064 nm wavelength
by oxyhemoglobin requires use of significantly higher ener­
gies to achieve desired effects. The 1064 nm wavelength is
poorly absorbed by melanin, which reduces the risk of epi­
dermal ­injury in patients with darker skin types.
Pulsed Nd:YAG lasers are potentially useful for treating
larger, deeper vessels such as reticular leg veins. Complete
clearance of facial reticular veins has been reported in eight
patients treated with a 1064 nm Nd:YAG in combination with
epidermal cooling.40 In an evaluation of treatment of leg ­vessels
with a diameter of 0.5–3 mm diameter (50 sites treated on 30
patients), most improved by 75% 12 weeks after a single treat­
ment.41 While immediate epidermal injury was not ­observed,
post-treatment hyperpigmentation developed in 42% of pa­
tients, which resolved in 83% at the 3-month ­follow-up.
Multiple wavelength lasers
Laser irradiation of blood results in the transient ­formation
of methemoglobin from oxyhemoglobin and clot. Methemo­
globin and clot are not present in normal tissue and absorbs
near-infrared radiation much more strongly than does oxyhe­
moglobin. Systems have been developed to capitalize on meth­
emoglobin formation. A dual-wavelength Nd:YAG/KTP laser
that emits simultaneously at 1064 and 532 nm has been shown
to effectively treat PWS at a significantly reduced fluence than
the 532 nm laser alone with no loss of efficacy.42 It has been
proposed that to maximize on the effects achieved as a result
of the formation of methemoglobin and clot, it may be ad­
vantageous to delay the second Nd:YAG pulse. The Cynergy
(Cynosure, Westford, MA) is a two-laser device which has a
595 nm pulsed dye laser and a 1064 nm Nd:YAG ­laser that
are fired sequentially. Preliminary reports have shown that this
combined wavelength laser provides greater depth of treat­
ment and significant improvement in recalcitrant vessels with
lower fluences. In a study evaluating treatment of facial and
leg telangiectases, Tanghetti et al. showed >75% improvement
in 73% of lesions and noted that blebbed port-wine stains
­(frequently difficult to treat) had impressive response.43
Device type product
name (supplier)
Wavelength (nm)
Pulse duration
Comments
Intense pulsed light devices—cont’d
Cynergy PL (Cynosure)
569–950
5–50 ms
Spot 46 × 18 mm / 46 ×
10 mm / 21 × 10 mm
Quadra Q4
500–1200
10–110 ms
Lumenis One PDL (Lumenis)
515–1200
3–100 ms
Contact cooling
Solarus (Novalis)
520–1200
20, 40, 60 ms
MediLux/Starlux System (Palomar)
470–1400
10–100 ms
Contact cooling; photon
­recycling
Prolite II (Quantel Medical)
530–1200
20–72 ms
Spot 20 × 10 mm
Profile (Sciton)
400–1400
Up to 200 ms
Spot 15 × 30 mm; contact
cooling
Table 11-3  Some lasers and pulsed light devices available for vascular lesion treatment—cont’d

142
Chapter 11
Cosmetic surgery procedures and techniques
Intense pulsed light (IPL) sources
Intense pulsed light sources (IPLs) are intense, non-laser
flashlamp devices that produce incoherent, multiwavelength
light from 515 to 1200 nm (visible to infrared light). A series
of filters is used to cut off the output below a predetermined
wavelength, depending on patient skin type and lesion depth.
Light is delivered through a large rectangular handpiece.
Millisecond pulses are produced via a sequence of single,
double, or triple pulses separated by a variable delay. A thin
layer of cold aqueous gel is applied to the skin to protect the
epidermis and improve light coupling to the skin. In addition,
an attachable cooling bracket or built-in contact cooling can
be used for added epidermal protection.44
IPLs have been used to successfully treat a variety of vascu­
lar lesions, including PWS,45–47 hemangiomas, venous malfor­
mations,48 poikiloderma of Civatte,49and telangiectases.49,50
In general, an increased number of sessions is required to
clear vascular lesions compared with the PDL. The advan­
tage of the IPL is its versatility given its wide range of wave­
lengths, pulse durations, and pulse sequences. In addition, its
large spot size permits rapid treatment. Purpura is usually not
produced; however, it may occur with use of high fluences or
short pulse durations.
A disadvantage of IPLs is that they deliver some wave­
lengths that are preferentially absorbed by melanin. This may
account for the increased incidence of adverse effects such as
pigmentary change, blistering, and scarring in some ­reports.51
Further, IPLs produced by different manufacturers differ in
spectral wavelength output and filter effectiveness, making it
difficult to make generalized comments about these devices.
Clinical studies: laser treatment
of ­specific vascular lesions
Port-wine stains
The pulsed dye laser is currently the treatment of choice for
most PWS, especially those that are macular or only mildly
hypertrophic (Fig. 11-5). Many studies have demonstrated the
safety and efficacy of PDL in combination with epidermal cool­
ing for PWS treatment.52–64 In one study of 76 patients with
PWS, overall clinical improvement of 79% was achieved after
an average of nine treatments.55 Multiple treatments (25+)
may be necessary to achieve maximum lightening of some le­
sions.65 While most PWS can be lightened with the PDL, com­
plete clearing is infrequent, occurring in fewer than 20% of
cases,54,59,65 and some lesions are resistant, demonstrating lim­
ited response even after multiple treatments (Fig. 11-6). A recent
study53 evaluated efficacy of PWS therapy in patients referred
to a tertiary care center. Fifteen percent of subjects achieved
lightening of 75% or greater after an average of 4.3 treatments,
10% were evaluated to have lightening of 50–74%, 15% had
lightening of 25–49%, and 60% had less than 25% lightening.
It is difficult to predict which PWS will respond most favo­
rably to laser treatment. However, some studies have provided
guidelines regarding lesion response. Garden et al. evaluated
52 patients and found that purple, nodular lesions were in
many cases resistant to treatment.52 Poor response is likely due
to large red blood cell content in very ectatic vessels which
may shield deeper vessels from laser light. Deeper vessels may
also be present that are beyond the effective penetration depth
of the PDL.
B
A
Fig. 11-5  Facial PWS
(A) before and (B)
after treatment with the
pulsed dye laser.

143
Lasers in the treatment of vascular lesions  •  Chapter 11
A group of studies report that young children require fewer
treatments for clearance and achieve more lightening per treat­
ment than older patients.53–57 Pediatric PWS may respond
more favorably because of smaller vessel diameter, more su­
perficial vessel location, smaller lesional size and ­perhaps even
improved epidermal optics (thinner epidermis). However,
pediatric PWS responsiveness remains controversial. One pro­
spective study of 100 pediatric and adult patients found no
significant difference in PWS lightening between age groups.
No patient in this study achieved complete lesion clearance.58
Anatomic location is another potential predictor of treat­
ment response.59,60 PWS located on the face and neck ­often
­respond favorably as compared to trunk and extremity
­lesions.61 Centrofacial lesions (medial cheek, upper lip, and
nose) generally respond less favorably than those on other
­facial areas. Lesions localized to dermatome V2 are often
more resistant than PWS in V1, V3, and C2/C3 distributions.
Lesions located on the upper and lower extremities generally
respond poorly.59,61,62
Lesional size may also help predict laser therapy
­response,63,64 with smaller lesions generally responding ­better.
PWS vessel characteristics, including depth, number, and
­diameter, are also relevant.61,65 PWS with a reticulate ­pattern
and superficial vessels appear to respond more ­favorably.65
One study found that poor responders had significantly
smaller (mean vessel diameter 19 μm) and greater number of
vessels as compared to moderate and good ­responders.65
Absorption of laser energy by epidermal melanin inhibits
light delivery to targeted PWS vessels making it more difficult to
treat patients with darker skin types. Temporary or sometimes
permanent pigmentary changes can occur in these patients.
We believe that in an ideal PWS treatment protocol, wave­
length and pulse duration should be varied, in order to tar­
get vessels of different size and depth throughout the lesion.
Some of this variation can be achieved with PDL devices that
have varied wavelength (585–600 nm) and pulse duration
(0.45–40 ms). Resistant lesions may also benefit from use of
alternative laser devices.
Dierickx and colleagues used a pulsed, 532 nm laser to treat
11 patients with nonfacial, pink to purple PWS.66 The laser
was used with a computer-driven scanner that placed 127 spots
of 1 mm diameter in a hexagonal pattern. Pulse ­durations of
3, 5, 10, and 15 ms were compared. The best results were
obtained with 3 or 5 ms pulse widths at a fluence of 15 or
20 J/cm2. Immediate clinical response was transient blanch­
ing without purpura, but delayed purpura occurred at all sites
within several days. Other studies have shown >50% improve­
ment in facial and neck PWS in 95% of patients treated with
a 532 nm laser at 9.5–20 J/cm2 and 15–20 ms pulse width,67 as
well as lightening of previously treated, PDL-resistant PWS at
18–24 J/cm2 and pulse widths of 9–14 ms.68
IPLs have also been reported to effectively treat both un­
treated45,47 and treated but nonresponsive PWS.46 In a retro­
spective study, 70–100% clearance was achieved in 28 of 40
PWS treated with an IPL device.45 Although better results
were seen with pink and red PWS, good clearance (70–99%)
was achieved in 6 of 11 purple lesions. Treatment parameters
were not standardized, but the most frequently used parame­
ters were cut-off filters of 515 and 550 nm, pulse durations of
2.5–5 ms, and fluences of 24–60 J/cm2. Purpura developed in
most patients, while crusting was seen in 20%, and superficial
blistering in 8%. No scarring was observed in this study.
Yang et al.69 treated PWS three times with a 1064 nm Nd:
YAG laser using a 5 or 7 mm spot size, radiant exposures of
40–130  J/cm2 and pulse durations of 4–10 ms. Performing
treatments in conjunction with contact cooling and using
non-overlapping pulses, the authors achieved good blanching
results without adverse effects when energies were kept at or
below the minimum purpura dose. Six percent had more than
75% clearing, 31% had 51–75% clearance, 25% had 26–50%
clearance, and 38% had clearance of 25% or less. Scarring
was noted in one patient who was treated at energies above
A
B
Fig. 11-6  Resistant PWS after four treatments with the pulsed dye laser.

144
Chapter 11
Cosmetic surgery procedures and techniques
the minimum purpura dose. Histologic analysis of biopsies
confirmed that deeper vessels could be treated with the Nd:
YAG (>2 mm) as compared to the PDL (1 mm).
Facial telangiectases and other small vessel
disorders
Selection of device and treatment parameters for telangiectases
requires consideration of vessel diameter, anatomic location,
patient age, and patient expectations regarding results and
post-treatment healing.
Small-diameter vessels on the face usually respond favorably
to any of the millisecond duration lasers previously discussed.
The PDL represents an excellent treatment modality for ­facial
telangiectases (Figs 11-7, 11-8), even more difficult to treat
­lesions such as those associated with collagen vascular disease
or Osler-Weber-Rendu syndrome.70 Spot sizes (up to 12 mm)
allow confluent treatment of large areas. Alternatively, larger
telangiectases may be treated individually along their length
with an elliptical spot. The primary disadvantage of PDL
use is the potential occurrence of purpura immediately after
treatment, which may last up to 2 weeks. This is minimized
or eliminated completely by use of longer pulsed durations
(>6 ms). However, significantly longer pulse durations might
also limit treatment response, thereby increasing the number
of required treatment sessions.71 To improve response with
use of longer pulse durations, multiple passes or judicious
pulse stacking over the same area can be used.72
Pulse stacking improves results by several different mecha­
nisms. When a targeted vessel is hit with a laser pulse the intra­
vascular temperature increases. If the same vessel is hit again
with another laser pulse before the temperature has returned
back to normal, another incremental increase in vascular tem­
perature occurs. If this is done repeatedly with pulse stacking,
the intravascular temperature continues to slowly increase and
cause a greater thermal effect on the targeted endothelial cells
of the vessel wall and therefore a greater clinical response.
By increasing the temperature slowly in this manner, there is
only a minimal increased risk of purpura. There is, however,
a greater risk of postoperative edema. Also, when a red blood
cell is hit with a laser pulse and is heated, it undergoes a
­conformational change and its shape becomes elongated. As
in sickle cell anemia, the elongated red blood cells (RBCs) do
not flow as well through the blood vessel and tend to sludge in
the area. This creates a greater mass of RBCs and therefore
a more rich target for subsequent laser pulses. In addition, as
oxyhemoglobin is hit with a laser pulse, it can be transformed
into methemoglobin. Methemoglobin has greater absorption
of both 532 and 595 nm light and therefore makes a better
target with subsequent pulses. All of these factors lead to the
greater response of stacked laser pulses in the treatment of
vascular lesions. Rohrer et al. noted a 30% improvement
when nonpupuric stacked pulses were compared to nonpur­
puric single pulses.72
Facial telangiectases also respond favorably to millisecond-
pulsed 532 nm green light lasers.31 Pulsed green light lasers
coagulate small- and medium-diameter vessels with minimal
or no purpura. The target vessel can be traced with a laser
beam with a spot size that approximates the diameter of the
vessel or the entire field may be treated with larger spot sizes
(10 mm). Many of these devices use contact cooling for epi­
dermal protection. It is imperative that good contact be main­
tained throughout treatment, especially in high-risk areas such
as the ala and alar grooves; compromise of contact can result
in depressed scars. One study found the 532 nm KTP to be
more effective and less painful but have a higher incidence of
edema than PDL treatment of telangiectases.73
IPLs are another effective treatment modality for facial
telangiectases. Purpura is minimal or absent and handpieces
allows confluent treatment of large areas. However, more
treatments may be required for desired results as compared to
B
A
Fig. 11-7  Facial telangiectasia (A) before and (B) after one treatment with the 595 nm pulsed dye laser.

145
Lasers in the treatment of vascular lesions  •  Chapter 11
laser devices. In a small study, Raulin and colleagues reported
good to excellent clearing of telangiectases (mostly facial) after
an average of 4.4 treatments.49 Clementoni and colleagues
reported 88% of patients had >75% clearance of facial
­telangiectases after an average of 1.69 treatments.74
Spider and cherry angiomas typically respond after one
or two treatments with the PDL (Fig. 11-9).75 One pulse with
the 3 or 5 mm spot size usually treats the entire lesion. Pulsed
532 nm lasers are also effective, but higher fluences may be
necessary. For spider angiomas, treatment of the central
­feeding vessel followed by irradiation of the peripheral vessels
achieves the best results. Spider and cherry angiomas may also
respond to IPL; however, their large spot size makes ­treating
small superficial targets more difficult. In children, the use
of a PDL is preferable for telangiectases or spider angiomas
given the high therapeutic safety index.
Large blue vessels often present in the periorbital area. Due
to their size and depth, these vessels do not respond well to
A
B
A
B
Fig. 11-8  Large facial telangiectasia
(A) before and (B) after two treatments
with the 595 nm pulsed dye laser
Fig. 11-9  Angioma (A) before and
(B) after one treatment with the 595 nm
pulsed dye laser.

146
Chapter 11
Cosmetic surgery procedures and techniques
the PDL. They may be effectively treated with long-pulsed
infrared devices such as the long-pulsed alexandrite laser
or long-pulsed Nd:YAG lasers. Care must be taken when
long-pulsed lasers are used in the periorbital region as eye
injuries have occurred even when proper eye protection was
used.76 As such, these vessels are best treated by someone
with appropriate experience and knowledge of laser–tissue
­interactions.
Hemangiomas
Treatment of hemangiomas has long been a source of con­
troversy. Because of the natural history of these lesions and
the potential for involution, many lesions do not need to be
treated. Treatment may be indicated if the hemangioma is
rapidly proliferating, ulcerating, or is affecting important
structures such as the eyes or mouth. Treatment may also be
indicated for hemangiomas on the nose, lip, or ear because
they are more likely to heal with scarring or with permanent
anatomic distortion.77
The PDL has been the treatment of choice for super­
ficial hemangiomas selected for laser therapy.78,79 Use of a
PDL with longer wavelength (595 nm) and pulse duration
(1.5 ms or longer) may be more effective due to a greater
depth of penetration. Typically, the laser produces light­
ening and flattening of hemangiomas as well as a slowing
of proliferation and improvement in ulceration. Multiple
treatment sessions are usually required to achieve the
maximum benefit; treatment of lesions that are rapidly
proliferating should be repeated at 2–3-week intervals,
and those that are not rapidly proliferating should be re­
peated at 4–6-week intervals. Because of limited penetra­
tion depth (about 1.2 mm),25 PDL is not useful for ­lesions
with only a deep component.78 Further, PDL treatment
may have limited effect for proliferating hemangiomas
that have acquired significant thickness or depth. Whereas
lesions that are raised 3 mm or less off the skin surface
often achieve significant response, those raised more than
4 mm may lighten with therapy, but show less diminution
in thickness.80
Thicker hemangiomas are often better treated with longer
wavelength lasers such as the 755 nm alexandrite or 1064 nm
Nd:YAG lasers. The longer wavelengths of these lasers will
penetrate more deeply into these thick lesions and have a
greater clinical response (Fig. 11-10).
Once hemangiomas are in the involutional phase, the
PDL can be used to hasten resolution of the superficial
­component.81 Although these lesions are in a stage of regres­
sion, they are often slow to resolve and may persist beyond
school age, prompting a desire by the patient or parents for
treatment. The response to therapy is often rapid (within
two to four sessions), and lesions may be treated every 6–8
weeks.
B
A
Fig. 11-10  Hemangioma (A) before and (B) after two treatments with a long-pulsed 755 nm alexandrite laser.

147
Lasers in the treatment of vascular lesions  •  Chapter 11
PROCEDURES AND TECHNIQUES
Preoperative clinical considerations
Anesthesia
Most patients experience a well-tolerated, transient sting­
ing sensation during laser or IPL vascular lesion treatment.
As such, for most patients, anesthesia is not required. For
­sensitive patients, a thick layer of a topical lidocaine prepa­
ration ­under occlusion for 60 minutes is generally adequate
anesthesia. Alternatively, local infiltration or a regional
nerve block with lidocaine can be used. Epinephrine should
be avoided, as it will constrict vessels, diminishing the tar­
get and limiting efficacy. The exception is for nerve blocks
where epinephrine significantly potentiates block effective­
ness. Premedication with hypnotics, sedatives, or analgesics
are generally not required, but may be helpful for anxious
patients.
General anesthesia should be considered for treatment of
lesions in infants and children that require multiple pulses.
While use of general anesthesia is somewhat controversial,
we feel it is preferable, especially since children with ­vascular
birthmarks often require many treatments. In addition, protec­
tive eyewear is required during laser therapy (see below) and
may frighten conscious children. Finally, it is safer to use the
laser with the child immobilized under anesthesia. Frequently,
the anesthesiologist uses a laryngeal mask airway or mask
inhalation with sevoflurane as the anesthetic. Older, more
mature children may undergo intravenous induction. General
anesthesia for pediatric patients for these brief procedures is
generally safe; one study reported no serious adverse events in
881 procedures perfomed.82
Laser safety
Appropriate, wavelength specific safety goggles must be worn
by all personnel in the treatment room. Patients must also
wear protective eyewear appropriate for the procedure. For
treatment of nonfacial areas, patients may wear the same gog­
gles worn by assisting personnel, provided they are the type
that have complete contact with the skin and seal the entire
periocular region off from reflected laser light. If the face but
not the periorbital area is treated, then folded gauze with over­
lying metal goggles can be used. Corneal shields inserted with
the aid of ocular anesthetic drops are required for treatment
of the periorbital area, including the eyelid. Confirmation of
adequate size and correct placement of eyewear is crucial.
Several cases of eye injury have been reported when long-
pulsed, longer-wavelength lasers were used within the bony
orbit, even though eye protection was utilized. As such, use
of these devices in the periorbital area should be avoided or
approached with extreme caution by someone trained in such
procedures.
Although extremely rare, lasers have been reported to
cause flash fires.83 To minimize this risk, makeup should be
removed prior to treatment, and if alcohol is used to clean the
skin or laser handpiece, it must be allowed to dry completely
before treatment. Whenever possible, lasers should be used
with room air only. If oxygen use is required, then a closed
airway system should be used to avoid oxygen leakage. Water
and a fire extinguisher should be immediately available.
Device-specific procedural techniques
Pulsed dye laser
Port-wine stains
Test areas   For practitioners with limited experience, it may
be useful to perform test areas prior to treatment of an entire
PWS, in order to determine optimal fluence and prepare the
patient for the postoperative course, especially the purpura
(Fig. 11-11). An area should be chosen that is representative
of the entire lesion. Several test spots may be performed using
different fluences to determine the best therapeutic response.
Purpura should be produced, as subpurpuric doses are less
effective.84
• Use largest spot size possible to insure maximal
light penetration into tissue.
• PDLs should always be used with epidermal
cooling during treatment of vascular lesions.
• The laser handpiece should be held perpen­
dicular to the skin, with the attached spacer
resting on the skin.
• Best results are achieved when pulses are over­
lapped slightly.
• Purpura is required for PWS treatment but
can be avoided during treatment of facial
telangiectases by using longer pulse durations
(>6  ms).
• Judicious pulse stacking and multiple passes
optimize results when using long pulse
­durations.
• Wavelength and pulse duration should be varied
in the course of PWS treatment to target vessels
of varying diameter and depth.
Pearls
• Failure to overlap may result in a checkerboard
pattern of lesion resolution.
Pitfalls

148
Chapter 11
Cosmetic surgery procedures and techniques
Test areas should be evaluated in 4–6 weeks for degree
of lightening as well as for undesired textural or pigmen­
tary ­sequelae. If noticeable lightening has occurred without
­adverse effects, then treatment can proceed using the fluence
that produced the best results. Absence of lightening indicates
that higher fluences, alternative pulse widths, or different
wavelengths should be considered.
Treatment  It may be helpful to treat facial PWS with the
patient in the Trendelenburg position to increase blood flow
to the PWS and presumably increase the chromophore tar­
get. Treatment of infants and young children is generally ini­
tiated at 5–8 J/cm2 (depending on Fitzpatrick skin type) and
increased by 0.5–1.0 J/cm2 with each treatment, if no adverse
effects are noted. Lower radiant exposures are used for the eye­
lid, neck, and upper lip because these areas are more prone
to scarring. Beam profiles differ among available PDLs and,
thus, different fluences may be required to achieve equivalent
tissue ­responses.85 We commonly utilize shorter pulse durations
(0.45–3 ms) with a spot size of about 7 or 10 mm. Larger spot
sizes offer more uniform energy transmission, deeper penetra­
tion, and rapid treatment and, thus, the largest spot size which
will permit the desired radiant exposure should be chosen. PDLs
should always be used with epidermal cooling during treatment
of vascular lesions. Cryogen spray cooling parameters are in
the range of 30–50 ms spurt duration with a 20–30  ms delay
between the end of the spurt and laser pulse onset.
During treatment, the handpiece is moved across the PWS
in a methodical fashion. The laser handpiece should be held
perpendicular to the skin, with the attached spacer resting on
the skin. Best results are achieved when pulses are overlapped
by 10–20%, avoiding the checkerboard pattern of lightening
seen when spaces are left between pulses. Skipped areas can
be filled in at the end of the treatment. During treatment, an
erythematous flare often develops that obscures the margins
of the PWS. To avoid this problem, one should treat the edges
of the PWS first (the resulting purpura will outline the mar­
gins) or use a skin marking pen to delineate the border of the
lesion prior to treatment.
We believe that in an ideal PWS treatment protocol, wave­
length and pulse duration should be varied during treatment
course, in order to target vessels of different size and depth
throughout the lesion. Some of this variation can be achieved
with different PDL devices. Physicians and patients must
understand that multiple treatment sessions are required for
PWS and complete removal can not be guaranteed.
Postoperative clinical considerations  Post-treatment, pat­
ients experience local swelling, purpura (see Fig. 11-10) and pain
which is similar to a sunburn sensation. Ice packs and elevation
of the treated area for the first day after treatment will diminish
swelling. Cooling soaks, mild analgesics such as acetaminophen,
and the application of emollients (aloe vera gel or Aquaphor
Healing Ointment –Beiersdorf Inc., Norwalk, CT) can be
used to minimize discomfort. Mild crusting, which develops in
approximately 20% of patients, should be treated twice a day
with gentle washing and application of an ointment. Vesicula­
tion and thick crusting is abnormal and may be a sign of infec­
tion. To minimize hyperpigmentation, avoid treating when the
patient is tan. Patients should be instructed in good sun pro­
tective practices and can be prescribed bleaching creams (such
as hydroquinone-containing agents) to be started once bruising
has resolved. Treatments are repeated at 6–12 week intervals
and multiple treatments (3–15 or more) are typically required.
If a patient wishes to conceal purpura or skin discoloration,
makeup may be applied if crusting is not present. Makeup
with a green base may be helpful; although most discoloration
can be concealed completely only by using opaque makeup.
When makeup is removed, the skin should not be wiped, and
astringents or irritants should be avoided.
When PDL treatment of PWS is performed with appro­
priate fluences, correct technique and epidermal cooling,
serious postoperative complications are rare. Cutaneous de­
pressions or atrophic scarring, which have been reported in
up to 4% of patients,86,87 may be due to excessive fluences,
excessive spot overlap, trauma, or failure to use epidermal
cooling. Hypertrophic scarring is distinctly uncommon but
has been reported to occur on the face,88 neck,87 and chest,89
and in patients taking isotretinoin.90 In most cases, textural
changes are transient and resolve spontaneously within 1 year.
Transient hyperpigmentation, which occurs in about 25% of
patients,86,91 is associated with sun exposure and darker skin
types. Hypopigmentation is uncommon but risk is highest in
patients with actinic bronzing and skin types III or higher.
Fig. 11-11  Purpura 1 hour after pulsed dye laser treatment (short
pulse duration) of a facial port-wine stain.

149
Lasers in the treatment of vascular lesions  •  Chapter 11
Facial telangiectases and spider angiomas
Treatment  Test areas are generally not necessary. Treatment
technique is similar to that used for PWS treatment (includ­
ing use of epidermal cooling), except that good results can
be obtained without creation of purpura. Purpura can be
­avoided by use of longer pulsed durations (6–20 ms). Treat­
ment end point is vessel disappearance or a darkening of the
vessel. Judicious pulse stacking can be used to achieve the
desired end point. Whitening or blistering of the skin are signs
of epidermal damage and should be avoided.
The elliptical spot may be useful for treatment of linear tel­
angiectases. When using the elliptical spot, the handpiece should
be positioned at one end of the vessel and moved progressively
along its length so that the entire vessel is treated with minimally
overlapping pulses. The direction of treatment either in or against
the direction of blood flow is unimportant. Reactive erythema
often develops in the irradiated areas during treatment, making
it difficult to see residual vessels. Patients should be informed that
multiple treatments will be necessary for optimal results.
When treating spider angiomas, a spot size large enough to
cover the entire lesion should be used when possible. The radi­
ating ‘legs’ should be treated even if they appear to blanch after
treatment of the central papule. Treatment may be ­performed
through a glass slide compressed against the skin to target the
deeper component. Care must be taken to avoid breaking the
slide and the clinician must remember that the glass slide will
hinder or block epidermal cooling and ­treatment parameters
must be adjusted accordingly. If significant blood flow persists
within the angioma after irradiation, it may be necessary to
repeat treatment immediately, using higher fluence.
Postoperative clinical considerations
Postoperative care is similar to that described for PWS al­
though again purpura may not be necessary for treatment
results. Most telangiectases and spider angiomas respond very
well to PDL treatment. Smaller telangiectases resolve ­almost
completely after one treatment. Larger vessels and those
located in the nasal folds may require several treatments.
Hemangiomas
Treatment.  Anesthesia is usually not required, although use of
topical, intralesional, or even general anesthesia may be use­
ful during treatment of large lesions. Test spots can be consid­
ered but will delay full treatment by at least 2 weeks and some
hemangiomas appear to respond only when they are treated in
their entirety. Best results may be obtained using large spots size
and lower fluences (for example, a 10 mm spot and 6 J/cm2)
and once again, use of epidermal cooling is crucial.92 PDLs
with longer wavelengths (595 nm) and pulse durations (1.5 ms or
longer) may be optimal, especially for thicker lesions. Alterna­
tively, longer wavelength lasers such as the 755 nm alexandrite
or 1064 nm Nd:YAG may be used for even deeper penetra­
tion. Generally, two to six treatments are required for adequate
clinical response. Treatments are ­usually repeated at 2–8-week
intervals, with shorter intervals used for proliferating lesions.
Postoperative clinical considerations.  Postoperative care
is similar to that described for PWS and telangiectases. Ulcera­
tive hemangiomas may respond to application of bio-­­occlusive
dressings such as Duoderm (ConvaTEC, Princeton, NJ).
When the appropriate technique is used, complications are
not common, although ulceration and hypopigmentation
have been reported.93
Pulsed 532 nm Lasers
Port-wine stains
Treatment   Anesthesia considerations are the same as dis­
cussed above for PDL. Treatment may be accomplished via
the freehand or scanning technique. For the freehand method,
the largest laser beam spot size that delivers sufficient fluence
should be used. The handpiece should be held perpendicularly
to the skin surface, and the handpiece spacer should be placed
on the skin. Magnification of at least 5–10 times is needed to
visualize the individual vessels that make up PWS. The most
effective devices for visualizing intradermal vessels are polar­
ized magnified light sources (Syris Scientific, Gray, ME).
The vessels should be traced at a speed that seals the ves­
sel without causing overlying epidermal injury. If the vessel
does not disappear, then the handpiece should be moved
more slowly or the fluence should be slowly increased until
threshold fluence for vessel disappearance is reached. It may
also be necessary on some systems to adjust the pulse width
independently of the fluence. Optimal clearing of PWS has
• Higher melanin absorption at the 532 nm wave­
length increases potential for adverse effects in
patients with darker skin types.
• Incomplete epidermal cooling and adverse
­effects can result if the cooling tip is not in
good contact with the skin at all times.
Pitfalls
• The laser handpiece should be held perpendicu­
lar to the surface, with the handpiece spacer in
good contact with the skin.
• Vessels should be traced at a speed that seals
vessels without causing overlying epidermal
injury.
• If vessels do not disappear, then the handpiece
should be moved more slowly or the fluence can
be slowly increased until vessel disappearance
is achieved.
• If epidermal whitening is noted, then the fluence
is too high, the vessel is being traced too slowly,
or excessive overlapping is occurring.
• Avoid pulse stacking.
• Minimal pressure should be applied with the
cooling tip so vessels remain patent and the
target is not diminished.
Pearls

150
Chapter 11
Cosmetic surgery procedures and techniques
been reported at a pulse width of 3 or 5 ms.66 Larger-­­diameter
­vessels may ­require the use of longer pulse widths to achieve
desired vessel coagulation.
If epidermal whitening is noted, then the fluence is too
high, the vessel is being traced too slowly, cooling is inade­
quate, or excessive overlapping is occurring. Once the optimal
fluence, pulse duration, and tracing speed have been deter­
mined, the rest of the vessels of that caliber, depth, and color
can be treated with these parameters. Repeated tracing may
be required to coagulate some vessels, especially large-caliber
deep vessels. However, any one area should be treated only
once with each pass.
The scanning technique is performed with a scanning de­
vice that is attached with fiberoptics to the laser. The scanning
handpiece should be held perpendicular to the skin surface.
The fluence should be slowly raised until the threshold flu­
ence, defined as subtle blanching of the skin, is reached. The
scanner should not be moved until the entire scanning pattern
has been delivered. The handpiece should then be moved in
a methodical fashion to an adjacent area, taking care not to
overlap previously treated areas.
Postoperative clinical considerations  Post-treatment dis­
comfort can be lessened with the application of ice, cold tap
water-soaked gauze or hydro-occlusive dressings (e.g. Vigilon,
Bard Medical, Murray Hill, NJ). Postoperative edema can
be significantly reduced with application of ice for the first
6 hours after treatment. Erythema usually subsides within
24 hours. Crusting may develop within 1–2 days and last for
7–14 days; it occurs more commonly when patients with
­darker skin phototypes are treated.
Purpura is much less common with pulsed 532 nm lasers as
compared to PDLs, but mild purpura may develop with the
use of high fluences and short pulse durations.
Patients should wash the treated area gently with a
mild soap and water twice a day and then apply an oc­
clusive ­ ointment such as Aquaphor Healing Ointment
(Beiersdorf Inc., Norwalk, CT). Post-treatment sun protec­
tion is important to minimize the risk of postinflammatory
­hyperpigmentation. Repeat treatments should be delayed
by at least 6 weeks to ­allow maximal lightening and ensure
complete healing, ­including fading of postinflammatory hy­
perpigmentation.
Facial telangiectases and spider angiomas
Treatment  Anesthesia is usually not required. The spot size,
pulse duration, and fluence are determined by vessel size
and depth. The spot size should be slightly wider than the
­vessel diameter and the pulse duration slightly longer than
the ­thermal relaxation time of the vessel. Alternatively, an
entire area may be treated with a 10 mm spot size and then
any residual vessels may be traced out. The laser handpiece
should be held perpendicular to the surface, with the hand­
piece spacer in contact with the skin. Use of a polarized
magnifying device improves visualization of dermal vessels.
Vessels should be traced at a speed just slow enough to
cause sealing and vessel disappearance without ­ producing
­epidermal damage such as whitening. Using too high a
­repetition rate increases the risk for double-pulsing sites, rais­
ing the risk of side effects such as epidermal necrosis and scar­
ring. Particular caution should be used when treating the nasal
ala and alar creases, as these sites are prone to atrophic scar­
ring. If vessel disappearance does not occur during treatment,
then the fluence and pulse duration should be increased incre­
mentally, or the handpiece should be moved more slowly.
When using a laser with a cooling tip, the handpiece should
be held perpendicular to the surface with the cooling tip flat
and in direct contact with the skin. A thin layer of aqueous gel
applied to the skin will facilitate moving the tip and prevent it
from fogging up. Minimal pressure should be applied with the
cooling tip so that vessels remain patent. If too much pressure
is applied, then the vessel may be blanched, making treatment
less effective.
When treating spider and cherry angiomas, the spot size
should be selected to match the diameter of the target ­lesion.
The technique used is similar to that for telangiectases. With
spider angiomas the radiating vessels must also be treated.
When large cherry angiomas or high-flow spider angiomas
are treated, it may be necessary to use higher fluences that
coagulate the epidermis to ensure sufficient thermal damage
to the target vessels. The immediate end point of treatment is
disappearance of the lesion or superficial whitening.
Postoperative clinical considerations  Postoperative care
is similar to that described for treatment of PWS. Reactive
erythema that develops around the treated area usually fades
within 24 hours. Crusting occurs rarely, but when present can
last 3–14 days. Crusting is usually a sign of overly aggressive
treatment, except in the case of deep or wide-caliber vessels
that respond only to aggressive therapy.
Although facial telangiectases generally respond well to
treatment, multiple treatment sessions may be required to
achieve optimal clearing. Occasionally, recanalization and
vessel reappearance occurs after treatment. Re-treatment may
be safely performed 6 weeks after the original treatment if the
treatment area is completely healed.
Intense pulsed light sources
• Patients with darker skin phototypes should be
treated with a longer wavelength filter and
a longer pulse delay.
• Single pulses should be used for small vessels,
double pulses for medium vessels, and triple
pulses for large vessels.
• Lower fluences (20% below those recommended
by the manufacturer) should be used initially
until the skin response has been observed.
• After the pulse is delivered, gel should be wiped
off to observe the skin response.
Pearls

151
Lasers in the treatment of vascular lesions  •  Chapter 11
Treatment
Intense pulsed light sources require operators to select a
number of treatment parameters, including filter, pulse
mode (single, double, or triple), pulse duration, pulse delay,
and fluence. Software provides suggested treatment param­
eters based on lesion type, skin type, and predicted vessel
depth, but parameters may be changed based on individual
experience.
The cut-off filter should be chosen according to the pa­
tient’s skin type and lesion depth. A shorter wavelength filter
(e.g. 515 nm) should be used on type I skin only for superficial
and smaller vessels. A longer wavelength filter (e.g. 570 nm)
should be used for those deeper and larger vessels. Patients
with darker skin phototypes should be treated with a longer
wavelength filter and a longer pulse delay. Theoretically, use
of a longer pulse delay allows the epidermis to cool between
pulses, reducing the risk of epidermal injury. Single pulses
should be used for small vessels, double pulses for medium
vessels, and triple pulses for larger vessels. The theoretical
­advantage of multiple pulses is the ability to damage larger
and deeper vessels through additive heating.45 Pulse delays
should be longer for larger vessels to allow uniform heating of
the entire vessel. Conversely, pulse delays should be very short
for small vessels.
Before commencing treatment, a layer of cooling gel should
be applied on the area to be treated. If available, epidermal
cooling should be utilized. The handpiece should be placed
perpendicular to the skin surface. Lower fluences (20% below
those recommended by the manufacturer) should be used ini­
tially until the skin response has been observed. After the pulse
is delivered, the gel should be wiped off to allow inspection of
the tissue response. If the targeted lesion appears ­unchanged
and there are no epidermal changes, then the fluence may
be increased and an adjacent area treated. If no response
is observed, then the fluence can again be increased. If the
­desired tissue change is not seen, then the pulse width should
be ­increased, leaving the fluence the same.
Postoperative clinical considerations
Reactive erythema may develop in the treated area but typi­
cally subsides within 24 hours. Postoperative care is similar
to that described above for PDL and 532 nm lasers. Crusting
is an uncommon occurrence and is seen mostly in patients
with darker skin types or with the use of excessive fluence or
short wavelength filter. Again, post-treatment sun protection
is important.
Conclusion
Treating vascular lesions is one of the most common and
­effective uses of laser surgery. When currently available laser
and light source devices are used properly, they can lighten
or remove vascular lesions achieving significant patient
­satisfaction.
REFERENCES
  1. Requena L, Sangueza OP. Cutaneous vascular anomalies, part I:
hamartomas, malformations, and dilatation of preexisting vessels.
J Am Acad Dermatol 1997; 37:523–549.
  2. Mulliken JB, Glowacki J. Hemangiomas and vascular malformations in
infants and children: a classification based on endothelial characteristics.
Plast Reconstr Surg 1982; 69:412–422.
  3. Waner M, Suen JY. A classification of congenital vascular lesions.
In: Waner M, Suen JY, eds. Hemangiomas and vascular malformations
of the head and neck. New York: Wiley-Liss; 1999:1–12.
  4. Braverman IM. Ultrastructure and organization of the cutaneous
microvasculature in normal and pathologic states. J Invest Dermatol
1989; 93:2S–9S.
  5. Anderson RR, Parrish JA. Microvasculature can be selectively damaged
using dye lasers: a basic theory and experimental evidence in human
skin. Lasers Surg Med 1981; 1:263–276.
  6. Edstrom DW, Hedblad MA, Ros AM. Flashlamp pulsed dye laser and
argon-pumped dye laser in the treatment of port-wine stains: a clinical
and histological comparison. Br J Dermatol 2002; 146:285–289.
  7. Finley JL, Noe JM, Arndt KA, et al. Port-wine stains: morphologic
variations and developmental lesions. Arch Dermatol 1984; 120:
1453–1455.
  8. Requena L, Sangueza OP. Cutaneous vascular proliferations, part II:
hyperplasias and benign neoplasms. J Am Acad Dermatol 1997;
37:887–920.
  9. Smolinski KN, Yan AC. Hemangiomas of infancy: clinical and
biological characteristics. Clinical Ped 2005; 44:747–766.
10. Einstein A. Zur Quantentheorie der Strahlung. Physiol Z 1917;
18:121–128.
11. Dixon JA, Huether S, Rotering R. Hypertrophic scarring in argon laser
treatment of port-wine stains. Plast Reconstr Surg 1984; 73:771–777.
12. Gilcrest BA, Rosen S, Noe JM. Chilling port wine stains improves the
response to argon laser therapy. Plast Reconstr Surg 1982; 69:278–283.
13. Anderson RR, Parrish JA. Selective photothermolysis: precise
microsurgery by selective absorption of pulsed radiation. Science 1983;
220:524–527.
14. Mulliken JB, Young AR. Vascular birthmarks – hemangiomas and
malformations. Philadelphia: WB Saunders; 1988.
15. van Gemert MJC, Welch AJ, Amin AP. Is there an optimal laser
treatment for port wine stains? Lasers Surg Med 1986; 6:76–83.
16. Ross EV, Ladin Z, Kreindel M, et al. Theoretical considerations in laser
hair removal. Dermatol Clin 1999; 17:333–355.
17. Nelson JS, Milner TE, Anvari B, et al. Dynamic epidermal cooling in
conjunction with laser-induced photothermolysis of port wine stain
blood vessels. Lasers Surg Med 1996; 19:224–229.
18. Chang CJ, Nelson JS. Cryogen spray cooling and higher fluence pulsed
dye laser treatment improve port-wine stain clearance while minimizing
epidermal damage. Dermatol Surg 1999; 25:767–772.
19. Chang CW, Reinisch L, Biesman BS. Analysis of epidermal protection
using cold air versus chilled sapphire window with water or gel during
810 nm diode laser application. Lasers Surg Med 2003; 32:129–136.
20. Hammes S, Raulin C. Evaluation of different temperatures in cold air
cooling with pulsed-dye laser treatment of facial telangiectasia. Lasers
Surg Med 2005; 36:136–140.
21. Greve B, Hammes S, Raulin C. The effect of cold air cooling on 585 nm
pulsed dye laser treatment of port-wine stains. Dermatol Surg 2001;
27:633–636.
• IPLs require operators to select a number of
treatment parameters, including filter, pulse
mode (single, double, or triple), pulse duration,
pulse delay, and fluence.
Pitfalls

152
Chapter 11
Cosmetic surgery procedures and techniques
22. Levine VJ, Geronemus RG. Adverse effects associated with the 577- and
585-nanometer pulsed dye laser in the treatment of cutaneous vascular
lesions: a study of 500 patients. J Am Acad Dermatol 1995; 32:613–617.
23. Garden JM, Polla LL, Tan OT. The treatment of port wine stains by the
pulsed dye laser: analysis of pulse duration and long-term therapy. Arch
Dermatol 1998; 124:889–896.
24. Morelli JG, Tan OT, Garden J, et al. Tunable dye laser (577 nm)
treatment of port wine stains. Lasers Surg Med 1986; 6:94.
25. Tan OT, Murray S, Kurban AK. Action spectrum of vascular specific
injury using pulsed irradiation. J Invest Dermatol 1989; 92:868–871.
26. Geronemus RG. High-radiant exposure modified pulsed dye laser
photocoagulation with dynamic cooling of port-wine stains in infancy.
Arch Dermatol 2000; 136:942–943.
27. Kauvar ANB, Lou WW, Zelickson B. The effect of cryogen spray
cooling on 595 nm, 1.5 ms laser treatment of port wine stains. Lasers
Surg Med 2000; (suppl):24.
28. Goldberg DJ, Marcus J. The use of the frequency-doubled Q-switched
Nd:YAG laser in the treatment of small cutaneous vascular lesions.
Dermatol Surg 1996; 22:841–844.
29. Dierickx CC, Casparian JM, Venugopalan V, et al. Thermal relaxation
of port-wine stain vessels probed in vivo: the need for 1–10-millisecond
laser pulse treatment. J Invest Dermatol 1995; 105:709–714.
30. Dierickx CC, Farinelli WA, Anderson RR. Clinical and histological
responses of blood vessels to long (msec) 532 nm laser pulses. Lasers Surg
Med 1996; 18(suppl 8):48.
31. Goldberg DJ, Meine JG. A comparison of four frequency-doubled
Nd:YAG (532 nm) laser systems for treatment of facial telangiectases.
Dermatol Surg 1999; 25:463–467.
32. Clark C, Cameron H, Moseley H, et al. Treatment of superficial
cutaneous vascular lesions: experience with the KTP 532 nm laser.
Lasers Med Sci 2004; 19:1–5.
33. Chowdhury MMU, Harris S, Lanigan SW. Potassium titanyl phosphate
laser treatment of resistant port wine stains. Br J Dermatol 2001;
144:814–817.
34. No D, Dierickx C, McClaren M, et al. Pulsed alexandrite treatment of
bulky vascular malformations. Lasers Surg Med 2003; 15:26.
35. McDaniel DH, Ash K, Lord J, et al. Laser therapy of spider veins:
clinical evaluation of a new long pulsed alexandrite laser. Dermatol Surg
1999; 25:52–58.
36. Kauvar ANB, Lou WW, Quintana AT. Effect of cryogen spray cooling
on treatment of leg telangiectasia with 585 nm, 1.5 msec and 755 nm,
3 msec lasers. Lasers Surg Med 1999; 11(suppl):19.
37. Dierickx CC, Duque V, Anderson RR. Treatment of leg telangiectasia
by a pulsed, infrared laser system. Lasers Surg Med 1998; 10(suppl):40.
38. Garden JM, Bakus AD, Miller ID. Diode laser treatment of leg veins.
Lasers Surg Med 1998; 10(suppl):32.
39. Carniol PJ, Price J, Olive A. Treatment of telangiectasias with the
532-nm and the 532/940-nm diode laser. Facial Plastic Surg 2005;
21:117–119.
40. Eremia S, Li CY. Treatment of face veins with a cryogen spray variable
pulse width 1064 nm Nd:YAG Laser: a prospective study of 17 patients.
Dermatol Surg 2002; 28:244–247.
41. Weiss RA, Weiss MA. Initial results with a new synchronized pulsed
1064 nm laser for larger leg telangiectasias. Lasers Surg Med 1999;
11(suppl):21.
42. Ahcan U, Zorman P, Recek D, et al. Port wine stain treatment with a
dual-wavelength Nd:Yag laser and cryogen spray cooling: a pilot study.
Lasers Surg Med 2004; 34:164–167.
43. Tanghetti EA, Sherr E, Sierra R, et al. Sequential 595 nm 1064 mn
treatment for bleb port wine stains and leg veins. Lasers Surg Med 2005;
(supp):74.
44. Weiss RA, Weiss MA. Epidermal cooling crystal collar (E3C) device for
improved results on leg veins using intense pulsed light. Lasers Surg Med
1999; 11(suppl):20.
45. Raulin C, Schroeter CA, Weiss RA, et al. Treatment of port-wine stains
with a noncoherent pulsed light source: a retrospective study. Arch
Dermatol 1999; 135:679–683.
46. Raulin C, Hellwig S, Schonermark MP. Treatment of a nonresponding
port-wine stain with a new pulsed light source (Photoderm VL). Lasers
Surg Med 1997; 21:203–208.
47. Cliff S, Misch K. Treatment of mature port wine stains with the
Photoderm VL. J Cutan Laser Ther 1999; 1:101–104.
48. Raulin C, Werner S. Treatment of venous malformations with an
intense pulsed light source (IPLS) technology: a retrospective study.
Lasers Surg Med 1999; 25:170–177.
49. Raulin C, Weiss RA, Schonermark MP. Treatment of essential
telangiectasias with an intense pulsed light source (Photoderm VL).
Dermatol Surg 1997; 23:941–946.
50. Goldman MP, Eckhouse S. Photothermal sclerosis of leg veins.
Dermatol Surg 1996; 22:323–330.
51. Green D. Photothermal removal of telangiectases of the lower
extremities with the Photoderm VL. J Am Acad Dermatol 1998;
38:61–68.
52. Garden JM, Polla LL, Tan OT. The treatment of port-wine stains by
the pulsed dye laser: analysis of pulse duration and long-term therapy.
Arch Dermatol 1988; 124:889–896.
53. Kelly KM, Choi B, McFarlane S, et al. Description and analysis of
treatments for port wine stain birthmarks. Arch Facial Plast Surg 2005;
7:287–294.
54. Reyes BA, Geronemus R. Treatment of port-wine stains during
childhood with the flashlamp-pumped pulsed dye laser. J Am Acad
Dermatol 1990; 23:1142–1148.
55. Alster TS, Wilson F. Treatment of port-wine stains with the flashlamp-
pumped pulsed dye laser: extended clinical experience in children and
adults. Ann Plast Surg 1994; 32:478–484.
56. Goldman MP, Fitzpatrick RE, Ruiz-Esparza J. Treatment of port-wine
stains (capillary malformation) with the flashlamp-pumped pulsed dye
laser. J Pediatr 1993; 122:71–77.
57. Ashinoff R, Geronemus RG. Flashlamp-pumped pulsed dye laser for
port-wine stains in infancy: earlier versus later treatment. J Am Acad
Dermatol 1991; 24:467–472.
58. Van der Horst CMAM, Koster PHL, de Borgie AJM, et al. Effect of
the timing of treatment of port-wine stains with the flash-lamp-pumped
pulsed-dye laser. N Engl J Med 1998; 338:1028–1033.
59. Orten SS, Waner M, Flock S, et al. Port-wine stains: an assessment
of 5 years of treatment. Arch Otolaryngol Head Neck Surg 1996;
122:1174–1179.
60. Renfro L, Geronemus RG. Anatomical differences of PWS in response
to treatment with the pulsed dye laser. Arch Dermatol 1993;
129:182–188.
61. Onizuka K, Tsuneda K, Shibata Y, et al. Efficacy of flashlamp-pumped
pulsed dye laser therapy for port wine stains: clinical assessment and
histopathological characteristics. Br J Plast Surg 1995; 48:271–279.
62. Lanigan SW. Port wine stains on the lower limb: response to pulsed dye
laser therapy. Clin Exper Dermatol 1996; 21:88–92.
63. Morelli JG, Weston WL, Huff C, et al. Initial lesion size as a predictive
factor in determining the response of port-wine stains in children
treated with the pulsed dye laser. Arch Pediatr Adolesc Med 1995;
149:1142–1144.
64. Yohn JJ, Huff JC, Aeling JL, et al. Lesion size is a factor for determining
the rate of port-wine stain clearing following pulsed dye laser treatment
in adults. Cutis 1997; 59:267–270.
65. Fiskerstrand EJ, Svaasand LO, Kopstad G, et al. Laser treatment of
port wine stains: therapeutic outcome in relation to morphological
parameters. Br J Dermatol 1996; 134:1039–1043.
66. Dierickx CC, Farinelli WA, Flotte T, et al. Effect of long-pulsed 532 nm
Nd:YAG laser on portwine stains (PWS). Lasers Surg Med 1996;
18(suppl 8):33.
67. Pence B, Aybey B, Ergenekon G. Outcomes of 532 nm frequency-
doubled Nd:YAG laser use in the treatment of port-wine stains.
Dermatol Surg 2005; 31:509–517.
68. Chowdhury MM, Harris S, Lanigan SW. Potassium titanyl phosphate
laser treatment of resistant port-wine stains. Br J Dermatol 2001;
144:814–817.