Phẫu Thuật Da Liễu: Khía Cạnh Ngoại Khoa (Surgery of the Skin)

533
Chapter 31  Microdermabrasion and Dermabrasion
The depth of abrasion can be monitored by closely observ-
ing the abraded surface. As the epidermis is removed, the
papillary dermis appears as a glistening white surface. Corn
rows of pinpoint bleeding can be seen as the vascular loops
of the rete pegs are interrupted. As the depth of abrasions
proceeds further into the dermis, the points of bleeding
become larger.41 The yellow globules of sebaceous glands are
seen with deep abrasion of acne scars in the mid-cheek or
rhinophyma of the nose. The hemostasis of tumescent
anesthesia reduces the visibility of points of bleeding as does
the diamond fraise, so this cannot be used as a sole end point.
Nevertheless, these surgical landmarks together provide a
reliable means of following the depth of abrasion. The dermal
fibrosis produced by acne scars will crumble and become
friable with abrasion. The peripheral margin of the abraded
regions should be feathered to create a natural-looking transi-
tion zone. The arciform strokes should be parallel to the
border of the abraded areas to avoid jagged stop and start
streaks, much like coloring with crayons in a direction paral-
lel with a borderline rather than perpendicular to it.
 POSTOPERATIVE CARE
Upon completion of a full-face dermabrasion procedure,
most of the abraded areas are no longer bleeding. However,
the application of gauze soaked with 1% lidocaine with epine-
phrine 1 : 100 000 completes hemostasis and soothes any
postoperative stinging. Postoperative edema can be reduced
by intramuscular triamcinolone acetonide 40 mg given imme-
diately postoperatively. Propoxyphene N-100 pills (100 mg)
every 4–6 hours as needed eliminates postoperative stinging
or discomfort.
The abraded surface is dressed with a semipermeable dress-
ing (i.e. Vigilon, CR Bard, Murray Hill, NJ; 2nd Skin, Spenco
Medical, Waco, TX), which is held in place with paper tape
and backed with non-adherent pads and gauze. Surgilast
netting (Western Medical Ltd, Tenafly, NJ) secures the mask
and is much less bulky than Kling wrap or ACE bandages and
contours to the face. The patient returns to the office for the
full-face dressing to be changed every day for 5 days. With
the use of full-face dressings, patients experience very little
postoperative discomfort. Antiviral prophylaxis is continued
for 14 days and antibiotics or antifungal medications are only
necessary in the rare event of a secondary infection.
Close and meticulous attention to the sequential events of
wound healing during the postoperative course will allow for
the early detection and intervention of any postoperative
complications. The development of pain with or without ero-
sions is the sine qua non for a postoperative herpetic infec-
tion. The herpes virus requires viable epidermal cells in which
to propagate, therefore this infectious complication is usually
seen 5–10 days after surgery. The pain is usually accompanied
by punched out ulcerations or erosions in the new skin which
may or may not heal with residual scarring (Fig. 31.6). Anti-
viral medication (valacyclovir 1 g three times daily for 7 days
or famciclovir 500 mg three times daily for 7 days) is neces-
sary to treat these lesions.
Superinfection by bacteria or fungi is much less common
following dermabrasion (Fig. 31.7). Daily dressing changes
with careful debridement contributes to the low incidence of
secondary infections. Like the herpetic outbreaks, bacterial
or fungal infections will present as painful, non-healing ero-
sions. Consequently any painful or non-healing erosions
the skin, whereas counterclockwise rotation brushes the bris-
tles over the surface of the skin more gently.
The body of the hand engine is held with the forefingers
and the neck of the dermabrader is stabilized with the thumb.
The abrading endpiece is passed over the skin in arciform
strokes perpendicular to the direction of endpiece rotation.
To abrade, the hand engine is pulled rather than pushed over
the skin surface. The outer peel of an orange or grapefruit
provides a good surface upon which to develop a feel for using
a hand-held dermabrader. During surgery, the patient is
supine and the skin surface being abraded should be parallel
to the floor so that the surgeon’s hand can move freely back
and forth without obstruction.
Direction of rotation is only important when a wire brush
is used. For deep resurfacing of acne scarring on the mid-
cheek, traumatic or surgical scars, or debulking large nodules
of rhinophyma, clockwise rotation is more efficient and
requires a frozen or tightly tumesced surface upon which to
abrade. Counterclockwise rotation is more easily controlled
in that the brushing action of the bristles is less likely to gouge
the skin or grab the free edge of the lip or nose. In fact, wire
brush dermabrasion with counterclockwise rotation as well as
fraise surgery can be performed without the use of spray
refrigerants. In performing full-face procedures, it is not
uncommon to alternate between the fraise and the wire brush
as well as between the direction of rotation of the wire brush
endpiece from clockwise to counterclockwise.
For full-face procedures, it is best to start abrading along
the jawline or the preauricular area and progress toward the
center of the face and nose. This allows bleeding from the
abraded areas to flow away from the skin being abraded.
Three-point retraction of the skin produced by the two hands
of the assistant and the non-dominant hand of the surgeon
stabilizes the area being abraded. When using spray refriger-
ant, the scar or rhytide should be frozen in its unstretched
position, then three-point retraction is applied while abrading.
Figure 31.4  Arciform strokes are performed by pulling the hand
engine perpendicular to the direction of the rotating endpiece.
Figure 31.5  Abrasive endpieces: wire brush (left), diamond
fraise (middle), pear-shaped or cone fraise (right).

534
Part 3  Aesthetic Surgical Procedures
topical petrolatum ointment. The ointment should be applied
three to four times daily until re-epithelialization is complete.
The open wound produced by dermabrasion heals by the
well-described mechanism of second intention wound healing.
Re-epithelialization occurs as new cells migrate in a ‘leap-
frog’ fashion from the skin appendages and the periphery of
the wound over the denuded surface. Typically, regions
rich in sebaceous glands such as the nose and mid-cheek re-
epithelialize more quickly than the more peripheral skin over
the bony prominences of the forehead, malar cheek, and
mandible. Clinically, the pink new skin can be seen as it
replaces the eroded surface.
During the remodeling phase of wound healing, fibroblasts
lay down new collagen fibers in an organized fashion parallel
to the surface the skin (see Chapter 7). The initial deposition
of fibronectin and type III collagen fibers is replaced by type
I collagen fibers as stromal reorganization proceeds. In der-
mabrasive wounding, the collagen fibers align parallel to lines
of tension before intermolecular cross-linkages are complete.
This is believed to produce a smoother contour than was
present in the original scar. Similarly the re-establishment of
a more normal epidermis after the abrasion of scars is facili-
tated by alterations in the extracellular formation of integrins
and tenascin. Following dermabrasion, increased integrin
expression may promote cellular migration while tenascin
mitigates the epithelial mesenchymal interaction of wound
healing.43 As wound healing progresses, intradermal edema
continues to dissipate for up to 3 months. After the edema
has resolved, rhytides and depressed scars may appear to have
returned. However, as the remodeling phase of wound healing
continues, new collagen is laid down parallel to the surface
of the skin, with continuing improvement of skin surface
irregularities and depressions for 6–12 months following
surgery. Consequently, it is best to wait 1 year before con-
sidering retreatments.
Re-epithelialization is usually complete within 7–10 days
following surgery. The application of tretinoin cream 0.05%
to the skin several weeks before the dermabrasion has been
shown to decrease the time required for re-epithelialization.44
Additionally the use of semipermeable dressings has reduced
the time for re-epithelialization by up to 40% compared to
open techniques of wound care. These dressings maintain a
critical plane of humidity which enhances epithelial cell
migration.45
Patients can apply make-up once re-epithelialization is
complete. Green- and yellow-based foundations are espe-
cially well suited for camouflaging the ensuing postoperative
erythema. Typically the bright red color of new epithelium
fades to pink and returns to normal skin tone within 2–3
months. It is during this period of postoperative erythema
that complete sun avoidance is required. Despite compliance
with this request, most patients will develop some degree of
transient postinflammatory hyperpigmentation over the malar
prominences and jawline. This darkening reliably responds to
topical hydroquinone and tretinoin cream applied either sep-
arately or together once to twice daily. This bleaching regimen
is tolerated with minimal irritation beginning the third or
fourth week after surgery and continued for 4–8 weeks or
until the hyperpigmentation resolves.
Permanent pigmentary alteration, which is seen as a loss of
normal skin tone, occurs in 20–30% of patients. Skin types
III and IV are more likely to develop this complication than
light-skinned patients (types I and II) or dark-toned indi-
should be presumed to be herpetic and treated with zoster
doses of antiviral medications, but cultures for bacteria and
fungi should also be performed. Appropriate systemic anti­
biotics or antifungal medications as directed by the culture
results will clear these lesions.
The presence of bright erythema after the first 2–3 post-
operative weeks is the first sign of early scar formation and
should be treated with topical high-potency steroid ointment
or Cordran tape (Oclassen Pharmaceuticals, Inc, San Rafael,
CA) applied once or twice daily. These areas should be fol-
lowed every 1–2 weeks so that pulsed-dye laser intervention
can be employed, which has been shown to decrease ery-
thema and scar induration.42 Intralesional steroid injections
(5–40 mg/mL triamcinolone acetonide) can be given if any
induration, elevation, or hypertrophy develops. Early and
aggressive management of scar formation will prevent pro-
gression to scar contracture and disfigurement. Small focal
areas of hypopigmentation are usually the final outcome of
successful aggressive scar management.
The patient returns to the office daily for 3–5 days to have
the mask dressing changed. After the first 48 hours, there is
a significant decrease in the amount of transudate and oozing
such that the non-adherent pads and gauze are no longer
needed. With each visit, crusting, coagulum, and fibrin build
up are debrided. Following 3–5 days of wearing a full-face
mask, an open wound care technique can be employed with
Figure 31.6  Viral infections present as painful punched out
lesions 7–10 days following surgery after epithelialization is
complete.
Figure 31.7  Bacterial infections present with crusting at
postoperative day 3 or 4.

535
Chapter 31  Microdermabrasion and Dermabrasion
Dermabrasion
A test spot dermabrasion is recommended in patients with a
history of keloids and/or koebnerizing conditions such as
psoriasis, lichen planus, or pyoderma gangrenosum.
An atopic diathesis or immunosuppression may cause
delayed wound healing or an increased risk of postoperative
infection. Patients with viral hepatitis and HIV infections are
also at increased risk for delayed wound healing and postop-
erative infection. Because of the aerosolized viral particles
produced by dermabrasion, all healthcare personnel should
observe universal precautions in performing dermabrasion.
The development of pain with or without erosions is the
sine qua non for a postoperative herpetic infection. Superin-
fection by bacteria or fungi is much less common following
dermabrasion. Daily dressing changes with careful debri­
dement contributes to the low incidence of secondary
infections.
 SUMMARY
Microdermabrasion was developed as a blood-free, safe tech-
nique with less healing time than dermabrasion and no down-
time for the patient. It is painless, quick, easy to perform,
and has few associated risks. Microdermabrasion has been
widely used to treat photodamage, dyschromias, acne, scars,
and stretch marks. However, the clinical benefits of treat-
ment are subtle and it is important to make this clear to
patients so that reasonable expectations are set. The available
literature principally examines the effectiveness of microder-
mabrasion on photoaging. Further investigation is needed to
understand the long-term benefits, if any, of this treatment
for aging skin as well as for other indications including acne,
dyspigmentation, and stretch marks.
In this era of ever-expanding resurfacing treatments, der-
mabrasive resurfacing continues to offer a uniquely effective
approach for a well-defined subset of defects. Specifically,
sharp-shouldered scars of acne and varicella as well as ady-
namic, deep rhytides can be efficiently improved by non-
thermal mechanical dermabrasion. Similarly, traumatic and
surgical scars and rhinophyma can be beautifully recontoured
with the diamond fraise or wire brush endpieces. As with any
resurfacing procedure, careful attention to surgical technique
and close monitoring of patients during the postoperative
viduals (types V and VI). The mechanism for this loss of
pigment is not completely understood but is thought to be
caused by a loss of normal melanocytic function. Some
progress in re-establishing skin tone has been made with the
308-nm excimer laser.46
Another postoperative sequela, known as pseudohypopig-
mentation, is seen when a normally repigmented abraded skin
is seen to have a different tone and appearance than adjacent
non-abraded skin. For example, the lentigines and telangiecta-
sias of the non-abraded area contrast with the smooth, even
pigmentation of the dermabraded skin. This disparity can be
reduced by combination procedures such as superficial- or
medium-depth chemical peels of the non-abraded areas to
blend treated and non-treated sites. There has also been great
progress seen with the use of non-ablative lasers and intense
pulsed light sources in treating the hyperpigmentation and
telangiectasias of photodamaged skin. These serve as alterna-
tives to chemical peeling to minimize color mismatch of
dermabraded and non-dermabraded skin.
Increased milia formation is an expected postoperative
sequela, and best treated by gentle extraction after sturdy
epithelium has developed (usually after 1 week). Care must
be taken not to cause excessive trauma of this fragile skin,
which could result in scarring. Acne flares following derma-
brasive surgery are usually due to the occlusive nature of the
postoperative wound care. These can be managed with
routine acne regimens utilizing topical medications (usually
tolerated 2 weeks following treatment) and oral antibiotics.
Ultimately, both of these postoperative events – milia and
acne flares – are transient and patient reassurance is very
helpful.
 OPTIMIZING OUTCOMES
Optimizing outcomes
 Discuss the patient’s goals and objectives within the bounds
of reasonable surgical outcomes.
 Carefully examine the skin and its defects and obtain a
complete medical history.
 Review the advantages and disadvantages of a variety of
available resurfacing options.
 Encourage realistic outcome expectations by reviewing
before and after photographs.
 Review the events before and during surgery and the
postoperative routine of dressing changes to prepare patients
and their caretakers for dermabrasive surgery.
 Scar formation: treat bright erythema after the first 2–3
postoperative weeks with topical high-potency corticosteroid
ointment or Cordran tape (Oclassen) applied once or twice
daily, and follow every 1–2 weeks so that pulsed-dye laser
intervention and intralesional corticosteroids can be given if
necessary.
 Permanent pigmentary alteration: 308-nm excimer laser has
shown some progress in re-establishing skin tone in these
patients.
 Pseudohypopigmentation: can be reduced by combination
procedures such as superficial- or medium-depth chemical
peels of the non-abraded areas to blend treated and
non-treated sites.
 Increased milia formation: best treated by gentle extraction
once sturdy epithelium has developed (usually after 1 week).
 Acne flares: manage with routine acne regimens.
 PITFALLS AND THEIR MANAGEMENT
Pitfalls and their management
 Postoperative infections: prescribe prophylactic antibiotics to
patients with a history of impetigo and prophylactic antiviral
medication to patients with a history of herpetic infections.
 Postoperative herpetic infection: prescribe antiviral
medications.
 Delayed re-epithelialization and hypertrophic scarring in
patients during or shortly after isotretinoin therapy: postpone
dermabrasion for 6–12 months after a course of isotretinoin.

536
Part 3  Aesthetic Surgical Procedures
21. Yarborough JM Jr. Ablation of facial scars by programmed dermabrasion.
J Dermatol Surg Oncol 1988;14:292–294.
22. Alster TS, West TB. Resurfacing of atrophic facial acne scars with a high-
energy, pulsed carbon dioxide laser. Dermatol Surg 1996;22:151–154,
discussion 154–155.
23. Roenigk HH Jr. Dermabrasion for miscellaneous cutaneous lesions
(exclusive of scarring from acne). J Dermatol Surg Oncol 1977;3:322–
328.
24. Clabaugh WA. Tattoo removal by superficial dermabrasion. Five-year
experience. Plast Reconstr Surg 1975;55:401–405.
25. Coleman WP 3rd, Yarborough JM, Mandy SH. Dermabrasion for prophy­
laxis and treatment of actinic keratoses. Dermatol Surg 1996;22:17–21.
26. Hanke CW, O’Brian JJ, Solow EB. Laboratory evaluation of skin refriger-
ants used in dermabrasion. J Dermatol Surg Oncol 1985;11:45–49.
27. Rubenstein R, Roenigk HH Jr, Stegman SJ, et al. Atypical keloids after
dermabrasion of patients taking isotretinoin. J Am Acad Dermatol
1986;15:280–285.
28. Roenigk HH Jr, Pinski JB, Robinson JK, et al. Acne, retinoids, and derm­
abrasion. J Dermatol Surg Oncol 1985;11:396–398.
29. Katz BE, MacFarlane DF. Atypical facial scarring after isotretinoin
therapy in a patient with previous dermabrasion. J Am Acad Dermatol
1994;30:852–853.
30. Roenigk HH Jr, Pinski JB, Robinson JK, et al. Acne, retinoids, and derm­
abrasion. J Dermatol Surg Oncol 1985;11:396–398.
31. Hanke CW, O’Brian JJ. A histologic evaluation of the effects of skin
refrigerants in an animal model. J Dermatol Surg Oncol 1987;13:664–669.
32. Hanke CW, Roenigk HH Jr, Pinksi JB. Complications of dermabrasion
resulting from excessively cold skin refrigeration. J Dermatol Surg Oncol
1985;11:896–900.
33. Coleman WP 3rd, Klein JA. Use of the tumescent technique for scalp
surgery, dermabrasion, and soft tissue reconstruction. J Dermatol Surg
Oncol 1992;18:130–135.
34. Goodman G. Dermabrasion using tumescent anesthesia. J Dermatol Surg
Oncol 1994;20:802–807.
35. Rifat SL, Eastwood MR, McLachlan DR, et al. Effect of exposure of
miners to aluminum powder. Lancet 1996;336:1162–1165.
36. McLachlan DR. Aluminum and Alzheimer’s disease. Neurobiol Aging
1986;7:525–532.
37. Candy JM, Oakley AE, Klinowski J, et al. Aluminosilicates and senile
plaque formation in Alzheimer’s disease. Lancet 1986;1:354–357.
38. Sittig M. Aluminum and aluminum oxide. In: Sittig M, ed. Handbook of
toxic and hazardous chemicals and carcinogens, vol 1, 3rd edn. Park
Ridge, NJ: Noyes Publications 1991; 175–177.
39. Alt TH. Technical aids for dermabrasion. J Dermatol Surg Oncol
1987;13:638–648.
40. Yarborough JM Jr. Dermabrasion by wire brush. J Dermatol Surg Oncol
1987;13:610–615.
41. Burks JW, Thomas CC. Wire brush surgery. Springfield, IL: Charles C
Thomas; 1956.
42. Alster T. Laser scar revision: comparison study of 585-nm pulsed dye
laser with and without intralesional corticosteroids. Dermatol Surg
2003;29:25–29.
43. Harmon CB, Zelickson BD, Roenigk RK, et al. Dermabrasive scar revision
– an immunohistochemical and ultrastructural evaluation. Dermatol Surg
1995;21:503–508.
44. Mandy SH. Tretinoin in the preoperative and postoperative management
of dermabrasion. J Am Acad Dermatol 1986;15:878–879, 888–889.
45. Pinski JB. Dressings for dermabrasion: occlusive dressings and wound
healing. Cutis 1986;37:471.
46. Grimes PE, Bhawan J, Kim J, et al. Laser resurfacing-induced hypopig-
mentation: histologic alterations and repigmentation with topical photo-
chemotherapy. Dermatol Surg 2001;27:515–520.
period will improve surgical outcomes and decrease the rate
of complications.
 REFERENCES
1. Hopping S. The power peel: its emergence and future in cosmetic
surgery. Int J Cosmet Surg 1999;6:98–100.
2. Tsai R, Wang C, Chan H. Aluminum oxide crystal microdermabrasion:
a new technique for treating facial scarring. Dermatol Surg 1995;21:
531–542.
3. Shim EK, Barnette D, Hughes K, et al. Microdermabrasion: a clinical and
histopathologic study. Dermatol Surg 2001;27:524–530.
4. Freedman BM, Rueda-Pedraza E, Waddell SP. The epidermal and dermal
changes associated with microdermabrasion. Dermatol Surg 2001;27:
1031–1034.
5. Hernandez-Perez E, Ibiett EV. Gross and microscopic findings in patients
undergoing microdermabrasion for facial rejuvenation. Dermatol Surg
2001;27:637–640.
6. Tan MH, Spencer JM, Pires LM, et al. The evaluation of aluminum oxide
crystal microdermabrasion for photodamage. Dermatol Surg 2001;27:
943–949.
7. Rajan P, Grimes PE. Skin barrier changes induced by aluminum oxide
and sodium chloride microdermabrasion. Dermatol Surg 2002;28:390–
393.
8. Karimipour DJ, Rittie L, Hammerberg C, et al. Molecular analysis of
aggressive microdermabrasion in photoaged skin. Arch Dermatol 2009,
in press.
9. Karimipour DJ, Kang S, Johnson TM, et al. Microdermabrasion: a molec-
ular analysis following a single treatment. J Am Acad Dermatol 2005;
52:215–223.
10. Karimipour DJ, Kang S, Johnson TM, et al. Microdermabrasion with
and without aluminum oxide crystal abrasion: a comparative molecular
analysisi of dermal remodeling. J Am Acad Dermatol 2006;54:405–
410.
11. Fang JY, Lee WR, Shen SC, et al. Enhancement of topical 5-
aminolevulinic acid delivery by erbium:YAG laser and microderma­
brasion: a comparison with iontophoresis and electroporation. Br J
Dermatol 2004;151:132–140.
12. Katz BE, Truong S, Maiwald DC, et al. Efficacy of microdermabrasion
preceeding ALA application in reducing the incubation time of ALA in
laser PDT. J Drugs Dermatol 2007;6:140–142.
13. Gerritsen MJ, Smits T, Kleinpenning MM, et al. Pretreatment to
enhance protoporphyrin IX in photodynamic therapy. Dermatology
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14. Freedman BM. Topical antioxidant application enhances the effects of
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15. Kurtin A. Surgical planing of the skin. Arch Dermatol Syphilol 1953;68:
389–397.
16. Robbins N. Dr Abner Kurtin, father of ambulatory dermabrasion. J Der-
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17. Orentreich D, Orentreich N. Acne scar revision update. Dermatol Clin
1987;5:359–368.
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J Dermatol Surg Oncol 1986;12:260–265.
19. Solotoff SA. Treatment for pitted acne scarring – postauricular punch
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1995;21:543–549.

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32
Laser Treatment of Tattoos and
Pigmented Lesions
Emmy M Graber MD, Vivek Iyengar MD, Thomas E Rohrer MD, and Kenneth A Arndt MD
Summary box
 Various lasers and light sources effectively treat pigmented
lesions and tattoos with minimal downtime and superior
cosmetic outcomes.
 Q-switched lasers with extremely short pulse durations
are best suited for the selective destruction of commonly
encountered pigmented lesions.
 Intense pulsed light sources can improve pigmentary and
vascular components of photodamaged skin.
 Multiple treatments with fractional photothermolysis can
improve pigmented lesions with minimal downtime.
 Adjusting the fluence for each patient based on observed
clinical end points will give the best results.
 Proper patient selection and patient postoperative education
will optimize outcomes.
 INTRODUCTION
Most lasers used in dermatology today are based on the prin-
ciple of selective photothermolysis.1 According to this theory,
using the proper wavelength can cause light energy to be
preferentially absorbed by a target chromophore in the skin
and transferred into heat energy. Different chromophores in
the skin, such as melanin in pigmented lesions, oxyhemo-
globin in vascular lesions, and water in all cells, preferentially
absorb certain wavelengths of light. By designing a laser to
produce a wavelength of light that is better absorbed by the
target chromophore than the surrounding tissue, it is possible
to selectively heat that chromophore to the point of irrevers-
ible damage. By limiting the time that the laser is fired into
the chromophore (the pulse duration), it is possible to contain
the damage to the selected chromophore. If the laser is fired
in a time shorter than the target’s thermal relaxation time
(the time required for the target to lose 50% of heat), the
generated heat will cause selective damage to the target
chromophore. If the laser pulse duration is too long (greater
than the chromophore’s thermal relaxation time), the heat
produced in the chromophore will have time to spread to
surrounding structures, causing non-selective damage that
may lead to scarring. Choosing an appropriate wavelength and
pulse duration makes it possible to selectively heat and
destroy certain chromophores in the skin without damaging
surrounding structures. In this manner, vascular lesions, pig-
mented lesions, and hair may all be selectively targeted and
destroyed.
The chromophore targets in lentigines, and most pigmented
lesions, are tiny melanosomes.2 Melanosomes, the intracyto-
plasmic organelles found in melanocytes, are the sites of
melanin biosynthesis. After formation in the melanocytes,
melanosomes and their melanin are transferred to surround-
ing keratinocytes. Since melanosomes are extremely small,
they cool very quickly when heated (i.e. have a short thermal
relaxation time). The estimated thermal relaxation time
of a melanosome is approximately 250–1000 nanoseconds.3
Therefore, lasers with very short pulse durations, in the nano-
second domain, are ideally suited to target the small melano-
some chromophore. Such short-pulsed lasers are called
Q-switched (QS) lasers, indicating ‘quality-switched.’ These
lasers store large amounts of energy in the laser cavity through
the use of an optical shutter. When the laser fires, the shutter
is then able to release a high-powered pulse with an extremely
short pulse duration, in the nanosecond range.
The delivery of an exceptionally high-energy laser pulse
within a very short time span results in rapid heating of the
target melanosome (estimated at 10 million degrees per
second), causing it to explode.4 While electron microscopy
has confirmed highly-selective destruction of melanosomes
within melanocytes and melanized keratinocytes, it is not
known precisely how the pigment-containing cells are
destroyed. It is believed that melanocytes and melanized
keratinocytes are destroyed due to mechanical damage
from acoustic waves that emanate from the absorbing
melanosome.5,6
By inducing damage to the melanosome through the use of
laser radiation, a number of commonly encountered pig-
mented lesions can be treated with excellent cosmetic out-
comes. There are many lasers that can be employed to treat
pigmented lesions (Table 32.1). As a target chromophore,
melanin has a broad absorption spectrum within the ultravio-
let, visible, and near-infrared (NI) light range (Fig. 32.1).
Ideal wavelengths to treat pigmented lesions would be those
with greater absorption by melanin than by oxyhemoglobin.
However, melanin light absorption decreases with increasing
wavelength. Therefore longer wavelengths penetrate deeper,
but are absorbed less by melanin. Given that the pigment in
lentigines is very superficial, pigmented lasers with shorter
wavelengths, such as pulsed-dye (510  nm), QS potassium
titanyl phosphate (KTP) (532 nm), and QS ruby (694 nm)
lasers are typically used. The shorter wavelength only allows

538
Part 3  Aesthetic Surgical Procedures
of Ota and tattoos. QS alexandrite (755 nm) lasers, with an
intermediate wavelength, may be used for both superficial
and deep pigment.
Longer pulse width ruby, alexandrite, and Nd:YAG lasers,
predominantly used for hair removal, have the same wave-
lengths as the QS versions used in the treatment of pig-
mented lesions. However, they operate in a non-QS mode
resulting in laser energy delivery over a longer time interval
– milliseconds rather than nanoseconds. The longer pulse
width creates somewhat less confined thermal damage, but
with higher energies and less epidermal cooling than used
during hair removal, they are capable of removing some pig-
mented lesions in the epidermis. The longer pulse widths also
allow for higher fluences so that larger structures such as hair
follicles and nests of pigmented cells may be targeted. Their
use in the treatment of congenital and acquired nevi remains
under investigation. Other longer pulse duration lasers (in the
millisecond range), such as the KTP (532 nm) and the pulsed-
dye laser (585 nm), can be used to treat lentigines because
of their excellent melanin absorption.
Another option for treating superficial pigmented lesions is
intense pulsed light sources. Unlike laser devices with a col-
limated beam at a specific wavelength, these devices emit
polychromatic light ranging from 515 to 1200 nm with filters
to cut off light below a predetermined wavelength.1,7 There
is a diversity of different intense pulsed light sources that
differ in their wavelengths by using varying cut-off filters. By
providing light energy over broader wavelengths, the intense
for limited penetration depth of the laser radiation and is
thus not optimal for the treatment of dermal pigmented
lesions or deeper vascular lesions. Longer wavelength
pigmented lasers, such as the QS neodymium:yttrium-
aluminum-garnet (Nd:YAG) (1064 nm), are used for lesions
where the pigment is located in the dermis such as nevus
Table 32.1  Lasers used in the treatment of pigmented lesions
DEVICE
MANUFACTURER
LASER TYPE
WAVELENGTH
(nm)
PULSE
DURATION
SPOT
SIZE (mm)
MAXIMUM
RATE (Hz)
Aura
Laserscope (San
Jose, CA)
KTP
532
1–50 ms
1–4
10
Spectrum
RD-1200S
Palomar (Burlington,
MA)
QS ruby
694
28 ns
5, 6.5
0.8
EpiTouch
Lumenis (Santa Clara,
MA)
QS ruby
694
25 ns
5
0.8
RubyStar
Aesculap Meditec
(Jena, Germany)
QS ruby
694
40 ns
1.5, 3, 4
1
AlexLAZR
Candela
QS alexandrite
755
50 ns
2, 3, 4
5
HT 10
Cynosure
(Chelmsford, MA)
QS alexandrite
755
45–75 ns
2, 4
10
VersaPulse VPC
Lumenis
FD Nd:YAG
532
2–50 ms
2–10
6
QS FD Nd:YAG
532
4 ns
2–6
10
QS Nd:YAG
1064
5 ns
2–6
10
QS alexandrite
755
45 ns
2–6
10
Medlite CG
Continuum (Santa
Clara, CA)
QS FD Nd:YAG
532
5–7 ns
2, 3, 4, 6
10
QS Nd:YAG
1064
5–7 ns
3, 4, 6, 8
10
Quantum
Lumenis
IPL (Flashlamp)
515–1200
0.5–25 ms
8 × 15, 8 × 35
1 pulse/8 seconds
SkinStation
Radiancy
(Orangeburg, NY)
Flashlamp
35 ms
22 × 57
1 pulse/8 seconds
Starlux
Palomar
Flashlamp
500–670 and
870–1200 (LuxG
handpiece)
10 × 15
Starlux
Palomar
Flashlamp
525–1200 (LuxY
handpiece)
46 × 16
FD, frequency-doubled; IPL, intense pulsed light; KTP, potassium titanyl phosphate; Nd:YAG, neodymium:yttrium-aluminum-garnet; QS, Q-switched.
Wavelength (nm)
UV
Visible
Near IR
Absorption coefficient (cm–1)
Ruby laser
Melanin
Oxyhemoglobin
400
500
600
700
800
900
1000
101
102
103
Absorption spectrum diagram
Figure 32.1  Absorption spectrum diagram.

539
Chapter 32  Laser Treatment of Tattoos and Pigmented Lesions
etrate more deeply than shorter wavelengths and produce
relatively less epidermal damage with the same dermal effect.
Patients with ‘suntans’ should not be treated because they
are at a higher risk of spotty hypopigmentation, which may
persist for weeks to months after treatment.
Before treatment, a thorough medical history should be
taken. If there is any history of poor wound healing,
postinflammatory hyperpigmentation, bleeding disorders, or
isotretinoin use in the preceding 6 months, caution should be
exercised. Any of the above conditions may cause a prolonged
recovery or scarring. Pigmented lesions should also be prop-
erly diagnosed before laser treatment. If there is any doubt
that a lesion is benign, a biopsy should be performed in order
to assure that there is no significant atypia or malignant
potential. Furthermore, biopsies may be helpful in determin-
ing the depth of pigment present (i.e. epidermal versus
dermal) and possibly the type of pigment in a lesion caused
by foreign body implantation. Finally, patients should be
counseled appropriately with regard to having realistic expec-
tations in that multiple treatments may be necessary and that
all lesions may not clear completely.
Safety
Of primary concern in the use of pigmented lesion lasers (as
with other laser devices) is ocular safety. Retinal injury is the
primary hazard and all personnel in the room must wear
protective goggles. The ‘light’ from these lasers is out of the
visible range and is deeply penetrating and of great intensity.
Hence, these lasers are potentially even more dangerous than
visible light lasers. The patient must have appropriate eye
wear and the placement of intraocular metal eye shields
should be considered when treatment is in the immediate
periocular area. Furthermore, reflective surfaces and windows
should be covered, no flammable materials should be present,
and access to the procedure room should be limited during
laser treatment.
QS lasers, and especially the QS 1064-nm Nd:YAG laser,
can cause some tissue and blood splatter. As such, universal
precautions and the use of the protective plastic cone attached
to the hand piece should be employed to prevent splatter.
Alternatively, a clear film (i.e. Second Skin, Spenco Medical,
Waco, TX; Tegaderm, 3M Healthcare, St Paul, MN) may be
placed on the skin over the treatment area to eliminate
outward splatter. However, it must be noted that this tech-
nique results in a slightly reduced laser light transmission and
may increase the risk of ocular injury as a result of reflection
from the surface of the dressing. When using this technique,
an additional 0.5–1.0 J/cm2 is required to achieve equivalent
target absorption.
Of paramount importance in the preoperative preparation
of the patient is thorough removal of all make-up, creams,
topical anesthetics, sunblocks, etc. These products can hinder
the delivery of laser energy to the target and may contain
ingredients with the potential to ignite. Furthermore, the use
of alcohol in cleaning the area must be followed by assurance
that alcohol is not present on the surface of the skin at the
time of laser energy delivery because alcohol is a potential
source for flash fire development. Flammability can also
occur when the laser is used in the presence of oxygen (e.g.
nasal cannula). Drapes, towels, and sponges may be flamma-
ble, thereby necessitating the use of wet or non-flammable
material.
pulsed light is advantageous since it can improve both the
vascular and pigmentary component of photodamage.
There are also lasers that do not rely on the theory of
selective photothermolysis to remove pigment but instead
non-selectively eliminate pigment in the skin. Such lasers
ablate the skin and any associated pigment is destroyed as a
secondary event. These types of lasers include the carbon
dioxide
(CO2)(10 600  nm),
erbium:yttrium-aluminum-
garnet (Er:YAG) (2940  nm), yttrium-scandium-gallium-
garnet (YSGG) (2740  nm), and the fractional lasers. The
newer fractional lasers (available in both ablative and non-
ablative wavelengths) damage columns of the epidermis and
dermis while leaving interspersed areas unaffected. In this
manner, there is faster healing as the surrounding normal
tissue migrates into the areas of damage to heal each irradi-
ated column. Because only fractions of the pigmented epider-
mis and dermis are affected at a time, a series of treatments
is necessary to achieve the desired result. Another non-selec-
tive method to eliminate pigment is through plasma skin
resurfacing. This is not a laser but is a device that utilizes
radiofrequency energy to convert nitrogen gas into plasma.
The plasma gives up energy to the skin causing rapid heating
down to the dermis, consequentially destroying any pigment-
laden cells.8 Another older non-selective method of removing
superficial pigment is the use of chemical peels.
 HISTORY
The use of lasers for pigmented lesions began in 1963 when
Leon Goldman and colleagues found that 0.5-ms pulses of
ruby laser radiation were selectively absorbed by pigmented
skin.9 Two years later, these investigators also discovered the
specific utility of the QS ruby laser. They found that the
threshold radiant exposure for epidermal damage was 10–100
times lower for a QS ruby laser with a short pulse duration
of 50 ns.10 Despite these early findings, the ability of the QS
ruby laser to selectively target pigment was not initially
appreciated. Instead, for many years, pigmented lesions were
treated with non-selective continuous wave sources such as
the argon11 and CO2 lasers.12 In the late 1980s, Anderson
et al.13 demonstrated that pigment could be selectively dimin-
ished by using the QS Nd:YAG laser pulses at 1064, 532,
and 355 nm. This group also showed that the longer wave-
lengths (which are less well absorbed by melanin) required a
higher energy fluence to be effective. Over the last 20 years,
after further investigation, pulsed lasers and intense pulsed
light sources have become the treatment of choice for epi-
dermal, and pulsed lasers the choice for dermal, pigmented
lesions and tattoos.
 PREOPERATIVE PREPARATION
Patient evaluation
When treating any pigmented lesion, careful attention should
be paid to each patient’s skin type. Lower fluences should be
used in the treatment of patients with darker skin types, since
the threshold response will likely occur at a lower fluence.
When treating both epidermal and dermal pigmented lesions,
patients with darker skin are at greater risk for postoperative
hyperpigmentation or hypopigmentation. For these patients,
it may be preferable to use a longer wavelength device, such
as the 1064-nm Nd:YAG laser, since longer wavelengths pen-

540
Part 3  Aesthetic Surgical Procedures
effective in the treatment of some flat seborrheic keratoses.
Slightly thicker seborrheic keratoses, however, usually require
adjunctive cryotherapy. The response of CALMs and ephe-
lides to laser treatment is often unpredictable (Fig. 32.3).
Multiple treatments may result in clearance and some light-
ening but recurrence is common. Furthermore, transient
hyperpigmentation in the treatment of CALMs in darker skin
phototypes can be problematic. Recently, some have
described the use of Er:YAG superficial resurfacing of CALMs
for better longer-term clearance.18
In our practice, we find that fair-skinned photodamaged
patients with both mild vascular and pigmentary changes are
the best suited for treatment with intense pulsed light
devices. We prefer to treat patients with more significant and
larger lentigines with a selective QS laser device.
Dermal pigmented lesions
The advent of QS lasers revolutionized the treatment of
dermal melanocytosis and tattoos. Before this development,
only non-selective treatments such as dermabrasion, excision,
cryosurgery, and other procedures were available. Because
of their deeper penetration, QS alexandrite (755  nm) and
Nd:YAG (1064  nm) are typically the most effective for
deeper dermal pigment and tattoos.
Melanocytic lesions
QS lasers are extremely helpful in treating nevus of Ota,
which histologically demonstrates dermal dendritic melano-
cytes. It is most common in Asian populations, occurring in
Caucasians at lower incidence rates. Clearance of 70% or
more is reported in patients treated at least five times with
the QS ruby laser19 (Fig. 32.4). Successful treatment of nevus
of Ota has also been demonstrated with QS alexandrite and
QS 1064-nm Nd:YAG lasers.20,21 There are also anecdotal
reports demonstrating the efficacy of the newer fractionatal
technologies, such as the 1440-nm Nd:YAG (Affirm, Cyno-
sure, Inc) in treating nevus of Ota.22 With any modality, the
Anesthesia
Typically, neither infiltrative nor topical anesthesia is required
for the vast majority of treatments using laser or light source
energy in the treatment of pigmented lesions. However, one
must take into account the location, size, and depth of the
lesion as well as the individual pain threshold of the patient.
In our practice, neither topical nor infiltrative anesthesia is
routinely employed in the treatment of lentigines and photo-
damage with either the intense pulsed light source or QS
lasers. For the treatment of larger tattoos, lesions containing
large amounts of dermal pigment (such as nevus of Ota), or
when ablative lasers are used, infiltrative local anesthesia or
regional nerve blocks are employed.
 TECHNICAL ASPECTS
Epidermal lesions
The QS ruby (694 nm) lasers, QS alexandrite (755 nm) lasers,
532-nm lasers, short pulsed-dye (510 nm) lasers, and intense
pulse light devices have all demonstrated efficacy in the treat-
ment of various epidermal lesions including lentigines, café-
au-lait macules (CALMs), and ephelides.1,7,14–16 In addition,
intense pulsed light and the 532-nm pulsed lasers have both
demonstrated benefit for pigmentation from photodamage.
Shorter wavelength lasers are generally well suited for the
treatment of epidermal lesions as a result of their high absorp-
tion by melanin and limited depth of penetration (Fig. 32.2).
However, their efficacy in the treatment of dermal pigmented
lesions is limited because of this limited penetration depth.
Conversely, the longer wavelength lasers such as the 1064-nm
QS Nd:YAG penetrate deeper into the skin for dermal lesions
but have less melanin absorption. Thus, the 1064-nm QS
Nd:YAG is perhaps slightly less effective than shorter wave-
length QS lasers in the treatment of epidermal pigment.
The QS laser has been shown to be superior to both 35%
trichloroacetic acid and cryotherapy in the treatment of len-
tigines.17 QS lasers and 510-nm pulsed-dye lasers are reliably
A
B
Figure 32.2  Solar lentigines of the right
lower cheek (A) before and (B) after one
treatment with 532-nm KTP laser.

541
Chapter 32  Laser Treatment of Tattoos and Pigmented Lesions
to as pseudomelanoma.29,30 Despite this, there has never been
a report of true malignant transformation of a benign pig-
mented lesion following laser treatment.31 Theoretically, laser
treatment of melanocytic lesions may decrease the risk of
malignant transformation of a benign pigmented lesion simply
by reducing the population of existing potentially premalig-
nant cells. One study reported that no significant malignant
markers (such as proliferation cell nuclear antigen, pyrimi-
dine dimers, 8-OhdG, and p53) were found following treat-
ment of nevi with QS lasers.32 While these findings are
notable, additional study is needed to assess the outcome of
QS laser treatment of nevi. Until more is known, it is prudent
to perform a biopsy prior to laser treatment to confirm the
benign nature of the nevus. Laser treatment should not be
performed on nevi in patients with a personal or family
history of malignant melanoma.
When treating nevi, multiple treatments and a high rate of
recurrence are typical, with thicker lesions being more resist-
ant to treatment. Congenital nevi with nests residing deeper
in the dermis and around adnexa are particularly difficult to
treat with laser therapy. One group of investigators has
obtained impressive clearance with non-QS lasers with pulse
widths in the millisecond domain.33 The wider pulse width
allows for less selective thermal damage and perhaps better
delivery of energy to entire nests rather than to individual
pigmented cells.
degree of lightening is usually directly proportional to the
number of treatments performed. Acquired nevus of Ota-like
macules (also known as Hori’s nevus) differ from the classic
nevus of Ota in that they are bilateral, spare mucosa, and
occur later in life. Various QS lasers have been reported
effective in treating nevus of Ota-like macules.23–25 Manus-
kiatti et  al.24 demonstrated greater clearing of bilateral
nevus of Ota-like macules with a combination CO2 and QS
ruby laser treatment than with QS ruby laser alone. Laser
treatment of any pigmented lesion is often complicated by
postinflammatory hyperpigmentation. A recent study of QS
Nd:YAG treatment for acquired nevus of Ota-like macules
suggests that epidermal cooling may be associated with an
increased risk of postinflammatory hyperpigmentation.26
Laser treatment of melanocytic nevi is controversial since
it is unclear whether laser irradiation has any potential to
induce malignant change in nevus cells. In-vitro studies of
melanoma cells treated with QS lasers have found changes in
cell surface integrin expression, with subsequent alteration of
cell migration.27 Another in-vitro study found a significant
increase in p16INK4a in p16-positive cell lines following
irradiation with QS laser light and suggested that sublethal
laser damage may increase DNA damage leading to an
increase in p16 expression.28 In clinical practice, benign-
appearing nevi that tend to recur following laser treatment
may show new-found clinical and histologic atypia, referred
A
B
Figure 32.3  Café-au-lait macule on the left thigh (A) immediately after and (B) 2 months following a test spot with a 755-nm
alexandrite laser with a 50-ns pulse duration.
A
B
Figure 32.4  Nevus of Ota (A) before and (B) after five treatments. (Photo courtesy of Dr Tadashi Tezuka.)

542
Part 3  Aesthetic Surgical Procedures
of tattoos, and is the most responsive part of the pigment to
the laser treatment. Unfortunately, no regulation exists at the
state and federal level with regard to standards in the com-
position or amount of pigment deposited at the time of tattoo
placement. As a result, the response to laser treatment of
professional tattoos is often difficult to predict.
QS lasers lighten the majority of tattoos, but clearance is
related to density, color, and composition of the tattoo. Typ-
ically, amateur, dark, uniformly-colored tattoos clear with
some reliability after three to five treatments (Fig. 32.5).
Professional multicolored tattoos do not respond predictably
and may not clear completely even after more than ten treat-
ments (Fig. 32.6). Tattoos with red, yellow, and orange are
particularly difficult to completely clear with most tattoo
lasers. Older tattoos, especially those that have started to
fade slightly on their own, tend to clear in fewer treatments
than the more densely pigmented new tattoos. Furthermore,
tattoos on distal extremities tend to be more resistant to
treatment as a result of decreased lymphatic drainage.50 The
fate of tattoo ink particles after laser irradiation remains
unclear. Possibilities include direct fragmentation of ink par-
ticles, release of ink into the extracellular dermal space,
partial elimination of ink in a scale crust when present,
rephagocytosis of laser-altered residual tattoo ink particles,
and increased ink elimination via the lymphatics.51
Laser treatment of melasma, postinflammatory hyperpig-
mentation, and periorbital pigmentation is difficult. QS laser
treatment often paradoxically increases dermal melanophages
and is generally not recommended as first-line treatment of
melasma or postinflammatory pigmentation.34,35 Repeated
treatments with fractional photothermolysis utilizing the
1550-nm laser (Fraxel, Reliant Technologies) has shown
some benefit for melasma.36 Periorbital pigmentation may
result from dermal melanin deposition, chronic dermatitis,
chronic edema, or prominent superficial blood vessels. When
secondary to dermal melanin deposition, the QS ruby laser
is effective37 as is the QS alexandrite laser immediately fol-
lowing CO2 laser treatment.38
Medication-induced pigmentation
Numerous medications may cause unusual skin pigmentation.
The most commonly encountered in dermatology is minocy-
cline-induced pigmentation. This condition is seen after long-
term minocycline use and pigment found within dermal
macrophages typically stains positively for melanin and occa-
sionally iron.39 Although pigmentation typically resolves with
cessation of therapy, it may take years for total resolution.
As such, treatment with a variety of QS lasers is reported to
be effective and may be warranted.40–44 Limited reports have
also documented success of fractional photothermolysis for
minocycline hyperpigmentation.45
Less commonly encountered medication-induced hyperpig-
mentation is that due to imipramine, amiodarone, or topical
hydroquinone (causing exogenous ochronosis). These dermal
hyperpigmented disorders have all been successfully treated
with QS lasers.46–49
Tattoos
In amateur tattoos, pigment is typically present in lower
concentrations and located in various levels of the dermis. In
contrast, professional tattoos have dense pigment that is
implanted at the junction of the papillary and reticular
dermis.5 Commonly used pigments in professional tattoos
include cinnabar and cadmium red (red), cadmium sulfide
(yellow), chromium salts (green), cobalt salts (dark blue),
titanium dioxide (white), and iron oxide (red–brown) (Table
32.2). All tattoos contain carbon, which adds to the dark hue
Table 32.2  Tattoo pigments
COLOR
PIGMENT
LASER
Red
Cinnabar
Cadmium red
QS 510-nm pulsed-dye/
QS KTP
Red–brown
Iron oxide
QS KTP
Yellow
Cadmium sulfide
QS KTP
Green
Chromium salts
QS ruby/QS alexandrite
Dark blue
Cobalt salts
QS ruby/QS alexandrite/
QS Nd:YAG
Black
Carbon
QS rubs/QS alexandrite/
QS Nd:YAG
White
Titanium dioxide
Any QS laser
A
B
Figure 32.5  Amateur black India ink tattoo (A) before and (B) after two treatments using a 755-nm alexandrite laser with a 50-ns
pulse duration. Note the clearing of amateur tattoo with only two treatments.

543
Chapter 32  Laser Treatment of Tattoos and Pigmented Lesions
presumed to be gas bubbles and gradually disappear over 20
minutes, correlating to the disappearance of the clinical ash-
white color over the same period of time.53 The exact content
of the gas bubbles is not known, but may be water vapor,
nitrogen, or other gases. The adequate laser exposure dose
for melanosome damage correlates well with the clinical
threshold for immediate skin whitening. In other words, if
the clinical ash-white color is not visible, the laser exposure
dose is not sufficient. Darker skin has a lower threshold for
whitening due to a higher epidermal melanin content.53 If the
fluence is too low, whitening may be imperceptible. With
higher fluences, solid whitening with epidermal disruption and
pinpoint bleeding may occur. At fluences less than threshold,
paradoxical hyperpigmentation may occur as a result of
melanocyte stimulation. Excessive fluences can result in a
thermal burn with tissue sloughing, prolonged wound healing,
hypopigmentation, hyperpigmentation, textural changes, and
scarring. For darker phototypes, lower fluences with test
spots should be employed. Similarly, patients with a suntan
should postpone treatment because of the higher risk of
 OPTIMIZING OUTCOMES
Epidermal lesions
As outlined previously, preoperative considerations are of the
utmost importance. Anesthesia is not typically required but
the area to be treated should be thoroughly cleaned to remove
any creams, make-up, etc. The laser must be calibrated before
operation and the hand piece should be held perpendicular
to the skin with an attached plastic cone or guide on the skin.
The parameters selected depend on laser type, skin photo-
type of the patient, and melanin content of the target lesion.
Table 32.3 outlines common treatment parameters for various
epidermal pigmented lesions. Generally, lower fluences are
used for darker lesions with abundant target chromophore.
When treating pigmented lesions, QS lasers generate an
immediate ash-white color at the site of impact (Fig. 32.7).
The cause of this tissue response is due to heat-induced steam
cavities in melanosomes which cause a scattering of visible
light, producing a white color.52 These steam cavities are
A
B
Figure 32.6  Multicolor tattoo (A) before and (B) after ten treatments.
A
B
Figure 32.7  Immediate whitening of
epidermal pigment following treatment
with a QS 694-nm ruby laser; (A) before
and (B) after treatment.

544
Part 3  Aesthetic Surgical Procedures
Table 32.3  Standard treatment parameters for pigmented lesions and tattoos
LESION
LASER
SPOT SIZE (mm)
FLUENCE (J/cm2)
RETREATMENT
Lentigines
QS ruby
6.5
2.0–4.0
4–8 weeks
QS Nd:YAG (532 nm)
3
0.7–1.0
QS alexandrite
4
4.0–6.0
Pulsed dye (510 nm)
3
2.5
CALMs
QS ruby
6.5
3.0–4.5
4–8 weeks
QS Nd:YAG (532 nm)
3
1.0–1.5
QS alexandrite
4
4.0–6.0
Pulsed dye (510 nm)
5
2.0–3.5
Er:YAG
3–7
5.0–10
Becker’s nevus
QS ruby
6.5
3.0–4.5
4–8 weeks
QS Nd:YAG (532 nm)
3
1.5–1.8
QS Nd:YAG (1064 nm)
3
4.0–5.0
QS alexandrite
3
4.0–9.0
Nevus spilus
QS ruby
6.5
3.0–4.5
4–8 weeks
QS Nd:YAG (532 nm)
3
1.5–2.0
QS Nd:YAG (1064 nm)
3
4.0–4.4
QS alexandrite
3
6.0–9.0
Nevus of Ota
QS ruby
6.5
5.0–6.0
6–12 weeks
QS Nd:YAG (1064 nm)
3
4.0–5.0
QS alexandrite
3
6.0–9.0
Tattoos
QS ruby
5
7.0–10.0
6–12 weeks
QS ruby
6.5
3.0–6.0
QS Nd:YAG (532 nm)
3
2.0–3.5
QS Nd:YAG (1064 nm)
3
4.0–8.0
QS alexandrite
3
6.0–9.0
Pulsed dye (510 nm)
3–5
2.5–3.5
spotty pigmentation abnormalities, which may persist for
months. Typically, treatments are spaced 4–6 weeks apart.
Lentigines often require only one to two treatments, while
CALMs or ephelides may require multiple treatments.
Treatment of CALMs with Er:YAG resurfacing typically
requires only one treatment with a fluence sufficient for
complete removal of the epidermis. However, Er:YAG treat-
ment does carry a higher risk of scarring than treatment with
more selective QS lasers. If an Er:YAG resurfacing laser is
used to treat CALMs, infiltrative anesthesia is necessary.
Many patients are more comfortable with the use of preop-
erative topical anesthesia.
Unlike treatment with laser devices in which ‘specific’
lesions are treated, patients undergoing intense pulsed light
treatments typically have the entire face or large subunits
treated. The practitioner must take special precautions to
ensure that the contact cooling device is placed in the ‘on’
position while treating. Unlike QS lasers, cooling is vitally
important to minimize the risk of significant epidermal injury.
To ensure proper cooling, a coolant medium (e.g. ultrasound
gel) should be applied liberally to the area to be treated. The
hand piece is then placed in direct contact with the coolant
medium on the skin surface and the area is treated with
slightly overlapping pulses. Areas may be single, double, or
triple pulsed according to the user’s discretion. At least six
treatment sessions spaced 4–6 weeks apart are recommended
to achieve optimal results. One of the benefits of this series
of treatments is the improvement in subtle vascular telangiecta-
sia and skin texture. The practitioner should take extra care
to turn off the cooling device and wipe the hand piece clean
of any residual coolant gel when not in ‘treatment mode.’ If
not, the gel may freeze and harden on the hand piece.
Dermal lesions
Unlike epidermal lesions, dermal lesions may require the use
of anesthetic. A topical anesthetic or nerve blocks may be
used for patient comfort. For local tissue infiltration around
the eyes, a mixture of equal parts 2% lidocaine with
1 : 100 000 epinephrine, 0.5% bupivacaine, and 75U of
hyaluronidase can be used. The addition of hyaluronidase
facilitates tissue diffusion and bupivacaine provides long-
lasting anesthesia.
As with epidermal lesions, the surface to be treated should
be thoroughly cleansed and the laser must be calibrated
before operation. The parameters selected depend on laser
type, skin phototype of the patient, and melanin content of
the target lesion. Generally, higher fluences are employed for
dermal lesions than for epidermal lesions. Uniform whitening
is the desired end point after treatment with an approxi-
mately 10% overlap (Fig. 32.8). Fluences that are too low
may cause a paradoxical hyperpigmentation, whereas exces-
sive fluences may result in epidermal sloughing, prolonged
wound healing, pigmentary abnormality, and scarring. Patients

545
Chapter 32  Laser Treatment of Tattoos and Pigmented Lesions
lowing treatment, with treatment intervals typically 6–8
weeks apart.
No single laser is capable of eliminating all tattoo colors.
QS ruby55 and alexandrite lasers56 are best for black, blue,
and green pigments, whereas QS Nd:YAG (1064  nm)57 is
best for blue and black, but not green pigments. Shorter
wavelength lasers such as the 510-nm pulsed dye58 and QS
532-nm KTP5 are best for red and yellow pigments. Practi-
tioners should be wary of treating cosmetic tattoos with
shades of white, red, orange, tan, or brown as is often seen
in make-up tattoos (e.g. lip liner). These tattoos may contain
iron oxide or titanium dioxide that when treated with QS
lasers are at risk of immediate irreversible darkening of the
pigment. This darkening is a result of the conversion of ferric
oxide to ferrous oxide in these pigments. If this occurs,
the therapeutic armamentarium includes multiple additional
treatments, resurfacing, or surgical excision. Reports of
multiple treatments with single-pass resurfacing laser have
demonstrated success in treating these tattoos with minimal
risk of pigment darkening.59,60 In addition to partially or com-
pletely removing the cosmetic tattoo pigment, perioral
rhytides may be significantly improved (Fig. 32.9).
 POSTOPERATIVE CARE
AND COMPLICATIONS
Postoperatively, cool compresses, emollient application, and/
or the use of occlusive dressings (i.e. Vigilon, CR Bard,
Murray Hill, NJ; Second Skin, Spenco Medical) can provide
some pain relief. The whitening caused by laser irradiation
typically fades within 20–30 minutes. Some patients may
develop an urticarial reaction with edema and pruritus, which
will subside within the hour but can be treated with oral
antihistamines. Treated areas may appear darker and develop
crusting in the first 7–10 days after treatment. Patients should
be instructed to gently clean treated areas daily, apply occlu-
sive emollient ointments to hasten healing, and allow crusts
with darker phototypes require the use of lower fluences and
are probably best treated with longer wavelength lasers such
as the 1064-nm Nd:YAG. The 1064-nm wavelength with its
decreased melanin absorption and deeper penetration may
allow for sparing of epidermal melanocytes. Multiple treat-
ment sessions spaced 6–8 weeks apart are typical. Because
the clearing of dermal pigment is in large part a function of
phagocytosis, clearing is slow and gradual. Patients continue
to see lightening of their lesions for many months following
treatment.
Tattoos
Infiltrative anesthesia with 1% lidocaine and epinephrine is
preferred for larger tattoos. Preoperative skin preparation and
technique are very similar to that used for dermal lesions.
One exception may be the use of an occlusive dressing over
the tattoo during treatment. An occlusive dressing acts as a
heat sink (closer index of refraction) and may help protect
the epidermis. It also acts as a barrier to tissue splatter. Treat-
ment is performed through the dressing with slight overlap
of pulses to avoid untreated fragments of tattoo. When pulses
are spaced too far apart, the treated tattoo often takes on a
‘honeycomb’ appearance, which is cosmetically unappealing.
Treatment with the highest possible fluence is generally rec-
ommended. Lesions should be treated with one or two pulses
to determine the tissue response. The desired response is
immediate, bright tissue whitening (see Fig. 32.8). Epidermal
disruption or bleeding represents excessive fluence and should
be adjusted accordingly. However, some pinpoint bleeding is
acceptable. For tattoos with darker, dense pigment, lower
fluences are recommended for initial treatments. As the
pigment lightens, higher fluences can be used. In darker
skinned patients, the 1064-nm Nd:YAG laser is recom-
mended for blue or black pigment so that the longer wave-
length can target dermal tattoo pigment while selectivity
sparing epidermal melanin.54 Similar to dermal pigmented
lesions, tattoo pigment may lighten for several months fol-
Figure 32.8  Immediate whitening and
some mild pinpoint bleeding of tattoo
following treatment using a 755-nm
alexandrite laser with a 50-ns pulse
duration.

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Part 3  Aesthetic Surgical Procedures
 SUMMARY
Various pigmented lesions and tattoos can be treated safely
and effectively with pigment-selective laser irradiation. These
lasers can provide superior cosmetic outcomes compared
with older, standard non-selective therapies. Proper patient
selection and preoperative safety are essential. Adjusting laser
fluences to desired immediate clinical end points will result
in optimal results while minimizing untoward effects. Intense
pulsed light and fractional photothermolysis provide another
option to treating pigmented lesions. Future directions may
include the use of combinations of devices, longer pulse
widths for larger pigmented structures, and the addition of
photodynamic therapy.
to slough on their own. Furthermore, patients need to avoid
excessive sun exposure and apply appropriate sunscreens.
Patients treated with the 532-nm KTP or 510-nm pulsed-dye
lasers may develop purpura for 7–10 days as a result of the
significant absorption of hemoglobin at these wavelengths.
Given the more aggressive nature of the treatment of
dermal lesions and tattoos versus epidermal lesions, postop-
erative changes can be more pronounced. When treating
tattoos, pinpoint bleeding is seen immediately after treat-
ment. Vesiculation may occur with shorter wavelength
QS laser treatment of tattoos, but typically heals without
scarring or textural changes. However, the development
of blistering in the treatment of dermal lesions typically
indicates the use of excessive fluences. Ice packs, cool
compresses, and hydro-occlusive dressings will reduce
postoperative stinging and pain. Daily cleansing of treated
areas with soap and water and frequent application of occlu-
sive ointments are recommended.
Patients should also be counseled with regard to sun pro-
tection and avoidance to minimize the risk of unwanted hypo-
and/or hyperpigmentation. Although the risk of scarring and
permanent hypopigmentation is very low, the risk is slightly
higher when treating tattoos. Factors that may increase risk
include excessive fluences using small spot sizes, tattoos con-
taining ‘double ink’ (i.e. two tattoos on top of one another),60
pulse stacking, too frequent treatments, and treatment of
tattoos in areas more prone to scar such as the ankle, deltoid,
and chest areas. In addition, textural changes that may be
present but camouflaged before laser treatment may become
more apparent after treatment. The use of preoperative pho-
tographs may be helpful and essential in this regard.
Pigmented lesions treated with non-selective lasers such as
the CO2 and Er:YAG may have an occlusive dressing placed
on the wound for the first few days postoperatively. Subse-
quently, daily cleansing, soaks to minimize crusting, and fre-
quent application of occlusive emollients is required. After
re-epithelialization, erythema may persist for some time,
which may require prolonged patient reassurance.
In those patients treated with intense pulsed light devices,
postoperative reactions are less pronounced. There will be
some mild postoperative erythema and burning, which can
be soothed with cool compresses. Pigmented lesions will
A
B
Figure 32.9  Cosmetic tattoo of the vermilion border (A) before and (B) 4 weeks after treatment with a combined CO2 and Er:YAG
laser resurfacing procedure.
Pitfalls and their management
 Patients should be counseled with regard to sun protection
and avoidance before and after treatment to minimize the risk
of unwanted hypopigmentation or hyperpigmentation.
 Patients should have realistic expectations as to the number of
treatments and the potential outcomes.
 The development of blistering in the treatment of dermal
lesions typically indicates the use of excessive fluences.
 Postoperative stinging and pain can be reduced with the use
of ice packs, cool compresses, hydro-occlusive dressings,
daily cleansing of treated areas with soap and water, and
frequent application of occlusive ointments.
 Patients treated with intense pulsed light devices often require
multiple treatments to achieve the desired result. They may
develop some mild postoperative erythema and burning,
which can be soothed with cool compresses.
darken for up to 1 week. Similar to the intense pulsed light
devices, there is also minimal recovery time with fractional
photothermolysis. Some swelling and erythema can be seen
for 2–3 days after treatment, and there is a low risk of postin-
flammatory hyperpigmentation.
 PITFALLS AND THEIR MANAGEMENT

547
Chapter 32  Laser Treatment of Tattoos and Pigmented Lesions
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vitro. Lasers Surg Med 1996;18:63–71.
28. Chan HH, Xiang L, Leung JC, et al. In vitro study examining the effect
of sub-lethal QS 755  nm lasers on the expression of p16INK4a on
melanoma cell lines. Lasers Surg Med 2003;32:88–93.
29. Dummer R, Kempf W, Burg G. Pseudo-melanoma after laser therapy.
Dermatology 1998;197:71–73.
30. Hwang K, Lee WJ, Lee SI, et al. Pseudomelanoma after laser therapy.
Ann Plast Surg 2002;48:562–564.
31. Grevelink JM, van Leeuwen RL, Anderson RR, et al. Clinical and histo-
logical responses of congenital melanocytic nevi after single treatment
with Q-switched lasers. Arch Dermatol 1997;133:349–353.
32. Goldberg DJ, Stampien T. Q-switched ruby laser treatment of congeni-
tal nevi. Arch Dermatol 1995;131:621–623.
33. Ueda S, Imayama S. Normal-mode ruby laser for treating congenital nevi.
Arch Dermatol 1997;133:355–359.
34. Taylor CR, Anderson RR. Ineffective treatment of refractory melasma
and postinflammatory hyperpigmentation by Q-switched ruby laser.
J Dermatol Surg Oncol 1994;20:592–597.
35. Yoshimura K, Sato K, Aiba-Kojima E, et al. Repeated treatment protocols
for melasma and acquired dermal melanocytosis. Dermatol Surg
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36. Rokhsar CK, Fitzpatrick RE. The treatment of melasma with fractional
photothermolysis: a pilot study. Dermatol Surg 2005;31:1645–1650.
37. Lowe NJ, Wieder JM, Shorr N, et al. Infraorbital pigmented skin.
Preliminary observations of laser therapy. Dermatol Surg 1995;21:767–
770.
38. Manuskiatti W, Fitzpatrick R, Goldman MP. Treatment of facial skin
using combinations of CO2, Q-switched alexandrite, flashlamp-pumped
pulsed dye, and Er:YAG lasers in the same treatment session. Dermatol
Surg 2000;26:114–120.
39. Argenyi ZB, Finelli L, Bergfeld WF, et al. Minocycline-related cutaneous
hyperpigmentation as demonstrated by light microscopy, electron micro-
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180.
40. Alster TS, Gupta SN. Minocycline-induced hyperpigmentation treated
with a 755-nm Q-switched alexandrite laser. Dermatol Surg 2004;30:
1201–1204.
41. Collins P, Cotterill JA. Minocycline-induced pigmentation resolves after
treatment with the Q-switched ruby laser. Br J Dermatol 1996;135:317–
319.
42. Green D, Friedman KJ. Treatment of minocycline-induced cutaneous
pigmentation with the Q-switched alexandrite laser and a review of the
literature. J Am Acad Dermatol 2001;44(2 Suppl):342–347.
43. Greve B, Schonermark MP, Raulin C. Minocycline-induced hyperpig-
mentation: treatment with the Q-switched Nd:YAG laser. Lasers Surg
Med 1998;22:223–227.
44. Tsao H, Busam K, Barnhill RL, et al. Treatment of minocycline-induced
hyperpigmentation with the Q-switched ruby laser. Arch Dermatol
1996;132:1250–1251.
45. Izikson L, Anderson RR. Resolution of blue minocycline pigmentation of
the face after fractional photothermolysis. Lasers Surg Med 2008;40:
399–401.
46. Atkin DH, Fitzpatrick RE. Laser treatment of imipramine-induced hyper-
pigmentation. J Am Acad Dermatol 2000;43:77–80.
47. Karrer S, Hohenleutner U, Szeimies RM, et al. Amiodarone-induced
pigmentation resolves after treatment with the Q-switched ruby laser.
Arch Dermatol 1999;135:251–253.
48. Wiper A, Roberts DH, Schmitt M. Amiodarone-induced skin pigmenta-
tion: Q-switched laser therapy, an effective treatment option. Heart
2007;93:15.
49. Bellew SG, Alster TS. Treatment of exogenous ochronosis with a
Q-switched alexandrite (755  nm) laser. Dermatol Surg 2004;30:555–
558.
50. Fitzpatrick RE, Goldman MP. Tattoo removal using the alexandrite laser.
Arch Dermatol 1994;130:1508–1514.
51. Anderson RR. Laser–tissue interactions. In: Goldman MP, Fitzpatrick R,
eds. Cutaneous laser surgery: the art and science of selective photother-
molysis. St Louis: Mosby 1994; 14–15.
52. Dover JS, Margolis RJ, Polla LL, et al. Pigmented guinea pig skin irradi-
ated with Q-switched ruby laser pulses. Morphologic and histologic find-
ings. Arch Dermatol 1989;125:43–49.
53. Kossida T, Farinelli W, Flotte T. Mechanism of immediate whitening
during tattoo removal. Lasers Surg Med 2006;18:70.
54. Grevelink JM, Duke D, van Leeuwen RL, et al. Laser treatment of tattoos
in darkly pigmented patients: efficacy and side effects. J Am Acad Der-
matol 1996;34:653–656.
55. Taylor CR, Gange RW, Dover JS, et al. Treatment of tattoos by
Q-switched ruby laser. A dose–response study. Arch Dermatol 1990;126:
893–899.
 REFERENCES
1. Anderson RR, Parrish JA. Selective photothermolysis: precise microsur-
gery by selective absorption of pulsed radiation. Science 1983;220:524–
527.
2. Polla LL, Margolis RJ, Dover JS, et al. Melanosomes are a primary target
of Q-switched ruby laser irradiation in guinea pig skin. J Invest Dermatol
1987;89:281–286.
3. Murphy GF, Shepard RS, Paul BS, et al. Organelle-specific injury to
melanin-containing cells in human skin by pulsed laser irradiation. Lab
Invest 1983;49:680–685.
4. Levins PC, Anderson RR. Q-switched ruby laser for the treatment of
pigmented lesions and tattoos. Clin Dermatol 1995;13:75–79.
5. Taylor CR, Anderson RR, Gange RW, et al. Light and electron micro-
scopic analysis of tattoos treated by Q-switched ruby laser. J Invest
Dermatol 1991;97:131–136.
6. Ara G, Anderson RR, Mandel KG, et al. Irradiation of pigmented
melanoma cells with high intensity pulsed radiation generates acoustic
waves and kills cells. Lasers Surg Med 1990;10:52–59.
7. Weiss RA, Goldman MP, Weiss MA. Treatment of poikiloderma of
Civatte with an intense pulsed light source. Dermatol Surg 2000;26:823–
827, discussion 8.
8. Alster TS, Konda S. Plasma skin resurfacing for regeneration of neck,
chest, and hands: investigation of a novel device. Dermatol Surg 2007;
33:1315–1321.
9. Goldman L, Blaney DJ, Kindel DJ Jr, et al. Effect of the laser beam
on the skin. Preliminary report. J Invest Dermatol 1963;40:121–
122.
10. Goldman L, Wilson RG, Hornby P, et al. Radiation from a Q-switched
ruby laser. Effect of repeated impacts of power output of 10 megawatts
on a tattoo of man. J Invest Dermatol 1965;44:69–71.
11. Ohshiro T, Maruyama Y. The ruby and argon lasers in the treatment of
naevi. Ann Acad Med Singapore 1983;12(2 Suppl):388–395.
12. Dover JS, Smoller BR, Stern RS, et al. Low-fluence carbon dioxide laser
irradiation of lentigines. Arch Dermatol 1988;124:1219–1224.
13. Anderson RR, Margolis RJ, Watenabe S, et al. Selective photothermoly-
sis of cutaneous pigmentation by Q-switched Nd:YAG laser pulses at
1064, 532, and 355 nm. J Invest Dermatol 1989;93:28–32.
14. Lee MW. Combination 532-nm and 1064-nm lasers for noninvasive skin
rejuvenation and toning. Arch Dermatol 2003;139:1265–1276.
15. Taylor CR, Anderson RR. Treatment of benign pigmented epidermal
lesions by Q-switched ruby laser. Int J Dermatol 1993;32:908–912.
16. Kilmer SL, Wheeland RG, Goldberg DJ, et al. Treatment of epidermal
pigmented lesions with the frequency-doubled Q-switched Nd:YAG
laser. A controlled, single-impact, dose-response, multicenter trial. Arch
Dermatol 1994;130:1515–1519.
17. Li YT, Yang KC. Comparison of the frequency-doubled Q-switched
Nd:YAG laser and 35% trichloroacetic acid for the treatment of face
lentigines. Dermatol Surg 1999;25:202–204.
18. Alora MB, Arndt KA. Treatment of a café-au-lait macule with the
erbium:YAG laser. J Am Acad Dermatol 2001;45:566–568.
19. Watanabe S, Takahashi H. Treatment of nevus of Ota with the Q-switched
ruby laser. N Engl J Med 1994;331:1745–1750.
20. Alster TS, Williams CM. Treatment of nevus of Ota by the Q-switched
alexandrite laser. Dermatol Surg 1995;21:592–596.
21. Tse Y, Levine VJ, McClain SA, et al. The removal of cutaneous pig-
mented lesions with the Q-switched ruby laser and the Q-switched
neodymium:yttrium-aluminum-garnet laser. A comparative study. J Der-
matol Surg Oncol 1994;20:795–800.
22. Kouba DJ, Fincher EF, Moy RL, et al. Nevus of Ota successfully treated
by fractional photothermolysis using a fractionated 1440-nm Nd:YAG
laser. Arch Dermatol 2008;144:156–158.
23. Lam AY, Wong DS, Lam LK, et al. A retrospective study on the efficacy
and complications of Q-switched alexandrite laser in the treatment of
acquired bilateral nevus of Ota-like macules. Dermatol Surg 2001;27:937–
941, discussion 41–42.
24. Manuskiatti W, Sivayathorn A, Leelaudomlipi P, et al. Treatment of
acquired bilateral nevus of Ota-like macules (Hori’s nevus) using a com-
bination of scanned carbon dioxide laser followed by Q-switched ruby
laser. J Am Acad Dermatol 2003;48:584–591.
25. Polnikorn N, Tanrattanakorn S, Goldberg DJ. Treatment of Hori’s
nevus with the Q-switched Nd:YAG laser. Dermatol Surg 2000;26:477–
480.
26. Manuskiatti W, Eimpunth S, Wanitphakdeedecha R, et al. Effect of cold
air cooling on the incidence of postinflammatory hyperpigmentation after
Q-switched Nd:YAG laser treatment of acquired bilateral nevus of Ota
like macules. Arch Dermatol 2007;143:1139–1143.
27. van Leeuwen RL, Dekker SK, Byers HR, et al. Modulation of alpha 4
beta 1 and alpha 5 beta 1 integrin expression: heterogeneous effects of

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Part 3  Aesthetic Surgical Procedures
59. Mafong EA, Kauvar AN, Geronemus RG, et al. Surgical pearl: removal
of cosmetic lip-liner tattoo with the pulsed carbon dioxide laser. J Am
Acad Dermatol 2003;48:271–272.
60. Alora MB, Arndt KA, Taylor CR. Scarring following Q-switched laser
treatment of ‘double tattoos.’ Arch Dermatol 2000;136:269–270.
56. Kilmer SL, Anderson RR. Clinical use of the Q-switched ruby and the
Q-switched Nd:YAG (1064  nm and 532  nm) lasers for treatment of
tattoos. J Dermatol Surg Oncol 1993;19:330–338.
57. Kilmer SL, Lee MS, Grevelink JM, et al. The Q-switched Nd:YAG laser
effectively treats tattoos. A controlled, dose–response study. Arch
Dermatol 1993;129:971–978.
58. Grekin RC, Shelton RM, Geisse JK, et al. 510-nm pigmented lesion dye
laser. Its characteristics and clinical uses. J Dermatol Surg Oncol 1993;
19:380–387.

549
33
Energy-based Treatment of the Aging
Face for Skin Resurfacing: Ablative and
Non-ablative Lasers, Photodynamic
Therapy of Photoaging, and
Actinic Damage
Anne M Chapas MD, Roy G Geronemus MD, and Elizabeth K Hale MD
Summary box
 Many aspects of cutaneous photodamage are amenable to
treatment with a variety of ablative and non-ablative lasers
and light sources.
 Ablative laser skin resurfacing offers the most substantial
clinical improvement, but is associated with several weeks of
postoperative recovery.
 Non-ablative laser skin remodeling is a good alternative for
patients who desire modest improvement of photodamaged
skin with a limited post-treatment recovery period.
 Fractionated laser systems provide the benefits of higher
energy treatments with fewer side effects than traditional
lasers.
 With ongoing advancements in laser technology and
techniques, improved clinical outcomes with minimal
postoperative recovery will be realized.
 INTRODUCTION
Years of damaging UV light exposure manifests clinically as
a sallow complexion with roughened surface texture, and
variable degrees of dyspigmentation, telangiectasias, wrin-
kling, and skin laxity.1,2 Histologically, these extrinsic aging
effects are usually limited to the epidermis and upper papil-
lary dermis and are therefore amenable to treatment with a
variety of ablative and non-ablative lasers and light sources.3
The armamentarium of lasers and light-based sources avail-
able to treat cutaneous photodamage is larger than ever
before (Table 33.1). The most appropriate technique will
depend upon the severity of photodamage and rhytides, the
expertise of the laser surgeon, and the expectations and life-
style of the individual patient.
 ABLATIVE LASER SKIN RESURFACING
Preoperative preparation
Ablative lasers, such as carbon dioxide with an emission of
10 600 nm and erbium:yttrium-aluminum-garnet (Er:YAG)
with an emission of 2940  nm, are selectively absorbed by
water and act to vaporize skin in a controlled manner. Remov-
ing the epidermis and part of the dermis in this way stimu-
lates wound remodeling with new collagen and elastin
formation and subsequent healthier, firmer, and tighter skin.
Although the results can be dramatic, wounds of this nature
can take weeks to months to completely resolve and may be
associated with scarring and pigmentary alteration. The ideal
patient for ablative cutaneous laser resurfacing is one with a
fair complexion (skin phototype I or II), cutaneous lesions
that are amenable to treatment with a resurfacing laser, and
realistic expectations of the resurfacing procedure. For
patients unable or unwilling to tolerate extended postopera-
tive healing, a short-pulsed Er:YAG laser or application of
non-ablative laser procedures may be more suitable choices.
Currently, there is no consensus among laser experts
regarding the most appropriate preoperative regimen for abla-
tive laser skin resurfacing patients. The use of topical retinoic
acid compounds, hydroquinone bleaching agents, or α-hydroxy
acids for several weeks before ablative cutaneous resurfacing
has been touted as a means of speeding recovery and decreas-
ing the incidence of postinflammatory hyperpigmentation.4
Topical tretinoin enhances penetration of chemicals through
the skin and has been shown to accelerate postoperative re-
epithelialization after dermabrasion or deep chemical peels.5
However, because ablative laser-induced wounds are intrinsi-
cally different from those created by physically destructive
methods, skin penetrated with a laser is not typically affected
by the topical application of any of these medications. In
addition, since postinflammatory hyperpigmentation is rela-
tively common after ablative cutaneous laser resurfacing,
many laser surgeons originally believed that the preoperative
prophylactic use of topical bleaching agents would reduce the
incidence of this side effect. After the initial trial period,
investigators demonstrated that the preoperative use of
topical tretinoin, hydroquinone, or glycolic acid had no effect
on the incidence of postablative laser hyperpigmentation.6
Due to the moist, de-epithelialized state of ablative laser-
resurfaced skin and the possibility of bacterial contamination
and overgrowth, many laser surgeons advocate oral antibiotic
prophylaxis; however, this practice remains controversial. A
controlled study demonstrated no significant change in the
postlaser resurfacing infection rate in patients treated with
prophylactic antibiotics.7 Since laser resurfacing can reacti-
vate herpes labialis, some believe that all patients, regardless
of whether they have a history of herpes labialis, should
receive prophylactic oral antivirals such as acyclovir, famci-
clovir, or valacyclovir starting 1 day prior to resurfacing and
continuing for 10 days postoperatively.

550
Part 3  Aesthetic Surgical Procedures
fewer laser passes, and laser resurfacing of non-facial areas
(e.g. neck, chest) should be avoided due to the relative
paucity of pilosebaceous units in these areas.18 To reduce the
risk of excessive thermal injury, partially desiccated tissue
should be removed manually with wet gauze after each laser
pass to expose the underlying dermis.17
The clinical and histologic benefits of cutaneous laser resur-
facing are numerous. With the carbon dioxide laser, most
studies have shown at least a 50% improvement over baseline
in overall skin tone and wrinkle severity.19–24 The biggest
advantages associated with carbon dioxide laser skin resurfac-
ing are the excellent tissue contraction, hemostasis, prolonged
neocollagenesis, and collagen remodeling that it provides.
Histologic examination of laser-treated skin demonstrates
replacement of epidermal cellular atypia and dysplasia with
normal, healthy epidermal cells from adjacent follicular
adnexal structures.8,13 The most profound effects occur in the
papillary dermis, where coagulation of disorganized masses of
actinically induced elastotic material are replaced with normal
compact collagen bundles arranged in parallel to the skin’s
surface.25,26 Immediately after carbon dioxide laser treat-
ment, a normal inflammatory response is initiated, with gran-
ulation tissue formation, neovascularization, and increased
production of macrophages and fibroblasts.13
Absolute contraindications to carbon dioxide laser skin
resurfacing include active bacterial, viral, or fungal infection
or an inflammatory skin condition involving the skin areas to
be treated. Isotretinoin use within the preceding 6–12-month
period or history of keloids are also considered contraindica-
tions to carbon dioxide laser treatment because of the unpre-
dictable tissue healing response and increased risk for
scarring.27,28
Erbium:yttrium-aluminum-garnet laser
The Er:YAG laser is a more precise ablative tool than the
carbon dioxide laser and emits 2940-nm wavelength light that
corresponds to the 3000-nm absorption peak of water. The
absorption coefficient of the Er:YAG is 12 800 cm−1 (com-
pared with 800 cm−1 for the carbon dioxide laser), making it
12–18 times more efficiently absorbed by water-containing
tissue than is the carbon dioxide laser.29 The pulse duration
(mean 250 ms) is also much shorter than the carbon dioxide
laser, resulting in decreased thermal diffusion, less effective
hemostasis, and increased intraoperative bleeding which
often hampers deeper dermal treatment. Because of limited
thermal skin injury, the amount of collagen contraction is also
reduced with Er:YAG treatment (1–4%) compared to that
observed with carbon dioxide laser irradiation.4,30
The erbium laser’s efficient rate of absorption, short expo-
sure duration, and direct relationship between fluence deliv-
ered and amount of tissue ablated leads to 2–4 µm of tissue
vaporization per J/cm2, producing a shallow level of tissue
ablation. Much narrower zones of thermal necrosis, averaging
only 20–50 µm, are therefore produced.29,31–33 Laser-induced
ejection of desiccated tissue from the target site produces a
distinctive popping sound. Thermal energy is confined to the
selected tissue, with minimal collateral thermal damage.
Because little tissue necrosis is produced with each pass
of the laser, manual removal of desiccated tissue is often
unnecessary.
The short-pulsed erbium laser fluences used most often
range from 5 to 15 J/cm2, depending on the degree of pho-
Technical aspects
Carbon dioxide laser
The Ultrapulse 5000 (Lumenis Corp, Yokneam, Israel), one
of the first high-energy pulsed-laser systems developed, emits
individual carbon dioxide pulses (ranging from 600  µs to
1  ms) with peak energy densities of 500  mJ, whereas the
SilkTouch (Lumenis Corp), another high-energy pulsed-laser
system, is a continuous-wave carbon dioxide system with a
microprocessor scanner that continuously moves the laser
beam so that light does not dwell on any one area for more
than 1  ms. The peak fluences delivered per pulse or scan
range from 4 to 5 J/cm2, which are the energy densities nec-
essary for complete tissue vaporization.8–11 Studies with these
and other pulsed and scanned carbon dioxide laser systems
have shown that after a typical skin resurfacing procedure,
water-containing tissue is vaporized to a depth of approxi-
mately 20–60  µm, producing a zone of thermal damage
ranging from 20 to 150 µm.8,10,12–14
The depth of ablation is directly correlated with the number
of passes performed and usually is restricted to the epidermis
and upper papillary dermis.15 However, stacking of laser
pulses by treating an area with multiple passes in rapid suc-
cession or by using a high overlap setting on a scanning device
leads to excessive thermal injury with subsequent increased
risk of scarring.16,17 An ablative plateau is reached, with less
effective tissue ablation and accumulation of thermal injury.
This effect is most likely caused by reduced tissue water
content after initial desiccation, resulting in less selective
absorption of energy.17 The complete removal of partially
desiccated tissue and avoidance of pulse stacking is para-
mount to prevention of excessive thermal accumulation with
any laser system.
The objective of ablative laser skin resurfacing is to vapor-
ize tissue to the papillary dermis. Limiting the depth of pen-
etration to this level decreases the risk for scarring and
permanent pigmentary alteration. When choosing treatment
parameters, the surgeon must consider factors such as the
anatomic location to be resurfaced, the skin phototype of the
patient, and previous treatments delivered to the area.9,18 In
general, areas with thinner skin (e.g. periorbital) require
Table 33.1  Lasers and light sources for skin rejuvenation
LASER TYPE
WAVELENGTH (nm)
Ablative
resurfacing
Carbon dioxide
(pulsed)
10 600
Erbium: YAG (pulsed)
2940
Fractionated
10 600 and 2940
Non-ablative
remodeling
Pulsed dye
585–595
Nd:YAG (Q-switched;
normal mode)
1064
Nd:YAG, long-pulsed
1320
Diode, long-pulsed
1450
Erbium: glass
1540
Intense pulsed light
source
515–1200
Non-ablative
Fractional resurfacing
1550, 1540, 1320, 1440
Nd, neodymium; Q-switched, quality-switched; YAG, yttrium-aluminum-garnet.

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Chapter 33  Energy-based Treatment of the Aging Face for Skin Resurfacing
resurfacing for deeper rhytides. However, for mild photo-
damage, improvement of approximately 50% is typical.
Ablative fractional resurfacing
While ablative lasers remove 100% of the epidermis and
varying levels of underlying dermis, ablative fractional resur-
facing devices have the ability to achieve comparable clinical
results while keeping the majority of epidermis intact, thus
allowing quicker recovery periods and an improved safety
profile. Fractional energy is delivered through microscopic
zones of thermal injury, leading to coagulation necrosis and
resultant new collagen formation. A pattern of annular coag-
ulation of dermal collagen occurs, with increasing fluences
resulting in increasing treatment depths. This annular coagu-
lation leads to collagen contraction and tissue shrinkage,
which accounts for the improvement in laxity, appearance of
pores, and scars. The deep dermal ablated zones are sur-
rounded by zones of sparing, which result in quicker recovery
times than traditionally seen after ablative resurfacing.
Improvement in textural abnormalities, dyschromias, and
mild skin laxity can be achieved in as little as a single treat-
ment (Fig. 33.1).
Several devices employ ablative fractional resurfacing. The
Fraxel repair (Reliant Technologies, Inc, Mountain View,
CA) system is a fractionated carbon dioxide laser which
allows for treatment energies up to 70 mJ/cm2. The ActiveFX
(Lumenis Ltd, Yokneam, Israel) is another fractionated
carbon dioxide device using a computerized pattern generator
(UltraScan Encore CPG) with a 1.3-mm spot for moderate
effects on tone, texture, and tightening with low downtime.
The individual treatment spots are scanned without overlap-
ping and leave surrounding zones of untreated tissue to
support the wound healing process. The ActiveFX used with
CoolScan mode offers non-linear scanning to increase patient
comfort and reduce erythema. DeepFX, another computer-
ized pattern generator used with UltraPulse Encore (Lumenis
Ltd) carbon dioxide laser, delivers 0.1-mm diameter spots;
therefore, it enables tightening of skin with deep wrinkles and
scars more effectively than other methods of skin resurfacing.
The spots of the DeepFX are laid down in a fractional mode,
covering a treated surface up to 25% greater than other frac-
todamage and anatomic location. When lower fluences are
used, it is often necessary to perform multiple passes to ablate
the entire epidermis. The ablation depth with the short-
pulsed Er:YAG does not diminish with successive passes,
because the amount of thermal necrosis is minimal with each
pass. It takes three to four times as many passes with the
short-pulsed Er:YAG laser to achieve similar depths of pen-
etration as with one pass of the carbon dioxide laser at typical
treatment parameters.3,4 To ablate the entire epidermis with
the short-pulsed Er:YAG laser at 5  J/cm2, at least two or
three passes must be used, which increases the possibility of
uneven tissue penetration. Deeper dermal lesions or areas of
the face with extreme photodamage and extensive dermal
elastosis may require up to nine or ten passes of the short-
pulsed Er:YAG laser, whereas the carbon dioxide laser would
reach similar levels of tissue ablation in two or three
passes.8,10,29
Pinpoint bleeding caused by inadequate hemostasis and
tissue color change with multiple Er:YAG passes can impede
adequate clinical assessment of wound depth. Treated areas
whiten immediately after treatment and then the white color
quickly fades. These factors render it far more difficult for
the surgeon to determine treatment end points and thus
requires extensive knowledge of laser–tissue interaction.
Conditions amenable to short-pulsed Er:YAG laser resur-
facing include superficial epidermal or dermal lesions, mild
photodamage, and subtle dyspigmentation. The major advan-
tage of short-pulsed Er:YAG laser treatment is its shorter
recovery period. Re-epithelialization is completed within an
average of 5.5 days, compared with 8.5 days for multiple-pass
carbon dioxide laser procedures.10,31 Postoperative pain and
duration of erythema are reduced after short-pulsed Er:YAG
laser resurfacing, with postoperative erythema resolving
within 3–4 weeks. Because there is less thermal injury and
trauma to the skin, the risk of pigmentary disturbance is also
decreased, making the short-pulsed Er:YAG laser a good
alternative in patients with darker skin phototypes.3,34 The
major disadvantages of the short-pulsed Er:YAG laser are its
limited ability to effect significant collagen shrinkage and its
failure to induce new and continued collagen formation post-
operatively.3,31,35 The final clinical result is typically less
impressive than that produced by carbon dioxide laser skin
A
B
Figure 33.1  Perioral rhytides (A) before and (B) several months after fractionated carbon dioxide laser skin resurfacing.

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Part 3  Aesthetic Surgical Procedures
Optimizing outcomes
Side effects associated with ablative skin resurfacing vary and
are related to the expertise of the laser surgeon, the body
area treated, and the skin phototype of the patient (Table
33.2). Certain tissue reactions, such as erythema and edema,
are expected in the immediate postoperative period and are
not considered adverse events. Erythema can be intense and
may persist for several months after traditional ablative pro-
cedures. The degree of erythema correlates directly with the
depth of ablation and the number of laser passes performed.3,39
It may also be aggravated by underlying rosacea or dermatitis.
Postoperative erythema resolves spontaneously but can be
reduced with the application of topical ascorbic acid which
may serve to decrease the degree of inflammation.40,41 Its use
should be reserved until at least 4 weeks after the procedure
in order to avoid irritation. Similarly, other topical agents
such as retinoic acid derivatives, glycolic acid, and fragrance-
containing or chemical-containing cosmetics and sunscreens
should be strictly avoided in the early postoperative period
until substantial healing has occurred.3 Adequate preopera-
tive patient evaluation and education are absolute essentials
to avoid the pitfalls discussed below and optimize the clinical
outcome.
Minor side effects of laser resurfacing include milia forma-
tion and acne exacerbation, which may be caused by the use
of occlusive dressings and ointments during the postoperative
period, particularly in patients who are prone to acne.16,18,39,42
Milia and acne usually resolve spontaneously as healing
progresses and the application of thick emollient creams and
occlusive dressings ceases. Oral antibiotics may be prescribed
for acne flares that do not respond to topical prepara-
tions.24,39,42 Contact allergies and irritant reactions can also
develop from various topical medications, soaps, and moistur-
izers used postoperatively. Most of these reactions are irritant
in nature due to decreased barrier function of the newly
resurfaced skin.39,43
Wound infections associated with ablative laser resurfacing
include Staphylococcus, Pseudomonas, or cutaneous candidia-
sis and should be treated aggressively with an appropriate
systemic antibiotic or antifungal agent.44 However, the use of
prophylactic antibiotics remains controversial.7 The most
common infectious complication is a reactivation of labial
herpes simplex virus (HSV), which is most likely caused by
the thermal tissue injury and epidermal disruption produced
by the laser.16,39 After carbon dioxide resurfacing, approxi-
mately 7% of patients develop a localized or disseminated
form of HSV.39 These infections develop within the first
postoperative week and can present as erosions without intact
vesicles because of the denuded condition of newly lased
skin. Even with appropriate prophylaxis, a herpetic outbreak
tional lasers. The ablation depth and the residual thermal
damage depend on the energy density (micropulse laser
energy up to 50 mJ) and the number of stacked pulses (up
to 5) used. With increasing parameters, the postoperative
bleeding increases and the patient’s downtime will be pro-
longed. For a maximum effect, DeepFX is performed first
and can be combined with ActiveFX in the same operation
(TotalFX), leading to better results than either system alone.
Since the new UltraPulse Encore carbon dioxide laser can be
used to perform traditional skin resurfacing, usually overlap-
ping of individual spots up to 50%, the fractional and non-
fractional ablative skin resurfacing can be combined in the
same patient depending on the actinic damage. Using the
same device, the operator can perform traditional resurfacing
periorally, DeepFX periorbitally and ActiveFX for the rest of
the face.
Other devices include a Lux 2940-nm fractional hand piece
(Palomar Medical Technologies, Inc, Burlington, MA), which
can be attached to a pulsed light laser system utilizing erbium
laser energy to deliver deep dermal ablative columns.36
These devices allow for quicker recovery than traditional
ablative devices; however, when compared to their non-
ablative counterparts, downtime can be considerably greater,
lasting on average 5–7 days. The procedure is generally toler-
ated after topical anesthesia has been applied for 1 hour and
local nerve blocks are administered. Patients are usually
offered an oral pain medication. If the patient is accompanied
by a capable escort, an anxiolytic may be given. A forced air
cooling system can be utilized to further minimize procedural
pain. Most patients experience erythema, edema, and crust-
ing which usually resolves within 7 days. Some patients expe-
rience temporary bronzing, acneiform eruptions, or milia
formation. Patients are given oral corticosteroids in the peri-
operative period to minimize associated edema. Antiviral and
antibiotic prophylaxis is given for 7 days, beginning on the
day prior to surgery.
Results from a single treatment are fully realized 3–6
months after the procedure, after the process of collagen
remodeling is complete. Most patients receive only one or
two treatments, but selected patients with significant photo-
damage or acne scarring may require more. Several features
of ablative fractional resurfacing represent true advances over
traditional ablative lasers. First, ablative fractional resurfacing
can be performed safely on the neck and chest. To date, there
have been no reports of scarring or pigmentary alteration after
the use of fractional devices in any anatomic location. Stand-
ard ablative resurfacing has been limited to treating facial skin
since treatment of non-facial areas has an increased risk for
scarring and pigmentary alterations. Recent reports have
documented the absence of hypopigmentation following
ablative fractional resurfacing.37,38
Table 33.2  Side effects and complications of ablative laser skin resurfacing
EXPECTED SIDE EFFECTS
Complications
MILD
MODERATE
SEVERE
Erythema
Edema
Pruritus
Extended erythema
Milia
Acne
Contact dermatitis
Infection (bacterial, viral, fungal)
Hyperpigmentation
Hypopigmentation
Hypertrophic scarring
Ectropion

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Chapter 33  Energy-based Treatment of the Aging Face for Skin Resurfacing
decrease the incidence of post-treatment hyperpigmenta-
tion.6 Postoperative hypopigmentation is often not observed
for several months and is particularly difficult because of its
tendency to be intractable to treatment. The use of an
excimer laser or topical photochemotherapy to stimulate re­
pigmentation has proven successful in some patients.46,47
Postoperative care
Wound care during the immediate postoperative period is
vital to the successful recovery of ablative laser-resurfaced
skin. During the re-epithelialization process, an open or
closed wound technique can be prescribed. Partial-thickness
cutaneous wounds heal more efficiently and with a much
reduced risk of scarring when maintained in a moist environ-
ment because the presence of a dry crust or scab impedes
keratinocyte migration.47 Although there is consensus on this
principle by laser surgeons, disagreement exists regarding the
optimal dressing for the laser-ablated wound. The ‘open’
technique involves frequent application of thick healing oint-
ment to the de-epithelialized skin surface, whereas occlusive
or semiocclusive dressings are placed directly on the lased
skin in the ‘closed’ technique. While the open technique
facilitates easy wound visualization, the closed technique,
using, for example, Silon-TSR (Bio Med Sciences, Allentown,
PA), requires less patient involvement and may also decrease
postoperative pain. Proposed advantages of closed dressings
include increased patient comfort, decreased erythema and
edema, increased rate of re-epithelialization, and decreased
patient involvement in wound management.48,49 On the other
hand, additional expense and a higher risk of infection have
been associated with the use of these dressings.3,41,43
In addition to the prescribed wound care, ice-pack applica-
tion and anti-inflammatory medications should be used during
this time. Furthermore, pain medication is particularly impor-
tant for ablative laser-resurfaced patients during the first few
postoperative days.
Pitfalls and their management
Proper patient selection  While a variety of epidermal
and dermal signs of facial photodamage are amenable to laser
still can occur in up to 10% of patients and must be treated
aggressively.9 Oral antiviral agents, such as acyclovir, famci-
clovir, and valacyclovir are effective agents against HSV
infection, although severe (disseminated) cases may require
intravenous therapy. Patients should begin prophylaxis by the
day of surgery and continue for 7–10 days postoperatively.
The most severe complications associated with ablative
cutaneous laser resurfacing include hypertrophic scar and
ectropion formation.16,39 Although the risk of scarring has
been significantly reduced with the newer pulsed systems
(compared to the continuous wave lasers), inadvertent pulse
stacking or scan overlapping, as well as incomplete removal
of desiccated tissue between laser passes, can cause excessive
thermal injury that could increase the development of fibro-
sis. Focal areas of bright erythema, with pruritus, particularly
along the mandible, may signal impending scar formation.18,45
Ultrapotent (class I) topical corticosteroid preparations
should be applied to decrease the inflammatory response. A
pulsed-dye laser (PDL) also can be used to improve the
appearance and symptoms of laser-induced burn scars.45
Ectropion of the lower eyelid after periorbital laser skin
resurfacing is rarely seen, but if encountered it usually
requires surgical correction.18 It is more likely to occur in
patients who have had previous lower blepharoplasty or other
surgical manipulation of the periorbital region. Preoperative
examination is essential to determine eyelid laxity and skin
elasticity. If the infraorbital skin does not return briskly to its
normal resting position after a manual downward pull (snap
test), then ablative laser resurfacing near the lower eyelid
margin should be avoided. In general, lower fluences and
fewer laser passes should be applied in the periorbital area to
decrease the risk of lid eversion.
Hyperpigmentation is one of the more common side effects
of cutaneous laser resurfacing and occurs to some degree in
all patients with darker skin tones (Fig. 33.2).18,39 The reac-
tion is transient, but its resolution can be hastened with the
postoperative use of a variety of topical agents, including
hydroquinone, retinoic, azeleic, and glycolic acid. Regular
sunscreen use is also important during the healing process to
prevent further skin darkening. The prophylactic use of these
products preoperatively, however, has not been shown to
A
B
Figure 33.2  Periorbital rhytides and infraorbital hyperpigmentation (A) before and (B) several months after erbium laser skin
resurfacing.

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Part 3  Aesthetic Surgical Procedures
resurfacing with appropriate topical or systemic antibiotics.
Occlusive ointments used in the immediate postoperative
period may induce acne and complicate the postoperative
course.
Does the patient have realistic expectations of the
procedure and will he/she be compliant with
postoperative instructions?  Patients who believe that
every rhytide will be removed with the ablative laser resurfac-
ing procedure are not good treatment candidates. Further-
more, those who cannot physically or emotionally handle the
prolonged postoperative course should also be dissuaded
from pursuing ablative laser skin resurfacing procedures.
Summary
Ablative laser skin resurfacing has revolutionized the approach
to photodamaged facial skin. Technology and techniques con-
tinue to evolve, further enhancing the ability to achieve sub-
stantial clinical improvement of rhytides and dyspigmentation
with reduced postoperative morbidity. Utilizing proper tech-
nique and treatment parameters, excellent clinical results can
be obtained with any one or a combination of ablative laser
systems. Therefore, the best choice of laser ultimately
depends on the operator’s expertise, clinical indication, and
individual patient characteristics. Regardless of the type of
ablative resurfacing laser used, the importance of careful
postoperative follow up cannot be overemphasized.
 NON-ABLATIVE LASER
SKIN REMODELING
Preoperative preparation
Proper patient selection is critical to the success of non-
ablative laser skin remodeling. Patients with mild to moderate
facial photodamage with realistic expectations of treatment
are the best candidates for non-ablative procedures. Patients
seeking immediate improvement in photodamaged skin or
those who desire a dramatic result may be less than satisfied
with the overall clinical outcome.
For patients with a strong history of herpes labialis, pro-
phylactic oral antiviral medications should be considered
when treating the perioral skin. Reactivation of prior herpes
simplex infection can occur after non-ablative laser skin
remodeling due to the intense heat produced by the laser or
light source. Prior to non-ablative laser procedures, sun expo-
sure should be avoided, particularly when using shorter wave-
length systems such as the PDL or intense pulsed light (IPL)
source. Unwanted absorption of irradiation by activated epi-
dermal melanocytes can increase the risk of side effects,
including crusting, blistering, and dyspigmentation.
Technical aspects
Non-ablative laser systems stimulate collagen production
and dermal remodeling without wounding the epidermis.
These systems include mid-infrared lasers, visible light
lasers, and IPL systems. Devices which emit light within the
infrared portion of the electromagnetic spectrum (1000–
1500 nm) are weakly absorbed by superficial water-contain-
ing tissue, thereby effecting deeper tissue penetration.50
Since non-ablative remodeling involves creation of a dermal
wound without epidermal injury, all of these laser systems
skin resurfacing, clincially suspicious growths, especially pig-
mented lesions, should be biopsied for histologic examination
prior to laser irradiation.
Has the patient ever had the areas treated before? 
Ablative laser resurfacing may unmask hypopigmentation or
fibrosis produced by prior dermabrasion, cryosurgery, or
phenol peels. In addition, the presence of fibrosis may limit
the vaporization potential of ablative lasers, thereby decreas-
ing clinical efficacy. Patients who have had prior lower
blepharoplasties (using an external approach) are at greater
risk of ectropion formation after infraorbital ablative skin
resurfacing.
What is the patient’s skin phototype?  Pale skin tones
have a lower incidence of undesirable postoperative hyper-
pigmentation compared to patients with dark skin tones.
Does the patient have a history of herpes labia-
lis?  Reactivation and/or dissemination of prior herpes
simplex infection can occur with laser resurfacing. The de-
epithelialized skin is also particularly susceptible to primary
inoculation by herpes simplex virus; therefore all patients
should be treated with prophylactic antiviral medication prior
to ablative laser skin resurfacing.
Does the patient have an autoimmune disease or
other immunologic deficiency?  Because the postop-
erative course associated with ablative skin resurfacing is
prolonged, intact immunologic function and collagen repair
mechanisms are necessary to optimize the tissue-healing
response. In addition to possible delayed wound healing,
patients with scleroderma, lupus erythematosus, and vitiligo
may also exhibit worsening of their conditions after ablative
skin resurfacing.
Are there other dermatologic conditions present
which could potentially spread after treatment? 
Psoriasis, verrucae, and molluscum contagiosum are but a few
conditions that could conceivably undergo koebnerization
after ablative laser skin resurfacing. Thus, the skin should be
carefully inspected to rule out the presence of these and
other inflammatory or infectious cutaneous lesions so that the
final clinical result is optimized.
Is the patient taking any medications that are
contraindicated?  Concomitant isotretinoin use could
potentially lead to an increased risk of postoperative hyper-
trophic scar formation due to its detrimental effect on wound
healing and collagenesis. Because the alteration in healing is
idiosyncratic, a safe interval between the use of oral retinoids
and ablative laser skin resurfacing is difficult to calculate;
however, most practitioners delay the treatment for at least
6–12 months after cessation of the drug.
Does the patient have a tendency to form hyper-
trophic scars or keloids?  Patients with a propensity to
scar will be at greater risk of scar formation after laser resur-
facing, independent of the laser’s selectivity and the opera-
tor’s expertise.
Is the patient prone to acne?  Complete control of
acne eruptions should be obtained prior to ablative laser skin

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Chapter 33  Energy-based Treatment of the Aging Face for Skin Resurfacing
intracellular water and penetrates tissue to a depth of 0.4–
2 mm.50 The 1540-nm wavelength has the least amount of
melanin absorption compared with the 1320-nm and 1450-nm
laser systems – a potential advantage of this system when
treating tanned or darker-skinned patients. Fournier and col-
leagues treated 42 patients (skin phototypes I–IV) with five
consecutive 1540-nm diode laser treatments at 6-week inter-
vals.52 Patients were evaluated using clinical data, patient
satisfaction surveys, digital photography, ultrasound imaging,
and profilometry data from silicone imprints. The majority of
patients demonstrated modest improvement in objective and
subjective measurements which remained stable throughout
the 14-month evaluation period.
Visible light lasers
Pulsed-dye laser
Clinical studies have demonstrated the ability of 585-nm and
595-nm PDLs to reduce mild facial rhytides with few side
effects.53 The most common side effects of PDL treatment
include mild edema, purpura, and transient postinflammatory
hyperpigmentation. Although increased extracellular matrix
proteins and types I and III collagen and procollagen have
been detected following PDL treatment, the exact mecha-
nism whereby wrinkle improvement is effected remains
unknown.54 One theory states that vascular endothelial cells
damaged by the yellow laser light release mediators that
stimulate fibroblasts to produce new collagen fibers.55
Intense pulsed light source
Several investigators have shown successful rejuvenation of
photodamaged skin after IPL treatment.56,57 The IPL source
emits a broad, continuous spectrum of light in the range of
515–1200 nm. Cut-off filters are used to eliminate shorter
wavelengths depending on the clinical application, with
shorter filters favoring heating of melanin and hemoglobin.
Bitter57 showed improvement in wrinkling, skin coarseness,
irregular pigmentation, pore size, and telangiectasia in the
majority of 49 patients treated with a series of IPL treatments
(fluences 30–50  J/cm2). In a retrospective review of 80
patients with skin phototypes I–IV, Weiss and colleagues
reported signs of photoaging, including telangiectasias and
mottled pigmentation of the face, neck, and chest, improved
by a series of IPL treatments.58 While substantial clinical
improvement of dyspigmentation and telangiectasia associ-
ated with cutaneous photodamage is often seen, neocollagen-
esis and dermal collagen remodeling with subsequent
improvement in rhytides following IPL treatment has been
more modest. The effect on dermal collagen is thought to be
induced by heat diffusion from the vasculature with subse-
quent release of inflammatory mediators stimulated by vessel
heating.59
Non-ablative fractional resurfacing
The first non-ablative fractional resurfacing device was a
1550-nm erbium-doped, mid-infrared fiber laser system that
produced microscopic treatment zones (MTZs) utilizing a
scanning hand-piece device. The scanning hand piece allows
for deposition of MTZs in a random pattern through a con-
tinuous beam, which allows for uniform treatment. Tissue in
these coagulated zones is not vaporized, and the epidermis is
left intact, allowing for rapid repopulation of the ablated
employ unique methods to ensure epidermal preservation
during treatment. These methods typically include contact
cooling hand pieces or dynamic cryogen devices capable of
delivering variable duration spray spurts either before, during,
and/or after laser irradiation. In general, treatment of facial
photodamage with non-ablative technology does not produce
results comparable to those of ablative carbon lasers; however,
many patients are willing to accept modest clinical improve-
ment in exchange for fewer associated risks and shorter
recovery times.
Mid-infrared lasers
1320-nm Nd:YAG laser
The 1320-nm Nd:YAG laser (CoolTouch, ICN Photonics,
Costa Mesa, CA) was the first commercially available system
marketed solely for the purpose of non-ablative laser skin
remodeling. The 1320-nm wavelength is associated with a
high scattering coefficient that allows for dispersion of laser
irradiation throughout the dermis. The latest model is capable
of delivering energy densities up to 24  J/cm2 with a pulse
duration of 350 ms through a 10-mm spot size hand piece.
The 1320-nm Nd:YAG laser hand piece contains three
portals: the laser beam itself, a thermal feedback sensor that
registers skin surface temperature, and a dynamic cryogen
spray apparatus used for epidermal cooling. When skin surface
temperatures are maintained at 40–45°C, dermal tempera-
tures reach 60–65°C during laser irradiation, thereby effect-
ing collagen contraction and neocollagenesis. In order to
prevent unwanted sequelae (e.g. blistering) from excessive
heat production, it is imperative that epidermal temperatures
be kept lower than 50°C. A series of three or more treatment
sessions are scheduled at regular intervals (typically once a
month) for maximum mitigation of fine rhytides.50 Side
effects of treatment are generally mild and include transient
erythema and edema.
1450-nm Diode laser
The 1450-nm mid-infrared-wavelength diode laser (Smooth-
beam, Candela, Wayland, MA) targets dermal water and
penetrates the skin to an approximate depth of 500 nm. This
low-power laser system achieves peak powers in the 10–15 W
range with relatively long pulse durations of 150–250  ms.
Because of these long exposure times, epidermal cooling must
be delivered in sequence during the application of laser energy
in order to avoid excessive thermal build up within the super-
ficial layers of the skin. In a controlled clinical and histologic
study, Tanzi et  al.51 demonstrated improvement in mild to
moderate perioral or periorbital rhytides in 25 patients
treated with four consecutive 1450-nm diode laser treat-
ments. Peak clinical improvement was seen 6 months after
the series of laser treatments. The periorbital area was more
responsive to laser treatment than the perioral area – a finding
consistent with results obtained using other non-ablative laser
systems.51 Side effects were limited to transient erythema,
edema, and postinflammatory hyperpigmentation.
1540-nm Erbium:glass laser
The 1540-nm erbium-doped phosphate glass laser is another
mid-infrared-range laser that has also been used for ameliora-
tion of fine facial rhytides and atrophic facial scars. Similar
to other infrared laser systems, the erbium:glass laser targets

556
Part 3  Aesthetic Surgical Procedures
damaged dermal components, like dermal elastin in the form
of solar elastosis. Clinically, the extrusion is manifest as
superficial exfoliation, which imparts a rough, sandpaper-like
feel to the face. The skin often appears bronze during this
reparative phase, which is why treatment of complete
cosmetic units, if not the whole face en masse, is generally
recommended.
The intact stratum corneum acts as a form of biologic dress-
ing which promotes rapid re-epithelialization and a barrier
against secondary bacterial or viral colonization. The biologic
response to fractional photothermolysis is characterized by a
complex wound healing process, whereby the MTZs are com-
pletely replaced by new collagen over the course of 3 months.
Usually a series of treatments with non-ablative technology
is recommended, but the patient needs to be assured that the
final clinical effects will not be attained for at least 3 months
after the last treatment, due to the time course of collagen
regeneration and remodeling.
Treatment parameters
The two treatment variables are the treatment energy and
the treatment density, that is the total number of MTZs per
square centimeter. The density is usually represented by a
‘treatment level,’ which corresponds with percent of total
coverage. In selecting treatment parameters, one needs to
consider the treatment application as well as the skin type of
the patient. Generally speaking, for scarring purposes, higher
treatment energies are used with lower treatment densities.
For textural improvement like rhytides, a medium energy
level is utilized. Pigmentary distrurbances are best treated
with lower treatment energies which allow for more superfi-
cial penetration. Darker skin phototypes can be treated effec-
tively and safely by reducing the total treatment density while
maintaining the desired energy setting for the particular indi-
cation.38 It is important to note that melasma does have the
potential to paradoxically darken following fractional photo-
thermolysis, so patients must be cautioned about this possi-
columns of tissue.36 The density between these MTZs at any
given fluence can be varied, and the depth of the MTZ can
be increased by increasing the fluence.38 The potential for
bulk heating can be minimized by decreasing the density per
pass at a given fluence.
The original Fraxel SR (Reliant Technologies) was approved
for use by the FDA in 2003 for soft tissue coagulation. In
2007, the Fraxel SR 1500 was approved, yielding energies up
to 70 mJ/cm2. The higher energies allow for deeper penetra-
tion (up to 1.4  mm), which is useful for treating deeper
rhytides and both acne and surgical scars (Fig. 33.3).36 With
this newer device, a roller tip utilizing a scanning LED was
incorporated to facilitate the scanning hand-piece technology.
However, not all fractional devices utilize a scanning hand
piece. One approach uses a ‘stamping’ method to deliver the
fractionated infrared laser beam to the skin. Other devices
include the Lux 1540 Fractional (Palomar Medical Tech-
nologies), a device which contains a fractional hand piece
which can be attached to a pulsed light laser system. The
advantages of this device include its versatility and relatively
small size; however, treating large areas like the face or neck
can be time-consuming and less practical. Another fractional
resurfacing device is the Affirm (Cynosure, Inc, Westford,
MA), which sequentially emits 1320-nm and 1440-nm wave-
lengths at fixed intervals.36 Through utilization of two distinct
alternating wavelengths, superficial and deeper depths can be
achieved simultaneously.
Biology of fractional photothermolysis
Overlying the MTZs created, the stratum corneum is left
intact, while a small split confined to the sub-basilar region
is evident overlying the zone of thermal coagulation.38
Re-epithelialization is completed within 1 day following
treatment, and healing takes place through extrusion of
microepidermal necrotic debris (MEND), which represents
damaged epidermal components, like melanin and non-viable
keratinocytes. It is thought that the MEND also contains
A
B
Figure 33.3  Acne scars (A) before and (B) several months after non-ablative fractional treatment.

557
Chapter 33  Energy-based Treatment of the Aging Face for Skin Resurfacing
Summary
For those patients who desire a less aggressive approach to
photorejuvenation than ablative laser skin resurfacing, non-
ablative dermal remodeling represents a viable alternative for
patients willing to accept modest clinical improvement in
exchange for ease of treatment and a favorable side-effect
profile. Treatments are typically delivered at monthly inter-
vals with final clinical results taking several months after laser
irradiation to be realized. Although clinical outcomes with
these non-ablative systems are not yet comparable with those
of ablative carbon dioxide lasers, they do improve overall skin
texture, tone, and elasticity – subjective findings often diffi-
cult to represent in photographs. None of the non-ablative
laser systems has yet emerged as being clearly superior – each
produces similar degrees of improvement in dermal pathology
after multiple sessions at standard treatment parameters.
With continued research efforts focused on non-ablative laser
skin remodeling, it is possible that further refinements and
advances in this technology will more closely approximate the
effects of ablative laser treatment without its associated com-
plications and risks.
 PHOTODYNAMIC THERAPY
The application of the topical photosensitizers, 20% aminole-
vulinic acid (ALA) solution and methyl aminolevulinate
(MAL) cream, prior to non-ablative laser treatment, has been
shown to boost their rejuvenation effects. Both ALA and
MAL are strongly absorbed into sun-damaged cells, non-
melanoma skin cancers, and the pilosebaceous unit where
they are transformed by the heme pathway into their active
form, protoporphyrin IX (PpIX). Activation of PpIX by a
variety of light sources results in the production of reactive
oxygen species and local tissue destruction followed by a
wound healing response. In 1999, the United States Food and
Drug Administration (FDA) approved the first photodynamic
therapy (PDT) modality for the treatment of non-hyperkera-
totic solar keratosis on the face and scalp, which utilizes a
20% topical hydroalcoholic solution of ALA and a blue light
source of 417 nm peak output. In 2008, the FDA approved
a second PDT method for the treatment of actinic keratoses
which involves application of MAL cream under occlusion for
3 hours followed by illumination with a red light source of
630-nm peak output.
PDT was first described for photo rejuvenation in 2002
where Ruiz-Rodriguez and colleagues treated 17 patients with
a combination of actinic keratoses and photodamage.60 Appli-
cation of 20% ALA mixed in an oil-in-water emulsion for 4
hours was followed by treatment with a pulsed light device
(Epilight, ESC/Sharplan Medical Systems, Needham, MA)
using a 615-nm cut-off filter and a total fluence of 40 J/cm2
in a double-pulse mode of 4.0 ms with a 20-millisecond inter-
pulse delay. After 2 treatments, 1 month apart, approxi-
mately three-quarters of the actinic keratoses and adjacent
photodamaged skin resolved; however, post-treatment crust-
ing and erythema persisted up to 10 days.
Dover et al.61 showed that PDT using IPL in a randomized,
controlled, split-face study could improve global photodam-
age, mottled pigmentation, and fine lines better than IPL
alone. In this study, 20 patients underwent a series of three
split-face treatments in which half the face was pretreated
with topical 20% ALA solution (Levulan Kerastic DUSA
bility and must practice strict sun avoidance before initiating
treatment.
Adverse effects
The procedure is generally well tolerated after a topical
anesthesia has been applied for 1 hour. Topical preparations
containing tetracaine should be avoided in patients with a
known allergy to sulfa-containing medications. A forced air
cooling system can be utilized to further minimize procedural
pain. Most patients experience erythema, edema, and xerosis
which usually resolve within 4 days. Some patients experi-
ence temporary bronzing, acneiform eruptions, or milia for-
mation. Most patients can return to full social activity within
2 days. Patients can be offered oral corticosteroids to mini-
mize downtime.
Optimizing outcomes
Rarely, postoperative hyperpigmentation can develop several
weeks after non-ablative skin remodeling and is more likely
to be experienced by patients with darker skin tones. In some
cases, investigators demonstrated an association of post-
treatment hyperpigmentation with excess intraoperative epi-
dermal cryogen cooling.51 Although always transient, topical
bleaching agents and light glycolic acid peels may hasten the
resolution of postinflammatory hyperpigmentation.
In the weeks following a series of non-ablative laser proce-
dures, follow-up visits can help identify patient concerns and
increase the overall satisfaction with treatment. Clinical
improvements after a series of non-ablative laser procedures
may take weeks to realize; thus reassurance by the laser
surgeon regarding the patient’s progress can be particularly
important.
Postoperative care
Since the epidermis remains intact following non-ablative
laser skin remodeling, postoperative care is minimal. Some
patients experience mild erythema and edema lasting less
than 24 hours.
Pitfalls and their management
Is the amount of photodamage amenable to non-
ablative laser skin remodeling?  Patients with mild to
moderate facial photodamage are the best candidates for non-
ablative procedures. Patients with severe rhytides and skin
laxity may be disappointed with the overall clinical outcome.
Does the patient have a history of herpes labialis? 
Reactivation of prior herpes simplex infection can occur with
perioral non-ablative laser skin remodeling due to the intense
heat produced by the laser. Patients with a strong history of
herpes simplex labialis may require prophylactic oral antiviral
medication to avoid an outbreak.
What is the patient’s skin phototype?  Although the
majority of current non-ablative systems used are within the
mid-infrared range of the electromagnetic spectrum and not
avidly absorbed by epidermal melanin, patients with darker
skin phototypes may develop postinflammatory hyperpig-
mentation after non-ablative laser treatment. This temporary
reaction most likely develops following inflammation created
by concomitant cryogen-spray epidermal cooling.

558
Part 3  Aesthetic Surgical Procedures
improve fine lines, tactile roughness, and skin tightness.
Patients with moderate photodamage but without actinic
keratoses were randomized to receive MAL (Metvix, Gal-
derma, Ft Worth, TX) applied to half the face for 1 hour and
the other half for 3 hours prior to irradiation with the red
lamp (Aktilite, PhotoCure ASA, Olso, Norway), a diode-
emission lamp with an average emission at 630 nm, for a total
dose of 37  J/cm2. Far greater improvement in fine lines,
texture, and skin tightness was observed in the side incubated
for 3 hours; however, more intense erythema, edema, and
scaling were also observed in the postoperative period on this
side. No improvement in hyperpigmentation or telangiecta-
sias was observed on either side.
Recent molecular and cellular studies have begun to eluci-
date the mechanism in which PDT stimulates dermal remod-
eling and skin rejuvenation. Orringer and colleagues65
examined skin samples after 3-hour application of 20% ALA
solution (Levulan Kerastick DUSA Pharmaceuticals, Inc) and
irradiation with a single pass of long-pulsed PDL (VBeam) at
595 nm at non-purpuric settings. Serial in-vivo biochemical
and immunohistochemical analyses over 6 months following
the treatment showed stimulation of epidermal proliferation
and increased epidermal thickness. Upregulation of dermal
collagen production was demonstrated by increases in procol-
lagen I mRNA, procollagen III mRNA, and procollagen I
protein levels. The peaks in procollagen gene expression after
PDT with PDL were roughly twice the levels previously
reported with PDL alone.66
Technical aspects
Patient selection
PDT rejuvenation is the ideal choice for patients with actinic
keratoses with or without mild to moderate photodamage.
Treatment protocols can be tailored to each patient’s specific
cosmetic concerns. Patients with multiple actinic keratoses
and mild to moderate rhytides are best treated with diffuse
topical application of ALA or MAL followed by exposure
with blue or red light sources. PDT using non-purpuric PDL
Pharmaceuticals, Inc, Wilmington, MA) for 30–60 minutes
prior to full-face treatment with a pulsed light device (IPL
Quantum SR, Lumenis, Inc, Santa Clara, CA) with a wave-
length of 515–1200 nm, fluences from 23–28 J/cm2, pulse
durations of 2.4 and 4.0 ms with a 15-ms pulse delay. The
shorter incubation time resulted in far fewer side effects than
previous reports, with most erythema, purpura, and edema
resolving within 1–2 days post treatment.
Alexiades-Armenakas & Geronemus62 demonstrated that
PDL could activate 20% ALA solution (Levulan Kerastick
DUSA Pharmaceuticals, Inc) in order to resolve actinic kera-
toses on the face and scalp. In their study, 41 patients were
randomized to receive either 3-hour or overnight incubation
with 20% ALA solution followed by long-pulsed PDL (VBeam
Laser Corp, Candela, Wayland, MA) at 595 nm, at fluences
of 4–7.5 J/cm2, 10-ms pulse duration, 10-mm spot size, with
a 30-ms cryogen-spray application followed by a 30-ms delay
prior to each laser pulse. Treatment of actinic keratosis on
the head was safe and efficacious at both the shorter and
longer incubation time periods.
Recently, this PDT method has been shown in split-face
study to improve fine lines, skin texture, erythema, and pig-
mentation.63 Split-face treatments in which 20% ALA solu-
tion (Levulan Kerastick DUSA Pharmaceuticals, Inc) was
applied to half the face 60 minutes before full-face treatment
with long-pulsed PDL (VBeam) at 595 nm at the previously
described settings. After three treatments, 3 weeks apart,
participants showed greater improvement in several measures
of photodamage on the side of the face pretreated with 20%
ALA solution than in the side treated with PDL alone (Fig.
33.4). The treatments were well tolerated, with most patients
experiencing only transient erythema in the postoperative
period.
Although widely used to treat cancerous and precancerous
conditions, the combination of MAL and red light has only
recently been shown to improve photodamage. Ruiz-
Rodriguez and colleagues64 showed, in a split-face comparison
study of 10 patients, that three treatments of MAL cream
application followed by illumination with red light can
A
B
Figure 33.4  Facial rhytides and
erythema (A) before and (B) 3 months
after a series of three ALA plus PDL
treatments 3 weeks apart.

559
Chapter 33  Energy-based Treatment of the Aging Face for Skin Resurfacing
sources have been compared directly for rejuvenation. For
patients with significant actinic keratoses, activation with
continuous-wave broadband red or blue light sources is pre-
ferred since broadband light has been shown to induce more
significant PDT effect than IPL or PDL on normal skin.68
Patients with fewer actinic keratoses and global photodamage
are best treated with the appropriate laser. Treatments should
be repeated monthly until desired cosmetic results are
achieved. Given that PDT can sometimes unmask non-
melanoma skin cancers, any lesions remaining after treatment
should be biopsied.
Postoperative care
Following light activation, the skin should be thoroughly
cleansed with mild soap and water. Since inactivated PpIX
may remain in the skin for up to 48 hours, strict sun protec-
tion must be followed. Sunscreens containing physical block-
ers, such as titanium or zinc oxide, are preferred since they
effectively block the large spectrum of light which can acti-
vate PpIX. Wearing wide-brimmed hats and staying in a dim
room will further limit phototoxic reactions.
Pitfalls and their management
Can the patient adhere to strict sun and light
avoidance for 48 hours?  PDT is a relatively safe and
well-tolerated therapy with most postoperative side effects,
such as erythema, scaling, and crusting, resolving within the
first week after treatment. Patients who are exposed to bright
lights or sun within 48 hours after the treatment will feel a
burning or stinging sensation indicating further activation of
PpIX. Should this activation continue, phototoxicity will
develop. Phototoxicity should be treated urgently with sys-
temic corticosteroids, emollients, and ice to avoid scarring or
pigmentation alterations.
Summary
PDT is useful for augmenting the rejuvenation potential of
non-ablative laser and light devices. With the availability of new
photosensitizers and light sources, there are ever-increasing
options to help patients achieve their desired goals. Further
study is needed to identify the optimum photosensitzer,
incubation time, and light sources for a variety of conditions.
Better quenching of excess PpIX may limit the photosen-
sitivity period following each treatment and increase tolera-
bility. Broad application of PDT could help prevent
non-melanoma skin cancers by eliminating non-visible pre-
cancerous lesions, thus improving the health and appearance
of the skin.
can help resolve actinic keratoses as well as facial erythema.
Patients with multiple actinic keratoses, solar lentigines, and
facial erythema may benefit most from PDT using IPL as a
light source. Regardless of the PDT strategy, patients must
be able to adhere to strict sun and bright light avoidance for
48 hours after the treatment to limit redness, swelling, and
crusting associated with phototoxicity. Patients should not
undergo any form of PDT if they have a porphyrin disorder,
a photosensitivity disorder, or are taking photosensitizing
medications. Patients with peanut allergies are not candidates
for MAL PDT protocols since the cream contains peanut oil.
Since PDT protocols have not been studied extensively in
pregnant or lactating women, they should not undergo any
form of PDT.
Anesthesia
No topical anesthesia is required prior to application of the
light course. Since light activation of MAL or ALA to PpIX
can be associated with burning or stinging, forced air cooling
devices may be used to alleviate any discomfort. During the
illumination, short breaks with cold water mists can also help
patients better tolerate the procedure. In rare cases of severe
photodamage, nerve blocks or narcotics may be indicated for
pain relief.
Technique
After thorough cleansing of the skin, several strategies may
remove the stratum corneum and allow for more uniform
penetration of the photosensitizer. Microdermabrasion, vibra-
dermabrasion, and topical application of 40% urea cream,
alcohol, or acetone have all been used prior to application of
the photosensitizer. There is much debate about which pho-
tosensitizer, ALA of MAL, is more effective for photorejuve-
nation. Methylating the ALA molecule makes the MAL
molecule more lipophilic and better able to penetrate cutane-
ous structures.67 Comparisons between ALA and MAL in
patients with actinic keratoses have shown that MAL is more
specific for neoplastic lesions; however, ALA induced more
porphyrin production. No trials have directly compared the
efficacy of topical photosensitizers for rejuvenation.
After applying the photosensitizer broadly to the skin,
patients should be kept in a room with dim lighting prior to
activation with a light source. MAL should be occluded with
plastic wrap to increase penetration. Incubation time will vary
from 30 minutes to 3 hours based on desired results. MAL
cream should be removed prior to light activation and appro-
priate eye protection should be applied. The variety of light
sources for activation of photosensitizers and PDT protocols
are summarized in Table 33.3; however, none of the light
Table 33.3  Photodynamic therapy protocols for rejuvenation
APPLICATION OF
PHOTOSENSITIZER
Treating Condition
ACTINIC KERATOSIS
ACTINIC KERATOSIS +
ERYTHEMA
ACTINIC KERATOSIS ±
ERYTHEMA + DYSCHROMIA
MAL 3 hours under occlusion or
ALA 1–3 hours
Blue or red 411 nm or 630 nm
PDL 595 nm
IPL 515–1200 nm

560
Part 3  Aesthetic Surgical Procedures
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34
Laser and Light Treatment of Acquired
and Congenital Vascular Lesions
Arielle NB Kauvar MD FAAD and Agneta Troilius MD PhD
Summary box
 Lasers and light sources are the treatment of choice for
congenital and acquired cutaneous vascular lesions.
 Lasers produce selective photocoagulation of vessels using
wavelengths of light that are well absorbed by hemoglobin,
and pulse durations equal to or shorter than the thermal
relaxation time (or cooling time) of the vessels.
 Larger-diameter and deeper vessels require longer
wavelengths of light and longer pulse durations.
 Laser and light source treatment carries minimal risks and
minimal downtime, and provides superior outcomes.
 Lesions treated with lasers and light sources include vascular
malformations, hemangiomas of infancy, telangiectasia, facial
erythema, poikiloderma, as well as hypertrophic scars and
striae.
 INTRODUCTION
The development and refinement of laser technology pro-
vided, for the first time, an acceptable and effective means
of treatment for many congenital and acquired cutaneous
vascular disorders. Early efforts in the 1970s and 1980s cen-
tered around investigating the argon and other continuous-
and quasi-continuous-wave lasers for port-wine stains (PWSs),
hemangiomas, and telangiectasia.1–4 These laser treatments
often produced excellent lightening or clearance of these
lesions, but with an unacceptable rate of scarring and pigmen-
tary alteration. Macular lesions and pale, immature PWSs
were at highest risk for these complications.
The formulation of the theory of selective photothermoly-
sis, and its application to the development of the pulsed-dye
laser in the 1980s, revolutionized the treatment of cutaneous
vascular lesions. The principles of selective photothermolysis
describe the requirements for lasers or light energy to produce
selective heating and destruction of a targeted skin lesion,
such as a blood vessel, without damaging nearby structures.5
The pulsed-dye laser quickly emerged as the gold standard of
treatment for PWSs, hemangiomas, and facial telangiectasia.
Laser treatment produced excellent clinical efficacy with an
incidence of scarring less than 1% even after multiple, repet-
itive treatments.6,7 A deeper understanding of the complex
laser–tissue interactions and advancements in laser technol-
ogy further refined laser therapy over the past decade.
Lasers and light devices now being applied to the treatment
of cutaneous vascular lesions include the potassium titanyl
phosphate (KTP), pulsed-dye, alexandrite, diode, and neo­
dymium:yttrium-aluminum-garnet (Nd:YAG) lasers, as well
as intense pulsed light (IPL) (Table 34.1).
Principles of laser–tissue interaction
Electromagnetic radiation
The term laser is an acronym for Light Amplification by the
Stimulated Emission of Radiation. Albert Einstein introduced
the concept of stimulated light emission in 1917 when he
proposed that a photon of electromagnetic energy can stimu-
late emission of an equivalent photon from atoms or mole-
cules that are in an excited state.8 Laser light is emitted as a
single discrete wavelength, which is determined by the laser
medium which may be a solid (e.g. alexandrite crystal), liquid
(pulsed dye) or gas (carbon dioxide). All the effects of light
on tissue begin with the absorption of electromagnetic radia-
tion. The photobiologic effects of lasers or light on skin
results from absorption and excitation. When discussing elec-
tromagnetic radiation, energy is measured in units of joules
(J). The amount of energy that is delivered per unit area is
the fluence (or dose) and is measured in J/cm2. Power is the
rate at which energy is delivered, and is measured in watts
(W). By definition, 1 watt is 1 joule per second (W = J/sec).
Selective photothermolysis
Anderson and Parrish inaugurated a new era in the application
of lasers to cutaneous disease with their development of the
concept of selective photothermolysis in 1983. The term
selective photothermolysis describes the production of
site-specific, thermally-mediated injury of microscopic, pig-
mented tissue targets by selectively absorbed pulses of
radiation.
Three requirements must be met to achieve selective pho-
tothermolysis. First, the wavelength of light must be prefer-
entially absorbed by the desired target structures, and must
be capable of penetrating the tissue sufficiently to reach that
structure. Light deposits energy only in sites of absorption.
Atoms or molecules that absorb energy from light are termed
chromophores. The major chromophores in skin are hemo-
globin, melanin, and water.9,10 When targeting a vascular
lesion, the wavelength of light chosen should be well absorbed
by hemoglobin and poorly absorbed by melanin. When light

564
Part 3  Aesthetic Surgical Procedures
is absorbed by these structures, heat is produced and con-
tained within these structures.
The second requirement for selective photothermolysis is
that the pulse duration or laser exposure time is less than or
equal to the time necessary for cooling of the target struc-
tures. The goal is to selectively heat these structures without
allowing diffusion of thermal energy to the surrounding tissue
structures, which could result in damage to epidermal and
dermal components, and eventuate in scarring. When selec-
tive photothermolysis is achieved, light is absorbed by the
structure, and heat is produced and confined to the structure.
Selective heating of the target is produced when the energy
is deposited at a rate faster than the rate for cooling of the
target structure. Heat is dissipated by conduction and radia-
tive transfer as soon as it is created.
The last requirement for selective photothermolysis is that
sufficient fluence, or energy density, is used to reach a dam-
aging temperature in the target.
Wavelength
The wavelength of light chosen must be capable of reaching
the target structure. For a given wavelength, the optical pen-
etration into skin depends on absorption and scattering.11 For
wavelengths in the ultraviolet to near-infrared spectrum,
absorption and scattering are stronger for shorter wave-
lengths. In the dermis, collagen fibers produce strong wave-
length-dependent scattering. Light penetration into dermis is
primarily determined by this scattering. The most penetrating
wavelengths are in the 650–1200 nm red and near-infrared
region. The least penetrating wavelengths are in the far-ultra-
violet, where protein absorption dominates, and the far-infra-
red, where water absorption dominates. The depth of
penetration therefore gradually increases with longer wave-
lengths (Fig. 34.1).
In order to target vascular lesions, the wavelength of light
chosen must be preferentially absorbed by blood vessels.
Blood absorption is dominated by oxyhemoglobin and reduced
hemoglobin absorption.12 Hemoglobin is present at high con-
centrations within blood vessels. Oxyhemoglobin has major
absorption peaks at 418, 542, and 577 nm, in the blue, green,
and yellow wavelengths (Fig. 34.2). Melanin normally occurs
in the epidermis and hair follicles, and absorbs broadly across
the visible light spectrum. Despite strong absorption by blood
in the blue band (418 nm), wavelengths in this region are less
Table 34.1  Lasers and light sources for vascular lesions
LASER/LIGHT
SOURCE
WAVELENGTH
(nm)
PULSE
DURATION (ms)
Pulsed KTP
532
1–200
Pulsed dye
585
0.45
Long-pulsed dye
585, 590, 595, 600
1.5–40
Long-pulsed
alexandrite
755
3–20
Diodes
800, 810, 940
1–250
Long-pulsed
Nd:YAG
1064
1–100
Intense pulsed light
source
515–1200
0.5–30
532 nm
595 nm
694 nm
810 nm
1064 nm
Longer wavelengths penetrate skin more deeply
Figure 34.1  For a constant laser spot size and fluence, longer
wavelengths penetrate skin more deeply.
Absorption (log scale)
Wavelength (nm)
UV
Visible
IR
300
500
700
1000
Oxyhemoglobin
Melanin
Water
Nd: YAG
Diode
Ruby
Alexandrite
2000
Absorption spectra: major chromophores
Figure 34.2  Absorption spectra for the three major
chromophores: hemoglobin, melanin, and water.

565
Chapter 34  Laser and Light Treatment of Acquired and Congenital Vascular Lesions
Fluence and epidermal protection
Sufficient fluence must be supplied to produce irreversible
damage to the target, when targeting dermal blood vessels.
Increasing the fluence produces more effective photocoagula-
tion, but may lead to an increase in side effects. Absorption
by epidermal melanin and heat transfer from dermal targets
can result in inadvertent epidermal injury. Ideally, the epi-
dermis should remain unaffected to prevent adverse clinical
outcomes. Recently developed skin cooling methods mini-
mize tissue injury by extracting heat from the epidermis.20–25
Cooling the skin before, during, and after laser pulse impact
reduces tissue injury. Cooling the skin before and after laser
exposure tends to reduce pain and swelling. Cooling the skin
during laser treatment decreases epidermal heating. Skin
cooling devices extract heat from the epidermis by means of
conduction. Cold ice cubes may be applied to the skin before
or after treatment. During laser treatment, the application of
a cold gel or a liquid medium provides a more conductive
material than air, and increases heat dissipation. Cold sap-
phire laser tips extract even more heat than cold gels or
liquids (Fig. 34.3). Excellent heat extraction from the epi-
dermis is also provided by the application of a liquid cryogen
spray during laser treatment (Fig. 34.4).
Vascular lesion removal by selective
photothermolysis
Since the development of the first pulsed-dye laser, newer
developments in laser technology based on improved knowl-
edge of laser–tissue interactions have led to better treatment
responses with greater margins of safety. A wide variety of
laser and light systems are now used for vascular lesions (see
Table 43.1).
The theoretical formulation of selective photothermolysis
predicted that a 577-nm, 1-ms pulse duration was ideal for
immature PWSs.26 For vessels 10–50  µm in diameter, the
thermal relaxation time should be 0.1–10 ms, with an average
of 1.2  ms.14 Pickering et  al.27 demonstrated that exposure
times of 0.1–0.3  ms are required to irreversibly damage
100-µm diameter vessels with wall thicknesses of 3–6 µm. In
early studies, shorter pulse durations of 1–20 µs were tested
at a wavelength of 577  nm in normal human and animal
skin.28,29 Laser treatment produced selective vascular injury
but extensive vessel rupture and hemorrhage resulted from
erythrocyte explosion.30 This was consistent with mechanical
desirable because of limited penetration and interference by
melanin absorption. The yellow band (577 nm) of oxyhemo-
globin absorption was initially chosen for targeting superficial
small vessels using the flashlamp-pumped pulsed-dye laser.13
The wavelength of this laser was subsequently increased to
585  nm and later 595  nm to provide increased depth of
penetration into tissue. Pulsed KTP lasers emit at 532 nm in
the green light spectrum. Green light is absorbed by hemo-
globin approximately as well as yellow light and has roughly
the equivalent depth of penetration through fair skin.
There is also a broad oxyhemoglobin band around 900 nm
that provides preferential hemoglobin absorption, with
minimal interference from melanin, and much greater depth
of penetration. Lasers in the near-infrared region have recently
been applied to the treatment of cutaneous vascular lesions,
and include the alexandrite (755 nm), diode (800 nm), and
Nd:YAG (1064  nm) lasers. IPL sources use high-intensity
pulsed flashlamps that produce broadband emission from
500–1100 nm. The broad emission spectrum provides absorp-
tion by oxygenated and deoxygenated hemoglobin and deep
penetration into the skin for larger-diameter, more deeply
situated vessels.
Pulse duration and thermal relaxation time
An important concept underlying selective photothermolysis
is that the exposure time or pulse duration of the laser deter-
mines the confinement of heat and extent of thermal injury
produced in tissue.11,14–17 The thermal relaxation time (TRT)
refers to the time needed for significant cooling of the micro-
scopic tissue target. Maximal thermal confinement occurs
when the laser exposure time is less than the TRT. The
cooling of microscopic tissue structures is determined by heat
conduction. Conduction is the transfer of heat between two
interacting systems, and is driven by a temperature gradient
between the systems. The thermal relaxation time for heat
conduction is proportional to the square of the object size. It
is approximated by the formula TRT = d2/4κ where d is the
diameter of the object or thickness of the tissue layer and κ
is the thermal diffusivity. Thermal diffusivity is a material
property that expresses the ability of heat to diffuse. The
cooling time of an object depends on its shape owing to dif-
ferences in volume and surface area. In general, for a given
thickness of tissue, spheres cool faster than cylinders, which
cool faster than planes. Smaller objects cool more quickly
than larger objects. For objects of the same shape and mate-
rial, an object one-half the size cools in one-quarter of the
time and an object one-tenth the size cools in one-hundredth
of the time.
Spot size
The optical penetration of laser light is determined in part by
the beam diameter, or spot size.18,19 With smaller spot sizes,
a greater fraction of photons scatter outside the beam area
and are rendered ineffective. Larger spots allow more photons
to remain within the diameter of the incident beam of light.
The increased scattering within the beam diameter produces
higher fluences at a given depth within tissue. The ratio of
dermal to epidermal damage increases as the spot size
increases. Treatment fluences are therefore decreased with
larger spots compared to smaller spot sizes. A 7- and 10-mm
spot size requires only one-half to two-thirds the fluence for
a 5-mm spot with the 585-nm pulsed-dye laser.
Figure 34.3  Water-cooled sapphire laser chill tip on a pulsed-
KTP laser. (Courtesy of Lumenis, Inc.)

566
Part 3  Aesthetic Surgical Procedures
globin approximately as well as 585 nm light, and has roughly
the equivalent depth of penetration through fair skin. With
pulse durations in the 1–200 nm range, purpura is precluded
by the more uniform heating of blood vessels. Most of the
available laser systems use grouped nanosecond-domain
Q-switched pulses to produce millisecond exposure times.
The longer pulse durations minimize photomechanical
injury and, clinically, reduce post-treatment purpura. Pulse
durations greater than 1 ms produce gentle vaporization of
blood. Rather than producing explosive vessel rupture, evac-
uation of blood from the vessel produces an empty, thermally
coagulated blood vessel.42 Lengthening the pulse duration of
the pulsed-dye laser to 1.5 ms significantly reduced the inten-
sity and duration of purpura. Studies of adult PWSs with
a 595-nm, 1.5-ms pulsed-dye laser demonstrated reduced
purpura compared to the 585-nm, 450-µs laser.43 Lengthen-
ing the pulse duration also minimizes epidermal damage.
Melanosomes are less efficiently heated with longer pulses;
they cool during laser pulse delivery because of their small
size.
Longer wavelengths provide deeper penetration into the
skin and enable treatment of larger-diameter and deeper
blood vessels. The absorption coefficient of blood decreases
with increasing wavelengths beyond 577 nm. However, highly
selective microvascular injury can be achieved by increasing
the fluence to produce the same heating of the blood vessels.
Longer wavelength pulsed-dye lasers at 595 nm work well for
treating PWSs and telangiectasias, as long as higher fluences
are used. Pigment cell injury is minimized by the use of longer
pulse durations (1.5 ms) and active or passive skin surface
cooling.
IPL systems are high-intensity flashlamps that emit a broad
spectrum of polychromatic light from 500 to 1200  nm.44
Cut-off filters are used to match the spectrum of delivered
light to the required depth of optical penetration and to
maximize absorption by the targeted chromophores. By filter-
ing out shorter visible wavelengths, deeper or larger-diameter
blood vessels are more effectively targeted. The pulses are
delivered as single or multiple synchronized pulses with expo-
sure times of 0.5–80 ms. The pulse duration is matched to
the thermal relaxation time of the vessels being treated. The
interpulse delays allow cooling of the epidermis and smaller
vessels while heat is retained in the larger vessels.
More recently, the near-infrared wavelengths have been
applied to the treatment of vascular lesions. Alexandrite
(755  nm), diode (800, 940  nm), and Nd:YAG (1064  nm)
lasers rely on the broad oxyhemoglobin absorption band in
the 800–1000  nm spectrum, and provide greater depth of
penetration. These longer wavelength lasers and light sources
are being used to treat larger vessel vascular anomalies, as well
as larger leg veins (1–5 mm).
 PRACTICAL APPLICATIONS
The practical applications for vascular lasers and light sources
are listed in Box 34.1.
Port-wine stains
PWSs are congenital capillary malformations that occur in
0.3–0.5% of live births, grow commensurately with the child,
and never regress.45 Histopathology reveals an increased
number of ectatic blood vessels in the dermis. Their etiology
rupture of blood vessels from vaporization of blood. The
pulse duration of the pulsed-dye laser was then lengthened
to maximize thermal coagulation of vessels and minimize
vaporization injury. Longer pulse durations minimized the
hemorrhage, but required higher threshold fluences to achieve
vessel coagulation.31 Based on these studies, a 400-µs, 577-nm
pulsed-dye laser was developed and produced excellent clin-
ical lightening with a low risk of scarring in pediatric and adult
patients.32,33
The wavelength of the pulsed-dye laser was subsequently
increased to 585 nm, which provided similar vascular selec-
tivity and doubled the depth of penetration in tissue.32,34
Extensive clinical experience with the 585-nm, 400-µs
pulsed-dye laser demonstrated excellent clearing of PWSs
with a high safety profile in infants, children, and adults.35–40
Clinically, this laser produces transient blue–black purpura
due to hemorrhage and a delayed vasculitis. Histologic exam-
ination shows selective intravascular and perivascular coagula-
tion necrosis with epidermal injury in fair skin.40 In the 1990s,
newer pulsed-dye lasers were developed with pulse durations
greater than 1 ms because the 0.5-ms pulse width was theo-
retically too short for most PWSs, and produced disfiguring
purpura for as long as 10 days following treatment. Dierickx
et al.41 performed a landmark in-vivo study of PWS thermal
relaxation time in 1995, and experimentally demonstrated
that the thermal relaxation time for vessels approximately
60 µm in diameter was between 1 and 10 ms.
Millisecond-duration pulsed-KTP lasers were introduced in
the 1990s. Pulsed-KTP lasers emit at 532 nm in the green
light spectrum. KTP crystals are convenient to work with and
highly reliable. The 532-nm KTP light is absorbed by hemo-
Laser beam
Epidermis
Dermis
Blood vessel
Dynamic cooling device
Figure 34.4  The Dynamic Cooling Device (DCD; Candela Laser
Corp) provides a brief spurt of cryogen that selectively cools
the epidermis during Vbeam laser application. (Courtesy of
Candela Laser Corp, Wayland, MA.)

567
Chapter 34  Laser and Light Treatment of Acquired and Congenital Vascular Lesions
periorbital region may obstruct vision, and in the periorbital
and nose region may interfere with eating or breathing.52 Soft
tissue and skeletal hypertrophy occur in some facial PWSs,
and may require surgical correction or orthodontic treat-
ment.53 PWSs can have profound psychosocial consequences;
many patients report low self-esteem and difficulties in their
personal and professional relationships attributed to their
vascular lesions.
With the documentation of psychosocial morbidity associ-
ated with PWSs, especially with increasing age, some groups
have conducted studies of the potential benefits of early laser
treatments of the cutaneous lesions. In a study evaluating 231
young patients with PWSs before and after laser treatments
for psychosocial consequences, Troilius et  al.54 found that
75% of respondents found that their PWS had negative
impacts on their lives, 47% suffered low self-esteem, 28%
reported that their PWS made school life more difficult, and
76% of families thought the patient was negatively impacted
by their PWS.
All of these symptoms, however, decreased significantly
after successful laser treatment. Patients reported better
social relationships, fewer problems with the opposite sex,
and fewer negative reactions from peers. Based on these
results, Troilius et al.55 advocate treatment of PWSs as early
as possible to avoid the high psychosocial morbidity associ-
ated with the lesion. Treatment of PWS can prevent many
of these complications. The preponderance of evidence sug-
gests that treatment early in life is not only safe but also
enables more rapid clearing; however, there may be partial
return of the PWS 5–10 years after treatment. The greater
lesional clearance observed in children can be attributed to
thinner skin allowing better laser penetration, smaller vessel
diameter, and smaller lesional surface area.
Pulsed-dye laser treatment of port-wine stain
The safety and efficacy of the pulsed-dye laser for the treat-
ment of PWS in children and adults has been well established
in the literature. Gradual clearing of the PWS is produced
with successive laser treatments usually performed at 4–6-
week intervals. Early studies demonstrated 75% or more
lightening in approximately 36–44% of adult patients with
PWS, and at least 50% lesional lightening in 75% of pediatric
patients after a total of four treatments.30–34,56 With the
pulsed-dye laser, damage to vascular tissue is so selective that
there is inconsequential absorption by melanin in fair-skinned
individuals. Epidermal damage is, therefore, rarely seen fol-
lowing pulsed-dye laser treatment, and the laser can be used
safely in skin types I–IV. In a study of 500 patients, atrophic
scarring was reported in less than 0.1% of patients, spongiotic
dermatitis in 0.04%, hyperpigmentation in 1%, and hypopig-
mentation in 2.6% of patients.6 Treatment of darker skin is
not performed because the higher density of melanin results
in decreased vascular absorption and the possibility for epi-
dermal damage.57 Newer studies of cryogen cooling tech-
niques suggest that safe treatment of darker skin phototypes
may be possible in the near future.58
Advances in pulsed-dye laser include the use of larger spot
sizes, longer wavelengths, and longer pulse durations. The use
of larger 7- and 10-mm spot sizes improved PWS treat-
ment.59,60 Increased clearance was achieved at lower fluences,
purpura is reduced, and there was less post-treatment reticu-
lation of the skin. Longer wavelengths and longer pulse
is unknown, but there is an altered or even absent neural
modulation of the vascular plexus46 with a decrease in both
sympathetic and sensory nerve innervation of the papillary
plexus.47 Chang et al.48 showed a decrease in the nerve density
in facial PWS using confocal microscopy PWS specimens, and
overexpression of vascular endothelial growth factor (VEGF)
and its receptor.49 PWSs begin as flat, pink cutaneous patches
predominantly located on the head or neck. Most PWSs are
isolated lesions, but they may be associated with complicated
syndromes requiring prompt diagnosis and intervention. The
most common of these syndromes are Sturge–Weber50 and
Klippel–Trenaunay.51 PWSs are characterized histologically
by ectatic vascular channels with normal turnover of endothe-
lial cells. PWSs are usually present at birth and grow propor-
tionately to the individual. With age, PWSs darken in color
and become increasingly nodular.
By the fifth decade of life, up to 65% of patients develop
hypertrophy or nodularity of the lesion, and these changes
are associated with a risk of spontaneous bleeding or hemor-
rhage with injury to the site. Hypertrophy of lesions in the
Box 34.1  Practical applications for vascular
lasers and light sources
Capillary malformations
Infantile PWS
Macular PWS in adults
Hypertrophic PWS in adults
Hemangiomas
Superficial hemangiomas
Mixed-type hemangiomas
Involuting hemangiomas
Venous malformations
Telangiectasias
Spider angiomata
Actinic telangiectasia
CREST syndrome
Essential telangiectasia
Hereditary hemorrhagic telangiectasia
Radiation dermatitis
Rosacea
Facial erythema
Associated with rosacea
Flushing and blushing
Cherry angiomas
Venous lakes
Poikiloderma of Civatte
Other lesions treated with vascular lasers
Angiokeratomas
Glomus tumors
Pyogenic granulomas
Adenoma sebaceum
Blue rubber bleb nevi
Hypertrophic and erythematous scars
Striae distensae
Warts

568
Part 3  Aesthetic Surgical Procedures
dye laser treatment, the mean decrease in lesion size was
greatest for the smaller lesions: a 67% decrease for lesions
<20 cm2, compared to a 23% decrease for lesions >40 cm2.
In a histological study, Fikerstrand et al.69 showed that lesions
with a poor response to a 585-nm, 450-µs pulsed-dye laser
had small vessels. Moderate responses were observed for
PWSs with deeper and larger vessels. The best response was
seen in superficially located, larger-diameter vessels.
Vessel morphology correlated with PWS color.70 Pink
lesions had the smallest-diameter vessels, and purple lesions
had the largest. Red lesions were composed of more superfi-
cially located vessels than pink or purple ones. Red color
predicted a good response, while pink color predicted a poor
response to laser therapy. Using videomicroscopy, Motley
et  al.71 demonstrated two types of vascular ectasia within
PWSs. One type showed ectasia localized to the capillary
loops, and the other was composed of ring-like, dilated,
ectatic vessels in the superficial horizontal plexus. The first
type correlated with a poor response to pulsed-dye laser
treatment, and the second type correlated with a good
response. Kauvar et al.72 showed that even slowly responsive
PWSs continue to clear with repetitive pulsed-dye laser treat-
ment with no increased risk of adverse effects.
Several studies of pulsed-dye laser treatment for PWS
during infancy indicate that not only is early treatment safe
but also more rapid clearance is possible. In a study of 35
children ages 3 months to 14 years of age, Tan et al.73 found
that children less than 7 years old required fewer treatment
sessions than older children for PWS clearance. A study of
73 children reported that patients between 3 months and 6
years showed increased lightening of their PWS after one
treatment than patients between 7 and 14 years of age.40
Pulsed-dye laser treatment of PWS in 83 children resulted in
complete clearance in 32% of children who began treatment
before 1 year of age compared to 18% of children treated
after 1 year of age.74 Alster & Wilson reported 87% PWS
clearance in patients less than 2 years and 73% in patients 16
years and older.75 Similarly, a study of 133 patients found the
highest percentage of good and excellent results in those aged
0–10 years.76 In contrast, a study by Van der Horst et al.77
found no difference in treatment results between age groups.
However, in this study, only partial treatment of PWS lesions
was performed during each treatment session, and treatment
durations improve PWS clearance. In a side-by-side com-
parison study, Kauvar found increased clearance of PWS in
patients treated with a 595-nm, 1.5-ms pulsed-dye laser
as compared to a 585-nm, 450-µs pulsed-dye laser.61 The
longer wavelengths provide more deeply penetrating light to
target deeper vessels. The longer pulse durations enable more
even heating of larger-diameter vessels and minimize post-
treatment purpura.
Another advance in the laser treatment of PWS has been
the addition of skin cooling methods. Nelson et al.21 demon-
strated that selective cooling of the epidermis could be
achieved while maintaining the temperature of the laser-
heated dermal blood vessels by applying millisecond duration
cryogen spurts preceding each laser pulse. The use of cryogen
spray in conjunction with the 585-nm, 450-µs pulsed-dye
laser decreased patient discomfort during treatment without
compromising efficacy.62 When cryogen spray cooling was
used in conjunction with a 595-nm, 1.5-ms pulsed-dye laser,
an overall decrease in recovery time from 9.5 to 5 days was
achieved with reduced edema, erythema, and crusting.63 This
study also demonstrated that a laser fluence of 10 J/cm2 could
be administered safely in infants, children, and adults because
of the epidermal protection afforded by the skin cooling.
Based on these results, studies were undertaken evaluating
higher fluences (up to 15 J/cm2) in the treatment of PWS in
infants and adults with a 595-nm, 1.5-ms pulsed-dye laser
(Fig. 34.5). Dramatic clearing of PWS was achieved in fewer
treatments with the safe use of higher laser fluences afforded
by the cryogen spray cooling used to protect the epidermis.64,65
Factors affecting pulsed-dye laser treatment response
for port-wine stain
The response of a PWS to pulsed-dye laser treatment
depends, in part, on its size, anatomic location, and the types
of vessels that comprise the lesion. Among PWSs located on
the head and neck, lesions that are present in the central
facial area or in a V2 dermatomal distribution respond more
slowly than PWSs located elsewhere on the head and neck.66
PWSs located on the extremities respond more slowly to
laser therapy than lesions on the trunk, and lesions on the
distal extremities respond the slowest.67 In a study of 91
consecutive patients, Nguyen et al.68 found that with pulsed-
Figure 34.5  Infantile port-wine stain (A) before and (B) after four treatments with a 595-nm, 1.5-ms pulsed-dye laser. (Reprinted with
permission. Arch Derm 2000;136:942.)

569
Chapter 34  Laser and Light Treatment of Acquired and Congenital Vascular Lesions
pulsed-dye laser (see Laser and intense pulsed light safety
procedures, below).80 Endotracheal tubes and laryngeal masks
provide better seals than face masks and are preferred for this
purpose. As an added measure of precaution, the airway tube
and mouth region should also be covered with wet drapes.
Port-wine stain recurrence
Pulsed-dye laser treatment does not achieve complete clear-
ing of PWSs in all patients, and some lesions recur years after
completing therapy. Although there are reports of high recur-
rence rates 5–10 years after laser treatment,81,82 the patients
in these studies were treated with less advanced laser tech-
nology and the authors did not take into account factors that
affect treatment outcomes such as anatomic location. Even
among those patients who have recurrences, however, the
size of the recurring lesion is usually a fraction of the area of
the original PWS, and they are significantly lighter in color.
In the author’s experience, these lesions usually require very
few additional treatment sessions to achieve excellent clear-
ing, and a good cosmetic outcome can be maintained with
periodic laser treatments.
Intense pulsed light treatment
of port-wine stains
IPL devices are broadband filtered xenon flashlamps that
work on the principles of selective photothermolysis. The
emission spectrum of 515–1200 nm is adjusted with the use
of a series of cut-off filters, and the pulse duration ranges
from approximately 0.5 to 100 ms, depending on the technol-
ogy. The first commercial system, Photoderm VL (Lumenis,
Yokneam, Israel) became available in 1994, and has been used
to treat vascular anomalies. There are now many other IPL
systems available and the appropriate parameters for treating
congenital vascular lesions are being developed. The IPL has
been used successfully to treat PWSs (Fig. 34.6),83–85 but, in
general, the pulsed-dye laser produces the best clinical
outcome with the lowest risk of complications and remains
the treatment of choice.
IPL technology has also been used to treat pulsed-dye laser-
resistant PWSs. In a study by Bjerring and associates, seven
out of 15 patients achieved >50% lesional lighting after four
IPL treatments.83 The majority of these patients had lesions
involving the V2 dermatome (medial cheek and nose), which
are relatively more difficult to lighten. Six out of seven of
these patients showed >75% clearance of their PWS. A 550–
950-nm filter was used with 8–30-ms pulse durations and
fluences of 13–22 J/cm2 to achieve tissue purpura. The 530–
750-nm filter can also be used with double 2.5-ms pulses,
with a 10-ms delay and fluence of 8–10  J/cm2. Epidermal
cooling was not required. Treatment resulted in immediate
erythema and edema, and occasional crusting. Hypopigmen-
tation was observed in three patients, hyperpigmentation in
one patient, and epidermal atrophy in one patient.
Other lasers
The KTP laser provides relatively equivalent absorption and
depth of penetration to the pulsed-dye laser, and has been
used for PWSs with proper cooling and treatment tech-
nique,86 but the overall rate of adverse side effects is high
compared to the pulsed-dye laser as a result of its higher
absorption by melanin. Long-pulsed alexandrite and Nd:YAG
intervals were long.78 The greater success of the pulsed-dye
laser treatment in infants and young children can be attrib-
uted to decreased skin thickness allowing better laser pene-
tration, smaller vessel diameter, and smaller lesional surface
area. In a recent study, 49 infants who initiated pulsed-dye
laser treatment before 6 months of age tolerated high fluence
treatment with cryogen cooling with no incidence of atrophy
or scarring.79
Treatment technique
Treatment of PWS with the 585-nm, 0.45-ms laser is usually
performed with the largest spot size available to prevent
reticulation. Typical treatment fluences are 5.0–7.0  J/cm2
with a 7-mm spot and 5.0–6.0 J/cm2 with a 10-mm spot size,
depending on the age of the patient and thickness of the
lesion. Using the 595-nm, 1.5-ms pulsed-dye lasers in con-
junction with cryogen spray cooling, fluences of 8.0–11.0 J/
cm2 are used with a 7-mm spot size, and fluences of 5.0–
8.5 J/cm2 are used with the 10-mm spot in infants and chil-
dren. The Dynamic Cooling Device (DCD; Candela Laser
Corp) is generally used with a 20–30-ms spray and a 30-ms
delay. For adults with hypertrophic lesions, fluences up to
13 J/cm2 can be used with a 7-mm spot size and fluences up
to 8.5  J/cm2 with a 10-mm spot size, in conjunction with
cryogen cooling. Cooling can also be achieved with cold air
devices and contact cooling.
Determination of the appropriate fluence and DCD param-
eters should be assessed with test sites performed during the
initial evaluation. A test end point of graying indicates the use
of too high a fluence resulting in epidermal disruption. If
tissue graying results, the skin should be immediately cooled
with ice packs to avoid epidermal necrosis, crusting, and the
possibility of scarring. Treatment should be performed with
the lowest possible fluence that produces purpura without
tissue graying or whitening. When skin cooling is employed
during laser therapy, the patient is observed for several
minutes after treatment to visualize the final tissue reaction,
which may be delayed.
Immediately after treatment with the 585-nm, 0.45-ms
pulsed-dye laser, intense purpura develops for approximately
7–10 days. At equivalent fluences, the intensity and duration
of purpura is significantly lower using pulse durations of
1.5 ms. If crusting occurs, patients are instructed to apply a
topical antibiotic such as bacitracin or polysporin ointment
daily until it resolves. Following the resolution of purpura,
lesional lightening takes place over a period of 4–8 weeks,
when repeat treatments are performed. The subsequent
treatment session should be delayed until all traces of reactive
erythema have subsided.
The development of various skin cooling methods has obvi-
ated the necessity for local or general anesthesia in most
cases. With the exception of young children, most infants,
teenagers, and adults tolerate the treatment well with the use
of a topical anesthetic cream such as 4–5% lidocaine cream.
The topical anesthetic creams should be carefully washed off
several minutes before laser treatment to avoid interference
with the transmission of the laser light. The topical anesthetic
products have maximal limits based on patient weight, which
are provided in the manufacturers’ drug information. When
general anesthesia is used, care must be taken to avoid leakage
of flammable anesthetics in the operating field, which can
promote the ignition of a fire on hair-bearing skin by the

570
Part 3  Aesthetic Surgical Procedures
life. They can increase rapidly in both height and lateral
spread, sometimes reaching gigantic proportions. After
approximately 1 year, hemangiomas undergo a slow period of
involution that takes 5–10 years. Involution may not be com-
plete, and approximately 50% of patients are left with resid-
ual telangiectasias, redundant fibrofatty tissue, and epidermal
atrophy.101,102
Hemangiomas are further classified by their depth in tissue
and extent of involvement.97,103 Superficial hemangiomas
appear as bright red vascular papules or plaques when fully
developed. Deep hemangiomas appear as a bluish-colored
nodule within the skin and have only a subcutaneous compo-
nent without the superficial red plaque. Compound heman-
giomas have both a superficial and a deep component.
Hemangiomas may also be focal or diffuse. Focal lesions
present as solitary masses and represent 85% of lesions. They
appear to occur along the lines of embryological fusion.
Diffuse lesions are segmental in distribution. They usually
present as superficial or compound lesions and carry a high
risk of ulceration. Although hemangiomas regress during
childhood, involution is usually incomplete, and lesions persist
in 35–50% of school-age children. Laser therapy, often in
conjunction with other modalities, is useful in treating
these lesions during the periods of both proliferation and
involution.
The natural history of an individual hemangioma is variable
and unpredictable. Patients with hemangiomas require close
observation, and for complicated or aggressive lesions, patients
are best served by multidisciplinary evaluation and treatment.
Lasers are often used as monotherapy for superficial or thin,
mixed-type proliferating hemangiomas as well as involuting
hemangiomas. They are also used adjunctively with intrale-
sional or systemic treatments for more complicated lesions.
Pulsed-dye lasers prevent lesional enlargement, promote
involution, induce re-epithelialization of ulcerations, and
reduce vascular ectasia.
lasers are effective in treating hypertrophic or nodular PWS,
but the alexandrite laser has a higher incidence of postinflam-
matory hyperpigmentation compared to the pulsed-dye laser,
and the Nd:YAG laser can produce bulk heating and necrosis
if used too aggressively.87–90 Small pilot studies using hybrid
Nd:YAG/KTP lasers91 and Nd:YAG/pulsed-dye lasers92
achieved good lesional clearing using lower laser fluences, but
larger studies are needed to assess the relative safety and
efficiency of these approaches.
Hemangiomas
Hemangiomas are common benign vascular lesions of child-
hood and are present at birth in 2–3% of newborns,93 up to
12% of infants by 1 year of age, and up to 22% of preterm
infants weighing less than 1000 g.94 Hemangiomas occur in
females three times as often as in males95 and 60–70% are
localized to the head and neck. Hemangiomas are differenti-
ated from other vascular malformations such as PWSs, venous
malformations, arteriovenous, and lymphatic malformations,
by their rapid proliferation.96,97 Unlike PWSs, infantile
hemangiomas are true tumors rather than malformations.
They share many characteristics with syngeneic fetal pla-
centa.98,99 They are composed of myriad small blood vessels
and infiltrating vascular endothelial cells that express GLUT-1
and other molecular markers similar to placental trophoblasts.
There are several theories explaining their etiology including
placental embolization (and hence their high incidence fol-
lowing chorionic villus sampling) and underdeveloped vascu-
lature in the embryo with an altered capacity for proliferation.
This may explain the recent finding of an increased incidence
of hemangiomas in low-birth-weight babies.100
Infantile hemangiomas initially appear as white or pink
macules, or telangiectasia with surrounding vasoconstriction,
and then undergo a period of rapid proliferation out of pro-
portion to the growth of the infant during the first year of
A
B
Figure 34.6  Port-wine stain (A) before and (B) after five treatments with an IPL.

571
Chapter 34  Laser and Light Treatment of Acquired and Congenital Vascular Lesions
the use of skin cooling. Most studies of pulsed-dye laser treat-
ment of hemangiomas use the same treatment parameters as
they do for PWSs, aimed at photocoagulating the vessels.
Hemangiomas differ from PWSs histologically. They are
composed of densely-packed small vessels with almost no
intervening connective tissue, and these aggressive laser
parameters may induce necrosis, according to Anderson.116 In
the author’s experience, proliferating hemangiomas respond
best to fluences of 5.5–6.0  J/cm2 with spot sizes of 10–
12 mm and the adjunctive use of skin cooling. Laser treat-
ment should be aimed at damaging the vascular endothelium,
according to Anderson,116 without significant injury to the
rest of the vessel. More deeply penetrating near-infrared
lasers that can cause selective endothelial cell damage may
prove more effective and safer than present technologies.
Laser treatment of ulcerated hemangiomas
Ulcerations are the most common complication of hemangi-
omas.117,118 Ulceration usually occurs during the first few
weeks of life or during periods of rapid proliferation. Approx-
imately 12% of focal lesions and 65% of diffuse or segmental
hemangiomas ulcerate. Ulcers may heal and reappear, and
usually eventuate in a scar. Ulcerations may be painful, par-
ticularly in the anogenital region. Ulcerated hemangiomas are
managed with multiple modalities, including local wound
care, intralesional and systemic corticosteroids, and pulsed-
dye laser therapy.119 Ulcers respond well to pulsed-dye laser
treatment if the ulceration is limited and the hemangioma is
not undergoing rapid proliferation. Laser treatment induces
rapid re-epithelialization, decreases pain, and accelerates
involution.107,120,121 Despite the general success using pulsed-
dye laser therapy for ulcerated lesions, there have been
several reported cases of laser treatment leading to ulceration
in segmental hemangiomas treated early in the growth phase.
Systemic steroids are therefore recommended for this group
of hemangiomas when they ulcerate.119
Laser treatment of compound or deep
hemangiomas
Pulsed-dye lasers have little effect on the subcutaneous com-
ponent of hemangiomas because of their limited depth of
penetration. Interstitial laser therapy has been successfully
used by several groups to shrink large hemangiomas.111,122,123
A 600-µm quartz fiber coupled to a near-infrared diode or
Nd:YAG laser is introduced into the substance of a heman-
gioma percutaneously or transmucosally. Low-intensity light
(1–2 W) is delivered to the interstitium of the lesion for a
Laser treatment of proliferating hemangiomas
There are multiple reports of successful treatment of infantile
hemangiomas. Sherwood & Tan reported complete resolution
of superficial hemangiomas after several pulsed-dye laser
treatments.104–112 In a series of 10 children, superficial and
involuting lesions responded well but results were mixed for
thick proliferating lesions. Similar results were found by
others treating with a 585-nm pulsed-dye laser and a 5-mm
spot.106,107 Garden et al.108 found that the thicker the lesion,
the less the response, and thin lesions less that 1 mm in height
responded best. Waner induced early involution of superficial
proliferating hemangiomas with up to six pulsed-dye laser
treatments.109 Barlow et al.110 achieved some decrease in the
thickness of mixed-type proliferating lesions. In a study of
225 hemangiomas treated with a pulsed-dye laser, the super-
ficial hemangiomas involuted more completely than mixed-
type hemangiomas.111 Mixed-type hemangiomas lightened
but persisted. Hemangiomas treated early in the prodromal
phase responded better than those treated during active pro-
liferation; 13 of 74 initially flat, superficial hemangiomas
showed proliferation of the subcutaneous component. All of
these studies were performed with a 585-nm, 300–450-ms
pulsed-dye laser.
As with PWSs, recent improvements in pulsed-dye laser
technology have led to improved results for hemangiomas.
Longer wavelengths, millisecond pulse durations, and the
addition of skin cooling improve treatment efficacy (Fig.
34.7). Lou et al.112 showed faster clearing of hemangiomas
with a 595-nm, 1.5-ms pulsed-dye laser compared to his-
torical controls using the 585-nm, 450-ms laser. Chang
et al.113 found that the 595-nm, 1.5-ms laser used in conjunc-
tion with cryogen cooling produced more improvement in
lesion volume and texture and required fewer treatments
compared to the 585-nm, 450-ms laser. The addition of
cryogen cooling enabled the safe use of light doses of 9–10 J/
cm2 compared to 5.5–8 J/cm2 used with the 585-nm laser.
Laser treatment of proliferating hemangiomas is an area of
great controversy. It is clear that laser treatment usually slows
the proliferation of the superficial component and promotes
early regression. However, there are reports of inducing side
effects with laser treatment. Batta et al.114 found that pulsed-
dye laser treatments induced early complete clearance of
hemangiomas in a large, prospective, controlled trial, but also
found an increased risk of hypopigmentation and atrophy.
Witman et al.115 recently reported a series of hemangiomas
that ulcerated, bled, and scarred after laser treatment. In
both of these studies, however, the author used similar
parameters to those used for PWS treatment, often without
A
B
Figure 34.7  Proliferating mixed-type
hemangioma (A) before and (B) after
eight treatments with a 595-nm, 1.5-ms
pulsed-dye laser used with cryogen
cooling.

572
Part 3  Aesthetic Surgical Procedures
produce excellent results in one to two treatment sessions,
but induce purpura lasting 7–14 days.129 Treatment is per-
formed by applying contiguous laser pulses with approxi-
mately 10% overlap. The newer, millisecond-duration
pulsed-dye lasers, used at 6–10 ms, clear facial telangiectasia
without purpura production (Fig. 34.9). Effective treatment
usually requires stacking of three to four laser pulses with an
end point of vessel blanching or transient thrombosis.130 The
532-nm KTP laser produces excellent results for the treat-
ment of facial telangiectasia in one to three treatment ses-
sions.131,132 Contiguous laser pulses are applied directly over
the vessels, with additional pulses, if necessary, to achieve
visible vessel blanching. Treatment parameters used for tel-
angiectasia are pulse durations of 15–40 ms with spot sizes
of 2–4 mm and fluences of 10–16 J/cm2. Lower-power con-
tinuous-wave KTP lasers are used to trace out the vessels
with small spot sizes less than 2 mm. One high-power KTP
system (Gemini, Iridex Corporation, Mountain View, CA) is
equipped with cooled sapphire hand pieces that enable easy
gliding of the laser tip over the skin, when used with cold gel,
and relatively painless treatment. This KTP laser was used to
treat 30 subjects with rosacea-associated erythema and tel-
angiectasia, who underwent up to three laser treatments at
monthly intervals. After one to three treatment sessions, all
subjects showed 50–90% in reduction of erythema and tel-
angiectasia with no reported side effects.133 In another study,
15 subjects underwent three split-face treatments with a KTP
or pulsed-dye laser for facial telangiectasia. The 532-nm
device was at least as effective as the 595-nm laser in all
subjects. On average, the KTP laser achieved 62% clearing
after the first treatment and 85% clearing 3 weeks after the
third treatment, compared to 49% and 75% for the pulsed-
dye laser, respectively.134
Long-pulsed Nd:YAG lasers (Fig. 34.10), used with spot
sizes of 1–3 mm and fluences of 120–250 J/cm2, can clear
facial telangiectasia without purpura production,135,136 but
must be used with caution. Bulk tissue heating occurs with
the use of higher fluences and proper skin cooling and avoid-
ance of pulse stacking are necessary to prevent epidermal
damage, particularly around the nasal ala. The long-pulsed
Nd:YAG lasers are particularly useful for the treatment of
the larger-caliber paranasal vessels that often require multi-
ple, repetitive treatments with the shorter-wavelength lasers.
Venulectasia commonly seen on the lateral cheeks following
period of 500–1000  s to achieve photocoagulation. Since
there is a 15-mm zone of coagulation expected around the
emission point of the fiber, epidermal damage remains a risk.
This can be minimized by ultrasound-guided placement of
the fiber or cooling the skin surface with ice.
Laser treatment of involuting hemangiomas
Residual vascular ectasia often persists during involution
along with residual fibrofatty tissue, hypopigmentation, and
atrophic scarring. In addition to the pulsed-dye lasers, pulsed-
KTP lasers and the IPL can be used to treat these skin
changes. Carbon dioxide lasers, and long- and short-pulsed,
erbium (Er):YAG lasers, produce excellent improvement in
the atrophic scarring and textural change that accompany
involution.124 These lasers ablate the epidermis and superficial
dermis, and produce intraoperative collagen shrinkage.125–128
Re-epithelialization is accompanied by the production of a
new layer of collagen that undergoes remodeling for a period
of 12–18 months.125,126 The textural changes improve and the
scarring is diminished.
Telangiectasia
Most patients seek treatment for facial telangiectasia because
of cosmetic concerns. Techniques used to treat facial tel-
angiectasia in the past included electrosurgery, sclerotherapy,
and treatment with continuous-wave and quasi-continuous-
wave lasers, but these methods may produce textural and
pigmentary irregularities. The development of pulsed lasers
and light sources enabled efficient, effective, and low-risk
treatment of these common skin lesions.
Telangiectasia are capillaries, venules, or arterioles that
measure 0.1–1.0 mm in diameter and are visible as superficial
cutaneous vessels. Facial telangiectasia are common, and in
fair-skinned individuals they are often associated with rosacea
or actinic damage. Other etiologies include collagen vascular
disease, genetic disorders, hormonal, primary cutaneous
disease, and radiation dermatitis (Fig. 34.8). Spider angi-
omata are telangiectasia with a central feeding arteriole,
typically appearing in preschool and school children with a
peak incidence between the ages of 7 and 10.
A wide variety of vascular laser systems produce excellent
clearance of facial telangiectasia. The 585- and 595-nm
pulsed-dye lasers with 0.45- and 1.5-ms pulse durations
A
B
Figure 34.8  Radiation dermatitis before and after three pulsed-dye laser treatments at fluences of 3–4 J/cm2.

573
Chapter 34  Laser and Light Treatment of Acquired and Congenital Vascular Lesions
of these laser systems, including the newer pulsed-dye lasers
used with 6–10-ms pulse durations, and the IPL devices.
Multiple treatment sessions (two to six) may be necessary to
achieve good clinical results. An improvement in the associ-
ated symptoms or warmth and burning usually accompanies
the reduction in erythema.
The pulsed-dye lasers are used with a 10-mm spot. Flu-
ences of 4.0–5.0 J/cm2 are used with the 585-nm, 0.45-ms
laser. Fluences of 6.0–8.0 J/cm2 are used with the 595-nm
laser with pulse durations of 1.5–10.0 ms. The longer pulse
durations do not produce purpura, but require higher treat-
ment fluences and/or additional laser passes for equivalent
efficacy. The KTP lasers are used with millisecond-duration
pulses, larger spot sizes, and a painting technique for this
purpose.
Poikiloderma
Poikiloderma is treatable with lasers and light sources.
Poikiloderma of Civatte is relatively common in fair-skinned,
actinically-damaged individuals. Clinically, poikiloderma
appears as a combination of telangiectasia, irregular pigmenta-
rhytidectomy often usually clear in one treatment session.
Visible facial veins have also been treated with Nd:YAG
lasers, but extreme caution must be exercised to avoid laser
exposure within the orbital rim with this deeply penetrating
wavelength. Treatment is limited to veins outside the orbital
rim, and metal ocular shields must be used. The large-spot
IPL devices also clear facial telangiectasia, but multiple treat-
ment sessions may be necessary.137,138 A recent prospective
study of a broadband light source emitting at 500–635 nm in
12 patients used with a 6.35-mm diameter spot size (Acutip,
Cutera, Brisbane, CA) with contact cooling showed clearance
rates for telangiectasia that were comparable to results seen
with the KTP and pulsed-dye laser.139
Facial erythema
Facial erythema with or without associated telangiectasia is a
common cosmetic concern. The erythema is usually a mani-
festation of rosacea or a flushing or blushing disorder. Effec-
tive treatment can be achieved with the pulsed-dye lasers,
pulsed-KTP lasers, IPL sources, using large spot sizes to avoid
reticulation.139,140 Purpura-free treatment is possible with all
Figure 34.9  Rosacea-associated telangiectasia before and after treatment with a 595-nm pulsed-dye laser using a 20-ms pulse
duration. (Courtesy of Giuseppe Scarcella MD and Candela Laser Corp.)
Figure 34.10  Facial venulectasia before and after one treatment with a long-pulsed Nd:YAG laser. (Courtesy of Altus Laser Corp.)

574
Part 3  Aesthetic Surgical Procedures
Striae distensae
Low-fluence, pulsed-dye laser therapy also improves the
appearance of striae.146 Striae rubra shows the best response,
and can sometimes be entirely eliminated with early laser
intervention. Treatment fluences are used just at or below
the purpura threshold; 3.5–4.5  J/cm2 are used with the
585-nm, 0.45-ms pulsed-dye laser with a 10-mm spot. The
595-nm, 1.5-ms laser is used with a 10-mm spot fluence of
5.0–5.5  J/cm2, in conjunction with cryogen cooling. Pulses
are applied in a contiguous pattern. Three to five treat-
ment sessions are usually required, and are performed at 6–8
week intervals. Laser treatment clears the erythema and
improves the skin texture, but has no effect on the hypopig-
mentation. The skin textural irregularities in striae can some-
times be improved with pulsed-dye laser treatment and other
non-ablative lasers and light sources. The mechanism of
improvement is presumed to be via fibroblast activation and
induction of collagen production. Excimer lasers and narrow-
band UVB light sources have been used to repigment striae,
but upwards of 10 treatments are required, and the results
are short lived.
Warts
Pulsed-dye lasers are very effective in treating the cutaneous
lesions of human papillomavirus, including condyloma
acuminata, plantar warts, periungual wart, flat warts, and
verrucae vulgaris.147–149 The mechanism of improvement
appears to be via thermal alteration of the virally-infected
tissue. Laser treatment appears to be more effective than
conventional wart therapy, and carries a minimal risk of scar-
ring, even when used on deep plantar warts, and subungual
and periungual lesions. Treatments are performed using the
585- or 595-nm pulsed-dye laser at 0.45 or 1.5  ms using
a 5- or 7-mm spot at fluences of 6.0–9.0  J/cm2 without
cooling, following paring of hyperkeratotic lesions. Recalci-
trant warts require three to four repetitive treatments, at 3–4
week intervals. Uncomplicated warts usually respond in one
session.
tion, and atrophic changes. The treatment of this diffuse
condition is best accomplished using the pulsed-dye lasers
(Fig. 34.11) or IPL devices with large spot sizes to avoid
reticulation.44,141,142 Overly aggressive treatment with any
laser or light source can produce atrophy and hypopigmenta-
tion. Treatment should not be performed on individuals with
evidence of suntanned skin, as this will increase the risk of
epidermal damage and hypopigmentation; treatment should
be delayed for a minimum of 4 weeks following sun exposure.
Compared to the treatment of telangiectasia, fluences
should be lowered by approximately 25–30% to avoid adverse
effects. The 585-nm, 0.45-ms pulsed-dye laser is generally
no longer used because of the increased risk of hypopigmen-
tation. The best results are achieved using the pulsed-dye
laser with 6–20-ms pulse durations which produce excellent
results without the development of purpura and with a lower
risk of complications. Contiguous laser pulses are applied
with minimal overlap. IPL systems are generally used with
515–550-mm cut-off filters, pulse duration of 5–20 ms and
fluences of 15–30  J/cm2, depending on the manufacturer.
During treatment, a thin layer of gel is applied to the skin
surface to aid in skin cooling. Erythema and edema may be
present for 2–3 days after treatment with any of these
devices.
Hypertrophic and erythematous scars
Pulsed-dye laser therapy can be used to improve erythema-
tous and hypertrophic scars. Clinical response rates are 57–
83%.143–145 The pulsed-dye laser reduces erythema by
eliminating the underlying dilated microvasculature. Scar
height and skin surface texture changes are improved, pre-
sumably by altering collagen production. Multiple treatment
sessions are often necessary, particularly with thicker scars,
and adjunctive treatment with intralesional corticosteroid
injections is useful. The best results are achieved using the
585-nm or 595-nm lasers with a 10-mm spot size, fluences
of 4–5 J/cm2 without skin cooling and 5–6 J/cm2 with skin
cooling. Treatment intervals are typically 6–8 weeks in
duration.
A
B
Figure 34.11  Poikiloderma of Civatte
(A) before and (B) after treatment with
a 10-ms pulsed-dye laser used with
cryogen cooling. (Courtesy of Stephen
Eubanks and Candela Laser Corp.)

575
Chapter 34  Laser and Light Treatment of Acquired and Congenital Vascular Lesions
pulse duration and requires approximately 10 days for resolu-
tion. At 1.5 ms, the purpura usually resolves within 1 week.
With the use of epidermal cooling techniques, blistering or
crusting is a rare event. If crusting occurs, a topical antibiotic
ointment such as bacitracin or polysporin is applied twice
daily until it resolves. When prolonged purpura or crusting
does occur, subsequent treatment fluences should be lowered
accordingly.
At pulse durations greater that 6 ms, purpura is not pro-
duced. Laser pulse impact results in urticarial papules that
resolve over several hours. Head elevation and the application
of ice packs immediately after laser treatment help reduce
swelling. Most vascular lesions require multiple treatment
sessions. PWSs and hemangiomas usually require multiple
laser treatments (see above). Small telangiectasia usually
clear after one treatment, but larger vessels may require two
or more treatments. High-flow spider angiomas may require
several treatments, and may recur months later. Treatment
results are assessed at 4–6 weeks after treatment and repeat
treatment is performed if necessary. Sunscreen with an SPF
>15 should be used prior to treatment if the individual is at
risk of developing a suntan. Treatment of suntanned indi-
viduals should not be performed because of the risk of
absorption by epidermal pigment leading to hypopigmenta-
tion. Sunscreen with an SPF >15 should be used for 4 weeks
following treatment to prevent the development of postin-
flammatory hyperpigmentation.
Pulsed-dye laser light at wavelengths of 585–600 nm is well
absorbed by melanin. Suntanned patients and individuals
with skin types V and VI should not be treated with these
wavelengths because of the risk of epidermal damage and the
possibility of a poor clinical response due to shielding of the
laser light by epidermal melanin. Individuals with skin type
IV and the absence of a suntan can be treated safely by an
experienced clinician with higher fluences and skin cooling.
Pulsed-KTP lasers
Facial telangiectasia and erythema respond well to millisec-
ond-duration KTP lasers. The spot sizes and fluences used
vary depending on the size of the vessel. Individual vessels
are best traced with the laser beam, applying contiguous or
minimally overlapping pulses. Facial erythema is treated using
large spot sizes (4–10 mm) with a painting technique. Pulse
stacking should be avoided because of the risk of epidermal
damage. Patients with suntans or skin types V and VI cannot
be treated with this wavelength because of it strong absorp-
tion by melanin.
Anesthesia is rarely required for these procedures. Topical
anesthetic creams such as 4–5% lidocaine may be used for
those patients sensitive to pain. Lasers that are equipped with
a sapphire chill tip require direct contact with the skin, but
only minimal pressure is applied so as to avoid blanching of
the vessels. A thin layer of gel applied to the skin surface
prevents fogging of the lens and facilitates movement of the
hand piece over the skin. Treatment of non-planar surfaces
of the face such as the nasal ala and alar crease requires
extreme care to maintain skin contact with the chilled hand
piece.
Following treatment, there may be erythema and urticarial
edema of the treated skin lasting up to 24 hours. Cool dress-
ings, ice, and the application of a mid-potency topical corti-
costeroid immediately after treatment will reduce the redness
 TECHNIQUES AND
POSTOPERATIVE CARE
Laser and intense pulsed light
safety procedures
The treatment room should be free of all reflective surfaces,
and windows should be covered. The door must bear ‘laser-
in-use’ signage and be locked from within. Flammable anes-
thetic gases or materials may not be present. All personnel in
the treatment room and the patient must wear laser surgery
glasses that specifically absorb the wavelength being used.
Treatment around the eyes requires intraocular metal eye
shields that are placed after the installation of an ophthalmic
topical anesthetic agent. The IPL and near-infrared lasers
should not be used to treat within the orbital rim, and the
beam should always be directed away from the orbit when
treating in the eye region.
The pulsed-dye laser is capable of igniting a fire in the pres-
ence of oxygen and nitrous oxide. Leakage of gases from the
edge of the face mask has been reported to ignite the hairs.80,150
The safest way to deliver inhalational anesthetics is by means
of endotracheal intubation or by using a laryngeal mask which
fits over and seals the larynx. Wet drapes are placed around
the mouth area and tubing, and the surrounding hair-bearing
skin is lubricated with a non-flammable ointment such as
Surgilube (Fougera, Melville, NY).
Anesthesia
Vascular lasers and light sources produce a brief stinging or
burning sensation and most patients tolerate treatment with
minimal anesthesia requirements, but cumulative laser pulses
can produce increasing discomfort. Young children or adults
with larger lesions may require topical anesthetics, such as
4–5% lidocaine cream or a eutectic mixture of prilocaine and
lidocaine. Topical anesthetic preparations should be washed
off several minutes before treatment to reduce vasoconstric-
tion and avoid interference with light transmission. Local
anesthesia with lidocaine or nerve blocks was often used in
the past for the treatment of facial PWSs, but is generally
unnecessary with the availability of epidermal cooling methods
and topical anesthetic preparations. Intravenous sedation or
general anesthesia is usually reserved for children who require
immobilization, or highly anxious patients with extensive
lesions.
Pulsed-dye lasers
The pulsed-dye laser is used with short pulse durations (0.45
and 1.5 ms) to treat PWSs. Test areas are performed in areas
representative of the entire lesion using several fluences to
determine the parameters with the best therapeutic responses,
and are evaluated at 4–6 weeks. Beam profiles vary among the
different manufactures of the pulsed-dye laser, and laser flu-
ences should be chosen accordingly. Larger spot sizes produce
greater efficacy and reduce the potential for reticulation
between treatment sessions. Using the chosen fluence, pulses
are applied contiguously or with minimal overlap. Treatment
fluences can be increased with the use of air cooling and
cryogen cooling devices that are equipped with these systems.
Shorter pulse durations (<3  ms) produce an immediate
ashen-gray color with laser impact. Gradually, the color turns
to purplish–red. The purpura is most intense with the 0.45-ms

576
Part 3  Aesthetic Surgical Procedures
layer of gel. Test spots with increasing fluences should be
performed carefully inspecting for signs of epidermal damage
until the desired end point of faint erythema is achieved. The
individual pulses are applied contiguously with minimal
overlap. A second pass may be performed with the axis of
the light guide perpendicular to the first pass, in order to
avoid reticulation.
Reactive erythema and edema develop for 24 hours after
treatment. Cold dressings, ice, and the application of a mid-
potency corticosteroid reduce the burning, erythema, and
edema. As with the laser devices, suntanned individuals
should not be treated, and sunscreen with an SPF >15 should
be used for 4 weeks prior to and after light treatment.
 PITFALLS AND THEIR MANAGEMENT
and swelling. Crusting develops infrequently, but may occur
with overly aggressive therapy, treatment with improper
cooling techniques, or treatment of tanned skin. When crust-
ing occurs, a topical antibiotic ointment such as bacitracin or
polysporin should be applied twice daily until it resolves. Sun-
screen should be used for 4–6 weeks after laser treatment.
Scarring rarely occurs, but may result from excessive
fluence, overlapping of laser pulses, or inadequate skin cooling,
which results in non-selective thermal damage to the epider-
mis or dermis.
Pulsed Nd:YAG lasers
Several new Nd:YAG lasers are now available that use high
fluences and millisecond pulse durations. The Nd:YAG
laser can be used with large spot sizes (usually 10 mm) in a
painting technique for the treatment of facial erythema. The
Nd:YAG laser is not a first-line device for treatment of super-
ficial telangiectasia. Venulectasias are treated with smaller
spot sizes (1–3 mm) and high fluences (>100 J/cm2). Larger
paranasal and preauricular telangiectasia and venulectasia,
that may not clear with green and yellow light, respond well
to this wavelength because of its great depth of penetration.
The Nd:YAG laser produces bulk tissue heating. Laser pulses
should never be stacked as this can lead to ulceration and
necrosis. Extreme caution must be exercised when treating
vessels in the periorbital region with the 1064-nm wave-
length. Internal metal ocular shields are used and treatment
is limited to outside the orbital rim.
Anesthesia is usually not required, but treatment of larger-
caliber vessels may be more painful. Topical anesthetic
creams such as lidocaine 4–5% are useful for this purpose.
Non-specific thermal damage leading to scarring may result
from treating with excessive fluence or overlapping of laser
pulses. The nasal ala and alar crease are difficult anatomic
areas to treat. Proper skin cooling techniques are required,
whether it be cryogen spray or contact cooling. When a
chilled sapphire hand piece is being used, a thin layer of gel
is applied to the skin surface and there should be good contact
with the cooling plate.
Erythema and urticarial edema develop after treatment and
last up to 24 hours. Cold dressings or ice and the application
of a mid-potency corticosteroid immediately after treatment
will minimize these changes. Antibiotic ointment should be
applied twice daily if crusting develops. Sun protection is
required for 4–6 weeks after treatment.
Intense pulsed light sources
IPL devices deliver non-coherent, pulsed white light from
515 to 1200  nm, with multiple pulse modes and fluences
ranging from 3 to 90 J/cm2, through a large rectangular foot-
print. The range of wavelengths delivered can be altered with
a series of cut-off filters to correspond with the patient’s skin
type and lesion depth.
In general, shorter wavelength filters (515  nm) and the
single pulse mode are used on skin type I with fine, superficial
vessels. Larger and deeper vessels are treated with longer
cut-off filters (570 nm or 590 nm) and double or triple pulse
modes. Longer wavelengths and longer interpulse delays are
used for darker skin types. Parameters will vary based on the
system.
A thick layer of cool water gel is applied to the skin surface.
The light guide is gently placed over the skin atop a 1–2-mm
Pitfalls and their management
 Treatment of vascular lesions with visible-light lasers or
pulsed-light sources should not be performed on suntanned
skin or phototype V and VI because of the risk of epidermal
damage.
 When using higher fluences, skin cooling techniques are
essential to avoid epidermal damage.
 Whitening of the skin or blister formation may occur with pulse
stacking or the use of excessively high fluences.
 Pulse durations of 10 ms or higher are generally required to
avoid purpura formation.
 Laser-treated skin should be protected with a broad-spectrum
sunscreen for at least 4 weeks.
 Post-treatment erythema and edema can be reduced by using
ice compresses for 10–15 minutes immediately after laser
treatment.
 SUMMARY
Appropriate treatment begins with the correct diagnosis. The
choice of laser type and treatment parameters must be set
according to the type of lesion being treated. Vessel size and
depth, blood flow, skin type, melanin content, recent suntan,
natural behavior of the lesion, recurrence rate, and medical
history of the patient are just a few of the factors which must
be assessed prior to treatment with lasers or IPL. In the
future, we need to find ways to effectively treat deeper vas-
cular lesions with minimal risks of scarring.
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with a non coherent pulsed light source. A retrospective study. Arch
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86. Chowdhury MM, Harris S, Lanigan SW. Potassium titanyl phosphate
laser treatment of resistant port wine stains. Br J Dermatol 2001;144:
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87. Chotzen VA, McClaren M, Kilmer SL. Treatment of bulky congenital
vascular malformations with long pulsed lasers. Lasers Surg Med 2002;
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88. Li L, Kono T, Groff WF, et al. Comparison study of a long-pulse pulsed
dye laser and a long-pulse pulsed alexandrite laser in the treatment of
port wine stains. J Cosmet Laser Ther 2008;10:12–15.
89. Izikson L, Anderson RR. Treatment endpoints for resistant port wine
stains with a 755 nm laser. J Cosmet Laser Ther 2008; 13:1–4.
90. McGill DJ, MacLaren W, Mackay IR. A direct comparison of pulsed
dye, alexandrite, KTP and Nd:YAG lasers and IPL in patients with
previously treated capillary malformation. Lasers Surg Med 2008;40:
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91. Tanghetti EA, Sherr E, Sierra R, et al. Sequential 595  nm, 1064  nm
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92. Ahcan U, Zorman P, Recek D, et al. Port wine stain treatment with a
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94. Amir J, Metzker A, Krikler R, Reisner SH. Strawberry hemangiomas in
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140. Angermeier MC. Treatment of facial vascular lesions with intense
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142. Wheeland RG, Applebaum J. Flashlamp-pumped pulsed dye laser
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143. Weiss RA, Goldman MP, Weiss MA. Treatment of poikiloderma of
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144. Alster TS, Kurban, AK, Grove GL, et al. Alteration of argon laser-
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145. Alster TS. Improvement of erythematous and hypertrophic scars by the
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146. Alster TS, Williams CM. Improvement of hypertrophic and keloidal
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35
Sclerotherapy of Varicose Veins
Eberhard Rabe MD PhD, Franz X Breu MD, and Felicitas Pannier MD
Summary box
 The aim of sclerotherapy is the transformation of a treated
vein into a fibrous cord.
 Liquid sclerotherapy is the method of choice for telangiectasia
and reticular veins.
 Foam sclerotherapy has been shown to be effective in
saphenous veins and tributaries.
 Large-diameter veins are not expected to respond to
sclerotherapy.
 INTRODUCTION
Sclerotherapy involves the injection of a sclerosant for tar-
geted elimination of intracutaneous, subcutaneous, and/or
transfascial varicose veins (perforating veins) as well as the
sclerosing of subfascial varicose vessels in venous malforma-
tions. The various sclerosants markedly damage the vascular
endothelium and may possibly damage the entire vascular
wall. After successful sclerotherapy, the vein is permanently
transformed into a fibrous cord, a process known as sclero-
sis.1–3 The purpose of sclerotherapy is not merely to achieve
thrombosis of the vessel, which may be amenable to recanali-
zation, but definitive transformation into a fibrous cord. This
cord cannot recanalize and the functional result is equivalent
to the surgical removal of a varicose vein.
Indications
The objectives of sclerotherapy are:
• treatment of varicosities and prevention of possible
complications of varicosities
• reduction or elimination of existing symptoms
• improvement of pathologically altered hemodynamics
• achievement of a good result that satisfies aesthetic and
functional criteria.4
While in principle, all types of varicose veins are amenable to
sclerotherapy, those that are particularly amenable to treat-
ment are:
• truncal veins (long saphenous vein and short saphenous
vein) (Fig. 35.1)
• collateral veins
• varicose veins associated with perforator incompetence
• reticular varicose veins (Fig. 35.2)
• spider veins
• residual and recurrent varicose veins after interventions
to eliminate varicosities
• genital and perigenital varicose veins
• veins causing leg ulcers5–7
• venous malformations.8
Sclerotherapy is considered to be the method of choice for
the treatment of small-caliber varicose veins (reticular vari-
cose veins, spider veins).4 For the obliteration of varicose
collateral veins and incompetent perforating veins, sclero-
therapy competes with percutaneous phlebectomy and with
ligation of perforating veins or endoscopic dissection of per-
forating veins.9,10 In the treatment of varicose truncal veins
involving elimination of the proximal leakage point and of the
incompetent venous portion, surgery is considered to be the
method of choice. Nevertheless, treatment of truncal veins
by sclerotherapy is also possible.11–13 This applies in particular
to foam sclerotherapy, as has been demonstrated by studies
conducted in recent years.14–18
Contraindications
Absolute contraindications are:3,4,13
• known allergy to the sclerosant
• severe systemic disease
• acute deep vein thrombosis
• local infection in the area of sclerotherapy or severe
generalized infection
• permanent immobility and confinement to bed
• advanced peripheral arterial occlusive disease (stage III
or IV)
• hyperthyroidism (in the case of sclerosants containing
iodine)
• pregnancy (unless a compelling medical reason exists).
Relative contraindications are:3,4,19
• leg edema, uncompensated
• late complications of diabetes (e.g. polyneuropathy)
• arterial occlusive disease, stage II
• poor general health
• bronchial asthma
• marked allergic diathesis
• known thrombophilia or hypercoagulable state with or
without a history of deep vein thrombosis.20–22
Additional relative contraindications for foam sclerotherapy
are: