The Unfavorable Result in Plastic Surgery_ Avoidance and Treatment (2018, Thieme)

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Lower Eyelid Effects
When treating crow’s-feet and lower lid rhytids, injections
made too close to the lower lid margin can result in scleral
show. Injections that weaken the overlying orbicularis oculi
muscle may worsen the appearance of pseudoherniated fat
pads of the lower lids. A patient’s preexisting malar edema
may worsen after relaxation of the pumping action of the
orbicularis oculi. Lower lid tone should be assessed by a
“snap test” before injection near the lid margin. Careful
assessment is necessary to avoid these adverse effects, be­
cause the neurotoxin effect is not reversible.
Dry Eye Syndrome (Xeropthalmia)
Dry eye syndrome may develop when botulinum neuro­
toxin is repeatedly injected into the lateral canthal region
for aesthetic correction of crow’s-feet.68 Early symptoms
of this condition include mild eye irritation, foreign body
sensation, and epiphora. If injections are continued, wors­
ening of these symptoms may occur.69 It may result from
paralysis of the orbicularis oculi muscle causing decreased
tone and blink strength or direct diffusion of the toxin into
the lacrimal gland affecting tear production.68 Case reports
suggest that the snap-back test may identify patients at risk
of this syndrome because of a preexisting orbicularis oculi
muscle weakness.69
Lip Asymmetry
Asymmetrical Lip Animation
Upper lip asymmetry may result from relaxation of the
orbicularis oris to eliminate vertical lip rhytids. This re­
sults from uneven distribution of the toxin after a limited
number of depot injections. I place toxin using a retrograde
threading technique across the upper lip to evenly deposit
the toxin. If disharmonious motion is noted after toxin in­
jection to the upper lip, it can be corrected with additional
1- to 2-unit injections where necessary.
Lower lip asymmetry while smiling can result from in­
advertent paralysis of the depressor labii inferioris when
attempting to treat the depressor anguli oris. On smiling the
affected side will remain higher, making the smile crooked.
This can be masked by injection of a small number of units
of botulinum toxin into the untreated depressor labii inferi­
oris. This adverse event can be avoided by proper injection
technique and an understanding of the location of under­
lying musculature. Injection into the depressor anguli oris
must be placed at least 1 cm lateral and 1.5 cm inferior to
the oral commissure. Crooked smiles may also result from
injections that affect the zygomaticus major and are typi­
cally a result of periocular injections to treat crow’s feet that
are placed too inferior.
0.025%/pheniramine 0.3%. This results in contraction of the
adrenergically innervated Müellers’ muscle, which in turn
elevates the lid. The drug provides symptomatic relief and
must be continued on an as needed basis until the ptosis
has resolved. A recent report indicates that apraclonidine
drops can be used at the time of initial assessment to pre­
dict the relative longevity of ptosis.65 After a 1-week trial,
responders can be advised that ptosis is likely to resolve in
4 to 6 weeks, whereas nonresponders should be counseled
that resolution may take longer than 6 weeks.65 The closer
to the time of botulinum toxin treatment the ptosis occurs,
the longer it is likely to last (number of units diffusing down
to the levator muscle).
Eyebrow Ptosis
Eyebrow ptosis and undesirable eyebrow shape are re­
lated to paralysis of the frontalis muscle from the neuro­
toxin treatment. The frontalis muscle is very sensitive to
toxin and should be treated cautiously and conservatively.
Before any treatment the patient should be asked to force­
fully elevate the brows and the injector should note the de­
gree of medial, central, and lateral brow elevation as well
as the shape of the brow arch. The patient should then be
asked to relax the forehead and close the eyes, and the de­
gree of brow ptosis is assessed. The greatest excursion of
the frontalis muscle occurs in the portion 2 cm superior
to the brow. In patients with existing brow ptosis, injec­
tions should be confined to the superior forehead. A par­
tially paralyzed frontalis muscle will cause compensatory
elevation of the brow. A patient who arches the brow before
treatment will be more likely to overarch the brows after
treatment, and those with little medial elevation will likely
overelevate the lateral brow (diablo brow). If brow ptosis
occurs it can be minimally elevated by weakening the de­
pressors either medially (depressor supercilii) or laterally
(orbicularis oculi). Brow peaking can be treated by injecting
1 to 2 units at the peak of the brow at the level of the second
horizontal rhytid (see Fig. 16.19). In all cases it is better
to undertreat initially and add additional toxin at 2 weeks
rather than to have to wait for brow ptosis to resolve.
Diplopia
The treatment of crow’s-feet wrinkles with botulinum
toxin can affect the extraocular muscles, resulting in dip­
lopia. Paralysis of the extraocular muscles can be caused
by poor technique, diffusion of toxin through the orbital
septum, or infiltration caused by large volumes of low-con­
centration toxin.66 If diplopia occurs, the patient should be
referred to an ophthalmologist as soon as possible for ap­
propriate management. This may include use of ocular oc­
clusion, glasses with prismatic lenses, or botulinum toxin
injection into the antagonist muscle.67 This is a rare adverse
event and is avoidable by use of proper injection technique.

167
Chapter 16 Dermal Fillers and Neurotoxins
Deoxycholic Acid
Deoxycholic acid was approved by the FDA as a treatment
for moderate to severe submental fullness in April 2015 un­
der the name Kybella (Kythera Biopharmaceuticals).72 The
active ingredient is a synthetic, highly purified version of
deoxycholic acid (10 mg/mL), which occurs naturally in bile
and aids in the digestion of dietary fat. Deoxycholic acid, a
cytolytic agent, causes adipocyte lysis by destruction of the
cell membrane and an inflammatory tissue reaction lead­
ing to fat cell reduction and limited fibrosis.73 Endogenous
deoxycholic acid is a product of cholesterol metabolism and
is excreted intact in feces. Deoxycholic acid is not metabo­
lized to any significant extent under normal conditions. De­
oxycholic acid from Kybella joins the endogenous bile acid
pool in the enterohepatic circulation and is excreted along
with the endogenous deoxycholic acid.
Suitable candidates for treatment are adults with firm
elastic skin and excess subcutaneous submental fat. Use in
patients with flaccid skin and prominent platysma bands
may lead to unaesthetic results. Kybella is injected into sub­
cutaneous fat tissue in the submental area using an area-ad­
justed recommended dose of 2 mg/cm2. A single treatment
consists of a maximum of 50 injections (10 mL). The treat­
ment does not produce immediate effects, and most patients
require two to four treatments, spaced no less than 4 weeks
apart. The most common adverse reactions (more than 20%
of subjects in the pivotal trial) include injection site edema or
swelling, hematoma, ecchymosis, pain, numbness, erythema,
and induration. Adverse reactions that lasted more than 30
days and occurred in more than 10% of subjects were injec­
tion site numbness (42%), injection site edema or swelling
(20%), injection site pain (16%), and injection site induration
(13%). Rare side effects include difficulty swallowing during
the first few days (believed to be a result of the neck swell­
ing); marginal mandibular nerve injury (4%) causing ipsilat­
eral lower lip depressor muscle weakness or paralysis (all
cases so far reported have recovered spontaneously, range 1
to 298 days, median 44 days); local skin hyperpigmentation;
and for men, beard alopecia. The treatment is contraindicated
in the presence of infections at the injection sites.72
In my experience and that reported by my colleagues,
some of the postinjection adverse sequelae can be miti­
gated by reducing the dosage to 1 mg/cm2. If no untoward
sequelae occur the dosage can be increased on the subse­
quent treatments. Where the fat layer is thicker, 2 mg/cm2
should be used; with a thinner fat layer 1 mg/cm2 should be
used. Injection should be avoided immediately subdermally,
because this can cause skin ulceration; the correct plane is
only within the preplatysmal fat layer. Keep injections 1.5
cm inferior to the mandibular border and superficial to the
platysma to avoid injury to the marginal mandibular nerve.
Difficulty Swallowing (Dysphagia)
and Neck Weakness
Botulinum toxin injections are used off-label to improve
platysma bands and ringlet lines in the neck. Given the
large span of platysmal muscle fibers, doses of 50 units or
more of toxin may be needed. Diffusion of the toxin may
rarely affect the deeper musculature, resulting in difficulty
swallowing or vocal function disturbance. There is no treat­
ment to relieve these complications once they occur; the
patient must wait until neural function returns.
Precise injection into the platysmal bands themselves to
avoid inadvertent injection of deeper muscles will help to
prevent these complications. Patients may also experience
weakness when elevating their head from the supine posi­
tion after treatment of lateral platysma bands. This occurs
as a result of weakening the laterally adjacent sternocleido­
mastoid muscles, either from direct injection or diffusion.
This is more common in women with long thin necks. These
adverse effects too can be avoided by using the lowest ef­
fective doses and precisely placing toxin into the platysma.
Lack of Treatment Effect
A rare complication associated with botulinum toxin injec­
tions is formation of antibodies (less than 1%), which can
render treatments ineffective. In its original form, botuli­
num toxin is present as a complex, formed by the neuro­
toxin and accessory proteins. The latter play a role in the
oral toxicity of the botulinum toxin, allowing it not to be
broken down by stomach acid and to pass through the in­
testinal epithelial barrier and thereby enter the systemic
circulation but are not required for the therapeutic effect
of injected toxin. Theoretically, the increased protein load
of the complexing proteins could generate an antibody re­
sponse greater than the neurotoxin (150 kD protein) alone.
These neutralizing antibodies may result in partial or com­
plete treatment failure. Aesthetic medicine uses much lower
doses of botulinum toxin preparations than the therapeu­
tic field, but today’s cosmetic patients start their aesthetic
treatments at younger ages and are commonly treated for
multiple indications, resulting in increased frequency and
dose of toxin used over a lifetime. Although rare, cases of
treatment failure linked to neutralizing antibody forma­
tion after the administration of botulinum toxin containing
complexing proteins are increasingly reported.70 The botu­
linum toxin preparations approved by the U.S. Food and
Drug Administration (FDA) vary in their nontoxin protein
content (Xeomin has less than Botox, which has less than
Dysport). Most experts currently recommend reducing the
frequency of exposure by avoiding booster injections and
waiting at least 3 months between treatments.71

SECTION IV AESTHETIC SURGERY
168
in-depth knowledge of the commercially available prod­
ucts’ characteristics, facial anatomy, and injection tech­
niques to ensure patient safety and satisfaction. Although
most adverse events are minor and temporary, more se­
rious complications can occur. Most are preventable and
are technique-dependent. All injectors providing aesthetic
treatments should have the ability to recognize, treat, and
avoid complications.
Postinjection pain can be reduced using local anesthetic in­
filtration before injection placement.
Conclusion
Dermal fillers, botulinum toxins, and deoxycholic acid
have an overall excellent safety record but do carry risks
of complications. These procedures require a clinician with
References
1. American Society for Aesthetic Plastic Surgery (ASAPS). Cos­
metic surgery national data bank statistics 2014. Available
from:
pdf. Accessed November 2015.
2. Alam M, Kakar R, Nodzenski M, et al. Multicenter pro­
spective cohort study of the incidence of adverse events
associated with cosmetic dermatologic procedures: la­
sers, energy devices, and injectable neurotoxins and fill­
ers. JAMA Dermatol 2015;151(3):271–277
3. Flynn TC, Sarazin D, Bezzola A, Terrani C, Micheels P. Com­
parative histology of intradermal implantation of mono
and biphasic hyaluronic acid fillers. Dermatol Surg 2011;
37(5):637–643
4. Bass LS, Smith S, Busso M, McClaren M. Calcium hydroxyl­
apatite (Radiesse) for treatment of nasolabial folds: long-
term safety and efficacy results. Aesthet Surg J 2010;30(2):
235–238
5. Fitzgerald R, Vleggaar D. Facial volume restoration of the
aging face with poly-l-lactic acid. Dermatol Ther (Hei­
delb) 2011;24(1):2–27
6. Pallua N, Wolter TP. A 5-year assessment of safety and aes­
thetic results after facial soft-tissue augmentation with
polyacrylamide hydrogel (Aquamid): a prospective mul­
ticenter study of 251 patients. Plast Reconstr Surg 2010;
125(6):1797–1804
7. Shah NS, Lazarus MC, Bugdodel R, et al. The effects of
topical vitamin K on bruising after laser treatment. J Am
Acad Dermatol 2002;47(2):241–244
8. Cohen JL, Bhatia AC. The role of topical vitamin K oxide
gel in the resolution of postprocedural purpura. J Drugs
Dermatol 2009;8(11):1020–1024
9. Davis EC, Callender VD. Postinflammatory hyperpigmen­
tation: a review of the epidemiology, clinical features,
and treatment options in skin of color. J Clin Aesthet Der­
matol 2010;3(7):20–31
10. Heath CR, Taylor SC. Fillers in the skin of color population.
J Drugs Dermatol 2011;10(5):494–498
11. Hirsch RJ, Narurkar V, Carruthers J. Management of inject­
ed hyaluronic acid induced Tyndall effects. Lasers Surg
Med 2006;38(3):202–204
12. Douse-Dean T, Jacob CI. Fast and easy treatment for re­
duction of the Tyndall effect secondary to cosmetic use of
hyaluronic acid. J Drugs Dermatol 2008;7(3):281–283
13. Bailey SH, Cohen JL, Kenkel JM. Etiology, prevention, and
treatment of dermal filler complications. Aesthet Surg J
2011;31(1):110–121
14. Hypolite T, Grant-Kels JM, Chirch LM. Nontuberculous
mycobacterial infections: a potential complication of cos­
metic procedures. Int J Women Dermatol 2015;1:51–54
15. Rousso JJ, Pitman MJ. Enterococcus faecalis complicating
dermal filler injection: a case of virulent facial abscesses.
Dermatol Surg 2010;36(10):1638–1641
16. Christensen LH. Host tissue interaction, fate, and risks of
degradable and nondegradable gel fillers. Dermatol Surg
2009;35(Suppl 2):1612–1619
17. Monheit GD, Rohrich RJ. The nature of long-term fillers and
the risk of complications. Dermatol Surg 2009;35(Suppl 2):
1598–1604
18. Narins RS, Coleman WP III, Glogau RG. Recommendations
and treatment options for nodules and other filler com­
plications. Dermatol Surg 2009;35(Suppl 2):1667–1671
19. Dayan SH, Arkins JP, Brindise R. Soft tissue fillers and bio­
films. Facial Plast Surg 2011;27(1):23–28
20. Bjarnsholt T, Tolker-Nielsen T, Givskov M, Janssen M,
Christensen LH. Detection of bacteria by fluorescence in
situ hybridization in culture-negative soft tissue filler le­
sions. Dermatol Surg 2009;35(Suppl 2):1620–1624
21. Grippaudo FR, Pacilio M, Di Girolamo M, Dierckx RA, Si­
gnore A. Radiolabelled white blood cell scintigraphy in the
work-up of dermal filler complications. Eur J Nucl Med Mol
Imaging 2013;40(3):418–425
22. Cassuto D, Marangoni O, De Santis G, Christensen L. Ad­
vanced laser techniques for filler-induced complications.
Dermatol Surg 2009;35(Suppl 2):1689–1695
23. Leonhardt JM, Lawrence N, Narins RS. Angioedema acute
hypersensitivity reaction to injectable hyaluronic acid.
Dermatol Surg 2005;31(5):577–579
24. Van Dyke S, Hays GP, Caglia AE, Caglia M. Severe acute lo­
cal reactions to a hyaluronic acid-derived dermal filler. J
Clin Aesthet Dermatol 2010;3(5):32–35
25. Geisler D, Shumer S, Elson ML. Delayed hypersensitivity
reaction to Restylane®. Cosmetic Dermatol 2007;20:784–
786
26. Arron ST, Neuhaus IM. Persistent delayed-type hypersen­
sitivity reaction to injectable non-animal-stabilized hyal­
uronic acid. J Cosmet Dermatol 2007;6(3):167–171
27. Sclafani AP, Fagien S. Treatment of injectable soft tissue fill­
er complications. Dermatol Surg 2009;35(Suppl 2):1672–
1680
28. Voigts R, Devore DP, Grazer JM. Dispersion of calcium hy­
droxylapatite accumulations in the skin: animal studies
and clinical practices. Dermatol Surg 2010;36:798–803
29. Vrcek IM, Malouf P, Gilliland GD. A novel solution for su­
perficially placed calcium hydroxylapatite (Radiesse) in
the inferior eyelid. Orbit 2012;31(6):431–432
30. Reddy KK, Brauer JA, Anolik R, et al. Calcium hydroxyl­
apatite nodule resolution after fractional carbon dioxide
laser therapy. Arch Dermatol 2012;148(5):634–636

169
Chapter 16 Dermal Fillers and Neurotoxins
49. Hilton S, Schrumpf H, Buhren BA, Bölke E, Gerber PA. Hy­
aluronidase injection for the treatment of eyelid edema: a
retrospective analysis of 20 patients. Eur J Med Res 2014;
19:30
50. Pessa JE, Rohrich RJ. Facial Topography: Clinical Anatomy
of the Face. New York: CRC Press; 2012
51. Beleznay K, Carruthers JD, Humphrey S, Jones D. Avoiding
and treating blindness from fillers: a review of the world
literature. Dermatol Surg 2015;41(10):1097–1117
52. Park SW, Woo SJ, Park KH, Huh JW, Jung C, Kwon OK.
­Iatrogenic retinal artery occlusion caused by cosmetic ­facial
filler injections. Am J Ophthalmol 2012;154(4):653–662.
53. Kim YJ, Kim SS, Song WK, Lee SY, Yoon JS. Ocular ischemia
with hypotony after injection of hyaluronic acid gel. Oph­
thal Plast Reconstr Surg 2011;27(6):e152–e155
54. Silva MT, Curi AL. Blindness and total ophthalmoplegia
after aesthetic polymethylmethacrylate injection: case
report. Arq Neuropsiquiatr 2004;62(3B):873–874
55. Coleman SR. Avoidance of arterial occlusion from ­injection
of soft tissue fillers. Aesthet Surg J 2002;22(6):555–557
56. DeLorenzi C. Complications of injectable fillers, part
2: vascular complications. Aesthet Surg J 2014;34(4):
584–600
57. Cohen JL, Biesman BS, Dayan SH, et al. Treatment of hy­
aluronic acid filler-induced impending necrosis with hy­
aluronidase: consensus recommendations. Aesthet Surg J
2015;35(7):844–849
58. Carruthers JD, Fagien S, Rohrich RJ, Weinkle S, Carruthers
A. Blindness caused by cosmetic filler injection: a review
of cause and therapy. Plast Reconstr Surg 2014;134(6):
1197–1201
59. Hayreh SS, Podhajsky PA, Zimmerman B. Nonarteritic an­
terior ischemic optic neuropathy: time of onset of visual
loss. Am J Ophthalmol 1997;124(5):641–647
60. DeLorenzi C. Transarterial degradation of hyaluronic acid
filler by hyaluronidase. Dermatol Surg 2014;40(8):832–
841
61. Kleydman K, Cohen JL, Marmur E. Nitroglycerin: a review
of its use in the treatment of vascular occlusion after soft
tissue augmentation. Dermatol Surg 2012;38(12):1889–
1897
62. Sung HM, Suh IS, Lee HB, Tak KS, Moon KM, Jung MS.
Case reports of adipose-derived stem cell therapy for
nasal skin necrosis after filler injection. Arch Plast Surg
2012;39(1):51–54
63. Kang BK, Kang IJ, Jeong KH, Shin MK. Treatment of gla­
bella skin necrosis following injection of hyaluronic ac­
id-filler using platelet-rich plasma. J Cosmet Laser Ther
2015;8:1–5
64. Careta MF, Delgado L, Patriota R. Report of allergic reac­
tion after application of botulinum toxin. Aesthet Surg J
2015;35(5):NP102–NP105
65. Steinsapir KD, Groth MJ, Boxrud CA. Persistence of upper
blepharoptosis after cosmetic botulinum toxin type A.
Dermatol Surg 2015;41(7):833–840
66. Aristodemou P, Watt L, Baldwin C, Hugkulstone C. Diplo­
pia associated with the cosmetic use of botulinum toxin a
for facial rejuvenation. Ophthal Plast Reconstr Surg 2006;
22(2):134–136
67. Isaac CR, Chalita MR, Pinto LD. Botox® after Botox®—a
new approach to treat diplopia secondary to cosmetic
botulinic toxin use: case reports. Arq Bras Oftalmol 2012;
75(3):213–214
31. Heinz BC, Ladhoff U, Kahl Ch, Rzany B, von Mallek D. [Sur­
vey of incidents associated with injectable dermal fillers
reported to the German Medical Devices Vigilance Sys­
tem]. Bundesgesundheitsblatt Gesundheitsforschung Ge­
sundheitsschutz 2008;51(7):787–792
32. Alijotas-Reig J, Fernández-Figueras MT, Puig L. Inflamma­
tory, immune-mediated adverse reactions related to soft
tissue dermal fillers. Semin Arthritis Rheum 2013b;43(2):
241–258
33. Alijotas-Reig J, Fernández-Figueras MT, Puig L. Late-onset
inflammatory adverse reactions related to soft tissue filler
injections. Clin Rev Allergy Immunol 2013;45(1):97–108
34. Beleznay K, Carruthers JD, Carruthers A, Mummert ME,
Humphrey S. Delayed-onset nodules secondary to a
smooth cohesive 20 mg/mL hyaluronic acid filler: cause
and management. Dermatol Surg 2015;41(8):929–939
35. Maharjan AS, Pilling D, Gomer RH. High and low molecu­
lar weight hyaluronic acid differentially regulate human
fibrocyte differentiation. PLoS One 2011;6(10):e26078
36. Cyphert JM, Trempus CS, Garantziotis S. Size matters: mo­
lecular weight specificity of hyaluronan effects in cell bi­
ology. Int J Cell Biol 2015;2015:563818
37. Lemperle G, Gauthier-Hazan N, Wolters M, Eisemann-
Klein M, Zimmermann U, Duffy DM. Foreign body granu­
lomas after all injectable dermal fillers: part 1. Possible
causes. Plast Reconstr Surg 2009;123(6):1842–1863
38. Lemperle G, Gauthier-Hazan N. Foreign body granulomas
after all injectable dermal fillers: part 2. Treatment op­
tions. Plast Reconstr Surg 2009;123(6):1864–1873
39. Alijotas-Reig J, Garcia-Gimenez V, Miró-Mur F, Vilardell-
Tarrés M. Delayed immune-mediated adverse effects of
polyalkylimide dermal fillers: clinical findings and long-
term follow-up. Arch Dermatol 2008;144(5):637–642
40. Chrastil-LaTowsky B, Wesley NO, MacGregor JL, Kaminer
MS, Arndt KA. Delayed inflammatory reaction to bio-al­
camid polyacrylamide gel used for soft-tissue augmenta­
tion. Arch Dermatol 2009;145(11):1309–1312
41. Sachdev M, Anantheswar Y, Ashok B, Hameed S, Pai SA.
Facial granulomas secondary to injection of semi-perma­
nent cosmetic dermal filler containing acrylic hydrogel
particles. J Cutan Aesthet Surg 2010;3(3):162–166
42. Wiest LG, Stolz W, Schroeder JA. Electron microscopic
documentation of late changes in permanent fillers and
clinical management of granulomas in affected patients.
Dermatol Surg 2009;35(Suppl 2):1681–1688
43. Brody HJ. Use of hyaluronidase in the treatment of granu­
lomatous hyaluronic acid reactions or unwanted hyal­
uronic acid misplacement. Dermatol Surg 2005;31(8 Pt 1):
893–897
44. Funt DK. Avoiding malar edema during midface/cheek
augmentation with dermal fillers. J Clin Aesthet Dermatol
2011;4(12):32–36
45. Griepentrog GJ, Lucarelli MJ, Burkat CN, et al. Periorbital
edema following hyaluronic acid gel injection: a retro­
spective review. Am J Cosmet Surg 2011;28:251–254
46. Surek CC, Beut J, Stephens R, Jelks G, Lamb J. Pertinent
anatomy and analysis for midface volumizing procedures.
Plast Reconstr Surg 2015;135(5):818e–829e
47. Pessa JE, Garza JR. The malar septum: the anatomic ba­
sis of malar mounds and malar edema. Aesthet Surg J
1997;17(1):11–17
48. Codner M, McCord D. Eyelid and Periorbital Surgery, 2nd
ed. New York: CRC Press; 2016

SECTION IV AESTHETIC SURGERY
170
num toxin type A—evidence-based review, emerging con­
cepts, and consensus recommendations for aesthetic use,
including updates on complications. Plast Reconstr Surg
2016;137(3):518e–529e
72. KYBELLA. (deoxycholic acid) injection, for subcutaneous
use. Prescribing Information. Available from:
sumers.mykybella.com/~/media/Unique%20Sites/Kybella/
Documents/KYBELLA-Combined-FINAL-Labeling.ashx.
Accessed April 2016
73. Walker P, Fellmann J, Lizzul PF. A phase I safety and
pharmacokinetic study of ATX-101: injectable, synthet­
ic deoxycholic acid for submental contouring. J Drugs
­Dermatol 2015;14(3):279–287
68. Arat YO, Yen MT. Effect of botulinum toxin type a on tear
production after treatment of lateral canthal rhytids.
Ophthal Plast Reconstr Surg 2007;23(1):22–24
69. Ozgur OK, Murariu D, Parsa AA, Parsa FD. Dry eye syn­
drome due to botulinum toxin type-A injection: guideline
for prevention. Hawaii J Med Public Health 2012;71(5):
120–123
70. Torres S, Hamilton M, Sanches E, Starovatova P, Gubanova
E, Reshetnikova T. Neutralizing antibodies to botulinum
neurotoxin type A in aesthetic medicine: five case re­
ports. Clin Cosmet Investig Dermatol 2013;7:11–17
71. Sundaram H, Signorini M, Liew S, et al.; Global Aesthetic­
sConsensus Group. Global Aesthetics Consensus: Botuli­
Discussion by Karol A. Gutowski
The expanding popularity of minimally invasive aes­
thetic procedures is expected to continue as options
such as injectable dermal fillers and neurotoxins pro­
vide a more convenient and less expensive facial re­
juvenation alternative to surgical procedures. These
injectable products also enhance surgical treatments
and offer solutions to problems for which traditional
surgery is less effective. However, as with any proce­
dure, risks and adverse outcomes need to be consid­
ered. Unfortunately, most patients and some physi­
cians view injection treatments as having little to no
risk. Likewise, without proper education, patients are
commonly unaware of the limited results that injec­
tions can offer and are surprised when normal conse­
quences (such as bruising or swelling) or more serious
events occur.
With proper training and experience, a skilled and
qualified injector can reduce adverse outcomes, but we
do not have enough information to completely eliminate
injection-associated complications. The growth in the
number of individuals providing injectable treatments
who are not physicians aesthetic specialists or who are
support staff who have completed only a 1- or 2-day
training course is likely to result in more plastic sur­
geons seeing patients with adverse outcomes referred
for evaluation and treatment. A comprehensive over­
view on avoidance and treatment of injectable compli­
cations is mandatory for anyone offering these thera­
pies and should be reviewed regularly as a reminder that
even a simple product injection can cause significant
morbidity.
My approach to minimizing risk and unfavorable
outcomes starts with the basics:
•• Proper patient assessment and education
•• Individualized patient treatment plans
•• Comprehensive understanding of the products being
used
•• Standardization and protocols for procedures
•• Assessment of outcomes for each patient with
emphasis on future improvement
•• Analysis of any unfavorable outcomes with a focus
on future prevention and quality improvement
Following these principles, particularly in a practice
with multiple physicians and support staff (nurses,
physician assistants, nurse practitioners) offering in­
jection treatments, unfavorable outcomes may be re­
duced and better managed.1
Causes of adverse outcomes, including patient dis­
satisfaction, may be categorized as follows:
•• Patient selection
•• Undertreatment
•• Anatomic site
•• Product selection
•• Technique
•• Judgment (overfill/undercorrection)
•• Patient expectations
•• Tissue damage
Combining the basic approach listed previously with
minimizing the causes of adverse outcomes can grow
a minimally invasive practice, increase patient satisfac­
tion, and reduce unfavorable results.
Patient Assessment, Education, and
Selection
In addition to a standard medical intake document,
each consultation starts with a comprehensive facial
examination and history of past facial treatments. A
“top–down” analysis with the patient looking in a mir­
ror while the physician points out areas for improve­
ment enhances patient education. Starting at the top of
the face (temple hollowness, forehead lines, low brows,

171
Chapter 16 Dermal Fillers and Neurotoxins
glabellar creases, etc.) and working down (jowls,
­prejowl sulcus, neck bands, submental fullness, etc.)
allows for a standardized assessment and reduces the
likelihood of missing an area of possible treatment.2 At
this point, a patient can be informed of the “Four Rs of
Facial Rejuvenation” (Box 16D.1).
Once this evaluation is completed, a customized
treatment plan is recommended.3 This is the first oppor­
tunity for reducing unfavorable outcomes. Patients are
commonly surprised at the amount of injectable prod­
ucts needed to achieve their desired results. A single sy­
ringe of a filler often leads to undercorrection (particu­
larly in the midface), so an undertreated patient may
feel that the injection “did not work.” Likewise, a patient
hoping for an injection in the nasolabial folds may be
surprised to hear that an injection in the malar area may
be better at reshaping the face and minimizing central
facial fullness while highlighting the cheek bones and
correcting the malar descent that is contributing to the
nasolabial folds.
Using anatomic diagrams of facial aging and images
of patients with similar facial aging before and after in­
jection treatment are useful educational tools that help
patients understand the possible outcomes and set re­
alistic expectations. When appropriate, before and after
images of similar patients who had surgical treatments
should also be reviewed, because a patient may prefer
a more dramatic improvement than injectable prod­
ucts alone can provide. When a patient demonstrates
her expectations by pulling back her cheeks with her
finger tips, this is a sign that she wants the results of a
facelift and that injectable fillers may not meet her ex­
pectations.
Finally, appropriate alternatives to injectable prod­
ucts should be discussed. New products tend to offer
overly optimistic promises. Direct-to-consumer adver­
tising can lead to patients requesting an injectable treat­
ment that often offers results inferior to other minimally
invasive treatments, sometimes at higher costs. For ex­
ample, deoxycholic acid (Kybella [Kythera Biophar­
maceuticals]) injections are appropriate for improving
submental fullness.4 However, many patients are bet­
ter served with submental liposuction, which requires
fewer treatment sessions and has a lower cost.
Before any treatment is performed, a detailed
­informed consent is reviewed together by the clini­
cian and patient. Although it may not prevent a com­
plication, it serves as an educational tool and offers
protection if complications lead to legal actions. Stan­
dard ­patient digital photographs are taken (without
makeup) ­before treatment. In the event of patient dis­
satisfaction, ­reviewing before and after treatment im­
ages helps assure the patient that the results are appro­
priate. ­Without photo documentation, unsatisfactory
outcomes, real or perceived by the patient, cannot be
defended.
Treatment Plan
For patients having their first injection treatment, a
conservative approach is often better than a full injec­
tion session. Injecting enough filler or neuromodulator
to see an acceptable result should be balanced against
an overcorrection that will surprise the patient and
cause dissatisfaction. Patients should understand that
undercorrection is simple to treat, but overcorrection
is a much harder issue to resolve.
All neuromodulator patients should be encouraged
to return for a follow-up visit 2 weeks after treatment to
measure outcomes. More neuromodulator may be given
at that time. This is also the time for the injecting clinician
to get feedback and assess the results, noting whether
more or less product, or different injection points, should
be used in the future. Common consequences of over­
treatment such as a dropped brow can be reduced with
critical clinician self-assessment and patient review.
Because the results of injectable fillers last longer
than those of neuromodulators, it is even more impor­
tant to prevent overtreatment. Experienced injectors
know that edema that occurs during the injection may
alter the appearance of the filler results and lead to dif­
ficulty in determining whether more product is needed.
If this happens, it is better to stop the injection at that
site and have the patient return in 1 to 2 weeks for more
treatment. If there is unused product in the syringe, it
can be saved for a brief time if handled appropriately.
Replacing the injection needle or cannula with a sterile
unused needle and placing the syringe in a sealed and
labeled envelope with proper storage allows for comple­
tion of the injection a short time later.
Certain areas, particularly the tear troughs and
lips, tend to have more edema and are less forgiving,
especially when water-absorbing hyaluronic acid fillers
are used. In these cases, it is better to achieve an 80%
correction and reassess in 1 to 2 weeks whether more
­treatment is needed.
Box 16.D1
•• Relax the lines with neuromodulators.
•• Refill the lost facial volume with injectable
fillers.
•• Resurface the skin with lasers or chemical
peels, and introduce skin care maintenance.
•• Relift the sagging structures with surgery.
The Four Rs of Facial
Rejuvenation

SECTION IV AESTHETIC SURGERY
172
For patients who are having their first injection or
are apprehensive about their treatment, it is better to
start with one area where a significant improvement can
be seen with one injection. Correcting midface volume
loss with 1 mL of hyaluronic acid filler is not likely to re­
sult in visible improvement and may leave the patient
disappointed. However, simple malar and nasolabial fold
enhancement using 1.5 mL of calcium hydroxylapatite,
which has a high G′, or “lift capacity,” will be easily no­
ticeable and more likely to enhance patient satisfaction
and willingness for more treatments.5
It is useful for patients to view themselves in a mir­
ror after one side of the face is treated so they can see
the result and compare it against the nontreated side.
Treatment Sites, Product Selection,
and Injection Technique
Proper skin preparation is an aspect of filler injections
that is often neglected. Although infections thankfully
are rare, they can be devastating and difficult to treat.
Removal of makeup in and around the injection site
and a proper skin antiseptic is required. Betadine or
other products that leave the skin discolored should be
wiped away with an alcohol pad to allow for skin color
observation in case skin blanching or an intravascular
injection occurs.
Getting the right match of filler product to anatomic
site and deformity is critical to treatment success. Al­
though the hyaluronic acid fillers have many similarities
and, at times, are interchangeable, understanding their
unique physical properties (G′, water absorption) allows
for tailoring a customized treatment plan.6 Low-G′ fill­
ers are better for fine lines and creases, areas of thin­
ner skin, and for more superficial injections (Fig. 16D.1).
Higher-G′ products should be used for more aggressive
corrections where more “lift” is needed and injected in
a deeper tissue plane (Fig. 16D.2).
Nonhyaluronic acid fillers (Sculptra [Galderma], Bel­
lafill [Suneva Medical], Radiesse) have longer durations
of effect, cannot be reversed with hyaluronidase, and
should not be used in some anatomic areas (lips, areas
of thin skin). Therefore they should be used by more
experienced clinician injectors. The proper injection
technique partially depends on each clinician’s experi­
ence, but the following general guidelines may reduce
adverse events.
For superficial injections, controlled small injec­
tion volumes tend to be better. Multiple series of linear
threading or layers of cross-hatching of fanning are less
likely to produce palpable lumps, granulomas, discolor­
ation, and tissue distortion. For deeper injections, larger
volumes may be used, but bolus injections (0.1 mL each)
are best left for deeper injections at the supraperiosteal
level. Some products can be “molded” after injection to
achieve better filler placement.
For example, Radiesse injected in the dorsum of the
hand is easy to spread through the loose connective tis­
sue planes to yield diffuse volumization (Fig. 16D.3).
Bellafill, on the other hand, should not be placed in bo­
Fig. 16D.1 Before (a) and after (b) injection with Juvéderm Ultra Plus (Allergan), a low-G′ filler, for mild tear troughs.
a
b
Fig. 16D.2 Before (a) and after (b) injection with Radiesse (Merz Aesthetics), a high-G′ filler, for malar augmentation.
a
b

173
Chapter 16 Dermal Fillers and Neurotoxins
lus injections, because permanent nodules may form
(Fig. 16D.4). Instead, multiple small-volume injections
should be performed to leave only very tiny amounts
of Bellafill at each injection point. This may require 40
to 50 passes of a 0.8-mL syringe using a blunt injection
cannula with constant pressure on the syringe plunger
to achieve proper product placement (Video 16.1).
Sculptra also requires a special injection technique
with a higher reconstitution volume to reduce the risk
of nodule and granuloma formation.
Recent availability of disposable blunt injection can­
nulas may reduce the risk of intravascular filler injec­
tion. Although these cannulas have additional cost and
require some modification in injection technique, this
may be offset by the lower risk of complications.
Outcome Assessment
The best way to improve results is with regular criti­
cal assessment of a clinician’s outcomes. This requires
time spent with each patient a few weeks after treat­
ment to obtain honest feedback. Review of before- and
after-treatment photos (Fig. 16D.5) can help plan for
treatment changes for future injection sessions. Con­
Fig. 16D.3 Before (a) and after (b) injection of Radiesse for dorsal hand enhancement.
a
b
Fig. 16D.4 Upper lip nodules after improper Bellafill injection.
This is difficult to treat and may be permanent.
Fig. 16D.5 Before (a) and after (b) facial volu­
mization with two sessions of Bellafill. Proper
assessment before and after each injection ses­
sion allowed for an optimal aesthetic outcome
without an “overdone” appearance.
a
b

SECTION IV AESTHETIC SURGERY
174
Box 16.D2
•• Meet your individual injectable product industry representative and ask for actual published data or
data submitted to the U.S. Food and Drug Administration (FDA) for each product you plan to use. Set
up training sessions by experienced injectors for all clinician injectors for each product you plan to use
in your practice. Get to know the actual physicians who work with each manufacturer who can help in
the event of adverse outcomes.
•• Novice injectors should start with short-acting, reversible hyaluronic acid fillers and progress to
longer-acting and nonreversible products after gaining more experience, education, and mentoring.
•• New injectable products should be introduced thoughtfully into a practice. The FDA rightfully sets
a high bar before approving a product for use. This has kept some inferior products from being
used. However, some fillers have made it past the regulatory process and were later found to have
unacceptable complication rates.
•• Do not rush through the injection session, and maximize patient comfort. Use of local anesthetics at
injection points, tissue cooling with ice packs, and slow injections with narrow-bore blunt cannulas
when feasible may result in fewer complications.
•• Although it is best to avoid injections in patients taking known anticoagulants (aspirin, warfarin,
antiplatelet medications), normal use of nonsteroidal anti-inflammatory drugs or supplements (fish
oil, vitamin E, St. John’s Wort, garlic tablets, ginkgo biloba, ginseng) is a minimal concern for bruising
or bleeding.
•• Give patients proper instructions for what complications they should expect and what to do in such
an event. In some cases, signs of vascular occlusion after an injection were misinterpreted by a patient
and attributed to “bruising,” leading to a delay in diagnosis, treatment, and tissue salvage. Patients
should be able to reach their clinician injector directly in the event of a possible complication and not
have to rely on the internet to determine the cause of their concerns.
•• When serious complications occur, give the patient priority and see them frequently. Infection and
intravascular injection may require aggressive therapy with frequent monitoring, along with patient
handholding (which should not be dismissed). Consultation with other experts (other experienced
injectors or specialists in infectious disease, immunology, hyperbaric oxygen, dermatology,
ophthalmology, etc) should be done early.
•• Even a practice with occasional use of injectable fillers should plan for a serious complication.
Adequate hyaluronidase should always be available and the filler “crash cart” be properly stocked and
easily accessible.9,10
•• Respect the inferior orbital area and be conservative with filler injections for treating tear troughs
and infraorbital hollowness. Periorbital and malar edema can be long lasting, is very distressing to
patients, and is difficult to treat. Use only small amounts of reversible hyaluronic acid fillers and
undercorrect with a plan to bring to full correction if needed.
•• Customize your treatment plans to fit each individual patient’s realistic goals and clinical needs.
Two similar patients may have different expectations after a neuromodulator injection—one may
want to maintain some upper facial expression, whereas the other may want no forehead and brow
movement. It is better to discuss this in advance than to deal with a dissatisfied patient 2 weeks
later. Educate patients that some forehead movement after neuromodulator injection is better than
overtreatment that results in brow ptosis.
•• During the patient evaluation, point out all asymmetries and areas that cannot be corrected or
improved. Patients need to be reminded of what is realistic and what is not.
•• For patients who have a short duration of neuromodulator effect (less than 3 months) despite proper
dosing and injection technique, consider using a zinc and phytase product (Zytaze [OcuSoft]) before
the next treatment session.11
Avoiding Unfavorable Results and Complications in Injectable Treatments

175
Chapter 16 Dermal Fillers and Neurotoxins
stant feedback and self-assessment can improve a
­clinicians’ judgment and minimize undercorrection
and ­overtreatment in patients.
Preventing and Treating
Complications and Suboptimal
Outcomes
Obviously, prevention of complications is better than
having to deal with them afterward. Safer injections
should be implemented by all clinician injectors. As
with all areas of medicine, some recommendations
have stronger scientific support (or at lease consensus
recommendations), whereas others are more theoreti­
cal or seem like a good idea but are not supported by
science (usually because of lack of good studies).7,8 My
personal experience and interpretation of published
studies and filler product manufacturer data offer ad­
ditional suggestions, outlined in Box 16D.2.
Conclusion
Despite being considered simple office treatments with
minimal risk, injectable aesthetic products require
careful attention to detail and proper training to mini­
mize unfavorable results and serious complications.
Because these procedures are commonly performed
by nonphysicians and without direct physician super­
vision, it is important that these principles and guide­
lines be implemented and understood by everyone in­
volved in the care process.
References
1. Lemperle G, Rullan PP, Gauthier-Hazan N. Avoiding
and treating dermal filler complications. Plast Recon­
str Surg 2006;118(3, Suppl)92S–107S
2. Lam SM, Glasgold R, Glasgold M. Analysis of facial
aesthetics as applied to injectables. Plast Reconstr
Surg 2015;136(5, Suppl)11S–21S
3. Wilson AJ, Taglienti AJ, Chang CS, Low DW, Percec I.
Current applications of facial volumization with fill­
ers. Plast Reconstr Surg 2016;137(5):872e–889e
4. Humphrey S, Sykes J, Kantor J, et al. ATX-101 for reduc­
tion of submental fat: a phase III randomized controlled
trial. J Am Acad Dermatol 2016;75(4):788–797.e7
5. Shi XH, Zhou X, Zhang YM, Lei ZY, Liu T, Fan DL. Com­
plications from nasolabial fold injection of calcium
hydroxylapatite for facial soft-tissue augmentation: a
systematic review and meta-analysis. Aesthet Surg J
2016;36(6):712–717
6. Hee CK, Shumate GT, Narurkar V, Bernardin A,
­Messina DJ. Rheological properties and in vivo
­performance characteristics of soft tissue fillers.
­Dermatol Surg 2015;41(Suppl 1):S373–S381
7. DeLorenzi C. Complications of injectable fillers, part 1.
Aesthet Surg J 2013;33(4):561–575
8. DeLorenzi C. Complications of injectable fillers, part
II. Aesthet Surg J 2014;34(4):584–600
9. Cohen JL, Biesman BS, Dayan SH, et al. Treatment of hy­
aluronic acid filler-induced impending necrosis with
hyaluronidase: consensus recommendations. Aesthet
Surg J 2015;35(7):844–849
10. Rzany B, DeLorenzi C. Understanding, avoiding, and
managing severe filler complications. Plast Reconstr
Surg 2015; 136(5 Suppl)196S–203S
11. Koshy JC, Sharabi SE, Feldman EM, Hollier LH Jr,
­Patrinely JR, Soparkar CN. Effect of dietary zinc
and phytase supplementation on botulinum toxin
­treatments. J Drugs Dermatol 2012;11(4):507–512

CHAPTER
17

Laser Facial Resurfacing
Mark S. Nestor, Mitchell Manway, and Paige Paparone
Over the past two decades, laser facial resurfacing has
served as a valuable method toward the goal of achieving
facial rejuvenation. The ability to effectively combat the
normal and inevitable consequences of aging, such as rhyt­
ides, lentigines, alterations in skin texture, and scarring,
remains paramount, and practitioners are always search­
ing for effective nonsurgical means. Luckily, many advance­
ments in laser technology have been made since the rela­
tively primitive ruby and CO2 lasers were developed in the
early 1960s, and new technologies have increased efficacy
while minimizing adverse effects.1 Four broad categories of
laser resurfacing have formed from such innovations. These
consist of the novel ablative nonfractionated type, the less
dramatic but undeniably safer nonablative nonfractionated
type, the hybrid nonablative but fractionated type, and the
ablative fractionated type used by carbon dioxide (CO2) and
erbium-doped: yttrium aluminum garnet (Er:YAG) sys­
tems. Although some of these categories of lasers maintain
higher safety profiles over others, all types of ablative treat­
ments have a risk for complications.
When discussing laser resurfacing, understanding the
fundamental differences between these categories is essen­
tial. The term nonablative refers to a treatment that selec­
tively and often minimally damages the dermal tissue while
sparing the epidermis, achieving less dramatic results, but
maintaining a higher safety profile. This is in contrast with
ablative lasers, which essentially vaporize the epidermal
layer while stimulating the dermis, necessitating far more
downtime and a more difficult recovery but achieving signif­
icantly superior results. The term fractionated refers to the
ability of the laser to target a specific proportion of treated
skin, creating discrete and separated columns of affected tis­
sue instead of acting on the entire skin surface. This allows
the surrounding untreated skin to contribute to the healing
process through epithelial migration.2,3
Although the exact biochemical processes by which la­
ser resurfacing acts to improve cosmetic appearance are still
not fully determined, the relationship between the wave­
length that the laser emits and a high absorption coefficient
for tissue water is what allows highly controlled thermal
damage to the desired skin layer. For example, the CO2 la­
ser emits a wavelength of 10,600 nm, which is strongly ab­
sorbed by tissue water. It is hypothesized that through this
the CO2 laser targets the appropriate depth in the skin and
causes immediate contraction of the ablated area by dena­
turing existing old collagen.4
Subsequently, new collagen formation is stimulated,
and in conjunction with ablation of the epidermis, cos­
metic enhancement is achieved over time through con­
trolled wound healing as new epidermal and dermal tissue
takes the place of the photoaged and damaged skin. Com­
pared with the CO2 laser, the Er:YAG laser emits light at the
2,940-nm wavelength. At this frequency, the peak absorp­
tion range of water is more closely approximated, and as
such the Er:YAG laser possesses an absorption coefficient
for water 16 times greater than the CO2 laser.2 Despite this,
both systems can achieve similar efficacy, especially with
the advent of the long-pulse erbium laser. Past comparative
studies have shown the Er:YAG laser may cause fewer se­
vere side effects,5 and thus many practitioners have chosen
to only use this modality. However, many patients’ desired
cosmetic outcome or individual tolerance may not require
or allow for ablative laser resurfacing, and nonfractionated
and nonablative lasers are still widely used for various in­
dications.
Comparatively, ablative laser resurfacing does cause
more side effects, and additional minor and occasionally se­
vere complications can occur. The following sections detail
potential side effects, complications, and unfavorable results
and how best to avoid them.
176

177
Chapter 17 Laser Facial Resurfacing
the most predictable and notable associated complications
involving patient selection is those patients with ethnic
skin or those with Fitzpatrick types IV to VI. Again, caution
and a conservative approach must be observed to prevent
postinflammatory hyperpigmentation and other pigmentary
changes in these individuals.1
An important consideration for laser resurfacing should
be the planned method of adequate anesthesia. Ablative
resurfacing in particular causes significant stimulation to
dermal nerve fibers, resulting in substantial discomfort
and pain. When only small, localized, or superficial areas
of treatment are involved, methods such as oral sedation,
topical anesthetics combined with or without nerve block,
or cryoanesthesia may be sufficient. However, if deep resur­
facing of the entire face is planned, additional approaches
such as monitored intravenous sedation may be warranted.
Injected nerve blocks combined with topical and oral prepa­
rations are often preferred, negating the need for supervised
anesthesia, but drawbacks include potential tissue distor­
tion, increased procedure time, and inadequate pain con­
trol.8 Ultimately, appropriate methods of anesthesia must be
tailored to patient tolerance and preference and the comfort
level of the provider.
Intraoperative Considerations
The provider must also possess an adequate knowledge of
the different capabilities and adjustable settings of the pro­
posed device. All lasers have inherent and adjustable prop­
erties such as pulse duration, spot density and diameter,
and depth of penetration. Perhaps the most important ad­
Avoiding Unfavorable Results
and Complications in Laser
Resurfacing
Patient Selection and Preoperative
Planning
First and foremost, as with any cosmetic procedure, patient
selection must only involve individuals who not only pos­
sess the ability to thoroughly understand the procedure and
its associated risks, but also hold realistic expectations for
the end result. Depending on the type of laser used, patients
must be able to accept that most ablative laser resurfacing
may result in significant downtime and an extended period
of recovery. In addition, appropriate screening must be per­
formed so as to exclude those individuals who may lack the
diligence or ability to perform adequate postoperative care
to prevent complications during the wound-healing stage.
Without question, proper wound management is impera­
tive to achieve successful results. Likewise, patients with
medical conditions involving poor wound healing, a history
of collagen vascular disorders, conditions with propensity
to koebnerize, or past facial keloids or hypertrophic scarring
may be unfit candidates to undergo laser resurfacing.
Recent isotretinoin therapy within 6 months up to a year
or a history of radiation within the treatment area should
also be considered an increased risk for scarring compli­
cations. Although a recent study found that concomitant
isotretinoin was safe in an Asian population, I urge consider­
able caution based on personal experience.6,7 Perhaps one of
Summary Box
Expected Short-Term Side Effects
Erythema
Edema
Pain
Pruritus
Minor oozing
Minor bleeding
Minor crusting
Complications
Contact dermatitis
Acne/milia
Viral/bacterial/fungal infection
Sharp demarcation lines
Persistent erythema
Hyperpigmentation
Hypopigmentation
Side Effects and Complications of Ablative Laser Resurfacing
Hypertrophic scarring
Delayed healing
Tooth enamel damage
Corneal damage
Ectropion formation

SECTION IV AESTHETIC SURGERY
178
ser-induced tissue injury. Swelling and edema after resur­
facing usually peaks around 2 to 3 days and should resolve
within around 1 week. Increased blood flow, inflammation,
metabolic activity, and collagen remodeling are likely re­
sponsible.1 However, persistent erythema, considered to
be erythema which lasts up to 6 months or more, is not
common and is most often seen with CO2 lasers as a result
of more extensive residual thermal necrosis of the dermis.
Other factors that can increase the likelihood of persis­
tent erythema are multiple laser passes, pulse stacking, me­
chanical abrasion and rubbing of the skin intraoperatively,
postoperative infection, and patient susceptibility because
of preexisting conditions or therapies. These susceptibilities
include a history of rosacea, previous resurfacing or use of
acid peels, or use of retinoic acid derivatives.11 Other very
common aftereffects witnessed after resurfacing include mi­
nor crusting, oozing, and bleeding. Adequate wound care
and strict application of petroleum-based products will im­
prove the skin barrier and epithelialization, which in turn
promotes more pleasing aesthetic outcomes. When ery­
thema persists and is associated with pruritus, contact der­
matitis should be considered, although often it is difficult to
distinguish. This is usually irritant as opposed to allergic in
nature; recently resurfaced skin is particularly sensitive to
topical products and chemicals, and thus sunscreens, oint­
ments, and topical antibiotics should be avoided.12
Proper post-resurfacing wound care consists of liberal
application of petroleum-based products such as Aquaphor
to the entire treated area. Patients should be instructed to
avoid the urge to scratch or irritate the area while the skin
is in this vulnerable state. Some studies have shown that oc­
clusive dressings can be used up to the first 4 days after the
procedure and may contribute to a decreased incidence of
crusting, pruritus, erythema, and postoperative pain com­
pared with controls.13 Others have investigated the use of
occlusive silicone dressings, the application of platelet-rich
plasma, and even adipose-derived stem cells, all of which
showed potential for significant reduction in length of time
for erythema and edema and appeared to hasten wound
healing.14–16 However, any type of occlusive medium, with
a dressing or without, can contribute to the development
of infection, acne, and milia, which are very common af­
ter laser resurfacing, especially in patients who are already
acne-prone.
Laser-induced injury to the pilosebaceous apparatus
may also occur and contribute to aberrant follicular epi­
thelialization manifesting as acne and milia.11 These flares
tend to develop within the first few weeks after treatment
for acne-prone individuals, and at around 6 weeks for those
without prior history.17
Whether prophylactic antibiotics to prevent postoper­
ative infection are necessary with laser resurfacing is un­
clear. Investigations into the potential benefit of adminis­
tering prophylactic doses show a wide array of results and
varying recommendations. Bacterial infections during the
immediate postoperative phase are likely caused by strep­
tococcal and staphylococcal species. However, fungal in­
fection such as candidiasis has been documented and may
justable parameter is laser fluence, or the laser energy per
unit area of tissue. Cosmetic outcome and the rate of com­
plications are significantly related to the fluence and the
number of laser passes. Unquestionably, there is a direct
relationship between greater fluence, depth of penetration,
and number of passes with longer healing time. With the
advent of short-pulse and long-pulse Er:YAG lasers, dra­
matic results and increased coagulation of the dermis that
was previously only achieved with CO2 lasers is possible,
with the potential benefit of decreased side effects. With
fractionated lasers, microspot density is very important
when balancing the desired aesthetic results with risk of
complications. As mentioned previously, fractionated la­
sers cause discrete columns of tissue injury, and the degree
of fractionation can usually be adjusted. This leaves the
surrounding untreated skin with the ability to contribute
to the wound-healing process through epithelial migra­
tion. In addition, the unaffected areas allow adequate heat
transfer and help prevent excessive dermal bulk heating,
which has also been proven directly proportional to the
rate of complications.3 Finally, an experienced practitioner
can increase the effective area of ablation through multiple
passes and overlap of pulses, optimizing aesthetic results.
The ideal surgical goal may vary from patient to patient,
but minimizing photoaging, rhytids, and scars with as few
complications as possible is the ultimate objective. Increas­
ing the effective degree of ablation will cause greater der­
mal contraction and collagen stimulation, which in turn can
generate more dramatic results and improve deeper rhytids,
but also carries greater risk of complications. Also, differ­
ent areas of facial skin have varying levels of tolerance for
delivered fluence. For instance, perioral areas and cheeks
will traditionally tolerate higher fluences. In contrast, the
lateral aspects of the cheeks and the preauricular skin are
vulnerable to prolonged erythema and hyperpigmentation,
and thus lower fluences should be used. Similarly, although
the glabella may require more energy to achieve desired re­
sults, the rest of the forehead does not usually require com­
parative energy.
Caution is important around the eyelid skin, but the lat­
eral canthal areas have shown greater tolerance for more ag­
gressive fluences.9 Other areas of the body such as the neck
must be approached with extreme care because of the lack
of pilosebaceous units, decreased vascularity, and skin thick­
ness; multiple cases of hypertrophic scarring have been re­
ported.10 If only the face is to be resurfaced, sharp lines of
demarcation may result, and thus feathering of the neck and
hairline should be performed. Sharp transition zones are
more often problematic in men, because women are better
able to hide abrupt alterations with makeup and foundation.
Postoperative Complications
There are many possible short-term side effects with laser
resurfacing, and many cannot be prevented, but every ef­
fort to prevent further complications should be made. Ery­
thema and edema are inescapable side effects with ablative
laser resurfacing and are considered normal reactions to la­

179
Chapter 17 Laser Facial Resurfacing
serious and permanent complication and does not usually
manifest until 6 to 12 months postoperatively. It most com­
monly results from resurfacing performed too deeply into
the reticular dermis (Fig. 17.2).24 Particularly susceptible
facial areas include those adjacent to photodamaged skin,
such as the mandible.11 Because photodamaged tissue is re­
moved, and new nondamaged skin will replace the damaged
epidermis and dermis, almost all patients experience some
relative hypopigmentation. Despite advances in fractionated
technology, caution and conservative treatment is empha­
sized in darker-toned patients.
Scarring, particularly hypertrophic scarring, is also an­
other serious potential complication of laser resurfacing.
Multiple factors can influence the incidence of hypertro­
phic scarring. These include excessive thermal energy to
the skin or postoperative bacterial, fungal, or viral infec­
tions. Untreated contact dermatitis can also cause hyper­
trophic scarring. Furthermore, recent use of isotretinoin, a
history of keloid formation, and previous radiation therapy
can predispose patients to scarring complications.26,27 Par­
ticularly susceptible areas are those nonfacial regions with
less vasculature and blood supply, such as the neck, chest,
infraorbital region, and mandible. The least amount of pos­
sible pulse energy, pulse stacking, density, treatment frac­
be difficult to diagnose because it resembles acne or milia
formation. Those at risk for fungal infection include those
with diabetes, angular cheilitis, immunosuppression, and
vaginal candidiasis.11 Some studies have shown virtually no
incidence of bacterial infection with different prophylactic
treatment regimens—intraoperative cephalexin and postop­
erative azithromycin or dicloxacillin.18,19 On the other hand,
one study showed the rate of pseudomonal and serratia in­
fections was significantly higher in patients routinely given
such prophylaxis.20 As a result, no general consensus exists
on the use of prophylactic antibiotics, and many practition­
ers choose open wound healing combined with vigilant ob­
servation for any evidence of infectious process.
Any postoperative infection can place the patient at in­
creased risk for permanent scarring and further complica­
tions. In contrast with the risk of bacterial and fungal in­
fection, viral prophylaxis against the reactivation of herpes
simplex virus type 1 (HSV-1) is almost universally indicated,
regardless of previous history. Reactivation of HSV-1 is one
of the most common disruptions of proper wound healing
and increases the risk of secondary bacterial infection (Fig.
17.1). Because of the incomplete epithelial barrier, classic
vesicles are unlikely to form; instead erythematous erosions
associated with pain, fever, and malaise may encompass the
presentation.21 Reactivation and rarely primary HSV-1 infec­
tion is likely secondary to the disturbance of the normal skin
barrier and stimulation around mucocutaneous areas by la­
ser damage and trauma. To prevent this complication, ade­
quate prophylaxis usually consists of antivirals such as vala­
cyclovir or acyclovir given at least 1 day before the procedure
and usually continued up to 7 to 10 days afterwards.22 Most
patients and physicians prefer the use of valacyclovir be­
cause of its easier dosing.
Serious and concerning complications include dyschro­
mia and altered skin pigmentation, hypertrophic scar devel­
opment, delayed healing, and ectropion formation. Dyschro­
mia is a well-documented adverse effect after resurfacing
and is more common in dark-skinned patients and those of
higher Fitzpatrick types because of higher melanin concen­
tration. Because dark skin absorbs electromagnetic energy
much better than fair skin, the risk of thermal injury is in­
creased. Moreover, melanin’s wide absorption spectrum of
visible light and near-infrared light increases the risks for
any laser treatment and can result in permanent compli­
cations.23
Hyperpigmentation in fair-skinned individuals is usu­
ally a result of excessive sun exposure to vulnerable skin
after the procedure.24 Postinflammatory hyperpigmentation
is usually transient and relatively common within the first
month after laser treatment and will usually resolve spon­
taneously. In the past, some physicians attempted to pre­
vent hyperpigmentation preoperatively with 6 weeks of skin
therapy using topical tretinoin, alpha hydroxy acids, or 4%
hydroquinone bleaching cream in an effort to suppress mela­
nocytes, but newer studies have shown no statistical benefit
of these practices.21,25 Unlike hyperpigmentation, hypopig­
mentation witnessed after laser resurfacing is a potentially
Fig. 17.1 Bacterial infection 1 week after resurfacing.
a
b
Fig. 17.2 Hypopigmentation. (a) Two years after resurfacing.
(b) After multiple narrow-band ultraviolet A treatments.

SECTION IV AESTHETIC SURGERY
180
ing.28 Associated often but not always with deeper laser
procedures, this “delayed healing” syndrome is believed to
result from a combination of infection and potentially au­
toimmune phenomenon that prevents normal reepitheli­
alization. Documented cases usually involve patients with
Fitzpatrick type I or II skin, and after a prolonged healing
course of around 8 to 10 months, significant scarring is evi­
dent29 (Fig. 17.5).
tion, and laser passes is recommended when treating these
areas (Figs. 17.3 and 17.4). The first indicators of poten­
tial impending scar formation during the wound-healing
phase are focal areas of induration and intense erythema.
Immediate recognition is vital to prevent permanent scar
development.11
For reasons not entirely clear, occasionally patients ex­
perience great difficulty with healing after laser resurfac­
Fig. 17.3 Scarring. (a) Six months after resurfacing. (b) One year after resurfacing after multiple pulsed-dye laser treatments.
a
b
Fig. 17.4 Scarring. (a) Four months after resurfacing. (b) Six months after resurfacing after multiple pulsed-dye laser treatments.
a
b
Fig. 17.5 Delayed healing syndrome. (a) Six months after resurfacing. (b) One year after resurfacing after multiple pulsed-dye laser treat­
ments.
a
b

181
Chapter 17 Laser Facial Resurfacing
the adverse event and the underlying cause. Proper wound
management during the initial healing phase has already
been mentioned, and erythema is unavoidable; however,
persistent erythema may require treatment to prevent pos­
sible scar formation (Fig. 17.6). This can be accomplished
by administering a strong class 1 topical corticosteroid.
Additional studies have shown that topical vitamin C, also
known as ascorbic acid, may decrease postlaser erythema
through its anti-inflammatory effects. However, adminis­
tration of vitamin C should be reserved until reepithelial­
ization has finished, and the risk of irritation to the area
may outweigh the potential benefit.
When erythema and pruritus worsen, and contact or
irritant dermatitis is suspected, a thorough history must be
obtained to make sure that the patient has been following all
postoperative instructions and that potential irritants such
as home remedies, sensitizing topical antibiotics, or other
fragrant moisturizers have not been applied. As mentioned
previously, patients should be instructed to avoid further
mechanical irritation or scratching to the area to prevent
further crusting and poor cosmetic outcome. Some patients
may require a course of oral antihistamines such as diphen­
hydramine or hydroxyzine. These can be used in conjunction
Although cosmetic complications are of paramount
importance, one functional adverse event requires special
attention. Ectropion formation of the lower eyelid is a real
concern, especially in patients with a history of previous
lower blepharoplasty. A “snap test,” which involves manual
downward pull of the lower eyelid, can be used to detect
increased risk. If the lower eyelid does not quickly return to
its normal resting position within 3 seconds, laser surfac­
ing should not be performed around this area.11 Damage to
the cornea and tooth enamel can and should always be pre­
vented with proper protection and metal shielding for the
patient. If proper precautions are not taken, tooth enamel
may be fractured by the impact of the laser or subsequent
heat production.24
Managing Unfavorable Results
and Complications in Laser
Resurfacing
When unfavorable results and complications occur, the
treatment varies depending on the type and severity of
Fig. 17.6 Persistent erythema. (a) Eight months after resurfacing. (b) One year after resurfacing after multiple pulsed-dye laser treatments.
a
b
Fig. 17.7 Secondary fungal infection. (a) One week after resurfacing. (b) Resolution of infection.
a
b

SECTION IV AESTHETIC SURGERY
182
glycolic acid preparations may be administered. In addi­
tion, sun avoidance and adequate sunscreen or ultraviolet
protection should be emphasized.11 Other recent investi­
gations have indicated that the use of orally administered
Polypodium leucotomos extract may help improve postin­
flammatory hyperpigmentation because of its antioxidant
and photoprotective properties.31 In contrast, areas of hy­
popigmentation, which usually appear after a significant
delay after laser resurfacing, can be extremely conspicu­
ous and the cause of much dissatisfaction, particularly in
darker-toned patients and those of higher Fitzpatrick types
such as IV to VI. Unfortunately, there are not many effective
treatments against hypopigmentation, although glycolic
acid peels or light trichloroacetic acid peels can be used to
lighten surrounding areas in conjunction with makeup in
an effort to camouflage the affected areas.
Scarring
Many sequelae can cause hypertrophic scars after laser
resurfacing, and early detection is crucial to achieve the
most favorable cosmetic outcome. An initial approach for
mildly visible hypertrophic scars may involve the appli­
cation of steroid-impregnated tape, low-potency steroid
creams or lotions, or topical silicone or silicone sheeting.
Should these treatments prove ineffective, high-potency
steroids such as clobetasol propionate 0.5% can be used,
but many unwanted side effects are associated with longer
duration of use. Finally, should topical treatment lack ef­
ficacy or should severity of hypertrophic scarring dictate
aggressive measures, intralesional steroid injection with 5
to 10 mg/mL triamcinolone acetonide may be performed
at 3- to 4-week intervals.21 In addition, pulsed-dye laser
treatments, administered at 6- to 8-week intervals, have
also proven very effective at treating erythematous, hyper­
trophic burn scars.32
On the rare occasion that a patient exhibits delayed
healing for unknown reasons, treatment should include a
broad, comprehensive approach. A combination of oral an­
tibiotics, oral antivirals, and open wound care with gentle
topical treatment using betamethasone dipropionate has
been met with some success, and resultant scarring can be
treated with traditional methods (Fig. 17.8).29
If ectropion formation is witnessed postoperatively de­
spite appropriate initial evaluation of lower eyelid laxity and
adherence to conservative fluence during resurfacing, cor­
rection often ultimately requires surgical intervention. If it is
mild, however, a trial of topical corticosteroid preparations
combined with massage can be attempted.11,21
Conclusion
Although many strides have been made in laser resurfac­
ing techniques to effectively manage dermatologic condi­
tions and achieve less-invasive means of cosmetic rejuve­
nation, many complications and adverse events are still
with cool, wet compresses in addition to mild topical corti­
costeroids. In some severe cases, systemic steroids may be
necessary to control pruritus and inflammation.11
For most cases of acne and milia formation, treatment
is unnecessary and eruptions are usually mild. Flares usu­
ally improve with the cessation of thicker barrier ointments
and occlusive dressing. If acne and milia persist or worsen,
a course of oral antibiotics such as tetracycline or doxycy­
cline can be prescribed. If needed, topical retinoids can be
safely administered around 1 month postoperatively. Poten­
tial options include topical tretinoin or glycolic and azelaic
acid compounds.
Infection
Any surgical procedure has an inherent risk of infection,
but diagnosing and treating infections after laser resurfac­
ing requires special consideration. Opportunistic infection
may be bacterial, fungal, or viral in origin. Infections will
typically develop between postoperative days 2 and 5 and
may show evidence of purulence, discolored crusts, and
malodorous transudates. Other signs of infection such as
pain or fever may also be associated.
All suspected bacterial infections should be swabbed
and cultured to determine species and susceptibilities.
While awaiting culture, empiric treatment should include
regular water rinses, compresses with or without a 0.25%
acetic acid solution, and frequent dressing changes if occlu­
sion is desired, in addition to an antibiotic with gram-posi­
tive, gram-negative, and pseudomonal coverage, such as an
oral cephalosporin. If fungal or Candida albicans infection is
suspected, a simple potassium hydroxide (KOH) examination
should show evidence of fungal presence, and appropriate
antifungals such as oral fluconazole should be administered
for 5 to 7 days21 (Fig. 17.7). Latent viral reactivation prophy­
laxis has already been discussed in length in the previous
section. Nevertheless, should HSV-1 develop, a Tzanck smear
should be obtained and the patient’s prophylactic dosage
should be increased to herpes zoster doses or be switched to
a different antiviral agent. The appropriate treatment dosage
of valacyclovir is 1 to 2 grams twice daily for 5 days. Hospi­
talization and administration of intravenous antiviral ther­
apy may become necessary should dissemination occur.30
Pigmentation Alterations
Although almost all patients have some evidence of pig­
mentary alteration after laser resurfacing, detection should
be difficult if margins were appropriately treated and feath­
ered. Focal areas of postinflammatory hyperpigmentation
are usually transient and resolve spontaneously over the
course of a few months. However, patients may express
dissatisfaction with the conspicuous nature of this adverse
event and request treatment to hasten resolution. After the
first month, when reepithelialization is complete, topical
medications such as hydroquinone or retinoic, azelaic, or

183
Chapter 17 Laser Facial Resurfacing
tivity, and collagen remodeling. When significant erythema
persists for more than 6 months, treatment may be indicated
to hasten resolution.
Other very common side effects include some degree
of crusting, oozing, and bleeding, but strict postoperative
wound care and liberal application of petroleum-based
products, with or without occlusion, will help curb these
side effects and alleviate discomfort and pruritus. Occlusion
by dressing or petroleum increases the chance of acne and
milia formation in susceptible patients. Topical treatment
may begin around 1 month postoperatively, once sufficient
epithelium has reformed. Contact dermatitis can occur and
is usually a result of irritation as opposed to allergy. Ces­
sation of potentially sensitizing and irritating products in
addition to topical steroids is usually sufficient treatment.
Conversely, when irritation and pain are associated with
purulence, discolored crusts, and malodorous transudate,
infection must be suspected, and prompt wound culture
should be obtained to assess bacterial, viral, or fungal or­
igin. Empiric treatment must begin immediately, because
any infection, especially HSV-1 reactivation, can cause sig­
nificant impairment of wound healing and result in perma­
nent scarring.
Other more serious complications can include pigment
alterations. Although postinflammatory hyperpigmentation
is usually transient and resolves spontaneously, focal areas
of hypopigmentation are often permanent and very diffi­
cult to treat. Patients with Fitzpatrick skin types IV to VI are
particularly susceptible, and aggressive resurfacing must be
avoided. Every attempt to mitigate the incidence of hyper­
trophic scarring must be made, and areas of greater suscep­
tibility such as the neck must be taken into consideration.
Finally, preoperative assessment of the lower eyelid must be
performed to prevent ectropion formation and functional
impairment of the eyelid.
Ultimately, with awareness of potential hazards, appro­
priate patient selection, and an individualized treatment
plan, remarkable improvement in cosmetic appearance and
photoaging can be obtained without using historically inva­
sive procedures.
possible. Though the technology of fractionated lasers adds
increased safety to the dramatic potential of ablative and
nonablative therapy, a strong knowledge base and cautious
approach must be used to individualize each treatment.
Ablative resurfacing involves complete vaporization of
the epidermal layer and controlled damage and heating of
the dermal layer, causing dermal contraction and promot­
ing new collagen formation. Effective preoperative planning
must first and foremost involve appropriate patient selec­
tion and indication. A patient with conditions involving
healing impairment or propensity for hypertrophic keloi­
dal scars is likely not a good candidate for laser resurfacing.
Those with a higher Fitzpatrick type must be made aware
of the significant and permanent risks of hypopigmenta­
tion. Likewise, once informed consent is obtained, it must
be clear that patients possess realistic expectations and are
expected to be able to comply with long-term postopera­
tive wound care.
Considerations of adequate anesthesia must be deter­
mined and depend on the extent of laser resurfacing. Al­
though topical and injectable methods of pain control
prevent the need for help and supervision for monitored
anesthesia care, the complexity of nerve blocks, tissue dis­
tortion, and inadequacy of pain control may dictate such
need. In addition, the operator must have a deep and thor­
ough understanding of laser settings and parameters; each
brand and model of laser may differ in capabilities depend­
ing on the manufacturer.
Adjustment in fluence, spot density, pulse duration, and
number of passes will be variable depending on many fac­
tors, and only through experience will a practitioner be able
to anticipate and balance optimal cosmetic outcome with
increased risk of adverse events. Similarly, efforts must be
made to prevent sharp lines of demarcation, and with ad­
justment of laser parameters, feathering and tapering of
margins can be achieved.
Even with flawless technique and mastery of laser resur­
facing, certain postoperative side effects are simply unavoid­
able. A certain degree of erythema and edema is anticipated
and signifies increased blood flow, increased metabolic ac­
Fig. 17.8 Delayed healing syndrome. (a) Eight months after resurfacing. (b) One year after resurfacing.
a
b

SECTION IV AESTHETIC SURGERY
184
18. Bernstein LJ, Kauvar AN, Grossman MC, Geronemus RG.
The short- and long-term side effects of carbon dioxide
laser resurfacing. Dermatol Surg 1997;23(7):519–525
19. Nanni CA, Alster TS. Complications of carbon dioxide laser
resurfacing. An evaluation of 500 patients. Dermatol Surg
1998;24(3):315–320
20. Walia S, Alster TS. Cutaneous CO2 laser resurfacing infec­
tion rate with and without prophylactic antibiotics. Der­
matol Surg 1999;25(11):857–861
21. Demas PN, Bridenstine JB. Diagnosis and treatment of
postoperative complications after skin resurfacing. J Oral
Maxillofac Surg 1999;57(7):837–841
22. Gilbert S. Improving the outcome of facial resurfacing—
prevention of herpes simplex virus type 1 reactivation. J
Antimicrob Chemother 2001;47(Suppl T1):29–34
23. Arosarena O. Options and challenges for facial rejuvena­
tion in patients with higher Fitzpatrick skin phototypes.
JAMA Facial Plast Surg 2015;17(5):358–359
24. Apfelberg DB. Side effects, sequelae, and complica­
tions of carbon dioxide laser resurfacing. Aesthet Surg J
1997;17(6):365–372
25. West TB, Alster TS. Effect of pretreatment on the inci­
dence of hyperpigmentation following cutaneous CO2
laser resurfacing. Dermatol Surg 1999;25(1):15–17
26. Avram MM, Tope WD, Yu T, Szachowicz E, Nelson JS. Hy­
pertrophic scarring of the neck following ablative frac­
tional carbon dioxide laser resurfacing. Lasers Surg Med
2009;41(3):185–188
27. Katz BE, Mac Farlane DF. Atypical facial scarring after
isotretinoin therapy in a patient with previous dermabra­
sion. J Am Acad Dermatol 1994;30(5 Pt 2):852–853
28. Rendon-Pellerano MI, Lentini J, Eaglstein WE, Kirsner RS,
Hanft K, Pardo RJ. Laser resurfacing: usual and unusual
complications. Dermatol Surg 1999;25(5):360–366, dis­
cussion 366–367
29. Rigel DS, Weiss RA, Lim HW, Dover JS. Photoaging. New
York: CRC Press; 2004:416
30. Alster TS, Nanni CA. Famciclovir prophylaxis of herpes
simplex virus reactivation after laser skin resurfacing.
Dermatol Surg 1999;25(3):242–246
31. Nestor M, Bucay V, Callender V, Cohen JL, Sadick N, Wal­
dorf H. Polypodium leucotomos as an adjunct treat­
ment of pigmentary disorders. J Clin Aesthet Dermatol
2014;7(3):13–17
32. Alster TS, Nanni CA. Pulsed dye laser treatment of hyper­
trophic burn scars. Plast Reconstr Surg 1998;102(6):2190–
2195
References
1. Janik JP, Markus JL, Al-Dujaili Z, Markus RF. Laser resur­
facing. Semin Plast Surg 2007;21(3):139–146
2. Preissig J, Hamilton K, Markus R. Current laser resurfacing
technologies: a review that delves beneath the surface.
Semin Plast Surg 2012;26(3):109–116
3. Carniol PJ, Hamilton MM, Carniol ET. Current status
of fractional laser resurfacing. JAMA Facial Plast Surg
2015;17(5):360–366
4. Ross EV, McKinlay JR, Anderson RR. Why does carbon
dioxide resurfacing work? A review. Arch Dermatol
1999;135(4):444–454
5. Newman JB, Lord JL, Ash K, McDaniel DH. Variable pulse
erbium:YAG laser skin resurfacing of perioral rhytides
and side-by-side comparison with carbon dioxide laser.
Lasers Surg Med 2000;26(2):208–214
6. Ramsdell WM. Fractional carbon dioxide laser resurfac­
ing. Semin Plast Surg 2012;26(3):125–130
7. Kim HW, Chang SE, Kim JE, Ko JY, Ro YS. The safe delivery
of fractional ablative carbon dioxide laser treatment for
acne scars in Asian patients receiving oral isotretinoin.
Dermatol Surg 2014;40(12):1361–1366
8. Gaitan S, Markus R. Anesthesia methods in laser resurfac­
ing. Semin Plast Surg 2012;26(3):117–124
9. Jasin ME. Achieving superior resurfacing results with the
erbium:YAG laser. Arch Facial Plast Surg 2002;4(4):262–
266
10. Goldman MP, Fitzpatrick RE, Manuskiatti W. Laser resur­
facing of the neck with the Erbium: YAG laser. Dermatol
Surg 1999;25(3):164–167, discussion 167–168
11. Alster TS, Lupton JR. Treatment of complications of laser
skin resurfacing. Arch Facial Plast Surg 2000;2(4):279–
284
12. Lowe NJ, Lask G, Griffin ME. Laser skin resurfacing. Pre- and
posttreatment guidelines. Dermatol Surg 1995;21(12):
1017–1019
13. Newman JP, Koch RJ, Goode RL. Closed dressings after
laser skin resurfacing. Arch Otolaryngol Head Neck Surg
1998;124(7):751–757
14. Batra RS, Ort RJ, Jacob C, Hobbs L, Arndt KA, Dover JS.
Evaluation of a silicone occlusive dressing after laser skin
resurfacing. Arch Dermatol 2001;137(10):1317–1321
15. Kim H, Gallo J. Evaluation of the effect of platelet-rich
plasma on recovery after ablative fractional photother­
molysis. JAMA Facial Plast Surg 2015;17(2):97–102
16. Zhou BR, Xu Y, Guo SL, et al. The effect of conditioned
media of adipose-derived stem cells on wound healing
after ablative fractional carbon dioxide laser resurfacing.
BioMed Res Int 2013;2013(X):519126
17. Ratner D, Tse Y, Marchell N, Goldman MP, Fitzpatrick RE,
Fader DJ. Cutaneous laser resurfacing. J Am Acad Derma­
tol 1999;41(3 Pt 1):365–389, quiz 390–392

185
Chapter 17 Laser Facial Resurfacing
Discussion by Lawrence S. Bass and Jason N. Pozner
Obtaining excellent results with laser resurfacing
while minimizing the risk of complications requires
careful pretreatment counseling, appropriate laser
parameter selection, and vigilant aftercare. This must
be a conceptual process rather than a fixed set of rules
because of the wide variation in skin types and indi­
cations treated and the diversity in laser technologies
and parameter sets available. Many processes would
work reasonably well; this discussion explains my pre­
ferred approach.
Avoiding Unfavorable Results
and Complications in Laser Facial
Resurfacing
The most important aspect of laser facial resurfacing is
completely controlling exactly what is being done with
the patient’s skin—which products are being used and
the exact care instructions being followed. We do not
permit patients to use any products that we are not
aware of on their skin during the time leading up to the
laser treatment, after consultation, and for a minimum
of 6 weeks, preferably 3 months, after full epithelializa­
tion is obtained. If the examination reveals any prob­
lem in healing, changes can be made in management
with a full understanding of the situation and the typi­
cal issues that may be product-related based on previ­
ous experience.
Similarly, careful instruction on skin care, cleans­
ing, and protection is essential. Patients are discouraged
from any deviation from provided instructions. Often
a seemingly irrelevant variation or patient-initiated
“improvement” can be the start of a significant heal­
ing problem. Attention to these issues allows almost all
problems to be prevented and makes diagnosing and
treating problems easier. In the absence of a well-con­
trolled process, healing problems and adverse outcomes
can abound despite a well-executed laser treatment.
This is similar to hand surgery, for which vigorous com­
pliance to a carefully structured postoperative program
of occupational therapy is a key to excellent outcomes.
Time points for various changes in care, such as
maintenance of topical occlusive ointment, washing
three times daily, or resumption of topical retinoid or
glycolic acid preparations, cannot be readily stated in
numbers or days. The spectrum of laser treatments per­
formed currently varies greatly in the depth and density
of exposure, creating a wide range of healing responses.
With modern ablative treatments, time to epitheliali­
zation varies from 2 to 3 days to as much as 14 days.
Transition from one management step to another de­
pends more on reaching clinical milestones such as full
epithelialization or loss of erythema rather than a spe­
cific point in time.
Recurrent clinical examination by an experienced
provider (ideally the treating surgeon) is essential to
correctly identifying these landmarks, reinforcing the
desired home care management, and maintaining sur­
veillance for emerging complications such as hyperpig­
mentation and nascent hypertrophic scarring.
Preoperative Planning and Patient
Selection
Our only pretreatment requirement is to know specifi­
cally what products the patient uses.
We do not believe pretreatment retinoid use puts
the patient at increased risk of healing difficulty, and
long-term retinoid users tend to heal a day or 2 earlier,
in my experience. Patients who have been on retinoid or
glycolic acid preparations are asked to stop these several
days before the treatment.
Patients who are at high risk for healing difficulties
should not be offered laser treatment; in some cases a
minimal regimen of fractional laser exposure may be
used. This includes patients who have recently taken a
course of isotretinoin. The time before treatment var­
ies from 3 months to 2 years from the cessation of this
therapy. I typically use a 6-month interval, although this
can be modified based on the dose of isotretinoin used
and the number of courses of therapy in the past, each
of which affect the degree of permanent alteration in
the function of adnexal structures.
Active bacterial, viral, or fungal infection in the
treatment area is an absolute contraindication to resur­
facing. Patients with a history of oral herpetic outbreaks
require increased dosing and length of prophylactic
medication before treatment. Keloid formers should also
be avoided. Extensive electrolysis and skin grafts from
previous trauma or tumor reconstruction are relative
contraindications which should not be treated with full-
field resurfacing, although they may be acceptable for
fractional options. The current use of fractional ablative
and nonablative resurfacing to treat hypertrophic scars
and other traumatic and surgical scarring problems il­
lustrates the relative safety of these options. Multiple
previous deep peels with any modality or regional re­
surfacing in dark-skinned individuals are scenarios that
need to be approached with caution, as are individuals
with a history of multiple skin allergies or hypersensi­
tive skin.
Patients who have Fitzpatrick skin types IV to VI
are at increased risk of pigmentary abnormalities and

SECTION IV AESTHETIC SURGERY
186
require preoperative counseling and modified param­
eters. A careful history of previous hyperpigmentation
in reaction to inflammatory stimuli is essential. Patients
who form pigment around wounds, surgical scars, or
insect bites require caution, as do hyperpigmentation
reactions to hormone replacement therapy and preg­
nancy (mask of pregnancy). Any patient with a history
of melasma may have a florid worsening of their condi­
tion, which may take as long as 2 years to fade or may
never be meaningfully controlled with current options.
Prevention of eye or tooth injuries from the laser
and the potential for incineration of surgical drapes
require familiarity with laser safety precautions. Eye
safety when treating the face or periorbital region man­
dates the use of metal corneal shields. Fire risk increases
dramatically when supplemental oxygen is in use, so
this must be discontinued enough in advance of laser
application to allow clearance from the environment
around the face. The surgeon must remain vigilant re­
garding the exposure of drapes, hair, and endotracheal
tubes and laryngeal mask airways.
A detailed review of treatment parameters is be­
yond the scope of this discussion, but parameters must
be specific to the laser hardware selected. Modern laser
technologies do not have generic settings; parameters
suitable for one manufacturer’s fractional carbon diox­
ide (CO2) laser resurfacing device may produce scarring
or a healing delay when used in a competitor’s fractional
CO2 laser resurfacing device despite a comparable safety
record with appropriate device-specific parameters. De­
tailed training by the manufacturer and mentoring from
a physician experienced with the specific device brand
is essential to success.
Postresurfacing Care
Although many programs of post–laser resurfacing care
may work equally well, we have used a very simple pro­
gram that fosters compliance, increases patient com­
fort, and minimizes healing risks.
After treatment, the exposed skin is covered copi­
ously with Aquaphor or petroleum jelly. This is reap­
plied as needed on the day of treatment to minimize
discomfort. Starting the day after treatment, the patient
will wash three to four times daily with a superfatted
soap (e.g., Basis, Aveeno, or Ivory) or with a Cetaphil-
type cleanser. This involves gently lathering the area
with the fingertips, avoiding the use of nails, or with a
gauze pad. The skin is rinsed and patted dry with a clean
towel or gauze, and fresh Aquaphor ointment is applied.
Preferably, the washing is done standing under a gentle
stream of lukewarm water in the shower, which gently
but thoroughly debulks any ointment, exudate, or eschar
that is ready to separate.
Once epithelialization is complete, the patient re­
sumes normal washing and applies a nonmedicated
moisturizer during the day and Aquaphor at night for
another week. Then Aquaphor is discontinued. Differ­
ent petrolatum products have been tried, and despite
their resemblance, Aquaphor has been selected as the
best balance for adequate occlusion. A preparation that
is too heavy will produce a higher rate of acne outbreaks
and milia. Inadequate coverage will increase discomfort
in the early healing period and may promote erythema.
Medication to suppress hyperpigmentation is used
for high-risk patients (Fitzpatrick types IV and higher)
and those manifesting signs of hyperpigmentation start­
ing 1 to 2 weeks after full epithelialization and is con­
tinued for 6 weeks to 3 months depending on response.
Sun exposure needs to be strictly avoided during the
period of erythema and ideally for a month after. This
minimizes the risk of hyperpigmentation and protracted
erythema. Retinoid and glycolic acid preparations may
be resumed 6 to 8 weeks after epithelialization if ery­
thema is largely resolved, but a break-in process is usu­
ally best.
Success in the management of laser resurfacing
complications hinges on early diagnosis and interven­
tion. Even small delays can produce permanent scar­
ring or complications that can require months or years
to manage. Although plastic surgeons are experienced
wound-healing experts, laser resurfacing wounds don’t
visually resemble their surgical counterparts. A differ­
ent set of guidelines is needed to signal trouble. A typi­
cal laser resurfacing wound may have blood or fibrin­
ous debris on the surface and be oozing blood or serum.
Ideally, the wound is moist. Purulence is detectable if
pronounced but sometimes is hard to distinguish from
routine effluvia. Signs and symptoms that reliably in­
dicate complications include increasing redness, pain.
or edema or a previously epithelialized wound that has
reopened. Any of these findings should immediately pro­
duce a careful examination and probably a full spread
of empirical antimicrobial therapy after any necessary
tissue cultures are obtained.
Managing Laser Resurfacing
Complications
Infection
Bacterial
Open treatment of the laser resurfacing wound has
made bacterial infections uncommon. Although rare,
bacterial infections are possible even after nonablative
resurfacing.1 Washing is best performed by flushing
the open areas with a gentle stream of lukewarm wa­

187
Chapter 17 Laser Facial Resurfacing
ter from the showerhead for several minutes three to
five times a day. A superfatted soap or gentle facial skin
cleanser can be applied and then rinsed off. This pro­
cess removes debris, allows eschar to float off without
mechanical trauma, and minimizes bacterial counts
on the wound surface. We have found no advantage
to any other solution for irrigation, good results being
more dependent on frequent, high-volume, gentle la­
vage than on solution content. If a bacterial infection is
suspected, broad-spectrum coverage for gram-positive
skin flora, for example with a second-generation ceph­
alosporin, is a typical first-line approach. Pseudomonas
has also been seen, particularly under closed dressings.
With the rise in incidence of methicillin-resistant
Staphylococcus aureus (MRSA), some consideration must
be given to this possibility. It may be difficult to obtain
a meaningful culture by swabbing the wound surface. If
MRSA is suspected but the treatment was provided in an
office setting, community-acquired MRSA is typically re­
sponsive to doxycycline or trimethoprim/sulfamethoxa­
zole. If the patient was treated in a hospital setting or
works in a health care setting, intravenous vancomycin
or linezolid or rifampin may be needed.
The use of prophylactic antibiotics for laser resur­
facing is controversial. One study has failed to find a re­
duction in infection rate with prophylactic antibiotics.2
Viral
Whereas a clinical bacterial infection is uncommon, vi­
ral infections are not. All patients receive prophylaxis
with acyclovir 800 mg orally three times a day or vala­
cyclovir 500 mg orally twice a day, starting the day be­
fore treatment if there is no prior history of oral herpes
and 3 days before in patients with a prior history. Ther­
apy is continued for 10 days or until the wound is fully
epithelialized, whichever is longer. Freshly healed epi­
thelium after laser resurfacing is still highly susceptible
to herpetic infections. Patients need to be meticulous
about washing their hands before touching the face
and avoiding contact with anyone actively showing a
cold sore. If infection does occur, it typically produces
multiple punched-out lesions across the wound bed of
the associated resurfaced area (Fig. 17D.1). Diagnosis
usually relies on this clinical finding, which is highly
characteristic; however, small ulcerations that are less
well circumscribed are possible. The lesions tend to be
painful or have the typical burning sensation usually
associated with cold sores, although this is not always
distinguishable from the sensation of the wound. Treat­
ment of an active viral infection requires higher doses
(Table 17D.1), and local wound care must be contin­
ued. No fixed dressings can be used in these circum­
stances, only open wound care.
Fungal (Yeast)
The most common fungal infection is caused by Can­
dida yeasts. Affected skin exhibits redness, discharge,
and patchy raised reddish papular areas, often with
whitish or superficial pustules (Fig. 17D.2). Occasion­
ally, fungal infections manifest as perioral fissures that
reopen weeks or months after epithelialization of the
laser resurfaced areas (Fig. 17D.3). Fungal infections
are usually effectively treated with a topical agent such
as nystatin, clotrimazole, or miconazole applied twice
daily. In more severe cases or to prevent excessive
manipulation of the skin surface, fluconazole 100 mg
orally once daily may be given for few doses or up to 1
to 2 weeks.
Table 17D.1 Prophylactic and therapeutic dosing of antiviral agents
Medication
Prophylactic dosing (for 10–14 days)
Therapeutic dosing
Acyclovir
800 mg orally three times daily
800 mg orally five times daily
Famciclovir
250 mg orally twice daily
500 mg orally every 8 hours
Valacyclovir
500 mg orally twice daily
1–2 g orally every 12 hours
Fig. 17D.1 Lesions of the treated areas often indicate infection.
Punched-out circular lesions are typical of herpetic infection.

SECTION IV AESTHETIC SURGERY
188
As a practical issue, initial therapy is commonly a
combination of these treatments to cover all possible
options. Any wound that remains open and is not heal­
ing is likely infected, especially if proper wound care has
been confirmed. Previously closed wounds that reopen,
increasing redness, or increasing discomfort are also
signs of a likely infection. Infectious disease consulta­
tion is always an option if forward progress toward heal­
ing does not resume within several days after initiation
of empirical therapy.
Pigmentary Alterations
Hyperpigmentation
Hyperpigmentation after laser resurfacing is an in­
flammatory process that typically resolves but may
take weeks or months. Hydroquinone 4% cream topi­
cally twice daily may be started 1 to 2 weeks after full
epithelialization if hyperpigmentation is noted. Treti­
noin cream 0.1% topically each night is a good pigment
blender later in treatment and may be started 6 to 8
weeks after resurfacing with a progressive schedule of
application.
Sun avoidance and daily use of sunblock is essen­
tial. A lack of compliance to sun avoidance will doom
all efforts to suppress postinflammatory hyperpigmen­
tation. Resistant cases can be treated with Q-switched
alexandrite or neodymium-doped: yttrium aluminum
garnet (Nd:YAG) lasers (nanosecond pulse widths) or
with the newer picosecond pulse-width lasers if avail­
able. Postinflammatory hyperpigmentation is composed
of melanin pigment that resides superficially and may
be distinguished from melasma, which has a superficial
and deep pigmentary component or more confluent pig­
ment across depths, by using a Wood’s lamp, which will
show fluorescent enhancement for superficial pigment.
Hypopigmentation
Hypopigmentation is a known risk of all laser treat­
ments but is more likely to result in deeper or highly
coagulative treatments. True hypopigmentation is not
merely the removal of accumulated sun damage in the
form of solar lentigines and skin bronzing, which usu­
ally slowly reaccumulates over several months anyway.
If the skin tone is lightened compared with unexposed
body skin, such as the upper inner arm or buttock, then
hypopigmentation has resulted. Fortunately, most hy­
popigmentation with modern resurfacing devices and
settings is partial or mild. However, there are few treat­
ment options. Multiple treatments with excimer lasers
may provide some amelioration of this problem but
require maintenance treatments to preserve the result.
Fractional nonablative laser resurfacing has also been
reported to sporadically produce some mild repigmen­
tation of hypopigmented scars and skin areas when ap­
plied repeatedly.
Acne, Milia, and Hypersensitivity
Heavy occlusive ointment can produce an outbreak
of acne or milia in the first few weeks after epitheli­
alization. This is seen particularly in younger patients
having acne scars treated with resurfacing. Milia,
small whitish or yellowish concretions within the skin
without purulence, result from retention of sebaceous
secretions beneath the skin. A transition away from
heavy ointment to lighter emollient moisturizers is
usually all that is needed. If the outbreak is severe,
glycolic acid, clindamycin pads, Retin-A, or oral tetra­
cycline or doxycycline can be used depending on skin
tolerability to the topical agents. Milia can be unroofed
with a 30-gauge needle.
During the first few months after resurfacing, skin
is typically very sensitive and reactive. Manifesting as
allergic dermatitis or irritant dermatitis, this can be ex­
acerbated by exposure to sensitizing agents in the skin
products used. Allergies to parabens used as a preserva­
tive in skin products or to bacitracin are common. Red­
ness and skin irritation should raise suspicions of a pos­
Fig. 17D.2 Appearance of a common posttreatment fungal in­
fection.
Fig. 17D.3 Perioral fissures, which may be a sign of a fungal
infection.

189
Chapter 17 Laser Facial Resurfacing
sible allergy, which can be treated by discontinuation of
the offending agent along with 1 to 2 weeks of a topical
low-potency steroid cream, such as 1% hydrocortisone
cream, if needed.
Protracted Erythema
The degree and duration of erythema after epitheli­
alization is complete varies based on skin type, the
depth of resurfacing (depth of tissue ablation), and the
degree of coagulation (depth of coagulated tissue un­
derlying the ablated crater). The greater the duration
from the resurfacing treatment to full epithelialization,
the greater the erythema as well. Prevention centers
around good wound care to prevent a healing delay
and good planning with the patient regarding what
duration of erythema is acceptable and how well this
correlates with the aesthetic needs. Patients with deep
rhytids will require some interval of erythema to get
a meaningful improvement in rhytids. Nonetheless,
some patients will have continued erythema signifi­
cantly longer than anticipated. Treatment options in­
clude low-potency steroids like hydrocortisone cream
1% topically twice a day for 1 to 2 weeks and pulsed-
dye laser treatments.
Synechiae
Synechiae in the skin of the lower eyelid can form
from edema and inadequate occlusion when two de-
epithelialized skin edges stick together trapping a fold
of skin underneath. Synechiae are more common with
erbium-doped: yttrium aluminum garnet (Er:YAG) re­
surfacing than with CO2 resurfacing. During early office
visits, usually in the first 2 to 3 weeks, these can be de­
tected by observing a crease in the lower eyelid skin
(Fig. 17D.4a). Synechiae are treated by applying gentle
traction on the skin above and below the crease with
cotton applicators to distract the adherent skin edges.
A bleeding raw surface results (Fig. 17D.4b) and must
be treated with a continuation of heavy occlusive oint­
ment and multiple daily rinsing even if the remainder
of the resurfaced areas have epithelialized.
Ectropion
Ectropion can result from cicatrization of the anterior
lamella structures (Fig. 17D.5). Before laser resurfac­
ing of the eyelids, a careful examination and history for
lid laxity, horizontal excess, and diminished tear pro­
duction should be performed, similar to the appropri­
ate evaluation before blepharoplasty. Diminished tear
production or borderline tear production should warn
the surgeon against deep full-field resurfacing unless
accompanied by lid support procedures, such as can­
thoplasty or canthopexy.
Full-field laser resurfacing should not be performed
in any patient undergoing an anterior approach to the
lid with skin or skin muscle flap blepharoplasty. Trans­
conjunctival blepharoplasty does allow treatment of the
lid skin with resurfacing with similar parameters as a
stand-alone procedure. Usually, mild ectropion will re­
solve over several months with massage of the eyelid
and eye protection with moisturizing drops as needed
during the day and application of moisturizing gel or
ointment or use of a moisture chamber while sleeping.
Referral to an oculoplastic specialist is an option if the
Fig. 17D.4 (a) This crease in the lower lid area can be a syn­
echia. (b) After release, the resulting raw surface requires care­
ful treatment.
a
b
Fig. 17D.5 Ectropion. Scleral show and an effaced lid margin
are evident.

SECTION IV AESTHETIC SURGERY
190
plastic surgeon is not familiar with the surgery for and
management of this problem.
Hypertrophic Scar
Scarring can occur several ways. Anything that results
in the propagation of tissue injury in a broad-based
fashion (not fractional) into the reticular dermis is
likely to heal with a scar. This can result from inappro­
priate parameter selection creating too deep a tissue
injury, infection increasing the depth of tissue necrosis,
or an obsessive picker who mechanically traumatizes
the healing wound. Delayed healing can amplify the in­
flammatory response, resulting in protracted erythema
or a hypertrophic scar in susceptible patients.
Hypertrophic scars are most common after laser re­
surfacing in the perioral, preauricular, or jawline areas.
During follow-up visits, especially in the 2 to 3 weeks
after epithelialization, a nascent hypertrophic scar may
appear as a minimal dermal thickening, papule, or but­
ton of tissue. This is a harbinger of a full-blown hyper­
trophic scar, which can sometimes be aborted with ag­
gressive treatment (Fig. 17D.6).
Vigilance and early treatment will greatly diminish
the magnitude and duration of problems. Twice daily
application of a topical high-potency steroid such as clo­
betasol propionate 0.05%, intralesional injection of ste­
roids (such triamcinolone acetonide) or antimetabolite
antiinflammatories (such as 5-fluoruracil), or treatment
with a pulsed-dye laser are common options. Topical ap­
plication should be discontinued after 2 weeks to pre­
vent skin atrophy. Treatment with pulsed-dye lasers has
also been reported to abort early hypertrophic scarring
and to soften and flatten established hypertrophic scars.
Combined Facioplasty and Full-Face
Laser Resurfacing
Combining treatments with surgery is routine for
plastic surgeons, posing additional challenges com­
pared with stand-alone procedures. Mastery of this
combined approach is essential to achieve global facial
rejuvenation. Early experiences with full-field CO2 re­
surfacing taught surgeons the need for caution when
treating undermined skin and nonface areas like the
neck.3,4 Parameters must be moderated to ensure heal­
ing on a normal time schedule and with a similar in­
cidence of complications to stand-alone procedures.
More recent articles have suggested that resurfacing
can be performed with similar risks and results.5 Care­
ful examination of the articles reveals several impor­
tant distinctions. Fractional resurfacing techniques are
used in many of the more recent articles and are known
to have shorter, more reliable healing and a much lower
incidence of complications.6,7
Scheuer et al7 compared the incidence of complica­
tions and time to healing in three zones of the face af­
ter variable pulse Er:YAG laser resurfacing concomitant
with facioplasty. Central and perioral areas showed no
particular issues. Lateral areas, the areas beneath the fa­
cioplasty flaps, had more healing complications.7
The typical approach used now for full-face laser
resurfacing during rhytidectomy divides the face into
treatment zones (Fig. 17D.7). Central and perioral ar­
eas (zone I) can be treated using typical full-field pa­
rameters. Because most of the deepest rhytids reside in
these areas, a meaningful treatment can be obtained.
Lateral areas must be treated in a graded fashion with
modified parameters. The lateral area, or area beneath
the facioplasty flaps, is at risk of increased complica­
tions because of the interruption of cutaneous circula­
tion produced by undermining. The lateral zone must
be treated with modified parameters and in a progres­
sively lighter fashion (less depth, density, and coagula­
tion) from medial to lateral. A typical pattern is one or
two ablative-only superficial Er:YAG passes or fraction­
ated Er:YAG or CO2 treatment in this zone (zone II), stop­
ping 3 to 5 cm from the preauricular incision (zone III),
which is not resurfaced, creating a subtotal rather than
full-facial laser resurfacing. The lateral zone is exposed
to create pigment and texture blending rather than cor­
rection of deep rhytids. If deep rhytids are present in the
lateral zone, consideration should be given to a second
treatment at a later time or a stand-alone resurfacing
Fig. 17D.6 Hypertrophic scar, before and after treatment.

191
Chapter 17 Laser Facial Resurfacing
treatment. Thin parchment-like skin or thin flaps would
mitigate toward more conservative laser parameters and
a wider untreated area (zone III).
Undermined neck skin should not be exposed, or
to only conservative settings of fractional ablative or
nonablative resurfacing. Neck skin has 1,000-fold fewer
adnexal structures to serve as a reservoir for healing of
full-field resurfacing, which should never be attempted
in undermined skin on the neck.
Although these techniques routinely produce an ap­
proximately comparable healing profile to the two pro­
cedures individually, there clearly is more potential for
complications. A greater incidence of skin loss, epithelial
slough, and delayed healing can be expected if anything
goes amiss during early recovery. For this reason, careful
patient counseling, compliance, and monitoring during
early healing is even more important to a safe result.
Dressings and compression are possible over laser
resurfaced areas during the first 24 hours but are often
omitted for patient comfort and ease of care for the de-
epithelialized skin surface. If a gentle compression dress­
ing is considered essential to facelift management, this
may affect the size of the zone that is resurfaced.
Conclusion
Laser resurfacing is a safe, predictable treatment in the
hands of surgeons who have developed a process for
providing surveillance and management of the result­
ing open wound.
I
I
II
II
III
III
II
III
Fig. 17D.7 Treatment zones I, II, and III.
References
1. Xu LY, Kilmer SL, Ross EV, Avram MM. Bacterial
­infections following non-ablative fractional laser
­treatment: a case series and discussion. Lasers Surg
Med 2015;47(2):128–132
2. Walia S, Alster TS. Cutaneous CO2 laser resurfacing in­
fection rate with and without prophylactic antibiotics.
Dermatol Surg 1999;25(11):857–861
3. Goldman MP, Fitzpatrick RE, Manuskiatti W. Laser
resurfacing of the neck with the Erbium: YAG ­laser.
Dermatol
Surg
1999;25(3):164–167,
discussion
167–168
4. Avram MM, Tope WD, Yu T, Szachowicz E, Nelson JS.
Hypertrophic scarring of the neck following ablative
fractional carbon dioxide laser resurfacing. Lasers Surg
Med 2009;41(3):185–188
5. Wright
EJ,
Struck
SK.
Facelift
combined
with
­simultaneous fractional laser resurfacing: Outcomes
and ­complications. J Plast Reconstr Aesthet Surg
2015;68(10):1332–1337
6. Graber EM, Tanzi EL, Alster TS. Side effects and
­complications of fractional laser ­photothermolysis:
experience with 961 treatments. Dermatol Surg
2008;34(3):301–305, discussion 305–307
7. Scheuer JF III, Costa CR, Dauwe PB, Ramanadham
SR, Rohrich RJ. Laser resurfacing at the time of
­rhytidectomy. Plast Reconstr Surg 2015;136(1):27–38

192
CHAPTER
18

Chemical Peels
Gustavo A. Rubio and Thomas J. Baker
Chemical skin peeling remains among the most common
cosmetic procedures performed by plastic surgeons and
dermatologists. Chemical resurfacing has been safely and
effectively used for decades to rejuvenate facial skin from
the effects of aging and photodamage. Chemical peeling
involves producing a controlled skin injury to promote epi­
dermal regrowth with even melanin deposition to rejuve­
nate the facial skin. They are available in an ever-expanding
variety of formulations that produce superficial, medium,
and deep wounds. Deeper peels are the most effective in
resurfacing skin but are also associated with more compli­
cations and are not appropriate for some patients. Physi­
cians performing chemical peels should be knowledgeable
about the properties, safety profile, and indications of the
different available chemical peeling agents. Excellent re­
sults can be achieved in the treatment of photodamage,
dyschromias, rhytides, and acne with chemical resurfac­
ing in experienced hands. Chemical peels thus remain a
mainstay modality of skin rejuvenation, even in the age of
laser resurfacing. This chapter explores the most common
complications associated with chemical peeling and offers
recommendations for their prevention and management.
Avoiding Unfavorable Results
and Complications of
Chemical Peels
Summary Box

Major
•• Contact dermatitis
•• Hyperpigmentation
•• Hypopigmentation
•• Hypertrophic scarring
•• Infections (bacterial,
fungal, viral)
•• Cardiac arrhythmia
(phenol peels)
•• Laryngeal edema
Minor
•• Milia
•• Persistent erythema
•• Pruritus
•• Ocular injury
Complications of Chemical Peeling

193
Chapter 18 Chemical Peels
Postinflammatory Hyperpigmentation
A history of postinflammatory hyperpigmentation (PIH)
puts patients at higher risk for this complication after chem­
ical peeling.1,4,5 Patients should be counseled appropriately
regarding this possible side effect. Patients with darker skin
types (Fitzpatrick IV–VI) have a higher tendency to develop
PIH.1,4 Medium and deep chemical peeling pose a higher risk
for undesirable pigmentary changes than superficial peels.
Patients at higher risk for PIH should undergo preoperative
skin conditioning with bleaching agents, as described in the
next section. Strict sun precautions must also be followed to
decrease the risk of hyperpigmentation.
Darker Skin Types
Fitzpatrick skin types IV to VI are generally at increased
risk for unfavorable results after chemical peeling.1,3 The
most common side effects include pigmentary changes
(transient hyperpigmentation or permanent hypopigmen­
tation) and abnormal wound healing with potential scar­
ring. These patients are best treated with superficial peels,
or medium peels in carefully screened patients.3
Isotretinoin Use
Recent oral isotretinoin use before chemical resurfacing
can result in severe hyperpigmentation and hypertrophic
scarring because of isotretinoin’s inhibitory effects on seba­
ceous gland secretion, which is necessary for normal wound
healing.6 The current recommendation is to stop taking oral
isotretinoin at least 6 months before any skin resurfacing
procedure.5 Skin should be examined for return of normal
oil production before attempting chemical peeling.1
Photosensitizing Drugs
The medication history should be recorded with special
attention to drugs known to have photosensitizing effects,
such as estrogen-containing drugs (hormone replacement
therapy, oral contraceptives) and nonsteroidal anti-inflam­
matory drugs (NSAIDs).1,3 These drugs should be stopped if
clinically appropriate before chemical peeling to decrease
the risk of postoperative hyperpigmentation.
Unrealistic Expectations or Noncompliant
Patients
Details regarding the procedure, prepeel and postpeel care,
signs and symptoms to expect postoperatively, and realistic
expectations of results and possible complications should
be thoroughly discussed with patients. Patients should
have their questions and concerns addressed properly. Phy­
sicians must screen patients whom they suspect will not be
compliant with the necessary regimen to ensure optimal
results and prevent complications.
Preoperative Planning and Patient
Selection
Patient Selection
Achieving desired results and avoiding complications with
chemical skin resurfacing begins with proper patient se­
lection. Patients should undergo a thorough history and
physical examination to identify risk factors for unfavor­
able results. The indications for chemical peeling should be
carefully reviewed with the patient, and realistic expecta­
tions should be discussed in detail. Certain patient risk fac­
tors and contraindications exist for facial resurfacing with
chemical peeling.
Sun Exposure and Occupation
A history of sun exposure and outdoor occupations should
be reviewed with every patient. Patients must adhere to
strict sun precautions starting 6 weeks before the peel and
continuing postoperatively. Use of broad-spectrum sun­
screens (SPF 30) and sun avoidance is critical to preventing
undesirable effects such as postinflammatory hyperpig­
mentation, hypopigmentation, persistent erythema, and
scarring.1 Patients who are not able or willing to adhere to
this regimen will be at high risk for adverse outcomes and
should not undergo facial chemical peeling.
Infections
Active bacterial, fungal, or viral infections are an absolute
contraindication to chemical peeling. Appropriate treat­
ment should be completed before planning resurfacing
procedures. In addition, patients with a history of herpes
labialis are at increased risk of an outbreak postoperatively,
which may result in abnormal wound healing and perma­
nent scarring.2 All patients undergoing chemical peeling
should be given antiviral prophylaxis. Patients with a his­
tory of herpes outbreaks should be followed closely and
must adhere to antiviral prophylaxis.
Inflammatory Dermatoses
Patients with a history of atrophic dermatitis, psoriasis, or
other dermatologic conditions should be screened carefully
before chemical resurfacing is offered.3 These conditions
can be exacerbated with chemical resurfacing.
Abnormal Wound Healing
Patients with a history of abnormal wound healing, includ­
ing hypertrophic scarring or keloid formation, are at in­
creased risk for poor healing and scarring after chemical re­
surfacing. These patients should be screened carefully and
a more conservative depth of peel should be considered to
minimize the risk of postoperative scarring.

SECTION IV AESTHETIC SURGERY
194
are instructed to wash their face with mild soap and wa­
ter on the night before and on the morning of the proce­
dure. Cosmetics should not be applied on the day of the
­procedure.
Application of Chemical Peel
Superficial Peels
The most common superficial peeling agents include gly­
colic acid (30 to 70%), Jessner’s solution, resorcinol (40 to
50%), and lower concentrations of TCA (10 to 30%). The
face should be cleansed with soap and water, followed by
degreasing with acetone.3,16 Petroleum gel is applied to the
inner canthi and nasolabial folds to protect from accidental
spillage. Peels are applied in cosmetic units using a cotton-
tipped applicator, usually starting with the forehead (Fig.
18.1). The peel is “feathered” at edges such as the mandibu­
lar border to prevent lines of demarcation with surround­
ing skin.1 Glycolic acid peels require neutralization with
10 to 15% sodium bicarbonate solution after the desired
length of application.3 TCA peels are applied until an even
frost appears and can be neutralized with cold water. Cool
saline compresses can be applied afterward to reduce in­
flammation and discomfort.
Medium-Depth Peels
Products such as 30 to 50% TCA, 70% glycolic acid, and sev­
eral combination peels (e.g., 35% TCA with Jessner’s solu­
tion) can achieve penetration into the upper reticular der­
mis. Medium-depth peels are typically used to treat Glogau
category I to III skin damage16 (Fig. 18.2). Care should be
taken when mixing and handling peel solutions to ensure
that the desired concentration is achieved. Other precau­
tions include having saline flushes available in case of
­accidental spillage into the eyes and avoiding passing any
solutions over the face.
Systemic Disease
Patients undergoing deep chemical peels with phenol
should be evaluated for systemic diseases. Phenol has been
associated with a risk of cardiac arrhythmias, and patients
with cardiac, renal, or liver disease are at increased risk
of systemic toxicity and should not undergo deep phenol
peeling.7,8 Patients should be screened with appropriate
preoperative laboratory tests and electrocardiogram dur­
ing evaluation for deep phenol peeling.9
Pregnancy
In general, elective cosmetic procedures including chemical
peeling are delayed until after delivery in pregnant patients.
Certain skin conditions such as melasma appear during
pregnancy for which patients may seek treatment. In ad­
dition, patients may undergo chemical peeling during their
first trimester before they are aware of their pregnancy.
There is a lack of clinical trials investigating the safety of
chemical peeling during pregnancy.10 Salicylic acid (also
found in Jessner’s solution) is a U.S. Food and Drug Admin­
istration (FDA) pregnancy category C drug. Aspirin is safe
during pregnancy and topical salicylic acid is available over
the counter without any adverse events reported. How­
ever, its safety as a chemical peel during pregnancy has not
been investigated. Topical trichloroacetic acid (TCA) (85%)
has been safely used during pregnancy for the treatment
of genital condylomas.11 TCA has minimal systemic ab­
sorption and is theoretically safe as a chemical peel during
pregnancy; however, there is a lack of studies examining its
safety. Moreover, high doses of TCA (1,000 mg/kg/day) have
been reported to cause intrauterine growth retardation.12
Deep chemical peeling requires intravenous sedation
with cardiac monitoring (phenol-based formulations) and
should be avoided during pregnancy because of the lack
of evidence-based recommendations. Given the paucity of
safety trials for chemical peels, these elective cosmetic pro­
cedures should be delayed until after pregnancy.
Technique
Preparation
Preoperative planning with careful individualized selec­
tion of the peeling agent and concentration are critical to
ensuring optimal outcomes. Patients should be given de­
tailed instructions regarding their prepeel regimen. “Prim­
ing” the skin with bleaching agents such as hydroquinone
2% or tretinoin 0.0025% is started 2 to 4 weeks before the
procedure to promote uniform peel penetration and reduce
the risk of undesired pigmentary changes.3,13,14 Patients
should exercise sun precautions, including daily use of
broad-spectrum sunscreen. Antiviral prophylaxis should be
started 1 to 2 days before peeling and be continued until
­reepithelialization is complete in 7 to 10 days.3,15 Patients
Fig. 18.1 Careful chemical peel application with a cotton-tipped ap­
plicator. Peels are applied in cosmetic units, usually beginning with
the forehead.

195
Chapter 18 Chemical Peels
toxicity, including cardiac arrhythmias. Patients should be
monitored for at least 1 to 2 hours postoperatively.
Postoperative Care
Proper wound care after chemical peeling is essential to
ensure adequate healing and optimal results. In the im­
mediate postpeel period, patients should only use mild
soap to clean their face. It is imperative that patients avoid
scratching, peeling, or picking at their skin to prevent
­mechanical trauma and poor results. Cold compresses,
calamine solution, and antihistamines may help reduce
itching and burning.16 During the reepithelialization period
(7–10 days), topical agents should be withheld because
of the risk of irritant dermatitis. After reepithelialization,
sunscreen and mild moisturizers are restarted. Continued
sun precautions are critical at this stage to prevent uneven
Deep Peels
Deep chemical peels provide the best results for treating
severely photodamaged skin (Glogau categories III–IV) in
appropriate patients (Fig. 18.3). Formulations that achieve
deep peels include classic Baker-Gordon’s formula, 50%
TCA, and combination peels with lower concentrations of
phenol or TCA, including Hetter’s croton oil–phenol for­
mulation.16–18 The risk of adverse outcomes is greatest in
this category of chemical peels. Monitored anesthesia care
with continuous vital sign and cardiac monitoring pro­
vides the safest setting for deep chemical peeling. Phenol
peels should be applied slowly, with a 10- to 15-minute
pause between cosmetic units to minimize systemic toxic­
ity.19 Operating suites are adequately ventilated to remove
­phenol fumes. Intravenous hydration is also recommended
to prevent increased systemic levels of phenols and prevent
Fig. 18.2 A patient with mild photoaging (Glogau I) before (a) and 1 year after (b) medium-depth chemical peel (trichloroacetic acid 35%).
a
b
Fig. 18.3 Optimal results with deep chemical peels are achieved with lighter skin types (Fitzpatrick types I–II). This patient with deep facial
rhytids preoperatively (a) is shown 1 year after (b) full-face resurfacing with a phenol peel.
a
b

SECTION IV AESTHETIC SURGERY
196
the resurfaced area without skin thickening, then patients
may be reassured that it will resolve spontaneously. Skin
induration in the setting of persistent postpeel erythema is
a warning sign for the development of permanent scarring.
Patients should be treated with topical corticosteroids; sys­
temic and intralesional steroids may be required in certain
cases.1 Pain, burning, or pruritus along with erythema may
indicate the development of contact dermatitis, irritant
dermatitis, or infections.
Contact Dermatitis
Exposure to allergens and irritants from commonly used
topical agents may result in contact dermatitis after chemi­
cal peeling. Type IV delayed hypersensitivity reactions af­
ter chemical peeling are uncommon and result from loss
of the epidermal protective barrier, exposing the dermis to
antigens.5 Although rare, they typically develop during the
reepithelialization process but may present up to 4 weeks
after peeling. Topical antibiotics, cleansers, moisturizers,
and even sunscreens have been implicated in allergic re­
actions after skin resurfacing with chemical peeling.1,5
­Irritant contact dermatitis is more common than allergic
reactions and may occur during reepithelialization or in
newly epithelialized skin. Irritants may include a variety
of topical agents such as tretinoin, glycolic acid, bleaching
agents, fragrances, and other common ointments.1,5 It is
thus important to counsel patients not to start any topi­
cal products other than the prescribed regimen. Patients
may experience burning, pruritus, prolonged erythema,
swelling, and skin eruptions. The presentation of contact
dermatitis may be indistinguishable from infections and
thus cultures are necessary to differentiate the two. Dis­
continuation of all possible offending agents is the first
and most important step in management. Cool compresses
pigmentary changes. Patients should be followed closely to
ensure proper wound care and detect complications early
to implement appropriate treatment.
Postoperative Complications
Pruritus
Patients may experience pruritus during the reepithelial­
ization process after facial chemical peeling. Patients should
be closely monitored to detect any warning signs associated
with pruritus, such as persistent erythema or vesiculopus­
tules, which may indicate a dermatitis or skin infection
requiring prompt treatment to prevent postinflammatory
hyperpigmentation or scarring. Cold compresses and cala­
mine lotion can be helpful in reducing pruritus.3 A short
course of topical steroids and oral antihistamines may be
required to reduce itching. Patients should be counseled
not to scratch their skin after peeling to prevent mechani­
cal trauma that may take weeks to resolve.
Persistent Erythema
Erythema is a normal characteristic of the healing phase
after chemical peeling (Fig. 18.4). The duration of the ery­
thema depends on the depth of the peel. Superficial and
medium-depth peels usually produce erythema for 7 to 14
days, but erythema can last up to 3 months after deep peels.
Erythema that persists beyond the normal course can be
a sign of delayed healing and potential scarring.1,4 Topical
tretinoin and oral isotretinoin use in the perioperative pe­
riod has been implicated as a cause of persistent erythema
and scarring, particularly in medium and deep peels.1,6
Certain individuals may have genetic susceptibility to per­
sistent erythema. If the erythema is consistent throughout
Fig. 18.4 Normal desquamation and erythema observed during reepithelialization 3 days (a) and 6 days (b) after a medium-depth chemi­
cal facial peel (35% trichloroacetic acid).
a
b

197
Chapter 18 Chemical Peels
After chemical peeling, strict sun precautions are neces­
sary to prevent and treat hyperpigmentation. Patients can
be reassured that the hyperpigmentation is typically tran­
sient even without treatment. Topical bleaching agents can
be used after reepithelialization, but excessive or prolonged
use can cause irritant dermatitis.1,5 These agents include hy­
droquinone, kojic acid, retinoic acid, azelaic acid, and ascor­
bic acid.1,20 In some resistant cases, superficial peeling with
glycolic acid (30 to 40%) or salicylic acid (30%) is indicated
to hasten resolution.1,5
Hypopigmentation
Hypopigmentation is a normal phenomenon of chemical
skin resurfacing as old photodamaged skin is replaced by
lighter skin. Darker-skinned patients (Fitzpatrick types III–
VI) may also experience transient hypopigmentation while
their skin regains its pigment.5 True permanent hypopig­
mentation is a major complication seen with deep chemi­
cal peels.1,4 It is usually a late complication that can become
apparent months after skin resurfacing5 (Fig. 18.5). Perma­
nent hypopigmentation is believed to be secondary to loss
of melanocyte function or dermal fibrosis with deep peels
that reach the reticular dermis.1,4,5 Darker-skinned patients
undergoing medium or deep chemical peeling are at risk
for this complication. Typically this is most apparent at the
jaw border where a line of demarcation is seen between
the resurfaced facial skin and the neck (Fig. 18.6).
Strategies to minimize the risk of permanent hypopig­
mentation are limited. Use of broad-spectrum sunscreen
and sun avoidance before and after the peel are important
in preventing any undesired pigmentary changes. Careful
selection in both the patient and depth of peel are the most
important determinants in mitigating the risk of perma­
nent hypopigmentation. For patients with darker skin types
(Fitzpatrick III or greater), a more conservative depth of peel
should be strongly considered. “Feathering” the edges of the
are ­helpful in ­relieving symptoms of pain and itching. Oral
antihistamines are used if allergic dermatitis is suspected.
Judicious use of topical corticosteroids is indicated to de­
crease inflammation and prevent severe irritation that can
lead to delayed wound healing and hypertrophic scarring.5
Hyperpigmentation
Hyperpigmentation is among the most common side ef­
fects of facial chemical peeling, occurring in up to 30% of
patients.1,4,5 It may become apparent as early as the first
week after peeling, or up to 2 to 3 months later.4 In most
cases the hyperpigmentation is transient, but long-term
sequelae can result if not treated appropriately. Patients
should be made aware that nevi and solar lentigines might
become more prominent in the initial postpeel period.1 Pa­
tients with darker skin types (Fitzpatrick types IV–VI) and
those with baseline dyschromia, melasma, or a history of
PIH are at an increased risk of this complication.1,4,5,9,20
Postoperative hyperpigmentation may also occur in
lighter skin types (Fitzpatrick types I–III) with excessive sun
exposure before or after chemical peeling.1,5 Certain photo­
sensitizing drugs including NSAIDs and oral contraception
may increase the risk of PIH. As with most chemical peel
complications, deeper peels are associated with a higher risk
for undesirable pigmentary side effects. Careful patient se­
lection and medical history is important in identifying those
patients with increased risk for hyperpigmentation. Preven­
tion includes a strict regimen of sun exposure avoidance and
use of broad-spectrum sunscreen 6 weeks (or longer in high-
risk patients) before the peel.5
Preconditioning with bleaching agents such as hydro­
quinone or tretinoin starting 2 to 4 weeks before the peel
is recommended in higher risk groups, especially patients
with darker skin types.1,5,13,14,20 In two separate small trials,
2% hydroquinone was more effective in preventing postpeel
hyperpigmentation than 0.0025% tretinoin.13,14
Fig. 18.5 Hypopigmentation with a perioral demarcation line pres­
ent 1 year after partial resurfacing of the perioral region.
Fig. 18.6 Line of demarcation present below the neckline in this
patient more than 1 year after deep chemical resurfacing with a
phenol peel.

SECTION IV AESTHETIC SURGERY
198
Bacterial
The incidence of bacterial infections after resurfacing pro­
cedures reported in the literature range from 4 to 12%.15
TCA and phenol peels are bactericidal, and thus bacterial
infections are rare with their use. Streptococcal and staph­
ylococcal infections are the most common. Pseudomonal
and Escherichia coli infections have also been reported.1,3,16
Antibacterial prophylaxis for skin resurfacing procedures
has been advocated in the literature,21 but there have been
no large randomized controlled trials to support this rec­
ommendation.
Careful attention to wound care is important in reducing
the incidence of bacterial infections. Use of thick occlusive
ointments and prolonged use of biosynthetic membranes
have been implicated in bacterial infections.1 Acetic acid
(0.25%) soaks and gentle débridement of crusts aid in pre­
venting and treating bacterial infections.1,16 Bacterial, viral,
and fungal infections and dermatitis may present similarly
after chemical peeling. If infection is suspected, Gram stains
and cultures should be obtained for diagnosis and to guide
antimicrobial therapy. Early detection and treatment of bac­
terial infections with topical and systemic antibiotics is es­
sential to prevent permanent scarring.
Viral
Reactivation of herpes simplex virus-1 (HSV-1) is a com­
plication common to all skin resurfacing modalities in­
cluding laser, dermabrasion, and chemical peeling. HSV-1
infection in this setting presents similarly to bacterial and
fungal ­infections, typically by days 3 to 10 after the pro­
cedure. ­Patients may experience pain, burning, or itching
and vesiculopustules, ulcerations, or persistent erythema
(Fig. 18.7). Infection in the setting of recent chemical peel­
ing can result in delayed wound healing and permanent
scarring. Patients with an active herpes outbreak should
facial peel with a lower concentration peel has been advo­
cated to minimize these lines of demarcation.1 Subsequent
superficial chemical peeling can be used to attempt to even
out the pigmentary changes at the edges from a prior deep
peel.5 In most cases, treatment is difficult. Continued use of
sunscreen and makeup may be the only options for patients.
Scarring
Permanent scarring is the most feared complication of skin
resurfacing procedures. Fortunately, it is a rare complica­
tion for experienced operators. It almost exclusively occurs
with deep peeling applications.4,5 Scarring may develop as
atrophic scars, hypertrophic scars, or keloids.5 The areas of
the face most prone to scarring after resurfacing include
the perioral area, periorbital area, chin, and mandibular
border.4,5
Several risk factors have been implicated in the devel­
opment of hypertrophic scarring. Patient factors that may
increase the risk of scarring after resurfacing include a his­
tory of keloid formation or hypertrophic scarring, smoking,
and thin skin, such as is seen in older persons.1 Recent use of
oral isotretinoin has been shown to increase the risk of post­
operative scarring, even in superficial chemical peeling.1,5,6
Oral isotretinoin should be stopped 6 to 12 months before
chemical peeling.5 Recent facial procedures such as laser hair
removal and facial surgery with significant skin undermin­
ing may also increase the risk of scarring after resurfacing.1
Patients should also be warned to avoid scratching, because
the mechanical trauma to the wound may result in abnor­
mal healing and scarring. Recognition of the early signs of
scarring and appropriate treatment affords the only chance
of avoiding this dreaded complication.
Patients who develop contact dermatitis, infections,
or persistent erythema should be treated appropriately to
prevent subsequent hypertrophic scarring. Patients with
delayed wound healing should be followed closely and
­examined for development of dermal thickening. Topical
corticosteroids should be started at the first sign of skin
­induration.1,5 Silicone gel sheeting should also be applied
daily. Intralesional steroids, such as triamcinolone injec­
tions, can be used in increasing doses in cases that do not
respond to topical steroids.1,4,5 Pulsed-dye laser therapy is
an option in more severe cases of postoperative hypertro­
phic scarring.1
Infections
All skin resurfacing procedures including chemical peeling
result in temporary loss of the protective epidermal barrier,
increasing the risk of infection. Patients may develop bacte­
rial, fungal, or viral infections in the postoperative period.
Signs and symptoms of infection in this setting include de­
layed wound healing, persistent erythema, folliculitis, ul­
ceration, superficial erosions, crusting, discharge, pain, and
itching.1,16 Patients should be followed closely after chemi­
cal peeling to detect and treat infections promptly to pre­
vent delayed wound healing and permanent scarring.
Fig. 18.7 Erythema and vesiculopustules from a herpes simplex viral
outbreak after full-face medium-depth chemical peeling.

199
Chapter 18 Chemical Peels
blockages of the sebaceous gland orifices during the heal­
ing process.1,25 Milia may be more common after skin re­
surfacing in patients with thicker skin.25 Inappropriate or
excessive use of ointments in the postoperative period may
also increase the risk of developing milia. Small milia often
resolve spontaneously with gentle cleansing of the skin.
Larger or persistent milia should be opened with a fine
needle and the contents gently expressed. Patients should
be counseled to avoid attempting to mechanically express
or brush the milia, which may lead to abnormal wound
healing.
Cardiotoxicity with Phenol Peels
Cardiac arrhythmias have been reported in up to 23% of
patients undergoing full-face peeling with phenol-based
solutions.7 Arrhythmias can include benign tachycardia,
premature ventricular contractions, bigeminy, or atrial and
ventricular tachycardia.7 Although phenol has been shown
to be directly cardiotoxic in animal studies, it is unclear
whether the cardiac arrhythmias seen during peeling are
caused by the procedure or are incidental. However, car­
diac monitoring during peeling and 1 to 2 hours postopera­
tively is recommended.8,26 Several authors have advocated
prophylactic use of antiarrhythmics such as intravenous
lidocaine and beta-adrenergic blocking agents (β-blockers)
before deep phenol-based peeling, although there are no
controlled trials to support this recommendation.8,27 Lan­
dau8 reported a 6.6% incidence of cardiac arrhythmias with
the use of prophylactic propranolol. Of patients with ar­
rhythmias, 66% required an intravenous antiarrhythmic for
control; the rest were self-limited.
Phenol is partially metabolized in the liver and mostly
excreted by the kidney. Animal studies have also shown
that intravenous hydration and diuresis decreases the sys­
temic levels of phenol and decreases cardiac toxicity.26
not undergo resurfacing procedures until the infection is
treated and has resolved. Those with a history of oral her­
pes outbreaks are at an increased risk of a postoperative
outbreak and should be treated with caution. Most adults
are seropositive for HSV-1, and approximately 20 to 40%
develop recurrent herpes labialis.15 Therefore any patient
undergoing chemical peeling or other skin resurfacing pro­
cedures is at risk for latent HSV reactivation and its adverse
outcomes.
The true incidence of HSV-1 infection in patients not
given antivirals prophylactically before skin resurfacing is
not known, but reports range from 3 to 9.4%.15 In one study
involving 907 patients undergoing carbon dioxide (CO2) la­
ser resurfacing, the rate of HSV-1 infection was 3% in un­
treated patients and less than 1% in those given acyclovir
prophylaxis.22 In another study, patients were randomized
to receive 500 mg of valacyclovir twice daily starting ei­
ther 1 day before or on the day of the resurfacing procedure
(laser, dermabrasion, chemical peeling, or combination) for
a total of 14 days, and there were no reports of HSV-1 in­
fection out of 84 cases.2 Given the risk of permanent scar­
ring and the safety profile of antiviral agents, administering
antiviral prophylaxis to all patients undergoing resurfacing
procedures including chemical peeling is common,2 despite
the lack of placebo-controlled trials. Recommended pro­
phylactic regimens in the literature are based on anecdotal
­evidence and small prospective trials. The most effective an­
tiviral, dosage, duration, and timing have not been investi­
gated in large randomized controlled trials. However, two of
the largest prospective trials demonstrated that oral valacy­
clovir given 500 mg twice daily on the day of procedure or
before and continued for 14 days postoperatively was 100%
effective in preventing HSV-1 outbreaks.15 Oral famciclovir
given 125 mg to 250 mg twice daily for 5 to 14 days postop­
eratively has also been proven effective.23,24
Fungal
Fungal infections are less common after skin resurfacing,
with reported incidence between 1.8% and 2.2%.15 The
most common pathogen is Candida albicans15,16 (Fig. 18.8).
Diabetes, recent use of oral antibiotics, and prolonged use
of topical steroids appear to increase the risk of fungal in­
fections after chemical peeling.1 Fungal infections may be
suspected when superficial pustules or white discharge
is present, although they may be indistinguishable from
other infections or dermatitis, and thus fungal cultures and
stains should be obtained for confirmation. Treatment with
systemic antifungals should be implemented as early as
possible to help prevent sequelae. Administration of pro­
phylactic antifungals for prevention of fungal infection in
chemical peeling has not been investigated in randomized
controlled trials.
Milia
Small white inclusion cysts called milia are common in the
first few weeks after chemical peels. They are the result of
Fig. 18.8 Postoperative Candida albicans infection can present with
persistent erythema similar to other infectious agents or contact
dermatitis.

SECTION IV AESTHETIC SURGERY
200
3 to 5 days.28,29 Management included antibiotic eye drops,
artificial tears, and NSAIDS for pain control and to reduce
inflammation.
Laryngeal Edema
Laryngeal edema is an extremely rare complication of phe­
nol chemical peeling that has only been reported in one
series with three index cases (1.2%).30 These patients devel­
oped stridor, hoarseness, and tachypnea within 24 hours
of the procedure. Warm mist therapy was provided and
in all cases the signs of laryngeal edema resolved within
24 to 48 hours without more invasive measures. To our
knowledge, this is the only report of laryngeal edema af­
ter phenol chemical peeling. The underlying mechanism
of this complication is unclear, but the authors suspected
that laryngeal irritation developed from a combination of
heavy smoking and exposure to phenol fumes.30 The au­
thors anecdotally reported that after implementing a regi­
men including a diuretic, antihistamine, and NSAID, they
did not encounter any more cases of laryngeal edema after
phenol peel.30
Conclusion
Chemical peeling remains a time-tested, cost-effective, and
safe modality for skin resurfacing. Appropriately selected
patients can benefit from the improved appearance and
texture provided by chemical peeling to rejuvenate their
facial skin. Excellent results with minimal side effects
can be achieved by following a few important guidelines.
Most serious complications from chemical peeling can
be avoided by appropriate patient selection and choice of
peeling agent. High-risk patients such as those with darker
skin types should be carefully screened and a conservative
peeling regimen should be selected to avoid unfavorable
results. Moreover, proper preoperative and postoperative
care is critical to ensuring optimal results and preventing
complications. Patients must adhere to a strict wound care
regimen with particular emphasis on sun precautions. Pa­
tients should be followed closely after chemical peeling.
Early detection of complications allows timely manage­
ment that can prevent serious and permanent adverse out­
comes such as hypertrophic scarring.
­Therefore some authors recommend the use of continuous
intravenous hydration throughout the procedure and the use
of diuretics.27 In addition, the incidence of cardiac arrhyth­
mias appears to be associated with the total area of phenol
application and the timing of application. The study by Price
in 199019 found that slower application of the phenol peel by
pausing 10 to 15 minutes between cosmetic units decreased
the incidence of cardiac arrhythmia to 10%.
Given the paucity of studies to support recommenda­
tions regarding strategies to prevent cardiac arrhythmias,
it is important to screen patients for underlying conditions
such as cardiac, renal, or liver disease that may increase
their risk of adverse cardiac events. We also advocate car­
diac monitoring, adequate room ventilation, slow applica­
tion over at least 60 minutes, and intravenous hydration to
minimize cardiac arrhythmias during deep phenol peels.
The use of prophylactic antiarrhythmics and diuretics need
to be further investigated before formal recommendations
are made. Despite this potential complication, phenol-based
deep peels remain a safe and effective option for skin re­
surfacing.
Ocular Complications
Ophthalmic injuries caused by accidental spillage of chemi­
cals during peels have been reported.28,29 Resultant corneal
damage is usually temporary, with no reported cases of
long-term adverse outcomes. Care must be taken during
the application of chemical peels. Protection of the perior­
bital region with petrolatum ointment or gel and avoiding
over-soaking cotton-tipped applicators with peeling solu­
tion can decrease the risk of accidental spillage. Inevitably,
small amounts of peeling solution may enter the eyes, but
the solution is diluted by tears without any adverse effect.
In cases of larger spillage of chemicals into the eyes, pa­
tients may report pain, burning, and a foreign-body sen­
sation, along with excessive tearing and redness.28 Prompt
flushing of the eyes with an isotonic solution is critical,
because time is a factor in the degree of injury. Attempt­
ing to neutralize the acidic peeling solution can result in
an exothermic reaction and worsen the injury. Timely oph­
thalmology consultation is advisable. In the two reported
cases of ocular injury caused by TCA spillage, patients
were successfully treated with complete resolution in
References
1. Nikalji N, Godse K, Sakhiya J, Patil S, Nadkarni N. Compli­
cations of medium depth and deep chemical peels. J Cu­
tan Aesthet Surg 2012;5(4):254–260
2. Gilbert S, McBurney E. Use of valacyclovir for herpes sim­
plex virus-1 (HSV-1) prophylaxis after facial resurfacing:
a randomized clinical trial of dosing regimens. Dermatol
Surg 2000;26(1):50–54
3. Khunger N; IADVL Task Force. Standard guidelines of care
for chemical peels. Indian J Dermatol Venereol Leprol
2008;74(Suppl):S5–S12
4. Camacho FM. Medium-depth and deep chemical peels. J
Cosmet Dermatol 2005;4(2):117–128
5. Zhang AY, Obagi S. Diagnosis and management of skin re­
surfacing-related complications. Oral Maxillofac Surg Clin
North Am 2009;21(1):1–12
6. Gerber PA, Kukova G, Bölke E, Homey B, Diedrichson E.
Severe hyperpigmentation and scarring following gly­
colic acid peel treatment in combination with low-dose
isotretinoin. Eur J Med Res 2014;19:60
7. Truppman ES, Ellenby JD. Major electrocardiographic
changes during chemical face peeling. Plast Reconstr Surg
1979;63(1):44–48

201
Chapter 18 Chemical Peels
19. Price NM. EKG changes in relationship to the chemical
peel. J Dermatol Surg Oncol 1990;16(1):37–42
20. Callender VD, St Surin-Lord S, Davis EC, Maclin M. Postin­
flammatory hyperpigmentation: etiologic and therapeu­
tic considerations. Am J Clin Dermatol 2011;12(2):87–99
21. Manuskiatti W, Fitzpatrick RE, Goldman MP, Krejci-Papa N.
Prophylactic antibiotics in patients undergoing laser resur­
facing of the skin. J Am Acad Dermatol 1999; 40(1):77–84
22. Roberts TL III, Weinstein C, Alexandrides JK, Yokoo KM.
Aesthetic CO(2) laser surgery: evaluation of 907 patients.
Aesthet Surg J 1997;17(5):293–303
23. Bisaccia E, Scarborough D. Herpes simplex virus prophy­
laxis with famciclovir in patients undergoing aesthetic
facial CO2 laser resurfacing. Cutis 2003;72(4):327–328
24. Wall SH, Ramey SJ, Wall F. Famciclovir as antiviral pro­
phylaxis in laser resurfacing procedures. Plast Reconstr
Surg 1999;104(4):1103–1108, discussion 1109
25. Spira M, Gerow FJ, Hardy SB. Complications of chemical
face peeling. Plast Reconstr Surg 1974;54(4):397–403
26. Wexler MR, Halon DA, Teitelbaum A, Tadjer G, Peled IJ.
The prevention of cardiac arrhythmias produced in an an­
imal model by the topical application of a phenol prepa­
ration in common use for face peeling. Plast Reconstr Surg
1984;73(4):595–598
27. Botta SA, Straith RE, Goodwin HH. Cardiac arrhythmias in
phenol face peeling: a suggested protocol for prevention.
Aesthetic Plast Surg 1988;12(2):115–117
28. Fung JF, Sengelmann RD, Kenneally CZ. Chemical in­
jury to the eye from trichloroacetic Acid. Dermatol Surg
2002;28(7):609–610, discussion 610
29. Ozturk MB, Ozkaya O, Karahangil M, Cekic O, Oreroğlu AR,
Akan IM. Ocular complication after trichloroacetic acid peel­
ing: a case report. Aesthetic Plast Surg 2013;37(1): 56–59
30. Klein DR, Little JH. Laryngeal edema as a complication of
chemical peel. Plast Reconstr Surg 1983;71(3):419–420
8. Landau M. Cardiac complications in deep chemical peels.
Dermatol Surg 2007;33(2):190–193, discussion 193
9. Anitha B. Prevention of complications in chemical peel­
ing. J Cutan Aesthet Surg 2010;3(3):186–188
10. Lee KC, Korgavkar K, Dufresne RG Jr, Higgins HW II. Safety
of cosmetic dermatologic procedures during pregnancy.
Dermatol Surg 2013;39(11):1573–1586
11. Schwartz DB, Greenberg MD, Daoud Y, Reid R. Genital con­
dylomas in pregnancy: use of trichloroacetic acid and laser
therapy. Am J Obstet Gynecol 1988;158(6 Pt 1): 1407–1416
12. Costet N, Garlantézec R, Monfort C, et al. Environmental
and urinary markers of prenatal exposure to drinking wa­
ter disinfection by-products, fetal growth, and duration
of gestation in the PELAGIE birth cohort (Brittany, France,
2002-2006). Am J Epidemiol 2012;175(4):263–275
13. Nanda S, Grover C, Reddy BS. Efficacy of hydroquinone
(2%) versus tretinoin (0.025%) as adjunct topical agents
for chemical peeling in patients of melasma. Dermatol
Surg 2004;30(3):385–388, discussion 389
14. Garg VK, Sarkar R, Agarwal R. Comparative evaluation of
beneficiary effects of priming agents (2% hydroquinone
and 0.025% retinoic acid) in the treatment of melasma
with glycolic acid peels. Dermatol Surg 2008;34(8):1032–
1039, discussion 1340
15. Gilbert S. Improving the outcome of facial resurfacing—
prevention of herpes simplex virus type 1 reactivation. J
Antimicrob Chemother 2001;47(Suppl T1):29–34
16. Friedman S, Lippitz J. Chemical peels, dermabrasion, and
laser therapy. Dis Mon 2009;55(4):223–235
17. Hetter GP. An examination of the phenol-croton oil
peel: part IV. Face peel results with different concentra­
tions of phenol and croton oil. Plast Reconstr Surg 2000;
105(3):1061–1083, discussion 1084–1087
18. Cortez EA, Fedok FG, Mangat DS. Chemical peels: panel dis­
cussion. Facial Plast Surg Clin North Am 2014;22(1):1–23
Discussion by James E. Zins and Ahmed M. Hashem
History
Early chemical peeling techniques were the purview
of nonphysician lay peelers. They dominated the scene
from as early as the 1920s using their so-called “secret
formula.” It was not until the early 1960s that plastic
surgery entered the scene.1,2 The original phenol–cro­
ton oil peeling formula used by the lay peelers was
simplified and popularized by Dr. Tom Baker.3 This
remained the dominant resurfacing technique for the
next 30 years.
Although chemical peeling became widespread and
long-term results were good, the pathophysiology of the
peel was only incompletely understood. Early teachings
suggested the following:
•• The technique was an all-or-none phenomenon.
That is, the peel resulted in coagulative necrosis and
a barrier to further dermal injury. The material was
painted on and went to a given depth.
•• Therefore weaker concentrations of phenol and
croton oil created a greater depth of injury.
•• Phenol was the active agent.
It was not until 2000 that Hetter4 proved these
­premises to be inaccurate, ushering in the modern era
of phenol–croton oil peeling. He clearly demonstrated
the following:
•• Phenol, rather than being an all-or-none
phenomenon, acted much like trichloroacetic acid
(TCA). Higher concentrations and additional layers
led to a deeper peel.
•• Increasing concentrations therefore led to deeper
injury. Hetter5 and Stone and Lefer6 suggested
reducing the phenol and croton oil concentrations
to minimize complications while maintaining an
effective peel. Current phenol–croton oil peeling
therefore allows the surgeon to vary the depth of
injury and minimize complications by varying both
the concentrations of phenol and croton oil and by
altering the number of layers applied.

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Misinformation Regarding
Phenol–Croton Oil Peeling
Phenol–croton oil, like TCA, is not only a deep-peeling
technique; it can be used as a light, intermediate, or
deep peeling modality, and both can treat a wide va­
riety of ages and facial aging conditions. Furthermore,
by altering the concentration and the technique of
­application, various areas of the face can be treated to
different depths. A light peel using 27.5% phenol and
0.01% croton oil can be used to safely peel the lower
eyelids superficially, whereas higher concentrations
can be used to peel deeper wrinkled areas such as the
perioral region.7,8
Complications
Complications after intermediate-depth chemical
peeling can result from errors in (1) preoperative evalua­
tion, (2) intraoperative technique, or (3) postoperative care.
This chapter reviewed patient selection and identified red
flags in the preoperative assessment that might lead to ad­
verse sequelae. Also important is any history of previous
dermabrasion, chemical peeling, laser resurfacing, or elec­
trolysis. All of these modalities can reduce the epidermal
progenitor cells needed to replace the epidermal layer and
can lead to delayed healing. Anything that leads to delayed
healing makes hypertrophic scarring more likely.
With regard to intraoperative misadventures, techni­
cal errors are the overwhelming cause of complications.
This includes overaggressive peeling and resultant hyper­
pigmentation or worse, scarring. Areas where the dermis
is thick, including the perioral and midforehead region,
provide a greater margin for error with regard to depth of
injury (Video 18D.1). Conversely, the eyelid area, with its
thin dermal layer, must be peeled superficially. Overag­
gressive peeling is most likely to result from the following:
1. High concentrations of phenol and croton oil or TCA
2. Too many layers of chemical application
3. Application of the peel solution with too wet an
applicator
It should be noted that the critical peeling end point de­
pends not on the concentration or number of applica­
tions, but on the density of the frost obtained (Fig. 18D.1).
Minor postoperative problems such as milia, contact
dermatitis, persistent erythema, and pruritus are easily
remedied as outlined in this chapter. However, several
postoperative sequelae can be quite troublesome. When
aggressively and properly treated, however, a favorable
outcome can be achieved in most cases.
Phenol–croton oil peeling fell out of favor in the
1990s, replaced by a variety of laser and light-based
modalities. This was in great part because of the hy­
popigmentation that was common with Baker-Gordon’s
formula.9 The recent recommendations to reduce both
phenol and croton oil has reduced this unwanted side
effect. Although Hetter claims that hypopigmentation
does not occur with croton oil concentrations of less
than 1.1%,5 it is our experience that subtle hypopig­
mentation occurs in most patients.7 For this reason, we
limit croton oil peeling to Fitzpatrick skin types I to III.
Hypopigmentation in these skin types tends not to be
debilitating. In fact, skin lightening can be advantageous
in areas such as the eyelid. Because of this bleaching ef­
fect, segmental peeling should be avoided in the darker
skin types (Fitzpatrick III) in favor of full-face peeling to
prevent a patchwork appearance.
Hyperpigmentation, as explained in the chapter, oc­
curs most commonly in darker skin types. This is exac­
erbated by sun exposure and is minimized by at least
6 weeks of preoperative skin care and melanin sup­
pression with Retin-A and hydroquinone treatment.
In our experience hyperpigmentation is particularly
troublesome and most likely to occur in dark-skinned
­individuals of mixed race origin. However, unlike
­hypopigmentation, hyperpigmentation is generally
­reversible. It generally begins at 4 weeks after peeling.
For patients with darker skin types Retin-A and hydro­
quinone are routinely begun 6 weeks preoperatively and
restarted at 4 weeks postoperatively to minimize postin­
flammatory hyperpigmentation.
Other common skin problems include long-term er­
ythema. Although it is related to the depth of the peel,
it is also significantly more likely in very light–skinned
individuals. Erythema can also be the harbinger of
­hypertrophic scarring. Running an examining hand over
the area of erythema will detect areas of induration. If
aggressively treated with dilute intralesional steroid
(triamcinolone 5 mg per mL) on a weekly rather than
monthly basis, the likelihood of hypertrophic scarring
will be minimized (Fig. 18D.2). In our clinical experi­
ence, areas most prone to hypertrophic scarring include
the perioral marionette lines and the geniomandibular
Fig. 18D.1 Periorbital area showing the degree of frosting
deemed appropriate after a phenol–croton oil peel with a for­
mula of 27.5% phenol and 0.105% croton oil.

203
Chapter 18 Chemical Peels
groove. It is suggested, but not proven, that peel solu­
tion may pool in these creases, leading to an increased
depth of injury.
Infection can lead to an increase in the depth of in­
jury and is a leading cause of scarring. Because the epi­
dermal barrier is removed, infection tends to be more
widespread and atypical in appearance. Cardinal signs
of bacterial, fungal, or viral infections include sudden
wound breakdown in a patient otherwise healing well
or inordinate onset of pain. Treatment should include
the following:
•• Immediate observation
•• Gram stain
•• Bacterial, fungal, and viral cultures
•• Immediate doubling of antiviral therapy
Bacterial and fungal infections are more common
in laser-treated patients when occlusive dressings
are applied and left in place for a prolonged period
(i.e., 1  week). With the advent of open treatment of
­chemical and laser peeling, this has decreased dramati­
cally. In addition, prophylactic treatment with antivi­
rals makes herpetic infections unusual. When they do
occur they are quite mild and easily treated by doubling
the ­prophylactic antiviral dose. Although ­prophylactic
antibiotics have been recommended by some, our
burn surgery experience has taught us that they fail
to ­prevent both wound infection and wound sepsis.
Therefore we do not use them.
Cardiac toxicity from phenol–croton oil peeling is
controversial. Although Baker has stated that in his ex­
perience arrhythmias were rare,9 others have reported
a real incidence.10,11 However, cause and effect has not
been proven. In fact, studies have shown that Holter
monitoring demonstrates asymptomatic arrhythmias
in a large percentage of patients.11 However, given the
possibility of cardiac toxicity, hydration and full-face
peeling over a minimum of 60 minutes proves to be
prudent.11
Finally, we recommend the following with regard
to ocular injury:
•• Mixing of the peeling agent is done by the surgeon
only
•• The bottles stay on the stand and are never passed
over the patient to avert spillage
•• Petrolatum is not placed in the eyes, because phenol
and croton oil can mix with the petrolatum, making
irrigation washout difficult
Fig. 18D.2 (a) Erythema and induration of the right chin 9 weeks after a perioral phenol–croton oil peel with a formula of 33%
phenol and 1.1% croton oil. (b) At 5 months after the peel. The erythema and induration resolved with three dilute intralesional
triamcinolone (5 mg per mL) injections performed every other week.
a
b

SECTION IV AESTHETIC SURGERY
204
Conclusion
Chemical peeling is effective, predictable, and long-last­
ing. It requires no expensive lasers or light-based modal­
ities and is therefore cost-effective. Minor complications
are easily treated. Major complications such as scarring,
although rare, can be minimized by judicious preopera­
tive, intraoperative, and postoperative care.
References
1. Hetter GP. An examination of the phenol-croton oil
peel: Part II. The lay peelers and their croton oil for­
mulas. Plast Reconstr Surg 2000;105(1):240–248, dis­
cussion 249–251
2. Hetter GP. An examination of the phenol-croton oil
peel: Part III. The plastic surgeons’ role. Plast Recon­
str Surg 2000;105(2):752–763
3. Baker TJ. Chemical face peeling and rhytidectomy. A
combined approach for facial rejuvenation. Plast Re­
constr Surg Transplant Bull 1962;29:199–207
4. Hetter GP. An examination of the phenol-croton oil
peel: Part I. Dissecting the formula. Plast Reconstr
Surg 2000;105(1):227–239, discussion 249–251
5. Hetter GP. An examination of the phenol-croton oil
peel: part IV. Face peel results with different concen­
trations of phenol and croton oil. Plast Reconstr Surg
2000;105(3):1061–1083, discussion 1084–1087
6. Stone PA, Lefer LG. Modified phenol chemical face
peels: recognizing the role of application technique.
Facial Plast Surg Clin North Am 2001;9(3):351–376
7. Ozturk CN, Huettner F, Ozturk C, Bartz-Kurycki
MA, Zins JE. Outcomes assessment of combination
face lift and perioral phenol-croton oil peel. Plast
­Reconstr Surg 2013;132(5):743e–753e
8. Orra S, Waltzman JT, Mlynek K, Duraes EFR, Kundu
N, Zins JE. Periorbital phenol-croton oil chemical
peel in conjunction with blepharoplasty: an evolving
technique for periorbital facial rejuvenation. Plast
Reconstr Surg 2015;136(4, Suppl):99–100
9. Baker TJ, Gordon HL. Chemical face peeling: an ad­
junct to surgical facelifting. South Med J 1963;
56:412–414
10. Landau M. Cardiac complications in deep chemi­
cal peels. Dermatol Surg 2007;33(2):190–193,
­discussion 193
11. Truppman ES, Ellenby JD. Major electrocardiographic
changes during chemical face peeling. Plast Reconstr
Surg 1979;63(1):44–48

205
CHAPTER
19

Fat Grafting for Facial Rejuvenation
Sydney R. Coleman and Riccardo F. Mazzola
Although fat grafting procedures have an established re­
cord of safety and reports of adverse outcomes are uncom­
mon, complications do occur with fat grafting, as with any
surgical procedure. The majority of complications are re­
lated to aesthetic appearance and are most often associated
with the location, manner, and volume in which the fatty
tissue is placed into recipient areas. These include overcor­
rection, undercorrection, visible irregularities, migration
of placed fat, and donor site problems.1 Improvement in a
patient’s facial or body contours is not always enough for
a successful result. One of the most difficult elements of
this procedure is reliably predicting what the patient de­
sires before the procedure and what result will make the
patient happy; often these are not the same.2 In addition,
if the patient is not psychologically prepared for changes in
the face or body, for the postprocedure course, or for possi­
ble unexpected events, an otherwise successful procedure
can be a disappointment. The operating surgeon must be
familiar with the complications of fat grafting and should
warn the patient about the problems that are most likely to
occur during a fat grafting procedure. Before the operation
starts, the patient should carefully read and understand the
informed consent, in which all the details of the planned
procedure are accurately explained along with the predict­
able outcome, the postoperative course, the patient’s re­
sponsibilities during recovery, and potential sequelae and
complications.
Structural fat grafting has other potential complications,
including infection; damage to underlying structures such as
nerves, muscles, and glands; necrosis; calcifications; oil cyst
formation; and the most dreaded, embolism.
Fortunately, the complication rate with fat grafting is ex­
tremely low compared with most open surgical techniques
and the incidence of unpleasant events decreases signifi­
cantly with surgeon experience.
Avoiding and Managing
Unfavorable Results and
Complications in Fat Grafting
Summary Box

Aesthetic
Complications
•• Insufficient volume
•• Resorption
•• Swelling
•• Irregularities, lumps,
calcifications, oil cysts
•• Fat migration
•• Donor site
complications
Major
Complications
•• Infection
•• Damage to underlying
structures
•• Intravascular
complications
○
○Embolization
○
○Stroke
○
○Blindness
○
○Central retinal
artery occlusion
○
○Skin necrosis
○
○Death
Possible Complications of Fat Grafting
Common Aesthetic Complications
Insufficient Volume
The goal of structural fat grafting is for the grafted fat to
survive evenly and predictably. The most common com­
plaint that patients have after the swelling subsides is that
they had expected more or less fullness in a specific area.

SECTION IV AESTHETIC SURGERY
206
of the refined material placed will not be viable. Even with
scrupulous technique, a portion of the fatty tissue will die
from the negative pressure, exposure to air, and mechanical
trauma sustained during harvesting and refinement proce­
dures of the fragile fatty tissue.
Reducing Trauma
Forcing the lipoaspirate through a small cannula places a
positive pressure and further mechanical trauma on the
fatty tissue parcels. This trauma can vary from patient to
patient. For instance, in thin patients the fat cells store
much less triglyceride, which makes them smaller. When
the tissue parcels are composed of smaller cells, they are
more likely to flow through the cannulas without ruptur­
ing. In heavier patients, the fat cells are engorged with tri­
glycerides and are therefore larger. These larger cells with
stretched cell walls can be more easily ruptured by the
mechanical maneuvers associated with harvesting, puri­
fication, and placement. It is difficult to predict the exact
percentage of tissue that will be lost in these steps.
Preserving Viability
Even under ideal circumstances a small portion of trans­
planted fat will die, but certain conditions increase the like­
lihood of fat necrosis. Ischemia represents the major cause4
(Fig. 19.1).
Placing Minimal Aliquots of Fat
It is essential to avoid creating a bolus, which induces ne­
crosis of the central portion of the transplanted adipocytes.
Death of adipocytes and progenitors causes fibrosis, calcifi­
cations, and oil cyst formation.5 On the contrary, placement
of minimal aliquots of fat maximizes the contact and favors
the successful take of the graft. Forcing too much tissue
into a limited recipient site such as the nose, or placing the
grafted fat in too thick a layer (e.g., to fill a deep sternal de­
fect) can result in necrosis, because the grafted tissue does
not receive adequate nutrition or respiration, as well as the
development of long-term tissue atrophy, oil cyst forma­
tion, and progressive calcification4 (Fig. 19.2).
There are numerous factors to consider when estimating
the volumes of fat to be grafted, including the resorption
rate and intraoperative edema. Obtaining the exact amount
of fullness that will satisfy a patient can be difficult. Careful
planning and fat preparation are essential. Even after the
physician and patient agree on the desired change, many
variables will affect the outcome. The surgeon who per­
forms the procedure is commonly asked how much of the
grafted fat will survive. At present it not possible to give a
satisfactory answer. A good approach is to look at the pho­
tographs of patients when they return for follow-up, ob­
serving the volume of fat that was grafted on that person
to produce a specific change. It is important to understand
what different amounts will do rather than focusing on the
question of how much will survive. Thus it is even more
important to know what 10 cc of fat placed in the face will
look like as compared with 20 or 30 cc.
Resorption
After the edema subsides, if the patient expected more full­
ness than was achieved, a difficult question is whether this
adverse outcome is related to insufficient placement or to
resorption. Indeed, resorption represents one of the main
drawbacks of the procedure, ranging from 25 to 80%.3 Nu­
merous means are available to restrain resorption rate as
much as possible:
•• Obtaining pure fat
•• Reducing trauma
•• Preserving viability
Obtaining Pure Fat
Ideally, the surgeon should obtain the purest fat possible
by eliminating the blood and oily component, along with
other debris, with minimal damage to adipose tissue. The
presence of blood, fatty acids, and other debris seems to
stimulate an inflammatory response, which induces re­
sorption. No matter how carefully the fat is prepared, it will
not be 100% pure. Varying degrees of oil, blood, and other
impurities, such as lidocaine, are present in the lipoaspi­
rate even after processing. Furthermore, a varying degree
Fig. 19.1 The importance of avoiding creation of a bolus in structural fat grafting. Placement of an excessive amount of fat as a bolus iso­
lates the transplanted cells in the center of the lump from the blood supply. Without nutrition and respiration, the cells of the central lump
may die indiscriminately. The end result is the formation of an oil cyst and fibrosis. (Reproduced from Coleman SR. Structural Fat Grafting.
New York: Thieme Medical; 2004.)

207
Chapter 19 Fat Grafting for Facial Rejuvenation
filtrated site should not be used as the sole criterion to de­
termine the amount of fat to be placed, which is why it is
important to estimate the volume to be infiltrated before
the procedure begins.
Irregularities, Lumps, Calcifications, and
Oil Cysts
One of the most distressing and common negative out­
comes of grafting fat is visible and palpable irregularities
and lumps. They are mainly the result of necrosis of the
grafted material, which induces fibrosis, calcifications, and
oil cyst formation. Kato et al7 demonstrated that although
a single dead adipocyte can be completely absorbed, the
extruded oil droplets are replaced by a cicatrization phe­
nomenon (collagen matrix formation), with chronic in­
flammation. If numerous tiny droplets (smaller than 1 mm)
Swelling
Postprocedure edema is the most common problem asso­
ciated with structural fat grafting. Patients need to be well
prepared in advance for their postoperative appearance so
they are not unduly alarmed by the degree of swelling that
occurs. It is also important to warn patients that this adverse
situation will continue to increase for up to 3 days after the
procedure so they do not panic when they notice this hap­
pening. The injection of local anesthetic into the tissues can
swell and “pump” the tissues full of solution. The amount of
local anesthetic should be minimized to the smallest volume
that will numb the area and obtain vasoconstriction with
a minimum of distortion. Use of electrotherapy devices for
5 to 7 days has been successful for reducing swelling after
rhytidectomy, liposculpture, and facial fat grafting.6
How Swelling Occurs
Forcing a blunt cannula through living tissue will imme­
diately provoke edema. To separate the tiny parcels of fat
from one another, hundreds of passes are made with a
blunt cannula; the end result is a significant amount of
edema4 (Fig. 19.3).
This edema obscures the visual clues that might be help­
ful for determining an end point. Also, because of individual
patient variations, it can be difficult to predict how a given
patient’s body will react during and immediately after the
injection of fatty tissue. The swelling will vary from patient
to patient, from area to area, and even from side to side in
the same patient.
This three-dimensional technique of placing refined fat
into the recipient sites creates the shape, volume, and struc­
tural changes defined in the operative plan. The fatty tissue
should be deposited in the desired location, shape, and vol­
ume with each pass of the infiltrating cannula.
Because the visual clues seen during infiltration of fat
can be deceptive, the intraoperative appearance of the in­
Fig. 19.3 Because the transplanted fat is often located at an incon­
sistent distance from a blood supply, it will die in an irregular fashion.
As the tissue necroses and resorbs, irregularities emerge. This may
happen as late as 4 or more months after the procedure, when swell­
ing subsides. Placement of a lump of tissue with the intent to mold
it into a specific shape commonly results in irregularities. (Repro­
duced from Coleman SR. Structural Fat Grafting. New York: Thieme
Medical; 2004.)
Fig. 19.2 (a,b) Many early authorities on fat grafting advocated molding of the fatty tissue after placement to create the desired shapes,
to distribute the fatty tissue evenly, and to smooth out any surface irregularities. After placement of as much as 1 or 2 cc of fat at each
pass, these surgeons recommend using digital pressure to redistribute the fatty tissues. Unfortunately, this type of maneuver affords little
control over the subdermal configurations of the manipulated volume, and the fat may even squirt in many directions to form irregular
pools of tissue. (c,d) Unequal access to nutrition and respiration can cause irregular survival of the fat, which results in surface irregulari­
ties. If a cyst or clump forms accidentally, digital manipulation can sometimes flatten such minor irregularities. However, the tissue should
never be placed with the idea that digital pressure can change the shape after placement. The edema that is created by fat placement and
subsequent manipulation creates the illusion that because the swollen skin surface initially appears smooth, the underlying graft has been
placed in a smooth layer. If the fat were all to survive, the surface would remain smooth; however, a portion of fat often dies. (Reproduced
from Coleman SR. Structural Fat Grafting. New York: Thieme Medical; 2004.)
a
b
c
d

SECTION IV AESTHETIC SURGERY
208
fer or bolus injection, and they occur mainly in the breast
and buttocks, where larger cannulas (16 to 18 gauge) are
used. They seldom occur on the face. According to Kato
et al,7 the sequence is as follows: The death of adipocytes
gives rise to oil droplets, followed by the formation of ne­
crotic, calcified tissue that eventually develops an oil cyst
with a tendency to grow. The solid wall around the cyst
prevents absorption of new oil within the cyst itself, the
size and configuration of which remains stable.8
Preventing Irregularities
Placement of fatty tissue so it creates a smooth fullness is
imperative for a successful result. However, smooth place­
ment demands that the physician have technical ability as
well as experience. This is especially true in recipient areas
with thin skin, as in the eyelid (see Fig. 19.3).
occur, the consequence is the development of palpable sur­
face irregularities. If the necrosis is more consistent (larger
than 10 mm), an oil cyst typically forms, again with chronic
inflammation.8 Once established, oil cysts are permanent,
with no tendency to reduce in size or to reabsorb9 (Figs.
19.4 and 19.5).
In critical areas, like the breast, the formation of oil
cysts and calcifications may induce diagnostic problems
with breast cancer.10 However, calcifications of fat necro­
sis origin are substantially different from those induced by
breast cancer. An expert radiologist can recognize the dif­
ference.
How Irregularities Occur
Fat necrosis after grafting basically depends on the tech­
nique. Oil cysts are most common after large volume trans­
Fig. 19.4 (a,b) This patient had fat grafting that included 7 cc of adipocytes placed in multiple tunnels to correct facial asymmetry. A left
unilateral fibrotic cyst was noticed on her jawline 1 month after surgery. (c,d) The cyst still had not reduced after 1 year. (Reproduced from
Coleman S, Mazzola RF. Fat Injection: From Filling to Regeneration. 2nd ed. New York: Thieme Medical; 2017.)
a
b
c
d
Fig. 19.5 Bilateral fibrotic cysts resulting from fat grafting to correct tear trough
deformity. A 19-gauge blunt-tipped cannula was used to place 0.5 cc of refined
less-dense fat per side. To prevent a depression ensuing from the cyst’s excision, a
midface lift was performed. (Reproduced from Coleman S, Mazzola RF. Fat Injection:
From Filling to Regeneration. 2nd ed. New York: Thieme Medical; 2017.)

209
Chapter 19 Fat Grafting for Facial Rejuvenation
Donor Site Complications
Removal of subcutaneous fatty tissue reduces support
and can result in irregularities, increased wrinkling, and
depressions at the donor site. For this reason, fat must be
suctioned with a 2- or 3-mm cannula; the surgeon should
extend the movements of the cannula in different direc­
tions to avoid aspirating fat from only a single specific area,
which inevitably results in an unpleasant depression that is
difficult to correct. For facial applications, fat is usually har­
vested from the lower abdomen, which is typically the best
site for obtaining the necessary volume of lipoaspirate. In
slender patients, the inner thigh or inner knee offer alter­
native sources of fat. If a large volume of fat is to be grafted,
other donor site areas may be selected, such as the dorsum,
flanks, peritrochanteric region, and others. However, if fat
is harvested from the flanks or peritrochanteric region, it
is essential to aspirate it bilaterally to maintain symmetry
and to prevent the donor area from having a different con­
tour than the contralateral side.
Care should be taken to choose concealed zones such
as the umbilical fold, suprapubic area, or inguinal fold for
the cannula’s entry point to avoid visible scars that might
become hypertrophic.9 When harvesting fat from the abdo­
men, it is essential to pinch up the skin to avoid perforating
the gut or internal organs with the cannula. This is more
likely to occur in slender patients or in those with an ab­
dominal hernia (Fig. 19.6).13,14
Major Complications
Infection
Patients undergoing structural fat grafting should be
treated with the same care as with any surgical procedure
to avoid the potential risk of infection. Although the pro­
cedure is considered relatively simple, adherence to key
principles of sterile technique is critical to avoid adverse
outcomes.15 As a preventive measure, it is advisable to use
Use of thin cannulas (e.g., 21 gauge), less-dense fat, a
spaghetti-like technique, and painstaking molding of the
grafted material can potentially help reduce the chance of
fat necrosis and the resultant unpleasant irregularities and
oil cyst formation.
Fat Migration
Fat migration occurs most often in areas where muscle mo­
tion is particularly evident, such as at the insertion of the
glabella into the midbrow skin above the eyebrow. After the
surgeon has infiltrated the midbrow with fatty tissue, the
skin surface appears relatively smooth, because the corru­
gator muscles are not contracting at that point. However,
once the patient is awake, depressions will develop when
the muscles move, such as when the patient grimaces. The
photographs may look great, but the forehead has distress­
ing irregularities upon motion. In these patients, continued
botulinum toxin (Botox [Allergan]) injections may be war­
ranted.
Botulinum toxin should be used judiciously before infil­
tration of fat into the glabella, nasion, and forehead. For deep
creases that are not relieved completely with the botulinum
toxin injection, the paralysis can be helpful by stenting the
mobility of the crease to create a predictable, stable cor­
rection of the creases. For shallow creases that are obliter­
ated by the induced paralysis, botulinum toxin should not be
used, because localization of the problem areas is difficult.
Superficial layering of fatty tissue into the submucosal
plane and immediately deep to the vermilion gives greater
stability to the transplanted fat. Placement into the lip for
eversion should reduce the effects of the powerful contrac­
tions of the orbicularis oris muscle.
Use of Frozen Fat
The use of frozen fat exposes patients to the risk of severe
infections, because it is composed of dead tissue.11,12 Re­
sults with frozen fat are variable, and most often the grafted
material resorbs almost completely. The use of autologous
banked fat should be strongly discouraged because of the
significant potential for clerical error. Incorrect documen­
tation could result in the inadvertent transmission of vi­
ruses such as HIV or hepatitis or the stimulation of an auto­
transfusion-type reaction. Physicians who intend to inject
stored autologous fat should be aware that specific safety
requirements are needed, and that both state and federal
government agencies have stringent guidelines concerning
tissue banking for autotransplantation.
However, the proposed strategies for cryopreservation of
harvested tissue show great promise. Cryoprotective agents
are added to the tissue, which is cooled at a controlled rate
to a low storage temperature. Studies have shown remark­
able maintenance of lipoaspirate viability when a careful
thawing protocol is followed. This may become an attractive
option for patients to have their tissue banked for future fat
grafting, as long as the fat is properly preserved and remains
sterile and viable.
Fig. 19.6 Pinching of the abdominal skin is necessary to harvest fat
from thin patients or in the presence of an abdominal hernia to avoid
the risk of gut and internal organ perforation. (Reproduced from
Coleman S, Mazzola RF. Fat Injection: From Filling to Regeneration.
2nd ed. New York: Thieme Medical; 2017.)

SECTION IV AESTHETIC SURGERY
210
Avoiding the Introduction of Foreign Bodies
Care should be taken to avoid inadvertently introducing
a foreign body into the harvested fat. This is most likely
to occur during the process of refining the fatty tissue4
(Fig. 19.8).
Woven cotton nasal packing or woven sponges are
sources of such contamination. Nonadherent gauze pads
and other wicking devices may be an alternative, although
most of them can release loose fibers after being cut into the
appropriate sizes. Obviously, fibers of cotton or other sub­
stances placed with the grafted fatty tissue can result in in­
flammation and scarring when they are transferred into the
donor site. Codman pads, commonly used by neurosurgeons,
are recommended for wicking the oil from the fatty tissue;
they seem to unravel or release fibers the least.
Damage to Underlying Structures
Nerve Injury
Sensory and motor nerve injuries that have occurred with
fat grafting as an isolated procedure have been related to
the use of a sharp needle or a pointed cannula to release a
scar or adhesion. Several patients have experienced tran­
a chlorhexidine scrub and to prep the donor and recipi­
ent sites with a povidone-iodine solution. Intraoperative
antibiotics are recommended in potentially contaminated
areas such as the lips, genital areas, and oral cavity (Fig.
19.7). In cases of delayed infection, a high index of sus­
picion should be maintained for mycobacterial or other
unusual infections.4
Avoiding Contamination
The following guidelines are applicable and should be fol­
lowed when dealing with potentially contaminated areas:
1. Patients should gargle with a chlorhexidine gluconate
0.12% oral rinse immediately before any procedure on
the face.
2. The lips are always infiltrated last to avoid inoculating
other areas with bacteria.
3. If the oral or nasal mucosa is perforated during infiltra­
tion near these areas, the cannula should immediately
be removed off the sterile field.
4. Patients should receive a prophylactic intravenous
injection of cephalosporin or other appropriate an­
tibiotics before incisions are made at a site in which
contamination from a mucosal surface is possible.
5. For nasal, vaginal, or anal areas the same prophylactic
methods should be considered.
6. In cases of delayed infection, a high index of suspicion
should be maintained for mycobacterial or other un­
usual infections.
Fig. 19.7 This patient had fat grafting first into the lips and then later
into the glabella. Four days later, she presented with a purulent in­
fection that required open drainage from her lips and glabella. Her
oral mucosa was likely perforated during the lip infiltration with a
contaminated cannula. (Reproduced from Coleman SR. Structural
Fat Grafting. New York: Thieme Medical; 2004.)
Fig. 19.8 Care should be taken to avoid introducing cotton fibers
along with the grafted fat. (Reproduced from Coleman SR. Structural
Fat Grafting. New York: Thieme Medical; 2004.)

211
Chapter 19 Fat Grafting for Facial Rejuvenation
Fat infiltrated into the masseter can cause unsightly
bulges when the muscle is contracted during mastication,
causing trismus and an aesthetically unappealing increase
in the definition of the posterior mandibular border. Tissue
infiltrated into a muscle may produce changes in the appear­
ance of the muscle when it moves.
Placement of a space-occupying volume of tissue into
a functioning muscle or even near a muscle may influence
not only the appearance but also the function of muscles.
In particular, fat grafting in patients with prior or current
muscle or nerve impairments should be approached with
caution. Besides facial muscles, functional muscles can also
be influenced by the edema caused by adjacent structural
fat grafting (Fig. 19.10).
Salivary Gland Injury
When placing fat in the cheek and preauricular areas, the
surgeon should carefully avoid damage to the parotid gland,
even when using the most blunt cannula. There is a poten­
sient sensation loss, presumably from placement with a
sharp needle near the supraorbital or infraorbital nerve.
It is these temporary sensory deficits that prompted me
(S.C.) to design the blunt-tipped cannulas now in use. With
blunt cannulas alone, permanent motor nerve injuries are
rare and only minimal sensory nerve symptoms may occur,
most of them transient.
In our series of patients, four injuries of the facial nerve
have occurred: two transient marginal mandibular injuries
(S.C.) and one permanent (R.M.) and one transient frontal
branch injury (S.C.). The first may happen when sharp nee­
dles are used. I (S.C.) use sharp needles very superficially to
avoid intravascular injection and to minimize damage to the
nerves. I do not place the injections deep. In the second case,
a 2.1-mm suction cannula was used to remove tissue from a
jowl at the same time that fat was placed along the anterior
mandibular border. The action that precipitated the injury
most likely resulted from the aperture of the suction cannula
applying negative pressure during tissue removal. The third
case took place in an attempt to excise an adherent oily cyst
located along the course of the marginal mandibular branch,
a sequelae of previous fat grafting. A 19-gauge blunt cannula
was used to remove the cyst, but the movements of the can­
nula may have been responsible for damaging the nerve. At
2 years postoperatively, the situation remained unchanged.
A temporary injury to the frontal branch of the facial nerve
happened after placement of tissue in the temple and pre­
auricular regions. It resolved spontaneously within 4 weeks9
(Fig. 19.9).
Muscle Injury
Violation of muscle fibers of the face or body with needles
or cannulas can injure the muscle and cause restricted or
impaired motion. Great attention should be made not to
damage mimic and masticatory muscles.
Fig. 19.9 Permanent mandibular branch injury after an attempt to
remove an oil cyst on the jawline that resulted from fat grafting to
correct facial asymmetry (see Fig. 19.3). (Reproduced from Cole­
man S, Mazzola RF. Fat Injection: From Filling to Regeneration. 2nd
ed. New York: Thieme Medical; 2017.)
a
b
c
Fig. 19.10 (a) This patient experienced a transient worsening of ex­
isting left eyelid ptosis after fat injection into the supraorbital region,
presumably because the edema influenced the levator muscle.4 Her
subsequent appearance is shown at 1 month (b) and at 2 years (c),
by which time she had recovered her preprocedure state completely.
(Reproduced from Coleman SR. Structural Fat Grafting. New York:
Thieme Medical; 2004.)

SECTION IV AESTHETIC SURGERY
212
and travels as a column proximally past the origin of the
retinal artery9 (Fig. 19.12).
Once the surgeon stops placing pressure on the plunger,
the forced injection ceases. As the arterial systolic pressure
pushes the blood, this propels the filler into the branches
of the ophthalmic artery. A tiny amount of the filler slip­
ping into the retinal artery can precipitate a central retinal
artery blockage, usually resulting in permanent blindness9
(Fig. 19.13).
Avoiding Filler Embolization
To avoid such complications, it is crucial to have clear
knowledge of the vascular anatomy of the face and to un­
derstand key prevention and management strategies. Blunt
cannulas should be used when possible for placement of
soft tissue fillers into the subcutaneous tissues or deeper.
Sharp cannulas, small cannulas, and needles are much
more likely to perforate the wall of an artery and cannulate
the artery lumen than are the larger, blunter instruments.
Therefore extreme caution should be used when sharp
needles of any type are used to inject particulate matter
into the face. This includes all of the soft tissue fillers and
even injectable steroids.
The volume placed with each pass of the cannula should
also be limited. For a continuous column of filler to extend
back to the ophthalmic artery or internal carotid artery, a
volume of filler must be injected with one bolus. Therefore
if the surgeon limits the amount of filler injected to less than
0.1 cc with each pass, the probability of a column of filler
extending back to the ophthalmic artery is low. I recom­
mend the infiltration of less than 0.1 cc with each pass of
the cannula in the face. To be especially safe, I advocate in­
filtrating in aliquots of less than 0.03 and preferably 0.02 cc
in the periorbital region. A vasoconstricted artery is harder
to cannulate than a vasodilated one, so epinephrine should
be considered for use at the injection site for the placement
of fillers.
When using a larger syringe (5 or 10 mL) for infiltra­
tion of the fat, the surgeon has less control over the volume
injected compared with a smaller syringe, so it is easier to
mistakenly inject a larger amount or to inject with a high
pressure. For that reason, I strongly recommend that only
1-mL Luer-Lok syringes be used for subcutaneous infiltra­
tion into the face.
Blindness has also occurred after soft tissue injections
with assistive mechanical devices. Therefore I recommend
that surgeons avoid using any assistive devices that may cre­
ate strong pressures during the injection of soft tissues.
Since the first report published by Teimourian in 1988,16
numerous cases of unilateral blindness from central reti­
nal artery occlusion have appeared in the literature.13–28
Beleznay et al25 identified 98 cases of vision changes from
injected filler. Interestingly, the sites that were at high risk
for complications were the glabella (38.8%), nasal region
(25.5%), nasolabial fold (13.3%), and forehead (12.2%). Au­
tial risk of perforating the gland, which leads to the forma­
tion of salivary fistulas and parotitis4 (Fig. 19.11). Damage
to the submandibular gland may cause pain and edema of
the surrounding tissues.
Catastrophic Intravascular
Complications
Embolization After Intravascular Injection
Probably the most devastating potential complication of fat
grafting is embolization after intravascular injection. This
concern is not a new one: Conrad Miller first warned of the
dangers of intra-arterial injection of fillers in 1926.12 Obvi­
ously, fat parcels injected into a vein become pulmonary
emboli by traveling to the lung.
The injection of a particulate substance into an artery
can block the blood flow to a specific anatomic region and
precipitate necrosis of the tissues supplied. However, it is
possible for substances injected into an artery to enter the
central arterial system of the head and cause a stroke or
even blindness.
Injected Filler Causing Stroke or Blindness
The retinal artery and posterior ciliary arteries are proxi­
mal branches of the ophthalmic internal carotid arteries.
Many superficial arteries of the face are distal branches of
the ophthalmic artery (supraorbital, supratrochlear, dorsal
nasal, and angular artery of the nose). A needle or cannula
used to inject fat can accidentally perforate the wall of
one of these distal branches and enter the artery’s lumen.
When the plunger of the syringe is pressed to propel the in­
jectable filler out of the syringe, if the opening to the needle
is in the lumen of an artery, the filler will be injected into
the lumen of the cannulated artery. As more pressure is ap­
plied to the plunger, the filler displaces the arterial blood
Fig. 19.11 An 18-gauge sharp needle was used to release a scar in
this patient’s right posterior buccal region. She developed paroti­
tis, which was treated conservatively with antibiotics and hot com­
presses. (Reproduced from Coleman SR. Structural Fat Grafting. New
York: Thieme Medical; 2004.)

213
Chapter 19 Fat Grafting for Facial Rejuvenation
Management of Central Retinal Artery
Occlusion
Treatment of central retinal artery occlusion must be al­
most immediate. Minutes of anoxia will lead to irreversible
retinal degeneration. All treatments are aimed at dislodg­
ing the embolus to allow it to move to a more peripheral
location in the retina. The goal is to mitigate damage to the
retina; when the embolus is dislodged, it is possible to con­
vert the injury from full blindness to partial blindness.
tologous fat (47.9%) was the most common filler associated
with this complication, followed by hyaluronic acid (23.5%).
The most typical symptoms were immediate vision loss and
pain. Partial recovery after intra-arterial pharmacomechani­
cal thrombolysis in ophthalmic artery occlusion has been
reported by Park et al.22
Because the arteries are tiny, the volume of filler neces­
sary to reach even the internal carotid artery is small. Uni­
lateral blindness and brain infarction has been reported after
the injection of only 0.05 cc into a nasolabial fold.
Ophthalmic
artery
Anterior
cerebral
artery
Middle
cerebral
artery
Supratrochlear
artery
Internal
carotid
artery
Fig. 19.12 Accidental perforation with a needle or cannula of the wall of a distal artery branch can cause entry of injected material into
the artery’s lumen, causing blockage. (Reproduced from Coleman S, Mazzola RF. Fat Injection: From Filling to Regeneration. 2nd ed. New
York: Thieme Medical; 2017.)
Central
retinal
artery
Ophthalmic
artery
Supratrochlear
artery
Blistering of skin
Retinal artery
occluded
Internal
carotid
artery
Fig. 19.13 Even a small amount of filler can precipitate a blockage. (Reproduced from Coleman S, Mazzola RF. Fat Injection: From Filling to
Regeneration. 2nd ed. New York: Thieme Medical; 2017.)

SECTION IV AESTHETIC SURGERY
214
gic on the right side, and her left eye was amaurotic.29,30 An­
other case of internal carotid artery embolism was reported
by Wang et al.24
Death
In July 2015, the experience of plastic surgeons in Mexico
and Columbia was published reporting deaths from glu­
teal fat grafting in the two countries.31–33 They reported 13
deaths in Mexico over the previous 10 years, either during
or within 24 hours after fat grafting to the buttock. In Co­
lumbia, 9 deaths occurred during or immediately after the
injection of fat to the buttocks. The Columbian patients all
had autopsies that revealed damage to the gluteal veins. The
findings of the autopsies were otherwise variable but the
following were found on some of the autopsies: globules of
fat in the superior gluteal vein and macroscopic fat in the
inferior vena cava, right atrium, right ventricle, and lungs.
Furthermore, in March 2015 the Los Angeles County
Coroner’s Office reported on a death during the injection of
1200 cc of fat to the buttock with 60-mL Toomey syringes.32
The autopsy demonstrated that small vessels of both lower
lobes of the lungs contained multiple grossly visible plugs
of adipose tissue. They postulated that the gluteal varicose
veins in the patient were possibly a conduit for the emboli
to enter the venous system.
This problem is not new. Since 2009, reports have been
emerging in the media. There were three reported deaths
among patients undergoing gluteal fat grafting in Florida
clinics between 2010 and 2011, and additional such re­
ports have come in from California, New York, Florida, and
Georgia. All of the deaths occurred during the procedure or
within 24 hours afterward. If the blockage by the fat em­
boli is at the pulmonary level or the cardiac level, the death
is usually intraoperative. If smaller parcels of fat enter the
veins and are more gradually caught in the lung, death oc­
curs within 24 hours of the procedure.
This small epidemic should make surgeons reevaluate
what it means to ensure safety in fat grafting. Does the level
of fat infiltration matter? Can this problem be avoided by not
grafting fat into the gluteus muscle or by remaining superfi­
cial in the muscle? The most troubling question is whether
this can happen or has happened after injection into other
muscles: the pectoralis, calf, forearms, biceps, or triceps. Fi­
nally, what role did the placement of incisions for access,
the speed of injection, aliquots of injection, and volume of
injection play in creating these massive emboli?
Conclusion
Although fat grafting procedures have an established record
of safety and are classified as minimally invasive surgeries,
reports of adverse outcomes are uncommon; however, they
do occur, as with any surgical procedure.
Fat necrosis, which results in calcifications and oil cyst
formation, is one of the most typical complications. It is im­
portant to prevent cyst development, because once estab­
lished, they are difficult to manage and often require another
procedure to excise them. Therefore injecting a bolus should
Digital globe pressure can contribute to the dislodging
of the embolus. Increasing the patient’s carbon dioxide level
is an immediate means of creating vasodilation of the retina.
This can be accomplished by using an anesthesia machine
(if available) or by simply having the patient rebreathe air
into a bag.
Another strategy is to reduce the resistance on the central
retinal artery with medications such as carbonic anhydrase
inhibitors like acetazolamide by mouth or dorzolamide (Tru­
sopt) drops into the eye. Of course, the ultimate treatment
to reduce intraocular pressure is paracentesis of the globe.
Skin Necrosis
The same soft tissue filler can also embolize the arterial
supply of mucosa, the conjunctiva, or skin and result in
necrosis (Fig. 19.14). The most typical presentation men­
tioned in the literature is severe pain followed by skin loss.
Stroke
Just as the pressure on the plunger of a syringe can force a
column of soft tissue filler into the ophthalmic artery, a lit­
tle more pressure on the plunger of a syringe can force the
column back into the internal carotid artery. From there
the soft tissue filler can embolize into any area supplied by
the internal carotid area, and this may result in a stroke.
In 2010, a dramatic event occurred in a British hospital
when a small amount of fat (0.2 to 0.3 cc) was injected in
the posterior and lateral pharyngeal walls to treat velopha­
ryngeal incompetence (VPI) in an 18-year-old girl. The VPI
was a sequela of surgery for cleft palate. The fat was acciden­
tally introduced into the carotid artery. Instead of a blunt
cannula, the surgeon used a 14-gauge needle connected to
a 10-mL syringe. Sadly, immediately thereafter, the patient
suffered a massive stroke as a consequence of fat embolism.
Three years later, the patient was still aphasic and hemiple­
Fig. 19.14 Significant necrosis of the lower lip 1 year after intra-ar­
terial injection of frozen fat into the marionette region with a sharp
needle. The patient had received previous injections of fat into the
same marionette region by a dermatologist and returned for a sub­
sequent injection using frozen fat. During the injection of the frozen
fat with a 22-gauge needle, the patient complained of excruciating
pain in the left lower lip; she later developed full-thickness loss of the
skin and mucosa of the left lower lip. (From Coleman SR. Structural
Fat Grafting. New York: Thieme Medical; 2004.)