Phẫu Thuật Tạo Hình (Tập 2): Phẫu Thuật Thẩm Mỹ – Neligan (Ấn bản 4)

83
Complications
Disclosures
Drs. Cohen, Saad, and Leong have no financial relationships with any
commercial laser company discussed in this chapter. Dr. Ross receives
honoraria from Palomar, Lumenis, Candela, and Cutera; Dr. Ross receives
research support from Candela, Palomar, Sciton, Cutera, and Syneron.
Milia
Small inclusion cysts, sometimes called milia, can appear in
the healing process after a treatment. These usually appear
about 2–3 weeks after re-epithelialization and may be aggra­
vated by ointments, owing to occlusion of the sebaceous
glands.30,31
1. Alexander JT, Goldman MP, Roberts TL. Facial resurfacing. In:
Mathes J, ed. Plastic Surgery. Vol. 2. 2nd ed. Philadelphia, PA: WB
Saunders; 2006:339–384.
2. Smith L. Histopathologic characteristics and ultrastructure of aging
skin. Cutis. 1989;43:414.
3. Brody HJ. Chemical Peeling and Resurfacing. 2nd ed. St. Louis,
MO: Mosby-Yearbooks; 1997:29–38.
4. Anderson RR, Parrish JA. Selective photothermolysis: precise
microsurgery by selective absorption of pulsed radiation. Science.
1983;220:524–527.
5. Ross EV, Swann M, Soon S, et al. Full-face treatments with the
2790-nm erbium:YSGG laser system. J Drugs Dermatol.
2009;8:248–252.
6. Goldman L, Wilson RG, Hornby P, et al. Radiation from a
Q-switched ruby laser. Effect of repeated impacts of power output
of 10 megawatts on a tattoo of man. J Invest Dermatol. 1965;44:69–71.
11. Fitzpatrick RE, Goldman MP, Satur NM, et al. Pulsed carbon
dioxide laser resurfacing of photo-aged facial skin. Arch Dermatol.
1996;132:395–402. This is a blinded assessment of CO2 laser efficacy for
periorbital and perioral rhytids. CO2 laser was found to be useful in this
setting.
13. Manstein D, Herron GS, Sink RK, et al. Fractional photothermolysis:
a new concept for cutaneous remodeling using microscopic patterns
of thermal injury. Lasers Surg Med. 2004;34:426–438. A novel method
for skin resurfacing is presented. Microscopic treatment zones are targeted
for thermal injury.
28. Sadick NS. Update on non-ablative light therapy for rejuvenation: a
review. Lasers Surg Med. 2003;32:120–128. A review of non-ablative skin
resurfacing modalities is presented.
53. Goodman G. Post acne scarring: a review. J Cosmet Laser Ther.
2003;5:77–95. The acne scar is a historically difficult problem with
pathology that varies considerably within and between patients. The
authors emphasize the necessity of applying lesion-specific techniques in
their review of evolving technologies to address acne scars.
Access the complete reference list online at

83.e1
References
References
1. Alexander JT, Goldman MP, Roberts TL. Facial resurfacing. In:
Mathes J, ed. Plastic Surgery. Vol. 2. 2nd ed. Philadelphia, PA: WB
Saunders; 2006:339–384.
2. Smith L. Histopathologic characteristics and ultrastructure of aging
skin. Cutis. 1989;43:414.
3. Brody HJ. Chemical Peeling and Resurfacing. 2nd ed. St. Louis, MO:
Mosby-Yearbooks; 1997:29–38.
4. Anderson RR, Parrish JA. Selective photothermolysis: precise
microsurgery by selective absorption of pulsed radiation. Science.
1983;220:524–527.
5. Ross EV, Swann M, Soon S, et al. Full-face treatments with the
2790-nm erbium:YSGG laser system. J Drugs Dermatol.
2009;8:248–252.
6. Goldman L, Wilson RG, Hornby P, et al. Radiation from a
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69–71.
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for skin resurfacing is presented. Microscopic treatment zones are targeted
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14. Geronemus RG. Fractional photothermolysis: current and future
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19. Anderson RR. Dermatologic history of the ruby laser: the long story
of short pulses. Arch Dermatol. 2003;139:70–74.
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23. Ross EV, Sajben FP, Hsia J, et al. Nonablative skin remodeling:
selective dermal heating with a mid-infrared laser and contact
cooling combination. Lasers Surg Med. 2000;26:186–195.
24. Ross E, Anderson R. Laser tissue interactions. In: Goldman M, ed.
Cutaneous and Cosmetic Laser Surgery. Philadelphia, PA: Elsevier;
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25. Alam M, White LE, Martin N, et al. Ultrasound tightening of facial
and neck skin: a rater-blinded prospective cohort study. J Am Acad
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26. Kelly KM, Nelson JS, Lask GP, et al. Cryogen spray cooling in
combination with nonablative laser treatment of facial rhytides.
Arch Dermatol. 1999;135:691–694.
27. Lask G, Lee PK, Seyfzadeh M, et al. Nonablative laser treatment of
facial rhytides. In: Anderson RR, ed. Lasers in Surgery: Advanced
Characterization, Therapeutics, and Systems VII. Vol. 2970. San Jose,
CA: Society of Photo-Instrumentation Engineers; 1997:338–349.
28. Sadick NS. Update on non-ablative light therapy for rejuvenation: a
review. Lasers Surg Med. 2003;32:120–128. A review of non-ablative skin
resurfacing modalities is presented.
29. Cohen SR, Henssler C, Johnston J. Fractional photothermolysis for
skin rejuvenation. Plast Reconstr Surg. 2009;124:281–290.
30. Fabbrocini G Chemical peels. 2015. Online. Available at: http://
emedicine.medscape.com/article/1829120-overview.
31. Hilinski JM, Revis DR, Seagle MB Skin resurfacing – chemical peels.
Online. Available at:
32. Fitzpatrick RE, Goldman MP, Satur NM, et al. Pulsed carbon
dioxide laser resurfacing of photo-aged facial skin. Arch Dermatol.
1996;132:395–402.
33. Glogau RG, Matarasso SL. Chemical peels. Trichloroacetic acid and
phenol. Dermatol Clin. 1995;13:263–276.
34. Ross EV, Zelickson BD. Biophysics of nonablative dermal
remodeling. Semin Cutan Med Surg. 2002;21:251–265.
35. Saafan AM, Salah MM. Using pulsed dual-wavelength 595 and
1064 nm is more effective in the management of hemangiomas. J
Drugs Dermatol. 2010;9:310–314.
36. Kauvar AN, Rosen N, Khrom T. A newly modified 595-nm pulsed
dye laser with compression handpiece for the treatment of
photodamaged skin. Lasers Surg Med. 2006;38:808–813.
37. Soon SL, Ross EV. Letter: use of a perforated plastic shield for
precise application of intense pulsed light. Dermatol Surg.
2008;34:1149–1150.
38. Kono T, Manstein D, Chan HH, et al. Q-switched ruby versus
long-pulsed dye laser delivered with compression for treatment of
facial lentigines in Asians. Lasers Surg Med. 2006;38:94–97.
39. Taylor CR, Anderson RR. Ineffective treatment of refractory
melasma and postinflammatory hyperpigmentation by Q-switched
ruby laser. J Dermatol Surg Oncol. 1994;20:592–597.
40. Chan HH, Kono T. The use of lasers and intense pulsed light
sources for the treatment of pigmentary lesions. Skin Therapy Lett.
2004;9:5–7.
41. Negishi K, Kushikata N, Tezuka Y, et al. Study of the incidence and
nature of “very subtle epidermal melasma” in relation to intense
pulsed light treatment. Dermatol Surg. 2004;30:881–886.
42. Wattanakrai P, Mornchan R, Eimpunth S. Low-fluence Q-switched
neodymium-doped yttrium aluminum garnet (1,064 nm) laser for
the treatment of facial melasma in Asians. Dermatol Surg.
2010;36:76–87.
43. Hwang CY, Lin CS, Tseng ML, et al. Spotted leucoderma after
treatment of facial hyperpigmentation on hemodialysis patients
employing 1064-nm Q-switched Nd:YAG laser. J Cosmet Laser Ther.
2010;12:47–50.
44. Taylor MB, Prokopenko I. Split-face comparison of radiofrequency
versus long-pulse Nd:YAG treatment of facial laxity. J Cosmet Laser
Ther. 2006;8:17–22.
45. Trelles MA, Alvarez X, Martin-Vazquez MJ, et al. Assessment of the
efficacy of nonablative long-pulsed 1064-nm Nd:YAG laser
treatment of wrinkles compared at 2, 4, and 6 months. Facial Plast
Surg. 2005;21:145–153.
46. Prieto VG, Diwan AH, Shea CR, et al. Effects of intense pulsed light
and the 1,064 nm Nd:YAG laser on sun-damaged human skin:
histologic and immunohistochemical analysis. Dermatol Surg.
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83.e2
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CHAPTER 5.4 • Injectables and resurfacing techniques: Laser resurfacing
47. Lipper GM, Perez M. Nonablative acne scar reduction after a series
of treatments with a short-pulsed 1,064-nm neodymium:YAG laser.
Dermatol Surg. 2006;32:998–1006.
48. Jih MH, Friedman PM, Kimyai-Asadi A, et al. Successful treatment
of a chronic atrophic dog-bite scar with the 1450-nm diode laser.
Dermatol Surg. 2004;30:1161–1163.
49. Dahan S, Lagarde JM, Turlier V, et al. Treatment of neck lines and
forehead rhytids with a nonablative 1540-nm Er:glass laser: a
controlled clinical study combined with the measurement of the
thickness and the mechanical properties of the skin. Dermatol Surg.
2004;30:872–880.
50. Paithankar DY, Clifford JM, Saleh BA, et al. Subsurface skin
renewal by treatment with a 1450-nm laser in combination with
dynamic cooling. J Biomed Opt. 2003;8:545–551.
51. Goldberg DJ. Nonablative dermal remodeling: does it really work?
Arch Dermatol. 2002;138:1366–1368.
52. Jacob CI, Dover JS, Kaminer MS. Acne scarring: a classification
system and review of treatment options. J Am Acad Dermatol.
2001;45:109–117.
53. Goodman G. Post acne scarring: a review. J Cosmet Laser Ther.
2003;5:77–95. The acne scar is a historically difficult problem with
pathology that varies considerably within and between patients. The
authors emphasize the necessity of applying lesion-specific techniques in
their review of evolving technologies to address acne scars.
54. Yaghmai D, Garden JM, Bakus AD, et al. Comparison of a 1,064 nm
laser and a 1,320 nm laser for the nonablative treatment of acne
scars. Dermatol Surg. 2005;31:903–909.
55. Alster TS, Tanzi EL, Welsh EC. Photorejuvenation of facial skin with
topical 20% 5-aminolevulinic acid and intense pulsed light
treatment: a split-face comparison study. J Drugs Dermatol.
2005;4:35–38.
56. Richey DF. Aminolevulinic acid photodynamic therapy for
sebaceous gland hyperplasia. Dermatol Clin. 2007;25:59–65.
57. Gold MH. Eremia S, ed. Skin Tightening with the Aluma Skin
Tightening System in Office Based Cosmetic Procedures. Cambridge,
UK: Cambridge University Press; 2010:246–249.
58. Sadick NS, Shaoul J. Hair removal using a combination of
conducted radiofrequency and optical energies – an 18-month
follow up. J Cosmet Laser Ther. 2004;6:21–26.
59. Chess C. Prospective study on combination diode laser and bipolar
radiofrequency energies for the treatment of leg veins. J Cosmet
Laser Ther. 2004;6:27–31.
60. Hruza G, Taub AF, Collier SL, et al. Skin rejuvenation and wrinkle
reduction using a fractional radiofrequency system. J Drugs
Dermatol. 2009;8:259–265.
61. Gold MH, Foster A, Biron J. Clinical evaluation of a new
fractionated bipolar radiofrequency device for the treatment of
photoaging. J Am Acad Dermatol. 2011;64:AB171.
62. Kaplan H, Gat A. Clinical and histopathological results following
TriPollar radiofrequency skin treatments. J Cosmet Laser Ther.
2009;11:78–84.
63. Boisnic S, Branchet MC. Ex vivo human skin evaluation of localized
fat reduction and anti-aging effect of TriPollar radio frequency
treatments. J Cosmet Laser Ther. 2010;12:25–31.
64. Bass LS. Rejuvenation of the aging face using Fraxel laser treatment.
Aesthet Surg J. 2005;25:307.
65. Bernstein EF, Andersen D, Zelickson BD. Laser resurfacing for
dermal photoaging. Clin Plast Surg. 2000;27:221.
66. Saad AN, Lim S, Goodacre A, et al. Complications associated with
fractional lasers: a review of 716 patients treated by medically supervised,
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Montreal.
67. Palm MD, Butterwick KJ, Goldman MP. Mycobacterium chelonae
infection after fractionated carbon dioxide facial resurfacing
(presenting as an atypical acneiform eruption). Case report and
literature review. Dermatol Surg. 2010;36:1473–1481.

SECTION I • Aesthetic Surgery of the Face
5.5 
Injectables and resurfacing techniques:
Chemical peels
Suzan Obagi
SYNOPSIS
■ Skin resurfacing procedures have continued to increase in popularity.
■ Chemical peels continue to play a vital role in skin resurfacing.
■ Peels can be tailored to various patient ethnic backgrounds and to
various patient complaints.
■ Peels can be safely combined with a number of laser modalities to
enhance results.
Introduction
Skin resurfacing procedures have continued to increase in
popularity as the worldwide trend in non-invasive to mini­
mally invasive procedures increases. Chemical peels are a low
cost, yet highly effective means by which skin resurfacing can
be achieved. Peels are a great alternative to laser resurfacing
for certain indications and a great adjunct to laser resurfacing
in other instances. With the proper patient evaluation, skin
preparation, and correct treatment plan, skin rejuvenation
results can be remarkable.
cosmetic procedures have risen 154%.1 The most common
cutaneous concern in darker skinned patients is the issue of
dyschromia. The ability to safely resurface, with peels or
lasers, patients of a wide ethnic diversity hinges on the knowl­
edge of skin anatomy, the depth of the issue they present with,
and the proper performance of the procedure.
It is important to recognize that the skin undergoes aging
both intrinsically (chronologic passage of time) and extrinsi­
cally (environmental damage). Intrinsic aging shows that with
the chronologic passage of time, the epidermis and dermis
atrophy and the turnover of skin cells slows down. Collagen,
elastin, and glycosaminoglycan production declines steadily
through the years starting from about the age of 18. Further­
more, the combined effect of tanning and smoking is more
deleterious than either one alone.
Patient selection
Indications for chemical skin resurfacing include textural
changes such as acne scars, enlarged pores, and wrinkles, to
pigmentary concerns such as freckles/lentigines, and photo­
damage (Table 5.5.1 & Fig. 5.5.1). Additionally, peels have
been utilized in the management of precancerous changes in
the skin.
As with any cosmetic surgery procedure, the evaluation,
preoperative consultation, and proper patient selection are
crucial. Patients who seek treatment for barely noticeable skin
anomalies are likely to be unhappy with postoperative results,
even when the physician considers the outcome a success.
Patient history
A thorough history and physical exam should focus on medi­
cations and illnesses that could impact wound healing (Table
5.5.2). These would include medications such as prednisone,
immunosuppressants or D-penicillamine, along with condi­
tions such as diabetes or scleroderma. Smoking or “vaping”
(electronic nicotine use), or prior radiation treatment to the
Key points
1. Knowledge of skin anatomy is crucial for proper
resurfacing.
2. Chemical peels can be tailored to various patient concerns.
3. Knowledge of the various peeling agents allows for proper
selection of the peeling modality for each patient’s needs.
4. Proper performance of chemical peels allows patients of
darker skin types to be safely treated.
Chemical peels are increasing in popularity as the trend
towards non-invasive or minimally invasive procedures
grows. The American Society of Plastic Surgery (ASPS) 2014
Survey Data shows that surgical cosmetic procedures since
2000 have decreased 12%, and non-invasive outpatient
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85
Patient history
to a relapse of melasma or a temporary issue with PIH during
the healing stages of the procedure.
Concurrent or oral retinoid use within the last 6 months
has been generally considered an absolute contraindication to
resurfacing due to reports of prolonged healing and hypertro­
phic scarring. A number of recent studies have brought into
question the validity of this concern and challenge the con­
ventional thinking that isotretinoin impairs wound healing
with regard to skin resurfacing and laser treatments.2–6 Until
clear-cut guidelines emerge, the author stops isotretinoin 3–4
months prior to resurfacing does not restart it until 2–3 months
postoperatively. If the patient develops an acne or rosacea
flare, anti-inflammatory antibiotics (doxycycline) can be used
to quiet this down without impairing wound healing.
A similar question arises with regard to the safety of simul­
taneous skin resurfacing and cosmetic surgery. In the past, it
was thought that combining these procedures increased the
chance of impaired wound healing.7 Newer studies have
Table 5.5.1  Clinical indications for skin resurfacing
Anatomic
skin level
Clinical presentation
Treatment
options
Epidermis
Epidermal melasma
Actinic keratosis
Seborrheic keratosisa
Solar lentigines (sun spots)
Ephelides (freckles)
Topical products
Superficial peels
Pigment lasers
Dermis
Dermal melasma
Wrinkles – depth varies
Scars – depth varies
Telangiectasiasb
Sebaceous hyperplasiasa
Syringomasa
Medium-depth
resurfacing to
deep peels
Vascular lasers
Epidermis
and dermis
Mixed-type melasma
Medium-depth
resurfacing
aBest treated with electrodessication (using an epilating needle for dermal
lesions).
bBest treated with chromophore-specific lasers.
Fig. 5.5.1  Photoaged skin showing rhytides, dyschromia, and volume loss.
Table 5.5.2  Patient social and medical history
Pertinent history
Relative contraindications
Absolute contraindications
Medical
Medications
Systemic illnesses
Psychiatric illnesses
•  Depression
• OCD
• BDD
MRSA history
Radiation to the treated area
HSV or VZV tendency
Active acne, rosacea, CTD,
vitiligo
Bariatric surgery with nutritional deficiency
Diabetes
Isotretinoin use recently
Active infection at the treatment site
History of keloids at the treatment site – avoid
reticular dermis level procedures
Pregnancy
Social
Smoking history
Chronic sun exposure
Smoking/vaping/nicotine use
Inability to follow instructions
Unrealistic expectations
OCD, obsessive–compulsive disorder; BDD, body dysmorphic disorder; MRSA, methicillin-resistant Staphylococcus aureus; HSV, herpes simplex virus; VZV, varicella
zoster virus; CTD, connective tissue disease.
face and neck can also impair wound healing, as resurfaced
skin requires intact and functioning pilosebaceous units and
a good blood supply to re-epithelialize correctly. Furthermore,
smoking or tanning the skin diminishes the duration of any
improvement that is achieved.
The general health and nutritional status of the patient is
also an important consideration for appropriate wound
healing, especially in a time where the number of bariatric
surgery patients is increasing. Often, post-bariatric surgery
patients are deficient in vital nutrients or protein. The physi­
cian should inquire about previous poor wound healing,
hypertrophic or keloid scars, or a tendency to develop post-
inflammatory hyperpigmentation (PIH). Seborrheic dermati­
tis, atopic dermatitis, and rosacea indicates the presence of
inflammation in the skin, thus increasing the risk for postop­
erative complications secondary to alterations in the skin’s
normal barrier function. Melasma is a very common dyschro­
mia for which patients seek treatment (Fig. 5.5.2). However,
if the patient is taking estrogen or oral contraceptives, is using
a hormone-containing intrauterine device (IUD), or is exposed
to sun or heat during the recovery phase, she may be prone

86
SECTION I
CHAPTER 5.5 • Injectables and resurfacing techniques: Chemical peels
reported safe outcomes combining fractionated laser resurfac­
ing with short-flap rhytidectomy,8 full-face laser skin ablation
combined with rhytidectomy,9 fractionated CO2 laser has been
used to complement and enhance the results of endoscopic
eyebrow lifting and surgical blepharoplasty,10 and simultane­
ous facelift and laser resurfacing over skin flaps with decreased
laser energy settings and reduced number of passes has
achieved excellent aesthetic results.11
While most patients can safely undergo skin resurfacing,
absolute contraindications include pregnancy, active infection
at the treatment site, significant tendency to develop keloids,
and the inability to adhere to postoperative instructions.
Evaluating skin type
Older skin classification systems such as Fitzpatrick skin type
or Glogau skin type do not provide the physician all the
information needed to select the best treatment modality. In
particular, these scales were devised prior to the emergence
of non-ablative and fractionally ablative technologies and fall
short in addressing patients with thicker skin or darker skin
types. The author utilizes the Obagi Skin Classification (Table
5.5.3) to help with proper procedure planning.
Particular attention should be paid to the patient that has
skin that freckles, develops melasma, or is prone to PIH.
Regardless of ethnic background, the presence of these issues
heralds the risk of post-procedure hyperpigmentation. These
patients can be treated safely if the duration of both pre- and
Fig. 5.5.2  Melasma – hormonal pigmentation aggravated by heat, trauma, and
hormone supplementation.
Table 5.5.3  Obagi skin classification
Skin variable
Skin conditioning – pre- and post-resurfacing
Suitable procedures and potential complications
Color
Conditioning varies with skin color
More aggressive with darker Caucasian skin and
with lighter Asian or lighter African-American skin
Complications related to depth and skin color
Darker skin:
Hypopigmentation:
• Superficial procedure: rare
• Medium-depth procedures: possible
• Deep procedures: more likely
Hyperpigmentation:
• Common regardless of depth
Oiliness
Increased skin surface oil interferes with
effectiveness of skin conditioning
It may contribute to postoperative acne flares
Topical or systemic therapy to control or reduce
surface oiliness preoperatively*
Excessive oil hinders chemical peel acid penetration
Laser resurfacing is not affected by oiliness
Thickness
Thin skin needs papillary level procedures to
thicken the papillary dermal collagen layer
Thick skin needs reticular dermis level procedures
to effect a textural change
Thin skin: light to medium depth peels
Medium–thick skin: good for peels, dermabrasion, fractionated
lasers
Thick skin: deeper chemical peels, dermabrasion, fractionated
lasers
Laxity
Lax skin requires long-term collagen stimulation to
prevent further laxity
Differentiate between skin and muscle laxity:
Skin Laxity: medium-depth peel to the level of the papillary dermis
Muscle laxity: facelift alone or in combination with a medium-
depth peel (to correct any associated skin laxity)
Fragility
Goal is to maintain or possibly increase skin
strength
Fragility correlates with postsurgical scarring
Procedure depth should be limited to the papillary dermis in
fragile skin
*If systemic isotretinoin is used, it is prudent to delay medium or deep skin resurfacing by at least 3 months (medium-depth resurfacing) to 6 months (deeper
resurfacing).

87
Skin conditioning pre- and post-resurfacing
Photoprotection with sunscreens is important to protect the
skin against deleterious effects of ultraviolet (UV) radiation.
Additionally, there is new interest in the effects of visible light
on the aging process. Therefore, we may see an evolution in
sun protection to be effective in the visible light spectrum.
Sunscreens have been divided into chemical absorbers
(organic) and physical blockers (inorganic) on the basis of
their mechanism of action. In the author’s practice, physical
sunscreens are the only recommended type of photoprotec­
tion. These contain zinc oxide and titanium dioxide, which
are chemically inert and therefore less irritating and less
allergenic.
Newer, micronized zinc or titanium formulations have
improved the elegance of sunscreen products and may virtu­
ally replace moisturizers for patients.
The use of proper skin conditioning prior to a procedure
helps reduce the risk of hyperpigmentation afterwards. Fur­
thermore, the improved skin texture motivates patients to
proceed with further procedures to enhance their skin (Fig.
5.5.3A,B). Lastly, the ability of a patient to adhere to a skin
care regimen helps to predict which patients are most likely
to be compliant with postoperative instructions.
All patients should receive prophylaxis against herpes
simplex virus (HSV) or varicella zoster virus (VZV) to prevent
reactivation and potential scarring regardless of their personal
history of previous viral infection. Valacyclovir is the author’s
preferred medication; the usual dose is 500 mg twice daily,
starting the day before surgery and continuing until the skin
has fully healed (7 days for chemical peel resurfacing and 15
days for laser resurfacing). If a patient has a significant history
of HSV or VZV, a dose of valacyclovir 1 g twice daily is used.
This dose can be increased to three times a day if needed to
control an outbreak. Antibiotics and anti-Candida agents are
reserved for use only when an infection develops. However,
topical mupirocin ointment is prescribed to patients to apply
to the nares three times a day starting 1 week before their skin
resurfacing and to continuing until their skin is fully healed.
post-resurfacing skin conditioning is extended to at least 8–12
weeks.
Skin conditioning pre- and
post-resurfacing
Proper skin conditioning should be started at least 6 weeks
(8–12 weeks or longer for darker skinned individuals) prior
to resurfacing.12 Typically, the patient will use this regimen up
until the night before the procedure. Tretinoin 0.05–0.1%
or retinaldehyde 0.1% cream promotes collagen synthesis,
enhances hydroquinone penetration, restores normal epider­
mal thickness and maturation, and improves solar elastosis.13,14
Studies have shown faster wound healing from skin resurfac­
ing in patients pre-treated with tretinoin.15 Since many reti­
noids are photolabile, it is suggested that they be applied at
night. Patients are instructed to apply 0.5–1 g of tretinoin or
retinaldehyde to the entire face nightly including the lower
eyelids with feathering to the hairline, jawline, and preauricu­
lar areas. The corners of the eyes and mouth should be
avoided. The upper eyelids should be treated one to two times
per week. If there is significant retinoid dermatitis, the topical
agents can be stopped 4–7 days prior to skin resurfacing.
Hydroquinone 4% cream reduces the risk of post-
inflammatory hyperpigmentation. Since the half-life of
hydroquinone is 12 hours, it requires a twice-daily applica­
tion. Patients are instructed to apply 1 g twice daily to entire
face, with a second light application to areas of darkest pig­
mentation (sun spots, melasma).
A topical poly-hydroxy acid/lactobionic acid (PHA) or
alpha-hydroxy acid (AHA) 6–8% can be applied in the morn­
ings to help minimize acne flares and to enhance the penetra­
tion of hydroquinone or tretinoin. These are especially
important for patients with thick or oily skin. However, these
agents can oxidize tretinoin; thus it is not recommended to
apply them in the evenings along with the retinoids.
Fig. 5.5.3  Skin conditioning before (A)
and after (B) 6 weeks of a topical skin care
regimen consisting of tretinoin,
hydroquinone, alpha-hydroxy acid, and
sunblock.
A
B

88
SECTION I
CHAPTER 5.5 • Injectables and resurfacing techniques: Chemical peels
Table 5.5.4  Chemical peel formulas
Acid
properties
Commonly used concentrations and
formulations
Keratolytics
Salicylic acid peels 15–30%
Glycolic acid 50–70%
Jessner’s solution
Phenol 25–50%*
Protein
denaturants
Trichloroacetic acid 15–100%
Phenol 60–88%
Baker–Gordon phenol peel: 50% phenol, 2.1%
croton oil
Hetter phenol peels: 50% phenol, 0.7% croton oil
Hetter “all around”: 35% phenol, 0.4% croton oil
Hetter VL (neck & eyelid): 30% phenol, 0.1%
croton oil
Stone V-K: 62% phenol, 0.16% croton oil
Stone 2: 60% phenol, 0.2% croton oil
*Phenol at concentrations below 50% has keratolytic properties
Table 5.5.5  Key points for acid penetration
Enhanced penetration of peel solution
into the skin
Acid properties
Protein denaturants penetrate deeper than
keratolytics
Higher concentrations penetrate more than
lower concentrations
Higher volumes of acid applied penetrate
more than lower volumes
Keratolytics applied before protein denaturants
results in deeper acid penetration
Skin properties
Acid will reach deeper into the skin in thinner
skin
Properly retinized skin will absorb acid faster
and more evenly
Applying the solution with greater force results
in deeper penetration
Degreasing the skin enhances peel penetration
Open wounds in the skin will absorb the acid
quickest*
*Caution is required when combining peels with dermabrasion and laser
resurfacing. The peel should be performed first, the acid then washed off, then
the laser or dermabrasion is performed.
Treatment: chemical peel technique
Terminology
This chapter will categorize peels according to their depth of
penetration into the skin rather than strictly referring to the
acid used (Table 5.5.4). Exfoliation will refer to wounds con­
fined to the epidermis (basal layer and above). Peels reaching
the papillary dermis but not entering the reticular dermis will
be classified as light, while medium depth peels will refer to
peels that have entered the superficial aspect of the reticular
dermis. Deep peels extend into the mid-reticular dermis. It is
imperative to monitor the intraoperative signs to assess the
depth of penetration. This will be discussed further.
Mechanisms of action
There are a few key factors to be aware of with regard to
skin–acid interaction and penetration. These are the type of
acid used, the concentration of the acid, the force by which
the acid is rubbed into the skin, the volume of acid applied to
the skin, whether or not the skin is preconditioned properly
to enhance penetration, and in some cases, the duration of
contact of the acid on the skin16 (Table 5.5.5). Selection of
peeling agents should be based on the mechanism of action
of the solution, and not on acid concentration. Chemical
peeling agents are classified as keratolytics or protein dena­
turants. Keratolytics are primarily used for superficial, exfo­
liative procedures, whereas the protein denaturants can be
used for superficial or deeper peels. As will be discussed
below, keratolytics can be used in combination with protein
denaturants to enhance peel penetration.
Keratolytics
Keratolytics act as exfoliating agents based on their ability
to disrupt adhesions between keratinocytes. Glycolic acid,
salicylic acid, and Jessner’s solution are the most com­
monly used keratolytic peeling solutions. Jessner’s solution
is comprised of 14% each of resorcinol, salicylic acid, and
lactic acid mixed in ethanol. These agents are primarily used
for superficial conditions such as roughness, acne, and mild
dyspigmentation.
Salicylic acid and Jessner’s solution have an advantage
over glycolic acid in that salicylic acid is lipophilic. Therefore,
these two peel solutions penetrate acne lesions or oily skin
better than a hydrophilic agent such as glycolic acid. Another
advantage they have over glycolic acid is that salicylic acid
and Jessner’s solution do not have to have the skin contact
time closely timed.
All three of these peels have the benefit of little to no
“downtime”, no anesthesia requirement, and they are easy to
perform. Because of the superficial nature of these peels,
results are seen only after a series of peels, spaced several
weeks apart. However, due to the superficial nature of these
peels, deeper issues such as wrinkles, acne scars, or dermal
melasma will not improve with these, regardless of how many
peels are performed.
Protein denaturants
Trichloroacetic acid peels
Trichloroacetic acid (TCA) can be used to reach a variety of
depths and is therefore considered the “workhorse” of chemi­
cal peels. As TCA penetrates through the skin, it causes protein
coagulation and denaturation of the cells in the epidermis and
dermis as well as the blood vessels. TCA is self-neutralizing,
thus it is not one that can be neutralized. This means that
once TCA is applied to the skin, it will keep penetrating
until it has been used up during the coagulation of a certain
amount of protein. This is a key concept, because subsequent
applications of TCA will drive the peel deeper, regardless of
concentration, until the acid has coagulated proteins deeper
down in the skin. Based on this knowledge, it is incorrect
to refer to TCA peels as light or deep according to acid
concentration.

89
Techniques
and depigmentation is extremely high. This limits the utility
of this peel to a small subset of older, fair skinned individuals
with significant rhytides and laxity. Although any resurfacing
method that reaches the reticular dermis may cause perma­
nent hypopigmentation, the traditional Baker–Gordon peel
resulted in unacceptably high rates. Weaker solutions of
phenol (25–50%) can be used to achieve lighter peels; however,
the results are not better than TCA and there is still the risk
for systemic toxicity.
Modifications of the Baker–Gordon phenol peel formula
with reduced levels of croton oil have significantly reduced
the amount of postoperative hypopigmentation, postopera­
tive erythema, and scarring. Both Hetter and Stone indepen­
dently described modifications of phenol peels (lower phenol
acid concentration and/or lower croton oil concentrations)
that allow better control over depth of penetration,23,24 allow­
ing patients of a variety skin types to be treated. These newer
formulations have contributed to a renewed interest in phenol
peels, as they provide physicians with clinically and finan­
cially effective alternatives to laser resurfacing.
Techniques
Glycolic acid peels, salicylic acid peels,
Jessner’s peels
Another key point is that there are four ways in which TCA
can be formulated.17 Therefore, in order to avoid errors in
formulation, it is of utmost importance to purchase the acid
from a reliable source using the weight to volume (W : V)
method. The author uses a 30% TCA solution, which is then
modified as part of the Blue Peel to create a 15%, 20%, 22%,
or 25% solution.
While many physicians have switched from chemical peels
to the perceived “safety and reproducibility” of lasers, peels
can be approached in a systematic manner, making them very
powerful tools in skin rejuvenation. In an attempt to obtain
more consistent results while giving the physician more
control over the peel, variations of the TCA peel (Jessner–TCA
peel, glycolic acid–TCA peel, Blue Peel) have been devel­
oped. Anatomically, they are designed to peel through the
papillary dermis and into the most superficial aspect of the
reticular dermis. Their main indications are for epidermal
and upper dermal pathology: photodamage, actinic keratoses,
large pores, lentigines, ephelides, fine rhytides, and very
superficial, non-fibrotic scars. Deeper pathology such deep
wrinkles or deep scars are not amenable to correction with
these peels.
These combination TCA peels can be categorized as being
“accelerated” or “decelerated”. In an attempt to speed the
penetration and depth of TCA peels, two modified peels were
created that incorporate the use of a keratolytic agent. The
Jessner–TCA peel utilizes Jessner’s solution (keratolytic),
applied prior to the application of TCA.18 Application of the
Jessner’s solution allows for faster and deeper penetration of
the subsequently applied 35% TCA. A similar mechanism is
employed with the glycolic acid–TCA peel, which uses 70%
glycolic acid (keratolytic) prior to application of 35% TCA.19
The Blue Peel is unique in that instead of increasing the
speed and depth of the peel, the process is slowed down.20
This allows the physician better control of depth during the
peel. The Blue Peel incorporates a non-ionic blue dye, glycerin,
and a saponin with a specific volume of 30% TCA to yield a
15%, 20%, or higher percentage of TCA–Blue Peel solution.
Use of TCA, a colorless solution, requires close attention to
avoid reapplication over previously treated areas. Therefore,
the blue dye is advantageous as it stains the stratum corneum
and helps the physician to visualize even application of the
peel. Since TCA is hydrophilic, the use of a saponin as an
emulsifying agent creates a homogenous TCA–oil–water
emulsion that penetrates the skin in a slower and more even
fashion.
Phenol peels
Phenol peels are inherently categorized as deep peels due to
the predominant effect of phenol on the skin. Similar to TCA,
phenol works through protein denaturation and coagulation.
However, phenol differs from TCA in that it penetrates quickly
to the level of the reticular dermis.21 Phenol is partially detoxi­
fied by the liver and excreted through the kidneys. The per­
cutaneous absorption of phenol can lead to a rapid elevation
of serum phenol levels, resulting in systemic toxicity and
cardiac arrhythmias. Therefore, all patients should be cleared
from a cardiac, hepatic, and renal standpoint preoperatively.
In addition, intraoperative cardiac monitoring and at least 1 L
of intravenous (IV) hydration are imperative.22
Due to the depth of penetration of phenol peels into the
mid-reticular dermis, the risk of scarring, prolonged erythema,
Hints and tips
Glycolic acid peels, salicylic acid peels, Jessner’s peels
These lighter-peeling agents must be applied to clean skin.
Have the patients cleanse their skin of all make-up and
lotions. The skin is first degreased with 70% ethanol (ETOH).
However, if the desire is to push the peel deeper, the skin is
degreased with acetone instead.
Glycolic acid peels
Glycolic acid must be applied quickly (within 15–20 s) to the
treatment area, and the contact time must be measured. Gly­
colic acid is started at a lower concentration and with subse­
quent treatments, either a stronger concentration is applied or
the contact time with the skin is increased. Typically, 50–70%
glycolic acid is applied with gauze or a large cotton-tip appli­
cator swab. The acid is left in contact with the skin for 30 s,
and with subsequent treatments, the contact time is worked
up to 1–2 min. The peel is then diluted with copious amounts
of water or neutralized with sodium bicarbonate. Close timing
is important since a study has shown that glycolic acid left on
the skin for 15 min created a dermal wound identical to that
seen with 35–50% trichloroacetic acid.25
Salicylic acid peels
Salicylic acid is applied to acetone- or alcohol-cleansed skin
in concentrations of 20–35% using gauze or cotton-tip applica­
tors. Multiple applications can be applied to problematic areas
to enhance the depth of penetration. The peel is washed off
with water after 6 min. Salicylic acid does not need to be
neutralized as it precipitates into a powder on the surface of

90
SECTION I
CHAPTER 5.5 • Injectables and resurfacing techniques: Chemical peels
the skin after the solvent evaporates. Application to a large
surface area or the use of occlusion should be avoided due to
the risk of salicylism.
Jessner’s peels
Jessner’s solution is also applied to alcohol- or acetone-
cleansed skin. The solution is applied in multiple coats to
problem areas. After 6 min, the peel is washed off with water.
TCA peels
TCA is usually used to achieve medium-depth peels. The
recovery time can range from 5 to 10 days and the procedure
can be associated with significant discomfort while the peel
is performed. However, the pain usually subsides before the
patient goes home. Patients receiving intramuscular or IV
sedation tolerate the procedure better and allow the peel to
proceed at a faster speed. Additional pain control can be
achieve with the use of strong fans or cooling units with
refrigerated air and oral sedation. Topical anesthetics should
not be used prior to skin peels since they enhance the penetra­
tion of the TCA and may result in an undesirable depth of
peel.
Skin resurfacing, whether with peels or lasers, is all about
reading the skin depth signs properly. Regardless of the type
of TCA peel performed, the evolving clinical depth signs
remain the same. The only difference between the various
peels is the speed by which these signs appear.
Physicians with minimal peeling experience are encour­
aged to start with relatively slower peeling techniques prior
Fig. 5.5.4  (A) Level 1 frost: light, non-organized frost on right-hand side of forehead. (B) Level 2 frost: even frost with a pink background, “pink sign”, on right-hand side
of forehead. (C) Level 3 frost: solid frost with no pink background on lateral parts of forehead (arrows).
A
B
C
Fig. 5.5.5  Peel progression signs: (A) Minimal frost, no edema, no epidermal sliding sign. (B) Level 2 frost, minimal edema, almost solid frost, with pink background and
epidermal sliding. (C) Level 3 frost, deeper, frost more solid, edema present, epidermal sliding gone.
A
B
C
to proceeding to faster peels. Combination peels using a kera­
tolytic peel followed by a TCA peel will speed up the penetra­
tion of the TCA, therefore carrying the risk of penetrating
deeper than expected. Just like with laser resurfacing and
dermabrasion, physicians must keep in mind the anatomic
variations of skin thickness prior to resurfacing.
Residual oil or thick scale may lead to a patchy peel; there­
fore, it is essential to cleanse and degrease the face well prior
to proceeding. Clinical depth signs are very important to
monitor during the peeling process.26 Frost appears on the
skin gradually as a result of coagulation of epidermal and
dermal proteins by the action of trichloroacetic acid.20 As TCA
is first applied, a light, non-organized frost begins to form
(level 1 frost) (Figs. 5.5.4A & 5.5.5A).
Further application results in the frost being solid but with
a diffuse pink background (vasodilation; level 2 frost) (Fig.
5.5.4B); this level of frost indicates a peel to the level of the
papillary dermis. The pink background of the frost is referred
to as the “pink sign”20 (Fig. 5.5.5B). The “pink sign” will be
apparent as long as the blood vessels of the papillary dermis
are still intact with normal blood flow. This “pink sign” is the
endpoint for the standard, papillary dermis-level peel.
Additional chemical peel solution application will result in
further protein coagulation, a more solid white frost, and the
loss of the “pink sign” indicating coagulation of the papillary
dermis vascular plexus (level 3 frost) (Fig. 5.5.4C).
The “pink sign” is difficult to see in darker skin. When
peeling dark skinned individuals, the “epidermal sliding”
must be used to gauge depth.20 The “epidermal sliding” sign
shows up as exaggerated wrinkling of the skin that occurs

91
Postoperative care
Phenol peels
Hetter VL peels
The modified, lighter phenol peels, like the Hetter VL solu­
tion, can be used to treat a single cosmetic unit without the
need for cardiac monitoring or IV hydration. However, if a
larger area is to be treated, or a stronger solution of phenol is
used, the patient must have appropriate cardiac clearance,
good hepatic and renal function, and receive appropriate IV
hydration and cardiac monitoring.
The skin is degreased with alcohol. The phenol mixture
must be swirled before each application as the oil and water
components of the solution have a tendency to separate. The
solution is applied to the skin with a cotton-tipped applicator.
Care must be taken not to let the solution drip or run down
the face. Once the solution is applied, the skin will frost
quickly. The endpoint is an even white frost (Fig. 5.5.6). The
frost dissipates quickly, so one must pay close attention to
make sure that one does not apply more solution and peel the
skin too deeply.
Combination procedures
Chemical peels can be successfully combined with laser
resurfacing and surgery, with certain precautions. When
performing chemical peels with laser procedures, the follow­
ing guidance should be adhered to: (1) non-ablative or
minimally ablative lasers (vascular or pigment lasers) or
electrodessication is performed first; (2) the medium-depth
peel is performed next; (3) if a phenol peel is to be used in
certain cosmetic units, this is then performed; (4) the skin is
cleansed to remove all residual acids; and (5) the laser resur­
facing of certain areas can then be performed (Fig. 5.5.7). If
peels are done in combination with a facelift, care is taken to
avoid peeling beyond the superficial papillary dermis over
the undermined skin flap.
Postoperative care
Light peels
Patients will experience minimal erythema and a variable
amount of desquamation. They are instructed to avoid sun
prior to complete precipitation and coagulation of papillary
dermis proteins (see Fig. 5.5.5B). At this point, papillary
dermal edema and disruption of anchoring fibrils allows the
epidermis to be more freely movable, resulting in wrinkling
in an exaggerated fashion when the skin is pushed or pinched.
This sign will disappear when the papillary dermis protein
becomes coagulated and adherent to the epidermal coagu­
lated proteins, thus indicating that the peel depth has reached
the superficial reticular dermis (Fig. 5.5.5C). At this point, the
pink background also becomes lost. In thick skin, “epidermal
sliding” may not be very obvious and the “pink sign” alone
has to be used to indicate the peel depth.
Further TCA application will penetrate into the upper
reticular dermis and clinically shows a solid frost with a loss
of the pink background (level 3 frost) (see Fig. 5.5.4C) and the
presence of dermal edema upon pinching the skin. Reaching
this level implies that the whole papillary dermis is involved
with the peel and the upper reticular dermis has been reached
but not yet involved. This is the endpoint for most peels.
Beyond this level, the solid frost begins to take on a gray color
and this correlates with an increased incidence of scarring and
hypopigmentation.
Jessner–TCA peels
After the skin is cleansed, acetone is used to degrease the
face further. With either 2 × 2 gauze or cotton-tipped appli­
cators, the Jessner’s solution is applied evenly until a very
light frost develops. A small amount of 35% TCA is then
applied to the skin with either cotton-tipped applicators
or gauze in even strokes. Two minutes are allowed to pass
before further application so that one can assess the depth of
TCA penetration. Areas of inadequate frosting can be care­
fully retreated. Sharp demarcation lines should be avoided
by feathering out the solution to the hairline, ears, and
jawline.
Glycolic acid–TCA peels
The skin is first cleansed with soap and water only. Seventy
percent unbuffered aqueous glycolic acid is rapidly applied
to the skin and left on for 2 min. It is then washed off with
water. Next, a small amount of 35% TCA is applied in even
strokes to the face with gauze or cotton swabs. After allowing
2–3 min for the acid to neutralize, areas of poor frosting can
be carefully re-treated.
TCA–Blue Peels
The skin is gently cleansed with alcohol. The Blue Peel mixture
is then prepared by mixing the Blue Peel base with 2 mL,
4 mL, or 6 mL of 30% TCA to create a mixture of 15%, 20%,
or 22%, respectively. This mixture is applied evenly to one
quadrant of the face if the patient is awake or can be done on
the entire face if the patient is sedated. After a 2–3 min waiting
period, a subsequent coat is applied. The amount needed for
thinner skin will be less than that needed for thicker skin. An
even blue color, even frost, and a pink background indicate
that the papillary dermis has been reached. Additional coats
will result in loss of the pink background, thus indicating
penetration beyond the papillary dermis and into the super­
ficial reticular dermis. This is the maximum recommended
depth of a facial TCA–Blue Peel.
Fig. 5.5.6  Phenol peel frost – more solid frost on deeper scars, less solid frost at
periphery.

92
SECTION I
CHAPTER 5.5 • Injectables and resurfacing techniques: Chemical peels
exposure during the healing phase. Patients should gently
wash their face twice a day and apply a light moisturizer
and a sunscreen. They should hold off on applying their
retinoids or alpha-hydroxy lotions until the skin has fully
healed.
Medium-depth to deeper peels
Every patient will have a different postoperative course, but,
for the most part, patients should be fully healed within 7–8
days of the procedure (Fig. 5.5.8). Rarely, 10 days may be
needed in areas of deep resurfacing. Patients will experience
Fig. 5.5.7  Combination resurfacing: (A) TCA–Blue Peel performed first, (B) periorbital Hetter VL phenol peel is performed next, the skin is then cleansed, and
(C) fractionated laser resurfacing to the perioral and forehead region is performed last.
A
B
C
Fig. 5.5.8  Wound healing stages: (A) First 48 hours: medium-depth peel, swelling peaks. (B) Laser resurfacing and phenol peel areas show proteinaceous exudate
(periorbital). (C) Postoperative day 7 full-face medium-depth peel, neck still healing from electrodessication of lesions.
A
B
C
a moderate amount of facial edema between 24–48 h. If a
phenol solution or a resurfacing laser is used, those areas will
also have a fair amount of proteinaceous exudate. While every
physician will fine-tune the postoperative care to their patient,
the author’s 15 years of experience have resulted in a many
modifications and, ultimately, in simplification of the postop­
erative care.
Patients are instructed to begin topical mupirocin ointment
three times a day to the nostrils, starting 1 week prior to the
procedure and until the skin has fully healed. Patients will
wash their face twice a day with a gentle cleanser using only
their hands (no washcloths). In addition to the soap cleansing,

93
Complications
twice a day (at midday and late afternoon) patients perform
an astringent soak for 10 min using gauze soaked in Dome­
boro’s Solution (Moberg Pharma, Cedar Knolls, NJ). After
each wash or soak, patients apply an inert emollient to the
skin such as Vaniply Ointment (Pharmaceutical Specialties,
Rochester, MN) or Aquaphor Ointment (Beiersdorf, Hamburg,
Germany).
Patients continue this regimen until the skin is 100%
re-epithelialized. Once re-epitheliazed, patients can slowly
reintroduce their routine skin care. It is important during this
time that patients avoid exercise and sun exposure. Further­
more, they are instructed not to pick, rub, or scratch their skin
during the healing process (Table 5.5.6).
Outcomes
With the correct patient selection, skin preparation, and pro­
cedure performance, results can be very gratifying. Patients
will see more skin firmness, clarity, and a reduction in precan­
cerous changes (Figs. 5.5.9–5.5.11).
Table 5.5.6  Hints and tips: peels
Ways to enhance peel depth
Ways to enhance comfort
Degrease the skin with acetone
Apply firmer pressure when applying the peel solution
Apply more peel solution volume
Apply a higher acid concentration
Perform a light peel or microdermabrasion before applying the deeper peel
solutiona
Cooling air units or strong fans
Oral analgesics: ibuprofen, meperidine, hydrocodone
Music or relaxing atmosphere
Intravenous sedation
Nerve blocksb
aCaution is recommended with more aggressive techniques.
bMay not give complete analgesia.
Fig. 5.5.9  Skin resurfacing before and after
(A,B). Patient with melasma baseline and
after both skin conditioning and a
medium-depth Blue Peel.
A
B
Complications
Hints and tips
Whether the skin is treated with lasers, peels, or
dermabrasion, the complications are identical (Fig. 5.5.12).
Complications such as hypertrophic scarring, prolonged
erythema (over 3 months), and pigmentary changes are
related to wound depth, and not specifically to the modality
used. In contrast, complications such as infections and
contact dermatitis occur from the impaired skin barrier
function seen with resurfacing.
Infections need to be recognized and treated early to avoid
the risk of scarring. Infections are most commonly bacterial
(Staphylococcus
aureus,
community-acquired
methicillin-
resistant Staphylococcus aureus – MRSA) followed by virus
(herpes simplex virus, varicella zoster virus) and less so by
yeast (Candida).27 A potassium hydroxide (KOH) slide prep

94
SECTION I
CHAPTER 5.5 • Injectables and resurfacing techniques: Chemical peels
test (DFA) can quickly confirm a herpes or zoster infection.
However, patients should be treated with antiviral therapy
dosed as if treating a varicella zoster infection (i.e., valacyclo­
vir 1 g three times a day for 10 days) until results are
finalized.
Allergic contact dermatitis to the postoperative skin care
agents is often a challenging diagnosis. Patients will usually
complain of itching or burning of their skin along with
increased redness. Patients may have been healing well only
to show a setback in wound healing. The most likely culprits
are propylene glycol or lanolins. One must rule out an early,
disseminated viral infection or Candida. If an allergic contact
can be preformed in the office to confirm a yeast infection if
one is suspected. If a patient is on a systemic antibiotic and
develops an infection, consider Pseudomonas aeruginosa and
other Gram-negative organisms as the most common etiology.
Cultures and sensitivities should be performed as indicated
to identify the bacterial organism. Appropriate systemic
therapy should be directed at the most likely etiology while
results are pending.
Although the use of herpes prophylaxis has greatly
decreased the incidence of viral infection, some patients can
experience an outbreak even while on suppressive treatment.
If a viral infection is suspected, a direct fluorescent antibody
Fig. 5.5.10  Skin resurfacing before and
after (A,B). Patient before and after 3
months full-face medium-depth Blue Peel
and electrodessication of adnexal lesions.
A
B
Fig. 5.5.11  Skin resurfacing before and
after (A,B). Patient shown in Fig. 5.5.1,
before and 4 months after medium-depth
Blue Peel, fractionated laser forehead, and
perioral and periorbital Hetter VL peel.
A
B

95
Conclusion
dermatitis is still the most likely diagnosis, the patient should
stop all offending agents, cleanse the skin with water, and
apply only white petrolatum to the skin. A topical mid-potency
steroid ointment can be used, as long as it does not contain
propylene glycol. These patients need to be followed every
couple of days to monitor the wound healing process.
Hypopigmentation can be very disconcerting to the patient.
Any procedure that reaches the reticular dermis can result in
permanent hypopigmentation. While the color discrepancy
may not be as apparent in lighter skinned individuals, darker
skinned patients are more likely to notice any color discrep­
ancy. Therefore, patients with darker skin should be warned
of this possibility. This must be differentiated from the
pseudo-hypopigmentation that is seen in patients with heavily
photodamaged skin. Pseudo-hypopigmentation is when the
resurfaced skin looks lighter than the adjacent, un-resurfaced
skin, but this is because the sun damage has been removed,
and not because the skin is actually lighter.
Post-inflammatory hyperpigmentation (PIH) can occur in
all but the most fair of patients. PIH can overshadow the
results of resurfacing, thus it is better to anticipate this and
treat it before it manifests. PIH can be minimized or avoided
by having patients resume their skin reconditioning regimens
once the wound has healed fully. This is most often by post­
operative day 8 or 10. However, if PIH occurs and is resistant
to the topical agents alone, salicylic acid peels biweekly can
help speed up resolution.
Patients with acne or rosacea can experience a flare up
during the postoperative period. Systemic anti-inflammatory
antibiotics can help resolve this before scarring occurs. Sys­
temic anti-inflammatory antibiotics (tetracycline, doxycycline)
should be used in combination with appropriate topical thera­
pies to quickly quiet down these conditions.
Erythema lasting more than 2 weeks postoperatively is less
common with peels than with laser resurfacing. It is seen
commonly for several months following aggressive laser
resurfacing, dermabrasion, and modified phenol peels. Close
observation of areas of persistent erythema is important as it
can portend an impending scar. Usually this occurs at areas
where the wound has penetrated the reticular dermis (deeper
resurfacing) or at sites of infection and trauma. These areas
can be treated 2 days out of each week for several weeks with
a mid- to ultrapotent topical steroid (triamcinolone acetonide
or clobetasol). Too much steroid use can have adverse effects,
Fig. 5.5.12  Complications: (A) impetigo, (B) delayed wound healing, (C) hypertrophic scar formation.
A
B
C
therefore close patient monitoring is needed. The use of
pulsed dye laser (non-purpuric settings) early on can resolve
the erythema and halt the progression of scarring, often
without the need for a topical steroid. The laser treatments
can be spaced 2–4 weeks apart until the erythema resolves.
The most dreaded complication of skin resurfacing is scar­
ring and textural change. Scars can take a variety of mor­
phologies such as atrophic, hypertrophic, or keloid-like. As
was previously mentioned, areas of delayed healing or infec­
tion can then progress to scar formation. The importance
of early detection and intervention cannot be emphasized
enough. If the skin has already begun to thicken or become
fibrotic, it should be treated with an ultrapotent topical steroid
twice a day for 3–4 weeks. Care should be taken not to apply
the steroid to normal skin as it may result in atrophy, telangi­
ectasias, and skin fragility. Early intervention with a pulsed
dye laser should be the next step. This laser can greatly
improve skin texture, erythema, and can sometimes halt the
progression of scarring.
Intralesional steroid injections and manual massage should
begin if the topical steroids fail to improve the scar. The thicker
areas of the scar are injected at 2- to 4-week intervals with
triamcinolone acetonide 1–10 mg/mL. The concentration
used is based on scar thickness. A combination of triamcino­
lone acetonide and 5-fluorouracil can be used as well, with
the advantage of allowing for less steroid to be injected. The
5-fluorouracil is an antimetabolic agent that helps to slow
down scar fibrosis (Table 5.5.7).
Conclusion
There has been an increase in skin resurfacing procedures in
direct proportion to the rise in non-invasive procedures.
Advances in laser and skin-tightening devices has increased
awareness of newer treatment options for patients and awak­
ened interest in older modalities such as peels. As newer
procedures evolve, integrating them with current skin resur­
facing modalities will be key to successful rejuvenation.
Physicians should take into account all of the changes that
occur in the aging face and their etiologies. This allows for
meticulous tailoring of resurfacing procedures and thought­
fully planned skin conditioning regimens, to ensure the most
satisfied patients.

96
SECTION I
CHAPTER 5.5 • Injectables and resurfacing techniques: Chemical peels
Table 5.5.7  Complications of chemical peels
Complication
Comments
Infection
Bacteriala
Gram positive (Staphylococcus aureus)
Gram negative (if skin was occluded)
Viralb
Herpes simplex virus
Varicella zoster virus
Candidac
Contact dermatitis
Eliminate all possible offending topicals
Switch to water to cleanse and bland emollients
Consider a mid-potency topical steroid ointmentd
Scarring
Areas of delayed healing
Areas of “angry” redness
Consider intralesional steroids
Consider a mid-potency topical steroid ointment
Consider pulsed dye laser series
Dyschromia
Post inflammatory hyperpigmentation
Resolves with topical agents and light peels
Post inflammatory hypopigmentation
Can be permanent. May be improved with fractionated laser or microneedling.
aCulture and sensitivities necessary to rule out MRSA (methicillin-resistant S. aureus).
bDirect fluorescent antibody test gives a quick diagnosis.
cKOH prep of a skin scraping can help identify the presence of this yeast.
dVery cautious use of topical steroids during the re-epithelialization stage.
6. Obagi S, Obagi Z, Bridenstine JB. Isotretinoin use during chemical
skin resurfacing: a review of complications. Am J Cosmet Surg.
2002;19:9–13. A retrospective study of chemical peel patients looking at
the incidence of hypertrophic scarring in patients that recently took
isotretinoin, were on isotretinoin, or took isotretinoin during the
perioperative period. The study found that past, current, and postoperative
use of isotretinoin did not result in hypertrophic scarring if the depth of
the peel was kept to the papillary dermis.
12. Spencer L, Obagi S. Cosmetic dermatologic skin care: the essence of
our training. J Cosmet Dermatol. 2007;20:663–669.
14. Didierjean L, Tran C, Sorg O, et al. Biological activities of topical
retinaldehyde. Dermatology. 1999;199(suppl 1):19–24.
15. Hevia O, Nemeth AJ, Taylor JR. Tretinoin accelerates healing after
trichloroacetic acid chemical peel. Arch Dermatol. 1991;127:678–682.
18. Monheit GD. The Jessner’s–trichloroacetic acid peel. An enhanced
medium-depth chemical peel. Dermatol Clin. 1995;13:277–283.
Details the indications for Jessner’s-trichloroacetic acid peel and how to
perform the peel. Describes the rationale behind using Jessner’s solution
prior to TCA application.
19. Coleman WP, Futrell JM. The glycolic acid and trichloroacetic acid
peel. J Dermatol Surg Oncol. 1994;20:76–80.
20. Obagi Z, Obagi S, Alaiti S, Stevens M. TCA-based blue peel: a
standardized procedure with depth control. Dermatol Surg.
1999;25:773–780. Details the mechanism of action of TCA peels while
describing the rationale behind the TCA-based blue peel. In addition,
explains in detail how to perform the TCA-based blue peel.
23. Hetter GP. An examination of the phenol–croton oil peel: part I.
Dissecting the formula. Plast Reconstr Surg. 2000;105:227–239,
discussion 249–51. Describes the factors affecting the depth of
penetration of phenol acid peels. The author breaks down the various
components of the phenol peel solutions and identifies the role each of
them plays. He further details the important role of croton oil in driving
the phenol peels deeper.
24. Stone PA. The use of modified phenol for chemical face peeling.
Clin Plast Surg. 1998;25:21–44.
27. Zhang AY, Obagi S. Diagnosis and management of skin resurfacing-
related complications. Oral Maxillofac Surg Clin North Am.
2009;21:1–12. An overview of the common and rare complications
associated with skin resurfacing. Evaluation, diagnosis, and management
is discussed in detail. Photographs are shown to illustrate these
complications.
Access the complete reference list online at

96.e1
References
References
1. American Society of Plastic Surgeons. 2014 Plastic Surgery Statistics
Report. Available at: <
News/Statistics/2014/plastic-surgery-statistics-full-report-
2014.pdf>.
2. Khatri KA. Diode laser hair removal in patients undergoing
isotretinoin therapy. Dermatol Surg. 2004;30:1205–1207.
3. Chandrashekar BS, Varsha DV, Vasanth V, et al. Safety of
performing invasive acne scar treatment and laser hair removal in
patients on oral isotretinoin: a retrospective study of 110 patients.
Int J Dermatol. 2014;53:1281–1285.
4. Picosse FR, Yarak S, Cabral NC, et al. Early chemabrasion for acne
scars after treatment with oral isotretinoin. Dermatol Surg.
2012;38:1521–1526.
5. Kim HW, Chang SE, Kim JE, et al. The safe delivery of fractional
ablative carbon dioxide laser treatment for acne scars in Asian
patients receiving oral isotretinoin. Dermatol Surg. 2014;40:
1361–1366.
6. Obagi S, Obagi Z, Bridenstine JB. Isotretinoin use during chemical
skin resurfacing: a review of complications. Am J Cosmet Surg.
2002;19:9–13. A retrospective study of chemical peel patients looking at
the incidence of hypertrophic scarring in patients that recently took
isotretinoin, were on isotretinoin, or took isotretinoin during the
perioperative period. The study found that past, current, and postoperative
use of isotretinoin did not result in hypertrophic scarring if the depth of
the peel was kept to the papillary dermis.
7. Dingman DL, Hartog J, Sieminonow M. Simultaneous deep-plane
face-lift and trichloroacetic acid peel. Plast Reconstr Surg.
1994;93:86–93, discussion 4–5.
8. Taghizadeh F, Leibowitz A, Ellison T, et al. Short flap rhytidectomy
and fractional CO2 laser rejuvenation of the aging face. J Cosmet
Dermatol. 2013;12:49–56.
9. Jackson IT, Yavuzer R, Beal B. Simultaneous face lift and carbon
dioxide laser resurfacing: a proven technique. Plast Reconstr Surg.
2001;108:802–803.
10. Trelles MA, Brychta P, Stanek J, et al. Laser techniques associated
with facial aesthetic and reparative surgery. Facial Plast Surg.
2005;21:83–98.
11. Koch BB, Perkins SW. Simultaneous rhytidectomy and full-face
carbon dioxide resurfacing: a case series and meta-analysis. Arch
Facial Plast Surg. 2002;4:227–233.
12. Spencer L, Obagi S. Cosmetic dermatologic skin care: the essence of
our training. J Cosmet Dermatol. 2007;20:663–669.
13. Weinstein GD, Nigra TP, Pochi PE, et al. Topical tretinoin for
treatment of photodamaged skin. A multicenter study. Arch
Dermatol. 1991;127:659–665.
14. Didierjean L, Tran C, Sorg O, et al. Biological activities of topical
retinaldehyde. Dermatology. 1999;199(suppl 1):19–24.
15. Hevia O, Nemeth AJ, Taylor JR. Tretinoin accelerates healing
after trichloroacetic acid chemical peel. Arch Dermatol.
1991;127:678–682.
16. Moy LS, Howe K, Moy RL. Glycolic acid modulation of collagen
production in human skin fibroblast cultures in vitro. Dermatol Surg.
1996;22:439–441.
17. Bridenstine JB, Dolezal JF. Standardizing chemical peel solution
formulations to avoid mishaps: great fluctuations in actual
concentrations of trichloroacetic acid. J Dermatol Surg Oncol.
1994;20:813–816.
18. Monheit GD. The Jessner’s–trichloroacetic acid peel. An enhanced
medium-depth chemical peel. Dermatol Clin. 1995;13:277–283.
Details the indications for Jessner’s-trichloroacetic acid peel and how to
perform the peel. Describes the rationale behind using Jessner’s solution
prior to TCA application.
19. Coleman WP, Futrell JM. The glycolic acid and trichloroacetic acid
peel. J Dermatol Surg Oncol. 1994;20:76–80.
20. Obagi Z, Obagi S, Alaiti S, Stevens M. TCA-based blue peel: a
standardized procedure with depth control. Dermatol Surg.
1999;25:773–780. Details the mechanism of action of TCA peels while
describing the rationale behind the TCA-based blue peel. In addition,
explains in detail how to perform the TCA-based blue peel.
21. Brody HJ. Deep peeling. In: Brody HJ, ed. Chemical
Peeling and Resurfacing. 2nd ed. St. Louis, MO: Mosby;
1997:137–160.
22. Truppman ES, Ellenby JD. Major electrocardiographic
changes during chemical face peeling. Plast Reconstr Surg.
1979;63:44–48.
23. Hetter GP. An examination of the phenol–croton oil peel: part I.
Dissecting the formula. Plast Reconstr Surg. 2000;105:227–239,
discussion 249–51. Describes the factors affecting the depth of
penetration of phenol acid peels. The author breaks down the various
components of the phenol peel solutions and identifies the role each of
them plays. He further details the important role of croton oil in driving
the phenol peels deeper.
24. Stone PA. The use of modified phenol for chemical face peeling.
Clin Plast Surg. 1998;25:21–44.
25. Moy LS, Peace S, Moy RL. Comparison of the effect of various
chemical peeling agents in a mini-pig model. Dermatol Surg.
1996;22:429–432.
26. Johnson JB, Ichinose H, Obagi ZE, et al. Obagi’s modified
trichloroacetic acid (TCA)–controlled variable-depth peel: a study of
clinical signs correlating with histological finding. Ann Plast Surg.
1996;36:225–237.
27. Zhang AY, Obagi S. Diagnosis and management of skin resurfacing-
related complications. Oral Maxillofac Surg Clin North Am.
2009;21:1–12. An overview of the common and rare complications
associated with skin resurfacing. Evaluation, diagnosis, and management
is discussed in detail. Photographs are shown to illustrate these
complications.

SECTION I • Aesthetic Surgery of the Face
6.1 
Facelift: Facial anatomy and aging
Bryan Mendelson and Chin-Ho Wong
Introduction
The pathogenesis of facial aging is explained on an anatomical
basis, particularly the variations in the onset and outcome of
aging seen in different individuals. An anatomical approach
to surgical rejuvenation of the face provides the way to obtain­
ing a “natural” result that is lasting and with minimal
morbidity.
Fundamental to safety when operating in the face is a firm
grounding in the principles on which the facial soft-tissue
layers are constructed.1 Understanding the relations of the
facial nerve branches to these facial soft-tissue layers, retain­
ing ligaments, and soft-tissue spaces is crucial in predicting
the location of the facial nerves. This is most important in
addressing the overriding concern of the location and course
of the facial nerve branches when performing surgery.
Regions of the face
The traditional approach to assessing the face is to consider
the face in thirds (upper, middle, and lower thirds).2 While
useful in selecting surgical procedures in addressing patient’s
concerns, this approach limits conceptualization, as it is not
based on the function of the face. From a functional perspec­
tive, the face has an anterior aspect and a lateral aspect. The
anterior face is highly evolved for communication and facial
expression. In contrast, the lateral face predominantly covers
the structures involved in mastication.3 A vertical line descend­
ing from the lateral orbital rim is the approximate division
between the anterior and lateral zones of the face. Internally,
a series of facial retaining ligaments are strategically located
along this line to demarcate the anterior from the lateral face
(Fig. 6.1.1). The mimetic muscles of the face are located in the
superficial fascia of the anterior face, mostly around the eyes
and the mouth. This highly mobile area of the face is designed
to allow fine movement and is prone to develop laxity with
aging. In contrast, the lateral face is relatively immobile as it
overlies the structures to do with mastication – the temporalis,
masseter, the parotid gland and its duct – all located deep to
the deep fascia. The only superficial muscle in the lateral face
is the platysma in the lower third, which extends to the level
of the oral commissure.
Importantly, the soft tissues of the anterior face are subdi­
vided into two parts: the highly specialized sphincters overly­
ing the bony cavities and the part that overlies the skeleton.4
The soft tissues that overlie the orbital and oral cavities are
modified, as there is no deep fascial layer for support. As the
support cannot come from within the space immediately
behind, by way of “compensation” the support comes from
the rim of the bony cavities by a system of highly specialized
retaining ligaments. The fixation at these transitions zones
(between areas that overlie the skeleton and bony cavities),
while not seen in youth become increasingly evident with
aging.
Surgical anatomy of the face: SMAS,
facial spaces, and retaining ligaments
The five concentric layers of the face are1,4 (1) skin; (2) subcu­
taneous tissue; (3) musculo-aponeurotic layer (SMAS); (4)
loose areola tissue; and (5) deep fascia. This five-layered
arrangement is most clearly seen in the scalp and forehead
(due to expansion of the soft tissues as a result of evolutionary
expansion of the underlying cranial vault necessary to accom­
modate the highly developed frontal lobe in humans). The
scalp is an excellent place to study the principles of the layered
anatomy (Fig. 6.1.2). Layer 4 (the loose areolar tissue) is the
layer that allows the superficial fascia (defined as the compos­
ite flap of layers 1 through 3) to glide over the deep fascia
(layer 5), as noted with facial expression where the frontalis
functions independent of the deeper muscle of mastication,
the temporalis. The simplified anatomy over the scalp gives
the basic prototype of layer 4. There are no structures crossing
this plane, which is essentially an avascular gliding space. At
  Access video lecture content for this chapter online at expertconsult.com

98
SECTION I
CHAPTER 6.1 • Facelift: Facial anatomy and aging
producing melanocytes and antigen-presenting Langerhans
cells. A rich vascular plexus is an important component of the
dermis. The thickness of the dermis relates to its function and
tends to be inversely proportionate to its mobility. The dermis
is thinnest in the eyelids and thickest over the forehead and
the nasal tip. The thinner the dermis, the more susceptible it
is to qualitative deterioration aging changes like wrinkling
and formation of creases.
Layer 2 – subcutaneous tissue
The subcutaneous layer has two components: the subcutane­
ous fat, which provides volume, and the fibrous retinacular
the boundaries of the scalp along the superior temporal line
and across the supraorbital rim, the scalp and the forehead
are firmly anchored by ligamentous attachments. Vital struc­
tures such as nerves and vessels are always located in close
proximity to the retaining ligaments when transitioning from
deep to superficial in their course. In other parts of the face,
while the principles of construction remain the same, there is
considerably greater complexity. This is due to the compac­
tion resulting from the absence of forward projection of the
midface (as occurs in other species) and the predominance of
the orbital and oral cavities that limit the availability of a bony
platform for attachment of retaining ligaments and muscles.
To secure these five layers to the facial skeleton, an elaborate
system of retaining ligaments bind the dermis to the skeleton
(or deep fascia where the facial skeleton is covered by skeletal
muscles for mastication); the components of this system pass
through all layers (Figs. 6.1.3 & 6.1.4).5,6
Layer 1 – skin
The epidermis is a cell-rich layer composed mainly of differ­
entiating keratinocytes and a smaller number of pigment-
Fig. 6.1.1  Regions of the face. A vertical line of retaining ligaments (shown in red)
separates the mobile anterior face from the relatively fixed lateral face. The anterior
face is functionally adapted for facial expression while the lateral face passively
overlies the masticatory structures. The ligaments are, from above, temporal, lateral
orbital, zygomatic, masseteric and mandibular ligaments. The prezygomatic space
allows a functional separation of the crowded midcheek structures into two
separate, but overlapping, parts. The orbital-related structures, the orbicularis
retaining ligament and orbicularis oculi, are superficial, extending in the roof of the
prezygomatic space (shaded blue), while the perioral part is below and deeper
(shaded yellow). This includes the floor of the prezygomatic space and the
deeper structures, the zygomatic muscle origins and the zygomatic ligaments.
(© Dr. Levent Efe, CMI.)
Fig. 6.1.2  The five-layered basic construct of the facial soft tissues is most readily
understood in the scalp. While this same construct continues over the entire face,
there are significant regional modifications for functional purposes. Layer 4, the
most variable layer, contains soft-tissue spaces alternating with retaining ligaments.
In addition, the facial nerve branches travel through layer 4, where they remain
outside the spaces and then ascend to layer 3 in close relationship with retaining
ligaments. (© Dr. Levent Efe, CMI.)

99
Surgical anatomy of the face: SMAS, facial spaces, and retaining ligaments
subcutaneous tissue, the retinacular cutis lengthens signifi­
cantly, predisposing its fibers to weakening and distension
with aging. Within the subcutaneous tissue, the overall attach­
ment to the overlying dermis is stronger and denser than the
attachment to the underlying SMAS. This is a result of the
tree-like arrangement of the retinacular cutis fibers (see Fig.
6.1.3), with fewer but thicker fibers deep as its rises through
the SMAS that progressively divide into multiple fine micro­
ligaments as they reach the dermis. This explains why it is
easier to perform subcutaneous dissection in the deeper sub­
cutaneous level (just on the surface of the underlying SMAS)
than more superficially nearer the dermis, as there are fewer
retinacular cutis fibers and the subcutaneous fat here does not
attach directly to the outer surface of the underlying SMAS.
Furthermore, the retinacular cutis fibers are not uniform
across the face, but vary in orientation and density according
to the anatomy of the underlying deeper structures.7 As will
be apparent when the anatomy of the underlying layer 4 is
described, at the location of the retaining ligaments, the verti­
cally orientated retinacular cutis fibers are the most dense and
are the most effective in supporting the overlying soft tissues
and, in so doing, form boundaries that compartmentalize the
subcutaneous fat. These areas, such as the so-called McGregor’s
patch over the body of the zygoma, often require sharp release
to mobilize. In between these retaining ligaments in layer 4
are located the soft-tissue spaces of the face that facilitate the
mobility of the superficial fascia over the deep fascia. Where
the subcutaneous fat overlies a space, the retinacular fibers
are less dense and orientated more horizontally, as a result of
which, the tissues tend to separate with relative ease, often
with just simple blunt finger dissection (Fig. 6.1.5). This varia­
tion in the density and orientation of the retinacular cutis
fibers in the subcutaneous fat is the anatomical basis for
the so-called “superficial subcutaneous fat” compartments
recently described.9–11 In these studies, injection of dyes into
the subcutaneous fat results in staining of the fat in discrete
compartments. While the relevance of superficial subcutane­
ous fat compartments remains debated, anatomically it is part
of layer 2, with diffusion of the injected dye being limited
by the retaining ligaments at the boundaries of these
compartments.12
cutis that binds the dermis to the underlying SMAS of the
face.7,8 Of note, the retinacular cutis is the name given to that
portion of the retaining ligament that passes through the sub­
cutaneous tissues. The amount, proportion, and arrangement
of each component vary in different regions of the face. In the
scalp, the subcutaneous layer has uniform thickness and con­
sistency of fixation to the overlying dermis. In contrast, in the
face proper, the subcutaneous layer has significant variation in
thickness and attachments. In specialized areas such as the
eyelids and lips, this layer is significantly compacted such that
fat may appear non-existent. In other areas, such as the
nasolabial segment, it is very thick.4 In areas with thick
Fig. 6.1.3  The form of the retaining ligaments
can be likened to a tree. The “trunk” of the
ligaments attach the soft tissues to the
periosteum of the facial skeleton or deep
muscle fascia. The ligaments pass through all
soft-tissue layers, fanning out as multiple
branches through the SMAS to eventually
insert into the dermis. The ligamentous
component in the subcutaneous layer is seen
as the retinacular cutis. (© Dr. Levent Efe,
CMI.)
A
B
Fig. 6.1.4  The retaining ligaments of the face appear in three morphological forms:
adhesions, septae, and true ligaments. (© Dr. Levent Efe, CMI.)

100
SECTION I
CHAPTER 6.1 • Facelift: Facial anatomy and aging
and contains the following structures: (1) soft-tissue spaces;
(2) retaining ligaments; (3) deep part of the intrinsic muscles
where passing from their bone attachment to their more super­
ficial soft-tissue origin; and (4) facial nerve branches, passing
from deep to superficial. Functionally, a series of soft-tissue
spaces exist in layer 4 to allow independent movement of the
periorbital and perioral muscle of facial expressions (located
in the roof of the facial soft-tissue spaces) over the deep fascia
on the major muscles for mastication directly beneath (located
beneath the floor of the facial soft-tissue spaces).16 The retain­
ing ligaments of the face are strategically placed within the
boundaries between the soft-tissue spaces (Fig. 6.1.6). In
the lateral face, immediately in front of the ear, extending
25–30 mm forward of the ear cartilage to the posterior border
of the platysma, is a diffuse area of ligamentous attachment,
described by Furnas as the platysma auricular fascia (PAF).7
As no facial expression occurs here, the dermis, subcutane­
ous tissue, SMAS, and the underlying parotid capsule (layers
1–5) are bound together as an area of diffuse retaining liga­
ment. Layer 4 here is reduced to a layer of fusion without a
soft-tissue space, as mobility of the superficial fascia is not
required here. In contrast, in the anterior face where there
is considerable movement over and around the bony cavi­
ties, the ligaments are significantly compacted and arranged
around the edges of the bony cavities. These boundaries
provide the last position where there is underlying deep fascia
for the mobile shutters of the eyelids and lips to be supported.
Importantly for the surgeon, the retaining ligaments also act
as transition points for the facial nerve branches to pass from
deep to superficial on their way to innervate their target
muscles.
Layer 3 – musculo-aponeurotic layer
The muscles of facial expression are unique and fundamen­
tally different from skeletal muscles beneath the deep fascia
because they are situated within the superficial fascia and
they move the soft tissues of which they are a part. All muscles
of facial expression have either all or the majority of their
course within layer 3, and they are predominantly located
over and around the orbital and oral cavities. In the prototype
scalp, the occipital–frontalis moves the overlying soft tissue
of the forehead, while its undersurface glides over the subga­
leal aponeurotic space (layer 4). Layer 3 is continuous over
the entire face, although for descriptive purposes, different
names are given to certain parts according to the superficial
muscle within. It is called the galea over the scalp, the tempo­
roparietal (superficial temporal) fascia over the temple, the
orbicularis fascia in the periorbital region, the SMAS over the
mid- and lower face and platysma in the neck.13
Within layer 3, the facial muscles themselves have a
layered configuration, with the broad, flat muscles forming
the superficial layer that covers the anterior aspect of the face.
The frontalis covers the upper, obicularis oculi the middle,
and the platysma the lower thirds, respectively. The muscles
of this layer have minimal direct attachment to the bone,
stabilized to the skeleton at their periphery indirectly by
the vertically orientated retaining ligaments as noted earlier.
The frontalis is fixed along the superior temporal line by the
superior temporal septum, the obicularis oculi laterally by
the lateral orbital thickening and the main zygomatic liga­
ment at its inferolateral border, and the platysma at its upper
border by the lower key masseteric ligament. The deeper
muscles in layer 3 provide greater functional control of the
sphincters over the bony cavities. For the upper third, these
are the corrugators and procerus, and around the oral cavity,
the elevators (zygomaticus major and minor, levator labii
superioris, levator anguli oris) and levator labii superioris
alaeque nasi and the depressors (depressor anguli oris,
depressor labii inferioris) around the oral sphincter and the
mentalis.1
Layer 4
Layer 4 is the plane in which dissection is performed in
subSMAS facelifts.14,15 It is an area of significant complexity
Fig. 6.1.6  Topographical anatomy of layer 4 over the lateral face. Spaces (blue),
ligaments (red), and the areas of important anatomy (stippled). The largest area of
ligamentous attachment, the platysma–auricular fascia (PAF), overlies the parotid,
including its accessory lobe, and dominates the posterior part of level 4 in the least
mobile part of the face. At the vertical line of retaining ligaments, the lateral face
transitions into the anterior face. The spaces over the zygoma and over the lower
masseter allow for intermediate mobility. The triangular areas immediately above
and below the arch of the zygoma contain important anatomy, namely the temporal
and zygomatic branches of the facial nerve, respectively, that proceed from lateral
into the anterior face. The asterisk indicates the uppermost premasseteric area.
(© Dr. Levent Efe, CMI.)
Fig. 6.1.5  The effective strength of the retinacular cutis fibers varies in different
areas of the face. Overlying the retaining ligaments, the fibers are more densely
arranged and vertically oriented. As a result, surgically raising a subcutaneous flap
here usually requires sharp release. In contrast, in the subcutaneous compartments
overlying the subSMAS spaces, the retinacular fibers are less dense and more
horizontally oriented, so that a relatively easy blunt dissection is usually sufficient
to elevate the subcutaneous facelift flap here. (© Dr. Levent Efe, CMI.)

101
Facial spaces
the lamellae remain quite separate, i.e., the preseptal obicu­
laris does not have an attachment to the septum orbitale. This
is the anatomical basis for the surgically significant preseptal
space of the lower lid. In the upper lids, there is not an equiva­
lent space as the submuscular fat pad over the superior orbital
rim continues on the outer surface of the septum orbitale
where it is adherent to the overlying fascia on the underside
of the orbicularis almost down to where the levator crosses
into the orbicularis.
The extent of the vestibule of the oral cavity, covering the
maxilla and the mandible, has a major impact on the suscep­
tibility to aging of the overlying soft tissue. The skeleton
underlying the space is unavailable to provide ligamentous
attachment for support of the soft tissues that cover this large
area. The extreme mobility of the lip and adjacent part of the
cheek renders it susceptible to aging changes and the indica­
tion for a lower facelift is largely to correct aging changes in
this unsupported tissue.
Facial spaces
A large part of the subSMAS layer 4 consists of soft-tissue
“spaces”. These spaces have defined boundaries that are
strategically reinforced by retaining ligaments.4,6,21 Signifi­
cantly, these areas are by definition anatomically “safe spaces”
to dissect, as no structures cross within and all branches of the
facial nerve are outside these spaces. As the roof of each space
Fig. 6.1.7  The soft-tissue anatomy over the midcheek skeleton, showing the
arrangement of the spaces (preseptal, prezygomatic, and premaxillary) and the
related ligaments (orbicularis retaining, above, and zygomatic and maxillary, below)
to the bony, orbital, and oral cavities. (© Dr. Levent Efe, CMI.)
The soft-tissue spaces of the face are in two forms: (1) those
overlying bony cavities, such as the preseptal space of the
eyelid over the orbit and the vestibule of the oral cavity under
the lips and the lower nasolabial segment of the cheek; and
(2) those overlying bone, where the spaces allow the overlying
superficial fascia to glide freely over the deeper layer 5.
Layer 5
The deep fascia, the deepest soft-tissue layer of the face, is
formed by the periosteum where it overlies bone. Over the
lateral face, where the muscle of mastication (temporalis and
masseter) overlie the bone, the deep fascia is instead the
fascial covering of the muscles, the deep temporal fascia and
masseteric fascia above and below the zygomatic arch, respec­
tively. The parotid fascia is also part of the deep fascia. The
investing deep cervical fascia is the corresponding layer in the
neck where it covers the supraomohyoid muscles and splits
to form the submandibular space that contains the subman­
dibular gland. The deep fascia, although thin, is tough and
unyielding and gives attachment to the retaining ligaments of
the face. In the mobile shutters over the bony cavities, the
deep fascia is absent, being replaced by a mobile lining
derived from the cavities, that of the conjunctiva or oral
mucosa. The recently described “deep fat compartments” is
fat located in layer 5, having more generally been called
preperiosteal fat.11,12
Anatomy over the cavities
in the skeleton
The general pattern of the five-layered anatomy is modified
where the orbital, oral, and nasal cavities are present over the
anterior face (Fig. 6.1.7). Only the outer three-layer composite
continues into the soft tissue overlying the cavities. The SMAS
layer within this composite includes the sphincteric obicularis
muscles that extend to the free edge of the soft-tissue aperture
of the eyelids and lips. The retaining ligaments, which are
such a key feature of the five-layered anatomy, are not present
over the cavities. Thus, there are anatomical and functional
transitions from the relative stability over fixed areas to the
high mobility of the soft-tissue shutters over the cavities. In
order to support this composite, the retaining ligaments are
condensed and compacted along the bony orbital rim (Fig.
6.1.8). This is the anatomical basis for the periorbital ligament
around the orbit, of which the lower lid part is the orbicularis
retaining ligament, which stabilizes the orbicularis oculi to the
orbital rim periosteum.17–20 Around the oral cavity, the liga­
ments arise from the platform of the body of the zygoma and
from the deep fascia over the masseter.21
The deeper component of the eyelids and lips are derived
from the cavity they cover and are not an extension of the
facial soft tissues. In the eyelid, the deeper lid muscles
with their related aponeurosis (levator and capsulopalpebral
fasciae) and fat are retained by the fascial system of the septum
orbitale. The free edges of the upper and lower eyelids obtain
their ligamentous support from the tarsal plates, with their
canthal tendon attachments to the medial and lateral orbital
rims. In the pretarsal area, the superficial and deep lid struc­
tures, the anterior and posterior lamellae, merge. But in
between the orbital rim and the pretarsal area of the lower lid,

102
SECTION I
CHAPTER 6.1 • Facelift: Facial anatomy and aging
septum can be released sharply, taking care only to preserve
the lateral (deep) branch of the supraorbital nerve, which
runs parallel to the septum about 0.5 cm medial to it.17 The
inferior temporal septum provides a marker to the important
anatomy here as the temporal branches of the facial nerve are
located parallel to and immediately inferior to this septum.
To release the inferior temporal septum, the ceiling of the
space is gently lifted off the deep temporal fascia floor, which
three-dimensionalizes the septum in preparation for gentle
release at the level of the floor, bearing in mind the frontal
branches are located on the underside of the temporoparietal
fascia in the ceiling, under the roof of the lower temporal
area. Once released, the sentinel vein comes into view. The
sentinel vein is not a good landmark for locating the temporal
branches as they course cephalad to the vein, between it and
the inferior temporal septum, where they travel in a layer
of fat suspended on the underside of the temporoparietal
fascia.
Prezygomatic space
This triangular-shaped space overlies the body of the zygoma,
its floor covering the origins of the zygomatic muscles. The
space allows the independent displacement of the obicularis
oculi (pars orbitale) in its roof from the zygomatic muscles
is the least supported part, they are more prone to developing
laxity here with aging, compared to their ligament-reinforced
boundaries. This differential laxity accounts for much of the
characteristic changes that occur with aging. Once a space has
been surgically defined to its boundaries, the retaining liga­
ments in the boundary can then be precisely released under
direct vision to achieve the desired mobilization while pre­
serving the vital structures closely associated with the liga­
ments. A brief description of surgically significant facial
soft-tissue spaces is given below.
Upper temporal space
Overlying the temple are two compartments that are sepa­
rated by the obliquely oriented inferior temporal septum (Fig.
6.1.9). The upper compartment is a true space, and the lower
compartment is not a space, but an area containing important
anatomy.17 Both compartments are interposed between the
superficial temporal fascia (temporoparietal fascia) and the
deep temporal fascia (temporalis muscle fascia). Anatomi­
cally, the upper compartment is an extension of the forehead
anatomy down into the upper temple, and the lower compart­
ment is an upward extension of the upper cheek anatomy into
the lower temple.22
The upper temporal space is separated from the forehead
by the superior temporal septum (STS) along the superior tem­
poral line. Anteroinferiorly, the upper space is separated from
the lower triangular temporal area that contains important
anatomy, by the inferior temporal septum (ITS). These two
septi merge at the triangular-shaped zone of adhesion called
the temporal (orbital) ligament.17 The upper temporal space
readily provides safe surgical access to the lateral brow and
upper midcheek.23 The space can be readily opened by blunt
dissection to its boundaries. Once identified, the boundaries
are then released by precise dissection. The superior temporal
Fig. 6.1.9  Structures around the orbital cavity in level 4. Above is the upper
temporal space between the retaining ligaments of the temple, the superior
temporal septum (STS) and the inferior temporal septum (ITS), both being
extensions of the temporal ligamentous adhesion (TLA). There are no structures in
the upper temporal space. The TLA continues medially as the supraorbital
ligamentous adhesion (SLA). Below the bilaminar inferior temporal septum is the
triangular-shaped lower temporal area of important anatomy (stippled), where the
temporal branches of the facial nerve (TFN) course immediately inferior to the
septum on the underside of the temporoparietal fascia. Also crossing level 4 in this
area are the medial and lateral branches of the zygomatic temporal nerve (ZTN) and
the sentinel vein. The periorbital septum (PS, green) just outside the orbital rim
contains two areas of thickenings, the lateral orbital thickening (LOT) and the lateral
brow thickening (LBT). (© Dr. Levent Efe, CMI.)
Fig. 6.1.8  The system of retaining ligaments situated around the bony cavities
stabilizes the soft tissue, both over and around the cavities. (© Dr. Levent Efe,
CMI.)

103
Facial spaces
under the floor. Contraction of the overlying orbicularis
elevates the prezygomatic soft tissues, which results in
zygomatic smile lines (below the crows feet) (Fig. 6.1.10).18
With aging laxity, the roof of the space rests at a lower level.
As a result, there is a now a greater amplitude of move­
ment on orbicularis contraction, which exaggerates the
zygomatic lines with aging. This aging of the prezygomatic
space, with bulging over its roof accentuated by its well-
supported boundaries, is the anatomical basis for the clinical
entity variously described as malar mounds, bags, or malar
crescent. This deformity indicates the presence of significant
laxity, and the treatment is directed to tightening the laxity of
the roof.
Premaxillary space
This quadrangular space (medial to the prezygomatic space)
overlies the maxilla.24 Its floor is formed by the levator labii
superioris. The space allows the independent displacement of
the obicularis oculi in its roof from the lip elevators under the
floor. Fig. 6.1.11 details the anatomical relations of the premax­
illary space. This space is clinically significant in that laxity
over its roof contributes to the deepening of the nasolabial
fold with aging.
Fig. 6.1.10  The prezygomatic space overlies the body of the zygoma. The origins
of the zygomatic muscles extend under the floor between preperiosteal fat. The roof
is formed by the orbicularis oculi lined by the thin suborbicularis oculi fat (SOOF).
The upper ligamentous border, formed by the orbicularis retaining ligament, is not
as strong as the zygomatic ligament-reinforced lower border. (© Dr. Levent Efe,
CMI.)
Fig. 6.1.11  The anatomy and key relations of the premaxillary space. TTL, tear
trough ligament; ORL, orbicularis retaining ligament. (© Dr. Levent Efe, CMI.)
Lower premasseter space
This space overlies the lower half of the masseter and is
analogous to the temporal space in that it overlies the deep
fascia of a muscle of mastication (Fig. 6.1.12).21 This gliding
soft-tissue plane allows opening of the jaw without restriction
and avoids excessive distortion of the overlying soft tissues.
The roof of this space is formed by the platysma. The lower
premasseter space has profound clinical significance as it
is the anatomical basis for the development of jowls with
aging. Laxity in the roof of the space, particularly where
it has a weakened attachment to the anterior masseter by
the masseteric ligaments and its inferior boundary where
there is no ligament, manifests as the labiomandibular fold
and jowl, respectively. The relatively stable fixation at the
anteroinferior corner of the premasseter space provided by
the mandibular ligament accounts for the dimple that is com­
monly seen separating the labimandibular fold above and the
jowl below.
Middle premasseter space
The middle premasseter space is a rectangular space cepha­
lad to the lower premasseter space (Fig. 6.1.13).25 Its floor is
formed by the masseteric fascia and its roof by the SMAS,
but the platysma in the roof of the lower space does not
extend up to this level. It is an important facial soft-tissue
space in subSMAS facelift as it is an anatomical safe area to
dissect, with the facial nerve branches located immediately
outside the space within its superior and inferior boundar­
ies. The parotid gland and the duct are closely associated
with the upper boundary of the middle premasseter
space.

104
SECTION I
CHAPTER 6.1 • Facelift: Facial anatomy and aging
key retaining ligament of the upper midcheek.28 It is located
just outside the orbital rim and closely follows the edges of
the rim. This retaining ligament system separates the bony
cavity (the orbit) from the bony platform (that of the midcheek
skeleton) below, functioning to stabilize and secure the soft
tissues of the lower eyelid where it transitions from the rela­
tive stability over the bone to the mobile area over the orbital
cavity.
The tear trough ligament is a true osteocutaneous ligament
originating from the maxilla and inserting into the dermis of
the tear trough, passing through and binding all five soft-
tissue layers together.28 As previously shown, this retaining
ligament is the anatomical basis for the tear trough deformity
(Fig. 6.1.14). Laterally, the tear trough ligament continues as
the orbicularis retaining ligament. The orbicularis retaining
ligament has previously been demonstrated to be the ana­
tomical basis for the palpebromalar groove. The continuity of
the tear trough ligament with the orbicularis retaining liga­
ment then explains the observation that with more advanced
aging, the tear trough becomes continuous with the palpebro­
malar groove, forming the prominent cutaneous groove
sometimes called a prominent “lid–cheek junction”. This
demonstrates the key role that facial soft-tissue retaining liga­
ments play in the cutaneous grooves seen with aging.
Facial nerve branches
The danger zones for facial nerve injury have been well
described in the literature, but this is of limited value to the
surgeon due to the topographical two-dimensional perspec­
tive this gives of the expected course of the nerve relative
to surface landmarks.29–31 Confidence when approaching the
nerve surgically comes from (1) an understanding of the
three-dimensional course of the nerve relative to the layered
anatomy as described above and (2) by visually identifying
the nerves in relation to defined landmarks (Fig. 6.1.15).32 The
facial nerve branches exit the parotid gland and remain deep
Buccal space
This is one of the deep facial spaces, being like the subman­
dibular space (which contains the submandibular gland),
deep to the deep fascia (layer 5).26,27 The buccal space is located
in the anterior face, medial to the anterior border of the mas­
seter above the level of the oral commissure in youth. The
space and its contents, the buccal fat, facilitate movement of
the overlying nasolabial segment of the midcheek, as well as
buffering this area from excessive motion from jaw move­
ment. Aging and attrition of the boundaries, particularly of
the masseteric ligaments inferiorly, result in the platysma
being less firmly bound to the masseter. This allows the space
to enlarge, as a consequence of which the buccal fat prolapses
inferiorly, below the level of the oral commissure into the
lower face. As the buccal fat comes to overlie the anterior
border of the lower masseter, it results in increased promi­
nence of the labiomandibular fold and jowl.
Retaining ligaments of the face
To illustrate key concepts that retaining ligaments function to
bind all five layers of the facial soft tissues together and that
they are the anatomical basis for cutaneous grooves (seen
between areas of laxity/bulges), let’s examine the midcheek.
The tear trough–orbicularis retaining ligament complex is the
Fig. 6.1.13  The middle premasseter space is located within the concavity of the
parotid overlying the anterior masseter, above the lower space. The upper and lower
buccal trunks of the facial nerve course outside the space within its upper and
lower boundaries. The masseteric process of the buccal fat pad is the only content
and is variable. (© Dr. Levent Efe, CMI.)
Fig. 6.1.12  The rhomboid-shaped lower premasseter space overlies the lower half
of the masseter. The platysma forms the roof of the lower space but does not
extend over the middle space. The posterior border of the space is defined by the
anterior edge of the parotid, while the anterior border is reinforced by the
masseteric ligaments near the anterior edge of the masseter. The inferior boundary
is mobile, mesentery-like, and does not contain any ligament. Weakness of
attachment of the platysma roof at the lower anterior and inferior boundaries leads
to the formation of the jowl, which is immediately behind the strong mandibular
ligament. The buccal space containing the buccal fat is anterior to the key
masseteric ligaments. All facial nerve branches course around and outside the
space. The surgically important mandibular branch, after leaving the fixed platysma
auricular fascia (PAF), courses under the inferior boundary of the space then rises
onto the mobile outer surface of the membranous inferior border before reaching
the mandibular ligament. (© Dr. Levent Efe, CMI.)

105
Facial nerve branches
transition to under the temporoparietal fascia (layer 3) at a
distance of 1.5–3 cm above the zygomatic arch. The temporal
branch transitions to the underside of the temporoparietal
fascia before the nerve crosses the sentinel vein more cephali­
cally. Thus, once the sentinel vein is visualized from the
temporal incision, the temporal branches would be located in
the roof of the lower temporal compartment, in the wafer-like
layer under the temporoparietal fascia.17
The zygomatic branch exits the parotid gland deep to the
deep fascia just below the zygoma and cephalad to the parotid
duct. It travels horizontally on the masseter with the trans­
verse facial artery. The strong zygomatic retaining ligament
arises from the lower border of the body of the zygoma,
immediately lateral to the origin of zygomaticus major. Here,
the main zygomatic nerve continues beneath the muscle and
runs under zygomaticus major and minor, which it supplies
from the deep aspect.39–41 At the lateral border of the zygomatic
ligament, a small motor branch is usually given off to supply
the orbicularis oculi, entering the muscle at its inferolateral
corner.41 Careful dissection by vertical spreading of the scis­
sors is crucial to avoid damaging this branch here.
The upper buccal trunk exits the parotid, about in line with,
but superficial to, the parotid duct and continues deep to the
investing masseter fascia, close to, but outside, the upper
boundary of the middle premasseter space.25 Approaching the
anterior edge of the masseter, this branch leaves the floor
under the masseter fascia in close association with the upper
key masseteric ligament. The lower buccal trunk leaves the
parotid lower down, at about the level of the earlobe, and
remains under the masseter fascia floor of the lower premas­
seter space and approaches the lower boundary of the middle
premasseter space. Similarly, upon approaching the anterior
edge of the masseter, the lower buccal trunk transitions from
deep to gain the underside of the SMAS in close association
to layer 5 in the lateral face. As they approach the anterior
face, the branches traverse layer 4, ascending to reach the
underside of the mimetic muscles of the face. It is at these
transition points across layer 4 that the nerves are at greatest
risk of injury.25,33 The transitions occur at predictable locations,
in close association with retaining ligaments that provide
stability and protection for the nerves. The surgical release of
these ligaments to gain the needed mobility should be per­
formed with extreme care on account of the proximity of the
nerves.
The surface marking of the temporal branch of the facial
nerve is along the Pitanguy line, from a point 0.5 cm below
the tragus to a point 1.5 cm lateral to the supraorbital rim.34–37
It is traditional teaching that once the temporal branch exits
the parotid, it immediately runs superficially from the deep
fascia and comes to lie just deep to the SMAS as it crosses the
arch of the zygoma. Because of its superficial location, surgical
transection of the SMAS here, so-called “high SMAS transec­
tion” (i.e., at or above the arch), has been generally discour­
aged. It is now apparent that the nerve is deeper than was
previously thought as it crosses the zygomatic arch. A histo­
logical study confirmed that the temporal branches are in
transition from where they exit the parotid below the zygo­
matic arch to where they enter the underside of the temporo­
parietal fascia some 2 cm above the arch.38 They course in a
tissue layer (layer 4), just deep to the temporoparietal fascia
(layer 3) and immediately superficial to the periosteum, and
above that, the temporalis fascia (layer 5), all along protected
by a fascial, fatty layer, which is an upward prolongation of
the parotid–masseteric fascia and named the parotid–temporal
fascia. In another study, the temporal branch was noted to
Fig. 6.1.14  The tear trough ligament, the anatomical basis for the tear trough
deformity. TTL, tear trough ligament; ORL, orbicularis retaining ligament; OO,
orbicularis oculi; PZs: prezygomatic space; LLS, levator labii superioris; Zmj:
zygomaticus major; Zmi: zygomaticus minor. (© Dr. Levent Efe, CMI.)
Fig. 6.1.15  Illustration to emphasize the location of the facial nerve branches and
the alteration of their course relative to the spaces and ligaments. The nerves stay
deep to and outside the spaces at all times in the lateral face. As they approach the
ligamentous boundary into the mobile anterior face, the facial nerve branches
transition from beneath layer 5 to enter layer 3, always in close relationship with the
retaining ligaments forming the boundary. The interconnecting nerve branches
between adjacent nerve trunks are located immediately subSMAS. (© Dr. Levent
Efe, CMI.)

106
SECTION I
CHAPTER 6.1 • Facelift: Facial anatomy and aging
Skin
Skin aging is influenced by genetics, environmental exposure,
hormonal changes, and metabolic processes.46–52 With aging,
the supple skin of youth becomes thinned and flattened, with
loss of elasticity and architectural regularity. Atrophy of the
extracellular matrix is reflected by the decreased number of
fibroblasts and decreased levels of collagen (especially types
I and III) and elastin in the dermis. While chronological skin
aging and photoaging can be readily distinguished and con­
sidered as separate entities, both share important molecular
features, that of altered signal transduction that promote
matrix metalloproteinase (MMP) expression, decreased pro­
collagen synthesis, and connective tissue damage. Oxidative
stress is considered of primary importance in driving the
aging process, resulting in increased hydrogen peroxide and
other reactive oxygen species (ROS), and decreased anti-
oxidant enzymes. These changes result in gene and protein
structure alterations. Other environmental factors, notably
smoking, accelerate skin aging by 10–20 years. Increased col­
lagenase and decreased skin circulation have been suggested
as possible mechanisms. The muscles of facial expression flex
the skin in a specific pattern. As the underlying collagen
weakens and the skin thins, the dermis loses its capacity to
resist the constant force of the muscles and these lines become
etched in the skin, ultimately even at rest.
Subcutaneous tissue
The fibrous and fat components in the subcutaneous tissue
are not uniform but arranged in discrete compartments. Due
to the prominence of the subcutaneous fat in particular sites,
it has been given specific names such as the “malar fat pad”
and “nasolabial fat”.53,54 The boundary of these subcutaneous
compartments corresponds to the location of the retaining
ligaments, which pass superficially to insert into the dermis.
In youth, the transition between compartments is smooth and
non-discernable. With aging, a series of concavities and con­
vexities develop, which separates these compartments. These
changes have been attributed to a number of causes including
fat descent, selective atrophy and hypertrophy, and attenua­
tion of the retaining ligaments that cause fat compartment
malpositioning. It is, however, now apparent that fat descends
minimally with aging.55 Distinct compartmentalization by the
retaining ligaments holds the fat in its relative position.
Muscle aging
Skeletal muscles, in general, have been noted to atrophy up
to 50% with age.56 This is presumably applicable to the muscle
of mastication such as the temporalis and masseter as a result
of decreased demand and deterioration of the dentition with
aging. As yet, no specific study on the effect of aging on these
muscles has been reported. The mimetic muscle of the face,
in contrast to skeletal muscles, may not undergo the same
degree of degeneration with aging because of its constant use
with facial expression. The obicularis oculi has been noted to
remain histologically unchanged with no loss of muscle fibers,
adherence to surrounding tissues, or ptosis with aging.57 The
upper lip elevators, zygomaticus major, and levator labii
superioris were also noted to remain unchanged with aging,
based on magnetic resonance imaging (MRI) of their length,
thickness, and volume.58 In contrast, the upper lip orbicularis
with the lower key masseteric ligament. After the nerves reach
level 3, the zygomatic, upper and lower buccal trunks, and
mandibular branch send an interconnecting branch with each
other before continuing their course to innervate the mimetic
muscles of the anterior face. This accounts for the overlap in
muscles innervated by these nerves.
The temporal and mandibular branches are the most sig­
nificant in terms of surgical risks because of the lack of cross-
innervation of their target muscles. The marginal mandibular
nerve is at risk where it is fixed by its close association with
the retaining ligaments, both early in its course, around the
angle of the mandible, where it is within the PAF, and then
well anteriorly close to the mandibular ligament.42–45 Over
most of its course, the mandibular branch is mobile, being in
relation to the inferior boundary of the premasseter space. It
is not necessary to dissect in the vicinity of the nerve because
of the inherent mobility of the platysma where it overlies the
jaw and submandibular area. The mobility of the nerve as it
travels within the inferior membranous boundary of the
lower premasseter space accounts for the reported variability
of the location of this part of its course (occasionally below
the mandible).
Aging changes of the face
The youthful face has the general appearance of high, rounded
fullness, while the aging process is characterized by a look of
depletion and sagging, suggestive of tiredness. Changes with
aging occur at every level of the facial anatomy, starting with
the facial skeleton. Current understanding of the aging process
remains largely empirical, given that it is based on the effec­
tiveness of treatments designed to satisfy the requirements of
patients for a younger appearance. Historically, stretching of
loose facial skin (traditional facelift), removal of apparent
tissue excess (traditional blepharoplasty), tightening the
dermis and evening the complexion (early phenol peels and
CO2 laser resurfacing) and, in recent years, soft-tissue volume
augmentation (lipofilling and soft-tissue fillers) have all had
a positive impact on rejuvenating appearance. The success of
each is attributed to having reversed a cause of facial aging.
Yet, when each of these modalities is continued as the sole
treatment, to further reverse the aging appearance, the results
tend to be bizarre, leading to the conclusion that multimodal
therapy is required to further reverse, what must be, multiple
components of the aging process.
An understanding of the changes that occur in the layered
anatomy forms the basis for logical treatment. Changes of the
skin are readily observable, and changes in the skeleton affect­
ing layer 5 can also be observed radiologically. Because the
changes within the superficial fascia (layers 2 and 3) are not
directly measurable, empiricism has remained prevalent. A
correlation of the surface anatomy changes of aging with the
anatomy of layers 2, 3, and 4 indicates that bulging occurs
over the roof of soft-tissue spaces, which stand out in contrast
to the absence of bulging of the adjacent cutaneous grooves.
The grooves reflect the restriction imposed by the dermal
insertions of the retaining ligaments at the boundaries of the
spaces. The extent to which the bulging reflects true elonga­
tion from primary tissue degeneration and laxity and how
much it is “apparent” laxity secondary to loss of volume
(skeletal and soft tissue) has yet to be defined.

107
Aging changes of the face
atrophies with aging, with decreased muscle thickness,
smaller muscle fascicles, and increase in surrounding
epimysium.
Facial spaces and retaining ligaments
The multi-linked fibrous system attenuates with aging,
decreasing strength of the ligaments, and increasing laxity. In
general, the spaces expand with aging in proportion to the
amount of movement. This is greatest with the lower premas­
seter space and the related mandibular movement and least
over the zygoma. Expansion is related to the laxity that devel­
ops in the ligamentous boundaries and results in bulges
between areas of relative fixation. Accordingly, the spaces
dissect easily in older patients, and the boundaries widen as
the ligaments weaken. In young people, the spaces are more
potential that real and do not open quite so easily with blunt
dissection (Fig. 6.1.16).
Bone changes
The facial skeleton changes dramatically with aging (Fig.
6.1.17), and this has a profound impact on the appearance of
the face with aging (Fig. 6.1.18).59–71 At birth, the facial skeleton
is underdeveloped and rudimentary. This explains why
infants and toddlers often transiently have visibly distinct
midcheek segments (despite excellent tissue quality), which
disappear with the expansion of the midcheek skeleton as
they grow older. Peak skeletal projection is probably attained
in early adulthood. Thereafter, while certain areas continue
to expand, selective areas of the facial skeleton undergo
significant resorption. Areas with strong predisposition to
resorption include the midface skeleton, particularly that part
contributed by the maxilla including the pyriform area of the
nose, the superomedial and inferolateral aspects of the orbital
rim, and the prejowl area of the mandible.72,73 The resultant
deficiencies in the skeletal foundation have a significant effect
on the overlying soft tissues. In the midcheek in particular,
retrusion of the maxilla causes increased prominence of the
tear trough and the nasolabial folds. The retrusion of the facial
skeleton causes the origin of the multi-linked fibrous retaining
ligaments to be displaced posteriorly. This pulls the skin
Fig. 6.1.16  In youth, the spaces are tight glide
plane spaces. With aging, the spaces expand, and
to a greater extent where facial movement is greater,
namely in the lower face where the lower
masseteric ligament fence distends the most. The
weakened attachment of the platysma to the
masseter here allows this corner of the lower
premasseter space to expand to form the jowl. The
reduction of ligament tone also allows the buccal
fat to descend inferiorly into the labiomandibular
fold. (© Dr. Levent Efe, CMI.)
Fig. 6.1.17  The arrows indicate the areas of the craniofacial skeleton most
susceptible to resorption with aging and the relative degree according to the arrow
size. (© Dr. Levent Efe, CMI.)
inwards, exaggerating the concavity between the areas of rela­
tive convexity that develop with aging. Retrusion of the
midcheek with loss of projection gives the visual impression
of tissue descent with aging. Some patients have a congeni­
tally weak – thus, inadequately projecting – skeletal structure.
In such cases, the skeleton may be the primary cause of the
manifestations of premature aging. Accordingly, in patients
who suffer premature facial aging, a weakness of the relevant

108
SECTION I
CHAPTER 6.1 • Facelift: Facial anatomy and aging
corrugator supercilii moves the eyebrow medially and pro­
duces vertical glabella lines. The oblique head of the corruga­
tor, the depressor supercilii, and the medial fibers of the
obicularis oculi act in concert to depress the medial brow and
produce oblique glabella frown lines. The procerus, also a
brow depressor, causes transverse nasal skin lines. Laterally,
the action of the lateral fibers of the obicularis oculi with the
transverse head of the corrugator supercilii promotes lateral
brow ptosis. The ptosis of the lateral brow together with, to a
lesser extent, the laxity of the skin with aging produces a
pseudo-excess of the upper eyelid skin. Frontalis muscle
hypertonicity from lateral brow skin hooding and its reaction
to the action of antagonistic muscles (corrugator supercilii,
obicularis oculi, and procerus) result in the development of
transverse forehead skin lines.75 The medial brow, in contrast,
seldom descends with aging and in fact may rise.76–78 The
mechanism responsible for this includes the chronic activa­
tion of the frontalis muscle. This may either be to elevate the
brow/eyelid complex associated with clinical or subclinical
levator system weakness or to relieve visual field obstruction
due to excess lateral upper eyelid skin.75 Anatomically, the
frontalis muscle ends at approximately the temporal fusion
line (superior temporal septum). Lateral to this, there is not
an upward vector to counteract the downward pull of brow
depressors and gravity on the lateral brow, which may explain
why more descent occurs at the lateral brow.
Midcheek
The midcheek is the anterior part of the midface.4 It is trian­
gular in shape and bounded superiorly by the pretarsal part
of the lower eyelid, medially by the side of the nose and the
nasolabial groove below, and laterally around the lateral
cheek where the arch of the zygoma meets the body. A smooth,
rounded midcheek is a powerful image of youth and gives a
certain freshness to the face. With aging, the three midcheek
segments become clearly discernable, as they become sepa­
rated by the three cutaneous grooves of the midcheek: the
nasojugal, palpebromalar, and midcheek grooves. This “seg­
mentation” of the midcheek has a profound impact on
appearance that is responsible for giving the “tired” look we
associate with aging.
The soft tissues of the midcheek are structurally composed
of three segments or “modules”, with each overlying a specific
part of the midcheek skeleton (Fig. 6.1.19). The lid–cheek
segment overlies the prominence of the inferior orbital rim,
the malar segment overlies the body of the zygoma, and the
nasolabial segment overlies the anterior surface of the maxilla.
The skeletal foundation of the midcheek borders the three
bony cavities of the anterior face, the orbital, nasal, and oral
cavities. Because of the many spaces and limited bony support
available, the midcheek has some intrinsic structural weak­
nesses. Three factors make the midcheek susceptible to aging
changes. These are (1) the wedge shape of the soft-tissue of
the midcheek, which is thin above and thicker below; (2) the
natural posterior incline of the midcheek skeleton, from the
relative prominence of the infraorbital rim; and (3) the signifi­
cant retrusion that occurs with aging as a result of resorption
of the maxilla. This is not uniform, as the maxilla recedes more
medially and inferiorly.73 With early aging, the retrusion of the
maxilla, along with a slight descent of the wedge-shaped
cheek soft tissue results in an appreciable reduction of volume
part of the underlying skeleton is immediately suspect and
should be addressed in order to obtain better aesthetic results.
Regional changes observed with the
aging face
Temple and forehead
The skin of the temple differs from that of the forehead, being
thinner and less firmly supported to the underlying layers.
The loose attachment reflects the underlying temporal space,
which is extensive, as well as the nature of the surrounding
temporal ligaments. These are unlike other facial ligaments,
being septal-like, and do not continue through the thin, loose
subcutaneous layer 2 over the temple. This explains why
deep-layer procedures in the temple are not as effective in
toning the overlying skin as they are, for example, in the
cheek.
Corrugator muscle contraction is associated with the emo­
tional states of grief and sadness.74 The transverse head of
Fig. 6.1.18  Skeletal aging and its consequences. The stippled areas on the
skeleton indicate where bone is resorbed and the relative amount. On the right, the
stigmata of aging present in the facial soft tissues corresponds to the areas of
weakened skeletal support as a result of bone loss. (© Dr. Levent Efe, CMI.)

109
Considerations for correcting aging changes of the face based on the anatomy of the aging face
center of the “V”, the lowest and deepest part, has the naso­
jugal groove continuing down the cheek as the midcheek
groove that separates the cheek into the malar and nasolabial
segments. The reason why this contour demarcation changes
while the skin itself does not descend is explained by differ­
ence in the tissue layers. In level 4, the orbicularis retaining
ligament is not rigid where it is over the center of the inferior
orbital rim, so distension results in relative sliding between it
and layer 3, the orbicularis oculi. As the lid–cheek junction
becomes more prominent, it visually takes over from the
infratarsal groove and becomes the new separation between
the lower eyelid and the cheek. This is the basis for the com­
monly used but inaccurate phrase, “lengthening of the lid–
cheek junction with aging”, which is, in fact, the result of a
visual shift from the prominence of the infratarsal groove
in youth to the lid–cheek junction with age. Correction of
the aging of the lid–cheek segment of the midcheek, the
visibly descended contour of the lid–cheek junction and long
lower lid, is colloquially known as “blending the lid–cheek
junction”.
Lower face
The jowl and the labiomandibular fold in the lower face
are not present in youth and develop with aging. With the
description of the concept of soft-tissue spaces of the face, and
specifically the premasseter space, the mechanism for the
formation of the jowl can now be understood on an anatomi­
cal basis.21 With the onset of aging, laxity develops in the roof
of the premasseter space associated with attenuation of the
anterior and inferior boundaries. The major retaining liga­
ments (the key masseteric and mandibular), in contrast,
remain relatively strong, and at these locations the superficial
fascia remains firmly fixed to the underlying deep fascia.
Distension of the weaker masseteric ligaments at the anterior
border of the lower premasseter space (below the key mas­
seteric ligament) and inferior displacement of the buccal fat
(within the buccal space) is the anatomical basis for the devel­
opment of the labiomandibular fold. The mandibular ligament
demarcates the transition from the labiomandibular fold
above and medial and the jowl below. The jowl develops as a
result of distension of the roof of the lower premasseter space
with resultant descent of the tissues below the body of the
mandible. The more prominent the jowl, the more apparent
will be the cutaneous tethering provided by the mandibular
ligament. Accordingly, the anatomical solution to correcting
these aging changes is to reduce the inferiorly displaced
buccal fat and to tighten the roof of the premasseter space.
Considerations for correcting aging
changes of the face based on the
anatomy of the aging face
Dissection planes
The subcutaneous plane of dissection (level 2) is the most
commonly used plane in facelifts, either in isolation or more
commonly with some form of SMAS management from the
superficial aspect (Fig. 6.1.20).79–81 A distinction should be
of the upper cheek. The result is that the small amount of
orbital fat over the prominent edge of the infraorbital rim
(originally concealed by the volume of the upper cheek) now
becomes revealed, especially the underside of the lid fat bulge
over the middle part. The visual impression is of a “length­
ened” lower lid. At the same time, the increased thickness of
the soft-tissue mass over the lower cheek tends to conceal the
degree of maxillary resorption and gives the profound visual
impression that the soft-tissue mass has descended into the
lower part of the midcheek.
Of the three segments of the midcheek, the lower lid
segment changes the most dynamically with aging. It has two
distinct grooves across its surface that vary in their expression
during the aging process, often coexisting. The upper is the
infratarsal groove at the junction of the pretarsal and preseptal
parts of the eyelid. It defines the lower boundary of the pret­
arsal bulge. The pretarsal bulge in youth is the visual separa­
tion of the lid above and the cheek below. This so-called “high
lid–cheek junction” is located well above the infraorbital rim
and is a characteristic of youth. The infratarsal groove location
does not change with aging, although its contour usually
fades. The lower groove is the lid–cheek junction that relates
to the lower edge of the preseptal part of the lid. It is not
usually present in youth and appears with aging and then
progressively deepens and descends slightly over time. Its
shape when it first appears is a gentle “C” contour, but as it
“descends”, particularly in its central portion, its shape
changes to a progressively more angulated “V” shape with
the medial side being formed by the developing nasojugal
groove and the lateral side by the palpebromalar groove. The
Fig. 6.1.19  The midcheek has three segments, of which the lid–cheek segment
(blue) and the malar segment (green) are within the periorbital part. These are
adjacent to the nasolabial segment (yellow), which is in the perioral part overlying
the vestibule of the oral cavity. The boundaries of the three segments form three
grooves, which interconnect like the italic letter Y. The palpebromalar groove (1)
overlies the inferolateral orbital rim, and the nasojugal groove (2) overlies
the inferomedial orbital rim, then continues into the midcheek groove (3).
(© Dr. Levent Efe, CMI.)

110
SECTION I
CHAPTER 6.1 • Facelift: Facial anatomy and aging
example of this is the lower premasseter space. Subcutaneous
dissection is performed to approximately 30 mm anterior to
the tragus through the zone of fixation, the platysma auricular
fascia (PAF), where the SMAS is fused to the deep fascia
including the parotid capsule.83 Because the objective of the
surgery is to correct laxity in the mobile anterior face, the level
of dissection used in the lateral face is of secondary impor­
tance. A further benefit of leaving the PAF intact is that it is
strong and can be used for suture fixation. Once dissection has
proceeded beyond the PAF (indicated by the posterior border
of the platysma), the SMAS should then be incised to gain
direct access into the lower premasseter space. The space can
then be opened by gentle blunt dissection only, to define the
boundaries of the space. The premasseter space below and the
prezygomatic space above form a series of spaces in the ante­
rior face (Fig. 6.1.21). The boundaries of the spaces, reinforced
by retaining ligaments, are where the important anatomy is
located. These need to be precisely released to eliminate their
tethering effect on the soft tissues, which is more difficult in
drawn between subcutaneous dissection over the lateral face
from that over the anterior face. This plane of dissection is
perceived to be “safe” as dissection remains superficial to the
facial nerve branches at all times and is the main appeal of
level 2 dissection. The subcutaneous dissection can be per­
formed either in the superficial subcutaneous or deep subcu­
taneous level. In the former, there is more density of the
retinacular cutis fibers as the multi-linked ligaments branch
out before inserting into the dermis. In the latter on the outer
surface of the SMAS, there are fewer fibers, which tend to be
thicker and stronger. The deep subcutaneous layer is not
uniform in its tenacity: some areas, as over the facial spaces,
are inherently easier to dissect, while others, that overlie liga­
ments, are more strongly attached and require sharp surgical
release. For example, over the malar eminence at McGregor’s
patch, where the zygomatic ligaments are located, sharp
release is usually required and over the mandibular ligament.
In contrast, in the lower face over the premasseter space, the
subcutaneous layer separates quite readily, requiring only
blunt finger dissection.
SubSMAS dissection (level 4)
In the scalp, this is the preferred tissue plane for dissection,
as the scalp readily separates from the underlying periosteum
(level 5) through the avascular areolar tissue with ease and
inherent safety. Bruising and swelling is kept to a minimum
because of this anatomy. In the face proper, while the anatomi­
cal principles remain the same, level 4 is potentially the most
risky plane to dissect because of the facial nerve branches
that transition through this level from level 5 to supply the
facial muscles in level 3. However, it should be noted that
similar to the situation in the scalp where raising the flap at
level 4 gives a robust and structurally integrated composite
flap that can be effectively tightened, subSMAS dissection
in the face has the same advantages and potential benefits.82
Dissection can be performed safely in level 4 by applying
the understanding of the three-dimensional anatomy of the
face described earlier, the key being the facial spaces, which
provide safe access through this layer. Because these spaces
are “predissected”, access is quick, atraumatic, and easy. An
Fig. 6.1.20  Alternative levels for dissection and
redraping in facelifts. Dissection can be performed
through any one of three alternative layers, namely
subcutaneous (level 2), subSMAS (level 4), and
subperiosteal (level 6) for the upper two-thirds of
the face, while traction is applied either on the skin
(level 1), the SMAS (level 3), or the periosteum
(level 5). (© Dr. Levent Efe, CMI.)
Fig. 6.1.21  The subSMAS facial spaces interconnect for safe anatomical
dissection in composite flap facelifts. The premasseter spaces: 1, lower; 2, middle;
3, upper. 4, prezygomatic space; 5, upper temporal space.

111
Summary
Placement of sutures
While adequate surgical release is needed for mobility, it is
the surgical fixation that achieves the desired effect by holding
the mobilized soft tissue in its new position. The strength and
tenacity of the superficial fascia is not uniform. The areas
where the retaining ligaments are located have an inherent
ligamentous reinforcement, making them ideal for suture
placement. It is also the location in which traction gives the
most natural appearance, as these are the natural suspension
sites of the face. Accordingly, the suture fixation should be
placed where the retaining ligaments are located. Where fixa­
tion sutures are placed in the anterior face in subSMAS
surgery, they function as replacements for the retaining liga­
ments that have weakened or have been divided in order to
mobilize the composite flap. Accordingly, the replacement
sutures should replicate the quality of support provided by
the original ligaments as the “mobile” spaces remain. In this
respect, braided permanent sutures are advantageous as they
stimulate collagen and elastic deposition within the suture
similar to a ligament.89 The platysma auricular fascia, a diffuse
ligamentous area on the lateral face, provides an ideal area,
both anatomically and physically, to fix the facelift flap, due
to its inherent strength.
Summary
This chapter has been structured to assist the reader to
develop a conceptual understanding of facial anatomy and
how it changes with aging. It is the framework that unifies
the detailed anatomical information now available in the
literature. Once understood, this knowledge will serve as
the anatomical foundation for the logical and sound selec­
tion of surgical techniques for rejuvenation of the aging
face.
younger patients as the ligaments are denser and stronger.
Clear visualization, optimized by lifting the opened adjacent
facial spaces, is beneficial. When blunt scissors are used with
gentle vertical spreading of the blades, the surrounding fat
and areolar tissue separate to reveal the ligaments and the
facial nerve branches in relation to them. With further lifting,
the ligaments become more certainly defined as they tighten
further, at which time they can be safely released, while the
nerves, being obliquely orientated, dislodge out of the way,
unaffected by the controlled stretching. The subSMAS spaces
can be used to safely and atraumatically access various parts
of the face, the deep temporal space to the lateral brow, the
preseptal space to the lower eyelid, and the prezygomatic and
the premaxillary spaces to the midcheek.84
Level 5
Subperiosteal “lifts” have the appeal of safety as far as facial
nerve risk is concerned as they are superficial and the remote
nerves never cross this plane.85–88 However, there are inherent
limitations to subperiosteal lifts. The accumulated aging
changes across all five tissue layers are elevated as part of the
subperiosteal lift. Overcorrection is required to effect the
desired changes of soft-tissue shape and skin tone to compen­
sate for the “lift-lag” phenomenon, which is proportional to
the soft-tissue thickness and laxity. Accordingly, subperiosteal
lifting works best in areas where the layers are more com­
pacted as the lift-lag is minimized. An example of this is in
the brow where subperiosteal lifts are effective and popular.
Where the layers are thicker, such as the nasolabial segment
of the midcheek, the lift-lag phenomenon significantly limits
the improvement that can be achieved. Because of the unyield­
ing nature of the periosteum, extensive undermining beyond
the target area is needed or alternatively a “periosteal release”
immediately beyond the area that requires lifting is required
to isolate the area to a limited island of periosteum.
5. Stuzin JM, Baker TJ, Gordon HL. The relationship of the superficial
and deep facial fascias: relevance to rhytidectomy and aging. Plast
Reconstr Surg. 1992;89:441–449. A discussion of the concept of facial soft
tissue being arranged in concentric layers, and the SMAS as the
“investing” layer of the superficial mimetic muscles of the face. The
relationship between the deep and superficial fascias is described, with
acknowledgement of “areola” planes and areas of dense fibrous
attachments, including true osteocutaneous ligaments and other
coalescences representing the retaining ligamentous boundaries of the face.
Age-associated laxity of the retaining ligament was noted to be a key
component of facial aging.
17. Moss CJ, Mendelson BC, Taylor GI. Surgical anatomy of the
ligamentous attachments in the temple and periorbital regions. Plast
Reconstr Surg. 2000;105:1475–1490. A through description of the
retaining ligaments of the temporal and periorbital regions is given. The
term “ligamentous adhesion” is introduced to increase the understanding
of the system, and there is emphasis on the relations of the temporal
branch of the facial nerve and the trigeminal branches to structures
visualized in surgery rather than to less useful landmarks which are not.
A discussion of age-related changes to the region compliments one of
surgical approach with respect to the anatomy described.
21. Mendelson BC, Freeman ME, Wu W, et al. Surgical anatomy of the
lower face: the premasseter space, the jowl, and the
labiomandibular fold. Aesthetic Plast Surg. 2008;32:185–195. This
paper introduces the concept of the “premasseter” space, age-related
changes, and utility for safe subSMAS dissection. Distinction is made
between this space, over the lower part of the masseter, and another space
overlying the upper part of the masseter where the neurovascular
structures, the accessory lobe of the parotid gland and duct are located.
The true shape of the anterior border of the masseter muscle is described,
with the border ending anteroinferiorly at the mandibular ligament. This
description completes the picture of the retaining ligaments as a
continuous border separating the anterior and lateral parts of the face. The
relations of the facial nerve branches, particularly that of the lower buccal
trunk, to the masseter and its fascia are described.
73. Mendelson BC, Wong CH. Changes in the facial skeleton with
aging: implications and clinical applications in facial rejuvenation.
Aesthetic Plast Surg. 2012;36:753–760.
82. Mendelson BC. Surgery of the superficial musculoaponeurotic
system: principles of release, vectors and fixation. Plast Reconstr
Surg. 2001;107:1545–1552. This article highlights the importance of
adequate release of retaining ligaments of the SMAS in repositioning of
the composite flap. Inadequate release can lead to suboptimal advancement
of the flap, and worse, distortion of the flap if the direction of pull is
incorrect, due to unwanted rotation about the parts of the retaining
ligamentous system that have been left intact. The biomechanical function
of the retaining ligaments is described as “quarantining” sections of the
SMAS with less substantial fixation (areas now appreciated as subSMAS
facial soft-tissue spaces), preventing unwanted traction on areas of the face
distant to the desired action in facial expression. There is discussion on the
advantage of extensive SMAS mobilization in allowing multiple and
varied force vectors to be applied, which allows proper anatomical
repositioning of the soft tissue of the face.
Access the complete reference list online at

111.e1
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anatomic study. Plast Reconstr Surg. 2010;125:532–537.
38. Trussler AP, Stephan P, Hatef D, et al. The frontal branch of the
facial nerve across the zygomatic arch: anatomical relevance of the
high-SMAS technique. Plast Reconstr Surg. 2010;125:1221–1229.
39. Lowe JB 3rd, Cohen M, Hunter DA, et al. Analysis of the nerve
branches to the orbicularis oculi muscle of the lower eyelid in fresh
cadavers. Plast Reconstr Surg. 2005;116:1743–1749.
40. Ramirez OM, Santamaria R. Spatial orientation of motor
innervation of the lower orbicularis oculi muscle. Aesthetic Surg J.
2000;20:107.
41. Alghoul M, Bitik O, McBride J, et al. Relationship of the zygomatic
facial nerve to the retaining ligaments of the face: the sub-SMAS
danger zone. Plast Reconstr Surg. 2013;131:245e–252e.

111.e2
SECTION I
CHAPTER 6.1 • Facelift: Facial anatomy and aging
42. Dingman RO, Grabb WC. Surgical anatomy of the mandibular
ramus of the facial nerve based on the dissection of 100 facial
halves. Plast Reconstr Surg. 1962;29:266–272.
43. Nelson DW, Gingrass RP. Anatomy of the mandibular branches of
the facial nerve. Plast Reconstr Surg. 1979;63:479–482.
44. Conley J, Baker DC. Paralysis of the mandibular branch of the facial
nerve. Plast Reconstr Surg. 1982;70:569–577.
45. Huettner F, Rueda S, Ozturk CN, et al. The relationship of the
marginal mandibular nerve to the mandibular osseocutaneous
ligament and lesser ligaments of the lower face. Aesth Surg J.
2015;35:111–120.
46. Montagna W, Carlisle K. Structural changes in the aging skin. Br J
Dermatol. 1990;122(suppl 35):61–70.
47. Wulf HC, Sandby-Moller J, Kobayashi T, et al. Skin aging and
natural photoprotection. Micron. 2004;35:185–191.
48. Hall G, Phillips TJ. Estrogen and skin: the effects of estrogen,
menopause and hormone replacement therapy on the skin. J Am
Acad Dermatol. 2005;53:555–568, quiz 569–72.
49. Sander CS, Chang H, Salzmann S, et al. Photoaging is associated
with protein oxidation in human skin in vivo. Invest Dermatol.
2002;118:618–625.
50. Chung JH, Seo JY, Choi HR, et al. Modulation of skin collagen
metabolism in aged and photoaged human skin in vivo. J Invest
Dermatol. 2001;117:1218–1224.
51. Freiman A, Bird G, Metelitsa AI, et al. Cutaneous effects of
smoking. J Cutan Med Surg. 2004;8:415–423.
52. Haruko C, Okada HC, Alleyne B, et al. Facial changes caused by
smoking: a comparison between smoking and nonsmoking identical
twins. Plast Reconstr Surg. 2013;132:1085–1092.
53. Gosain AK, Klein MH, Sudhakar PV, et al. A volumetric analysis of
soft-tissue changes in the aging midface using high-resolution MRI:
implications for facial rejuvenation. Plast Reconstr Surg.
2005;115:1143–1152, discussion 1153–5.
54. Gosain AK, Amarante MT, Hyde JS, et al. A dynamic analysis of
changes in the nasolabial fold using magnetic resonance imaging:
implications for facial rejuvenation and facial animation surgery.
Plast Reconstr Surg. 1996;98:622–636.
55. Lambros V. Observations on periorbital and midface aging. Plast
Reconstr Surg. 2007;120:1367–1376.
56. Faulkner JA, Larkin LM, Claflin DR, et al. Age-related changes in
the structure and function of the skeletal muscles. Clin Exp Phamacol
Physiol. 2007;34:1091–1096.
57. Pottier F, El-Shazly NZ, El-Shazly AE. Aging of orbicularis oculi:
anatomophysiologic considerations in upper blepharoplasty. Arch
Facial Plast Surg. 2008;10:346–349.
58. Penna V, Stark GB, Eisenhardt SU, et al. The aging lip: a
comparative histological analysis of age-related changes in the
upper lip complex. Plast Reconstr Surg. 2009;124:624–628.
59. Hellman M. Changes in the human face brought about by
development. Int J Orthod. 1927;13:475–516.
60. Todd TW. Thickness of the white male cranium. Anat Rec.
1924;27:245–256.
61. Lasker GW. The age factor in bodily measurements of adult male
and female Mexicans. Hum Biol. 1953;25:50–63.
62. Garn SM, Rohmann CG, Wagner B, et al. Continuing bone growth
during adult life: a general phenomenon. Am J Phys Anthropol.
1967;26:313–317.
63. Kahn DM, Shaw RB Jr. Aging of the bony orbit: a three-dimensional
computed tomographic study. Aesthet Surg J. 2008;28:258–264.
64. Pessa JE, Chen Y. Curve analysis of the aging orbital aperture. Plast
Reconstr Surg. 2002;109:751–755.
65. Pessa JE, Zadoo VP, Mutimer KL, et al. Relative maxillary retrusion
as a natural consequence of aging: combining skeletal and
soft-tissue changes into an integrated model of midfacial aging.
Plast Reconstr Surg. 1998;102:205–212.
66. Pessa JE. An algorithm of facial aging: verification of Lambros’s
theory by three-dimensional stereolithography, with reference to the
pathogenesis of midfacial aging, scleral show, and the lateral
suborbital trough deformity. Plast Reconstr Surg. 2000;106:479–488.
67. Shaw RB Jr, Kahn DM. Aging of the midface bony elements: a
three-dimensional computed tomographic study. Plast Reconstr
Surg. 2007;119:675–681.
68. Mendelson BC, Hartley W, Scott M, et al. Age-related changes of
the orbit and midcheek and the implications for facial rejuvenation.
Aesthetic Plast Surg. 2007;31:419–423.
69. Zadoo VP, Pessa JE. Biological arches and changes to the curvilinear
form of the aging maxilla. Plast Reconstr Surg. 2000;106:460–466.
70. Pessa JE, Slice DE, Hanz KR, et al. Aging and the shape of the
mandible. Plast Reconstr Surg. 2008;121:196–200.
71. Shaw RB Jr, Katzel EB, Koltz PF, et al. Aging of the mandible and
its aesthetic implications. Plast Reconstr Surg. 2010;125:332–342.
72. Pessa JE, Zadoo VP, Yuan C, et al. Concertina effect and facial
aging: nonlinear aspects of youthfulness and skeletal remodeling,
and why, perhaps, infants have jowls. Plast Reconstr Surg.
1999;103:635–644.
73. Mendelson BC, Wong CH. Changes in the facial skeleton with
aging: implications and clinical applications in facial rejuvenation.
Aesthetic Plast Surg. 2012;36:753–760.
74. Schwartz GE, Fair PL, Mandel MR, et al. Facial electromyography
in the assessment of improvement in depression. Psychosom Med.
1978;40:355–360.
75. Knize DM. Anatomic concepts for brow lift procedures. Plast
Reconstr Surg. 2009;124:2118–2126.
76. Knize DM. Muscles that act on glabella skin: a closer look. Plast
Reconstr Surg. 2000;105:350–361.
77. Matros E, Garcia JA, Yaremchuk MJ. Changes in eyebrow position
and shape with aging. Plast Reconstr Surg. 2009;124:1296–1301.
78. Jelks GW, Jelks EB. The influence of orbital and eyelid anatomy on
the palpebral aperture. Clin Plast Surg. 1991;18:183–195.
79. Baker DC. Lateral SMASectomy. Plast Reconstr Surg. 1997;100:
509–513.
80. Tonnard P, Verpaele A. The MACS-lift short scar rhytidectomy.
Aesthet Surg J. 2007;27:188–198.
81. Aston SJ, Walden JL. Facelift with SMAS techniques and FAME. In:
Aston I, Steinbrech DS, Walden IL, eds. Aesthetic Plastic Surgery.
London: Saunders Elsevier; 2009:73–86.
82. Mendelson BC. Surgery of the superficial musculoaponeurotic
system: principles of release, vectors and fixation. Plast Reconstr
Surg. 2001;107:1545–1552. This article highlights the importance of
adequate release of retaining ligaments of the SMAS in repositioning of
the composite flap. Inadequate release can lead to suboptimal advancement
of the flap, and worse, distortion of the flap if the direction of pull is
incorrect, due to unwanted rotation about the parts of the retaining
ligamentous system that have been left intact. The biomechanical function
of the retaining ligaments is described as “quarantining” sections of the
SMAS with less substantial fixation (areas now appreciated as subSMAS
facial soft-tissue spaces), preventing unwanted traction on areas of the face
distant to the desired action in facial expression. There is discussion on the
advantage of extensive SMAS mobilization in allowing multiple and
varied force vectors to be applied, which allows proper anatomical
repositioning of the soft tissue of the face.
83. Labbé D, Franco RG, Nicolas J. Platysma suspension and
platysmaplasty during neck lift: anatomical study and analysis of
30 cases. Plast Reconstr Surg. 2006;117:2001–2007.
84. Wong CH, Mendelson BC. Midcheek lift utilizing facial soft tissue
spaces of the midcheek. Plast Reconstr Surg. 2015;136:1155–1165.
85. Le Louarn C. The concentric malar lift: malar and lower eyelid
rejuvenation. Aesthetic Plast Surg. 2004;28:359–372.
86. Sullivan SA, Dailey RA. Endoscopic subperiosteal midface lift:
surgical technique with indications and outcomes. Ophthal Plast
Reconstr Surg. 2002;18:319–330.
87. Ramirez OM. Three-dimensional endoscopic midface enhancement:
a personal quest for the ideal cheek rejuvenation. Plast Reconstr
Surg. 2002;109:329–340.
88. Rowe DJ, Guyuron B. Optimizing results in endoscopic forehead
rejuvenation. Clin Plast Surg. 2008;35:355–360.
89. Huggins RJ, Freeman ME, Kerr JB, et al. Histologic and
ultrastructural evaluation of sutures used for surgical fixation of the
SMAS. Aesthetic Plast Surg. 2007;31:719–724.

SECTION I • Aesthetic Surgery of the Face
6.2 
Facelift: Principles of and surgical
approaches to facelift
Richard J. Warren
SYNOPSIS
■ Age-related changes occur in all layers of the face, including skin,
superficial fat, SMAS, deep fat, and bone.
■ Patients presenting for facial rejuvenation surgery are usually middle
aged or older, thus increasing the chance of comorbidities. Risk
factors such as hypertension and smoking should be dealt with prior
to facelift surgery.
■ Careful preoperative assessment will provide the surgeon with an
aesthetic diagnosis regarding the underlying facial shape, the
age-related issues that predominate, and the appropriate surgical
procedures for every individual patient.
■ Almost all facelift techniques begin with a subcutaneous facelift
flap. Careful incision placement, tissue handling, and flap
repositioning are important in order to avoid the obvious stigmata
of facelift surgery.
■ In its pure form, the subcutaneous, skin-only facelift has a limited
effect on the position of heavier deep tissue.
■ In SMAS plication, a skin flap is created with suture manipulation of
the superficial fat and the underlying SMAS/platysma.
■ In loop suture techniques (MACS lift), a skin flap is created with long
suture loops taking multiple bites of superficial fat and platysma
– fixed to a single point on the deep temporal fascia.
■ The supraplatysma plane creates a single flap of skin and superficial
fat mobilized and advanced along the same vector.
■ SMASectomy involves a skin flap plus excision of superficial fat and
SMAS from the angle of the mandible to the malar prominence, with
direct suture closure of the resulting defect.
■ A SMAS flap raised with skin attached (deep plane) creates a flap of
SMAS/platysma, superficial fat and skin, all mobilized and advanced
along the same vector.
■ A separate SMAS flap (dual plane) creates two flaps, the skin flap and
the superficial fat/SMAS/platysma, which are advanced along two
different vectors.
■ The subperiosteal lift involves dissection against bone, with
mobilization and advancement of all soft-tissue elements.
■ Additional volume augmentation, and in some locations volume
reduction, should be considered in all cases of facelift surgery.
■ Facial aging is usually a pan-facial phenomenon. Therefore, in order to
obtain a harmonious result, patients will often benefit from surgery to
other components of their face.
■ The most common complication of facelift surgery is hematoma. This
problem should be dealt with promptly.
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Introduction
A complete discussion of facial rejuvenation would involve
the periorbital region, forehead, cheek, neck, and perioral
region. In this chapter, we will be dealing with the middle and
lower thirds of the face – the cheek and neck. Terminologies
for procedures that address these areas include rhytidectomy,
rhytidoplasty, meloplasty, and facialplasty, although in this
text, the more common term “facelift” will be used.
Facelift surgery was originally conceived as a method of
placing traction on the aging face by excising skin in the
periphery of the face and closing the resulting defect under
tension. Since that simple beginning over 100 years ago, the
procedure has evolved to encompass a wide range of tech­
niques which lift, augment, and rearrange facial tissues in an
attempt to rejuvenate the aging face.
Despite the development of many less invasive technolo­
gies, nothing can match a facelift in its ability to globally treat
the face, returning its basic architecture to a more youthful
configuration.
Anatomy and patient presentation
The classic stigmata of the aging face include:
■ Visible changes in skin, including folds, wrinkles,
dyschromias, dryness, and thinning
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112.e1
Historical perspective
Historical perspective
Facelift surgery dates from the early part of the 20th century.
Its colorful history has been thoroughly reviewed by Stuzin,1
whose summary is reproduced here.
In the past, the history of aesthetic facial surgery has been
reported by a number of authors, including Rogers,2,3 Rees
and Wood-Smith,4 Gonzalez-Ulloa,5 Rees,6 and Barton.7,8
There is still doubt as to who performed the first facelift,
but most sources date it to the first decade of the 20th
century.3,9,10 According to Rogers,3 Hollander11 reported in a
chapter entitled “Cosmetic Surgery” in Handbuch der Kosmetik
that “as a victim of the art of feminine persuasion”, he removed
pieces of skin at the margins of the hairline and in the natural
aging skinfolds of a woman to freshen up “her wrinkles and
drooping cheeks”. In this chapter, Hollander did not date the
procedure, but in 1932 he stated that his original procedure
had been performed in 1901 for a Polish aristocrat.12 Lexer,10
however, reported in 1931 that he had performed a facelift for
an actress in 1906 and that he was unaware of any such opera­
tion before that date. Joseph9 reported in 1921 that he had
performed an operation in 1912 for correction of aging cheek
tissues in a 48-year-old woman. By the time Hollander, Lexer,
and Joseph reported their first procedures, a number of other
prominent surgeons in Europe, such as Noel, Passot, Morestin,
Bourguet, and Lagarde, were busy performing cosmetic surgi­
cal procedures. In the United States, Miller and Kolle had
large cosmetic surgery practices. Passot13 in 1919 published an
illustrated article showing sites of elliptic skin excision of the
hairline, the forehead, and the temporal and preauricular
areas to tighten the skin and an elliptic excision of skin and
fat to reduce submental fat deposits. Bourguet14 reported
elliptic skin excisions similar to those of Passot. He was the
first to report fat excisions to correct herniated periorbital fat
pads (1924)15 and to publish preoperative and postoperative
photographs of fat pad excision (1925).16 Noel published a
book in 1926,17 La Chirurgie Esthetique: Son Role Social, describ­
ing facialplasty, blepharoplasty, forehead lifting, and correc­
tion of loose skin of the neck, burns, scars, protruding ears,
and laxity of the upper arms. Although her procedures were
not aggressive by modern standards, Noel was a true master
of that era.
Miller18 published the first book in medical history devoted
entirely to the subject of cosmetic surgery. Miller was described
by Rogers3 as a “quack” on one hand and at the same time,
“a surgical visionary years ahead of his academic colleagues
… medicine’s first truly cosmetic surgeon.” Miller was a
prolific writer. In 1906, he wrote the first article in the medical
literature describing an attempt to remove excess skin from
the eyelids.19 In 1907, he published the first article with a
photograph illustrating lower eyelid incisions,20 and he also
published three cosmetic surgery textbooks.18,21,22 Kolle was
born in Germany and practiced in New York. His book Plastic
and Cosmetic Surgery23 represented the second description of
cosmetic surgery in medical history. The book was more than
500 pages in length and contained hundreds of illustrations,
including preoperative and postoperative photographs of
protruding ears; it took a rather aggressive surgical approach
to the correction of excess skin of the eyelids. Bettman24 was
the first to publish preoperative and postoperative facelift
photographs and to describe a continuous temporal scalp,
preauricular, postauricular, and mastoid area incision. With
modifications, his incision is essentially that used for facial­
plasty today. Hunt25 published a book, Plastic Surgery of the
Head, Face and Neck, that included facelifting and forehead/
browlifting operations.
All the early facialplasty procedures were limited to skin
excision and wound closure without subcutaneous under­
mining. Bames26 described subcutaneous face and neck
undermining, skin redraping, and excision of excess skin. The
continuous incision described by Bettman24 and subcutaneous
undermining recommended by Bames26 essentially estab­
lished the basic facelift procedure for the next 40 years. As
discussed by Rees,6 a great deal of secrecy surrounded early
facelift procedures. Surgeons were reluctant to share their
techniques because of professional jealousy and greed. The
disdain for “vanity” surgery by both the medical profession
and the public restricted most facelift procedures to private
offices and small clinics. The extent of surgery in such settings
was necessarily limited. Many prominent plastic surgeons in
major medical centers were forced to perform their facelifts in
small clinics or to hide their cases by misnaming the proce­
dures on the operating schedule. Renowned plastic surgeons
after the First and Second World Wars, such as Gillies, Blair,
Davis, Pierce, McIndoe, Mowlem, Conway, and others, did a
great deal of cosmetic surgery but were reluctant to publish
on the subject.6 The conventional facelift operation (skin dis­
section only) failed to address the effect of aging and the force
of gravity on the structures (e.g., muscle, fat, and superficial
fascia) deep to the skin. Likewise, the classic skin dissection
facialplasty failed to account for the wide variation in facial,
jawline, and cervical deformities; in the location of fat depos­
its; in the asymmetry of anatomic structures; and in the
genetically determined deformities, such as microgenia and
the obtuse cervicomental angle.
Aufricht27 discussed the limitations of the subcutaneous
facelift, particularly its failure to correct submental fat depos­
its and platysma bands. Adamson and colleagues28 discussed
correction of the platysma bands in the submental area, and
Millard and co-workers29 recommended extensive submental
defatting. Pennisi and Capozzi30 and Baker and Gordon31
described suture plication of the deep tissues of the cheek and
lateral neck. Tipton32 challenged the deep suture techniques
in a study of 33 patients in whom he performed unilateral
plication. Two years postoperatively, there was no obvious
difference in the two sides of the face. Skoog33,34 described a
technique of dissection of the superficial fascial layer in the
face, in continuity with the platysma muscle in the neck and
advancement of the myofascial unit in a cephaloposterior
direction. This was the beginning of the modern era in facelift­
ing. Mitz and Peyronie35 used cadaver dissections to define
the limits of the superficial musculo-aponeurotic system
(SMAS) in the face and noted that tightening of this layer
would be beneficial in facialplasty. SMAS-platysma facelift­
ing, wide skin undermining, and extensive fat removal soon
gained worldwide popularity. Surgery of the tissue layers
deep to the skin of the face and neck is now established as an
essential part of cervical and facialplasty operations. Many
surgeons have described different SMAS-platysma techniques
to improve the cervicofacial area and to remedy problems not
corrected by conventional facialplasty.36–44 Furnas,45 in 1989,
described the retaining ligaments of the midface, which led to
a better understanding of anatomic areas where facial soft

112.e2
SECTION I
CHAPTER 6.2 • Facelift: Principles of and surgical approaches to facelift
tissue is supported and the involvement of these ligaments in
leading to the anatomic changes that occur with aging. These
ligaments were further defined by others46,47 who thought that
loss of the support from the retaining ligament system allowed
facial fat to descend inferiorly in the face, deepening the
nasolabial fold and forming facial jowls with aging. The
importance and location of the retaining ligaments led to
modifications in procedures involving retaining ligament
release in subSMAS dissection,47–56 the primary goal of these
procedures being to reposition descended facial fat to the
anatomic location of youth. Other surgeons, preferring sub­
periosteal rather than subSMAS dissection to reposition fat,
developed procedures whose similar goal is to resuspend
descended malar fat to the malar eminences using the sub­
periosteal plane.57–59 A combination of subperiosteal and
subcutaneous lifting has also been described.60
In concert with attempts to reposition facial fat, astute
observations were eventually made about the age-related
deflation of the human face.61–64 This led to the use of injected
fillers and injected fat (lipofilling), championed by Coleman,
in order to re-inflate the aging face, either independently or
at the same time as facelift surgery. Anatomic dissections
determined that facial fat is in distinct compartments both in
the superficial and deep layers of the face.61,65

113
Anatomy and patient presentation
Skin
Normal skin is directly adherent to underlying fat via the
retinacular cutis system. In certain predictable areas, the skin
is tethered to bone or underlying muscle by condensed areas
of connective tissue. In some places, these are string-like
cutaneous ligaments, and in other areas, these are ribbon-like
septae. Because nerves and vessels often reach the skin adja­
cent to these vertically running fibrous structures, dissection
of skin is more difficult and bloody where the skin is tethered;
McGregor’s patch is such an area because of its association
with the zygomatic cutaneous ligaments and a perforating
branch of the transverse facial artery.
Surface changes in facial skin are some of the most obvious
signs of aging. Skin aging is both intrinsic and extrinsic.
Intrinsic aging is the result of genetically determined apopto­
sis. The skin becomes thinner; there is a decrease in melano­
cytes, a reduced number of fibroblasts, and a loss of skin
appendages, leading to dryness. In the dermal matrix, there
is fragmentation of the collagen and impairment of fibroblast
function.66,67 Thinner skin becomes more susceptible to the
repeated contraction of underlying facial muscles, which
leads to permanent skin folds in predictable locations (Fig.
6.2.2). Extrinsic forces include sun exposure, cigarette smoke,
extreme temperatures, and weight fluctuations.
The net result is that aging facial skin becomes weaker,
thinner, and dryer. It also loses its ability to recoil, a condition
called elastosis. This has surgical implications, because firm
tight skin is youthful, and to varying degrees, the tightening
of loose facial skin is part of a good surgical result. However,
a facelift does not appreciably improve the quality or texture
■ Folds in the skin and subcutaneous tissue created by
chronic muscle contraction: glabellar frown lines, transverse
forehead lines, and crow’s feet over the lateral orbital rim
■ Deepening folds between adjoining anatomic units: the
nasojugular fold (tear trough), nasolabial folds,
marionette lines, and submental crease
■ Ptosis of soft tissue, particularly in the lower cheek, jowls,
and neck
■ Loss of volume in the upper two-thirds of the face, which
creates hollowing of the temple, the lateral cheek, the
central mid face and in the upper lip, premaxillary area
between the two nasolabial folds. The result is a more
skeletal appearance in the temple, the periorbita, and the
malar region as well as deepening of the nasolabial folds.
■ Expansion of volume in the neck and lateral jawline,
which leads to the formation of jowls and fullness of the
neck (Fig. 6.2.1).
The driving force behind our ability to explain these many
changes has been an improved understanding of facial anatomy
and how it changes over time. Facial aging occurs in all its
layers, from skin down to bone; no tissue is spared. For the
purposes of this discussion, the face will be viewed as a five-
layer structure as described in Chapter 6.1: skin, subcutaneous
fat, the superficial musculo-aponeurotic system (SMAS) and
muscles of facial expression, fascial spaces, and deep fascia.
Underlying everything is bone, except over the oral cavity. The
surgical significance of this concentric layer arrangement is
that dissection can be done in the planes between the layers.
Also, anatomical changes in each of the layers can be addressed
independently, as required to treat the presenting problem.
Fig. 6.2.1  The aging face exhibits changes in
the skin, superficial wrinkles, deeper folds,
soft-tissue ptosis, loss of volume in the upper
third and middle third and increased volume
in the lower third.
Perioral wrinkles
Buccal fat pad ptosis
Expansion and ptosis of jowl fat
Elongation and volume
loss in upper lip
Excess preplatysmal and
subplatysmal fat
Platysma muscle laxity
Malar fat descent
Frontalis contraction
Lateral brow ptosis
Temporal fat pad atrophy
Upper lid sulcus hollowing
Obicularis oculi laxity
Obicularis contracture
Lower lid laxity
Loss of midface fat
Transverse forehead creases
Temporal wasting
Crow’s feet
Tear trough
Cheek descent
Midface flattening
Nasolabial folds
Thinning lips
Marionette lines
Jowls
Transverse neck folds
Platysma bands
Vertical neck pleats

114
SECTION I
CHAPTER 6.2 • Facelift: Principles of and surgical approaches to facelift
SMAS and the muscles of facial expression.68 The superficial
fat is separated by vertical septae into five distinct compart­
ments: nasolabial, medial cheek, middle cheek, lateral tempo­
roparietal, and the inferior orbital fat (Fig. 6.2.4A).65
The two central fat compartments (medial and middle) are
the primary components of the malar fat pad.
The deep fat is also compartmentalized (Fig. 6.2.4B). The
most significant is the deep medial fat compartment, which
lies directly against bone and is bordered above by the orbi­
cularis retaining ligament, laterally by the zygomaticus major
and buccal fat pad and medially by the pyriform aperture61
(Fig. 6.2.4C).
The authors who identified this compartment propose that
age-related deflation of deep medial fat compartment leads to
“pseudoptosis” of the overlying superficial fat and skin –
ptosis that is real, but that is caused by lack of underlying
support.61 This is thought to cause deepening of the nasolabial
fold and development of the “inverted V deformity” below
the infraorbital rim.69 Adjacent and lateral to the deep medial
fat is the suborbicularis oculi fat (SOOF), which itself is
divided into a medial and lateral component.
Using sophisticated photographic analysis and facial aver­
aging, volume loss has also been demonstrated in the aging
upper lip area. This results is decreased projection of premax­
illary soft tissue and deepening of the nasolabial folds.70
Generally in youth, facial fat is tightly packed, creating
surface contours which undulate smoothly from convexity to
concavity. Cosmetic highlights rise above areas of depression.
The malar fat pad creates the principal cosmetic highlight
zone in the youthful face, immediately above the normal
depression overlying the buccal recess. Make-up artists
of the skin. Therefore, patients with good quality skin are
likely to enjoy better results from facelift surgery than patients
with poor quality skin. When skin quality is poor, options
such as injectable fillers and skin resurfacing may be more
appropriate for rejuvenation than facelift surgery. However,
in most cases of facial rejuvenation, medical and surgical
therapies can work in concert for a more complete result.
(These complementary therapies are reviewed in Chapters
5.1–5.4.)
Facial fat: ptosis, volume loss,
and volume gain
The face is carpeted in a layer of superficial fat that lies imme­
diately deep to the dermis. Between individuals, there is
much variability in the thickness of this superficial fat layer.
This has surgical implications, because a heavier patient will
have thicker, heavier tissues to reposition, but the dissection
of the facelift skin flap will be easier. Conversely, in a thin
patient, the weight of tissue to be lifted is less, but facial layers
are packed closely together, like an onion, necessitating
greater care if the surgeon wishes to separate skin from SMAS
and SMAS from underlying structures. Superficial facial fat
also varies in thickness depending on the area of the face. An
important zone is the malar fat pad, which overlies the zygo­
matic body.54 This is a triangular-shaped mass of fat bordered
by the nasolabial fold, the infraorbital arch, and a diagonal
line across the midcheek. Its apex is over the malar eminence.
The malar fat pad is present throughout life (Fig. 6.2.3).
One study looked at fat volume in the cheek and found
56% of the fat superficial to the SMAS and 44% deep to the
Fig. 6.2.2  Muscles of facial expression. The solid lines
demonstrate overlying skin creases caused by repeated
contraction of the underlying muscles. (Netter illustration
from © Elsevier Inc. All rights
reserved.)
Galea aponeurotica
Procerus
Corrugator supercilii
Nasalis
Zygomaticus minor
Zygomaticus major
Levator anguli oris
Buccinator
Masseter
Orbicularis oris
Frontalis
Orbicularis oculi, pretarsal portion
Orbicularis oculi, preseptal portion
Orbicularis oculi, orbital portion
Levator labii superioris alaeque nasi
Levator labii superioris
Auricularis anterior
Risorius
Depressor septi nasi
Platysma
Depressor anguli oris
Depressor labii inferioris
Mentalis

115
Anatomy and patient presentation
At the time of writing, it is unclear whether the cause of
superficial fat ptosis is gravitational due to relaxed fixation, or
if it relates to pseudoptosis caused by the loss of volume in the
deep fat compartments. Also, it is uncertain whether facial fat
volume is lost equally from the deep and superficial fat layers,
or if it is lost equally or differentially from the various identi­
fied fat compartments.61 This is an area of ongoing study.
In the lower face, the area of the jowl just posterior to the
marionette lines appears to thicken with age, making the
mandible appear wider. This phenomenon has been called
“radial expansion”.73,74 This may be due to fat accumulation,
or it may be caused by soft-tissue ptosis within the premas­
seteric space, a natural glide plane.75 Below the mandible,
a similar expansion often occurs in the neck as soft tissue
falls away from deep tissue attachments and fat tends to
accumulate.
Change in facial shape
The loss of facial volume is an important phenomenon that
surgeons recognized much later than the more obvious ptosis
of soft tissue. To arrive at this conclusion, astute observations
were made about changes in surface contours, which lead to
inferences about internal volume loss.61–64
The combination of volume loss in some areas, volume
gain in others, and soft-tissue ptosis creates a cascade effect
resulting in the loss of natural youthful curves (Fig. 6.2.5).
Gradually, there is a reversal of facial shape as the cheek
prominence of youth gives way to the jowl prominence of age.
Effectively, in youth, the cheeks are full, but with age, the
jowls and neck become full. The face changes from a heart
shape to a more rectangular shape, or from an egg sitting on
its narrow end to an egg resting on its broad end. This change
has been called losing the “inverted cone of youth”, and has
been likened to a reversal of the “Ogee” curve, a natural
S-shaped curve seen in architecture.60,76
Superficial musculo-aponeurotic system
Immediately deep to the subcutaneous fat is the superficial
musculo-aponeurotic system (SMAS), described by Mitz and
Peyronie in 1976.35 The SMAS, or its analogs, can be thought
of as a continuous fascial sheath encompassing the entire face
and neck. Superiorly, it continues into the temple as the
superficial temporal fascia (temporoparietal fascia) and then
into the scalp as the galea aponeurotica.77 Inferiorly, into the
neck, the SMAS continues as the superficial cervical fascia,
which envelopes the platysma muscle. Clinically, the thick­
ness and strength of the SMAS varies between patients, and
also varies in individual faces, being thicker and adherent
over the parotid and thinner anteriorly. In the surgical setting,
the SMAS is most tenuous under the malar fat pad where it
splits to encompass the zygomaticus major and the orbicularis
oculi.53,78 The SMAS has several important surgical implica­
tions. Its fibrous attachments to skin allow it to act as a carrier
for overlying subcutaneous fat; also it has been shown to be
much more resistant to stretch than skin.79 Furthermore, below
the zygomatic arch, all branches of the facial nerve are deep
to the SMAS.
The relationship of the SMAS (superficial fascia of the face)
to the deep fascia of the face involves areas of mobility inter­
spersed between areas of attachment. SMAS is tethered to the
accentuate this zone by highlighting the apex and simulating
a depression immediately below. In the aging face, fat is less
tightly packed, and facial contours become more abrupt. In
areas of tight ligamentous attachment, such as the preparotid
area, the anterior jowl border, and the zygomatic ligament
insertions, there appears to be an acceleration of volume loss
with indenting of the surface contour.62 With more advanced
aging, there is often malar fat atrophy, leading to a more
skeletal zygomatic appearance. Simultaneously there is
apparent ptosis of the malar fat pad which contributes to a
deepening of the nasolabial fold. Surgeons have traditionally
viewed superficial cheek fat as a ptotic layer requiring correc­
tion for facial rejuvenation to occur. In support of this theory,
it has been demonstrated that the primary muscles of facial
expression in the midcheek (zygomaticus major and minor)
do not change in length, while the overlying fat appears to
migrate inferiorly.71 Another study, using computed tomogra­
phy (CT) scans, confirmed the presence of facial fat compart­
ments and identified age-related inferior migration of the
midfacial fat compartments as well as inferior volume shift
within the individual compartments.72
Fig. 6.2.3  The malar fat pad is a triangular area of thickened superficial fat with
its base along the nasolabial fold and its apex over the superolateral malar
prominence.
Malar fat pad
Orbicularis oculi
Zygomaticus major

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CHAPTER 6.2 • Facelift: Principles of and surgical approaches to facelift
Fig. 6.2.4  (A) Superficial facial
fat is compartmentalized by
vertically running septae. In the
midcheek, from medial to lateral,
these compartments are the
nasolabial, medial, middle, and
lateral compartments. The
nasolabial and medial
compartments make up the malar
fat pad.
A
ORL
ORL
SCS
Nasolabial
Medial
Middle
Lateral
SOOF
ZM
deep fascia by retaining ligaments over the parotid gland, at
the inferior border of the zygomatic body, and along the
anterior edge of the masseter (see Chapter 6.1 and later in this
chapter). Between these areas of fixation, the SMAS is free to
move over the underlying deep fascia. These are the suprazy­
gomatic zone where superficial temporal fascia slides over the
deep temporal fascia, the midcheek where SMAS rides over
the parotid masseteric fascia (premasseteric space), and the
neck where the platysma lies unattached over the underlying
strap muscles.
Facial muscles
The muscles of facial expression are found in two layers:
superficial and deep. The superficial muscles are orbicularis
oculi, orbicularis oris, zygomaticus major, zygomaticus minor,
levator labii superioris, risorius, and depressor anguli oris. All
of these muscles are innervated on their deep surface by
branches of the facial nerve (VII). Consequently, surgical dis­
section on the superficial surface of these muscles will not
endanger their innervation. The only facial muscles inner­
vated on their superficial surface are the muscles in the deep
layer: mentalis, levator anguli oris, and buccinator. The three
facial muscles most important to surgeons are orbicularis
oculi and platysma – because they are often manipulated
during facelift surgery – and zygomaticus major – because
it is used as a landmark in certain facelift techniques (see
Fig. 6.2.2).
Most muscles of facial expression take their origins from
bone and insert into the dermis thus allowing for voluntary
and involuntary movement of facial soft tissues. Platysma is
a purely subcutaneous muscle taking its origin from the fascia

117
Anatomy and patient presentation
Fig. 6.2.5  This healthy 72-year-old woman
has never undergone facial surgery, has
gained 10 pounds, but has aged 50 years.
She appears to have lost fat in the
periorbital region and middle third of her
face, revealing underlying bone. The orbit
seems to have enlarged. Overall volume has
been lost in the middle third of the face.
The soft tissues that remain appear to be
ptotic, flattening her cheeks, and widening
her jawline. The heart-shaped face of youth
has become more rectangular.
A
B
B
C
(B) The deep facial fat is also compartmentalized by septae. The deep medial fat pad (here stained blue) is bounded above by the orbicularis retaining
ligament, medially by the pyriform aperture, and laterally by the zygomaticus major (labeled ZM) muscle and the buccal fat pad (labeled B). (C) Over the body of the
zygoma, the suborbicularis oculi fat (SOOF) is deep fat. It is seen here with a medial portion (yellow) and a lateral portion (stained blue). It is bounded medially by deep
medial fat pad (stained red). (A, Courtesy of Rohrich RJ, Pessa JE. The fat compartments of the face: anatomy and clinical implications for cosmetic surgery. Plast Reconstr
Surg. 2007;119:2219–2227; B,C Courtesy of Rohrich RJ, Pessa JE, Ristow B. The youthful cheek and the deep medial fat compartment. Plast Reconstr Surg.
2008;121:2107–2112.)
Fig. 6.2.4, cont’d
of the pectoralis and inserting into soft tissue of the face, with
a small bony insertion on the anterior mandible. It is also
tethered posteriorly to the sternocleidomastoid muscle via the
cervical retaining ligaments.80 The platysma interdigitates
with the depressor labii inferioris and in some individuals the
platysma provides some effect on the depression of the lower
lip. The platysma is thickest in the neck and can be visualized
when a patient grimaces. As the muscle courses superiorly,
crossing the mandibular border, it becomes much thinner. In
some individuals the platysma can be found extending well
into the midcheek, occasionally approaching the lower fibers
of the orbicularis oculi.
While most muscles of facial expression do not change
appreciably with age, the orbicularis oculi and the platysma
are thought to undergo age-related changes. Both muscles
have a large surface area and are relatively thin – a configura­
tion lending them to potential redundancy if they lose tone or
if their deep tissue attachment is attenuated. For example, in
some individuals redundancy develops in the lower half of
the orbicularis, a condition that is a speculated cause of lower
eyelid festoons.81 Some have suggested that it is the loss of
support of the orbicularis through attenuation of the orbicu­
laris retaining ligament (orbitomalar ligament) that contrib­
utes to deformities of the lower eyelid/cheek junction.69
Similarly, the paired platysma muscles, which are encased by
SMAS, appear to gradually fall away from their deep cervical
attachment carrying the overlying fat and skin. The net result
is a more obtuse cervicomental angle and the development of

118
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CHAPTER 6.2 • Facelift: Principles of and surgical approaches to facelift
facial fat, inserting into the dermis.45,46,48 Effectively, these liga­
ments attach the SMAS and overlying skin to the underlying
deep fascia and bone (Fig. 6.2.6).
There are two ligament systems. The first are true osteocu­
taneous ligaments, tethering skin to bone: the orbital, zygo­
matic, and the mandibular ligaments. The orbital ligament is
found at the junction of the superior and lateral orbital rims
and constitutes the inferior thickening of the temporal crest
line zone of fixation (zone of adhesion) (see Chapter 7). The
zygomatic ligament is actually a group of ligaments originat­
ing from the lower half of the zygomatic body to join the
zygomatic arch. The zygomaticus major bony origin is in this
location. These ligaments stabilize the overlying malar fat
pad, going through this structure to the overlying skin. In this
area, a perforating branch of the transverse facial artery
courses from deep to superficial, contributing to the clinical
bleeding seen when the zygomatic ligaments are released in
this area during superficial skin flap dissection (McGregor’s
patch). A branch of the zygomaticofacial nerve also
visible platysma bands at the anterior platysmal border.
Another issue common to orbicularis oculi and platysma is
that these are the only facial muscles that are undermined
during certain surgical procedures, thus imperiling some of
their motor innervation. Fortunately, the orbicularis has
multiple motor nerve branches providing a level of collateral
innervation.82 There is a less elaborate innervation to the
platysma; two or three cervical branches can be identified just
inferior and anterior to the angle of the mandible in the plane
between the deep cervical fascia and the undersurface of the
platysma. Preservation of these branches is potentially impor­
tant because the platysma acts as a support structure and also
influences lower lip depression, especially in those individu­
als with a “full dentition” smile.83
Retaining ligaments
Facial soft tissue and skin are held in place by retaining liga­
ments running from underlying fixed structures through
Fig. 6.2.6  Facial soft tissue is tethered to underlying bone by the orbital, zygomatic and mandibular ligaments. Soft tissue is tethered to underlying deep fascia by the
masseteric cutaneous ligaments and by an area of attachment anterior and inferior to the earlobe, known by a number of different terms: platysma auricular ligament
(Furnas), platysma auricular ligament (Mendelson), parotid cutaneous ligament (Stuzin), and a distinct area anterior to the earlobe known as Lore’s fascia.
Zygomatic ligaments
Temporal fat pad
Orbital ligaments
Masseteric ligaments
Temporalis
Mandibular ligament
Zygomaticus major
Platysma auricular fascia
Tympanoparotid (Lore’s) fascia
Upper edge of temporal fat
Cervical retaining ligament
Platysma
Sternocleidomastoid

119
Anatomy and patient presentation
available at this time. Either way, the tethering structures play
an important role in determining the way a face will age.
Furthermore, these same tethering structures can be manipu­
lated during facelift surgery, depending on the specific
indication.
Deep fascia
The deepest layer of the face is the deep fascia, covering deep
muscles and overlying the oral cavity (see Chapter 6.1). In the
face, this fascia is a continuation of the deep cervical fascia in
the neck, which covers the superficial surface of the strap
muscles and the sternocleidomastoid. The equivalent layer in
the temple is the deep temporal fascia covering the temporalis.
In the cheek, this fascia is found covering the masseter muscle,
where it is called masseteric fascia, and covering the parotid
gland, where it is called the parotid fascia or parotid capsule;
the combined complex is called the parotid masseteric fascia
(parotidomasseteric fascia). When the SMAS is raised surgi­
cally, just anterior to the parotid gland in the premasseteric
space, the parotid masseteric fascia can be seen as a thin shiny
membrane – an important landmark, because in the cheek
(unlike the neck and temple), all branches of the facial nerve
are deep to this deep fascial layer. Superficial to this layer, but
deep to the SMAS, there is often an additional thin layer of
fat, the subSMAS fat, which adds further protection to the
underlying nerves when the SMAS is raised. In Chapter 6.1,
this area is called the premasseteric space. As mentioned
earlier, in the neck where the platysma crosses the anterior
border of the sternocleidomastoid, the SMAS encompassing
the platysma is fused with the deep cervical fascia where
the deep fascia covers the sternocleidomastoid muscle – the
so-called cervical retaining ligament. This is an important
accompanies the ligaments in this area, coursing directly from
bone to skin, providing sensation to the skin of the malar
cheek prominence. As described in Chapter 6.1, the zygomatic
ligaments constitute the lower border of the prezygomatic
space and must be released if the malar fat pad is to be fully
mobilized and elevated. The mandibular ligament is a short
but strong structure originating from the parasymphysial
mandible, tethering the overlying skin and contributing to
formation of marionette lines.
The second ligament system involves tethering structures
not originating from bone, but rather tethering the SMAS to
the deep fascia. Along the anterior border of the masseter, the
masseteric ligaments extend in a line from the zygoma down
to the lower cheek.46 These ligaments support the anterior
cheek and are more clinically significant superiorly, where
they intermingle with the zygomatic ligaments. The most
superior fibers of the obliquely running platysma can be seen
terminating in the most superior masseteric ligaments. Over
the parotid gland, the superficial fascia is directly attached to
the deep fascia. This firm attachment continues inferiorly
where the superficial fascia encompassing the platysma is
attached directly to the deep fascia of the sternocleidomastoid;
this area has been termed the cervical retaining ligament.80
Some surgeons have identified the importance of the
fixated SMAS over the parotid and, with some subtle differ­
ences, different names have been applied to the same soft-
tissue attachment: platysma auricular fasica,84 platysma
auricular ligament,45 and parotid cutaneous ligament.46 Deep
to this area and attaching the SMAS to the bone of the ear
canal is Lore’s fascia.85,86 In the parotid area, the SMAS and
the overlying skin are tethered to such a degree that soft tissue
in this zone does not become ptotic with age. The primary
surgical significance of this area is that the SMAS is relatively
immobile and the so-called “fixed SMAS” can be used to
support the surgically mobilized portion of the more anterior
“mobile SMAS”. A number of facelift techniques depend on
this concept (Fig. 6.2.7).
The importance of retaining ligaments in aging is poten­
tially two-fold. One theory holds that with age, ligaments
relax, causing a gravitational shift of overlying superficial fat
and skin. In youth, these appear to be firmly adherent to
underlying bone and deep fascia, while with age the same soft
tissue appears to become ptotic. One area where this has been
proposed is along the infraorbital rim, where the orbicularis
retaining ligament may relax, leading to the V-deformity at
the lid–cheek junction.69,87–89 Over the malar highlight area, the
ligament relaxation theory suggests that the zygomatic liga­
ments become attenuated and the malar fad pad becomes
ptotic, causing a migration of fat medially and inferiorly,
contributing to the development of the nasolabial fold.
The second way that retaining ligaments become an issue
with aging is through their tethering effects. The concept of
“pseudoptosis” suggests that a loss of facial fat volume leads
to ptosis, but the ligaments tether the overlying skin, leading
to depressions and grooves in the surface contour of the face.
Examples of tethering include the midcheek groove, caused
by the zygomatic ligaments; the nasojugular groove, partly
caused by the orbicularis retaining ligament (orbitomalar liga­
ment); and the jowl/marionette line, caused by the mandibular
ligament.84–86,88
Both of these theories are likely in play – ptosis and defla­
tion, although conclusive proof of how faces age is not
Fig. 6.2.7  Mendelson’s interpretation of soft-tissue attachments (see Chapter 6.1).
The fixed posterior soft tissue is held in place by the platysma auricular fascia
(large red area). The anterior face is fixed by a vertical column of attachments:
orbital ligament, lateral orbital thickening (superficial canthal tendon), zygomatic
ligaments, masseteric ligaments, mandibular ligament). In the midcheek, there is
some mobility of these ligaments, while there is limited mobility over the platysma
auricular fascia. The so-called “fixed SMAS” is that portion attached to the parotid
and the posterior border of the platysma. Anterior to this, is the “mobile SMAS”.
(Courtesy of Dr. Levent Efe, CMI.)

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CHAPTER 6.2 • Facelift: Principles of and surgical approaches to facelift
Bone loss can be replaced with solid objects such as facial
implants (see Chapter 6.8), or with soft-tissue volume
enhancement such as with fat grafting (see Chapter 13).
Facial nerve
The facial nerve exits the stylomastoid foramen, separating
into an upper and lower division within the parotid glad.
Classically, there are five branches arising and exiting the
cover of the superficial lobe of the parotid: temporal, zygo­
matic, buccal, marginal mandibular, and cervical. There are
typically 2–3 temporal branches; 4–5 zygomatic branches; 3
buccal branches; 2–3 mandibular branches; and 2–3 cervical
branches.
In fact, there is considerable variation in the anatomy
of facial nerve branches. One study identified up to eight
branches exiting the parotid, with multiple connections
between these branches.97–99
The temporal branches exit the parotid superiorly, coursing
obliquely across the middle third of the zygomatic arch. Like
all other facial nerve branches, the temporal branches start out
deep to the deep fascia of the midcheek (parotid masseteric
fascia), but unlike all other facial nerve branches in the cheek,
factor, because a surgeon planning to mobilize a platysma flap
to address the neck will have to release the platysma’s attach­
ment to the sternocleidomastoid (Video 6.2.1
).80
Bone
The bony skeleton of the face was once thought to be quite
stable in volume and shape as the body aged. However, there
is ample evidence that atrophy in certain portions of the facial
skeleton is a factor in facial aging.90–95
Computed tomography of young and old skulls has shown
a retrusion of the infraorbital rim as well as recession of the
maxillary face below the infraorbital rim (Fig. 6.2.8).92 This has
been confirmed by others who have also demonstrated an
enlarging orbital aperture (Fig. 6.2.9).96
Loss of bone has surgical implications because it contrib­
utes to an overall loss of volume, and more specifically, to a
loss of soft-tissue support in critical areas such as the infraor­
bital rim. This contributes to development of the tear trough
deformity and age-related flattening of the anterior midface.
Fig. 6.2.8  Computed tomography of young and old skulls has demonstrated a
retrusion of the infraorbital rim. (Courtesy of Pessa JE. An algorithm of facial aging:
verification of Lambros’s theory by three-dimensional stereolithography, with
reference to the pathogenesis of midfacial aging, scleral show, and the lateral
suborbital trough deformity. Plast Reconstr Surg. 2000;106:479.)
Fig. 6.2.9  Computed tomography scan of (A) a male patient in the young age
group and (B) a male patient in the older age group. The image from the older age
groups shows significant bony remodeling (arrows) both superomedially and
inferolaterally. (Courtesy of Kahn DM, Shaw RB. Aging of the bony orbit: a
three-dimensional computed tomographic study. Aesthetic Surg J. 2008;28:258.)
A
B

121
Patient selection
they become more superficial. At a point 1.5–3.0 cm superior
to the zygomatic arch, the temporal branches transition from
deep to superficial, travelling at first on the undersurface and
then within the superficial temporal fascia (temporoparietal
fascia), staying there until they terminate in the frontalis
muscle, upper orbicularis, and corrugator supercilii. The
surgical implication is that an SMAS flap can be safely raised
from a point just superior to the zygomatic arch providing
that surgical dissection does not extend superiorly to the
level where the temporal branch transitions superficially.100
For this reason, the “high SMAS” procedure described in
Chapter 6.7 can be done safely without injury to the temporal
branch.
A classic external landmark for the course of the temporal
branch has been along a line drawn from a point 0.5 cm below
the tragus to a point 1.5 cm lateral to the lateral eyebrow.101
More recent studies have found that the temporal branch
actually consists of 2–5 individual branches that do not adhere
completely to this landmark. One study found that these
branches cross the middle third of the zygomatic arch, with a
posterior safe zone 1 cm anterior to the acoustic meatus, and
an anterior safe zone 2 cm posterior to the lateral orbital rim.
Once above the zygomatic arch, these branches were consis­
tently found anterior and inferior to the anterior branch of the
temporal artery, a palpable landmark in the temple.102
The zygomatic and buccal branches all exit the parotid
deep to the parotid masseteric fascia. As they travel anteriorly,
they often arborize with each other. Zygomatic branches
course parallel to the transverse facial artery. When they reach
the area of the zygomatic retaining ligament, they travel to
the undersurface of the muscles that they innervate: zygo­
maticus major, zygomaticus minor, and orbicularis oculi.
Deep to the parotid masseteric fascia, within the premasseteric
space, the parotid duct courses anteriorly along an imaginary
line from the tragus to the corner of the mouth. Accompany­
ing the duct is normally a buccal branch. Beyond the anterior
border of the masseter, a buccal branch can normally be seen
crossing the buccal fat pad (fat pad of Bichat). At this level,
the portion of buccal fat seen is the buccal extension, which
is the most inferior portion of the buccal fat pad.103
The mandibular branches exit the parotid approximately
near the angle of the mandible. They then travel anteriorly
near the mandibular border, until they encounter the facial
artery and vein, crossing those vessels and then turning more
superiorly. In Chapter 6.1, facial spaces are described, with the
mandibular branches coursing at the lower border of the
premasseteric space, which displaces inferiorly with age.
Consequently, in elderly patients in the supine position, they
have been found coursing well inferior to the mandibular
border.104
The cervical branches are the most inferior, exiting the
parotid at its inferior border and always coursing below the
mandibular border. The cervical branches innervate the pla­
tysma. There are usually two or three branches with consider­
able variation in branching patterns. A contribution from the
sensory transverse cervical nerve has also been described.83
Because the buccal and zygomatic branches are multiple
and interconnected, there is a reserve capacity in the event
of a single branch injury; therefore, permanent injury is
uncommon. However, the temporal and marginal man­
dibular branches enjoy less collateral innervation, making
permanent loss much more likely if these branches are
injured. Also, damage to the cervical branches can weaken
the platysma, leading to a “pseudo paralysis” of the lower lip
(Fig. 6.2.10).105
Sensory nerves
The great auricular nerve, a branch of the cervical plexus, is
sensory to the earlobe and lateral portion of the pinna. This
nerve wraps around the posterior border of the sternocleido­
mastoid and courses obliquely across the muscle in a superior
direction. The classic landmark for this nerve is at the midpor­
tion of the sternocleidomastoid, 6.5 cm below the external
auditory canal106 (Fig. 6.2.11).
It runs parallel and about 1 cm posterior to the external
jugular vein which also crosses the sternocleidomastoid
roughly along the same vector. The nerve is deep to the
superficial cervical fascia, but the platysma is usually absent
over the posterior sternocleidomastoid. Hence, the nerve is at
risk of injury during surgical dissection along the posterior
border of the sternocleidomastoid because, with lack of fascial
cover, it is technically subcutaneous.81,107
The auriculotemporal nerve, a branch of the trigeminal, is
sensory to the preauricular skin and the lesser occipital nerve
is sensory to the retroauricular scalp. The zygomaticofacial
nerve exits through its foramen in the body of the zygoma,
piercing the malar fat pad to provide sensation to the skin of
the malar prominence; this nerve is often transected when the
malar fat pad is surgically mobilized (Fig. 6.2.12).
Patient selection
Like any elective surgical procedure, the patient’s physical
and mental status must be appropriate to withstand the rigors
of surgery, recovery, and any potential complications. The
patient’s expectations must be explored to determine if they
are realistic and if they are technically achievable. The quality
of surgical result will be affected by many patient-related
factors including the facial skeleton, the weight of facial soft
tissue, the depth and location of folds, and the quality of the
skin. For every patient there are some issues that can be pre­
dictably reversed, others attenuated, and some may not be
correctable at all.
The patient presenting for facial rejuvenation will usually
be middle aged or older, thus increasing the chances of under­
lying medical problems. In an otherwise apparently healthy
individual, specific issues that must be addressed are blood
pressure, smoking history, and the use of medications or
supplements that can promote surgical bleeding.
Incipient hypertension is common in the general popula­
tion and can promote postoperative hematomas if it is not
identified prior to surgery. Hematoma is by far the common­
est complication in facelift surgery; therefore, uncontrolled
hypertension is a contraindication for surgery, while con­
trolled hypertension is not a contraindication. The labile
hypertensive can be the most insidious situation. If patients
have intermittent hypertension (the white coat syndrome), or
they are simply type A individuals who are easily excitable,
perioperative treatment with medications such as clonidine
should be considered.
Smokers can exhibit delayed wound healing due to micro­
vasoconstriction and abnormal cell function.108 One study

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CHAPTER 6.2 • Facelift: Principles of and surgical approaches to facelift
they see in the mirror. Nevertheless, it is important to
recognize what the patient can see is the patient’s primary
concern. To help focus the discussion, old photographs are
very useful in determining which aging changes predominate
and what features the patient would most like corrected. This
will help improve patients’ understanding of exactly how
they have aged and what, if any, rejuvenation they would
like to undergo. They will also gain a better understand­
ing of the magnitude of surgery required to accomplish
their goals.
Anatomic assessment
Before surgery, the entire face should be properly assessed.
This examination is conducted in a well-lit room with the
patient sitting vertically in a comfortable position. Examina­
tion should be orderly so that nothing is missed. The face is
examined with the patient in repose and in animation. Thus,
facial nerve function is clinically assessed. The face should be
assessed as a whole – looking for the equality of facial thirds,
the degree of symmetry, and the overall shape (round, thin,
wide). Classic tenants of facial shape are reviewed at the
completion of this chapter. Facial shape influences the choice
of surgical procedure.74 For example, a wide full face may be
more suited to soft-tissue excision, rather than overlapping
facial fat in the midface. Fat grafting may not be necessary.
reported a 12.5 times greater chance of having skin flap
necrosis in a smoking patient compared with a non-smoker.109
Long-term smokers have reduced arteriole function, which
may never return to normal. Nevertheless, there are signifi­
cant short-term effects that can be reversed by abstaining from
tobacco use for 2–3 weeks prior to surgery. Tests for the
metabolites of nicotine in the blood are available to confirm
abstinence from smoking.
Commonly used non-steroidal anti-inflammatory medica­
tions (NSAIDs) and the consumption of certain dietary supple­
ments may promote intraoperative and postoperative bleeding
based on platelet function inhibition. Patients should avoid
these medications for 3 weeks prior to surgery.
Female patients in the facelift age group may be on hormone
replacement and are therefore at increased risk for developing
postoperative deep vein thrombosis (DVT) and a potentially
lethal pulmonary embolism. For these patients, in addition to
all recognized preventative measures, consideration should
be given to stopping hormonal replacement 3 weeks prior to
surgery.
With respect to the surgical objectives in facelift surgery,
aging causes fundamental anatomical changes in all tissues
of the face. However, patients will typically present with
specific concerns about specific areas – often the soft-tissue
ptosis in the neck or jowls, or the visible wrinkles and folds
in the cheek and neck. Patients are usually unaware of the
underlying anatomic changes that are causing the problems
Fig. 6.2.10  (A) A cadaveric dissection of the facial nerve. The superficial lobe of the parotid gland is peeled away. The SMAS, platysma and parotid masseteric fascia have
been removed, revealing the facial nerve branches. (B) Diagram of the facial nerve. The facial nerve exits the stylomastoid foramen and normally divides within the parotid
gland into a superior and inferior division. Classically, five groups of branches are seen: temporal, zygomatic, buccal, mandibular, and cervical. There is arborization
between branches, particularly between the zygomatic and buccal branches. (A, Courtesy of Dr. Mario Pelle-Ceravolo.)
A
B
Parotid gland
Posterior
auricular nerve
Temporofacial division
Cervicofacial division
Marginal mandibular
branch
Cervical branch
Buccal branches
Zygomatic branches
Temporal branches

123
Surgery
Fig. 6.2.11  The great auricular nerve crosses the midportion of the
sternocleidomastoid at McKinney’s point, which is 6.5 cm inferior to the external
auditory canal. It usually travels about 1 cm posterior to the external jugular vein.
Anterior to McKinney’s point, the nerve is covered by the superficial cervical fascia
and the platysma (SMAS), but at the posterior border of the sternocleidomastoid,
the nerve is effectively subcutaneous. The most common point of injury is at the
posterior border of the sternocleidomastoid muscle.
Great auricular nerve
External jugular vein
6.5cm
McKinney’s point
Conversely, a long, thin face will require the preservation of
all soft tissue, overlapping it rather than excising it, and
potentially adding additional volume. Preoperative identifi­
cation of asymmetries is important and should be pointed out
to the patient because facelift surgery will make some asym­
metries more obvious.
Surgeons should develop an organized way to examine all
the zones of the face: forehead, eyelids, cheeks, the perioral
area, and the neck. In certain individuals, the appropriate
procedure will be a correction of only one of these areas, but
more commonly, all or most or the zones should be addressed
in order to achieve a harmonious result. Assessment of the
forehead and orbital area are discussed in Chapter 7. In the
cheeks, the surgeon should assess the shape and prominence
of the underlying skeleton, the volume and distribution of
facial fat, the degree of soft-tissue atrophy and ptosis, and the
relative mobility of the subcutaneous (superficial) fat. Any
significant hollowing or flattening should be noted, and
conversely, any radial expansion (fat deposition) in the jowl
and neck should be noted. With the diversity of surgical
techniques available, a surgeon should think like a sculptor
– considering the face in three dimensions with a view to
adding tissue in some areas, removing tissue in other areas,
and repositioning tissue to a more youthful location. In the
perioral area, the plumpness of the lips should be assessed,
and any elongation of the upper lip should be noted. On
smiling, the amount of dental show is observed. The skin
should be assessed, its quality noted, along with the depth of
wrinkles and folds, including the nasolabial fold and the
marionette lines.
Assessment of the neck is discussed in Chapter 12, but in
brief, the neck should be examined in various positions:
neutral, flexion, and turning side-to-side. The patient is asked
to contract the platysma by clenching the teeth and grimacing.
This will help identify the degree of platysma laxity, the
strength of the anterior platysma bands, and the amount of
subcutaneous fat superficial to the platysma. The amount of
subplatysmal fat is also estimated. Ptosis of the submandibu­
lar gland should be noted and pointed out to the patient
preoperatively; this condition, if untreated, will become more
obvious after facelift surgery.
The ear should be examined with a thought to the potential
placement of incisions. Important factors include the size and
orientation of the earlobe, the angle of attachment of the
tragus, the difference in character of the cheek skin and tragal
skin, and the size of the tragus. The density of the hair sur­
rounding the ear, the location of the hairline in the temple, the
sideburn, and posterior to the ear all influence incision choice.
Careful assessment of the overlying skin is also important
to determine if anything non-surgical is indicated – before,
during, or after facelift surgery. Assessment will include skin
type, skin quality, skin excess, the depth of folds, the degree
of fine wrinkling, and the amount of photoaging. In particular,
perioral rhytides should be examined as they are often a
significant concern for the patient. Issues with the skin should
be pointed out to the patient and options discussed because
facelift surgery itself will not improve the texture and quality
of the skin – a common misconception.
Excellent photographic documentation of the preoperative
face is very important, and should include frontal, oblique,
and profile views. Other optional views include the smile and
close-up views of the neck in repose and with platysma con­
tracture. Changes in the face from facelift surgery may be
more subtle than other aesthetic procedures, so a reliable
record of the surgical starting point is imperative.
Surgery
A facelift is a significant operation. It should be done under
excellent conditions, with appropriate medical staff, appropri­
ate equipment, and adequate back up. Anesthesia can be
safely done with many different approaches, including local
anesthetic with different levels of intravenous sedation and
with varying levels in the spectrum of general anesthesia. An
anesthesiologist can decide in consultation with the surgeon
what form of anesthesia is preferred for an individual patient.
There should be proper intraoperative patient positioning,
intraoperative monitoring, intraoperative warming, and
intraoperative DVT prophylaxis.
Technique
Historically, surgeons have been guided by the simple empiri­
cal finding that people look younger when soft tissue of the
lower cheek is shifted into the middle and upper cheek.
Patients see the same thing in a mirror when they manually
lift their cheek or when they lie on their back. Effectively, by

124
SECTION I
CHAPTER 6.2 • Facelift: Principles of and surgical approaches to facelift
direction.24,26 Still used today, this classic procedure tightens
excess skin and relies on skin tension to reposition the
underlying facial soft tissue against the force of gravity. The
advantages of a “skin-only” facelift are its relative simplicity,
a rapid postoperative recovery, and the use of a dissection
plane that does not risk damage to the facial nerve or other
deep structures. The inherent disadvantage of the “skin-only”
facelift is that a thin skin flap placed under tension to support
heavy underlying soft tissue will inevitably stretch, leading
to a loss of surgical effect. Therefore, the longevity of effect
is in question. Unfortunately, if the surgeon increases skin
tension in a misguided attempt to reposition ptotic deep
tissue, the shape of the face can be distorted. Skin tension
will flatten facial shape, negating the rounded contours of
youth. Also, patients in the facelift age group have usually
lost elasticity in their skin and therefore, with tension, are
prone to a stretched look with wrinkles and folds reoriented
in abnormal directions. Lastly, excess skin tension at the
incision line can cause malposition of the hairline, alopecia,
distorted earlobes, widened scars, and possible skin flap
necrosis.
Despite these issues, for the thin-faced patient with primar­
ily loose skin with minimal ptosis of deep soft tissue, this
procedure can be quite effective. It may also be a useful
technique in secondary or tertiary situations where the deep
tissues have previously been repositioned and the presenting
problem is a recurrence of skin laxity.
shifting volume from the lower face to the midface, a more
youthful facial shape is achieved. As we have seen, changes
in volume are a significant part of facial aging. Surgeons have
been able to improve the lower third of the face and neck by
removing excess volume, and in recent years, surgeons have
demonstrated that people may look younger with volume
augmentation alone.110,111 By combining these approaches –
adding volume in some areas, subtracting volume in others,
and repositioning ptotic tissue, the surgeon has the ability to
sculpt facial shape to restore the contours of youth.
The repositioning of ptotic tissue is the principle objective
that has interested surgeons since facelift surgery began.
Many methods have been described. The choice of technique
will depend on the individual patient’s aesthetic diagnosis,
the patient’s desires, and the surgeon’s comfort level with a
certain procedure. In this section, the classic subcutaneous
facelift will be described followed by a review of the various
methods surgeons use to manipulate the deeper soft tissue of
the face.
Subcutaneous facelift
The first facelift, dating from the early 20th century, was a
simple skin incision at the temporal hairline and anterior to
the ear; several authors have claimed this innovation.9–11 This
method evolved into a subcutaneous dissection of a large
random-pattern skin flap that was shifted in a superior–lateral
Fig. 6.2.12  Major sensory nerves of the
face.
Ophthalmic nerve V1
Zygomaticotemporal nerve
Zygomaticofacial nerve
Supraorbital nerve
Supratrochlear nerve
Infratrochlear nerve
External nasal nerve
Lacrimal nerve
Infraorbital nerve
Buccal nerve
Mental nerve
Auriculotemporal nerve
Maxillary nerve V2
Mandibular nerve V3