You are on page 1of 6

Postoperative Regimen

for Chemical Peeling:


A Clinical Approach
Wallace K. Dyer II, M.D., F.A.C.S.

To develop an effective postoperative treatment much more time than epithelialization, and ulti-

Downloaded by: Universite Laval. Copyrighted material.


regimen for chemical peels, it is necessary to under- mately the strength of the skin depends on the thick-
stand general wound healing principals, the perti- ness of the dermis.
nent anatomy and physiology of skin, and the depth
of injury that is being treated. Chemical peeling de-
scribes a wide range of wounding agents that, de- WOUND HEALING
pending on the desired result, will damage the skin
from the stratum corneum to the midreticular der- Controlled wounding with chemical peel agents
mis. This depth of injury may also be extended by produces a partial thickness wound that heals by
postoperative complications such as infections. Ulti- secondary intention. Golsen2 defines wound healing
mately, the depth of the injury determines the post- as "the interaction of a series of complex events that
operative care regimen. leads to the resurfacing, reconstitution, and propor-
tionate restoration of tensile strength of wounded
skin. Partial-thickness wounds penetrate partially
CUTANEOUS ANATOMY but not completely into the dermis. These defects
heal by reepithelialization from residual adnexal
After a chemical peel, the epidermis and dermis epithelium or epithelium derived from adjacent un-
both actively contribute to wound healing. Because injured skin. Healing is rapid and scarring is clini-
the basal layer remains intact, partial thickness cally imperceptible since contraction does not gener-
wounding, even to the level of the midreticular ally occur."
dermis, generally heals without visible scarring. Wound healing is accomplished in multiple phases
However, since melanocytes are found in the epi- that overlap over time (Fig. I).3 On injury, an imme-
dermis, deep chemical peel injuries may result in diate vascular and inflammatory response occurs.
pigmentary abnormalities. The epidermis contains The complex cellular response activated by the in-
no collagen fibers but has impressive growth poten- jury mediates the inflammatory phase, which nor-
tial, enabling epithelial cell migration often to cover mally persists for at least 1 week. Granulation tissue
wide wounds within a few days when given the begins to form, providing a temporary matrix over
appropriate conditions. Collagen is extensively cross- which epithelial cells and fibroblasts may proliferate
linked in the dermis and provides intrinsic strength within the wound. Polymorphonuclear leukocytes
to this layer.1 The process of laying down dermal stimulated by the cellular response remove bacteria
collagen matrix after superficial wounding requires from the wound. In a contaminated wound, poly-

Department of Surgery, Otolaryngology—Head and Neck Surgery, Emory University


Atlanta, Georgia
Reprint requests: Dr. Dyer II, 1218 W. Paces Ferry Rd., Suite 108, Atlanta, GA 30327
Copyright ©1995 by Thieme Medical Publishers, Inc., 381 Park Avenue South, New York, NY 10016. All rights reserved.

47
FACIAL PLASTIC SURGERY Volume 11, Number 1 January 1995

vasoeoAarmc~lon INFUMMAToRY PHASE

C.IIuIar Response
...............................
PROLIFERATIVE PHASE

I MATURATION I REMODELING PHASE

I I I I I I I I I I I I
P
$ $'
P ,f &?
. **
3
8
3
8'
,s,
*$
4
' . ha'
Figure 1. Phases of wound healing.
8

morphonuclear leukocytes persist and prolong the Bio-occlusive dressing


inflammatory phase. This extended inflammation
Moist exudate

Downloaded by: Universite Laval. Copyrighted material.


may account for more severe cellular damage, in-
creasing the original wound depth and resultant
scarring. Thus, it is important to minimize contam-
---- Wound surface

ination and inflammation to maximize the rate of


epithelialization. Macrophages also migrate to the
wound and are essential for phagocytosis and tissue
\ Migrating epithelial cells
debridement.4 During the proliferative phase of Figure 2. Epidermal migration beneath a moist wound.
wound healing, epithelial regeneration is maxi- (With permission of Dr. Jim English.)
mized. Fibroplasia, collagen formation, and neo-
vascularization also occur within this phase. Wound
contraction is often minimal in superficial injuries, the early postoperative period to enhance reepithe-
but may account for the tightening of skin demon- lialization. Numerous semiocclusive or occlusive
strated in medium to deep chemical peels. Epithe- dressings have been developed. Numerous types of
lialization begins within 24 hours of injury by migra- bio-occlusive dressings are delineated in Table
tion of epithelial cells from the surrounding wound Occlusive dressings not only encourage epithelial-
margins or from the deeper adnexal structures, such ization, but have the added advantage of promoting
as hair follicles or sebaceous glands.5 The rapidly fibroblast proliferation." However, bacteria also have
advancing front of epithelial cells continues until it the opportunity to proliferate under such dressings.
comes in contact with other epithelial cells. Simul- Contaminated states may lead to local bacterial
taneously, basal cells within the wound begin mitotic wound infection, and wound healing will be pro-
activities, thus thickening the new epithelial layer. It longed. Bacteria delay the normal healing phases by
has been shown that the rate of postoperative epi- directly damaging cells of wound repair, by pro-
thelialization may be increased by preoperative longing the inflammatory phase, and by competing
treatment of the skin with tretinoin 0.1% (Retin-A)in for oxygen and nutrients within the wound.12J3
a double-blind placebo study.6
It has been demonstrated by Maibach and Rovee7
that in a moist environment, wounds will heal ap-
proximately 40% faster than those that undergo dei-
iccation.819 If a wound is kept moist, particularly
with an occlusive dressing, epithelial migration pro-
ceeds more directly and efficiently. Conversely,wound
desiccation sipficantly impairs normal wound heal-
ing? When a desiccated crust forms over wounded
skin, the migrating epidermis takes a longer, less
I Normal scab

efficient route, thus delaying epithelialization (Figs.


2,3). Accordingly, most surgeons prefer to maintain Figure 3. Epidermal migration beneath a dry wound.
a moist environment for chemically peeled skin in (With permission of Dr. Jim English.)
REGIMEN FOR CHEMICAL PEELING-Dyer

Table 1. Bio-Occlusive Dressings* --

~e~meabilit~
Name Types of Composition Transparent Adherent Absorbent Gas Fluid Clinical Uses
Ob-Slte Polyurethane Yes Yes No Yes No Sutured wounds, cutaneous
ulcers, skln-graft sltes,
laser wounds
Tegaderm Polyurethane Yes Yes No Yes No Same as for Ob-Slte
B~oclus~ve Polyurethane Yes Yes No Yes No Same as for Ob-Slte
Ensure Polyurethane Yes Yes No Yes No Same as for Ob-Slte
Vlgllon Polyurethane ox~de/water Part~ally No Yes Yest Yest Dermabras~ons,laser
wounds
Spenco Second Polyurethane ox~de/water Part~ally No Yes Yest Yest Dermabras~ons,laser
Skln wounds, frlctlon bl~sters
Duoderm Hydrocollo~d No Yes Yes No No Cutaneous ulcers, sutured
wounds, dermabraslons,
frlctlon bllsters
Comfeel Ulcus Hydrocollord No Yes Yes No No Same as for Duoderm
Blobrane S~l~cone/nylon
wlth No No No Yes Yes Thermal burns,
collagen peptldes dermabras~ons
N-terface Monof~lamentplastic No No No Yes Yes Skln grafts, dermabraslons
*Modified from Wheeland.19
+Permeability of gas and fluid depends on the removal of one or both of the supportive polyethylene sheets.

Downloaded by: Universite Laval. Copyrighted material.


Therefore, it is imperative to change the dressings Systemic disease, genetic or acquired, can ad-
and cleanse the area beneath the dressing at least versely affect wound healing. The more common
every other day. genetic disorders include Ehlers-Danlos syndrome,
It has been shown that certain topical agents may cutis laxa, progeria, pseudoxanthoma elasticum,
affect epidermal migration (Table 214). All of the among others. Some diseases have both a genetic
agents noted within Table 2 promote hydration by and acquired basis, such as metabolic disorders, vas-
covering the peeled areas and reducing desiccation. cular disorders, keloid/hypertrophic scars, and im-
Those containing antibacterial properties tend to in- mune deficiencies.12J6 Infections represent an ac-
crease the relative healing rate and those without quired cause for poor wound healing. Infectious
similar antibacterial properties tend to decrease the etiologies with chemical peels include bacterial (most
healing rate. Providing a sterile environment along commonly Staphylococcus aureus and Pseudornonas
with hydration will help promote epithelialization. species), viral17 (most commonly herpes simplex),
Short-acting corticosteroids are often used to mini- and fungal (most commonly Candida). Iatrogenic
mize edema and inflammation within the immedi- causes of impaired cutaneous wound healing in-
ate postpeel period, but this would not be recom- clude radiation therapy and 13 cis-retonoic acid (Ac-
mended without the simultaneous use of antibiotic cutane). The use of 13 cis-retonoic acid has been
prophylaxis. Clinical morbidity is decreased with shown to impair wound reepithelialization and
low to moderate doses of corticosteroids, but high- should be avoided 6 to 12 months prior to chemical
dose corticosteroids are contraindicated due to a peeling or dermabrasion.18
direct inhibitory effect on early wound healing that
has been reported in the rat model.l5
A N APPROACH T O POSTOPERATIVE
CHEMICAL PEEL CARE

Table 2. Topical Agents By understanding the phases of wound repair,


That Affect Eaidermal Mieration* and the effects of medications, dressings, and sys-
Relative Healing temic agents on the skin, we are able to optimize the
Agent Ratet (%)
local environment for wound healing. Our approach
Neosporin ointment* +25 to postoperative chemical peel wound care and its
Silvadene creams f38
Eucerin cream +5 rationale are discussed (Table 3).
Petrolatum, USP -8 Preoperative patient selection for chemical peel-
Triamcinolone acetonide oiuntment, 0.l0/0 - 34
ing is very important, but, in all patients, preopera-
*Adapted from Geronemus et tive conditions that may optimize the cutaneous re-
+Guinea pig skin. sponse to wounding are considered. The patient's
*Contains neomycin sulfate, polymyxin B sulfate, and bacitracin
zinc. perioperative nutritional status is important, and
§Contains 1% sulfadiazine silver. they are encouraged to eat a well-balanced diet with
FACIAL PLASTIC SURGERY Volume 11, Number 1 January 1995

Table 3. An Approach to Chemical Peel Care


Preoperative Postoperative
2 Weeks 1 Day 24 Hours 2-7 Days 7-14 Days Extended Treatment
Medication
Vitamins x x x x As needed
Prophylactic acyclovir x x x x
Prophylactic antibiotics x x x x
Tretinoin cream x As needed
Lidocaine ointment x
Methylprednisolone x x As needed
Cortisone cream As needed As needed
Hydroquinone cream As needed As needed
Petrolatum ointment x As needed
Sunblock a30 SPF* x
Treatment
High protein diet x x x x x As needed
Oral hydration x x x x As needed
Occlusive ointment x x
Bio-occlusive dressing x
Wound debridement x As needed
*SPF: sun protection factor.

an emphasis on extra protein. Preoperatively, multi- for four different time frames: the first 24 hours, 2

Downloaded by: Universite Laval. Copyrighted material.


vitamins are begun to ensure that trace elements and to 7 days, 7 to 14 days, and from 2 weeks on.
enzymatic cofactors are adequate for protein syn- Immediately after the chemical peel procedure is
thesis. We believe that a high protein diet and vita- complete and during the first 12 to 24 hours, a thin
mins are important from 1 week preoperatively to l layer of lidocaine ointment 5% is applied to the
month postoperatively. Oral antibacterial and anti- wound as needed to decrease pain, provide wound
viral agents (cefaclor 250 mg three times daily and occlusion, and hydration. It is occasionally mixed
acyclovir 800 mg three times daily) are used pro- with petrolatum for better hydration. Oral methyl-
phylactically beginning 1 day preoperatively and prednisolone in a tapering dosage (Medrol Dose-
continuing until the completion of epithelialization. pac) is used to limit the inflammatory response.
The skin is prepared preoperatively with a 2-week During days 2 to 7, the wound care is directed
treatment of 0.05 to 0.1% tretinoin to enhance the toward removing the debris of the superficial skin
postoperative wound healing. This regimen is dis- slough. Patients are directed to wash the area every
continued 1day prior to chemical peeling. Preopera- 4 to 6 hours with water (shower) and gently mas-
tive hydration is also important, and patients are sage the skin with their fingertips. The use of cotton
encouraged to drink at least 1quart of liquid (prefer- balls, tissue paper, and washcloths to remove debris
ably Gatorade) the evening before surgery. is discouraged because cotton and wood fibers may
Postoperatively, wound treatment differs slightly easily be incorporated into the new epithelium, pro-

Figure 4. There is incomplete epi-


thelialization at 7 days postoperatively.
REGIMEN FOR CHEMICAL PEELING-Dyer

. Figure 5. Appearance with Duo-


derm bio-occlusive dressing applied.

Downloaded by: Universite Laval. Copyrighted material.


Figure 6. At 48 hours after Duo-
derrn application, epithelialization i s
complete.

longing the inflammatory phase. Hydration of the CONCLUSION


skin is maintained with a thick covering of pe-
trolatum. During the first 2 weeks, if a dramatic In treatment of the aging face, chemical peeling is
increase in pain is noted, herpes simplex virus infec- one of the most useful modalities available to com-
tion is the likely cause. Acyclovir is increased to plement incisional surgery. A requirement for pre-
double the prophylactic dosage, and symptoms usu- dictable results is a sound knowledge of the skin's
ally subside over 24 hours. At 7 days, most deep reaction to the peeling agents and a logical approach
peels are approximately 80% epithelialized, and to postoperative wound treatment. Appropriate pa-
most medium peels are completely resurfaced. tient selection and avoidance of complications by
Between 7 and 14 days postoperatively, bio-occlu- adequate patient follow-up are necessary to obtain
sive dressings (our choice is Duoderm; Figs. 4-6) are the best outcome. These principles should allow fa-
utilized to cover any areas yet to be epithelialized cial plastic surgeons to incorporate chemical peeling
completely. If there appears to be a persistent in- into their armamentarium and provide consistent,
flammatory response, a second course of methyl- predictable results.
prednisolone is given. Until the wound area is fully
epithelialized, the patient is maintained on systemic
antibiotics and acyclovir. Hytone cream may also be REFERENCES
added to the regimen to help treat the inflammatory
1. Saski GH, Krizek TJ: Biology of tissue injury and repair. In:
response. Any early hyperpigmentation may be Giorgiade NG, et a1 (eds): Essentials of Plastic Maxillofacial and
treated with hydroquinone (2%). Reconstructive Surgery. Baltimore: Williams & Wilkins, 1987
FACIAL PLASTIC SURGERY Volume 11, Number 1 January 1995

Golsen JB: Wound healing after cosmetic surgery. In: Cole- brane. J Invest Dermatol 84:153,1985
man WP, Hanke CW, Alt T, et a1 (eds):Cosmetic Surgery of the Carrico TJ, Mehrhof AI, Cohen IK: Normal and pathological
Skin. Philadelphia: BC Decker, 1991 wound healing. In: Giorgiade NG, et a1 (eds): Essentials of
Frodel JL: Wound healing. In: Facial Plastic and Reconstructive Plastic, Maxillofacial and Reconstructive Surgery. Baltimore:
Surgery. St. Louis: Mosby-Year Book, 1992 Williams & Wilkins, 1987
Diegelmann RF, Cohen IK, Kaplan AM: The role of macro- Goslen JB: Physiology of wound healing and scar formation.
in wound repair: a reGiew. Plast Reconstr Surg 68: In: Thomas Jr, Holt GR (eds): Facial Scars: Incision, Revision,
107.1981 and Camouflage. St. Louis: CV Mosby, 1989
~ r a w c z WS:
~ k The pattern of epidermal cell migration dur- Geronemus RG, Mertz PM, Eaglstein WH: Wound healing:
ing wound healing. J Cell Biol 49:247,1971 the effects of topical antimicrobial agents. Arch Dermatol
Hevia 0,Nemeth AJ, Taylor JR: Tretinoin accelerates healing 115:1311,1979
after trichloroacetic acid chemical peel. Arch Dermatol127: Ehrich HP, Hunt TK: Effects of cortisone and vitamin A on
678-682,1991 wound healing. Ann Surg 162342,1968
Maibach HF, Rovee DT: Epidermal wound healing. Chicago: Goodson WH, Hunt TK: Studies of wound healing in exper-
Year Book Medical Publishers, 1972 imental diabetes mellitus. J Surg Res 22:221,1977
Golsen JB: Wound healing for the dermatologic surgeon. J Rapaport MJ, Kamer F: Exacerbation of facial herpes sim-
Dermatol Surg Oncol 14(a):959,1988 plex after phenolic face peels. J Dermatol Surg dncol lo:
Hunt TK: The physiology of wound healing. Ann Emerg 57-58.1984
Med 1223,1988 Alt TH: Avoiding complications in dermabrasion and chem-
Winter GD: Effect of air drying and dressings on the surface ical peel. Skin Allergy News 2: 1990
of a wound. Nature 197:91,1963 Wheeland RG: The Miller surgical dressings and wound
Alper JC, Tubbetts LL, Sarazen AA: The in vitro response to healing. Dermatol Clin 5:400, 1987
the fluid that accumulates under a vapor-permeable mem-

Downloaded by: Universite Laval. Copyrighted material.

You might also like