Skin Resurfacing - Chemical Peels 

The use of chemical peels, termed chemoexfoliation, to rejuvenate skin is one of the most powerful tools available to facial plastic surgeons. The concept of using a chemical agent to resurface the skin for purposes of improved appearance dates as far back as ancient times. In fact, it has been reported that Cleopatra routinely bathed in sour goat's milk to help beautify her skin. Unbeknownst to her, the lactic acid contained in the milk was the active ingredient providing her with a rejuvenating peel.

The modern era of chemical peeling began at the turn of the century when George Miller MacKee, a dermatologist, began using phenol to treat facial scars. Over the ensuing decades, peeling was popularized by lay operators rather than by physicians. At the time, formulas were considered closely guarded secrets. Eventually, these procedures began to attract widespread attention because of the remarkable results that were achieved.

Scientific investigation was finally undertaken by plastic surgeons and dermatologists who legitimized their use for cosmetic enhancement of the face. This included delineating the indications and limitations of the procedures and improving their safety and efficacy.

Currently, a number of categories of chemical peeling agents available for rejuvenating the skin can be found. These range from superficial formulations available over-the-counter to deep chemical agents that should only be applied by a physician in a controlled setting. When used in the proper setting with appropriate technique, nearly all of these products have proven successful in improving quality and appearance of facial skin.

The goal of chemical peeling is to remove a predictable uniform thickness of damaged skin. Normal wound healing and skin rejuvenation follow while complications such as scarring and pigmentary changes are minimized.

Before embarking on chemical peeling, one must have a thorough knowledge of skin anatomy and normal wound healing. Skin covers the entire external surface of the human body and is the principle site of interaction with the surrounding world. The skin serves as a protective barrier, preventing exposure of internal tissues to trauma, ultraviolet radiation, temperature extremes, toxins, and bacteria. Other important functions include sensory perception, immunologic surveillance, thermoregulation, and control of insensible fluid loss.

The skin is composed of 2 mutually dependent layers, the epidermis and dermis, which rest on a fatty subcutaneous soft tissue. The epidermis contains no blood vessels and is dependent entirely on the underlying dermis for nutrient delivery and waste disposal. This occurs by diffusion through the so-called dermoepidermal junction. The primary function of the dermis is to sustain and support the epidermis.

Epidermal appendages are intradermal epithelial structures lined with epithelial cells that have the potential for division and differentiation. These structures are named from the fact that they develop as down-growths or diverticula of the epidermis into the dermis. These appendages serve an important role as a source of epithelial cells, which are responsible for re-epithelialization when the overlying epidermis is removed or destroyed. Chemical peeling is just one example of how the epidermis may be removed or destroyed. Others include include partial thickness burns, dermabrasion, traumatic abrasions, or split thickness skin graft harvesting.

Epidermal appendages include sebaceous glands, sweat glands, apocrine glands, mammary glands, and hair follicles. Sebaceous glands are highest in concentration on the face and scalp, where as many as 900 glands/cm² may be found. Epithelial appendages are located deep within the dermis. In the face, these appendages may also be located in the subcutaneous fat beneath the dermis. The deep location of these structures and their density in the face account for the remarkable ability of this area to re-epithelialize the deepest cutaneous wounds.

Atrophy of the skin is a well-known process that occurs with aging. This process typically begins during the fourth decade of life. The outermost portion of the epidermis, the stratum corneum, becomes disorganized and less effective as a protective barrier to the external environment. A gradual decline in the number of melanocytes populating the basal layer of the epidermis also occurs. The dermoepidermal junction becomes flattened because of a decrease in the number of dermoepidermal papillae. More significant changes can be seen within the dermis, where an overall loss of organization occurs as this layer begins to thin with age. The amount of ground substance decreases, and elastic fibers degenerate, making the skin less resistant to deformational forces. Collagen is also lost, and the relative proportion of Type I to Type III collagen is reduced.

Beyond the aging process, actinic damage, or photodamage, can produce further unwanted change in the skin. This commonly results in thickening of the skin. Actinic keratoses and lentigines are 2 examples of this process. Dermal elastosis results from the accumulation of thickened degraded collagen and elastic fibers. Ground substance is also increased, whereas mature forms of collagen are decreased. Facial rhytides are probably the multifactorial result of combined aging, photodamage, gravity, and repeated use of muscles of facial expression.

Chemical peeling is the process of applying chemicals to the skin to destroy the outer damaged layers. The epidermis regenerates from the epidermal appendages located in the remaining dermis. This process begins within 24 hours of wounding and is usually complete in 5-10 days. The new epidermis shows greater organization and vertical polarity, with the disappearance of actinic keratoses and lentigines. Dermal regeneration is a slower process but is usually complete within several months. The regenerated dermis demonstrates less elastosis and improved organization, with compact horizontally arranged bundles of collagen interspersed with elastic fibers. Ground substance is decreased and telangiectasias are absent. The overall result is soft supple skin that appears more youthful with fewer rhytides and dyschromias.

Different agents and formulations are chosen based on their depth of penetration and risk profile. Destruction confined to the epidermis results in rapid healing without scarring, although some pigmentation change may be present if melanocytes are damaged. This superficial wounding has the disadvantage of producing less dramatic results but is very safe. Deeper wounding, extending into the papillary and, sometimes, reticular dermis, produces more dramatic results. However, deeper penetration eradicates a portion of the epidermal appendages, making healing slower and scarring more likely. Penetration into the reticular dermis entails a very high risk of scarring. The more common categories of chemical peeling agents will be considered separately along with recommended preoperative and postoperative care.

Adequate evaluation and photographic documentation of the patient prior to peeling is absolutely essential. This includes consideration of the severity of actinic damage, depth and number of rhytides, and need for additional or alternative procedures. The patient with deep rhytides and excessive facial skin laxity is likely to respond better to traditional rhytidectomy. The patient with moderate-to-severe photodamage and medium-to-fine rhytides may be a more optimal candidate for chemical peeling. Some patients may benefit from both procedures because rhytidectomy addresses skin quantity, whereas peeling addresses skin quality. However, these procedures cannot be recommended as concurrent interventions. In general, for safety purposes, a minimum of 3 months is recommended between the procedures to allow for adequate wound healing.

A cornerstone of the evaluation of the patient for chemical peeling is Fitzpatrick's scale of sun-reactive skin types. This scale denotes patients' reactions to ultraviolet radiation and existing degree of pigmentation. Type I patients always burn and never tan. Type II patients tan only with difficulty and usually burn. Type III patients tan but sometimes burn. Type IV patients rarely burn and tan with ease. Type V patients tan very easily and very rarely burn. Type VI patients tan very easily and never burn. Patients with lighter skin types can expect to undergo peeling with minimal concern for abnormal pigment changes, whereas individuals with darker skin are at higher risk for unwanted hyperpigmentation or hypopigmentation.

A thorough medical history and review of systems should be completed in concert with the physical examination. Preexisting cardiac, hepatic, and renal disease may influence the treatment decision and choice of peeling agents.

The use of exogenous estrogens, oral contraceptives, and other photosensitizing medications are known to predispose to unpredictable pigment changes. Therefore, such agents should be avoided several weeks before and after a peel.

If the patient has a history of herpes simplex infection, the physician should provide antiviral prophylaxis several days before and after the peel. This will help minimize chances of unwanted viral reactivation as the re-epithelialization process occurs. Some authors, in fact, advocate prophylaxis in all patients. Toward this end, it is also advisable to allow any existing lesion to heal completely before proceeding with a chemical peel.

Patients must also be aware that cooperation and compliance with the postpeel regimen is required to ensure normal wound healing and to avoid complications. Patients likely to be noncompliant or unable to avoid sun exposure because of occupation are unsuitable candidates. In general, men are considered less optimal candidates because of thicker, oilier skin that risks uneven penetration of the peeling agent. Men are also less likely to be willing to use camouflage makeup in the event of pigmentary disturbances. Patients with a decreased number of epithelial appendages from prior radiation treatment or current isotretinoin (Accutane) use are also poor candidates because healing will proceed more slowly and scarring is more likely. Consider recent use of Accutane an absolute contraindication to medium and deep peels. One should wait at least 12 months after stopping Accutane to allow sufficient regeneration of epithelial appendages prior to peeling.

Although the technique of chemical peeling is relatively simple, the real challenge lies in proper patient and peeling agent selection. In general, the more severe the actinic damage or advanced the aging changes, the more aggressive the treatment should be. Once the patient is appropriately selected to undergo a chemical peel, informed consent, including a thorough discussion of possible complications, is obtained.

Preconditioning the skin is a useful adjunct to improving overall results. Trans-retinoic acid (Retin-A, Renova), an exfoliative agent, is believed to facilitate uniform penetration of the peeling agent and promote more rapid re-epithelialization. This may be applied nightly or every other night for several weeks prior to peeling, depending on the degree of skin irritation caused and patient tolerance. This promotes a thinning of the stratum corneum with shedding of keratinocytes while fibroblasts are stimulated.

Prior to the peel, the patient should thoroughly cleanse the face with non-residue soap on the evening before and morning of the procedure. The patient is instructed not to apply makeup or moisturizers in the interim. The skin is cleansed immediately prior to the procedure to remove any remaining traces of makeup or oils. Either acetone or isopropyl alcohol may be used for this purpose. This step is absolutely essential to prevent uneven penetration of the peeling agent.

Superficial chemical peels are typically accomplished with use of alpha hydroxy acids (AHA). This group of chemicals is largely comprised of naturally occurring fruit acids, including glycolic, lactic, citric, tartaric, and malic acid. Arguably the most popular physician grade AHA used is glycolic acid, which is derived from sugar cane. Most formulations include concentrations of 50% glycolic acid or higher. After application subsequent exfoliation occurs over several days. Over-the-counter AHA products contain 3-10% glycolic acid or one of the many other milder fruit acids. These formulations cause gradual exfoliation over several weeks and actually may be used as a pre-peel primer to potentiate the effects of a higher concentration peel. Unlike other peeling agents, penetration of glycolic acid is time dependent; thus, the agent is applied for a specific amount of time and then neutralized.

The systematic application of glycolic acid with a sponge typically proceeds from one facial region to another, dividing the face into 6-8 regions and treating each in succession. The length of time that glycolic acid is left on the skin relates to concentration, with increasing concentrations achieving the desired results in less time. Removal of the agent is achieved by washing the face with water or neutralizing it with an alkaline solution such as sodium bicarbonate.

Following application, an initial erythema may become frankly red, often accompanied by edema. White patches subsequently develop, indicating epidermolysis with separation of the epidermis from the underlying dermis. Development of a frost indicates deeper depth of destruction into the dermis and is not desirable, as this is meant to be a relatively superficial peeling agent. Exfoliation typically occurs over several days, and re-epithelialization is complete within 7-10 days. Multiple treatments may be required to achieve the desired results and should be spaced several weeks apart. Glycolic acid peels produce the least profound results but also are associated with the lowest frequency of complications.

Another agent used for superficial peeling is Jessner’s solution.^[1] This solution is comprised of 14 g of resorcinol, 14 g of salicylic acid, and 14 mL of 85% lactic acid mixed in enough 95% ethanol to bring the quantity to 100 mL. Jessner’s solution is usually applied with either cotton-tip applicators or sponge gauze. The Jessner’s solution is applied evenly with one or more coats to achieve a light but uniform frost. In some cases, 2-4 coats are necessary to achieve the desired level of resurfacing. The frosting achieved with Jessner’s solution typically results in the subjective feeling of heat with a mild discomfort that is easily controlled with a fan. After several minutes, a mild erythema appears with only faint evidence of scattered frosting over the skin surface.

Medium depth peels are usually performed with trichloroacetic acid (TCA) in concentrations ranging from 20-35%.^[2] Depth of penetration is increased as concentration increases, with formulations of 50% having a well-documented ability to penetrate into the reticular dermis. Such concentrations are not recommended because of the extremely high risk of scarring associated with this depth of penetration. Currently, 35% TCA is considered the high end of a medium-depth peel formulation. Trichloroacetic acid works as a keratocoagulant that produces a frost or whitening of the skin, which is dependent on the concentration used. Vigorous rubbing of the agent, as compared with blotting, yields a deeper penetration. This technique is not time dependent, and the agent does not require neutralization.

Combinations use of TCA and other peeling agents has been demonstrated to provide more effective skin resurfacing in some cases. For instance, application of Jessner’s solution immediately prior to use of 35% TCA has been shown to disrupt the epidermal skin barrier and promote deeper, more uniform penetration of the TCA. Similarly, Coleman has reported improved results with application of 70% glycolic acid prior to a 35% TCA peel.

The systematic application of TCA with a sponge also involves treating the face in a succession of 6-8 regions. TCA application is associated with an intense burning that usually resolves within 30 minutes. Administer appropriate analgesia prior to the procedure and consider regional nerve blockade with lidocaine. Patient comfort may also be improved by having a fan to cool the face and by applying sponges soaked in iced saline prior to moving from one facial region to another.

During the procedure, if the frosting is not uniform or complete, reapplication may be performed until frosting of a desired plateau is reached. Once completed, exfoliation proceeds for several days, and re-epithelialization is complete within 10-14 days.

The standard-depth depth chemical resurfacing procedure is a phenol peel. Phenol peels may be performed with various formulations, such as pure phenol (which is really 88%) or phenol mixed with soap, water, croton oil, and sometimes olive oil. These formulas have such names as Baker-Gordon, Venner-Kellson, Maschek-Truppman, and Grade. The classic Baker-Gordon formula is composed of 3 mL of United States Pharmacopeia (USP) phenol, 2 mL of tap water, 8 gtt of liquid soap, and 3 gtt of croton oil.

Phenol causes keratolysis and keratocoagulation. In contrast to other agents, increasing the concentration of phenol actually decreases the penetration up to a point. This is because the ensuing destruction forms a barrier to further penetration of the chemical. Pure phenol does not penetrate as deeply as the various formulations. Occlusion with a waterproof mask is reported to deepen the level of the peel, which increases the time required to fully re-epithelialize and increases posttreatment erythema. Following the peel, many physicians now apply a thick layer of petroleum jelly or other equivalent agent. Predictable but less profound results are produced, and penetration is less. Similar to trichloroacetic acid (TCA), the time spent applying the agent and the amount of sponge strokes used will be proportional to the depth of penetration. The addition of croton oil to the various formulations as a skin irritant also allows deeper penetration.

Although phenol produces the most remarkable resolution of actinic damage and wrinkling among the various chemotherapeutic agents, it also possesses some of the more significant morbidities. Many have abandoned phenol in favor of other agents or laser resurfacing. Marked hypopigmentation may result following the use of phenol and is correlated with the depth of penetration, use of the Baker-Gordon formula, and addition of croton oil. Hypopigmentation may occur in all skin types, noticeably lightening the skin of patients with darker skin and making lighter-skinned patients appear waxy or pale. A clear line of demarcation may be present between treated and untreated skin.

Phenol causes an intense burning upon application that may last 4-6 hours, which is much longer than the discomfort associated with other peeling agents. Administer appropriate analgesia prior to the procedure and consider regional nerve blockade with lidocaine. Patients also must be provided with sufficient oral analgesics and anxiolytics for use at home following the peel.

The toxicity of phenol may be significant. Phenol is absorbed through the skin, metabolized by the liver, and subsequently excreted by the kidneys. Some practitioners preload the patient with fluids to facilitate renal clearance. Overdoses may injure the liver and kidney and may lead to myocardial irritability, including arrhythmias. For this reason, monitor patients with telemetry during the procedure and in the immediate recovery period. The face is again divided into 6-8 regions, but 20 minutes must be allowed to elapse between treating subsequent regions. This allows for some degree of ongoing metabolism and helps avoid a toxic systemic dose.

Postoperative care is aimed at providing an ideal environment for moist wound healing. Initially, a generous amount of bland ointment (eg, white petrolatum, A&D ointment) is applied to the entire treated area. Crisco vegetable shortening historically had been used quite successfully but has been reformulated and now actually may be irritating to patients. Patients are instructed to reapply the ointment throughout the day, any time the face feels tight or dry. As the outer layers begin to shed, the patient is allowed to shower and gently wash the face with nonresidue soap using fingertips only. After showering, the face should be patted dry and a new coating of ointment applied. Instruct patients to not pick at the face during the recovery period.

Following chemical peeling, some practitioners use topical agents that contain platelet products or growth factors. While these products have been reported to improve wound healing in other clinical situations, no randomized controlled clinical trials presently support their use in this setting. This is an area in which further research is ongoing.

Understanding the process of re-epithelialization and the importance of compliance with the prescribed posttreatment regimen is essential information for every patient. This includes awareness of likely facial edema that may contribute to symptoms such as diplopia. If antiviral therapy is instituted, continue therapy until re-epithelialization is complete. In the early stages of wound healing, re-examine the patient within 48 hours and again every several days. Instruct patients to refrain from trans-retinoic acid, sunscreen, or makeup until the face is healed to the satisfaction of the treating physician.^[3]

Chemical peeling may result in a profound improvement in the quality of facial skin, but this treatment also has potential complications. Results and complications are generally related to the depth of wounding, with deeper peels providing more marked results and a higher incidence of complications. Complications are also more likely with darker skin types and certain peeling agents.^[4]

Erythema generally subsides within 90 days but may become prolonged and even manifest as hyperpigmentation. Patients at increased risk are those taking oral contraceptive pills, exogenous estrogens, or other photosensitizing medications. The application of topical hydrocortisone lotion and/or a short course of systemic steroids may lead to earlier resolution. Other treatment options for hyperpigmentation include trans-retinoic acid, glycolic acid, or hydroquinone.

Accompanying pruritus may be treated with oral antihistamines.

Following chemical peeling, the skin is typically sensitive to the sun, which also may be a source of hyperpigmentation. Instruct patients to use sunscreen daily for 6-12 months following a chemical peel. Patients should also be educated in the appropriate application of camouflaging makeup.

Hypopigmentation is the result of melanocyte destruction or inhibition. Melanocytes originate from neural crest cells and do not possess the ability to regenerate or divide. Hypopigmentation is encountered most frequently when phenol is used as the peeling agent, which has led many to abandon phenol in favor of other agents. Hypopigmentation is more noticeable on darkly pigmented patients. Hypopigmentation may be difficult to assess until erythema has subsided, at which point the condition unfortunately becomes permanent. The line of demarcation between treated and untreated skin is usually the most noticeable. Prior to the peel, with the patient in the sitting position, note the position of the skin draping over the mandibular border. The peel may be feathered at this line of natural shadowing to create a transition zone. This may be performed by using a less concentrated formulation or by applying less of the agent in these regions. Camouflage makeup may help conceal this and other pigmentary disturbances.

Delayed healing may lead to hypertrophic scarring, a devastating complication that requires close follow-up and aggressive early treatment. Topical or intralesional steroids, silicone sheeting, pressure application, and scar massage may improve outcomes. Scar excision or dermabrasion may be necessary in some cases of unsatisfactory results.

Infectious complications are unusual but also demand vigilance and aggressive therapy with oral and topical antibiotics. Pseudomonas infections are treated by washing the face with equal parts water and distilled vinegar. Herpes exacerbations are treated with oral and topical acyclovir until resolution. Most of these lesions respond rapidly and completely to this treatment and rarely cause scarring.