Disclosure
The desire to reverse the aging process has generated tremendous interest throughout history. Ancient texts describe the application of certain substances to the skin in an attempt to rejuvenate the appearance. The modern era of chemical peeling was introduced at the turn of the century beginning with MacKee, a dermatologist who began using phenol to treat facial scars. Over the ensuing decades, peeling became popularized by lay operators rather than by physicians, and formulas were 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 delineated the indications and limitations of these procedures and improved safety and efficacy. Several products are currently available for rejuvenating the skin, including over-the-counter superficial peeling agents and deeper peeling agents that should be applied only by a physician in a controlled setting. These products have proven very successful in improving the quality and appearance of facial skin. The goal of chemical peeling is to remove a controlled uniform thickness of damaged skin. Normal wound healing and skin rejuvenation follow, and complications of scarring and pigmentary changes are avoided.
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, extremes of temperature, 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 layer. The epidermis contains no blood vessels and is dependent entirely on the underlying dermis for nutrient delivery and waste disposal by diffusion through the 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 downgrowths 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. Situations that may remove or destroy the epidermis include partial thickness burns, chemical peeling, 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 the face to re-epithelialize the deepest cutaneous wounds. The skin undergoes atrophy 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 fewer dermoepidermal papillae. The most significant changes occur in the dermis, where an overall loss of organization occurs as the dermis thins 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. Actinic damage produces changes in the skin, resulting in thickened skin. Actinic keratoses and lentigines are formed. 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 rhytids are probably the result of a combination of aging, photodamage, gravity, and the repeated use of the 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 7-10 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 rhytids and dyschromias. Different agents and formulations are chosen for their penetration and potential complications. 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 commonly used agents will be considered separately, as well as the preoperative and postoperative regimens.
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 rhytids, and need for additional or alternative procedures. The patient with deep rhytids and excessive facial skin is likely to respond best to traditional rhytidectomy. The patient with severe photodamage and medium-to-fine rhytids may be an 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 for simultaneous application. In general, for safety purposes, a minimum of 3 months is recommended between the 2 procedures to allow for complete wound healing. A cornerstone of the evaluation of the patient for chemical peeling is Fitzpatrick's scale of sun-reactive skin types, which 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 pigmentation alteration, whereas individuals with darker skin are at a higher risk for hyperpigmentation or hypopigmentation. Other considerations highlight the importance of obtaining a thorough medical history and review of systems in addition to the physical examination. Preexisting cardiac, hepatic, and renal disease may influence treatment decisions and the choice of peeling agents. The use of exogenous estrogens, oral contraceptives, or other photosensitizing medications may predispose patients to pigmentary changes following chemical peeling. If the patient has a history of herpes simplex infections, the physician, in order to prevent an outbreak, needs to provide prophylaxis in the immediate pre-peel period until re-epithelialization is complete. Some authors, in fact, advocate prophylaxis in all patients. 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. Men are 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 a contraindication to medium or deep peels. Wait at least 12 months after stopping Accutane to allow some regeneration of epithelial appendages prior to peeling. While the technique of chemical peeling is relatively simple, the real challenge lies in appropriate patient and peeling agent selection. In general, the more severe the actinic damage, 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 in order to improve results. Transretinoic 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, and fibroblasts are activated. Prior to the peel, the patient thoroughly cleanses the face with nonresidue soap on the evening before and morning of the procedure. The patient is instructed not to apply makeup or moisturizers. The skin is cleansed immediately prior to the procedure to remove any remaining traces of makeup or oils. Ether, acetone, or isopropyl alcohol may be used for this purpose. This step is absolutely essential to prevent uneven penetration of the peeling agent. |
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The typical alpha hydroxy acid (AHA) peel involves the use of glycolic acid, which is derived from sugar cane, at concentrations of 50% or higher. Subsequent exfoliation occurs over several days. Over-the-counter AHA products containing 3-10% glycolic acid or other naturally occurring organic acids (lactic acid, citric acid, tartaric acid, malic acid) cause exfoliation over several weeks and actually may be used as a pre-peel primer to potentiate the effects of application of a higher concentration. 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 isachieved by washing off the agent 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 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.
Trichloroacetic acid (TCA) is typically used as an intermediate-to-deep peeling agent in concentrations ranging from 20-50%. Depth of penetration is increased as concentration increases, with 50% TCA penetrating into the reticular dermis. Concentrations higher than 35% are not recommended because of the high risk of scarring. TCA is 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 to blotting, yields a deeper penetration. This technique is not time dependent, and the agent does not require neutralization. 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. The application of topical lidocaine 4% immediately following the peel decreases the burning sensation and increases patient comfort. Once completed, exfoliation proceeds for several days, and re-epithelialization is complete within 10-14 days.
Phenol peels may be performed with various formulations, such as pure phenol (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 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, because the ensuing destruction forms a barrier to further penetration. 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 agent. Predictable but less profound results are produced, and penetration is less. Similar to 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 to the depth of penetration, use of the Baker-Gordon formula, and the 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 ongoing metabolism and avoids 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 and knowing what to expect, including facial edema that may cause diplopia, is essential for the patient. 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 not to reapply transretinoic acid, sunscreen, or makeup until the face is healed to the satisfaction of the treating physician.
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 certain skin types and certain peeling agents. Erythema generally subsides within 90 days but may become prolonged 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 include transretinoic 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. Instruct patients in the appropriate application of camouflage 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 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 outcome. Scar excision or dermabrasion may be necessary in 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.
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