Disclaimer: The information contained within the Grand Rounds Archive is intended for use by doctors and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No guarantees are made with respect to accuracy or timeliness of this material. This material should not be used as a basis for treatment decisions, and is not a substitute for professional consultation and/or peer-reviewed medical literature. Facial Chemical Peels The desire to reverse the aging process has generated tremendous interest throughout history. Today’s public has been inundated with advertising for cosmetic agents, over the counter chemicals, and treatment programs meant to rejuvenate the skin and erase the marks of sun damage and age. Options available to patients include: surgical intervention, chemical peeling, microdermabrasion, and laser resurfacing. Today, we will discuss chemical peeling. A case presentation: CB is a 60-year-old female who presented to the Baylor Facial Plastic Surgery clinic. She had an evidence of facial aging that she wanted reversed. In particular, she was concerned about the changes in the periorbital region. She is a Fitzpatrick skin type II and a glogau class III. She has signs of both intrinsic and extrinsic aging. She has significant pigmentary dyschromia, with patches of irregularly pigmented skin. She has both upper and lower lid dermatochalasis and fine rhytides in the periorbital and perioral areas. She underwent endoscopic brow lift, upper lid blepharoplasty, and lower lid transconjunctival blepharoplasty with skin pinch, a 15% trichloroacetic acid full face peel and a 35% trichloroacetic acid lower lid peel. These procedures had a large impact on her overall look. In focusing on the results of her peels, her skin appeared to be smoother and more even, with less pigmented irregularities. Also, the rhytides around her mouth and more significantly, her eyes appeared to improve. She was satisfied with the results of her procedures and the appearance of her post-peel skin has been stable. The oldest record of cosmetic treatment by physicians is the Ebers Papyrus written about 1560 BC, which outlined methods for removing wrinkles and other procedures for body beautification. The original chemoexfoliant was lactic acid, the active ingredient of sour milk, which was used topically by Cleopatra as part of an ancient skin rejuvenation regimen. In the middle ages, old wine with tartaric acid was used for the same purpose. In 1630, croton oil was brought to Europe. It was prepared from the seeds of Croton tiglium, a tree native to or cultivated in India and the Malay Archipelago. It was used as a purgative. Kate, in Steinbeck’s East of Eden, used it to slowly murder Faye and inherit her house of ill-repute. In the early 20 th century, interest in facial skin resurfacing experienced a revival. In 1903, MacKee, a dermatologist, is reported to have used liquefied phenol in the treatment of acne scars. In 1905, Kromayer pioneered the modern use of surgical planning of facial skin and is reported to have used rasps and rotating wheels in the treatment of acne scars, keratoses, and hyperpigmentation. Kromayer, credited as the father of dermabrasion, termed his technique “scarless surgery.” He noted that healing following dermabrasion, as in other forms of skin resurfacing, occurs from the epithelium of deep adnexal structures. It was his hypothesis that if resurfacing were not carried below the papillary layer of the dermis, healing would occur without the development of hypertrophic scarring. In 1920s-30s, Otolaryngologist Sir Harold Gillies , regarded as the founder of British plastic surgery, is reported to have used pure carbolic acid in a painting and taping technique for correction of “slight laxity of the lid.” In 1935, organic chemist Spies isolated croton resin from croton oil. He found that it caused vesiculation, and a severe burn requiring 2-3 weeks to heal when he tested it on his own skin. During the late 1940s and early 1950s, chemical peeling was popularized by lay peelers with reports of discovering the “fountain of youth.” Urkov in 1946 described his method of superficial exfoliation using a mixture of resorcinol and salicylic acid, which became the prototype for light or superficial peels. Brown et al in 1960 introduced phenol chemical peeling into the plastic surgery literature. During this same period, Ayres, a dermatologist in California, investigated the effects of trichloroacetic acid or TCA on acinically damaged skin as well as the use of dermabrasion in the treatment of epithelial dysplasia. In September of 1961, Litton presented 50 patients on whom chemical peels had been performed using a minute amount of croton oil in a 50% solution of phenol with glycerin and water. He had paid Coopersmith, a lay peeler in Fort Lauderdale, for the formula in 1958 or 1959. In 1962, Baker published a peel formula that essentially remained unchanged—to the exclusion of all others—for the next 35 years. Skin anatomy: The skin covers the entire external surface of the human body and is the principle site of interaction with the surrounding world. Among its functions, the skin serves as a protective barrier, preventing exposure of internal tissues to trauma, ultraviolet radiation, extremes of temperature, toxins, and bacteria. The skin is composed of 2 mutually dependent layers, the epidermis and dermis, which rest on a fatty subcutaneous layer. The epidermis is the outermost part of the skin; it is stratified squamous epithelium. Its thickness ranges from 0.05mm on the eyelids to 1.5mm on the palms and soles. 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 innermost stratum basale consists of a single row of columnar cells called basal cells. Basal cells divide to form keratinocytes, which comprise the stratum spinosum. The cells continue to flatten, forming the stratum granulosum. They finally die as they reach the surface to form the stratum corneum. Skin aging: There are two types of aging that the skin undergoes. First, intrinsic aging, which is largely determined by genetic factors, is the process of atrophy. 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 results in hypopigmentation in older skin. This is superimposed on focal proliferation of some melanocytes, particularly in sun-exposed areas, which produces hyperpigmented macules, solar lentigines, which coexist with hypopigmented areas. The rete ridges of the dermal–epidermal junction flatten, causing increased fragility and propensity to shear. The number of fibroblasts decreases as do their biosynthetic capability. The proliferative capacity further decreases as keratinocytes and fibroblasts become less responsive to growth factors. Sebaceous glands hypertrophy but produce less sebum, causing problems with skin dryness. The most significant changes occur in the dermis, where an overall loss of organization occurs. The amount of ground substance decreases, and elastic fibers degenerate, making the skin less resistant to deformational forces. The rate of collagen synthesis and the relative proportion of Type I to Type III collagen in the dermis decreases, causing dermal atrophy, and suboptimal wound healing, especially after age 60, is reduced. Cutaneous vasculature undergoes thinning and loses its integrity and wall strength causing easy bruising. The second type of skin aging is extrinsic aging, where a number of extrinsic factors act together to further age the skin. The result of long-term damage to skin from environmental stresses is a decrease in the water volume and increase in damaged cutaneous proteins. In particular, the elastic fibers tend to form tangled masses of nonelastic elastin remnants. This leads to increased volume of skin without functional elements. Sun damage, especially from UV-A wavelengths, causes ionization and oxidation of dermal elements and genetic information, resulting in premalignant and malignant skin lesions. Actinic damage produces changes in the skin, resulting in thickened skin and forming actinic keratoses and lentigines. Dermal elastosis results from the accumulation of thickened degraded collagen and elastic fibers. Cigarette smoking generates free radicals that destroy the texture of the skin by destroying the support collagen and elastic fibers. When combined with excessive exposure to UV light, there is elastic fiber degeneration resulting in sallow, pebbly appearance of the skin. Frequency: Chemical peeling is performed extremely frequently. Hundreds of thousands, and perhaps more than 1 million, phenol peels have been performed in the United States during the last 40 years. Patient selection: A cornerstone of the evaluation of the patient for chemical peeling is the Fitzpatrick skin typing system, which classifies degrees of pigmentation and ability to tan. In addition, this system classifies skin in terms of risk factors for complications during chemical peeling. The best candidates are the light skin types 1, 2, and 3, which have less chance for such complications as pigment dyschromia and scarring. Fitzpatrick skin types 5 and 6 are usually not ideal candidates for medium and deep peels and are at greater risk for pigmentary dyschromia—hyper or hypopigmentation after a chemical peel, and may need pre- and post-treatment with both sunscreen and bleaching to prevent those complications. Individuals with these skin types can be peeled using such superficial agents. The Glogau photoaging classification is a visual grading system used to quantify photodamage. Patients with photoaging type I are not good candidates for deep peeling because the peel may be more damaging than beneficial, while a superficial peel plus medical treatment would be more efficacious. Patients with type IV may benefit from deep peeling or resurfacing plus cosmetic surgical intervention for gravitation changes. Patients with skin types II and III ordinarily benefit from superficial or medium-depth peels depending on the exact circumstances concerning the patient Indications. There are many indications for chemical peeling. Upper epidermal defects, such as melasma, can be treated with superficial peels; while medium-depth defects, such as mild dermatoheliosis, require a medium-depth peel. Deep perioral rhytides may require a deep peel. Contraindications: Contraindications to chemical peeling include documented hypersensitivity to the peeling agent, any of the peel components, or any sedatives used. The procedure also is contraindicated in the presence of facial cancers There are also a number of relative contraindication: 2. Prior cosmetic surgery: Waiting several months following surgery involving the face is recommended. 3. General health: With respect to phenol peels, the patient should be in good general health since phenols can cause arrhythmias. Good kidney and liver function are necessary for adequate excretion and detoxification. ECG monitoring is necessary during the peeling process. 4. Mental health: Patients who are mentally unstable may be overly self-conscious and may not be prepared for their aesthetic appearance immediately following the peel. Patients likely to be noncompliant or unable to avoid sun exposure because of occupation are unsuitable candidates. 5. Medications: The use of exogenous estrogens, oral contraceptives, or other photosensitizing medications may predispose patients to pigmentary changes following chemical peeling. Patients taking blood thinners, such as coumadin, should avoid deep peels because of the possibility of blood oozing from the peel site. Patients taking aspirin usually do not have complications; but if the medication is not necessary, advising them to stop taking it 1 week prior to a deep peel is advised. 6. Herpes: Chemical peels are contraindicated in patients with active herpes infections. If the patient has a history of herpes simplex infections prophylaxis must be given in the immediate pre-peel period until re-epithelialization is complete. Some authors, in fact, advocate prophylaxis in all patients. 7. History of hypertrophic scarring: Patients need to be asked if they have a history of hypertrophic scarring. Patients with a history of hypertrophic scarring are not candidates for major skin resurfacing, such as laser or medium/deep peels. 8. Follicle unit density: Previous use of isotretinoin must be noted. Patients should wait 6-12 months after the last dose of isotretinoin to allow some regeneration of epithelial appendages prior to peeling and to reduce the risk of scarring. Patients with prior radiation treatment are also poor candidates for peels due to a decreased number of epithelial appendages and, as a result, slower healing and more likely scarring. Pre-procedure Care: Pretreatment of the skin has been very controversial over the past decade. Tretinoin is believed to facilitate uniform penetration of the peeling agent and promote more rapid re-epithelialization. This may be applied for several weeks prior to peeling. Some studies have shown that pretreatment with tretinoin promotes thinning of the stratum corneum with activation of keratinocytes, and fibroblasts and, as a result, decreasing time to re-epitheliazation and possibly decreasing the risk of hyperpigmentation. Hevia et al conducted a double-blind, placebo-controlled, prospective, randomized study to assess the effects of tretinoin pretreatment on healing after trichloroacetic acid (TCA) chemical peel. Sixteen male patients with actinically damaged skin were treated daily with 0.1% tretinoin and placebo creams to the left and right halves of the face and the left and right forearms and hands, respectively, for 14 days prior to the 35% TCA peel. In all regions, the mean area healed was significantly greater in skin that had been pretreated with tretinoin. After 7 days, 75% of the tretinoin-pretreated hemifaces were completely healed, as opposed to 31% of the placebo-pretreated hemifaces. By visual inspection, there was no appreciable cosmetic difference between tretinoin- and placebo-pretreated skin 2 weeks and 3 months after the TCA peel. Factors affecting peel depth: There are a number of factors that affect peel depth. They include: 1. Patient history: The amount of sun-induced damage, history of hypertrophic scarring or keloid formation, and a general medical history will affect the peel depth chosen. 2. Peeling agent concentration: The concentration and the volume of that particular concentration delivered will both affect peel depth. 3. Free acid availability: The pKa of the solution is the pH at which half is in acid form; therefore, a lower pKa means that more free acid is available. Many products advertise the acid percentage; however, pKa is a more accurate determinant of strength. 4. Application of peeling agent: The degree, intensity and number of strokes of peeling agent applied to the skin all affect the depth of the peel. The peel frost, or facial whitening indicating depth of epidermal damage, can aid in the determination of this number. 5. Contact time: How long the peeling agent is applied also determines the depth of the peel. After the appropriate time has passed, neutralization is performed. Some chemical peels, such as salicylic acid and trichloroacetic acid, do not require a neutralization step since the skin neutralizes the acid. Glycolic acid peels must be neutralized. 6. Occlusion: Products available, such as biosynthetic occlusive dressings, may decrease pain and speed healing. Examples include hydrogel membranes (consisting of cross-linked polyethylene oxide), polyurethane membranes; and silicone membranes which are nonadherent, permeable to oxygen and water vapor, and impermeable to bacteria and water. Petroleum jelly and other occlusive ointments may also act as occlusive barriers to a minor degree. 7. Rejuvenation regimen: Patients may treat the skin before and after a peel with such agents as tretinoin, hydroquinone, or an alpha hydroxy acid. These may help the skin heal faster and also allow the chemical peel agent to achieve better penetration. Defatting: The skin should be cleaned and excess fat removed with such agents as acetone, rubbing alcohol, or Septisol, or a combination of these agents. A thorough defatting of the skin is necessary for proper penetration of the peeling agent since most agents are not lipid soluble. Application: The peeling agent can be applied with 4 X 4 gauze, cotton swabs, or the foam applicator that comes with the peel kit. Popsicle sticks are good applicators for the paste form. Reapplication of the peeling agent may be necessary if the frost is uneven or is not white enough. Frost : The change in coloration of the skin to a whitish tint is called frost. This represents the end stage of the chemical peel and shows that keratin agglutination has occurred. Depending on the agent used, the white tint may vary from a brighter white in a superficial peel to a grayish white in a deep peel. Neutralization: Neutralization of the chemical peeling agent is an important step once the clinician has achieved the proper depth of the peel, which is determined either by the frost or how much time has elapsed. Neutralization can be achieved by cold water or wet, cool towels applied to the face following the frost. Peels for which this neutralization step is less important include salicylic acid, Jessner's, and phenol. Stages of Wound Healing after Chemexfoliation Inflammation and Coagulation: First, vascular permeability is temporarily increased to allow neutrophils, platelets and plasma proteins to infiltrate the wound. Vasoconstriction follows, in response to factors released by these cells. Coagulation then occurs as platelets aggregate with fibrin, which is deposited in the wound following its conversion from fibrinogen. Platelets release several factors, including platelet-derived growth factor (PDGF) and transforming growth factor ß, which attract PMNs to the wound, signaling the beginning of inflammation. After 48 hours, macrophages replace PMNs as the principal inflammatory cell. Together, PMNs and macrophages remove debris from the wound, release growth factors, and begin to reorganize the extracellular matrix. Inflammation produces a brawny, dusky erythema that progresses for the first 12 hours, while coagulation phase separates the epidermis, producing serum exudation, crusting, and pyoderma. Reepithelialization begins 48 hours after the peel and is usually complete by 10-14 days. The epidermis regenerates from the epidermal appendages located in the remaining dermis. The new epidermis shows greater organization and vertical polarity, with the disappearance of actinic keratoses and lentigines. Preventing scab formation is important for faster and more even healing. Biosynthetic occlusive dressings can be used to hasten the healing process. Granulation tissue: Granulation tissue usually appears the second day and consists of fibroblasts, inflammatory cells, fibronectin, glycosaminoglycans, and collagen. Angiogenesis: This process begins with endothelial cell migration to the wound site and is essential for wound healing. The erythema following a chemical peel primarily is caused by the new capillary growth in the area. Collagen remodeling: Collagen remodeling in the dermis is the main reason that chemical peels improve texture and rhytides. This process may continue for 3-4 months. The process of remodeling involves a reorientation of the collagen in a parallel fashion and begins as collagen is formed following the peel. 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. Chemical Peels Superficial peeling agents: Superficial chemical peeling is the exfoliation of the stratum corneum or the entire epidermis to encourage regrowth with less photodamage and more youthful appearance. Very superficial peels, which are limited to the stratum corneum, produce no or minimal frosting, while superficial peels produce mild erythema and scattered areas of frosting, when the peel is limited to the superficial epidermis. It usually takes repetitive peeling sessions to obtain maximal results. Superficial peeling on photoaged skin is subtle and will not produce a prolonged or noticeable effect on dermal lesions such as wrinkles and furrows. Salicylic acid has been used for several decades and is found in various medications. It is lipid soluble and, as a result, is able to penetrate the comedones better than other acids. The anti-inflammatory and anesthetic effects of the salicylate also result in a decrease in the amount of erythema and discomfort that generally is associated with chemical peels. The most common concentration used today is 20-30% Jessner's peel is a combination of salicylic and lactic acids, and resorcinol. It is thought to break intracellular bridges between keratinocytes. Dainichi et al evaluated the effects of chemical peeling with 30% salicylic acid on skin tumor formation in hairless SKH/hr1 mice irradiated with ultraviolet (UV) B for 14 weeks. Not only was the total number of tumors greatly reduced, but skin tumor development was also slower in the treated vs. the control mice. At week 18, the development of skin tumors in mice treated with salicylic acid was suppressed macroscopically. Alpha hydroxy Peel: Alpha hydroxy acids are nontoxic acids formed naturally in foods such as sugar cane (glycolic acid) and fermented apples (pyruvic acid). Today, alpha hydroxy acids used in peels include lactic acid, glycolic acid, citric acid, tartaric acid, and malic acid and are synthesized chemically for use in peels. They are composed of carbon backbones with one or more carboxyl groups and a hydroxyl group on the adjacent carbon to the carboxyl group. Various concentrations can be used, with 50 or 70% concentration used most commonly for facial peels. The exact mechanism of action of AHAs is not known; however, it has been demonstrated that AHAs applied topically in lower concentrations diminish corneocyte cohesion, which reduces stratum corneum thickness by causing dead cells to slough and new cell growth in the basal layer of the epidermis. At higher concentrations, the same acids cause epidermolysis. Glycolic acid has also been shown to increase dermal glycosaminoglycans and increased number and quality of elastic fibers and collagen, especially when used for long periods of time in higher concentration. The typical alpha hydroxy acid (AHA) peel involves the use of glycolic acid at concentrations of 50% or higher. Subsequent exfoliation occurs over several days. Over-the-counter AHA products containing 3% to 10% glycolic acid or other naturally occurring organic acids cause exfoliation over several weeks and may be used as a pre-peel primer to potentiate the effects of application of a higher concentration. These peels are both time and dose related; thus the longer the exposure to the skin and the more concentrated the solution, the deeper the peel. Removal of the agent is achieved by washing off the agent with water or neutralizing it with an alkaline solution such as sodium bicarbonate. In comparison to other treatments, the attractiveness of these peels is enhanced by their low cost and significantly decreased associated “downtime” and consequent effect on the patient’s daily activities. AHA peels can be performed quickly without sedation or anesthesia. There is no photosensitivity and complications are directly related to the depth of the peel. Studies have shown that glycolic acid peels improve mild photoaging of the skin. In a double-blind placebo controlled study conducted by Newman et al, forty-one volunteers had glycolic acid (50%) or placebo applied topically for 5 minutes to one side of the face, forearms, and hands, once weekly for 4 weeks. Significant improvements noted included decrease in rough texture and fine wrinkling, fewer solar keratoses, and a slight lightening of solar lentigines. Histology showed thinning of the stratum corneum, granular layer enhancement, and epidermal thickening. Some specimens showed an increase in collagen thickness in the dermis. TCA Peel: Trichloroacetic acid (TCA) is typically used as an intermediate-to-deep peeling agent in concentrations ranging from 20% to 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. Ten percent to 20% TCA produces a light whitening or frosting effect on the skin with a result of sloughing of the upper one half to one third of the epidermis. TCA is a keratocoagulant, causing protein denaturization with resultant desquamation. This reaction is perceived as frosting of the skin. The greater the concentration of acid, the more rapidly the frosting effect declares itself. There is a time delay or lag period between the time of application and the emergence of frosting, a concept vital to injury prevention. The agent does not require neutralization. The systematic application of TCA with a sponge involves treating the face in a succession of 6-8 regions. 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. El-Domyati et al evaluated the changes induced by serial TCA peeling with concentrations up to 30%. They found significant increase in mean viable epidermal and granular cell layer thickness with associated development of rete ridges with dermoepidermal junctions. There was also an increase in the amount and quality of elastic fibers as well as significant increases in both collagen types I and III. The results of this study suggest that beneficial effects of such modalities on facial skin were accomplished primarily by increasing the amounts of collagen I and collagen III and improving the morphologic appearance of collagen and elastic fibers. Medium-depth peels: Further destruction of the epidermis and induction of inflammation within the papillary dermis constitutes a medium depth peel. Medium depth peels achieve a level II to III frosting. Level II frosting is defined as white-coated frosting with erythema showing through, when the peel involves the entire epidermis. Level III frosting ,which is associated with penetration to the papillary dermis, is a solid white enamel frosting with no background of erythema. Most medium depth peels use a level II frosting, especially for eyelids and areas of sensitive skin. Healing is completed within 1 week to 10 days. The hallmark for this level peel is TCA 50%. It is seldom used today as a single agent because of a higher risk of scarring and the availability and effectiveness of the combination peels. Three combination peels are currently used, as these peels are as effective as TCA 50% with less chance of scarring and pigment dyschromia. Brody developed the use of solid CO2 applied with acetone to the skin as a freezing technique prior to the application of 35% TCA. This appears to break the epidermal barrier for a more even and complete penetration of 35% TCA. Monheit demonstrated the use of Jessner’s solution prior to application of 35% TCA. Jessner’s solution was found to be effective in destroying the epidermal barrier by breaking up individual epidermal cells. This also allowed more even and deeper application of 35% TCA. Similarly, Coleman demonstrated that the use of 70% glycolic acid prior to application of 35% TCA had a similar effect as use of Jessner’s solution prior to TCA application. Tse et al performed a clinical and histologic comparison of Coleman’s combination 70% glycolic acid versus Monheit’s combination of Jessner's solution as part of a medium-depth chemical peel using 35% trichloroacetic acid (TCA). Thirteen patients with actinic keratoses, solar lentigines and fine wrinkling were treated with 70% glycolic acid plus 35% TCA (GA-TCA) to the right face and Jessner's solution plus 35% TCA (JS-TCA) to the left face. Clinically, the GA-TCA peel was as effective in treating photodamaged skin as the JS-TCA peel. They were both found to be efficacious in removing actinic keratoses, causing neoelastogenesis, papillary dermal fibrosis and neovascularization. Deep peels: Deep peels are characterized by an inflammatory response in the deep reticular dermis which induces production of new collagen and ground substance. 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; the different formulations are as listed. Historically, the Baker-Gordon formula, with phenol diluted to 50% to 55%, was thought to penetrate deeper than full strength, undiluted phenol. The rationale for this was that full strength phenol presumably caused an immediate coagulation of epidermal keratin proteins and thus formed a barrier to further penetration. Moreover, the liquid soap Septisol was thought to act as a surfactant that reduces skin tension, allowing for more even penetration of phenol, while Croton oil was considered to be a vehicle for phenol in peel formulas. In 1999, Gregory P. Hetter wrote a four part series challenging the assumptions surrounding phenol-based chemical peeling. He found that increasing concentrations of phenol without croton oil caused skin reaction but no significant peeling effect. Moreover, he found that the depth of the peel was dependent on concentration of croton oil rather than phenol. There are two modalities for deep chemical peeling: Deep peels can be occluded or nonoccluded. The occluded method uses zinc oxide tape or other artificial barrier product to prevent evaporation of the phenol from the skin, thus enabling the solution to penetrate deeper. The tape is placed directly after the peel solution is applied to each individual cosmetic subunit. Tape occlusion increases the penetration of the Baker’s solution and is particularly helpful for deeply lined, “weather-beaten” faces. A taped Baker’s formula peel creates the deepest damage in the midreticular dermis. The unoccluded technique involves more skin cleansing and application of more peel solution. This technique, however. does not produce as deep a peel as the occluded method. Deep peels produce the most remarkable resolution of actinic damage and wrinkling among the various chemotherapeutic agents. However, it also possesses some of the more significant morbidities. Phenol causes an intense burning upon application that may last 6-8 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. Overdoses may injure the liver and kidney and may lead to myocardial irritability, including arrhythmias. Methods to limit these possible toxic effects include: 1) Giving IV hydration prior to and during the procedure. 2) Extending the time for a full face peel to more than 1 hour. Fifteen to 20 minutes must be allowed to elapse between treating subsequent cosmetic subunits. This allows for some ongoing metabolism and avoids a toxic systemic dose. 3. Monitor patients with telemetry during the procedure and in the immediate recovery period. A study by Butler et al used a recognized photo-aged animal model, the Skh:HR-1 hairless mouse, to quantify and qualify the changes that occur in collagen and glycosaminoglycan content after chemical peel. One hundred Skh:HR-1 hairless mice were photo-aged by use of chronic ultraviolet B irradiation for 14 weeks. After irradiation, the animals were randomly distributed into five groups of 20 mice each. Histological examination demonstrated an increase in dermal thickness in the 50% trichloroacetic acid and phenol groups in comparison with controls. All chemical peel groups demonstrated a reorganization of collagen and elastic fibers in the reticular and papillary dermis. The beneficial effects of chemical peels were due to a combination of two findings: a reorganization in dermal structural elements and an increase in dermal volume. Complications: 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. The main complications are: Pigmentary change: Hyperpigmentation following the chemical peel is more common and may be treated with various topical medications such as: topical tretinoin 0.1%, corticosteroids, or depigmenting agents such as hydroxyquinone 2-4%. Hypopigmentation, the result of melanocyte destruction or inhibition, is encountered most frequently with phenol/croton oil peels. 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. The peel may be feathered at the line of natural shadowing along the mandible to create a transition zone; this is important if the patient at a later date has a rhytidectomy. 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. Scarring: By matching the patient and peeling agent properly, the risk of scarring can be decreased. Patients with a history of keloids should not undertake medium or deep peels because of the risk of scarring. Medium and deep peels penetrate to the superficial and reticular dermis and, thus, may stimulate keloids. Weaker superficial peels that only exfoliate the stratum corneum or superficial epidermis can be used. When hypertrophic scarring occurs, aggressive early treatment with 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. Infection: Infectious complications are unusual but also demand vigilance and aggressive therapy with oral and topical antibiotics. The best deterrent for local infection is the continuous use of soaks to debride crusting and necrotic material. Acetic acid based facial washes are recommended to prevent Pseudomonal infections. Streptococcus and staphylococcus infections can occur under biosynthetic membranes or thick occlusive ointments. E coli or Candida infection can also develop, for which a short course of antibiotics should be administered. Herpes exacerbations are treated with oral and topical acyclovir until resolution. Herpes simplex infection is the result of reactivation of HSV on the face. A history of previous HSV infection should necessitate the use of prophylactic oral acyclovir (400 mg PO bid), beginning 2 days prior to the peel and continuing 7-14 days after the peel, as previously discussed. Prolonged erythema: Patients usually do not complain of erythema because it generally subsides in 30 to 90 days, but sometimes erythema continues. The erythema following a superficial peel resolves in 15 to 30 days, a medium depth peel within 60 days, and a deep peel in 90 days. It may be 2/2 contact dermatitis, contact sensitization, re-exacerbation of prior skin disease, or a genetic susceptibility to erythema, but it may also indicate potential scarring. Erythema is the result of angiogenic factors stimulation vasodilation which includes the phase of fibroplasia being stimulated for a prolonged period of time. For this reason, it can be accompanied by skin thickening and scarring. It should be managed promptly with topical and/or systemic steroids, intralesional steroids if thickening is occurring, and skin protection to eliminate the factors of irritancy and allergy. 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. Acne: Some patients develop acne after a chemical peel. This usually occurs between days 3 and 9. Cultures should be taken, and an antibiotic that covers gram-positive bacteria should be prescribed. If it is a true acne occurrence, then the appropriate topical treatment also should be started. If severe enough, isotretinoin may be initiated. Milia: Small inclusion cysts, sometimes called milia, can appear in the healing process after a chemical peel. These usually appear about 2 to 3 weeks after reepithelialization and may be aggravated by ointments due to occlusion of the sebaceous glands. Case Presentation: CB is 60 year-old female who presented to the Baylor Facial Plastic Surgery clinic. She had evidence of facial aging that she wanted reversed. In particular, she was concerned about the changes in the periorbital region. Her past medical history was significant for fibromyalgia. Currently she is taking hydrocortisone. She admits to being an occasional drinker. On physical examination, she is a Fitzpatrick skin type II and a glogau class III. She has significant pigmentary dyschromia, with patches of irregularly pigmented skin. She has both upper and lower lid dermatochalasis and fine rhytides in the periorbital and perioral areas. Treatment: She underwent Endoscopic brow lift, Upper lid blepharoplasty, Lower lid transconjunctival blepharoplasty with skin pinch, 15% TCA full face peel and 35% TCA lower lid peel. These procedures had a large impact on her overall look. In focusing on the results of her peels, her skin appeared to be smoother and more even, with less pigmented irregularities. Also, the rhytides around her mouth and more significantly, her eyes appeared to improve. She was satisfied with the results of her procedures and the appearance of her post-peel skin is stable. Bibliography: Alam M, Omura NE, Dover JS, Arndt KA. 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Ultrastructural study of the skin after facial chemical peels and the effect of moisturization on wound healing. Plast Reconstr Surg 1998;101:1374-1379. Coleman WP III. Dermal peels. Dermatol Clin 2001;19:405-411. Dainichi T, Ueda S, Isoda M, Koga T, Kinukawa N, Nose Y, Ishii K, Amanto S, Horii I, Furue M. Chemical peeling with salicylic acid in polyethylene glycol vehicle suppresses skin tumour development in hairless mice. Br J Dermatol 2003;148:906-912. Fanous N. A new patient classification for laser resurfacing and peels: Predicting responses, risks and results. Aesth Plast Surg 2002;26:99-104. Flynn TC, Coleman WP. Topical revitalization of body skin. JEADV 2000;14:280-284. Fulton JE Jr, Porumb S. Chemical peels: Their place within the range of resurfacing techniques. Am J Clin Dermatol 2004;5:179-187. Fung JF, Sengelmann RD, Kenneally CZ. Chemical injury to the eye from trichloroacetic acid. Dermatol Surg 2002;28:609-610. Giese SY, McKinney P, Roth S, Zukowski M. The effect of chemosurgical peels and dermabrasion on dermal elastic tissue. Plast Reconstr Surg 1997;100:489-498. Gentile RD. Multimodality aesthetic skin rejuvenation. Fac Plast Surg 2005;21:120-129. Ghadishah D, Gorchynski J. Airway compromise after routine alpha-hydroxy facial peel administration. J Emerg Med 2002;22:353-355. Hetter GP. An examination of the phenol-croton oil peel: Part I. Dissecting the formula. Plast Reconstr Surg 2000;105:227-239. Hetter GP. An examination of the phenol-croton oil peel: Part II. The lay peelers and their croton oil formulas. Plast Reconstr Surg 2000;105:240-248. Hetter GP. An examination of the phenol-croton oil peel: Part III. The plastic surgeons’ role. Plast Reconstr Surg 2000;105:752-763. Hetter GP. An examination of the phenol-croton oil peel: Part IV: Face peel results with different concentrations of phenol and croton oil. Plast Reconstr Surg 2000;105:1061-1083. Imayama S, Ueda S, Isoda M. Histologic changes in theskin of hairless mice following peeling with salicylic acid. Arch Dermatol 2000;136:1390-1395. Langsdon PR, Milburn M, Yarber R. Comparison of the laser and phenol chemical peel in facial skin resurfacing. Arch Otolaryngol Head Neck Surg 2000;126:1195-1199. Mandy SH, Monheit GD. Dermabrasion and chemical peels. In: Frodel J, Park SS, Holt GR, Sykes JM, Larrabee WF, Toriumi D, Nachlas N (editors). Facial Plastic and ReconstructiveSurgery, 2 nd edition. New York: Thieme; 2002; pp.223-240. Moetaz B, El-Domyati M, Attia SK, Saleh FY, Ahmad HM, Uitto JJ. Trichloroacetic acid peeling versus dermabrasion: A histometric, immunohistochemical, and ultrastructural comparison. Dermatol Surg 2004;30:179-188. Monheit GD. Chemical peels. Skin Therapy Ltr 2004;9:6-11. Monheit GD. Medium-depth chemical peels. Dermatol Clin 2001;19:413-425. Monheit GD. Consultation for photoaging skin. Dermatol Clin 2001;18:401-403. Most SP, Alsarraf R, Larrabee WF Jr. Outcomes of facial cosmetic procedures. Fac Plast Surg 2002;18:119-124. Nanda S, Grover C, Reddy BSN. Efficacy of hydroquinone (2%) versus tretinoin (0.025%) as adjunct topical agents for chemical peeling in patients of melasma. Dermatol Surg 2004;30:385-389. Sheeris DA, Otley CC, Bartley GB. Comprehensive treatment of the aging face-cutaneous and structural rejuvenation. Mayo Clin Proc 1998;73:139-146. TerKonda RP. Incorporating skin care into a facial plastic surgery practice. Fac Plast Surg 2004;20:3-9. Tung RC, Bergfeld WF, Vidimos AT, Remzi BK. α-Hydroxy acid-based cosmetic procedures. Guidelines for patient management. Am J Clin Dermotol 2000;1:81-88. Wolf R. Early repeeling—a matter of time. Int J Dermatol 1998;37:709-712. Grand Rounds Archive | Department Home page BCM Public | BCM Intranet | Privacy Notices | Contact BCM | BCM Site Map | ©2001-2006 Baylor College of Medicine
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