Chemical peels and dermabrasion

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CHAPTER 79 Chemical peels and dermabrasion

Physical evaluation

Table 79.1 Fitzpatrick skin classification

Type Color Reaction to sun exposure
I White Always burns/never tans
II White Usually burns/tans with difficulty
III White Sometimes mild burn/average tan
IV Moderate brown Rarely burns/tans with ease
V Dark brown Very rarely burns/tans very easily
VI Black Never burns/tans very easily

Data from Fitzpatrick TB. The validity and practicality of sun-reactive skin types I through VI. Arch Dermatol 1988;124:869.

Anatomy

The skin consists of three layers: the epidermis, dermis, and subcutaneous fatty tissue. Appendageal structures, including hair follicles, sebaceous glands, eccrine glands, and apocrine glands pierce these layers and are required for wound healing following partial-thickness injury. The efficiency of healing and re-epithelialization is related to the concentration of adnexal structures, which decreases with increasing depth of injury.

The most superficial portion of the skin is the stratum corneum, which is a non-viable layer of cornified cells serving as a protective barrier. It becomes disorganized and looser with aging and photodamage. The remainder of the epidermis consists of continually rejuvenating cells that migrate from the bottom of the epidermis toward the surface.

The dermis is a thicker layer consisting of the superficial papillary dermis and the deeper reticular dermis. It lies beneath the epidermis and contains a vascular network, hair bulbs and sebaceous, apocrine and eccrine glands. The subcutaneous tissue lies deep to the dermis.

Aging of the skin affects both the epidermis and dermis and is exacerbated by actinic damage. Aging causes epidermal hyperplasia, atrophy and dysplasia, producing an atrophic and flat epidermis. Dermal connective tissue shows progressive diminution with loss of much of the reticular dermis. Collagen fibers become degenerated and thickened. Reduction of the amount of collagen leads to thinning of skin. The dermis of actinically damaged skin exhibits elastosis, the presence of thickened, degraded elastic fibers. Separating the solar elastotic material from the epidermis is a thin zone of normal appearing dermis largely composed of collagen, called the Grenz zone. Additionally, aging causes loss of dermo-epidermal papillae and reduction in the melanocytes. These histological changes are responsible for the clinical signs of aging and sun damage including wrinkling, laxity, and pigment changes. Cutaneous resurfacing is intended to reverse these changes.

Technical steps

Pretreatment helps to minimize or prevent adverse pigmentation changes. Pretreatment consists of a 2–6-week course of 0.05% Retin-A once a day with topical 4% hydroquinone twice a day added for darker skin patients to decrease melanin formation and hyperpigmentation. Alpha-hydroxy acids in combination with Retin-A help to even out skin texture, improving the outcome of resurfacing. Routine skin care, including the use of cleansers, moisturizers and sunscreens, must be emphasized to improve skin quality.

Superficial peeling agents such as Jessner’s solution, Unna’s paste, salicylic acid and the alpha hydroxy acids penetrate to the epidermal–dermal junction. Trichloroacetic acid (35%) is a medium depth peel that penetrates deep to the epidermal–dermal junction. Phenol–croton oil peels and dermabrasion may penetrate into the upper to mid reticular dermis. In general, aesthetic improvement, morbidity and healing time are directly related to the depth of injury.

Trichloroacetic acid (TCA)

See Fig. 79.1.

Trichloroacetic acid (TCA) is a derivative of acetic acid that has been used in the treatment of aging skin since the early 1960s. Trichloroacetic acid is mostly commonly used in 35% concentration for medium depth peeling, penetrating the papillary and into the upper reticular dermis. In concentrations above 40%, TCA can penetrate the reticular dermis, providing deeper and increased morbidity and risk of scarring. TCA is not absorbed systemically. TCA is versatile and can be used in a wide range of skin types. TCA is useful for treatment of pigmentation disorders, dysplasias, photoaged skin and wrinkles. TCA produces limited neocollagen formation and some improvement in facial wrinkling but it is limited in treating deep facial wrinkles, especially in the perioral area.

Pretreatment for TCA peels improves the penetration of the acid and provides more consistent results. Prior to TCA peeling, the skin is degreased with acetone and/or alcohol to remove surface oils from the skin, which can decrease absorption and result in an uneven peel. Sedation is usually not necessary with 35% TCA. The solution is applied regionally to each facial unit with brush-like strokes. Adequate penetration of the solution usually occurs between one to two minutes. Trichloroacetic acid is a keratocoagulant and frosting is the key to judging the depth of the peel. Initial frosting is pink or white in color and progresses to more uniform white as penetration proceeds to the papillary dermis. A gray appearance can signal penetration to the reticular dermis and may cause abnormal healing. Once the desired degree of frosting occurs, the acid is washed with water. The water serves to dissipate some of the generated heat, but since trichloroacetic acid is an aqueous solution, it cannot be neutralized but only diluted. If after inspection the frost is not as deep as anticipated, it is appropriate to retouch those areas. During the entire peeling process, a fan can be used to aid in patient comfort.

Chemical peeling is a technique-dependent procedure. Depth of treatment correlates with the concentration of TCA, but variables such as skin type and thickness, concentration of sebaceous glands, pretreatment, skin degreasing, amount of acid applied and the rigor of application must be taken into account. Patients with thicker skin will tolerate higher concentrations of TCA or multiple reapplications of acid, but care must be taken in patients with dry and atrophic skin as penetration is increased. TCA has broad applications but the learning curve can be prolonged.

Phenol

See Fig. 79.2.

Phenol, also known as carbolic acid, is protein precipitant, causing extremely rapid denaturation and coagulation of surface keratin. It provides a relatively deep and predictable injury to the dermis, penetrating to the level of the upper reticular dermis. It has become a standard to which other resurfacing methods are compared. It treats both coarse and fine wrinkles and irregular pigmentation.

Phenol is detoxified in the liver and excreted by the kidney. Toxic doses of phenol can injure both the liver and the kidney and may depress respiration and the myocardium. Atrial and other arrhythmias can be seen after rapid phenol absorption.

Chemical peeling with phenol–croton oil is used to improve significant actinic damage and moderate wrinkling of the skin.

The Baker–Gordon formula is the standard phenol formula. It consists of 3 mL USP liquid phenol, 2 mL tap water, eight drops of liquid soap and three drops of croton oil (Table 79.2). Soap lowers the surface tension of the mixture and croton oil has been thought to act as a vesicant, increasing local inflammation and penetration of phenol. Water prepares a solution of 50% phenol concentration. It has been shown through histologic studies that the Baker–Gordon formula penetrates deeper than pure phenol (Stegman, 1980).

Table 79.2 Baker–Gordon formula

3 mL USP liquid phenol
2 mL tap water
8 drops liquid soap
3 drops croton oil

Data from Baker, TJ, Stuzin, JM, Baker TM. Facial skin resurfacing. St. Louis: Quality Medical Publishing, 1998.

Cardiac monitoring, pulse oximetry and accessible resuscitation equipment is recommended if the entire face is peeled. The skin is cleansed in a fashion similar to that discussed for TCA peels. The phenol solution is applied with a contact tip applicator with care being taken to avoid dripping. Missed spots must be avoided. After phenol application, the skin frosts a grayish white color and a burning sensation is experienced. Small subunits are peeled at 15- to 20-minute intervals with a full-face peel being completed in about 1 to 2 hours. An occlusive dressing applied to the treated area prevents evaporation and increases phenol penetration and depth of the peel. Either tape or a petroleum-based ointment dressing can provide occlusion, although the former may be more painful and morbid for the patient.

The depth of treatment with phenol does not correlate with its concentration. A lower concentration does not necessarily produce a lighter peel and higher concentrations may produce less of a peel because of keratin coagulation in the epidermis.

Hetter (2000) varied the concentration of croton oil and demonstrated that it was the concentration of croton oil and not the concentration of phenol that was the factor that controlled depth of penetration. He asserted that phenol is simply the carrier. Minute variations in the concentration of croton oil are critical to the outcome of the peel. The different proportions according to depth of peel desired and anatomic site are summarized in what Hetter calls “the heresy phenol formulas”. As a result of this work, phenol peels are probably more properly referred to as “phenol–croton oil” peels.

Dermabrasion

See Fig. 79.3.

Dermabrasion, which was developed in the 1950s, mechanically abrades the epidermis and upper portion of the dermis. It is technique dependent and the depth can be precisely controlled. The epidermis is entirely obliterated and there is partial removal of the dermis, which undergoes incomplete regeneration. Both coarse and fine wrinkling can be treated with dermabrasion. Wrinkles can be lowered and smoothed mechanically. For resurfacing, dermabrasion is most useful for perioral lines and particularly those of the upper lip. Baker (1998) describes the current technique of dermabrasion and reviews the various adjuncts, instruments, indications, contraindications, and complications of the procedure.

Dermabrasion patients may receive premedication and/or regional nerve blocks may be used. The hand-held dermabrader is motor-driven and operates at 12,000–15,000 rpm. There is a wide variety of diamond-tipped burrs, differing in shape, size and coarseness. Protection against aerosolized particular matter must be taken. Wrinkles are marked before infiltration of anesthesia and regions are treated according to anatomic subunits. The handpiece should be kept moving, with light pressure applied. The edges of treated areas are feathered to blend with those not treated. Providing treatment to the proper depth is important. After the epidermis is removed, the pink epidermal–dermal junction is encountered. As treatment continues, fine punctate bleeding indicates the level of the papillary dermis. At the papillary–reticular junction, bleeding is increased and the surface becomes rougher, indicating the endpoint of treatment for most patients. Following treatment, the entire face is covered with gauze soaked in lidocaine with epinephrine to provide both anesthesia and hemostasis. Once bleeding has stopped, ointment is applied and the treated area either covered with petroleum or xeroform gauze, or is left uncovered. There appears to be neocollagen formation following dermabrasion.

Postoperative care

Following TCA peel, the skin will feel tight and will darken. Starting after 24 hours, the patient should cleanse the treated areas several times a day with water and/or dilute hydrogen peroxide solution and apply ointment such as A&D or Aquafor to hasten re-epithelialization. After several days a moisturizer may be substituted for the ointment. Medium depth peels produce erythema and desquamation that lasts for 5 to 7 days. Once desquamation is complete, makeup can be applied. The peel can be repeated periodically to maintain youthful-looking skin.

Phenol peeling has a longer recovery period and increased morbidity. Either tape or a petroleum-based ointment dressing can provide occlusion. Ointment is more comfortable for the patient and also allows visualization of the wound. If used, tape is removed within 48 hours and gentle washing is permitted. The skin is kept moist with ointments to speed re-epithelialization, which is usually complete within 10 to 14 days. Erythema however, persists for several months. Bleaching agents are helpful to treat increased pigmentation.

After dermabrasion, the patient may clean the areas and apply ointment as needed. Re-epithelialization is usually completed within 7 to 10 days.

Following all resurfacing techniques, avoidance of sun exposure and use of broad-spectrum sunscreens against both UVA and UVB is important. After seven to ten days, a skin care regimen can be resumed, including use of a broad-spectrum sunscreen. Erythema can persist for several months.

Complications

The goals of chemical peeling are the controlled creation of a partial-thickness wound with minimal complications. Pigmentary problems are the most common complications. Hypopigmentation is seen with peels that destroy the entire epidermis. If pigment-producing melanocytes, located at the dermal–epidermal junction are destroyed, it is possible for permanent hypopigmentation to occur, which has no effective treatment. Hypopigmentation is more common after phenol peeling.

Hyperpigmentation is inflammatory in nature and results from melanocyte overstimulation secondary to trauma. In general, patients with darker skin types have a greater tendency to develop post-treatment hyperpigmentation, while patients with light skin are more prone toward post-treatment hypopigmentation. Darker skin patients in particular benefit from pretreatment with tretinoin and hydroquinone and may require post-peel treatment with bleaching agents because of hyperpigmentation. Hyperpigmentation can be increased by premature sun exposure.

Wound infections can occur, most of which are due to Staphylococcus and Streptococcus, but can include yeast (Candida), Pseudomonas or herpes viruses. In patients with a history of herpes infection, peeling may cause a herpes outbreak in the chemically damaged skin. These patients should be treated prophylactically with antiviral agents such as acyclovir or valacyclovir.

The most serious, but rare, complication of chemical peeling and dermabrasion is scarring. In general, the deeper the peel, the higher the risk of scarring. An increased risk of scarring is associated with injury to the deep reticular dermis and is most often seen in the perioral and mandibular areas. Full thickness injury to the skin cannot heal by re-epithelialization and permanent scarring is inevitable. Also, previous use of isotretinoin (Accutane) may lead to hypertrophic scarring. Scars are usually preceded by persistent erythema and should be treated with topical corticosteroids, which can reverse the process and prevent a scar from forming. Intralesional corticosteroids and/or silicone pressure dressings may be used and in severe cases, surgical revision may be necessary.

Overall, chemical peeling and dermabrasion are time-tested, safe and efficacious modalities for the treatment of facial aging.

The ideal method of skin resurfacing should be judged by long-term wrinkle improvement, predictability, accuracy of depth control, low morbidity, minimal complications, high patient acceptance and cost-effectiveness.

Summary of steps