CHAPTER 41 SKIN RESURFACING
FRITZ E. BARTON
LAYERS OF THE SKIN
In basic terms, the skin is divided into two layers: the epidermis and the dermis (Figure 41.1). The epidermis provides a water exchange barrier (via its lipid intercellular mortar) and sun protection (via pigment). A vertical series of oxytalan elastic fibers attach the epidermis to the underlying dermis (Chapter 13).
The dermis is the structural layer of the skin. The more superficial papillary dermis provides flexibility and elastic recoil. The deeper reticular dermis provides a thick, sturdy foundation.
Natural aging is a process of atrophy of all skin elements—epidermis, dermis, and appendages. Actinic damage, to the contrary, is a process of thickening—particularly of the epidermis. The face, neck, chest, and hands are the most sun exposed and the most frequent sites of skin resurfacing.
Common benign maladies of the skin surface include dyschromias (solar lentigines), keratoses (actinic and seborrheic), and wrinkles.
With age, asynchrony of keratinocyte proliferation can produce seborrheic keratoses. These lesions are usually individually curetted, since they involve only the superficial epidermis. Actinic keratoses commonly occur with chronic sun exposure. If few, they may be individually treated with cryotherapy or trichloroacetic acid (TCA). If diffuse, overall skin resurfacing may be required.
Skin pigmentation occurs from melanocytes that are principally distributed along the basement membrane. Each melanocyte normally controls the production and distribution of melanin to approximately 15 to 18 keratinocytes.
With age and irradiation-induced DNA damage, asynchrony of melanin production and/or distribution occurs. Thus, collections of excess pigment (lentigines) occur. Solar lentigines are common on the face, chest, and dorsal hands. Histologically, both increased number of basal melanocytes and increased deposition of melanin in keratinocytes are present. Cryotherapy is a common treatment for isolated lesions, since melanocytes are particularly susceptible to cold injury.1,2 Broader fields of lentigines are more conveniently treated with TCA peels or intense pulsed light treatments.3,4 Eradication requires destruction to the basal layer of the epidermis.
On rare occasions, abnormal pigment may be distributed into the dermis—a condition known as melasma. Melasma occurs most commonly in young females and is felt to be hormonally induced. Treatment is unpredictable. Topical Retin A and hydroquinone 2% to 4% to block melanin production is useful and is critical for avoiding recurrence. Dermal chemical peels, intense pulse light, and non-ablative laser treatments may also be useful.
The exact cause of fine lines and wrinkles remains undetermined. Changes in the epidermis, loss of oxytalan fibers at the dermal–epidermal (DE) junction, and “elastotic” thickening in the superficial dermis all seem to play a role. What empirically seems clear, however, is that correction of skin wrinkles requires some type of ablative therapy through the DE junction into the papillary dermis at least.5-7
The concept of resurfacing is to destroy the layers of the skin down past the level of the abnormality, followed by healing of the skin to replace the removed layers with fresh, healthy tissue.
If the level of destruction is confined to the epidermis, the re-epithelialization occurs from the basal layer of the epidermis. If the level of destruction removes the epidermis, re-epithelialization occurs from lateral migration of adjacent keratinocytes and vertical migration of epithelial cells from the underlying dermal appendages (sweat glands and hair follicles). Destruction into the dermis stimulates a healing response characterized by new collagen production. The type of collagen response varies with the injury mechanism.
For practical purposes, there are three methods of resurfacing: mechanical sanding (dermabrasion), chemical burn (chemical peels), and photodynamic treatments (laser ablation or coagulation).
There are several side effects of skin resurfacing that influence the choice of method and application: rate of healing, loss of skin texture, depigmentation, and potential for visible scarring.
Any injury that removes all epithelium and enters the dermis can cause scarring. The exact limits of dermal depth and injury type which exceeds the normal healing capacity and produces visible scarring are not known. However, it is apparent that the deeper the dermal injury, the greater the likelihood of scarring. In addition, certain topographic areas are more prone to scar—such as the mandibular border and neck where the dermis is thinner and there are fewer underlying skin appendages for re-epithelialization.
The vast majority of melanocytes occur along the basal epithelial layer, although some also reside in the hair follicles. Complete removal of the basal melanocytes by destruction or selective melanocyte injury (such as heat from coagulative lasers or phenol peel) can result in unwanted hypopigmentation.
The opposite can also occur. Freshly re-populating melanocytes are particularly sensitive to sunlight stimulation and “post-inflammatory hyperpigmentation” can occur for the first several months of healing.
Epidermal treatments usually focus on actinic keratoses, dyschromias, and dull skin from excess accumulation of old keratinocytes in the stratum corneum.
The skin abnormalities may be diffuse or patchy, but since the depth of treatment is superficial to the basement membrane, repair is rapid from migration of surface epithelium. Therefore, a complete coverage treatment is safe and effective.
FIGURE 41.1. Skin elements, cross section.
The most common superficial treatments are chemical peels (Chapter 13).
α-Hydroxy acids are naturally occurring acids derived from fruits and milk products.8 They are shown in Table 41.1.
Glycolic acid has received the most wide use in topical products, primarily due to the fact that its smaller molecular size (two carbon chain) makes it penetrate the epidermis most readily. Both the concentration and the pH influence its penetration. As a topical peel, the FDA has suggested limits of 30% concentration and pH 3.0 or greater. It has been used “off label” in concentrations of 50% and lower pH’s. From a practical standpoint, patchy or uneven penetration is a problem that limits its use as an epidermal peeling agent. For this reason, glycolic acid peels are often administered in a gel base rather than in aqueous solution.
Lactic acid is a three carbon chain. As such, it penetrates more slowly and perhaps more evenly than glycolic acid. It can be applied in concentrations up to 70%.
The “frosting” end point of effect in α-hydroxy acid peels is often indistinct. As a result, they are usually applied on a time of application basis, followed by dilution with water rinsing.
β-Hydroxy acids are a chemical variant with two carbons between hydroxyl groups, versus one carbon separating hydroxyl groups in α-hydroxy acids. The most commonly used β-hydroxy acid is salicylic acid. Salicylic acid in concentrations up to 30% can be used for peeling. Salicylic acid produces a visible white frost (even more visible under fluorescent light), which makes the end point easier to assess. It is particularly effective in acne skin patients. Historically, salicylic acid lost favor because of the side effect of tinnitus with higher concentrations.
The most commonly used superficial peeling agent is Jessner’s solution (formerly Coombes formula).9 It is a combination of α- and β-hydroxy acids, providing benefits of both, but each in low enough concentration to limit side effects. The formula is usually mixed as follows:
Premixed Jessner’s solution is commercially available. The mixture has several advantages. First, a light frost end point can be visualized. Second, it rapidly volatizes, so it does not need neutralization. Depth is controlled by the number of layers applied. Jessner’s peels are not only used alone as an epidermal peeling agent, but they are also commonly used for initial dekeratinization to facilitate the penetration of other chemical peels such as TCA.
TCA has been used as a variable depth skin peel since at least 1962.10 It is used in strengths of 15% to 20% for epidermal peels. Coagulation of keratinocyte protein produces a light white frost, which is easy to read as an end point. Epidermal TCA peels desquamate in approximately 5 days and are effective for correction of superficial actinic changes and dyschromias.
Wrinkles and fine lines involve at least the DE junction, if not the dermis itself. Correction requires a treatment that penetrates to the dermis and causes secondary fibroblastic production of collagen. While elastin replacement has been theorized, there is yet no predictable way to stimulate normal elastin replacement.
The more aggressive resurfacing methods—deeper peels, dermabrasion, and lasers—are most commonly employed for dermal problems. Scarring risk, however, increases significantly as the dermis is injured. The key to each of the dermal treatments is determining the depth of treatment—the clinical end point. Each technique has different visual signs and all the signs are relatively subtle. Experience is required to learn to accurately “read” those end points.
FIGURE 41.2. The frost of a papillary dermal trichloroacetic acid (TCA) peel.
The two most common dermal depth peels are TCA and phenol/croton oil. Both create a definite white “frost” by coagulation of epidermal proteins (Figure 41.2).
When used in a concentration of 35% to 42.5%,11 TCA is an excellent peeling agent for the face. One of the advantages of TCA is the ability to read the depth by clinical end points (Table 41.2).
Preparatory dekeratinization of the epithelium with either topical retinoic acid for several weeks or immediate dekeratinization with Jessner’s solution enhances uniformity of the depth of penetration. TCA does not volitize quickly, so continued depth of penetration is achieved with increased concentration as well as with friction in application. Postoperatively peeled skin is usually treated with ointment rather than an occlusive dressing until re-epithelialization is complete.
TCA is excellent for the cheeks, forehead, and eyelids (Figure 41.3). In general, it is less effective for deep perioral rhytids.
In the 1960s, phenol mixed with croton oil was popularized by the Baker-Gordon formula.12 This formula was the standard for many years, but the strength of the peel solution was suitable only for severely thickened, sun-damaged skin.
In response to the popularity of varying strength TCA peels, the roles of the Baker-Gordon ingredients were studied by Hetter.13,14 Hetter concluded that the croton oil is, in fact, the actual peeling agent. He went on to suggest varying concentrations for varying depths of correction (Figure 41.4, Tables 41.3 and 41.4).
FIGURE 41.3. Patient with severe sun-damaged skin. A. Before treatment; B. Four days after 42.5% TCA to face and dermabrasion of upper lip; and C. 6 weeks post peel.
FIGURE 41.4. Patient previously peeled with TCA wanted additional benefit. Shown on fourth post-peel day (A) and 3 months post peel (B).
A different, but equally analytical evaluation of the phenol/ croton oil peel was presented by Stone.15-17 Stone suggests that the phenol is of equal or greater importance and that the friction of application is a major factor. Stone suggested the formulas shown in Table 41.5.
As with TCA, the end point of treatment is determined by reading the appearance of the “frosted” tissue. While similar to TCA, the frosting from phenol/croton oil is more gray-white and is distorted somewhat by the erythema from the caustic croton oil component. Posttreatment care usually consists of ointment or occlusive dressing until re-epithelialization is complete.
Regardless of the formula of preference, phenol/croton oil remains the most aggressive of the clinically useful face peels and is more efficacious than any other peel for perioral rhytids.
FIGURE 41.5. Dermabrasion fraises (left) and brushes (right).
Surgical sanding—dermabrasion—was perhaps the first resurfacing method.
Most commonly it was used to correct acne scarring. The concept was to remove the skin thickness until the surrounding tissue was at the same level as the depth of the scar. The same concept has been applied to wrinkles.
Histologic studies have indicated that dermabrasion permanently reduces the thickness of the dermis, and that healing does not completely replace the lost thickness.18 This is in distinction to chemical peels and coagulative lasers that appear to produce compensatory dermal thickening.
Dermabrasion can be performed manually with sandpaper.19,20 However, it is mechanically awkward and sterility is an issue.
Microdermabrasion has been popularized as an office procedure. Course crystals are blown onto the skin and recollected. For practical purposes, microdermabrasion is a salon procedure that is confined to epidermal exfoliation.21
Surgical dermabrasion is usually performed with power rotary using either wire brush or diamond fraise (Figure 41.5). The fraise is less aggressive. The challenge with dermabrasion is adequate stabilization of the tissue for sanding. It is excellent for individual scars and along the lip borders, but dermabrading larger areas of the cheeks is more technically demanding. Dermabrasion cannot be performed on the eyelids. Temporary freezing of the skin to increase stiffness is commonly employed22,23.
The end points of dermabrasion are determined by dermal bleeding patterns. The superficial papillary dermis shows almost confluent bleeding points with a fine lattice stroma. As the sanding reaches the deeper reticular dermis, bleeding points become wider spaced and more discrete, and the stroma becomes coarse. In general, the depth of a wrinkle must be reached to correct it.
Posttreatment care usually consists of wet dressings for a few hours until bleeding stops, followed by ointment until re-epithelialized.
The use of light energy as a LASER (Light Amplification by Stimulated Emission of Radiation) began in the 1960s. Lasers are classified by their wavelength on the electromagnetic spectrum (Chapter 18). The refinement of medical laser application was facilitated by the identification of “selective photothermolysis,”24 meaning that different laser wavelengths are attracted to different biologic targets (“chromophores”). For practical purposes in skin resurfacing for fine lines and wrinkles, the chromophore is water in the skin. The two lasers most useful in targeting water are erbium:YAG and carbon dioxide.
The prototypical laser for skin resurfacing has been carbon dioxide. The earliest CO2 (10,600 nm) lasers used a continuous-wave technology. The duration of the heated pulse created char of the epidermis and superficial dermis. While very effective at ablating wrinkles, the side effects of scarring, depigmentation, and loss of skin texture largely extinguished its use.
The next major modification was pulsing the energy. Originally the pulses were long and exceeded the thermal relaxation time of skin (0.2 to 1 milliseconds). Gradual shortening of the pulses and patterning the cores of energy have refined the method. It should be noted that all of the original CO2 lasers were applied with overlap of the heat cores in order to achieve complete skin coverage. Collagen shrinkage and secondary proliferation occurred in the papillary and upper reticular dermis in response to heat coagulation injury. The exact depth of injury was dependent on energy and pulse duration. It is critical to recognize that pulse duration varies significantly among CO2 lasers, so comparison is difficult (Figure 41.6).
FIGURE 41.6. Typical epidermal and papillary dermal ablation of pulsed CO2 laser with complete coverage (Coherent Ultrapulse 5000): (A) untreated skin; (B) single pass removes epithelium and reaches papillary dermis; (C) second pass reaches the upper reticular dermis. Courtesy of Jeff Kenkel, MD.
FIGURE 41.7. Comparison of continuous (complete) coverage and fractionated coverage with laser.
Whether skin contraction after laser resurfacing is permanent remains controversial.25-27 Continuous (contiguous) coverage CO2 laser resurfacing is still the most effect laser method of wrinkle removal and is still widely used. However, prolonged recovery, delayed hypopigmentation, and the risk of scarring remain limiting factors.
The other major skin resurfacing laser to achieve widespread use is the erbium:YAG. As opposed to CO2, which is a heat-coagulative ablative laser, erbium can be calibrated to deliver either cool ablation or coagulation. In the cool ablation mode, erbium functions as a laser dermabrader. Specific depths of tissue can be removed with minimal heating of the tissue, due to the fact that erbium (at the 2,940 nm wavelength) has much greater affinity for water than CO2. As with dermabrasion, since there is minimal surrounding damaged collagen, the overall dermis could be thinner after treatment. Collagen response is proportional to the depth of the wound.28,29
In 2004 “fractionated photothermolysis” was introduced.30 The concept was to provide intermittent microscopic columns of thermal injury (“microthermal zones”) while sparring tissue between the columns. The hope was to preserve skin pigment, preserve skin appendages (skin texture), and promote rapid healing (minimal “downtime”) (Figure 41.7).
The first fractionated medical laser utilized erbium:glass at a 1,540 wavelength. Fractionated “microthermal zones” penetrated through the papillary dermis while leaving micro eschars of epithelium intact on the surface. A variety of non-ablative lasers in the erbium:YAG 1,540 to 1,550 wavelength have been developed. Their advantage is rapid healing (only 24 to 48 hours of erythema), but benefit in terms of reversal of significant wrinkling or actinic lines is minimal.
In 2007 the concept of fractionated delivery was applied to CO2 lasers, in an effort to achieve greater wrinkle correction,31 while preserving the rapid healing time. What followed was a marketing rush by companies to produce the devices. Spot sizes vary from 130 to 350 µm. Pulse durations, density of treatments, and pattern of application also vary. The two basic application types of fractionated lasers are striping and stamping (Figure 41.8).
To date, specific treatment parameters of fractionated lasers correlating to clinical results are lacking. It appears that “hot” lasers (CO2) may only need to reach the papillary dermis to correct wrinkles. “Cold” lasers (erbium:YAG), dermabrasion, and chemical peels may need to reach greater dermal depth to stimulate adequate contracture to efface wrinkles.
As of this writing the results from fractionated CO2 treatment are still not as good as the wrinkle effacement from complete coverage pulsed CO2 laser treatments.
Any procedure that disrupts the DE junction exposes the skin to infection. Post-resurfacing infections can be of three types: viral, fungal, and bacterial.
Herpes virus types HSV-1 (herpes simplex virus), HSV-2, and HH3 (Candida) infection can occur in facial resurfacing. Since the virus can lay dormant prior to resurfacing, prophylactic treatment is common. The response to antiviral agents is variable, but the most common prophylactic treatment is valcyclovir 500 mg po starting the day prior to treatment. Herpes infection usually appears as vesicles in patchy areas of moderate erythema. In the case of clinical infections, valcyclovir doses are increased to 2,000 mg per day (refer http://www.skintherapyletter.com/2005/10.1/1.html).
FIGURE 41.8. Ablative cores (“microthermal zones”) of fractionated CO2 laser (Courtesy of Solta Medical).
Bacterial infection can occur in resurfacing as with any open wound. Purulent exudate indicates secondary infection, but can be difficult to distinguish from normal desquamation. Immediate recognition is critical because secondary bacterial infection can deepen the wound and cause scarring. Gram stain of the exudate and culture diagnosis is imperative.
Candida albicans is a regular inhabitant of normal skin. The moist environment of resurfacing wounds can be a fertile bed for yeast infection. Clinically, the wound becomes fire red with fine vesicles. Treatment with topical antifungals such as nystatin, often combined with mild topical steroid, will usually eradicate the yeast infection without sequelae.
Skin pigmentary changes are not uncommon after resurfacing. Response may be over (hyperpigmentation) or under (hypopigmentation).
Source melanocytes reside in the basal layer of the epidermis as well as in hair follicles. Melanin in the skin is produced by the conversion of tyrosine by the enzyme tyrosinase. Production of melanin by melanocytes is stimulated by ultraviolet irradiation (particularly UVB) and by irritation.
In the early healing phase of a wound, there is little remaining protective melanin in the superficial epithelium to absorb ultraviolet irradiation stimulation. Thus, for up to 3 months after resurfacing, sunscreen protection is important. The use of a tyrosinase blocking agent, such as hydroquinone, is helpful. If rebound hyperpigmentation should occur, it can usually be corrected with topical bleaching agents.
Of greater potential significance is post-resurfacing hypopigmentation. Any procedure that destroys the basal layer of epithelium—that is, dermal treatments for wrinkle irradiation—can permanently alter pigmentation.
The risk is greatest with uniform (contiguous) injuries, such as dermabrasion, chemical peels, and dense laser treatments. Since the entire surface melanocyte population in area is removed, repigmentation is dependent upon melanocyte migration from the wound edges and from dermal appendages.
It appears that heat (CO2 laser), cold (liquid nitrogen), and phenol (chemical peel) may have selective melanocyte toxicity. Conversely, treatments of discontinuous injury (fractionated lasers) spare melanocytes in the untreated areas. Hypopigmentation may not be fully evident for several months after injury, and when it occurs, it is irreparable.
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