Complications of Chemical Peels, Dermabrasion, and Laser Resurfacing

Introduction

The number of aesthetic facial procedures continues to increase every year. Particularly in the area of facial resurfacing demand for these procedures has increased dramatically, with 550,000 chemical peels, 1 million microdermabrasion procedures and 400,000 laser resurfacing procedures performed in 2005 out of a total of 11 million aesthetic procedures in 2005, 9 million of which were nonsurgical.(1) Facial resurfacing is now an integral part of the aesthetic facial surgeon’s palette of techniques for facial rejuvenation. As in other areas of aesthetic surgery, patients who seek these procedures are not suffering from an illness or trauma but are seeking improvement in their physical appearance. The elective nature of these procedures imposes a different level of expectation with regard to outcomes and avoidance of complications when compared to medically essential treatments. Proper patient selection is paramount for success with facial resurfacing procedures. If the surgeon has questions about the patient’s likelihood of following preoperative and postprocedure care instructions and other recommendations, the best option is often to defer performing these procedures on that patient. As an example, patients must be willing to commit to applying topical emollients or ointments after a chemical peel procedure, potentially up to 6 times a day.

Patients who are seeking aesthetic surgery should participate in a thorough process of evaluation and discussion with their surgeon. Obtaining an appropriate medical history with focused attention to any medications or underlying medical conditions that may affect the surgical outcome is extremely important to avoid predictable complications and to select the right procedure for the patient. The patient’s habits including sun exposure expectations, cosmetic regimen, and lifestyle are all important factors in predicting the outcome of their procedure. A history of abnormal scarring, collagen vascular disease or previous surgery in the area undergoing treatment can predict possible abnormalities in postoperative healing. Previous radiation therapy may disturb the skin’s architecture and reduce the number of pilosebaceous units needed to heal after resurfacing and possibly impacting any efforts at recontouring. Assessment of the patient’s psychological stability may help to avoid performing procedures on potentially problematic individuals. At times a preoperative psychological consultation may be necessary. Many patients undergo resurfacing with high expectations of results. Demanding or imbalanced patients may have disturbed or unrealistic expectations. A recent study evaluated 212 patients undergoing ablative pulsed carbon dioxide laser resurfacing. There was an 89% overall satisfaction rate, i.e. “they would do it again”.(2) Predictors of patient satisfaction included expectations of mild to moderate improvement, hopes for improved appearance and healthier appearing skin. Correlates of dissatisfaction included preoperative expectation of improved self-esteem after therapy, a belief that the face was disfigured before treatment, and an expectation of complete or near-total improvement in the aging skin.(2)

After obtaining a thorough history, the physician must perform a thorough evaluation of the patient’s physical status. For patients seeking facial resurfacing, particular attention is paid to the condition and objective qualities of the facial skin. Analyzing the degree of skin changes, assessment of skin coloration and Fitzpatrck skin type, and degree of aging changes including assessment by the Glogau scale are parts of this evaluation.(3) The degree of skin pigmentation is a key predictor of an uneventful outcome of particular facial resurfacing procedures and the potential need for a preprocedure regimen of topical therapy. Photographs of the patient should be obtained, documenting problem areas and allowing for prospective evaluation of their improvement after the resurfacing procedure.

During their discussions about the upcoming procedure, the patient and surgeon should discuss the nature and limitations of the chosen procedure as well as the expected outcome. For example, those with relatively fine rhytids will often do well with a variety of procedures, including medium-depth peels or other resurfacing techniques while those with deeper rhytids can only achieve complete resolution of these with deeper resurfacing. The normal course of healing including routine symptoms such as erythema, swelling and ecchymosis should be reviewed including a reassurance to the patient that none of these symptoms represents a complication or untoward event. Some physicians recommend showing photographic examples of patients documenting the immediate postoperative appearance as well as the course of healing and the eventual outcome during the consultation This documentation should include outstanding results, average outcomes and suboptimal results so that the patient has a full understanding of what can be achieved.(4) During this discussion, the patient’s desired outcome and whether it can be achieved with the procedure being considered, expectations and level of commitment can be assessed. Reviewing possible complications of the procedure including their source, treatment and results is an in integral part of preoperative preparation. Complications although uncommon do occur after facial resurfacing and may be due to various factors, including surgeon inexperience or inattention, inadequate postoperative care, and patient variables such as skin type and coloration, UV exposure, and compliance with care instructions. (5) Patient satisfaction ultimately depends not just on how closely the physical result matches their expectations, but also on how strongly the physician-patient relationship has developed. The process of obtaining consent is crucial to the outcome of cosmetic surgery and in acceptance of potential complications.

Resurfacing Techniques

Chemical peels, dermabrasion, and laser resurfacing share a number of similarities including the types of problems treated with these techniques, the histologic basis behind them and their potential complications. These procedures in broad terms involve mechanical, thermal or chemical injury to the skin to produce a desired outcome through the process of healing and organized regeneration, usually a reduction in the signs of aging or sun-induced damage to the skin.(6) Chemical peels take advantage of certain organic acids’ ability to penetrate the skin and create a (fairly) predictable pattern of injury and subsequent repair. Modern chemical peeling includes the use of a variety of different compounds including alpha-hydroxy acids (AHA’s), trichloroacetic acid (TCA), phenol based formulae which most often incorporate phenol, croton oil, a potent vesicant, a soap such as Septisol and water along with vegetable oils or glycerin in some formulae, and several peel techniques utilizing more than one solution such as Monheit’s Jessner’s:TCA medium-depth peel. These combination peels use a keratolytic agent such as Jessner’s solution or glycolic acid to enhance penetration by the TCA peeling solution. Reepithelialization should be complete by 5 days for superficial resurfacing and 7-10 days for medium-depth treatments.(7)

Resurfacing procedures produce a level of injury to the skin that can be classified as superficial (through the epidermis to the papillary dermis), medium-depth (into the upper reticular dermis), and deep (to the mid-reticular dermis). Examples of superficial treatments would include AHA or Jessner’s chemical peels, light laser resurfacing or microdermabrasion. Medium-depth treatments include combination chemical peels and many laser treatment protocols. Deep level resurfacing includes phenol peels, more aggressive laser treatments and most dermabrasion procedures. The body’s natural process of healing produces the desired aesthetic result and the depth of injury can be tailored based on the problem to be corrected and to produce the desired outcome. (3) In general reepithelialization of the skin surface occurs by proliferation of epithelial remnants in the skin adnexae such as the hair follicles.(8,6) If these adnexae are suppressed as in the case of those on Accutane (isotretinoin) or after radiation treatment, then care must be taken before proceeding with certain techniques of skin resurfacing. At the microscopic level, after healing the epidermis thickens with increased ridging at the dermal-epidermal junction. After medium and deeper resurfacing, the dermis shows increased elastin and more organized collagen formation in contrast to the disorganized collagen found in sun-damaged skin.(9) Medium-depth and deep peels stimulation of a new band of collagen in the dermis further reduces the signs of aging. All of these modalities stimulate the body’s natural repair processes to replace damaged, aging tissue with more organized and histologically youthful features.

The depth of injury and thus the eventual result and risk of complications depends on several factors. Patient selection, choice of resurfacing technique including peeling agent (e.g. TCA, Jessner’s solution, phenol-based solutions, alpha-hydroxy acids, or one of numerous combination peels) or laser/dermabrasion technique, preoperative skin preparation, application technique, and postoperative care regimen and compliance can all affect the patient’s outcome and risk for untoward events.(10) For example, patients undergoing a Baker-Gordon phenol peel must accept certain expected results such as some degree of persistent hypopigmentation as well as a higher risk of complications during the healing process. Similarly, if the physician chooses to use higher-concentration TCA (50% or greater), he must understand the intrinsically greater risk of postoperative scarring.

Surgeons who employ these techniques must be well-versed in the characteristics of the different treatment techniques, their likelihood of success for the patient’s presenting clinical conditions and their potential to cause complications. Indications for treatment include dyschromias, fine and coarse rhytids, premalignant skin lesions, and acne scars. Laser resurfacing and other resurfacing techniques can be very effective in reducing the number of actinic lesions in those with widespread photoaging and precancerous lesions.(15) This can be a significant clinical problem because of the difficulty separating diffusely damaged skin from isolated lesions. Approximately 90% of patients may remain lesion free for one year and 60% for two years after a single treatment. Overall 95% of actinic keratoses can be eradicated with common resurfacing techniques which allow removal of the lesions as well as prophylactically treating surrounding sun-damaged skin.(16) The patient must be carefully evaluated so that the depth of peeling will be appropriate for the lesion being treated. The development of more superficial treatments has expanded the range of potential patient beyond the blond, blue-eyed, fair-skinned individual originally thought to be ideal for deep peels.(11) Some physicians are now treating even Fitzpatrick types III and IV skin with deep peels along with very vigorous postoperative care aimed at reducing hyperpigmentation.(11)

In contrast to chemical peels and dermabrasion, laser resurfacing relies on thermal energy to wound the skin. This thermal energy has the benefit of cauterizing potential bleeding sites, but can also damage adjacent tissue.(12) Early laser resurfacing procedures were performed with continuous wave carbon dioxide laser technology which led to more complications. Excessive laser energy delivery resulted in a higher incidence of scarring.(5) After high-energy short-pulse lasers became available in the early 1990’s, controlled ablation with acceptable incidence of complications became possible. This followed in parallel with the development of less aggressive and safer peeling regimens. With the newer laser technologies, surgeons could deliver high energy fluences in very short pulses resulting in effective cutaneous ablation with minimal collateral thermal damage. There are now a number of different protocols for laser resurfacing varying the type of laser, amount of energy, pulse mode and number of treatment passes.(13) Carbon dioxide ablative resurfacing techniques remain the standard for laser resurfacing. Primarily absorbed by intracellular water, carbon dioxide laser energy heats the cells to the boiling point. This results in vaporization and removal of the surface layer of cells and thermal coagulative necrosis of a band of cells and denaturation of extracellular proteins in the immediate area bordering the zone of vaporization.(14) High energy pulsed carbon dioxide lasers produce deeper penetration (20-60 microns) with each pass and 20-150 micron of collateral thermal damage. Er:YAG which also targets intracellular water, but with a higher coefficient of absorption, allows more shallow ablation in the range of 2-5 microns per pass and 20-50 microns of thermal spread.(17) With this technology the entire epidermis and variable amounts of dermis are removed resulting in a smoother and tighter appearance of the skin as it heals due to the heat-induced shrinkage of extracellular collagen. Deposition of heat from the laser does cause some tightening of the tissue and collagen fibril shrinkage by up to 30% which can help smooth surface skin irregularities.(4).

Reepithelialization is typically complete in 7-10 days for carbon dioxide laser and 5-7 days for Er:YAG treatments.(5) The importance of the broader thermal spread of carbon dioxide laser during recovery is that more pronounced and prolonged redness will usually be seen in these patients. The other main negative effects of laser resurfacing are posttreatment edema, erythema, pruritis and burning. Redness may last an average of 4 months. With most laser procedures today, the risk of complications depends on the number of passes performed, energy density, the degree of pulse and scan overlap, preoperative skin conditioning and the relative thickness of the skin in the anatomic area being treated.(5) Other results are similar to those of similar resurfacing techniques. Overall indications for laser resurfacing include: rhytides, photodamage, acne scars, actinic and seborrheic keratoses, actinic cheilitis, scar revision and rhinophyma.

Newer nonablative laser techniques have also been developed which selectively treat the aging dermis and increase collagen production but protect the epidermis through application of cooling to the skin surface during treatment and through the use of lasers with targeted absorption at various levels of the dermis. These lasers were selected based on the principles of selective photothermolysis.(18) They are becoming more popular due to patient demand for less discomfort, reduced downtime, and lower risk of complications along with faster recovery, and also offer a broader range of therapies to accommodate a wider spectrum of patients. Hence the ideal nonablative treatment protocol should have: no significant downtime, minimal discomfort, observable improvement in rhytids, and improvement in the skin’s appearance.(19) These techniques include a number of technologies such as the 585 and 595 pulsed dye laser, Er:glass 1540 nm, the Nd:YAG 1320-nm or 1450-nm diode lasers to produce histologic effects on the dermis but offer variable clinical improvement as does clinical application of intense pulsed light.(20,21) Multiple treatment sessions are most often needed to effect a significant result and the best patients for these treatments probably have a mild to moderate amount of photoaging skin with fine rhytids, superficial pigmentary changes or shallow scars.(22) Some authors report a 25-50% objective improvement in these patients but others report that more established techniques continue to offer greater improvement.(19). Others have had success extending the area of treatment to incorporate cervical rhytids. Due to the nature of the procedures, nonablative techniques are limited to laser techniques as chemical peel and dermabrasion procedures all require effacement of the surface epithelium.

With the advent of other procedures including laser resurfacing (both ablative and nonablative), chemexfoliation, and microdermabrasion, the popularity of dermabrasion has decreased.(23,24) Dermabrasion remains a valuable technique for reducing the cosmetic impact of traumatic or surgical scarring, acne and other surface irregularities, as well as an alternative for cosmetic facial resurfacing. The history of dermabrasion dates into the 1930’s and Kurten wrote the first thorough review of the technique. He recommended its use for conditions including acne scars, actinic lesions, keloids, lichenoid plaques, nevi, tattoos, traumatic scars,and rhytids.(23) For scar revision, dermabrasion can reduce the contrast between the depressed scar which lies in shadow and the surrounding skin,, possibly by beveling its edges and reducing the attention-drawing shadows cast by many scars.(25) Dermabrasion remains much more dependent on operative technique (requiring significant manual dexterity, and a strong and delicate touch developed through extensive training and experience) than either chemical peel or the computer-controlled laser therapies and thus more vulnerable to operator error. Variables affecting depth of injury during dermabrasion include the amount of pressure holding the instrument tip against the skin, speed of rotation, coarseness of the tip chosen, and the patient’s skin type and texture.(26) Full dermabrasion most often produces removal of 350 microns of tissue into the upper reticular dermis. Avoiding complications such as excessive removal of tissue is very dependent on training and experience. Laser techniques offer advantages in predictability and accuracy reducing reliance on the surgeon’s knowledge and experience compared to dermabrasion, which contributed to their rise in popularity.(8)

A number of different preoperative skin treatment regimens are available to help control the predicted outcome of the peeling session and further reinvigorate the skin. Pretreating regimens are used by many resurfacing practitioners (87% in an ASAPS survey).(27) Tretinoin is the most common agent used preoperatively for its effects on accelerating healing and also improving the skin quality and response to treatment. Glycolic acid preparations are also valuable for their exfoliating and rejuvenating effects. Some physicians prescribe a preoperative course of hydroquinones or Kligman’s mixture (Retin-A, hydroquinone and hydrocortisone) to try to reduce the risk of postoperative hyperpigmentation. Appropriate wound care after resurfacing is vital to success and leads to faster wound healing along with a faster resolution of minor postoperative symptoms. Most physicians rely on an open technique of treatment with frequent application of ointments (Aquaphor, Catrix-10, Recovery Hydra, or plain petrolatum for example). The open technique allows for better visualization of the healing process and better identification of problems at an earlier stage. Closed techniques of wound care involve application of a biosynthetic dressing material such as Flexzan, Biobrane, Silon TSR or Vigilon. These are left in place and then removed after from 2-7 days. Closed dressings can hide early infections and may even contribute to the owing to wound maceration.

At some point during the postoperative period, many patients require reassurance that the sequellae they are experiencing, are in fact normal processes and are not complications. One example of this situation is the need to remind some patients that improvement not elimination of skin problems such as scars, rhytids or pigmentary irregularities was the expected goal. Addressing the problem of unrealistic expectations may need to be done several times during the course of evaluation and treatment. Another example would be the postoperative pruritus experienced by up to 90% of patients undergoing resurfacing especially those treated with the laser.(28) In other cases, patients will need to be informed that they are experiencing an unexpected outcome and require extra care to ensure a good result. All of these conversations during the preoperative consultation, performance of the procedure and during the postoperative care are designed to eliminate one of the most difficult situations to manage: the dissatisfied patient. Complications of facial resurfacing include: premature peeling, infection, herpetic infection or reactivation, pigmentary abnormalities, milia, prolonged erythema, phenol toxicity, and scarring.

Premature Exposure of Peeled Areas and Delayed Healing

At times after resurfacing, the superficial layers of the skin will desquamate earlier than expected. Usually after a peel this layer of debris will function as a protective dressing, allowing healing to proceed predictably and premature exposure of the fragile, partially reepithelialized areas may increase the risk of inflammation, infection, or possible scarring. Early removal of this layer most often occurs from patients rubbing or scratching at the areas or even manually peeling off the strips of desquamating skin. If the underlying area has not yet reepithelialized, it may appear raw or moist. Intervention must be geared to reduce inflammation and protect the area thereby allowing normal healing to resume. Application of topical antibiotic ointments such as Bacitracin or Polysporin three to four times a day is the best approach. Treatment with oral antibiotics covering for Staphylococcus and Streptococcus, most often a cephalosporin may also be indicated. Area that have already reepithelialized but are not yet ready for exposure may also be uncovered by early removal of peel debris. The risk of infection is very low, but the new skin is extremely thin and fragile. There is a high risk for increased inflammation which may lead to hyperpigmentation or prolonged redness. The patient must be cautioned to treat the skin very carefully with no rubbing or mechanical trauma. Reducing any inflammation is a priority so a low potency steroid cream or ointment can be used such as DesOwen.

Delayed healing is defined as a nonreepithelialized area within the treatment zone that persists for more than 14 days. Usually laser resurfacing and chemical peel/dermabrasion patients will show complete reepithelialization within two weeks of the procedure, particularly if they have been treated with tretinoin preoperatively. The mainstay of treatment is to apply an occlusive dressing or ointment that protects the area and allows better epithelial cell migration. Care should also be taken to prevent some of the causes of delayed healing such as infections, herpetic outbreaks, poor postoperative care, and secondary tissue injury, e.g. from picking at the wound or scratching.

Infection

Infection is quite uncommon after chemical peeling and dermabrasion, occurring in less than 4-8% of patients.(29) Facial resurfacing leads to a wound which is easily colonized with bacteria and may become infected. Those who have an active bacterial or viral infection probably would be better managed by delaying treatment until they have recovered. Good postoperative hygiene with a reduction in the amount of surface coagulum and crusts reduces the ability of colonizing organisms to become a problem. Removal of the epidermal barrier between the patient and the environment makes the skin more susceptible to infection. Thus care should be taken when peels or dermabrasion are performed on patients with reduced immune function such as diabetics or those who are immunocompromised. Those who are unable to care for the treated area and perform the needed cleaning and application of topical preparations are at higher risk for infection. In many ways facial resurfacing procedures produce an injury that mimics that of a second-degree burn.(30) Since resurfacing wounds mimic burn injuries, some basis for treatment can be found in the burn literature. Most often burn surgeons avoid systemic antibiotics unless signs of infections develop. Several studies have shown that although the resurfacing wound is initially sterile, it is soon colonized with bacteria and occasionally yeast organisms.(31,32) Prophylactic antibiotic therapy has been associated with selection for pathogenic organisms and tendency to higher infection rates.(32) The antibiotic must also be in the patient’s bloodstream before initiating any surgical treatment, thus must be taken at least one hour before surgery if an oral medication is used. For this reason, the Centers for Disease Control do not recommend prophylactic antibiotics for patients with clean or clean-contaminated procedures such as facial resurfacing. Nevertheless, many surgeons still prescribe a cephalosporin or similar antibiotic with gram-positive coverage (usually a first-generation cephalosporin) for their patients.(33)In clinical practice, patients undergoing medium-depth or deep peels are often treated with antibiotics prophylactically, most often cephalosporins, as the most common infecting agent is Staphylococcus aureus. Pseudomonas aeruginosa and streptococcal spp. are less common causes of infections. Topical antibiotic use after facial resurfacing is less controversial.(30) The choice of agents is wide and includes bacitracin, silver sulfadiazine, and many others.

In rare cases staphylococcal toxins have been reported to induce toxic shock syndrome in phenol peel patients. This is a potentially lethal condition caused by release of toxic superantigens from S. aureus, which then induce cytokine release (most notably tumor necrosis factor and interleukin-1).(34) Manifestations of this problem include acute onset of hypotension, fever, and desquamating or scarlatiniform rash along with mental confusion and eventually multiple organ failure.(35) Initial symptoms most often include fever, diarrhea and vomiting followed by confusion and then syncopal hypotension.(34) This may be followed by acute tubular necrosis, hepatocellular inflammation and adult respiratory distress syndrome (ARDS or ‘shock lung’) and skeletal muscle breakdown with very high CPK levels on laboratory evaluation.. Treatment includes rapid intervention with hospital evaluation, initiation of high dose antistaphylococcal antibiotics, supportive care including fluid replacement and vasopressors as needed, and appropriate consultation with infectious disease specialists and intensivists.

Bacterial infection most often begins to appear 48-96 hours after the procedure. It manifests with pain and erythema at the treated areas and may be accompanied by some fever. Increased swelling and some crusting may also be seen as well as potentially malodorous exudate. Cultures can be obtained and may help guide eventual therapy. Most physicians initiate empiric treatment with topical cleaning possibly including 0.25% acetic acid soaks and appropriate antibiotics covering common skin pathogens and possibly Pseudomonas usually proving to be very effective. Initially, most patients are treated empirically with oral cephalexin in doses of 1000 to 2000 mg per day. This agent shows good activity against most gram-positive organisms and some effectiveness against gram-negatives as well. Clindamycin can be a good substitute in the penicillin or cephalosporin allergic patient. If a gram-negative infection such as Pseudomonas is likely, then oral ciprofloxacin 500 to 1000 mg a day must be considered. At times it can be difficult to determine what type of infection is present. Frequently these patients will be treated with both antibiotics and antiviral agents until culture results become available.

Candidal infections although uncommon can also occur and are promoted by the use of local or systemic antibiotics as is common with resurfacing procedures. Although not infrequently innocuous, Candidal infection has been reported after all three modalities of facial resurfacing and can manifest up to two weeks after the resurfacing procedure.(36,37) . Signs and symptoms typically include redness and itching, significant swelling, increased exudate and crusting, as well as occasionally vesicles or pustules. The most significant manifestation may well be delayed reepithelialization. Since Candida prefers a warm, moist environment, exposing the wound to cool, dry air can help reverse the infection. Topical ketoconazole (Nizoral) or clotrimazole and oral flucanozale (Diflucan) 150-200 mg daily for 5-7 days or ketoconazole are frequently effective in treating these infections. Most often the affected areas will clear without any sequellae over approximately on to two weeks. Acetic acid soaks may be equally as helpful in Candidal infection as they are in treating bacterial overgrowth.

Allergic dermatitis can also occur after peeling or dermabrasion and may be confused with an infection, but typically develops later after the procedure than most infections. Typically dermatitis begins about 7-10 days after the procedure and is associated with intense pruritis that extends beyond the area that was treated along with copious exudate and crusting. Postoperative dermatitis is usually irritative or allergic in nature and can occur in up to 65% of patients.(5) It seems to occur because the newly resurfaced skin does not have a protective epithelial barrier and thus is more vulnerable to irritation. Most patients do not give a history of sensitivity to any particular topical agents and thus offer few clues as to the source of the problem. Choosing products for topical therapy which include few preservatives and also avoiding neomycin which seems to affect a larger number of patients than other topical antibiotics may help reduce the incidence of postoperative dermatitis. Whenever patients present with an inflammatory reaction, they should be questioned about what topical agents they may be applying on their own and urged to discontinue those when appropriate. Treatment for dermatitis with mild topical steroid application and hypoallergenic soaps seems best. At times, oral antihistamines or short courses of steroids may be necessary to control the cutaneous inflammation and decrease risk of fibrosis.

Herpetic Outbreaks

Herpetic infection or reactivation is well-known after chemical peels and can occur after dermabrasion and laser resurfacing, occurring in up to 50% of patients with a known history of herpetic infection if no prophylaxis is given.(38,30,39) More typically herpetic lesions may be seen in 9-10% of all patients undergoing facial resurfacing. It appears that herpes virus elements latent within the trigeminal nerve ganglia are reactivated in some patients who have had either a known or subclinical infections in the past. During the preoperative consultation a detailed history including history of prior viral infections should be obtained. At one time previous HSV infection was a considered to be a contraindication to facial dermabrasion or chemical peel. With the advent of specific antivirals, these patients can now be treated effectively both on a prophylactic basis or if an infection develops. Prophylaxis for herpetic infection remains controversial but many surgeons pretreat all patients undergoing skin resurfacing. The primary concern leading to prophylactic therapy is the possibility of scarring in the areas affected by herpetic outbreaks during the healing process. Many surgeons will begin acyclovir 200-800mg four times daily or valcyclovir 500 mg twice a day one to two days preoperatively.(41) Most continue this for 5-7 days postoperatively up to as long as 10-14 days. McBurney and Gilbert found that a regimen of 500mg of valcyclovir begun one day preoperatively and continued 14 days was 100% effective at preventing herpetic lesions in a series of 84 patients. They prefer valcyclovir (an L-val ester prodrug of acyclovir) because its oral bioavailability is 3-5 times as great as acyclovir. Their choice to treat for 14 days was based on Perkins’ finding of outbreaks as late as day 12..(38) Reported histories of herpetic infection are given by 40-60% of patients but up to 80% will have serologic evidence of prior infection.(39). These results indicate that prophylaxis based on patient recollection may not be a valid approach. Beeson and Rachel compared 10 and 14 days valcyclovir regimens and found that 78% of their patients had IgG antibodies to HSV-1. They also found that 70% of their patients with negative history did in fact have positive serology.(39) They found no difference in outcome with 10 or 14 days treatment regimens.

Herpetic outbreaks typically present four to five days after peels or dermabrasion with intense, unusually severe pain and prominent redness often including superficial skin ulceration. Viral vesicles may not be seen due to the lack of complete reepithelialization and superficial erosions may be the presenting sign.(41) If material is available, Tzank preparations with Wright-Giemsa staining will confirm the diagnosis. Multinucleated giant cells are seen confirming infection with the virus.(39) In patients who have not been undergoing prophylactic antiviral therapy, treatment should be begun immediately with one of the following agents: Acyclovir, valcyclovir or famcyclovir, usually at a dose twice that used for prophylaxis. Cultures can be obtained from the area if possible. Fortunately, although these outbreaks are quite uncomfortable and appear severe, the incidence of scarring or longterm poor cosmetic outcomes is low.

Prolonged or Persistent Erythema

Almost all patients have some degree of erythema after their procedure. Initially the treated skin may be bright red which fairly rapidly fades to light red or pink. The length of time this takes to occur may vary from 7 to 14 days for light and medium-depth peels and up to 4 to 6 weeks for phenol peels. Patients who have undergone light or medium-depth peels usually do not have any significant residual redness after about 3 weeks. After phenol-based peels erythema may still be present up to 6 weeks after treatment. Redness may persist past these intervals without necessarily leading to any longterm problems, but a syndrome of prolonged posttreatment erythema occurring in up to 10% of phenol peel patients, has been reported with multiple causative factors being hypothesized.(42) The patients with this clinical syndrome also reported an increase in itching and burning in the peeled areas as well as some irregularity of skin texture and with a marked prolongation of postoperative erythema. These authors believe that the prolonged erythema represents a heightened inflammatory reaction and that has both intrinsic and extrinsic causes.(42) These may include: sensitivity to the peeling agent, allergic or contact dermatitis and a preexisting clinical disorder such as lupus or rosacea that might predispose to a stronger inflammatory response. Extrinsic factors might include previous skin treatments such as previous peels or topical agents, peeling techniques and use of sensitizing agents such as neomycin or certain cosmetics during the postoperative period. As noted above, the choice of agent frequently determines how long erythema will persist, but genetic predisposition as well as other factors such as sun exposure and alcohol consumptions and preoperative skin preparation may play a role.(35) Some authors report that the incidence of prolonged erythema is higher in patients undergoing laser resurfacing than chemical peels or dermabrasion.(43) Prolonged erythema after laser can be seen more often in patients treated with carbon dioxide laser due to its increased collateral thermal spread. Multiple laser passes, stacking of pulses and aggressive char removal can also contribute to a greater risk of prolonged erythema.

For all of these patients, reassurance is an integral part of their management and education should include discussing the fact that their prolonged erythema represents a heightening of the normal repair process without longterm implications. The application of low potency topical steroids such as 2.5% hydrocortisone or 0.25% hydrocortisone valerate (Westcort) can reduce the inflammatory response improving the skin’s appearance. It is important to maintain good sun protection along with possibly alcohol avoidance to reduce secondary vasodilation and further redness. Noncomedogenic cover preparations such as high quality foundation makeup can also be helpful to reduce their apparent cosmetic deficit. If there are still localized areas of persistent erythema after conservative treatment, these may be a precursor to scarring. Frequently these smaller areas are darker red or even purple in color rather than the more uniform erythema seen immediately after the peel was performed. These localized areas should be treated with Class I steroids topically (Similar to the treatment noted below for early hypertrophic scars). (44) Topical therapy is the best choice at this juncture and steroid injections are usually not required. The higher potency topical steroid ointments such as betamethasone (Diprolene), clobetasol (Temovate) or halobetasol (Ultravate) are all worthwhile choices. They will often produce noticeable benefits within 2 weeks of initiating twice a day applications to the affected areas. Patients should also be cautioned to avoid rubbing or picking at these areas to reduce the possibility of creating a full-thickness injury which will lead to scarring.

Phenol Toxicity

TCA and glycolic acids have no known systemic effects when used as peeling agents, but phenol has possible cardiac, renal, hepatic and neural toxicity. These toxicities have to do with the differences in metabolism between the various peeling agents. TCA and other organic acids are broken down within the skin and typically appear in the bloodstream as bicarbonate ions. Phenol is absorbed unchanged and then 80% is excreted by the kidneys while some is metabolized in the liver.(35) The most common signs of toxicity include an initial stimulation of the CNS with hyperreflexia, tremors and hypertension followed by cardiac arrhythmias, syncope, decreased respiratory function, and rarely coma or death. Phenol is absorbed through the skin and the majority is excreted unchanged by the kidney while some is metabolized in the liver. Patients who are to undergo phenol peels should be screened for preexisting cardiac, renal or liver disease.

All patients who will undergo phenol peels should have cardiac monitoring and have careful attention to their fluid status and hydration. Cardiac arrhythmias are by far the most common untoward occurrence and typically develop during phenol peels when the peeling solution is applied too rapidly resulting in absorption of excess phenol. Arrhythmias have been recorded in 23% of patients when full face phenol peels were completed in 30 minutes or less, due to systemic accumulation of phenol.(145) To avoid this problem each segment (cheeks, forehead, perioral, periorbital and nasal areas) of the face should be treated followed by a 15 minute delay before the next segment is treated. Thus a full-face phenol peel requires approximately one and a half hours to perform and the patient should be monitored for another 60 to 90 minutes. If an arrhythmia or other sign of complications occurs, the procedure is terminated and the patient treated with fluid and lidocaine.(7) Some physicians will resume the peel if the patient remains in sinus rhythm for 15 minutes, but increase the delay between segments to 20-30 minutes.

Hyperpigmentation

Pigmentary changes after facial resurfacing are particularly common with up to a third of patients having at least transient pigmentation changes which most often resolve within a few weeks to a few months.(29) This remains the most common complication occurring after resurfacing procedures and can manifest as blotchy irregular areas of pigmentation or as more homogeneous dyschromia involving the entire treated areas.(43) After resurfacing hyperpigmentation usually appears around 3-4 weeks after the procedure and may last for 2-3 months.(47,52) Postinflammatory hyperpigmentation is particularly common in darker skinned patients. Those with Fitzpatrick types IV-VI are more likely to experience prolonged and potentially permanent hyperpigmentation particularly with deeper peels with less but still significant risk in type III skin.(49) Some authors recommend superficial peels only for those with type V and VI skin and that any more ablative procedures be avoided, while others have found that deeper treatments can be performed safely with aggressive intervention for any postoperative pigmentary changes.(45,46)

The pathogenesis of hyperpigmentation is not clear but the culprit in these patients may be dermal injury producing significant inflammation leading to activation of the dermal melanocytes.(52) Pigmentary abnormalities can also occur in all patients particularly if postoperative instructions to avoid sun exposure are disregarded. Good postoperative skin care and rigorous use of sun screens can prevent many of these patients from suffering this complication. Patients are, in general, advised to avoid sun exposure for 3-6 months after their peel and to use a daily moisturizer with sunscreen at least sun protection factor (SPF) 15 in strength (preferably 30 or higher). Avoidance of oral contraceptives may also be suggested because of the hormonal effect on pigment production particularly in conjunction with UV light exposure. Photosensitizing drugs including certain antibiotics should be avoided during this period as well. If early increase in pigmentation is observed, it can frequently be stopped through application of steroid creams such as 2.5% hydrocortisone or 0.2% hydrocortisone valerate (Westcort) and possibly 4% hydroquinone cream. Fluorinated steroids have more of a tendency to cause skin atrophy, telangiectasias and hypopigmentation and should be avoided in this situation. It may take several weeks or months for mild hyperpigmentation to resolve even with appropriate therapy.

In more advanced cases, Klingman’s mixture can be used: hydroquinone 4%, tretinoin .05% and triamcinolone 0.1% applied twice a day to blotchy areas of hyperpigmentation. This preparation should be used for 8-12 weeks for optimal effectiveness. Hyperpigmented areas can also be repeeled approximately 3-6 months after the initial treatment with resolution of the pigmentary problems. Some have recommended a preoperative regimen incorporating tretinoin, alpha-hydroxy acids and 4% hydroquinone to increase the rate of epithelialization and suppress melanocytes function preoperatively.(53) This preconditioning can be particularly useful in Mediterranean, Fitzpatrick III-IV, skin by weakening the melanocytes ability to produce pigment and significantly reducing the likelihood of postprocedure dyspigmentation. Reported rates of post-inflammatory hyperpigmentation are around 20-30% for Fizpatrick type III skin and nearly 100% for type IV if no preoperative preparation is given.(47) Other studies, however, have failed to show any benefit from this regimen or others incorporating bleaching agents.(48) Use of a pigment-decreasing premedication regimen can help determine which patients tolerate hydroquinones without skin reactions. If postoperative pigmentation develops and the patient is among those who react poorly to hydroquinone, then they can be treated with topical azelaic or kojic acids (beta-hydroxyacids) with good results. Azelaic and kojic acids along with glucosamine inhibit tyrosinase and reduce pigment production. These agents are good choices for patients who cannot tolerate hydroquinone and in cases that are not responding adequately to less aggressive therapy. Topical vitamins C and E can be employed in their capacity of free radical scavengers which reduce inflammation and thereby decrease melanocytes stimulation and responsiveness to UV radiation.(47)

Hypopigmentation

Hypopigmentation is very common after phenol peel and other deeper resurfacing procedures, and should be presented to every patient as part of the expected outcome. Decreased pigmentation arises from deeper injury resulting in damage to the melanocytes and a potentially permanent reduction in pigment production. Phenol is reported to be melanotoxic and thus always produces some degree of skin lightening.(43) Melanocytes are derived from the neural crest embryologically and are lost to some extent with all dermal resurfacing procedures.(49) They do not replicate as well as epithelial cells, through which they migrate to provide pigmentation. Deeper injury into the dermis can damage melanocytes directly while the dermal fibrosis seen in deeper resurfacing adds to the hypopigmented appearance of these patients. In most cases of post-resurfacing hypopigmentation, this develops 4 to 6 weeks after the procedure, correlating with the maturing dermal fibrosis.(49) Fulton et al have proposed a treatment plan consisting of dermabrasion or laser-assisted chemabrasion to reduce the original scar and wound healing under occlusion to allow melanocytes to migrate back into the treated areas and reduce postoperative fibrosis.(49) Use of an occlusive dressing was critical to decrease the inflammatory response allowing faster cell migration and reducing the unwelcome fibrotic reaction. Their postoperative care includes use of Silon-TSR sheeting as an occlusive dressing for 5 days and then application of petrolatum ointment three to four times a day along with use of a gentle skin cleanser such as Cetaphil. After day 10 they recommend use of sunscreen moisturizers during the day and aloe vera/hydrocortisone cream at night. Another option is to use a pulsed topical corticosteroid treatment with clobetasol ointment for 1 week at weeks 6 and 12 postoperatively to prevent formation of dermal fibrosis. Areas of hypopigmentation can also be treated with a combination of topical application of 8-methoxypsoralen twice weekly with concurrent UV light application. 71% of the treated patients had clinical and histologic repigmentation with this regimen.(50)

The most common complaint about hypopigmentation is the line of demarcation between treated and untreated areas. Feathering the margins of treatment into the hairline and just into the area below the jaw can help reduce the cosmetic effect of this demarcation. This is accomplished by applying the peel agent with a semi-dry cotton applicator approximately 0.5 cm beyond the mandibular margin and into the hairline or by treating the borders of the area with lower laser energy levels.. For regional peels such as the lower lids, a semi-dry applicator can be used to apply a small amount of the peeling agent beyond the orbital rim. Patients who have undergone deep treatment may need to wear makeup to camouflage the demarcation between treated and untreated areas. Some surgeons recommend the use of single-pass CO2 laser in the neck to decrease the obvious demarcation at the margins of the peel.(51) In many cases hypopigmentation may improve with time. Patients can use make-up camouflage and occasionally cosmetic tattoing can be employed.(41)

Scarring

Scarring represents for most physicians and their patients, the worst complication of chemical peels and other resurfacing procedures, although luckily quite uncommon. The areas around the mandible and over the bony prominences of the malar area as well as the perioral areas are most commonly affected. Certain categories of patients are at higher than normal risk for scarring even with properly applied peels or dermabrasion. These include: those with a history of poor healing or keloid formation, those undergoing deep peels, patients having repeated peels without adequate time for full healing in between peels, those who have previously been treated with isotretinoin (Accutane), and those who develop an infection following their resurfacing procedure.(25) The most significant factors relating to potential for scarring remains the depth of injury achieved and the number and density of skin adnexae. Particularly if injury goes deeper than the midreticular dermis the risk of scarring increases. Superficial peels that do not penetrate beyond the papillary dermis are not associated with scarring nor is microdermabrasion. Lower concentration (10-35%) TCA and other superficial and medium-depth peeling agents rarely cause scarring because their depth of penetration (usually within the papillary dermis and not deeper than the superficial reticular dermis) does not foster scar formation to as great a degree as those producing injury to the mid-reticular or deep reticular dermis.(54) Scars can be fostered by factors promoting deeper penetration of the peel solution: use of phenol-based formulae (Baker’s solution which penetrates to the midreticular dermis), differences in skin preparation and postoperative care, occlusive taping, too-frequent applications of more superficial peeling agents and differences in technique, including overaggressive applications of peeling solutions, use of the dermabrader or laser.

Some surgeons use the appearance of the skin during chemical peels as a guide to the depth of penetration. Although not universally accurate, it can serve as a guide and a warning when the appearance changes to one indicating a deeper injury than appropriate. For example, diffuse erythema with small and scattered punctate whitish frosting indicates an epidermal injury, while light white frosting evenly over the treated area indicates injury to the epidermal/dermal junction. Dense pure white frosting shows a typical medium-depth peel into the papillary/reticular dermal junction. A grayish or yellowish frost can show injury to the deeper reticular dermis and delayed healing with a higher risk of scarring can be anticipated.(8) Scarring can also arise in the setting of excessive inflammation such as in keloid formation. Preoperative use of Accutane has been associated for years with a very high risk of postoperative scarring due to reduction in skin adnexal appendages and resultant problems with reepithelialization potential. As the use of this agent has decreased, the likelihood of this complication seems to be becoming more remote. For patients who have used Accutane in the past, a waiting period of at least 12 months before chemical peel or dermabrasion procedures seems prudent, which allows time for regrowth of epithelial appendages.(55) 50% TCA or higher concentrations is associated with deeper penetration and a particular increase in risk of scarring.(53,56) Excess thermal injury from carbon dioxide laser resurfacing can cause hypertrophic scarring in a small percentage of patients (usually less than 1% which also approximates the risk after a deep chemical peel). This is most often due to excessive energy setting, overlapping of pulses to too many passes in the same area.(58)

Dessication with superficial cell death can lead to a deeper than expected injury as can picking or denuding areas that have some superficial crusting. Pruritis after peel or dermabrasion can cause intense itching leading to excoriation of the treated area and increased chance of scarring. Several different forms of scarring can occur after chemical peel or dermabrasion. Hypopigmented, flat scars with a shiny surface and no induration are possible as are atrophic, depressed scars with sharply defined edges. Some patients will develop thickened and elevated scars with at least some persistent erythema, but these rarely become true keloids. This last category can most vividly develop features of truly hypertrophic, cosmetically unpleasant scarring

A special instance of scarring is lower eyelid retraction and scleral show. Preoperative evaluation includes assessment of lid tension or laxity and the amount of preoperative scleral show should be recorded. In most cases skin resurfacing can be delayed until three months after any procedures involving a skin flap such as traditional lower eyelid blepharoplasty. Simultaneous resurfacing and transconjunctival blepharoplasty is a safe approach and can produce excellent results. (60) Prevention of ectropion includes using less concentrated or semi-dry applicators for lower lid peeling or lower fluences for resurfacing. If some retraction begins to develop after resurfacing, massage, eyelid taping and topical or intralesional steroids all play a role in reducing the problem. Mild postoperative scleral show usually resolves spontaneously. Combined procedures incorporating elevation of a skin or skin-muscle flap and resurfacing (especially chemical peels) have been discouraged in the past because of concerns about blood supply and flap survival.(61) Koch and Perkins reviewed 30 patients who underwent simultaneous facelift and full-face carbon dioxide laser resurfacing and also performed a meta-analysis of over 450 similar patients previously reported. In their own series they found no instances of flap necrosis or other complications, no hypopigmentation, nor infection. Complications reported in their meta-analysis of other studies did not exceed those normally associated with rhytidectomy alone.(61)

The earliest signs of scarring are often persistent erythema and delayed healing. When this occurs the affected areas should be treated with nonfluorinated steroid creams and mechanical debridement such as over-aggressive cleaning should be stopped. If a scar forms massage and compression can help reduce the collagen deposition and cross-linking. Most often this will resolve early scars without progressing to need for intralesional steroids. but steroid-impregnated tape (Cordran) can be used when needed.

Once overt scarring begins to develop aggressive intervention is indicated, since early still-developing scars area easier to manage than fully mature ones will be later on. If persistent erythema does not resolve with less aggressive treatment, this may herald the beginning of scar formation, and a higher potency Class I steroid cream such as 0.5% clobetasol (Temovate) or Diprolene should be applied twice daily. If followed for more than two weeks, this regimen may lead to some skin atrophy and telangiectasia formation, but these side effects may be more desirable than the development of significant scarring. Usually incipient scars will respond quickly, often in a week or less, but if induration is significant, up to three or four weeks may elapse before the problem completely resolves. For this reason a trade-off between side effects of the steroid cream and the future cosmetic outcome may need to be balanced. Telangiectasias can be treated with laser therapy and any atrophy should respond to tretinoin (Retin-A) or AHA therapy. Steroid-impregnated (Cordran) tape can also be applied as can topical silicone gel, which often works better on the face than silicone sheeting. At times scars will not respond to topical therapy and will need to be treated with intralesional steroids such as triamcinolone (Kenalog) 10% at 4 week intervals. Higher concentrations up to 40% may be needed in some cases. Treatment with the 585 nm pulse dye and/or 1320 nm holmium-YAG lasers also has a role in improving this problem. Laser treatments can reduce redness and soften the scar tissue while reducing scar bulk and improving texture.(13) Laser treatments can be done every 6-8 weeks as needed and are done with similar settings as for cutaneous vascular lesions (e.g. 4-5 J/cm2 with a 10 mm spot size). After two to four treatments, a roughly 50% improvement in scar appearance can be expected.(59,24) If atrophic scarring occurs then use of soft tissue fillers such as collagen or Restylane can sometimes reduce the soft tissue deficit.

Skin Atrophy or Skin Texture Change

Depending on the depth of injury and the process of healing, certain changes in skin quality or texture may become apparent after chemical peel or dermabrasion. Pore size may change and nevi may darken. Small telangiectasias can also develop or increase in number. Laser ablation remains the best treatment for these vascular lesions.

Milia and Acne

Milia which appear as small whiteheads are tiny epidermal inclusion cysts that occur more commonly after dermabrasion than chemical peeling or laser therapy but still occur in up to 15% of patients.(62) They are usually self-limited and clear with facial hygiene. Alternatively they can be unroofed with an 18-gauge needle in the office if they persist. Pretreatment with tretinoin for 2-3 weeks before the peel or dermabrasion and then resuming application after epithelialization is complete, decreases formation of these lesions. Acne eruptions may occur after peeling occurs in up to 80% of resurfacing patients in some series.(62) Acne flare-ups can be treated in a routine fashion after the skin irritation from the peel resolves: topical cleaning and other topical therapies including topical clindamycin or erythromycin.(35) Oral antibiotics such as minocycline can be begun as soon as eruptions appear without having to wait for full healing to occur.

Unusual Reactions

A case of airway obstruction related to an AHA peel has been reported.(63) No obvious mechanism of injury was obvious in this patient although it appeared to be a direct result of deeper than expected burns from a citric acid peel. Clearly if patients become tachypneic or have difficulty breathing