Laser Management of Festoons

Key Points

•Correcting lower eyelid festoons adds greatly to overall rejuvenation of the lower eyelid–cheek complex.

•Traditional incisional techniques to correct festoons are often time intensive and yield suboptimal results.

•Festoons have been reported to result from damage to the skin, and potentially to oppositional underlying muscular forces in the tissue deep to the festoons. Our experience and results have substantiated the skin as a primary etiologic factor.

•Both CO2 and certain Er:Yag lasers can be used to treat lower eyelid skin folds and festoons effectively.

•It is important to distinguish between the relatively thin skin above the orbital rim and the relatively thick skin below the orbital rim when treating festoons with laser skin resurfacing.

•The lower eyelid skin should be treated more conservatively above the orbital rim and more aggressively below the rim.

•The end point for laser treatment of lower eyelid festoons is no further tissue shrinkage with the last laser application.

•It is important to create a transition zone with lighter laser ablations around the border of the more aggressively treated skin to avoid creating a demarcation line from the treated region to the untreated surrounding skin.

•Application of laser safety principles is critical when using lasers to improve festoons.

•Knowledge of postoperative laser skin healing care and possible complications is critical to the clinical and aesthetic outcome.

S.S. Baker (*)

Assistant Clinical Professor, Departments of Ophthalmology and Dermatology, University of Oklahoma College of Medicine, Oklahoma City, OK, USA

e-mail: sbaker@baker-holloman.com

19.1Introduction

Skin folds that may occur at the junction of the lower eyelid and cheek are known as festoons [1]. They are a difficult finding to treat in rejuvenation of the lower eyelid–cheek complex. While skin excision, muscle plication, canthal suspension, and judicious removal or translocation of orbital fat can improve the contour of the lower lid and midface, the quality of the overlying skin can often dramatically affect the final cosmetic outcome.

Clinically, festoons appear in the inferior area of the lower eyelid where the thin eyelid skin transitions into the thicker facial skin of the cheek. While festoons are often seen with prolapsed orbital fat, their distinguishing feature is redundant or ballotable skin caudal to this area of transition. Festoons can vary in severity from localized folds of skin in the inferior lower lid to protuberances on the cheek (Fig. 19.1). Furnas and others have suggested that laxity in the orbicularis oculi muscle of the lower eyelids is implicated as an etiology based largely on their intraoperative observations. This explanation seems counter-intuitive when considering the movement of the muscle itself.

The facial muscles of the lower eyelid and cheek are the orbicularis oculi muscles above and the upper lip elevators below. The skin and subcuticular tissues in this region are secured to deep structures by orbitomalar retaining ligaments which were demonstrated in convincing microscopic detail by Kikkawa et al. [2]. In their paper, Mendelson et al. [3] further expanded the anatomic definition of this area by describing a prezygomatic area bounded by the lower eyelid above, the lower temple superolaterally, the cheek laterally, and the infrazygomatic cheek below. Their cadaver studies led them to conclude that the zygomatico-cutaneous ligaments at the inferior border of the area are stronger than the orbicularis retaining ligaments at the superior border of this region. On the basis of these observations, we can surmise that festoons may form as a consequence of this comparative

weakness in the superior orbicularis retaining ligament, allowing the overlying lax skin to slide caudally over the relatively stronger support of the zygomatico-cutaneous ligament.

Festoons are predominantly found as a condition of aging. However, other factors such as solar elastosis, tobacco abuse, or other environmental factors contribute to skin laxity and festoon formation. Another possible explanation may be muscular in origin. Festoons tend to occur at the level of the junction of the orbital orbicularis oculi muscle, which contracts in a horizontal direction, and the upper lip elevators, which contract in a vertical direction. These two muscle groups act at approximate right angles to each other, which could damage intrinsic skin elasticity as well as stretch the deeper retaining ligaments.

Festoons may occur as a familial trait and can be exacerbated by allergies. Goldberg et al. [4] proposed that loss of skin elasticity in the malar eminence leads to festoon formation. While festoons are most often cosmetic concerns, they can rarely be significant enough to produce functional defects by compromising the inferior visual field. Esmaeli et al. described such a case of lower lid festoons, which occurred during treatment of chronic myelogenous leukemia [5].

Medical treatment of festoons with oral diuretics or steroid injections may produce minimal improvement, which is usually transient. Superficial skin procedures such as chemical peels can improve rhytids but are largely ineffective for festoons. Surgical treatment by creating large lower lid skin or skin muscle flaps has been described as being effective [1]. These flaps involve relatively extensive dissections that risk iatrogenic ectropion formation. In addition, they are often suboptimal in their results. Another surgical alternative is the direct resection of the festoon itself, but this surgery is seldom used because it has the potential to

create a visible scar on the midface [6]. Laser resurfacing is a relatively simple and effective alternative to these surgical flaps. One of us (SSB) initially presented and published the technique in the mid 1990 [7].

19.2Laser Tissue Interactions

Patel developed the CO2 laser [8], which emits at 10,600 nm. The concept of selective photothermolysis explains the tissue effect produced by lasers [9]. The chromophore or target in tissue for both the CO2 and Er:Yag lasers [9, 10] is water. Early incisional applications of the CO2 laser were developed chiefly by gynecologists and otolaryngologists. In 1984, the first extensive periorbital CO2 laser application was reported in as a series of blepharoplasties [11]. In1988, laser techniques were developed for tranconjunctival lower lid blepharoplasty [12]. In 1985, initial laser resurfacing techniques for facial lesions were reported for the treatment of actinic cheilitis [13]. Further uses of topical laser therapy were developed as resurfacing applications to treat periorbital facial rhytides [14]. Newer, pulsed, and high energy CO2 and Er:Yag lasers (emitting at 2,940 nm) have extended precision and predictability to laser skin resurfacing of the face by producing dermal changes in a controlled fashion [10, 15–21].

CO2 and Er:Yag lasers produce skin changes by vaporizing water in the skin. Skin, which is damaged to less than full thickness, will heal by forming new elastin and new more tightly cross-linked collagen. In their clinical applications, these lasers differ in their coefficient of absorption with the Er:Yag being more efficiently absorbed by water than the CO2 laser. Vaporization of water in the skin requires a fluence of 4.5–5.0 J/cm2 at the wavelength emitted by the CO2 laser while ablation from the Er:Yag laser requires

approximately 1.0 J/cm2. In terms of clinical relevancy, this means that more of a given ablative pulse of CO2 energy remains at the site of application in the form of sub-ablative thermal energy than an equivalent pulse of energy emitted by an Er:Yag laser. The duration of the laser pulse also determines how much thermal energy is conducted to adjacent tissue from the site of application. The thermal relaxation time of skin is about 800 ms. If ablation occurs in less than that time interval, most of the thermal energy produced during vaporization will not be conducted to adjacent tissue. The most reliable way to achieve that objective is to deliver the laser energy in the form of an ablative pulse of less duration than the thermal relaxation time of skin. The Er:Yag laser energy is emitted from a doped crystal, which is limited by its design to a pulsed emission of about 250 ms. CO2 lasers are gas lasers which emit in a continuous fashion. To generate time limited exposure to tissue, CO2 lasers must be rapidly swept across the target tissue or gated in some fashion to be effective at limiting thermal damage. Even in the limited exposure mode though, they still impart a moderate amount of thermal damage to the tissue adjacent to the wound because of their relatively less efficient coefficient of absorption. This factor can be used to the practitioner’s advantage in achieving festoon reduction. The same clinical result can be achieved from the Er:Yag laser by combining two pulses in rapid succession. The first pulse emits at a fluence higher than the ablative threshold while the second pulse emits at a sub-ablative fluence. This second pulse imparts thermal energy in a tunable fashion [10, 19–27].

Residual thermal energy at the site of the laser application accomplishes two objectives. First, bleeding from superficial vessels in the upper dermis is controlled by the cautery effect of that residual thermal energy. This control is necessary because the water in blood on the surface of the treated skin becomes the chromophore for successive passes of the laser, thereby limiting the effect of the laser to the surface of the target tissue. Second, thermal energy in skin produces relatively deep collagen fiber devitalization, and most importantly collagen contraction [22]. This becomes the framework for the new collagen formation in the healing skin.

areas of the face to be treated with the laser should be confirmed, and patients should be educated about the course and importance of their postoperative care.

Patients are informed of the traditional indications for laser skin resurfacing including improvement of sun damaged skin, including actinic keratoses and seborrheic keratoses; facial rhytids; dyschromia; and scar revision. They are then told how the laser can also be used to reduce, or eliminate, the prominence of their festoons.

Any suspicious skin lesions must be biopsied and treated appropriately before undergoing treatment with the laser. If either a frank or latent ectropion is noted on exam, plans should be made to correct that condition at the time of surgery. Patients should be shown photos of the actual daily healing progress of previous patients. This can be helpful in preparing the patient for what can be a challenging postoperative recovery.

The patient should be educated on all the possible complications and their treatment.

Photography of the treatment areas is critical and can be valuable in discussing the patient’s expectations. The goal is to improve facial rhytids and festoons. It is not appropriate to guarantee that these conditions can be fully resolved. The strategy of under promising and over delivering can serve the practitioner well.

Medical and dermatologic histories should be obtained. The pigmentation skin type should be noted. Fitzpatrick Class III skin types or darker have an increased risk of pigmentation change after the procedure. The healing of the skin after laser skin resurfacing depends on the density of the pilosebaceous appendages in the treatment area. Any factors which may affect the pilosebaceous glands such as previous facial radiation or use of oral retinoids for 1 year prior can put the patient at risk for poor healing after laser treatment. Active acne should be treated prior to resurfacing. Tobacco use can delay healing and should be avoided. Any interruption in healing can result in scarring. Other contraindications include active skin infections, vitiligo, pregnancy, and a history of keloids or hypertrophic scars.

Anti-virals should be started one day preoperatively and continued until full re-epithelialization occurs. Medications given before laser skin resurfacing to reduce the incidence of hyperpigmentation include topical retinoids and hydroqui-

Selection

Laser skin resurfacing is an excellent treatment option for festoons. However, it is an elective procedure requiring an interval of time for healing, with potential postoperative morbidity. As such, it is important to evaluate patients thoroughly and confirm that they have realistic expectations, and understand potential complications about the procedure. The

restarted after full re-epithelialization has been achieved. Patients should expect relatively long healing times (typically about 14–16 days to re-epithelialization) and persistent postoperative erythema when treating to the depth necessary to reduce festoons. Preoperative consultation with informed consent reviewing potential complications is crucial to the examination process. All potential anesthesia-related complications should be discussed as well.

19.4Treatment Protocols

Anesthesia is typically achieved with a mixture of 2% lidocaine with 1:100,000 epinephrine (AstraZeneca, LP) mixed in a 1:1 ratio with 0.75% bupivacaine (Hospira, Inc.). Two to four milliliters of this mixture is injected as a bolus transorally to block the infraorbital nerve. An additional 1–2 mL boluses are injected transcutaneously at the lateral orbital rim to block the zygomaticotemporal and the zygomaticofacial nerves. The patient is prepped with non-flammable solutions and draped with non-flammable drapes. Standard laser safety protocol is observed. Laser safe eye shields are placed to protect the eyes during the application of the laser.

When resurfacing the lower lid, it is useful to divide this area into two zones roughly demarcated by the inferior orbital rim. The upper zone (lid margin to orbital rim) includes the thin eyelid skin, which has relatively sparse subcutaneous tissue between the deep dermis and the orbicularis muscle. There is a risk of producing a cicatricial ectropion from overly aggressive treatment in this region. Therefore, resurfacing should be performed conservatively in this upper zone.

The second treatment zone extends from the inferior orbital rim caudally to the junction of the lid skin with the cheek skin overlying the malar eminence. Festoons lie within this lower zone. This lower zone is treated aggressively with multiple passes of ablative laser energy. For example, when using the Sciton Contour Er:Yag laser (Sciton, Inc.), multiple passes are made at an ablative fluence of 10–15 J/cm2 with 50–100 mm of nonablative coagulation. Table 19.1 shows representative laser settings for a few common lasers in use today. Between passes, the desiccated tissue residue can be removed by gentle debridement using saline soaked gauze.

However, mechanical removal of this residue is not a necessary component to achieve festoon resolution. Typically, the first two passes of laser ablation remove epidermis and most of the papillary dermis. These passes also substantially alter the water content of the remaining dermis. Subsequent passes do not produce much additional desiccated tissue debris but do continue to produce shrinkage of the residual reticular dermis. The laser passes are continued over the area of the festoon until the last application of laser energy no longer produces visible shrinkage of the festoon. The total number of passes typically ranges from seven to 10. The margins adjacent to the main treatment area should be lasered in a “feathering” fashion with declining fluences to avoid demarcation lines by blending the treated area with the untreated area.

Postoperative wound care is a critical factor in achieving the clinical results from this procedure. Many approaches to treating a second degree burn, which characterizes this postoperative wound, have been reported. Our preferred approach includes an oral antiviral medication (e.g., Valtrex®, GlaxoSmithKline) (500 mg po BID) to prevent the herpes simplex virus from interfering with wound healing. This is begun the day before and continued throughout the postoperative healing regimen. Immediately following the procedure, bioocclusive topical wound dressings (e.g., Flexzan®, Advanced Medical Solutions Limited) are applied for 1–3 days. During this time, the areas of treated skin not covered by the bioocclusive dressing are coated with a topical lubricant (e.g., Aquaphor®, Beiersdorf Inc.) (Figs. 19.2 and 19.3).

The Flexzan® bandages are removed by gentle soaking during a shower on the second post op day (Fig. 19.4).

The patient is followed closely with multiple postoperative clinic visits in order to help guide patient compliance with the healing regimen and observe for signs of compli-

cations. The healing regimen includes soaking the skin with a dilute solution of acetic acid (e.g., vinegar water) at the concentration of 1 teaspoon – 1 tablespoon per cup of water. Clean cloths are soaked in this solution and applied sopping wet to the healing skin for a half hour per application. The cloth can be resaturated during this half hour soak. The acetic acid facilitates the debridement of the thermally devitalized tissue and creates an acidic environment. The acidic washes reduce the growth of bacterial and fungal elements, which is why antibiotics or antifungals are rarely needed during the healing process. After soaking, the skin is coated with a topical lubricant (e.g., Aquaphor®) to prevent tissue desiccation and encourage epidermal healing until the next vinegar water application. These

cycles of vinegar water soaks followed by the application of healing ointments are constant throughout the healing process. The patient is encouraged to do the vinegar soaks 6–10 times per day. The authors tend to see the patient every 2–4 days until the skin is fully epithelialized (Figs. 19.5–19.10).

This frequency of follow-up allows observation of the wounds and early detection of wound healing problems. If herpes simplex virus is suspected to be interfering with wound healing, the dose of the antiviral can be increased to fight such an infection. Likewise, if bacterial or fungal infections are suspected, appropriate medications should be used. The treated area re-epithelializes generally in 14–16 days. Once the target area has fully epithelialized, the frequency of post