Facelift surgery or rhytidectomy, browlifts, and midface lifts are performed in an effort to redrape and suspend facial soft tissues to gain a more youthful appearance to the face. Facial aging has traditionally been attributed to the force of gravity causing soft tissue ptosis of the face as patient ages. The actual causes of facial aging are incompletely understood at this time, but the pathogenesis of the aging face continues to be a fascinating, hotly debated topic among physicians. In general, facial aging tends to occur in three dimensions and involves all tissue components of the face: skin, muscle and soft tissue, facial fat pads, and the bony facial skeleton.
Facial aging can be thought of occurring from superficial to deep, and tends to begin in the late twenties and thirties in the skin. Photodamage is defined as the functional and structural damage that occurs to skin after chronic exposure to ultraviolet radiation from the sun. The structural changes involve gradual thinning of the epidermis, flattening of the epidermal-dermal border, loss of collagen and thickness in the dermis, decrease in collagen Type I to Type III ratio, and reduction in the skin cellular and protein components. Lax skin with decreased collagen manifests through sagging and increased propensity to be wrinkled and furrowed.
Deeper into the facial soft tissues, muscle laxity and atrophy, as well as bony remodeling and resorption can potentiate the loss of facial, mandibular, and neck definition. These anatomic changes manifest clinically as brow ptosis, deepening of the nasolabial fold, jowling, blunting of the cervicomental angle, and platysmal banding (Figure 73–1). These features of the aging face are particularly amenable to correction with a rhytidectomy, platysmaplasty, midface lift, and/or browlift.
Characteristics features of facial aging: (a)—brow ptosis, (b)—descent of the midface, (c)—nasolabial fold, (d)—excessive jowling, (e)—Marionette line, (f)—prejowl sulcus, and (g)—platysmal banding
However, there are limitations to these surgical procedures. The surgeon must know that there are options to deal with aspects of the aging face for which a facelift or a browlift is not as effective. Although photodamage from the sun or tanning beds can increase the process of skin thinning, it causes fine skin wrinkling which may be more amenable to a skin treatment such as laser resurfacing or a chemical peel. Also, there is a gradual volume loss in the face which occurs over the time from change in facial fat pads and bony remodeling of the facial skeleton. Fat pads in the temporal and malar area lose volume, and the malar fat pad descends. Although a facelift may elevate the malar fat pad, additional augmentation of facial volume may be necessary with injections of autologous fat, fillers, or even implants.
The key to understanding facelift surgery is understanding the anatomy of the superficial muscular aponeurotic system (SMAS) (Figure 73–2). The SMAS is a fibromuscular fascial layer that invests and interlinks the muscles of facial expression. It maintains consistent relationships with the vessels and nerves. The SMAS is contiguous with the platysma inferiorly and the temporoparietal fascia superiorly. In the temporal region, the frontal branch and the superficial temporal artery pierce this layer and become superficial. Inferior to this, the nerves and vessels are all deep to the SMAS, with motor innervations coming from the undersurface. Around the eye, the SMAS interdigitates with the orbicularis oculi. Medially, it has attachments to the zygomaticus major and minor as well as the dermis of the upper lip. The SMAS also has fascial condensations which are adherent to the overlying dermis and underlying muscle and bone. While not true ligaments, they are termed as such and act as support for the soft tissues of the cheek. The major osseocutaneous ligaments include the zygomatic ligament (McGregor's patch) and mandibular ligament and the fascia–fascia retaining ligaments include the parotid and masseteric ligaments.
The superficial musculoaponeurotic system is a distinct layer between the parotid gland, skin, and subcutaneous fat.
The platysma is innervated by the cervical branch of the facial nerve, a branch deep to platysma, and assists the depressor anguli oris in depressing the lower lip. As mentioned previously, the SMAS and platysma are contiguous; however, the location of the superior extent of the platysma is controversial and can be found up to 4 cm above the mandibular line and 3 cm below the malar eminence.
Medially, at the level of the thyroid cartilage, the platysma fibers interdigitate forming an inverted “V.” The apex can be at the level of the chin, or slightly below at the level of the thyroid cartilage. Because of this, the submental area may or may not be covered by the muscle fibers. If there is laxity or dehiscence of the anterior borders of the muscle, it creates banding in the midline, which occurs with age. Patients may then also have a chin droop, as the submental area lacks tissue. Laxity of the platysma can lead to “turkey gobbler” deformity and a more obtuse cervicomental angle. Flaccidity of superolateral fibers of the platysma muscle may be a contributing factor to chin droop and submental laxity.
The facial nerve exits the stylomastoid foramen and courses through the parotid gland. It branches into five branches: temporal (or frontal), zygomatic, buccal, (marginal) mandibular, and cervical rami. (Figure 73–3) within the parotid gland, the main trunk usually divides a superior (temporofacial) and inferior (cervicofacial) branches. From there, the branching pattern becomes variable. There is frequent anastamosis between the zygomatic and buccal branches. After exiting the parotid gland in the face, the nerve ...