Introduction

The rising interest in cosmetic surgery among the general population is so widespread that cosmetic procedures, surgical, and non-invasive, have essentially entered the popular lexicon. With the purification of bovine collagen and its subsequent clearance for marketing by the US Food and Drug Administration (FDA), soft-tissue filling first became practical in the 1980s. As minimally invasive cosmetic procedures grew from an occasional medical novelty, the purview of the rich and famous, their use became widespread in the 1990s, eventually to a commonly sought means of cosmetic enhancement for millions of people. In 1992 the American Society of Plastic Surgeons reported 41 623 collagen injections, the only type of exogenous filler generally available in the USA. In 2006, 388 316 injections were reported by its members and their use had been accepted in mainstream culture. If data on botulinum toxin is included, the numbers go beyond 1 million per year.

The choice of the appropriate filler, however, has become increasingly difficult. With the ever-expanding number of fillers and filler types, the surgeon must, not only maintain an adequate knowledge of the physiochemical properties of the filler types, but also must understand the differences in injection levels and techniques for each of the fillers. A thorough aesthetic evaluation of the patient as well as a complete discussion of the patient’s aesthetic goals and treatment preferences must be performed in order to achieve a treatment plan that is safe and realistic.

Soft Tissue Loss in the Aging Patient

Some of the features that a youthful face exhibits include smooth contours, few wrinkles, except in dynamic expression, and full subcutaneous tissues with minimal or no soft-tissue atrophy (Fig. 3.1). Nasolabial, glabellar and crow’s feet skin folds are almost uniformly absent at rest, and minimally noticeable, even with muscular contraction. During aging of the normal, healthy adult, there is loss of soft-tissue fullness in the face, often beginning in the nasolabial folds and progressing inferiorly along the marionette lines. Lines in the upper face may show years earlier during dynamic expression than at rest. Lipoatrophy can distress the aging patient with resultant low self-image and self-esteem, depression and social isolation.^1,2 With the severe rise in obesity in recent years, loss of facial fat due to aging may be partially offset due to fatty accumulation after weight gain.

Fig. 3.1 Location of rhytids in the aging face.

In the normal aging face there is gravitational pull on sagging skin, flattening of the youthful contours, accompanied by solar degeneration, variation in pigmentation, an increase in rhytids, capillary break-down, loss of muscle tonicity and progressive thinning of the skin and subcutaneous tissues (Figs 3.2 and 3.3). One of the hallmarks of aging skin – and one for which we have essentially no topical or minimally invasive corrective solution – is poor elasticity, breakdown of elastic fibers and excess skin envelope. In essence, with an imbalance of soft tissue volume to skin envelope, there are three basic approaches: 1) fill up the lost tissue volume, 2) chemically peel, laser, or mechanical dermabrade or excise the excess skin, or 3) live with the difference. Because few patients have one isolated contributing factor, the ideal approach would often include volume restoration and treating the skin. However, many patients do not desire more aggressive treatment. Chemical peels and lasers chemically denude the superficial layers of the skin, but do not reduce the surface area of the skin sufficiently to balance the loss of soft tissue volume in any but the mildest conditions in the youngest patients. While they tighten the skin, in essence by cross-linking collagen and other proteins, they do not restore the elasticity of youth.

Fig. 3.2 The aging face: presence of rhytids and soft tissue descent.

Fig. 3.3 Architecture of rhytids.

Soft Tissue Loss in Disease Conditions

While less common, certain disease conditions cause premature loss of soft-tissue volume; some are genetic and some acquired. Congenital generalized lipodystrophy (autosomally recessive) results in lack of adipose tissue from birth. Familial partial lipodystrophy (autosomally dominant) causes progressive peripheral fat loss beginning at puberty and, typically, the facial fatty tissue will stay the same, or rarely gain fat, while the body atrophies. Mandibulosacral dysplasia (autosomally recessive) shows two forms: type A demonstrates peripheral fat loss with normal or excess facial fat, while type B shows generalized fat loss. Partial lipodystrophy (autoimmune mediated) presents during childhood or adolescence and the upper body, including the face, presents with fat loss. Excess fat is found in the legs and hips. Generalized lipodystrophy (immune mediated) presents during childhood or adolescence and shows generalized fat loss, including the face.

Acquired lipodystrophies arise from multiple mechanisms, but more commonly small localized areas of fat loss may occur from drug injections, local trauma or crush injuries, immune-mediated mechanisms, cancer or HIV, the most prevalent form. Highly active antiretroviral therapy (HAART) is associated with the condition, but its actual mechanism is unknown. There appears to be some interaction with protease inhibitors and nucleoside reverse transcriptase inhibitors. The HIV patient shows rapid loss of peripheral fat and fat in the face, occurring within 1 year of treatment.³ Fat paradoxically accumulates in the abdomen, breast and dorsocervical spine. In the face, the buccal and temporal fat pads are most locally affected; however, there is loss of fat diffusely in the face. Fat loss may be rapid and progressive and is often permanent, refractory to steroid administration and dietary intervention. The prevalence has been reported as variable (18-83%) due to differing definitions.⁴ Lipoatrophy in HIV patients can lead to compliance issues, reducing the effect of HAART and accelerating disease progression, fear of stigmatization and recognition.^5,6

Indications

Skin lines, wrinkles and folds

By far the most frequently injected area, the nasolabial fold (NL), may be best evaluated by the standardized Lemperle scale of severity (Fig. 3.4). Natural folds in the face are created by attachment of the facial muscles to the undersurface of the skin. No comparable scale is widely used in the marionette lines, the crow’s feet and/or other skin folds of the face. However, an appropriate approach would be to use the commonly accepted Lemperle scale. The NL fold may begin to appear in the early 20s and progresses with aging. While this scale is primarily focused on skin wrinkling, soft tissue loss is a contributing factor as well.

Fig. 3.4 Lemperle scale of nasolabial fold severity. A, Grade 0 contains no wrinkles or lines, but may show some minimal contour depression. B, Grade 1 shows just perceptible wrinkles. C, Grade 2 shows shallow wrinkles. D, Grade 3 shows moderately deep wrinkles. E, Grade 4 shows deep wrinkles with well-defined edges. F, Grade 5 shows very deep wrinkles with a redundant fold.

Facial lipoatrophy scale

A four-point grading system is commonly used to measure facial lipoatrophy (Fig. 3.5). Grade 1 is characterized by small localized areas of fat loss, especially in the nasolabial folds. Grade 2 includes mentolabial folds (marionette lines) and may include concavity of the lips. Grade 3 progresses to malar fat atrophy, preauricular hollowing and shadowing of the cheeks and mandibular ridge, while Grade 4 demonstrates malar fat ptosis, temporal hollowing and protruding musculature and bones.

Fig. 3.5 Facial lipoatrophy scale. A, Grade 1 facial lipoatrophy. B, Grade 2 facial lipoatrophy. C, Grade 3 facial lipoatrophy. D, Grade 4 facial lipoatrophy.

(Photos courtesy of Ute Bauer, MD, 2004.)

Contraindications

While there are many contraindications to surgical interventions, there are very few for injectables. This, along with their relatively low incidence of complications, is the factor contributing to their wide popularity. They are very easy to inject, but much more difficult to inject well. Careful attention to topical and deep anatomic detail is essential to avoid distortion of facial anatomy, lumps and nodules. In addition, even in patients with an undesirable outcome, effects rarely last longer than the prospective duration of the injection. This ranges from about 3 months with collagen to about 2 years for calcium hydroxyapatite, but may be permanent with polymethylmethacrylate synthetics. Patients with mild connective tissue diseases may be eligible for injection after a careful history and physical exam, but should be considered a relative contraindication. Active acne, psoriasis or eczema warrant withholding the procedure. A patient who has an apparent large softtissue volume loss may be corrected partially, but almost never should be fully corrected, as a significant portion of the defect may also be due to ptosis of soft tissues. To the extent the soft tissues have fallen they should be lifted; to the extent the soft tissues have atrophied, the volume should be restored.

Preoperative History and Considerations

Injectable Fillers

We have truly entered the ‘filler revolution’ and the number of new fillers on the market is constantly increasing.⁸ The first injectable filler that was approved by the FDA was bovine collagen (Zyderm/Zyplast; Inamed Aesthetics, Santa Barbara, CA). The need for skin testing and its lack of longevity were key issues hindering its widespread use.⁹ Since this time, many classes of fillers have been approved by the FDA, with more likely in the future. Listed in this section is a brief description of each of the major injectable fillers currently being utilized in the USA.