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Breast enlargement by autologous fat transfer (AFT) makes sense. We have all had patients who asked us: “Doctor, why can’t you take from there and put it here?” The procedure was attempted more than a century ago, but it was the introduction of liposuction in the early 1980s that made it practical. Bircoll, in 1984, reported his experience with autologous fat graft obtained using liposuction for breast augmentation. Unfortunately, his results were underwhelming, and the complications overwhelming. The xeromammograms of the time had difficulty discerning cancer calcifications from fat necrosis, and many unfortunate patients were permanently scarred from open biopsies. This led to an outburst of letters to the journal condemning the procedure and to the American Society of Plastic and Reconstructive Surgeons to issue a position statement in 1987 banning the procedure. For nearly two decades, the undisputed dogma remained, “no fat grafting to the breast”. It does not work, and it leads to dangerous calcifications and nodules indistinguishable from cancer. However, convinced that fat grafting has merit, Coleman persevered to refine the procedure and introduced the concept of micrografting. Along the way, improvements in breast imaging technology allowed radiologists to better differentiate fat necrosis from tumorous lesions. Later, in 2012, Rubin showed that the microcalcifications from fat grafting were benign and similar to the microcalcification that was observed with reduction mammaplasty but clearly distinguishable from the microcalcifications associated with malignancy. Spear broke the ban in 2005 when he published his series of breast reconstructions that were satisfactorily improved by fat grafting with minimal complications. Shortly thereafter, Rigotti made the seminal discovery that radiation fibrosis of the breast is reversed with lipoaspirate injections. Coleman that same year published his early experience with breast augmentation using his improved technique of fat grafting. Having figured out that the recipient size is the limiting factor in augmenting the small breast, Khouri pre-expanded the recipient with an external vacuum expander (EVE) and showed a reasonable amount of fat retention resulting in permanent breast augmentation with minimal complications. Realizing that if performed properly, the procedure has merit and no significant downside, an American Society of Plastic Surgery (ASPS) committee issued an updated position statement in 2009. The American Society for Aesthetic Plastic Surgery (ASAPS) then commissioned Dr. Spear to perform a prospective study of fat graft breast augmentation. He operated as best he could on 10 women, thoroughly recorded their preoperative and 1-year postoperative data and reported his autologous fat graft breast augmentation results in 2014. The results were modest but convincing, while the complications were minimal. Meanwhile, Yoshimura persevered with refining the procedure with the addition of stem cells. Yoshimura is also credited for elucidating in his lab the mechanism of avascular fat graft survival. Research from Orgill’s laboratory shed further light on the process of adipogenesis and graft angiogenesis. In 2014, Khouri and Rigotti published their experience with breast augmentation and reconstruction combining recipient pre-expansion and autologous fat transfer. As the procedure grew in popularity, a number of independent retrospective studies appeased the concerns that injected fat might be carcinogenic. Fat grafting the breast is in the process of becoming a well-accepted adjunct or alternative for breast augmentation and has clear benefits in the setting of breast reconstruction. Surgeons can now reply to the patient’s question by saying, “Yes, we can do that, but doing it right involves a bit more than inserting an implant”. In this chapter, we will expand on the lessons learned and the fundamental principles that lead to successful and safe breast augmentation with autologous fat grafting (AFT). Liposuction and fat re-injection are procedures readily accessible to many practitioners, but unless they performed by adequately trained surgeons, the danger of repeating the complications of the past remains.
In essence, fat grafting represents 3D cellular grafting. Compared with the familiar 2D skin grafting, the added dimension brings about new concepts and principles. We will first elaborate on the fundamental requirements for safe and successful application of the procedure.
To survive, avascular grafts need to revascularize. Survival is then a race between the slow neovascularization of capillaries sprouting into the graft versus the short graft survival time allowed by plasmatic imbibition. Yoshimura has elegantly described this process with the survival zones concept ( Fig. 4.1 ). He showed that a globule of grafted fat has three zones. The outermost, less than a mm thick, is where the adipocytes in direct contact with the recipient bed can rapidly revascularize and survive. Next is the regenerative zone where the adipocytes die, but where the accompanying stem cells that are more resistant to ischemia can wait a bit longer for the neovascularization to reach them and survive. Under the influence of local factors, these more resistant precursor cells then differentiate into mature adipocytes. This zone is about 1–1.7-mm thick. Deeper to this is the necrotic zone where everything dies from inability of the angiogenic process to reach them on time. Therefore, fat droplets larger than 3 mm in diameter will invariably suffer central necrosis. From this geometrical constraint, we calculate that only 50% of a tiny 1-mL spherical droplet of fat will survive.
The delivery of fat typically occurs during cannula retraction to leave behind graft ribbons. It follows from the above that for the injected grafts to survive, the ribbons should not be wider that 3 mm (see Fig. 4.1 ). Ribbons that are 3 mm wide have a cross-sectional area of about 10 mm 2 . To deliver 1000 mm 3 (1 mL) as ribbons 10 mm 2 thick, the ribbon needs to be 100 mm long (10 cm; Fig. 4.2 ). Therefore, the cardinal rule for adequate graft delivery should be: “Never inject more than 1 mL while simultaneously retracting the cannula for no less than 10 cm”. Injecting more than 1 mL/10 cm of cannula excursion will invariably leave behind thicker graft ribbons with tissue that is less likely to survive. Furthermore, pistoning back and forth through the same channel is counterproductive; thus, the surgeon should also ensure that each cannula passes in a separate channel. It should also be emphasized that the injection rate (mL) is a function of cannula travel distance (cm) through the tissues and is independent of the injection rate in mL/min. Shear forces that depend upon mL/min are minimal here. Furthermore, the 1 mL/10 cm rule is based upon simple geometry and volume conservation; the size of the ribbon is independent of the size/bore of the cannula delivering it.
Since surgeons typically inject by advancing the syringe plunger with their thumb, the smaller the syringe, the greater the accuracy of delivery. Most surgeons have about 1 cm precision in the thumb that controls the syringe plunger while they simultaneously drive the cannula through the tissues. A 1-cm plunger advance in a 60-mL syringe, for instance, delivers about 6 mL. This would require the surgeon to evenly travel the cannula a full 60 cm through the tissues while synchronizing a simultaneous 1-cm controlled thumb advance. Even with a 10-mL syringe, a 1-cm plunger advancement delivers 2 mL, requiring a simultaneously synchronized 20-cm cannula motion – a dexterity few surgeons are gifted with. While the ideal is a 1-mL syringe (as advocated by Dr. Coleman), the compromise is a 3-mL syringe, which would only require 4 cm of cannula travel per centimeter of plunger advancement.
Revascularization requires an intimate graft-to-recipient interface. This can best be achieved by using small syringes that are best at delivering micro-grafts. Larger syringes are much more prone to leave behind ribbons larger than 3 mm across, where only their outer shell survives, leaving behind necrotic lakes.
The problem, of course, is that injecting 600–800 mL of fat for a bilateral breast augmentation with a 3-mL syringe would require 200–300 syringe cannula swit-ches. Assuming a rate of 10 sec per switch, this would add 1 h of operating room and anesthesia time. Since speed in surgery is economy of motion, herein the advantage of a valve system that avoids switching, and instead, continuously aspirates from a graft reservoir to directly re-inject.
Other factors also come into play to complicate the issue. Rubin has shown that, everything else being equal, there is a wide patient-to-patient variation in the ability of grafted fat to revascularize and survive. He attributed this to the very wide patient-to-patient variation in stem cell content of their lipoaspirate. This variation seems to be an inherent individual patient attribute that could not be attributed to age, sex, or medical conditions.
Just like in the conventional 2D skin grafting, where it is counterproductive to graft more than the defect size, in 3D grafting the amount of fat graft should not exceed the capacity of the recipient site. The elasticity of the skin is dependent upon the mechanical compliance of the recipient. Healthy subcutaneous tissue is our buffer for excess fluid, it can accumulate edema and easily stretch up to 50% before the interstitial pressure build ups to choke the capillary circulation. While scarred, radiated tissue is much less compliant and is limited in its ability to accommodate the graft. It is important to note that percentage volume change is the critical element, and that beyond a certain point, the curve becomes near vertical such that a small percentage increase can lead to very large and prohibitive pressure increases ( Fig. 4.3 ).
Even with the most meticulous dispersion of the graft, making sure that there is no coalescence and that each tiny globule (or ribbon) is surrounded by recipient tissue, a tipping point will occur in which the tissue can no longer accommodate additional grafting without causing the interstitial tissue pressure to rise above capillary occlusion pressure resulting in cessation of circulation.
Another way to look at graft survival is the stoichiometry concept ( Fig. 4.4 ). A graft particle G has to combine with a recipient site R to yield a surviving graft-recipient complex GR. This important stoichiometry ratio must be respected. Adding more grafts, G, to an established recipient site containing a limited amount of R will not yield more surviving GR. Overgrafting will manifest as early volume increase; however, it is counterproductive as it will invariably resorb over the ensuing few months. Small, localized excess grafted fat will turn into tiny oil cysts that tend to resorb over time. This is why the grafted tissue tends to decrease in size within the first 6 months. In contrast, larger fat clusters will result in necrotic lakes that may calcify and become problematic nodules.
The shape of our soft tissues is largely determined by their intrinsic fibrovascular structural scaffold. Contour defects and volume deficiencies are therefore not solely due to the lack of filling substance. Whether endogenous or secondary to scar, all surface contours are tethered by a complex array of fibrous bands. Therefore, to augment the size of a dome such as the breast, it is not enough to pump in more filler because the fibrous structural framework must be stretched, and in some cases, loosened and released. Judicious release of these fibrous connective tissue bands is paramount if the contour defect is to be corrected and the volume is to be augmented beyond the intrinsic viscoelastic deformation limit of the fibrous scaffold. Rigotti used an 18-G hypodermic needle to spot release these restraining fibers, thus the term “Rigottomy” was coined to refer to this extremely useful maneuver of percutaneous mesh expansion ( Fig. 4.5 ).
The original Coleman grafting technique consisted of jackhammering back and forth with a blunt cannula, a maneuver that loosens the fibrous scaffold and allows the tissues to expand, while delivering tiny packages of graft with each stroke. This is an alternative to the Rigottomy technique, but it has limited effectiveness against denser scar fibers. Most fat grafting surgeons now use a combination of both techniques, starting with the jackhammer and then performing a limited Rigottomy to spot release the more resilient fibers (see Fig. 4.5 ). Since harmonic vibration (not power-assisted liposuction reciprocation) is a very effective and less traumatic method of loosening tissues, a harmonic vibrating cannula was recently introduced and found to be effective at transforming the fibrous structural scaffold into a putty that can be stretched and refashioned.
Loosening and re-structuring the fibrovascular framework is very beneficial because it softens fibrous scars and turns the stiff restrictive cicatrix to a recipient matrix that expands and softens with the inserted fat (see Fig. 4.5 ). However, as the connective tissues are loosened and released, it is important to recognize that these are also part of the delicate nutritive reticular framework that the graft depends upon for revascularization and survival. With excessive tissue trauma and aggressive Rigottomy, the scaffold may collapse and the graft may not survive resulting in a cavitary space. There is a fine line that should not be crossed as excessive release can also devascularize the entire recipient structure. Thus, for recipient sites with dense and tethered scar, it is safer to limit the release and stage the procedure a few weeks apart.
Releasing the restrictive fibers is beneficial by reducing interstitial pressure that results from grafting; however, this same release may also compromise the nutritive recipient scaffold. This is the primary reason why interstitial pressure measurement is not a good measure of tissue capacity. Most complications arise from excessive grafting or excessive release. The dilemma occurs because it is difficult to know when to stop because there is no reliable endpoint; therefore, less is best.
A chain is only as strong as its weakest link. It is common knowledge that surgical procedures often involve multiple steps. The rate-limiting step effect must be appreciated because outcome is constrained by the weakest step. Using microvascular free tissue transfer as an analogy, it is known that failure is not solely because of a poor anastomosis; these flaps can fail despite an excellent anastomosis due to a series of other factors such as compression, twists/kinks of the pedicle, traumatic dissection, or inadequate vessel selection. Autologous fat grafting can be considered in the same light because it is a multistep procedure that has a succession of factors linked in series, such that the weakest link can seal the outcome. Success in tissue augmentation with avascular grafts involves harvesting the graft, processing it, skillfully injecting the optimal amount as micro-ribbons, and providing adequate post-graft care. The least successful step determines the outcome, regardless of how perfect all others are.
Another analogy is to compare autologous fat grafting to farming. The four Ss of Successful crops are: the S eeds, the S oil, the S owing technique and the post-sowing Support . The very best Seeds crammed in a tiny, rocky recipient Soil will not yield much of a crop. The outcome will also be poor if excellent Seeds are piled up in the corner of a perfect large recipient Soil. They need to be carefully Sowed, one Seed at a time, evenly all over the Soil. Furthermore, the best Seeds perfectly sowed in an ideal Soil will not yield much either if they are traumatized, stamped or allowed to dry out. Lack of post-sowing Support can also lead to a suboptimal outcome.
Much of the literature in fat grafting focuses on the graft, the “seeds”. However, it must be recognized that investing heavily in maximizing a non-rate liming factor is futile. To optimize the results, the rate-limiting factors should be addressed first. In large-volume fat grafting, the rate-limiting step is most often a recipient site that is incapable of accommodating a large amount of graft.
The rate-limiting step effect explains why stem cell grafting, despite excellent results in the lab, has failed to show any significant improvement in the clinic ( Fig. 4.6 ). It is like adding horsepower to a car stuck in traffic. In heavy traffic, a good moped driver can beat a Ferrari. This bottleneck effect explains why experimental laboratory findings about an isolated factor do not necessarily correlate with the multifactorial clinical situations.
Another rarely discussed rate-limiting factor is the grafting craftsmanship that carefully, systematically, and meticulously teases the recipient site to insert in the 3D recipient site as many separate fine graft ribbons as possible without coalescence (see Fig. 4.13 ). Horsepower is not enough, the road condition should be good, and the driver also has to be skilled!
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