Chapter 45: Plastic and Reconstructive Surgery

1. Plastic surgery is the field of surgery that addresses congenital and acquired defects, striving to return form and function.

2. Plastic surgery has been a field of innovation. The future of the specialty likely includes advancements in the areas of regenerative medicine, fetal surgery, and reconstructive transplantation with composite tissue allotransplants.

3. Children diagnosed with cleft and craniofacial anomalies benefit from interdisciplinary care at a specialized center focusing on team care. Long-term follow-up during growth and development is critical for optimal outcomes.

4. Reconstructive surgery attempts to restore form and function through techniques that include skin grafting, use of muscle flaps, bone grafting, tissue expansion, free tissue transfer with microsurgery, and replantation.

5. Aesthetic surgery is surgery performed to reshape the normal structure of the body to improve the patient’s appearance and self-esteem. Patients undergoing aesthetic surgery present a unique challenge. The most important outcome parameter is patient satisfaction, and therefore, a thorough understanding of the patient’s motivations, goals, and expectations is critical.

The field of plastic surgery focuses on the restoration of form and function to those who have congenital and acquired deformities. Plastic surgery routinely addresses novel problems and challenges; therefore, the plastic surgeon must have an expert knowledge of anatomy and surgical technique to address new challenges.

The word plastic is derived from the Greek plastikos, meaning “to mold.” Although the term plastic surgery can be found in several medical writings from the eighteenth and nineteenth centuries, it was John Staige Davis who established the name of the specialty with the 1919 publication Plastic ­Surgery—Its Principles and Practice.

One of the earliest accounts of reconstructive surgery can be found in the Sushruta Samhita, an early text from the sixth or seventh century b.c. by the practitioner Sushruta. In this writing, the reconstruction of an amputated nose with a pedicled forehead flap and the reconstruction of the ear with cheek flaps were described. In addition, in the first century a.d., the Roman physicians Aulus Cornelius Celsus and Paulus Aegineta described operations for facial reconstruction.

The first textbook of plastic surgery is believed to be Gaspara Tagliacozzi’s 1597 publication De Curtorum Chirurgia per Insitionem. This text describes the reconstruction of the nose with a pedicled arm flap. The nineteenth century saw advances in reconstructive surgery, including Giuseppe Baronio’s successful grafting of sheepskin. The techniques for perfecting human skin grafting followed later in the nineteenth century.

Great advances in plastic surgery occurred as a result of the first and second world wars. Out of the fields of dental surgery, otolaryngology, ophthalmology, and general surgery, the discipline of plastic surgery was established. The founders of the field include Sir Harold Gillies, an otolaryngologist who established a center for the treatment of maxillofacial injuries in England; V. H. Kazanjian, a dental surgeon from Boston, who established a center in France for the treatment of facial injuries incurred in World War II; and Vilray P. Blair, from St. Louis, who established centers for the treatment of soft tissue and maxillofacial reconstruction for the U.S. Army. With the onset of World War II, centers of excellence for hand reconstruction appeared as well.

In the last 50 years, advances in plastic surgery have included the transplantation of both autologous and allogeneic tissue, tissue expansion, regional muscle and myocutaneous flap transfers, distant transfer of free flaps using microsurgery, replantation of traumatically amputated extremities and digits, and the emergence of craniofacial surgery. The future of plastic surgery will likely see further advances in the realms of regenerative medicine, fetal surgery, and reconstructive transplantation.

Skin Incisions

Human skin exists in a state of tension created by internal and external factors. Externally, skin and underlying subcutaneous tissue are acted on by gravity and clothing. Internally, skin is subjected to forces generated by underlying muscles, joint extension and flexion, and tethering of fibrous tissues from zones of adherence. As a result, when skin is incised linearly, it gapes to variable degrees. When a circular skin excision is performed, the skin defect assumes an elliptical configuration paralleling the lines of greatest tension. Carl Langer, an anatomist from Vienna, first fully described these tension lines in the mid-1800s based on his studies of fresh cadavers.¹ A. F. Borges described another set of skin lines that, different from Langer’s lines, reflect the vectors of relaxed skin tension.² Although the term Langer’s lines often is used interchangeably with the term relaxed skin tension lines, the former lines describe skin tension vectors observed in the stretched integument of cadavers exhibiting rigor mortis, whereas the latter lines lay perpendicular to and more accurately reflect the action of underlying muscle² (Fig. 45-1). Relaxed skin tension lines may be exploited to create incisions that minimize anatomic distortion and improve cosmesis. In areas of anatomic mobility, such as the neck or over joints, incisions are oriented less for aesthetic reasons and more with the goal of avoiding scar contractures and subsequent functional compromise. In general, incisions are placed perpendicular to the action of the joint.

There are situations, however, in which the direction of the incision has been preestablished, as in acute lacerations, burns, or old contracted and distorting scars. In these circumstances, the principles of proper incision placement can be combined with simple surgical techniques to reorient the scar and lessen the deformity. The Z-plasty technique uses the transposition of random skin flaps both to break up a linear scar and to release a scar contracture through lengthening (Fig. 45-2; Table 45-1). W-plasty is the technique of scar excision and reconstruction in zigzag fashion to camouflage the resulting scar.

Wound Healing

The fundamentals of plastic surgery are based on wound healing physiology. Wound repair consists of an exquisitely regulated symphony of molecular and cellular instruments that act in concert to restore the local tissue environment to prewound conditions. Metabolic imbalances in the wound milieu drive this orchestration and continue to direct it until healing resolves the disturbance. Although a detailed review of wound physiology is presented elsewhere in this text, it is useful to emphasize several points.

Tissue injury disrupts the tissue microenvironment and sets into motion a cascade of events that combine to reestablish the environmental status quo. Disrupted blood vessels fill the wound space with red blood cells and plasma. Injured cells release factor III (thromboplastin), which accelerates the clotting cascade. Clotting factors in the plasma are activated, and the coagulation cascade forms thrombin and eventually fibrin. Simultaneously, the complement system activates and produces chemoattractive complement protein fragments. Platelets, activated by thrombin and exposed collagen, release a number of growth factors and cytokines. Traumatized vessels contract in response to both direct physical stimulation and prostaglandins released by platelets. Intact local microvasculature vasodilates and leaks plasma in response to inflammatory mediators such as histamine, kinins, and serotonin. These early events, and others, establish inflammation and, finally, homeostasis.³

Platelet activation initiates the first major escalation in the inflammatory response. Within minutes, platelets release signaling molecules from their α-granules to attract macrophages, polymorphonuclear cells (PMNs), fibroblasts, and vascular endothelial cells. Within a few hours of injury, PMNs and macrophages invade the wound and remove tissue debris, coagulation proteins, and bacteria. Although both PMNs and macrophages begin to marginate early, PMNs dominate during the first few days. PMNs also constitute the primary defense against invading organisms that have breached the epithelial barrier. PMNs and macrophages, in concert with the complement system, form the basis of “natural” or “nonspecific” immunity. If there is no infection or foreign material, the neutrophil population diminishes by the second day, whereas macrophages continue to amass.³

Macrophages become the major population by the third day after injury. These cells then dominate the wound region for days to weeks. Macrophages are the “masterminds” behind the finely tuned array of repair events that characterizes the proliferative phase of healing. Like neutrophils, activated macrophages continue the task of wound débridement. They are a rich source of degradative enzymes that process the extracellular matrix to make room for remodeling. Tightly coordinated release of the many growth factors, colony-stimulating factors, interleukins, interferons, and cytokines gives the macrophage the ability to regulate migration, proliferation, and specific protein synthesis of multiple cell lines. Macrophages lead the procession of new tissue into the wound dead space. Immature, replicating fibroblasts follow the macrophages. Mature fibroblasts then advance into the wound and are, in turn, followed by newly forming capillary buds, the last cells in the procession.³

Thus, injury perturbs the microenvironment and leads to the autoamplifying inflammatory phase. As a result of these processes, three changes occur in the wound: the environment becomes hypoxic, acidotic, and hyperlactated. One biochemical pathway by which this low redox potential state can signal cells to take biologic action is the adenosine diphosphoribose (ADPR) system. Recent evidence has shown that alterations of the polyADPR system affect regulation of collagen and vascular endothelial growth factor (VEGF) transcription.³ Consequently, the metabolic state that is so deranged in the wound microenvironment is intimately linked to altered cellular function and leads to reparative cell phenotypes.

After inflammation has begun, fibroblasts are attracted by many stimuli and then proliferate and migrate into the site of injury. Fibroblasts are the major producers of collagen in the repair response. Substances that increase collagen deposition and maturation include lactate, oxygen, and growth factors. Lack of these agents as well as steroid treatments decrease collagen in wounds.

Macrophages also usher along angiogenesis, largely through the release of VEGF. VEGF production is upregulated by the same wound metabolic environment that stimulates collagen production. As neovascularization takes place, many of the conditions that signaled the start of the inflammatory and proliferative phases are resolved, and the wound healing response recedes.

Epidermal cells are attracted to the healing wound by the same cytokines that attract other wound cells. Epithelialization proceeds best in a moist environment with high oxygen tension.³

Preoperative, intraoperative, and postoperative interventions may be taken by the surgeon to minimize infection and optimize wound healing (Tables 45-2–45-4). These measures all draw on what we understand of the physiologic wound healing process.

Skin Grafts and Skin Substitutes

Skin is comprised of 5% epidermis and 95% dermis. The dermis contains sebaceous glands, whereas sweat glands and hair follicles are located in the subcutaneous tissue. The dermal thickness and concentration of skin appendages vary widely from one location to another on the body. The skin vasculature is superficial to the superficial fascial system and parallels the skin surface. The cutaneous vessels branch at right angles to penetrate subcutaneous tissue and arborize in the dermis, finally forming capillary tufts between dermal papillae.⁴

Skin grafting techniques date back >3000 years to India, where forms of the technique were used to resurface nasal defects in thieves who were punished for their crimes with nose amputation. Modern skin grafting methods include split-­thickness grafts, full-thickness grafts, and composite tissue grafts (Table 45-5). Each technique has advantages and disadvantages. Selection of a particular technique depends on the requirements of the defect to be reconstructed, the quality of the recipient bed, and the availability of donor site tissue.

Split-Thickness Grafts

Split-thickness skin grafting represents the simplest method of superficial reconstruction in plastic surgery. Many of the characteristics of a split-thickness graft are determined by the amount of dermis present. Less dermis translates into less primary contraction (the degree to which a graft shrinks in surface area after harvesting and before grafting), more secondary contraction (the degree to which a graft shrinks during healing), and better chance of graft survival. Thin split grafts have low primary contraction, high secondary contraction, and high reliability of graft take, often even in imperfect recipient beds. Thin grafts, however, tend to heal with abnormal pigmentation and poor durability compared with thick split grafts and full-thickness grafts. Thick split grafts have more primary contraction, less secondary contraction, and may take less hardily. Split grafts may be meshed to expand the surface area that can be covered. This technique is particularly useful when a large area must be resurfaced, as in major burns. Meshed grafts usually also have enhanced reliability of engraftment, because the fenestrations allow for egress of wound fluid and excellent contour matching of the wound bed by the graft. The fenestrations in meshed grafts reepithelialize by secondary intention from the surrounding graft skin. The major drawbacks of meshed grafts are poor cosmetic appearance and high secondary contraction. Meshing ratios used usually range from 1:1.5 to 1:6, with higher ratios associated with magnified drawbacks.

Full-Thickness Grafts

By definition, full-thickness skin grafts include the epidermis and the complete layer of dermis. The subcutaneous tissue is carefully removed from the deep surface of the dermis to maximize the potential for engraftment. Full-thickness grafts are associated with the least secondary contraction upon healing, the best cosmetic appearance, and the highest durability. As a result, they are frequently used in reconstructing superficial wounds of the face and the hands. These grafts require pristine, well-vascularized recipient beds without bacterial colonization, previous irradiation, or atrophic wound tissue.

Graft Take

Skin graft take occurs in three phases: imbibition, inosculation, and revascularization. Plasmatic imbibition refers to the first 24 to 48 hours after skin grafting, during which time a thin film of fibrin and plasma separates the graft from the underlying wound bed. It remains controversial whether this film provides nutrients and oxygen to the graft or merely a moist environment to maintain the ischemic cells temporarily until a vascular supply is reestablished. After 48 hours, a fine vascular network begins to form within the fibrin layer. These new capillary buds interface with the deep surface of the dermis and allow for transfer of some nutrients and oxygen. This phase, called inosculation, transitions into revascularization, the process by which new blood vessels either directly invade the graft or anastomose to open dermal vascular channels and restore the pink hue of skin. These phases are generally complete by 4 to 5 days after graft placement. During these initial few days, the graft is most susceptible to interference in engraftment caused by infection, mechanical shear forces, and hematoma or seroma.⁴

Composite Grafts

Composite tissue grafts are donor tissue containing more than just epidermis and dermis. They commonly include subcutaneous fat, cartilage and perichondrium, and muscle. Although less common than skin grafts, grafts of this type are particularly useful in select cases of nasal reconstruction. Excision of the thick skin of the nasal lobule may create too deep a defect to reconstruct with a full-thickness skin graft. The ear lobe composite graft provides thicker coverage with good color match and a fairly inconspicuous donor site (Fig. 45-3). Similarly, the root of the helix of the ear may be used to reconstruct the alar rim, providing skin coverage, cartilaginous support, and internal lining in a single technique.

Flaps

A flap is a vascularized block of tissue that is mobilized from its donor site and transferred to another location, adjacent or remote, for reconstructive purposes. The difference between a graft and a flap is that a graft brings no vascular pedicle and derives its blood flow from recipient site revascularization, whereas a flap arrives with its blood supply intact.

Random Pattern Flaps

Random pattern flaps have a blood supply based on tiny blood vessels in the dermal-subdermal plexus, as opposed to the discrete, well-described vessels of axial pattern flaps (Fig. 45-4).⁵ Random flaps are typically used to reconstruct relatively small, full-thickness defects that are not amenable to skin grafting. Unlike axial pattern flaps, random flaps are limited by their geometry. The generally accepted reliable length-to-width ratio for a random flap is 3:1. Exceptions to this rule abound, however. There are many different types of random cutaneous flaps that differ in geometry and mobility. A transposition flap is rotated about a pivot point into an adjacent defect (Fig. 45-5). A Z-plasty is a type of transposition flap in which two flaps are rotated, each into the donor site of the other, to achieve central limb lengthening (see Fig. 45-2). Another common transposition flap is the rhomboid (Limberg) flap (Fig. 45-6). Rotational flaps are similar to transposition flaps but differ in that they are semicircular (Fig. 45-7). Advancement flaps slide forward or backward along the flap’s long axis. Two common variants include the rectangular advancement flap and the V-Y advancement flap (Fig. 45-8). Like transposition flaps, interpolation flaps rotate about a pivot point. Unlike transposition flaps, they are inset into defects near, but not adjacent, to the donor site. An example of an interpolation flap is the thenar flap for fingertip reconstruction (Fig. 45-9).

Fasciocutaneous and Myocutaneous Flaps

The composition of a flap describes its tissue components. For example, a cutaneous flap contains skin accompanied by a variable amount of subcutaneous fat. A fasciocutaneous flap contains skin and fascia, whereas an adipofascial flap contains subcutaneous fat and fascia without overlying skin. A muscle flap contains muscle only, whereas a myocutaneous flap also contains the overlying skin and intervening tissues. An osseous flap contains vascularized bone only, whereas an osteomyocutaneous flap contains, in addition, muscle, skin, and subcutaneous tissues.

The contiguity of a flap describes its position related to its source. Local flaps are transferred from a position adjacent to the defect. Regional flaps are from the same anatomic region of the body as the defect (e.g., the lower extremity region or the head and neck region). Distant flaps are transferred from a different anatomic region to the defect. They may remain attached to the source anatomic region (pedicled flaps) or may be transferred as free flaps by microsurgery. These are completely detached from the body, and their blood supply is reinstated by microvascular anastomoses to recipient vessels close to the defect.

The term pedicle was originally used to describe a bridge of tissue that remained between a flap and its source, similar to how a peninsula remains attached to its mainland. However, as knowledge of flap blood supply and (micro)vascular anatomy has improved over the years, the term pedicle has increasingly become reserved for describing the blood vessels that nourish the flap. Thus its current use is, in essence, vascular pedicle in shortened form. As a refinement, it is possible to dissect the pedicle free of its surrounding tissues (termed skeletonization) to allow any tortuosity of the supplying blood vessels to be released in order to maximize their reach toward a given defect. This is usually performed in a retrograde direction starting from where the pedicle enters the flap tissues. Similarly, it is possible to detach the desired skin paddle circumferentially from all unneeded surrounding tissues in order to maximize the freedom with which the flap can be inset to reconstruct the defect. Hence, a pedicled island flap has had its cutaneous component circumferentially incised while preserving its vascular pedicle. Therefore, a free flap and a pedicled island flap differ only in that the former requires transection of the vascular pedicle for anastomosis to alternative recipient vessels, whereas the pedicle of the latter remains in continuity.

Such flaps that are supplied by an anatomically defined configuration of vessels are described as having an axial pattern blood supply and can be transferred as local, regional, or distant, and pedicled, island pedicled, or free flaps.⁶ Arising from the aorta are arteries that supply the internal viscera and other deep vessels that divide to form the main arterial supplies to the trunk, head, and extremities. They ultimately feed interconnecting vessels that supply the vascular plexuses of the fascia, subcutaneous tissue, and skin. These interconnecting vessels reach the skin via either fasciocutaneous (also called septocutaneous) vessels that traverse fascial septae between muscles, musculocutaneous perforators that penetrate muscle bellies, or direct cutaneous vessels that traverse neither muscle bellies nor fascial septae.⁷ Axial pattern flaps, incorporating suprafascial tissues, are supplied by these fasciocutaneous (septocutaneous), musculocutaneous, or direct cutaneous arteries. The internal viscera are also a source of axial pattern flaps, such as the jejunum flap and omentum flap. The circulation of bone- and muscle-containing flaps also is mainly axial in pattern. It also is possible to design local flaps, such as V-Y advancements and rhomboid flaps, as axial pattern flaps. In contrast to axial pattern flaps, random pattern flaps are only commonly transferred as local flaps by virtue of their lack of a defined vascular pedicle and cannot be transferred as island pedicled or free flaps. Axial pattern flaps may possess some areas with random pattern circulation, usually located at the flap periphery.

The volume of tissue reliably vascularized by the pedicle of an axial pattern flap defines its limits. In other words, the portion of a flap that extends beyond the capabilities of its vascular pedicle to perfuse it reliably will ordinarily undergo necrosis of that portion. This can be clarified conceptually. The arterial tree can be described in terms of its angiosomes.⁸ An angiosome is a block of tissue that is reliably supplied by a given artery. Neighboring angiosomes overlap, just as the dermatomes of neighboring nerves overlap. An anatomic angiosome is defined by the limits of an artery’s ramifications, where it forms anastomoses with a neighboring anatomic angiosome. The vessels that pass between these anatomic angiosomes are called choke vessels. In life, these may open or close in response to physiologic changes to increase or decrease, respectively, an artery’s dynamic angiosome momentarily. Accordingly, at any given time point, the dynamic angiosome of an artery may be approximated by the volume of tissue stained by an intravascular administration of fluorescein into that artery (indicating the reach of blood flow from that artery into tissues). The potential angiosome of an artery is the volume of tissue that can be included in a flap that has undergone conditioning (see below). Both the dynamic and potential angiosomes extend beyond the anatomic angiosome of an artery. Although the angiosomal concept provides some guidance to the size and volume limits of a flap harvest, there remains no quantifiable method to predict safe flap harvest limits exactly.

Conditioning refers to any procedure that increases the reliability of a flap by enlarging the angiosome of the pedicle artery from its dynamic toward its potential angiosome. Invoking the delay phenomenon, for example, has improved the survival of flaps that otherwise would more frequently be complicated by unpredictable partial necrosis, such as the pedicled transverse rectus abdominis myocutaneous (TRAM) flap. The procedure can be particularly useful in patients at higher risk, such as those who are obese, smoke, or have received radiotherapy. One method of delay for the pedicled TRAM flap is to divide a major portion of its blood supply, the deep inferior epigastric artery on both sides, approximately 2 weeks before transfer. In response, blood from the anatomic angiosome of the superior epigastric artery appears to flow into that of the interrupted deep inferior epigastric artery via intervening choke vessels. As a result, the flap becomes conditioned to rely on the superior epigastric artery. The TRAM flap can then be transferred based on the superior epigastric artery with less risk of its distal portions becoming ischemic and possibly necrotic. Several theories have been proposed to explain the delay phenomenon, including metabolic compensatory responses to relative ischemia and dilatation of choke vessels; however, its mechanisms remain incompletely understood.⁹

Further subclassifications of flap circulation have been introduced for muscular and fasciocutaneous flaps.¹⁰ Individual muscles have been classified by Mathes and Nahai into five types (I–V) according to their blood supply (Table 45-6). This classification is also applied to the respective myocutaneous flaps. Fasciocutaneous flaps also have been classified by these authors into types A, B, and C (Table 45-7). The inclusion of muscle in a flap may serve to increase flap bulk (so as to obliterate dead space) or to provide a functioning component with the harvest of its motor nerve for coaptation to a recipient motor nerve. The purported advantages of muscle-containing flaps over fasciocutaneous flaps for use in previously infected tissue beds or for fracture healing have been debated.

With progressive advancements in flap transfer techniques and in understanding of microvascular flap anatomy, plastic surgeons have steadily increased the number and variety of available flaps, thereby improving the results of flap reconstructions. In addition, this knowledge has reduced the morbidity associated with flap harvest. Perhaps the most important advancement in flap surgery within recent decades has been the introduction of the perforator flap.¹¹ Perforator flaps evolved from the observation that the muscle component of myocutaneous flaps served as a carrier of blood vessels to the overlying fasciocutaneous tissues. Prior to this, it had been deemed mandatory to include the muscle for reliable harvest of fasciocutaneous tissues supplied by musculocutaneous perforators, even if it was not necessary to include that muscle for the reconstruction. This unfortunately caused an unnecessary muscular deficit at the donor site, and for this reason, fasciocutaneous flaps that were supplied by musculocutaneous perforators instead of septocutaneous vessels were sometimes abandoned. The introduction of intramuscular retrograde dissection techniques, however, allowed the skeletonization of a musculocutaneous perforator from its encasement within a muscle belly, which spared that muscle from flap harvest and preserved its donor site function.^7,11 Further refinement of this concept gave rise to the harvest of cutaneous flaps based on any vessel that penetrated the fascia, which preserved the muscle (when the vessel was a musculocutaneous perforator) as well as the fascia (by suprafascial dissection). Within the last decade, free-style flap harvest has also been introduced.¹² With a handheld Doppler ultrasound probe, the surgeon is able to identify an arterial supply to almost any area of skin with the desired reconstructive characteristics and trace that pedicle in retrograde fashion along whatever direction it takes, preserving donor site fascia and muscle as necessary. Although the exact definition of what a perforator flap is remains contentious, its advantages remain clear: reduced donor site morbidity, reduced flap bulk, and increased flexibility in choosing desired flap components for reconstruction. The circulation of perforator flaps is axial in pattern; consequently, they can be transferred as pedicled island flaps or by microvascular free tissue transfer.

Free Tissue Transfer

A free tissue transfer, often referred to as a free flap procedure, is an autogenous transplantation of vascularized tissues. Any axial pattern flap with pedicle vessels of a suitable diameter can be transferred as a free flap. This involves three main steps: (a) complete detachment of the flap, with devascularization, from the donor site; (b) revascularization of the flap with anastomoses to blood vessels in the recipient site; and (c) an intervening period of flap ischemia. Flap circulation must be restored within a tolerable ischemia time.

Given the small diameter of most flap pedicle vessels (usually between 0.8 and 4.0 mm), these anastomoses are usually performed using an operative microscope that provides dedicated illumination and between 6× and 40× magnification. Any surgery performed with the aid of an operative microscope is termed microsurgery; such anastomoses are therefore termed microvascular anastomoses. High-magnification surgical loupes are usually used for flap harvest, especially for dissecting the flap pedicle, because they allow greater operator freedom. Aside from microvascular anastomosis, microsurgical techniques include microneural coaptation, microlymphatic anastomosis, and microtubular anastomosis.

The first successful free tissue transfer in humans was of a jejunal free flap for cervical esophagus reconstruction in 1957; however, the surgeons did not use microsurgery for the anastomoses. The first microvascular free tissue transfers in humans were carried out during the late 1960s and early 1970s. Free flaps were initially considered to be a last-resort option to reconstruct the most complex defects. However, as a result of improved microsurgical techniques and microinstrumentation, as well as proper patient and free flap selection and effective postoperative monitoring methods, the success rates have increased to exceed 95%.¹³ Today, free tissue transfer is often the first-choice treatment for many defects and is no longer considered the last-ditch effort. It is now ubiquitously used in appropriate patients by reconstructive plastic surgeons worldwide.

The predetermining factor in free flap failure is occlusion of its blood supply due to thrombosis. As enumerated by ­Virchow’s triad, any factors that alter normal laminar blood flow, cause endothelial damage, or change the constitution of blood (producing hypercoagulability) increase the risk of thrombosis (Table 45-8).¹⁴ Avoidance of this complication, therefore, begins with a thorough patient evaluation for the presence of acquired or inherited thrombophilic tendencies. The patient’s hemodynamic status influences that of the free flap and should be optimized. The effect of tobacco smoking on free flap success has been debated, with some larger retrospective studies reporting no difference in thromboembolic complications; however, smoking is well known to affect wound healing.^13,15 Smoking and the use of potentially vasoconstrictive agents, such as caffeine, should be avoided for several weeks before and after a free flap procedure. The restoration of normal laminar blood flow and avoidance of endothelial damage are addressed principally by careful flap insetting and meticulous microvascular surgical technique.

Planning a free flap goes beyond a simple calculation of matching flap and defect dimensions and tissue characteristics. The surgeon must, in addition, consider several important technicalities: what flap pedicle length and size are required (affected by flap choice); which recipient vessels to use; how to orient anastomoses (end to end or end to side), deal with mismatched donor and recipient vessel dimensions, overcome unhealthy donor and/or recipient vessels (e.g., traumatic dissection, scarred surgical field due to previous operation or radiotherapy), inset flap tissues (to maximize functional and cosmetic results without detriment to flap circulation), route the pedicle (to restore normal blood flow without pedicle kinking, twisting, or compression), position the patient (especially if the flap is to be inset over mobile soft tissue or joints), and place postoperative dressings (so as to produce no compression of the flap or pedicle); and what donor site morbidity will likely result (there is a risk-benefit decision between defect severity and flap choice).¹⁶ In addition, the surgeon must have a suitable backup plan to overcome intraoperative troubles; for example, insufficient pedicle length can be addressed with an interpositional vein graft adjoining the donor and recipient vessels, and iatrogenic vessel injury or severely aberrant anatomy may necessitate use of a backup flap or backup recipient vessels.¹³

A clear understanding of the blood supply to the free flap and its tissue components is a prerequisite to harvesting a viable free flap. Pedicle vessels must be identified and protected and handled minimally and atraumatically to avoid thrombogenic factors (see Table 45-8). Meticulous technique also reduces the risk of vasospasm, but the latter can be ameliorated by topical lidocaine or papaverine should it occur. Critical vessels connecting flap components must also be recognized and preserved. Under microscope magnification, the donor and recipient ­vessels should be dissected back to health. The presence of, for example, venous valves, atherosclerotic plaques, intimal trauma, and intraluminal prolapse of adventitial tissue at or adjacent to the anastomosis site increases the risk of thrombosis. The vessel ends should be cleared of periadventitial tissues for 3 to 5 mm with sharp dissection under the microscope. Periadventitial dissection should be limited to this extent, so as to avoid potential devascularization of the vessel wall by removal of the vasa vasorum and prevent the subsequent delayed development of a perianastomotic pseudoaneurysm. Adventitiectomy also helps relieve vasospasm by increasing compliance of the vessel wall and by inducing a local sympathectomy effect. The vessel ends usually are stabilized with a double approximating microvascular clamp for anastomosis. Interrupted sutures or, less commonly, continuous sutures can accomplish the anastomosis. The microneedle typically has a three-eighths circle curvature and is between 30 and 150 μm in size. Its monofilament microsuture is usually between 9-0 and 11-0 caliber. The dimensions of the vessels to be anastomosed define the choice of microneedle and microsuture. Less commonly, suture alternatives such as fibrin adhesives or laser welding (these remain largely experimental) and mechanical anastomotic devices (e.g., venous couplers) may be used. Triangulating or bisecting suturing techniques can help to achieve an even placement of sutures. Normally, each suture should include the full thickness of both vessel walls, none should catch the opposite vessel wall (which causes disastrous luminal occlusion and intimal trauma), and the size of each bite should approximate the vessel wall thickness. The configuration of the anastomosis can be either end-to-end (Fig. 45-10), if the distal circulation can be adequately preserved, or end-to-side (Fig. 45-11), if the distal circulation must be preserved, as in the case of an extremity supplied by one dominant vessel. An end-to-side orientation may also be useful to overcome dramatically mismatched donor-recipient vessel dimensions. Whatever the method chosen, microanatomic differences between the vessels should be respected so as to achieve accurately approximated intimal surfaces in a tension-free anastomosis, devoid of redundancy that might promote kinking.¹³

The clinical monitoring of a free flap should start during flap harvest, especially before its pedicle is divided. A free flap that is struggling to maintain normal perfusion characteristics during harvest most likely has insufficient circulation, which may be due to arterial or venous compromise or a combination of both (Table 45-9). Flap compromise may be due to reversible factors such as pedicle kinking, tensioning, or twisting; patient hemodynamic compromise; or an overly large flap harvest for the chosen pedicle vessels. If poor flap perfusion continues despite the absence or correction of all these factors, an inherent flap problem or a critical vascular injury to the flap or its pedicle must be considered, and it may not be safe to continue its harvest. This is one example of a situation in which a backup plan may require execution.

Clinical flap monitoring continues after successful restoration of arterial inflow and venous outflow. The mainstay of postoperative free flap monitoring is clinical assessment (see Table 45-9), although supplementary instrument monitoring also can be helpful. Doppler ultrasound assessment of arterial and venous signals is useful for monitoring buried or concealed flaps. If flap perfusion was healthy before division of its donor site pedicle, then poor perfusion after anastomoses is likely due to either a technical error or insufficient systemic hemodynamics. The latter usually is correctable by ensuring that the patient and the patient’s environment are suitably warm and by initiating intravenous colloid challenge or, if indicated, blood transfusion. Numerous potential technical errors, which have been described in the earlier paragraphs on planning and anastomosis technique, may occur. Routine postoperative patient monitoring includes measurement of total fluid inputs, urinary catheter output (which should be >1 mL/kg per hour), core temperature, and arterial blood pressure (systolic pressure should be >100 mmHg), as well as pulse oximetry. The patient and free flap are best monitored in an intensive care setting by experienced staff until both are stable enough for routine ward assessments.¹⁷

Occlusion of the anastomosis most commonly arises from intraluminal thrombosis or from external compression of the pedicle, such as from surrounding tissues, fluid accumulation (e.g., hematoma and tissue edema), or overly tight dressings or skin sutures. Because there is a threshold of ischemia beyond which a flap will sustain irreversible tissue and/or microcirculatory damage, it is important that the early signs of flap circulatory compromise be recognized as quickly as possible and the underlying problem diagnosed and corrected promptly if flap health is to be restored successfully.¹⁷ Different tissues tolerate differing durations of ischemia in correlation with their tissue-specific basal metabolic rate. Although cooling free flaps (to reduce basal metabolic rate) has a variably protective effect in experimental settings, it appears that this practice contributes little to improving free flap success in the clinical setting as long as warm ischemia times are kept to <4 hours for most tissues; exceptions include bowel flaps, which are more susceptible to ischemia.¹³

Given that the predisposing factor for free flap failure is thrombus formation, it is understandable that plastic surgeons have looked to anticoagulant therapies in an effort to improve success rates. Although such drugs, including the dextrans, aspirin, heparins, and also some fibrinolytics, appear beneficial in experimental settings, large clinical trials have failed to show any conclusive associations between their use and either free flap success or failure rates.¹⁸ It seems intuitive to use these drugs for failing free flaps as an adjunctive measure alongside operative reexploration and surgical intervention. The surgeon must be aware of their contraindications and recognize that their side effects, apart from bleeding, are occasionally serious. Venous congestion may be addressed by surgical measures as well as by application of medicinal Hirudo medicinalis leeches (with concomitant Aeromonas hydrophila prophylaxis) or by chemical “leeching” (topical heparin combined with dermal punctures).

Unfortunately, the “no-reflow” phenomenon is occasionally witnessed and leads to irreversible flap failure. This describes a situation in which no venous return drains into the pedicle vein of the flap, even though adequate arterial inflow passes the arterial anastomoses and is seen to enter the flap tissues. The no-reflow phenomenon sometimes follows an extended ischemic insult and appears to be a self-perpetuating cycle of endothelial cellular swelling, inflammatory vasoconstriction, impaired microcirculatory flow, stasis, microcirculatory thromboses, progressive ischemia, and flap failure.¹³

Despite these potential problems, free flap success rates exceed 95% in experienced hands. There is no doubt that increasing microsurgical experience is critical to improving free flap success rates. The laboratory setting is an excellent environment in which to progress beyond the early portion of one’s learning curve through supervised microsurgical training and execution of microvascular anastomoses and microvascular free flap procedures in small animals.

Tissue Expansion

Although skin grafts and local flaps are very useful in reconstructing many superficial defects, they are not without their drawbacks. Both leave donor site defects with cosmetic and/or functional sequelae. Grafts are limited in color match and durability, whereas local flaps may supply insufficient tissue and produce contour irregularities. The advent of tissue expansion has created the potential to increase the amount of local, well-matched tissue that can be advanced or transposed as a flap while decreasing donor site morbidity.

The most common method of skin expansion involves the placement of an inflatable silicon elastomer balloon with an integrated or remote port beneath the skin and subcutaneous tissue followed by serial inflation with saline. After completion of expansion, usually over weeks to months, the expander is removed and the redundant overlying skin may be advanced into an adjacent defect. Expanders are available in a multitude of shapes and sizes that can be tailored to the reconstruction. In breast reconstruction, the tissue expander is replaced with a permanent implant instead of using the tissue as a flap to re-create the volume of the breast mound. Histologically, expanded skin demonstrates thickened dermis with enhanced vasculature and diminished subcutaneous fat. Studies have shown that the skin expansion is due not merely to stretch or creep but also to actual generation of new tissue.¹⁹

The technique of tissue expansion comes with its share of potential complications, including infection, hematoma, seroma, expander extrusion, implant failure, skin necrosis, pain, and neurapraxia. Furthermore, an inflated expander is a very visible, albeit temporary, deformity that may cause patients much distress.

Despite these imperfections, tissue expansion has become a major treatment modality in the management of giant congenital nevi, secondary reconstruction of extensive burn scars, scalp reconstruction, and breast reconstruction. The technique has permitted the plastic surgeon to perform reconstructions with tissue of similar color, texture, and thickness with minimal donor site morbidity.

Cleft Lip and Palate

Orofacial clefting is the most common congenital anomaly and is known to occur in 1 in 500 live white births.²⁰ The incidence is lower in African Americans and higher in Native Americans and Asians. Clefting of the lip and/or palate is felt to occur around the eighth week of embryogenesis, either by failure of fusion of the medial nasal process and the maxillary prominence or by failure of mesodermal migration and penetration between the epithelial bilayer of the face. The cause of orofacial clefting is felt to be multifactorial. Factors that likely increase the incidence of clefting include increased parental age, drug use and infections during pregnancy, smoking ­during pregnancy, and a family history of orofacial clefting. The increased chance of clefting when there is an affected parent is approximately 4%.

The primary palate is defined as all tissue anterior to the incisive foramen, including the anterior hard palate (premaxilla), alveolus, lip, and nose. The secondary palate includes everything posterior to the incisive foramen, including the majority of the hard palate and the soft palate (velum). Clefting can involve the lip and nose, with or without a palatal cleft. Clefts of the lip and/or palate are first classified as unilateral or bilateral and then as complete or incomplete (Fig. 45-12). Complete clefts of the lip affect the entire lip and extend up into the nose. Incomplete clefts affect only a portion of the lip and contain a bridge of tissue connecting the central and lateral lip elements, referred to as Simonart’s band.

Treatment Protocol

Considerable controversy remains over the details of the timing, technique, and protocol for treating children with orofacial clefting. The treatment protocol described in this chapter is accepted at many large cleft centers around the United States. All infants born with cleft-craniofacial anomalies benefit from care by a specialized team dedicated to the treatment of congenital anomalies. Today, this is widely accepted as the standard of care. Often, patients are seen prenatally after a diagnosis is made using sophisticated antenatal ultrasonography. The prenatal consultation has proven to be beneficial to parents, serving to dispel fears and uncertainties, and assuring them that treatment exists. After the infant’s birth, a team evaluation occurs, and input is obtained from the surgeon, speech and language pathologist, social worker, craniofacial orthodontist, geneticist, otorhinolaryngologist, and pediatrician. For infants born with orofacial clefting, initial concerns relate to successful feeding and breathing. Infants with palatal clefts cannot generate negative pressure when suckling and therefore need milk dispensed into their mouths from a specialized nurser when they make suckling motions.

Once adequate nutrition and a safe airway are ensured, attention is turned to the cleft anomaly. Attempts to lessen the deformity and set the stage for the surgical repair of the lip and nose begin with a process known as presurgical infant orthopedics (PSIO), which includes procedures such as nasoalveolar molding (NAM) (Fig. 45-13). NAM repositions the neonatal alveolar segments, brings the lip elements into close approximation, stretches the deficient nasal components, and turns wide complete clefts into the morphology of narrow “incomplete” clefts. After PSIO with NAM, the definitive single-stage cleft lip and nose repair is performed at 3 to 6 months of age. With this initial operation, the lip deformity is repaired and a primary nasoplasty reconstructs the cleft lip nasal deformity. If the family does not have access to PSIO or have the resources for this time-intensive therapy, a cleft lip adhesion can be performed as an initial stage in the repair. The preliminary cleft lip adhesion unites the upper lip and nasal sill, truly converting complete clefts into incomplete clefts. A cleft lip adhesion is performed in the first or second month of life, and the definitive cleft lip and nose repair follows at 4 to 6 months. After the definitive cleft lip and nose repair, the cleft palate is repaired in a single stage at 9 to 12 months of age.

Unilateral Cleft Lip

The unilateral cleft lip is classically associated with a cleft lip nasal deformity. The cleft lip nasal deformity includes lateral, inferior, and posterior displacement of the alar cartilage. This results from the deficient and clefted underlying skeleton as well as the unopposed pull of the clefted orbicularis oris muscle abnormally inserted on the alar base (Fig. 45-14A). The maxillary minor segment (the smaller alveolar/maxillary ­segment on the clefted side) is collapsed medially. The process of unilateral cleft lip repair can be thought of as “philtral subunit reconstruction.” The goal of the operation is to level Cupid’s bow and reconstruct the central philtrum of the lip, ideally placing the incision and subsequent scar as close to the normal philtral column as possible. The surgical repair is performed under general anesthesia, and local anesthesia containing epinephrine is used. Many different techniques of cleft lip and nose repair have been proposed; however, most of the commonly used procedures are variations of a “rotation-advancement” procedure.²¹ The rotation-advancement procedure, as championed by Millard (Fig. 45-14B), rotates the philtral subunit of the central lip downward to level Cupid’s bow as the lateral lip element is advanced into the defect created by the downward rotation of the philtrum. Some surgeons choose to perform primary closure of the alveolar cleft at the time of primary lip and nose repair, called a gingivoperiosteoplasty. If the alveolar cleft is to be repaired, the gingivoperiosteoplasty is performed by raising mucoperiosteal flaps within the alveolar cleft margin and reapproximating them across the alveolar cleft defect. This creates a bony tunnel closed with periosteal flaps and facilitates the generation of bone in the alveolar defect. It is accepted today that some form of primary nasoplasty should be performed at the time of primary definitive lip repair. Techniques to release and reposition the nasal tip cartilages, as well as the ala, are performed with variations of tip rhinoplasties using suture methods. Some surgeons choose to use postoperative internal and/or external splints to maintain the nasal correction achieved at surgery during the healing process.

Bilateral Cleft Lip

In the complete bilateral cleft lip and nose deformity, the central lip element, called the prolabium, is entirely separate from the rest of the upper lip. The prolabium is displaced on top of the central alveolar segment, called the premaxilla, containing the unerupted four central incisors. Often, the premaxilla and prolabium are outwardly displaced. This is referred to as a flyaway premaxilla. For the child with a complete bilateral cleft lip and nose, PSIO is a very important step in preparing the child for definitive lip and nose surgery by retracting the premaxilla into the maxillary arch, repositioning the lip segments, and stretching the rudimentary columella. Bilateral cleft lip and nose repairs often are versions of straight-line repairs, with the Mulliken technique being the more commonly performed (Fig. 45-15). In the bilateral cleft lip deformity, the new ­philtrum is made from the prolabium and is united to the lateral lip elements on top of the repaired orbicularis oris muscle.²²

Cleft Palate

During the eighth to twelfth weeks of gestation, the mandible becomes more prognathic, the tongue drops from beneath the clefted lateral palatine processes, and the palatal shelves migrate upward into a more horizontal position and fusion occurs. A cleft palate results from the failure of fusion of the two palatal processes. As with labial clefting, isolated clefts of the palate are multifactorial in etiology, and isolated clefts of the palate are more likely to be associated with other anomalies. Between 8% and 10% of isolated clefts of the palate are associated with the 22q deletion of velocardiofacial syndrome.²³

The main goal of cleft palate surgery is to help the patient attain normal speech, which results from velopharyngeal competence. During speech, the soft palate, or velum, is moved posteriorly and superiorly, primarily by the levator palatini muscle sling that suspends the velum from the skull base. Velopharyngeal competence is obtained during attempted speech when the velum approximates the posterior pharyngeal wall, preventing air and liquid from regurgitating into the nasal cavity. Velopharyngeal competence allows intraoral pressure to be built up for speech sounds. A cleft palate precludes this from occurring and results in velopharyngeal incompetence (VPI). Because it is impossible for the oral and nasal cavities to be partitioned in the patient with a cleft palate, it is also difficult for the patient to develop negative intraoral pressure for an effective suck. Therefore, specialized nursers are used to dispense liquid into the infant’s mouth during the suckling motions. Children with clefts of the palate have an increased incidence of otitis media; this may be related to the abnormality of the velar musculature and ineffective function of the eustachian tube. The increased incidence of otitis media can result in hearing loss if not treated appropriately. In addition, VPI and nasal air escape during speech results in hypernasal speech.

As with the repair of cleft lip and nose, the timing, technique, and protocols for cleft palate repair are controversial. Most agree that palate repair should be performed before the development of speech. The cleft palate usually is repaired when the infant is between 6 and 18 months of age. Cleft palate repair also is performed under general anesthesia, with the head slightly hyperextended and a retractor, such as the Dingman mouth gag, placed intraorally to retract the tongue and endotracheal tube. An epinephrine solution is injected into the palate. Techniques of hard palate closure include the use of unipedicled hard palate mucoperiosteal flaps as in the Wardill-Veau-Kilner repair or bipedicled hard palate mucoperiosteal flaps as in the von Langenbeck repair. Both the unipedicled and bipedicled hard palate palatoplasty techniques rely on the greater palatine neurovascular pedicle. Soft palate or velar closure techniques are divided into straight-line and Z-plasty procedures. With either a straight-line or Z-plasty velar repair, the levator palatini muscle should be independently repaired; this is called an intravelar veloplasty. The clefted levator is identified coursing sagittally in an anterior-posterior direction, abnormally inserted onto the posterior edge of the hard palate. In intravelar veloplasty, it is released from the posterior edge of the hard palate in the midline and dissected free from abnormal attachments to the aponeurosis of the tensor veli palatini muscle and superior constrictor laterally. After its complete release, the levator palatini muscle is united in the midline, with reconstruction of the levator muscle sling that suspends the velum from the skull base and aids in velopharyngeal competence.

The authors prefer the double opposing Z-plasty technique of soft palate or velar reconstruction known as the Furlow palatoplasty.²⁴ The procedure uses four triangular flaps, two oral and two nasal, with the posteriorly based flaps containing the released levator muscles. The Z-plasty lengthens the soft palate, prevents longitudinal scarring from a straight-line repair, and produces a secondary pharyngoplasty effect by narrowing the velopharyngeal port (Fig. 45-16).

Complications of palatoplasty include wound healing problems resulting in a breakdown of the suture line and the development of a fistula. The literature reports fistula rates ranging from approximately 1% to 20%. Treatment of palatal fistulae is particularly challenging, because the recurrence rates have been noted to approach 96%. The second most common complication of palatoplasty is the incomplete correction of speech and the development of postoperative VPI. The literature reports postoperative VPI rates ranging from 10% to 40%. Some of the best rates of velopharyngeal competence have been reported with the Furlow double opposing Z-plasty palatoplasty. Postoperative VPI is treated with pharyngoplasty—either a posterior pharyngeal flap pharyngoplasty or a sphincter pharyngoplasty. A posterior pharyngeal flap is a static flap formed from the posterior pharyngeal wall including mucosa and a portion of the superior constrictor muscle. The midline superiorly based pharyngeal flap is inset into the posterior free edge of the soft palate, permanently attaching it to the posterior pharyngeal wall. The sphincter pharyngoplasty has been reported to involve creation of a dynamic sphincter made with the bilateral posterior tonsillar pillars containing the palatopharyngeus muscle. The superiorly based tonsillar pillars are elevated from the lateral pharynx and inset into a horizontal incision on the posterior pharyngeal wall at the level of the adenoid pad.

Craniofacial Anomalies

History, Overview, and Classification System

Craniofacial surgery is the subspecialty of plastic surgery dealing with hard and soft tissue deformities of the craniofacial skeleton, treating the congenital, developmental, and acquired defects of the cranial and/or facial skeleton. Craniofacial surgery addresses the functional and equally important appearance-related issues surrounding these deformities. Attempting to separate the functional impairment from the appearance-related issues is arbitrary, because it can be argued that the most important function of a face is to look like a face.²⁵ Numerous studies have established the importance of facial form and the significant emotional impact that facial deformities have on a person’s life and sense of self.

The field of craniofacial surgery finds its origins in the aftermath of the world wars and the need to treat massive facial injuries. In 1967, Dr. Paul Tessier, now recognized as the father of craniofacial surgery, first publicly presented his concepts of using wide exposure and a transcranial route to treating craniofacial deformities with large segmental movements of bone. An American disciple of Dr. Tessier, Dr. Linton Whitaker of the Children’s Hospital of Philadelphia, working with the Committee on Nomenclature and Classification of Craniofacial Anomalies of the American Cleft Palate-Craniofacial Association, presented a simple and practical classification system for craniofacial anomalies (Table 45-10).

It is the standard of care today that an interdisciplinary team of experts with specialized knowledge and training in treating children with craniofacial anomalies care for children who have such anomalies. The preoperative workup and evaluation must be thorough and should include imaging (computed tomography [CT], magnetic resonance imaging [MRI], and cephalography), photography, blood work, anesthesia consultation, and other components as the condition dictates. Craniofacial procedures are often long, complicated surgeries of significant magnitude, with an attendant risk of blood loss, serious morbidity, and even mortality. Significant blood loss is a realistic possibility, and preparation for blood conservation and transfusion must be made. The routine surgical approach to the craniofacial skeleton can be via a coronal incision, and after a bifrontal craniotomy, the orbital and facial skeleton can be addressed. Bone grafts for reconstruction can be split calvarial grafts or, alternatively, grafts from the ribs or iliac crest. Rigid fixation is obtained with bioresorbable plates, screws, and sutures. Despite the magnitude of the procedures, significant morbidity (e.g., blindness, brain injury, significant infection, cerebrospinal fluid leak, intracranial hematoma) or mortality is rare.

Craniofacial Clefts

The rare craniofacial clefts have been subclassified by Tessier (Fig. 45-17). The Tessier classification of craniofacial clefts considers the orbit as the center around which the clefts radiate as the spokes of a wheel, numbered from 0 to 14. The facial clefts (0 to 7) and their cranial extensions (8 to 14) are often associated and total 14 (Fig. 45-18). Treacher Collins syndrome (Fig. 45-19), also known as mandibulofacial dysostosis, is a type of craniofacial clefting disorder representing bilateral 6-7-8 clefts. This autosomal dominant disorder with variable penetrance has the following manifestations: hypoplasia of the zygomas, asymmetry and hypoplasia of the mandible, ear anomalies, and colobomas of the lower eyelids. Craniofacial microsomia, also known as hemifacial microsomia, can be classified as a form of clefting as well (Fig. 45-20). Manifestations of this anomaly usually involve the hard and soft tissue of one half of the craniofacial skeleton. Deformities range in severity from complete absence of an affected facial component (globe, mandible, ear) to mild asymmetries. Ear deformities range from complete absence of the ear to only preauricular skin tags. Similarly, the eye deformities range from complete absence of the globe to various anomalies including epibulbar dermoids. Hypoplasia of the temporal skull, maxilla and zygoma, and orbit are seen in varying degree and affect the underlying skeleton as well as the overlying soft tissues. The classical deformity of hemifacial microsomia affects the mandible. Hypoplasia of the hemimandible, as well as the maxilla, results in dental malocclusions (Fig. 45-20C). Mandibular hypoplasia may range from minor underdevelopment of otherwise normal components to complete absence of the condyle, ramus, and proximal body.

Treatment of hemifacial microsomia includes management of the airway and attention to other functional conditions. Treatment of the mandibular deformity includes distraction osteogenesis during growth and orthognathic procedures at skeletal maturity. Ear deformities are reconstructed with techniques using costal cartilage and local soft tissue. Soft tissue deficiencies of the hemiface can be treated with fat injections, dermal-fat grafts, or free tissue transfer. Orbital hypertelorism is yet another type of midline craniofacial (0-14) clefting. Orbital hypertelorism is defined as a lateralization of the entire orbit, increasing the intraorbital distance and resulting from midline conditions such as encephaloceles, frontonasal dysplasia, and syndromic craniosynostosis. The treatment of severe orbital hypertelorism includes a transcranial approach to four-wall orbital box osteotomies, resection or treatment of the abnormal midline process, mobilization, medialization of the orbital complexes, and nasal reconstruction with a cantilever nasal bone graft.

Craniosynostosis

The craniosynostoses are a group of disorders that result from the abnormal obliteration or premature fusion of the cranial sutures. The craniosynostoses can be subdivided into simple or single-suture craniosynostoses, and complex, syndromic, or multiple-suture craniosynostoses. The cranial sutures allow for the normal growth of the skull, and therefore, the classic presentation of craniosynostosis is an abnormal head shape. The resultant abnormal head shapes are secondary to an inhibition of skull growth at right angles to the fused suture and a compensatory overexpansion of the skull perpendicular to the fused suture into areas with open sutures. These abnormal head shapes provide a basis for the classification of craniosynostoses. In addition to appearance-related deformities resulting from craniosynostosis, important functional aspects include the potential for intracranial hypertension, which may result from brain growth restricted by an unyielding skull. The chances of intracranial hypertension increase with the number of sutures affected. Blindness and mental deficiencies secondary to an increase in intracranial pressure can likely be prevented by the surgical expansion of the cranium to release the fused suture, correct the abnormal head shape, and remodel the skull. The standard procedure used today in the correction of these synostotic deformities is fronto-orbital advancement. Fronto-orbital advancement, performed using a transcranial approach, includes a frontal craniotomy and orbital repositioning. The complex or multisutural synostoses are often syndromic, resulting from gain-of-function mutations of the fibroblast growth factor receptors (FGFR1, FGFR2, FGFR3). These syndromes of craniosynostosis include Apert’s, Crouzon’s, Pfeiffer’s, and Saethre-Chotzen syndromes. The syndromic craniosynostoses not only include bicoronal synostosis but also involve the midface, with resulting exorbitism and midface hypoplasia. Multilevel airway anomalies, obstructive sleep apnea, corneal exposure, intracranial hypertension, feeding difficulties, and severe malocclusion are some of the associated anomalies found in children with syndromic craniosynostoses. In addition to fronto-orbital advancement, facial osteotomies (i.e., Le Fort III craniofacial disjunction) are required to treat the orbital, midfacial, and occlusal deformities.

Atrophy and Hypoplasia

The categories of craniofacial atrophy and hypoplasia encompass many conditions such as Pierre Robin sequence and Romberg’s progressive hemifacial atrophy. Pierre Robin sequence is characterized by three pathognomonic findings: microretrognathia, glossoptosis, and respiratory distress. Pierre Robin sequence may or may not be associated with a palatal cleft. It is thought by some to occur secondary to a fixed and flexed fetal head position that inhibits mandibular growth and results in micrognathia. The micrognathia prevents the natural caudal migration of the tongue from between the clefted palatal shelves, and the resulting deformity as described earlier. The functional consequences include intermittent respiratory obstruction and obstructive sleep apnea that may affect feeding, growth, and safety of the airway. Treatment of a child mildly affected with Pierre Robin sequence may include simply positioning the child prone until the child “grows out” of the condition. However, if the child is severely affected and unable to feed adequately or has an unsafe airway, surgical intervention is required. For decades, tracheotomy was the initial and definitive treatment of choice; however, today many initially attempt a tongue-lip adhesion, treating the glossoptosis and alleviating respiratory obstruction by suturing the tongue tip to the lower lip. The tongue-lip adhesion is taken down at the time of palatoplasty. Should the tongue-lip adhesion not adequately correct the obstruction, then neonatal mandibular distraction can be used to correct the underlying microretrognathia and relieve the obstructive symptoms (Fig. 45-21). Another syndrome of atrophy and hypoplasia is Romberg’s progressive hemifacial atrophy, also known as Parry-Romberg syndrome (Fig. 45-22). Romberg’s disease is a disorder of unknown etiology, beginning in childhood or adolescence, in which hemifacial atrophy of the skin, subcutaneous fat, muscle, bone, and cartilage progresses for a variable period of time before spontaneously ceasing or “burning out” 2 to 10 years after beginning. Most believe treatment should be delayed until at least 1 year after the process of atrophy has ceased. Some hematologists and oncologists have treated the early presentation of Romberg’s disease with chemotherapy. After the cessation of atrophy, reconstruction of the craniofacial skeleton and soft tissues may begin with bone and/or cartilage grafts, alloplastic implants, dermal-fat grafts, fat grafting, and possibly free tissue transfers.

Hyperplasia, Hypertrophy, and Neoplasia

The categories of craniofacial hyperplasia, hypertrophy, and neoplasia encompass a wide variety of conditions affecting the craniofacial skeleton. These include vascular anomalies (discussed later in this chapter), neurofibromatosis, hemifacial hypertrophy, and bony conditions such as osteomas and fibrous dysplasia. Fibrous dysplasia can be monostotic, affecting a single location, or polyostotic, affecting more than a single location in the skeleton; it may be associated with skin pigmentation abnormalities and endocrine involvement, and be termed polyostotic or McCune-Albright syndrome. Treatment of fibrous dysplasia of the craniofacial skeleton includes block resection and reconstruction with bone grafts. If extensive involvement exists and block resection is not possible or feasible, partial resection and contouring of the affected bone is possible, as long as there is the understanding that long-term outcomes and the behavior of the disease are unpredictable.

Vascular Anomalies

Vascular anomalies are vascular birthmarks that all appear similar: flat or raised, in various shades of red and purple.²⁶ For centuries, they have been named by similarly colored food and drink (i.e., strawberry hemangioma, port-wine stain). Today these vascular birthmarks have been biologically classified as either hemangiomas or vascular malformations. The Greek suffix -oma means “swelling” or “tumor” and today connotes a lesion characterized by hyperplasia. Hemangiomas are congenital vascular anomalies that undergo a phase of rapid growth followed by slow regression, based on endothelial cell kinetics. Malformations are abnormal vascular channels lined with quiescent endothelium, usually are seen at birth, never regress, and have the potential to expand. The differential diagnosis of vascular anomalies is routinely made by a detailed accurate history and clinical examination. For deep lesions, radiographic studies may help determine the diagnosis. Biopsy is used if the diagnosis is uncertain or there is concern over the potential of malignancy.

Hemangiomas

The infantile hemangioma is the most common birthmark, affecting 10% to 12% of whites, with a 3:1 to 5:1 predilection for females and an increased incidence in preterm infants (23%) (Fig. 45-23). Hemangiomas are solitary in 80% of cases and multiple in 20%. In children with multiple (more than three) cutaneous hemangiomas, abdominal ultrasound is suggested to rule out hemangiomatosis with visceral involvement. Hemangiomas do not cause bleeding disorders; however, more invasive lesions such as kaposiform hemangioendothelioma can result in Kasabach-Merritt syndrome, characterized by platelet trapping and disordered bleeding.

Hemangiomas are usually first noted around 2 weeks of life as a flat pink spot, often confused with a superficial scratch. Around the second month of life, they enter the proliferating phase in which rapid growth is seen caused by plump, rapidly dividing endothelial cells. If the hemangioma is superficial, the skin becomes crimson and raised; if the lesion is deep, a dark blue or purple color is noted with less superficial swelling. Hemangioma growth frequently peeks before the first year, and then the lesions enter the involuting phase in which growth is commiserate with the child. The involuting phase is characterized by diminishing endothelial activity and luminal enlargement. The lesion begins to “gray,” losing its intense reddish color and taking on a purple-gray shade with overlying “crepe paper” skin. The involution phase continues until 5 to 10 years of age. Regression of the lesion is then complete. The involuted phase begins in 50% of children by 5 years of age and in 70% by 7 years. If there was cutaneous ulceration during the proliferative phase, a cutaneous scar may persist, along with the yellow-gray crepe paper–like skin with fibro-fatty deposition. In 50% of children, near-normal skin is restored.

The treatment of hemangiomas is largely observational, with reassurance of parents that regression and involution will occur. Cutaneous ulceration secondary to a proliferating hemangioma occurs in 5% of cases and more frequently with lip or urogenital lesions. Local wound care, topical application of lidocaine for pain, and laser cauterization may be beneficial treatment modalities. Problematic or endangering hemangiomas (i.e., periocular lesions threatening amblyopia, airway lesions, facially disfiguring lesions) occur in 10% of cases. The first-line treatment for problematic hemangiomas is systemic corticosteroid therapy, which is particularly effective (85% response rate). Second-line therapies include interferon and vincristine, each with its own attendant effectiveness and morbidity. Laser therapy has been claimed by some to be effective in the treatment of early hemangiomas; however, there has been no conclusive proof that laser therapy either diminishes lesion bulk or induces involution. Laser therapy has been effective in lightening affected skin. Surgery for hemangiomas in the proliferating phase is largely limited to treatment of problematic lesions (i.e., eyelid lesions threatening amblyopia). Hemangioma surgery usually is reserved for the treatment of secondary deformities and residual fibro-fatty depositions, among other indications.

Vascular Malformations

Vascular malformations are subclassified by vessel type, such as lymphatic, capillary, venous, or arterial, and by rheologic characteristics, such as slow flow and fast flow. Slow-flow lesions include capillary malformations (CMs) and telangiectasias, lymphatic malformations (LMs), and venous malformations (VMs). Fast-flow lesions include arterial malformations (AMs) and arteriovenous malformations (AVMs). In addition, there are combined malformations. One such combined lesion occurs in Klippel-Trénaunay syndrome in which CMs, LMs, and VMs are found and may be associated with soft tissue and skeletal hypertrophy in one or more of the limbs (Fig. 45-24A).

CMs are pink-red macular vascular stains that are present at birth and persist throughout life. These lesions tend to become more verrucous and darker throughout life. CMs are effectively treated with a pulsed-dye laser, and the results often are better with treatment in infancy and young childhood. Laser therapy often is repetitive and prolonged. CMs of the head and neck, historically called port-wine stains, may be associated with Sturge-Weber syndrome, which includes vascular involvement of the leptomeninges and ocular pathology (Fig. 45-24B).

LMs are anomalous lymphatic channels that never regress and have the potential to affect underlying muscle and bone, causing significant swelling and bony overgrowth. They have historically been called lymphangiomas or cystic hygromas (Fig. 45-24C). LMs can be classified as microcystic, macrocystic, or both. LMs expand or contract with the flow of lymph, infection, or intralesional hemorrhage. Superficial LMs that affect the skin often produce cutaneous vesicles that may coalesce and weep lymph fluid. Sclerotherapy remains a major treatment modality for LMs, and lesions that are macrocystic can be aspirated before sclerotherapy. Although surgery rarely removes the entire lesion, surgical resection is the only possibility for cure. These resections often are challenging, lengthy, and associated with significant blood loss, and the potential exists for regeneration of lymph channels and recurrence of the LMs postoperatively.

VMs are frequently bluish, soft, and compressible, and swell when dependent (Fig. 45-24D). VMs grow with the child, expand slowly, and may enlarge during puberty. Patients often complain about stiffness and pain with thrombosis. VMs can affect the skin, muscle, and bone. MRI is the modality of choice for imaging these lesions. Preoperative sclerosis followed by surgical extirpation is the treatment of choice for VMs that cause functional or appearance-related disability. VMs have the tendency to recanalize and re-expand. Use of elastic support stocking and low-dose aspirin therapy are important adjunctive treatment modalities for VMs involving the legs.

Pure AMs are rare and more commonly present as AVMs. AVMs appear as red violaceous skin with a palpable mass beneath. Local warmth, bruit, and thrill are frequently present. AVMs have the likely consequences of ischemic changes, ulceration, intractable pain, and intermittent bleeding. The natural history of AVMs has been described as consisting of four stages: quiescence, expansion, destruction, and decompensation. Usually, treatment for AVM is initiated when signs and symptoms of ischemic pain, ulceration, bleeding, or hemodynamic instability (stages 3 and 4) are evident. Surgical treatment includes arterial embolization to temporarily occlude the nidus 24 to 72 hours before surgical extirpation. The nidus and overlying affected skin must be widely excised, and reconstruction can be performed afterward.

Congenital Melanocytic Nevi

Congenital melanocytic nevi (CMNs) contain nevus cells and are usually present at birth. Lesions are frequently light to dark brown and round or oval, and vary greatly in size, pattern, and anatomic location. The most common location of CMNs is the trunk, followed by the extremities and head and neck. Frequently, larger lesions are associated with multiple smaller satellite lesions. Over time, these lesions may become less (or sometimes more) pigmented and develop hypertrichosis and a variegated texture, including nodularity. Small CMNs are <1.5 cm in diameter, and large ones are >10 cm. Giant CMNs usually are >20 cm in their greatest dimension in adulthood, and this correlates with a 9-cm scalp lesion or a 6-cm trunk lesion in an infant. All CMNs should be monitored for worrisome changes that indicate the need for biopsy, including ulceration, uneven pigmentation, change in shape, and nodularity. There is controversy over the actual incidence of malignant transformation of CMNs; however, most experts believe that melanoma may arise directly from a CMN. No convincing study to date has proven that excision of a CMN reduces the rate of malignant transformation to melanoma; however, many clinicians feel that excision serves at least to debulk the lesion. The reported lifetime risk for melanoma arising in small or large CMNs is between 0% and 5%; the risk for giant CMNs is estimated to be between 5% and 10%.²⁷ In addition to being at risk for melanoma, patients with large or giant CMNs are at risk for neurocutaneous melanocytosis (leptomeningeal melanosis), and this condition includes collections of melanocytes in the leptomeninges. Neurocutaneous melanocytosis carries a lifetime nonreducible risk of central nervous system melanoma and other morbidity and mortality from seizures, hydrocephalus, and other central nervous system conditions. MRI screening for infants born with large or giant CMNs is recommended to make the diagnosis of neurocutaneous melanocytosis.

Many different treatments have been advocated for the child with CMN; however, the overwhelming goals are to remove (or at least reduce) the risk of malignant transformation, preserve function, and improve cosmesis. Dermabrasion, chemical peels, and laser therapy have been reported to improve the appearance; however, none of these modalities completely removes nevus cells. To address malignant potential, only complete excision is a possible solution, and this is difficult, because nevus cells may extend beyond the skin and into the deep subcutaneous tissue and even the underlying muscle. The surgical options include direct excision and primary closure, serial excision, excision and skin grafting, and staged tissue expansion with subsequent lesion excision and flap reconstruction (Fig. 45-25). Treatment options have particular indications with respect to the location of the nevus. Scalp lesions are best treated with tissue expansion. Full-thickness skin grafting is best used for ear and eyelid reconstruction. Tissue expansion is associated with increased morbidity in lower extremity reconstruction, and therefore excision and grafting, even with previously expanded full-thickness skin grafts, is often the treatment of choice. In summary, CMNs often are treated surgically to decrease the risk of malignant degeneration to melanoma as well as to correct the significant appearance-related deformity.

Facial Reconstruction after Fracture

General Principles

As technologic advances raise the level of energy involved in modern systems of transportation, recreation, and weaponry, so follow increases in the degree of maxillofacial destruction related to misadventures with this technology. The first phase of care for the patient with maxillofacial trauma is activation of the advanced trauma life support protocol. Concomitant injuries beyond the face are the rule rather than the exception. The most common life-threatening considerations in the facial trauma patient are airway maintenance, control of bleeding, identification and treatment of aspiration, and identification of other injuries. Once the patient’s condition has been stabilized and life-threatening injuries treated, attention is directed to diagnosis and management of craniofacial injuries.

Physical examination of the face with attention to lacerations, bony step-offs, instability, tenderness, ecchymosis, facial asymmetry, and deformity guides the examiner to underlying hard tissue injuries. Traditional specialized radiography has largely been replaced by widely available high-resolution CT. Coronal, sagittal, and three-dimensional reconstructions of images further elucidate complex injuries.

Mandible Fractures

Mandibular fractures are common injuries that may lead to permanent disability if not diagnosed and properly treated. The mandibular angle, ramus, coronoid process, and condyle are points of attachment for the muscles of mastication, including the masseter, temporalis, lateral pterygoid, and medial pterygoid muscles (Fig. 45-26). Fractures are frequently multiple, and disturbances in dental occlusion reflect the forces of the many muscles of mastication on the fracture segments. Dental occlusion is perhaps the most important basic relationship to understand about fracture of the midface and mandible. The Angle classification system describes the relationship of the maxillary teeth to the mandibular teeth. Class I is normal occlusion, with the mesial buccal cusp of the first maxillary molar fitting into the intercuspal groove of the mandibular first molar. Class II malocclusion is characterized by anterior (mesial) positioning, and class III malocclusion is posterior (distal) positioning of the maxillary teeth with respect to the mandibular teeth (Fig. 45-27).

Nonsurgical treatment may be used in situations in which there is minimal displacement, preservation of the pretraumatic occlusive relationship, and normal range of motion. The goals of surgical treatment include restoration of pretraumatic dental occlusion, reduction and stable fixation of the fracture, and repair of soft tissue. Operative repair involves seating of the condyles within the glenoid fossa, achievement of maxillary-mandibular fixation with arch bars or intermaxillary screws to establish proper dental occlusion, and intraoral, extraoral, or combination surgical exposure of fracture lines. The mandibular plating approach follows one of two schools of thought: rigid fixation as espoused by the Association for Osteosynthesis/Association for the Study of Internal Fixation (AO/ASIF) and less rigid but functionally stable fixation (Champy technique). Regardless of the stabilization approach, one of the postoperative objectives is release from maxillary-mandibular fixation and resumption of range of motion as soon as possible to minimize the risk of ankylosis. Other potential complications include infection, nonunion, malunion, malocclusion, facial nerve branch injury, infra-alveolar or mental nerve injury, and dental fractures.

Orbital Fractures

Treatment of all but the simplest orbital injuries should include evaluation by an eye specialist to assess visual acuity and rule out globe injury. Orbital fractures may involve the orbital roof, floor, or lateral or medial walls. The most common orbital fracture is the orbital floor blow-out fracture caused by direct pressure to the globe and sudden increase in intraorbital pressure. Because the medial floor and inferior medial wall are made of the thinnest bone, fractures occur most frequently at these locations. These injuries may be treated expectantly if they are sufficiently small and without complication. However, larger blow-out fractures and those associated with enophthalmos (increased intraorbital volume), entrapment of inferior orbital tissues, or diplopia lasting >2 weeks generally require surgical treatment.²⁸ There are many approaches to the orbital floor, including the transconjunctival, subciliary, and lower blepharoplasty incisions. All provide access to the orbital floor and allow for repair with a multitude of different autogenous and synthetic materials. Late complications include persistent diplopia, enophthalmos, ectropion, and entropion.

Lateral and inferior orbital rim fractures also are not uncommon and are often associated with the zygomaticomaxillary complex fracture pattern, as discussed later.

Special mention should be made of two uncommon complications after orbital fracture. Superior orbital fissure syndrome results from compression of structures contained in the superior orbital fissure in the posterior orbit. These include cranial nerves III, IV, and VI, and the first sensory division of cranial nerve V. Compression of these structures leads to symptoms of eyelid ptosis, globe proptosis, paralysis of the extraocular muscles, and anesthesia in the cranial nerve V1 distribution. If the optic nerve (cranial nerve II) is also involved, symptoms include blindness and the syndrome is dubbed orbital apex syndrome. Both of these syndromes are medical emergencies, and steroid therapy and surgical decompression are considered.

Zygoma and Zygomaticomaxillary Complex Fractures

The zygoma forms the lateral and inferior borders of the orbit. It articulates with the sphenoid bone in the lateral orbit, the maxilla medially and inferiorly, the frontal bone superiorly, and the temporal bone laterally (Fig. 45-28). Zygoma fractures may involve the arch alone or many of its bony relationships. Isolated arch fractures manifest as a flattened, wide face with associated edema and ecchymosis. Nondisplaced fractures may be treated nonsurgically, whereas displaced and comminuted arch fractures may be reduced and stabilized indirectly (Gilles approach) or, for more complicated fractures, directly through a coronal incision.

The zygomaticomaxillary complex (ZMC) fracture involves disruption of the zygomatic arch, the inferior orbital rim buttress, the zygomaticomaxillary buttress, the lateral orbital wall, and the zygomaticofrontal buttress. The fracture segment tends to rotate laterally and inferiorly, creating an expanded orbital volume, limited mandibular excursion, an inferior cant to the palpebral fissure, and a flattened malar eminence. ZMC fractures are almost always accompanied by numbness in the infraorbital nerve distribution and subconjunctival hematoma. Displaced fractures are treated by exposure through multiple incisions to gain access to all of the buttresses requiring fixation. These include the upper eyelid incision (zygomaticofrontal buttress and lateral orbital wall), the subtarsal or transconjunctival incision (orbital floor and infraorbital rim), and the maxillary gingivobuccal sulcus incision (zygomaticomaxillary buttress). Again, significantly complex zygomatic fractures require wide exposure through a coronal approach.⁵

Naso-Orbital-Ethmoid Fractures

Naso-orbital-ethmoid (NOE) fractures are often part of a constellation of panfacial fractures and intracranial injuries. Anatomically, the fracture pattern involves the medial orbits, nasal bones, nasal processes of the frontal bone, and frontal processes of the maxilla. These injuries result in severe functional deficit and cosmetic deformity from collapse of the nose, ethmoids, and medial orbits; displacement of medial canthal ligament fixation; and nasolacrimal apparatus disruption. Telecanthus is produced by splaying apart of the nasomaxillary buttresses to which the medial canthal ligaments are attached. Treatment typically involves plating or wiring all bone fragments meticulously, potentially with primary bone grafting, to restore their normal configuration. Key to the successful repair of an NOE fracture is the careful re-establishment of the nasomaxillary buttress and restoration of the pretrauma fixation points of the medial canthal ligaments. If comminution is severe, this may be achievable using transnasal wiring of the ligaments.

Frontal Sinus Fractures

The region of the frontal sinus is a relatively weak structural point in the upper face. For this reason, it is a common location for fracture in facial trauma. The paired sinuses each have an anterior bony table that determines the contour of the forehead and a posterior table that separates the sinus from the dura. Each sinus drains through the medial floor into its frontonasal duct, which empties into the middle meatus within the nose. Treatment of a frontal sinus fracture depends on the fracture characteristics (Fig. 45-29).

Nasal Fractures

The nose is the most common facial fracture site due to its prominent location, and such fracture can involve the cartilaginous nasal septum, the nasal bones, or both. It is important to perform an intranasal examination to determine whether a septal hematoma is present. If present, a septal hematoma must be incised, drained, and packed to prevent pressure necrosis of the nasal septum and long-term midvault collapse. Closed reduction of nasal fractures may be performed under local or general anesthesia. Unfortunately, many, if not most, show some deformity upon final healing, requiring rhinoplasty if airway obstruction is present or if improved appearance is desired.

Panfacial Fractures

Fractures of multiple bones in various locations fall into the category of panfacial fracture. These may involve frontal and maxillary sinus fractures, NOE fractures, orbital and ZMC fractures, palatal fractures, and complex mandible fractures. The difficulty in the repair of these injuries lies not in the technical aspects of fixation but in the reestablishment of normal relationships between facial features in the absence of all pretraumatic reference points. Without proper correction of bony fragment relationships, facial width is exaggerated and facial projection is lost. The key point in approaching the patient with a panfacial fracture is first to reduce and repair the zygomatic arches and frontal bar to establish the frame and width of the face. The nasomaxillary and zygomaticomaxillary buttresses may then be repaired within this correct frame. Next, the maxilla may be reduced to this framework, followed by palatal fixation if needed. Finally, now that the midface relationships have been corrected, maxillary-mandibular fixation can be applied with the mandible in correct occlusion followed by plating of any mandibular fractures.²⁹

Ear Reconstruction

Acquired defects of the auricle have many causes, and many different choices for reconstruction are available. Reconstructive approach often is determined by the size and location of the defect. Small helical lesions may be simply excised as a wedge and closed primarily. Larger defects of the upper and middle thirds of the ear may use antihelical and conchal cartilage reduction patterns to reduce the circumference of the helix to allow primary closure. When helical defects are too large for this solution, local flaps may be used to close or re-create the missing tissue. Postauricular flaps created in staged procedures may be manipulated to create a skin tube mimicking the furled helix and bridging the gap of a defect. Alternatively, use of an Antia-Buch chondrocutaneous advancement flap combined with cartilaginous reduction allows for closure of defects³⁰ (Fig. 45-30). Even larger defects of the upper and middle thirds of the ear may be reconstructed with large local skin flaps combined with contralateral cartilage grafts or contralateral composite grafts. Although ear lobe defects are relatively simple to close primarily, lower third auricular defects that involve more than just the lobe are complex and require cartilaginous support, often combined with local skin flaps.

Nasal Reconstruction

Reconstruction of the nose requires appreciation of the nine aesthetic subunits that are defined by normal anatomic contours and lighting patterns (Fig. 45-31). In general, if a defect involves ≥50% of a subunit, the remainder of the subunit should be excised and included in the reconstruction. The nose can be thought of as being composed of three layers: skin cover, structural support, and mucosal lining. When a defect or anticipated defect is evaluated, it is useful to consider what layers of tissue will be missing so that a reconstruction can be devised that replaces each layer. Healing by secondary intention is successfully used in concavities such as the alar groove. Split- or full-thickness skin grafts may be used for superficial defects of the nasal dorsum or sidewall. Composite grafts may be used for the nasal tip or alar rim (see Fig. 45-3). Local random pattern flaps are useful in closing small defects of the dorsum and tip and may be combined with cartilage grafts if structural support is needed. Axial pattern flaps are commonly used for larger defects. These flaps have the advantage of being able to cover and revascularize underlying cartilage grafts and enjoy a close color match to surrounding skin. Workhorse flaps used in nasal reconstruction include the nasolabial flap and the paramedian forehead flap (Fig. 45-32). Even larger defects may require scalping flaps or free radial forearm flaps. Split calvarial cantilever bone grafts may provide the nasal dorsum support. Lining is generally achieved with scar tissue turnover flaps, mucoperichondrial flaps from within the nasal vestibule, or skin grafting of the underside of transposed flaps.

Lip Reconstruction

The lips are important for articulate speech, eating, maintenance of oral competence, facial expression, and aesthetic harmony of the lower face. Three layers of tissue form the upper and lower lips: skin, muscle, and mucosa. Blood supply is through the facial artery and its branches to the lip, the superior and inferior labial arteries. Lip defects can arise from trauma, burns, neoplasms, congenital lesions, clefts, or infection. As with almost all types of reconstruction, choice of technique is heavily dependent on defect size, location, and deficient structures. The goals of lip reconstruction are restoration of the competent oral sphincter with vermilion apposition, preservation of sensation, and avoidance of microstomia, all while preserving a near-normal static and dynamic appearance. In the upper and lower lip, vermilion-only defects can be corrected with advancement of the labial mucosa, often called a lip shave. In defects of less than one-third the horizontal length, enough redundancy is present to allow primary closure. More complex decisions must be made for defects that are between one-third and two-thirds of the total lip length.

The two categories of lip flap technique are transoral cross-lip flaps and circumoral advancements flaps. Cross-lip flaps include the Abbé flap and the Estlander flap. The Abbé flap was originally designed to reconstruct central upper lip (tubercle) defects with lower lip full-thickness tissue vascularized by one of the labial arteries (Fig. 45-33). The technique requires a second-stage procedure for division of the pedicle. The Estlander flap is similar in principle but is based laterally at the oral commissure and is used to reconstruct lateral upper or lower lip lesions. Both the Estlander and Abbé flaps are denervated, but sensation and perhaps even motor function return over months.³¹ The Karapandzic technique is an advancement-rotation flap technique designed for central lower lip defects. Although good function, sensation, and mobility are preserved, a side effect is reduction in the size of the oral aperture. The Webster-Bernard technique uses cheek tissue advancement flaps to replace defects with full-thickness or partial-thickness cheek incisions extended laterally from the commissure (Fig. 45-34). When performed bilaterally, both the Karapandzic and the Webster-Bernard methods can be used to reconstruct a complete upper or lower lip.

In addition, microvascular free tissue transfer reconstruction may be necessary in cases where there is no remaining lip. The radial forearm free flap is the most commonly used for this purpose, usually transferred with the palmaris longus tendon for lip support.

Eyelid Reconstruction

The eyelids protect the eye from exposure and are another crucial aesthetic structure of the face. They consist of an anterior lamella (skin and orbicularis oculi muscle) and a posterior lamella (tarsus and conjunctiva). The eyelid blood supply is robust, and ischemia is rarely a concern in reconstruction.

Upper Eyelid

Defects comprising <25% of the upper eyelid can generally be closed primarily in pentagonal approximating fashion (Fig. 45-35). For defects involving 25% to 50% of the upper eyelid, lateral canthotomy (release of the lateral canthal tendon) and cantholysis (release of the superior limb of the lateral palpebral tendon) can be performed to allow advancement and are often combined with use of a lateral semicircular flap (Fig. 45-36). Defects larger than 50% of the upper eyelid may be reconstructed with a Cutler-Beard full-thickness advancement flap or a modified Hughes tarsoconjunctival advancement flap (Fig. 45-37).

Lower Eyelid

Lower eyelid reconstruction considerations parallel those for the upper eyelid. In addition, special attention must be given to the prevention of scleral visibility and ectropion, which can arise from excessive vertical tension due to either technique or scarring. Similar reconstructive methods may be used, including direct closure, semicircular flaps and canthal release, and advancement flaps. Grafts may also be used if the defect is partial thickness. Full-thickness contralateral upper eyelid skin grafts are suitable for replacing the anterior lamella. The posterior lamella requires sturdy, nonkeratinized graft tissue, such as cartilage (tarsal, ear, or nasal septal) or hard palate mucosal grafts, to allow globe apposition.³²

Ptosis

In the normal eyelid, the orbicularis oculi muscle, Müller’s muscle, and levator palpebrae muscle act in concert to open and close the palpebral aperture and to maintain the level of the upper eyelid with respect to the pupil. Eyelid ptosis is created by derangement of this cooperative action. Ptosis may be congenital or acquired. Congenital ptosis is caused by lid anomalies, ophthalmoplegia, and synkinesis, whereas acquired ptosis can be neurogenic, myogenic, or traumatic in nature. Horner’s syndrome is a form of neurogenic ptosis caused by interrupted sympathetic innervation that leads to ptosis, miosis, and anhydrosis. A thorough evaluation of the ptotic patient includes a general eye and visual acuity examination, attention to signs of exposure or irritation, measurement of marginal-reflex distance, observation of the height of the supratarsal fold, and assessment of levator function. Severity of ptosis and degree of levator dysfunction are critical in deciding the appropriate corrective procedure (Table 45-11). Mild ptosis may be addressed with the Fasanella-Servat procedure, which involves excision of the superior tarsal edge, conjunctiva, and levator aponeurosis, and mullerectomy. Other corrections of mild ptosis usually involve variations on this procedure. Moderate ptosis with fair to good levator function may be treated with some form of a levator aponeurosis shortening procedure. Severe ptosis with poor levator function requires use of an alternate eyelid motor. The frontalis muscle fascial sling technique, which uses strips of fascial grafts sutured to the frontalis muscle, is one such solution.

Skull and Scalp Reconstruction

Scalp Reconstruction

The scalp is formed of five layers: Skin, subCutaneous tissue, galea Aponeurotica, Loose areolar tissue, and Pericranium (SCALP). The scalp is well vascularized bilaterally by branches of the external carotid artery, including the superficial temporal arteries, the occipital arteries, and the posterior auricular arteries. In addition, the bilateral supraorbital and supratrochlear arteries contribute to the ­forehead and anterior scalp blood supply. These vessels run in the subcutaneous tissue layer, just superficial to the galea. Because of this rich blood supply, scalp lacerations can lead to dramatic blood loss, an event that usually can be curtailed by a simple running/locking suture closure.

Partial-thickness scalp loss due to trauma usually occurs at the level of the loose areolar tissue plane and is treated initially with débridement of devitalized tissue. If a partial-thickness defect is small enough, primary closure or skin graft can be used. Although the cosmetic result is often less than desirable, all layers of the scalp will accept a skin graft, including the calvaria if it is burred down to its diploë. Because the scalp is relatively inelastic, scoring of the galeal layer often facilitates closure of full-thickness defects, but care must be taken to avoid lacerating the blood vessels just superficial to the galea. Larger areas of loss (4–8 cm) may be covered with large scalp flaps, as classically described by Orticochea.³³ Grafting of defects or donor sites leaves a visible area of alopecia. Tissue expansion has been very successful in replacing scarred or grafted regions with hair-bearing skin. Defects larger than 8 to 10 cm are best treated with microsurgical free tissue transfer. Total or subtotal scalp avulsions are rare injuries that usually occur when a person’s long hair becomes caught in rotating machinery. These potentially devastating injuries are ideally treated by scalp replantation, because the avulsed segment usually has preserved vessels (Fig. 45-38).

Calvarial Reconstruction

Autogenous bone remains the material of choice for reconstruction of skull defects. Its advantages include resistance to infection and ability to heal with strength. All autogenous bone sources have the disadvantage of donor site morbidity. Bone grafts can be harvested from a normal area of the calvaria, of which the outer table may be used as a graft for defects of limited size. Care must be taken during harvest to avoid compromise of the inner table. Rib bone may also be used, either as a split-rib graft or as a microsurgical free osseous flap. Unfortunately, use of ribs to reconstruct the skull may give an unappealing “washboard” appearance to the scalp. Another disadvantage of bone grafts, although not flaps, is graft resorption over time.

Alternative materials to autogenous bone exist for calvarial reconstruction, including methyl methacrylate, titanium, and hydroxyapatite (with or without bone morphogenic protein). Although they have the advantage of no donor site, these plastics and metals are associated with a higher risk of infection necessitating removal. Various formulations of calcium phosphate hydroxyapatites are being actively studied as bone replacement materials.

Head and Neck Reconstruction

The head and neck region has a compact arrangement of critical and complex structures encasing the essential routes to the gastrointestinal and respiratory systems. The tissues of the face, mouth, and cavities serve as a primary communication interface with the external environment through facial and verbal expression. Therefore, cancer resections with adequate safety margins can be severely and multiply debilitating. The management of head and neck cancer patients demands an integrated multidisciplinary team approach that includes the skills of ablative and reconstructive surgeons, medical and radiation oncologists, pathologists, nutritionists, and functional and psychological rehabilitation specialists.

Tumor-Ablative Surgery

The freedom available to the ablative surgeon to completely excise a tumor is limited, at least partly, by the capability of the reconstructive surgeon to restore anatomic continuity and achieve successful wound healing. A neck dissection to remove cervical lymphatics and nodes may be performed for prophylactic or curative intent, for more accurate prognostication by operative staging, and/or for solidification of plans for adjunctive treatments. It is important to be familiar with the tumor-node-metastasis (TNM) classification and staging of head and neck cancers. The N and M parameters are fairly constant for most head and neck cancers, whereas the T parameter varies according to tumor location.

Principles of Reconstruction

The reconstructive surgeon aims to restore lost anatomic components adequately. Residual deficits, seemingly inconsequential, may progress to psychological morbidity, societal malacceptance, and social withdrawal. Uncomplicated and timely wound healing is important to allow adjuvant therapies when indicated and smooth discharge to home and occupation.

Each defect can be addressed by a number of methods, but the technique must be decided for each individual patient. Although a more complex reconstruction might offer improved outcomes, it may bring an increased risk of complications. Some patients may therefore benefit from use of a simpler method with more acceptable anesthetic and operative risk rather than a gold-standard reconstruction. Such an approach may be appropriate, for example, for an elderly patient with an advanced T4 cancer and short life expectancy. Reconstruction is impossible for some functional losses, such as the enucleation of an eye, but replacement by a reasonably aesthetic prosthesis may be achievable.³⁴

Reconstructive Options by Region

Before the 1970s, autogenous tissue reconstructions were largely restricted to local or regional pedicled flaps, including the trapezius, pectoralis, and deltopectoral workhorse flaps. With microvascular free tissue transplantation, defects that were previously deemed nearly impossible to reconstruct can now be addressed in a single operation. Consequently, head and neck cancers that were historically unresectable have become more operable.

Intraoral Structures

The reconstructive choice for floor of mouth, tongue, and other intraoral defects is dictated by the dimension of the defect, the volume of tissue lost, and residual tongue mobility. The tongue and adjacent mucosal surfaces heal exceptionally well, so small defects may be treated by primary closure or even left to heal spontaneously. Smaller defects, less than one-fourth glossectomy, may be treated with a skin graft or perhaps primary closure if tongue mobility is preserved. Larger defects, more than one-third glossectomy, call for reconstruction by free tissue transfer, commonly a free radial forearm or anterolateral thigh flap for smaller- or larger-volume defects, respectively. Total glossectomy defects are a major challenge, and no ideal method exists to restore tongue motor functions. The primary goal is to protect the airway from aspiration. Swallowing and articulation are often suboptimal after total glossectomy reconstructions. Options include bulkier myocutaneous free flaps harvested from the anterolateral thigh, the back (latissimus dorsi), or the abdomen (rectus abdominis), or pedicled regional flaps (e.g., latissimus dorsi).³⁵

The reconstructive choice for other intraoral soft tissue defects should also take into consideration the specific characteristics of the defect, such as its thickness and dimensions, and involvement of the oral commissure, facial skin, and/or neck. Buccal defects, for example, may be adequately treated with a radial forearm free flap or a thin anterolateral thigh flap. Thicker defects may be more appropriately reconstructed with a fasciocutaneous anterolateral thigh free flap. Those that extend through the full thickness of the cheek to involve the external facial skin may be reconstructed with a cutaneous or myocutaneous anterolateral thigh free flap that has been folded to address the internal mucosal, external skin, and intervening soft tissue defects simultaneously.³⁶ When the contour of the neck is expected to be sunken and asymmetric after a neck dissection, it is possible to improve symmetry by insetting part of the flap into the neck. This maneuver also obliterates dead space and helps protect the adjacent major neurovascular structures.

Mandible and Midface

Mandibular defects may arise from the ablation of tumors involving the bone itself or from the need to satisfy clearance margins for adjacent soft tissue tumors. Segmental mandibular defects can be classified as isolated bone defects, compound defects (bone and oral lining or skin), composite defects (bone, oral lining, and skin), or extensive composite defects (bone, oral lining, skin, and soft tissues).³⁷ The primary goals of mandibular reconstruction are to restore bony continuity, masticatory (with accurate dental occlusion) and speech functions, and facial contour, and to maintain tongue mobility. Occasionally, a small segmental mandibular defect may be amenable to reconstruction with a nonvascularized bone graft, but these are poorly suited to the forces of mastication and are prone to resorption and failure amid radiotherapy or infection.

The best option for most segmental mandibular defects is the fibula bone free flap with an adjoined skin island supplied by reliable septocutaneous vessels (occasionally musculocutaneous perforators) from the peroneal artery and vein; this is termed a fibula osteoseptocutaneous free flap.³⁸ Its many desirable characteristics include (a) the ability to withstand multiple osteotomies (as long as the periosteal blood supply is protected) so that the bone can be folded to re-create the contour of any mandibular region, (b) an unmatched supply of sturdy bone length (22–26 cm in the adult) sufficient to reconstruct even angle-to-angle defects, (c) a bicorticocancellous structure that can tolerate the forces of mastication as well as the incorporation of osseointegrated dental implants, (d) acceptable donor site morbidity when the flap is appropriately harvested, and (e) a donor site location that allows a two-team approach for simultaneous tumor ablation and flap harvest.^39,40 Reasonable alternatives include vascularized bone flaps from the iliac crest, radius, or ribs. Extensive composite mandibular defects may demand more than one free flap (such as one anterolateral thigh free flap with one fibula osteoseptocutaneous free flap) to reconstruct the entire anatomy in one operation.⁴¹ Later, dental rehabilitation can be achieved with conventional dentures if alveolar ridge height and soft tissue quality allow. However, for select patients, osseointegrated dental implants offer a far superior alternative. These can be secured into the neomandible, either at the time of reconstruction (primarily; Fig. 45-39) or more commonly at a later stage (secondarily), and ultimately will support a dental prosthesis that can closely match the native dentition for excellent aesthetic and masticatory outcomes.⁴²

Similar principles are also applicable to other bony defects in the head and neck region, including maxillary and other midfacial defects, although non–load-bearing, facial, bone-only defects may be more amenable to nonvascularized bone grafting such as from the calvarium. The goals of midface reconstruction include the restoration of facial contour and projection, achievement of accurately occlusive maxillary dentition, provision of appropriate infraocular support, and sealed separation of adjacent nasal and oral cavities.

Esophagus and Hypopharynx

The goals of reconstruction for esophageal and hypopharyngeal defects, which may be circumferential or partial, are to maintain luminal patency, restore speech and swallowing, and avoid strictures, fistulas, and gastrointestinal anastomotic leaks. Reconstructive options for partial defects include primary closure, if luminal narrowing is insignificant, and skin (or dermal) grafts for partial-lining defects. A regional muscle flap may be useful for patching small full-thickness defects, but larger defects call for free tissue transfer of a jejunal flap or a tubed fasciocutaneous flap.⁴³ The jejunal flap involves the harvest of a proximal segment based on its mesenteric blood supply and inset into the neck in the isoperistaltic direction. Disadvantages of the jejunal flap include halitosis, slow swallowing transit times, and a “wet” voice. Tubed fasciocutaneous free flap options, including the anterolateral thigh and radial forearm flaps, are also popular; however, they may have a greater risk of stricturing than the free jejunal flap. Nevertheless, proponents of such flaps favor the resultant vocal qualities and faster transit times.

Recipient Vessels in the Head and Neck for Free Flaps

Commonly used recipient arteries for free tissue transfer in the head and neck include the ipsilateral superior thyroid, lingual, facial, superficial temporal, and transverse cervical arteries. End-to-side anastomosis with the carotid artery is associated with potentially lethal carotid blow-out injury. Anastomoses with contralateral vessels are useful when ipsilateral vessels are not available, such as in patients with recurrent cancer who have undergone previous free flap procedures or irradiation.³⁶ Vein grafts can be avoided by using carefully planned flaps that offer longer pedicles (such as the anterolateral thigh of fibula osteoseptocutaneous free flaps) but may occasionally be necessary. For venous drainage, tributaries of the superficial and deep jugular systems are convenient. Finally, protection of the major vessels and nerves of the neck is possible after neck dissection by overlaying residual free flap tissues. This also aids in improving the contour and symmetry of the neck for aesthetic purposes and obliterates any dead space.

Complications

Apart from the general complications that may be encountered with any major operation, there are several specific potential complications of head and neck ablative and reconstructive surgery. Specific intraoperative complications include air embolus, pneumothorax, and injuries to important vessels, lymphatics, or cranial nerves. Specific perioperative complications include carotid artery blow-out, flap necrosis, infections, saliva or chyle leakage, airway problems, and acute psychiatric disturbances. Examples of later complications are prolonged pain syndromes, fistulas, scar contractures, and problems associated with radiotherapy such as flap shrinkage (potentially with metalwork exposure) and osteoradionecrosis.

Facial Reanimation

Facial nerve paralysis is a debilitating and emotionally depressing condition that presents many functional and aesthetic problems. Loss of mimetic muscle activity leads to poor articulation and drooling from oral incompetence, exposure keratopathy from dysfunctional lacrimation and paralytic ectropion, and impaired socialization from facial disfigurement and difficulty expressing emotion. Facial nerve dysfunction has a number of possible causes, including oncologic resection, temporal bone or skull base surgery, trauma, congenital conditions (Möbius’ syndrome), and idiopathic origin. The main considerations in treatment are management of forehead and brow symmetry, eyelid closure, oral competence and symmetry, and smile dynamics. The long-term goals include normal static appearance, symmetry with movement, and restoration of voluntary muscular control. Although the best results usually require multistaged, complex surgeries, the elderly patient is better served by a single-stage procedure that provides immediate improvement.

Neural Techniques

Traumatic injuries to the facial nerve without segmental nerve loss are best treated with primary end-to-end neurorrhaphy of the facial nerve stumps. The success of this repair depends on accurate approximation of nerve ends and achievement of a tension-free epineural repair with fine sutures. In segmental facial nerve loss due to trauma or oncologic resection, interpositional nerve grafts lead to the most successful reconstruction and may approach the results of primary repair. Grafting ideally is performed at the time of the injury rather than in delayed fashion. Donor nerves include the cervical plexus, great auricular nerve, and sural nerve. Timing of reanimation after nerve repair depends on distance of the repair from the motor end plates. Axonal regeneration proceeds at approximately 1 mm/d, whereas motor end plates deteriorate at approximately 1% per week and are gone by 2 to 3 years. In general, facial tone returns approximately 6 months after repair and voluntary motion a few months later.⁴⁴ Problems associated with facial nerve repair and grafting are weakness, mass movement (synkinesia), and dyskinesia. If the proximal facial nerve stump is available but the distal stumps are not, the cervical plexus can be harvested and proximally anastomosed to the facial nerve stump and distally implanted into the mimetic muscles to allow neurotization and partial restoration of function.

Nerve transfer techniques borrow other local cranial nerves to innervate the distal facial nerve stump if grafting cannot be done. This requires the availability of distal facial nerve or nerve branch stumps. Typically used donor nerves include the ipsilateral hypoglossal nerve, spinal accessory nerve, and cross-face sural nerve graft from a contralateral facial nerve branch (redundant buccal or zygomatic branch). Disadvantages of this technique include those of nerve repair or grafting plus loss of donor nerve function and facial hypertonia. Transfer of the complete hypoglossal nerve creates ipsilateral tongue paralysis and hemitongue atrophy with mild to moderate intraoral dysfunction.⁴⁴

Muscle Transposition Techniques

All of the aforementioned neural techniques rely on the presence of a functional distal neuromuscular unit. When the distal neuromuscular unit is deficient, as in congenital facial paralysis or in situations in which reconstruction is not undertaken until 2 to 3 years after the original insult, muscle transposition is considered. Muscle transposition techniques require intense muscular retraining to achieve the intended dynamics. A classic muscle dynamic facial sling uses the temporalis muscle, innervated by the trigeminal nerve and perfused by the deep temporal branch of the internal maxillary artery. The muscle is released along with its aponeurosis from the temporal fusion line, reflected inferomedially, and attached to the modiolus at the oral commissure, the nasolabial fold, and potentially the orbicularis oculi. Disadvantages include lack of spontaneous movement, temporomandibular joint dysfunction, and soft tissue fullness over the zygomatic arch. Other transferable muscle units include the masseter muscle and the anterior belly of the digastric muscle.⁴⁴

Innervated Free Tissue Transfer

Microsurgical free innervated muscle transfer may be considered in the same situations as local muscle transfers but is especially appropriate when concomitant soft tissue augmentation is needed. Muscles described for this purpose include the gracilis, latissimus dorsi, serratus anterior, and pectoralis minor muscles. The procedure may be performed in a single stage if the proximal facial nerve stump is available for anastomosis or if a long enough donor muscle nerve is present to reach the contralateral facial nerve branches. Often, however, it is a staged procedure beginning with establishment of a local neural source via cross-facial nerve grafting. The extent of axonal regeneration through the graft is monitored using Tinel’s test. After sufficient axonal progression, approximately 6 to 12 months, the free muscle transfer is performed via vascular anastomoses to the superficial temporal or facial vessels, recipient and donor nerve coaptation, and fixation of the muscle to the zygoma superolaterally and to the nasolabial fold, upper lip orbicularis, and lower lip orbicularis inferomedially. Disadvantages of free muscle transfer include donor site morbidity, lengthy surgical times, and the need for specialized microsurgical skills.

Ancillary Procedures

One of the most important goals of treatment for facial paralysis is rehabilitation of the periocular region. This objective may be simply achieved with implantation of gold or platinum upper eyelid weights, which allows gravity to assist with lid closure. Static fascial slings are used to improve symmetry when comorbid conditions preclude more extensive and staged surgeries. Sling materials include tensor fasciae latae, Gore-Tex, and human acellular dermal allograft. Nonsurgical techniques play a significant role in improving facial symmetry, both as a primary intervention and an adjunct to surgery. Contralateral mimetic muscle hypertonicity is tempered with botulinum toxin injections. Finally, soft tissue rejuvenative techniques such as cervicofacial rhytidectomy, blepharoplasty, browlift, and midface lift can improve the soft tissue effects of facial nerve paralysis (Fig. 45-40).

Breast Reconstruction

Breast cancer is the most common malignancy and the second leading cause of cancer-related death among women in the United States. One in eight women will develop breast cancer sometime during their life. Breast reconstruction began as a means to reduce chest wall complications and deformities from mastectomy. Reconstruction has now been shown to benefit women in terms of psychological well-being and quality of life.⁴⁵ The goal of breast reconstruction is to re-create form and symmetry while avoiding delay in adjuvant cancer treatment. A number of studies have shown that breast reconstruction, both immediate and delayed, does not impede standard oncologic treatment, does not delay detection of recurrent cancer, and does not change the overall mortality associated with the disease.^46,47,48

Preoperative counseling of the breast cancer patient regarding reconstruction options should include discussion of the timing and type of reconstruction, alternatives to surgical reconstruction, and realistic expectations. The plastic surgeon and surgical oncologist must maintain close communication to achieve optimal results.

Timing of Reconstruction

Immediate reconstruction is defined as initiation of the breast reconstructive process at the time of the ablative surgery. This is usually done in patients with early-stage disease for whom there is low expectation of postoperative radiation therapy. Immediate reconstruction takes advantage of the preserved, supple skin envelope made possible by the skin-sparing mastectomy approach. In general, this allows a more aesthetically pleasing and symmetric reconstruction. It is also psychologically advantageous to the patient to avoid living with the mastectomy deformity, as in delayed reconstruction. Furthermore, the cost to the medical system is less with immediate reconstruction because fewer operations are required than for staged procedures. Disadvantages include the potential delay of adjuvant therapy due to surgical site complication, partial necrosis of mastectomy skin flaps, and the possibility that unanticipated postoperative radiation therapy is required. Breast reconstructions by all techniques are adversely affected by radiation therapy, and many surgeons feel reconstruction should be delayed until at least 6 months after treatment.

Delayed breast reconstruction is initiated at least 3 to 6 months after mastectomy. This approach avoids mastectomy flap unreliability and radiation therapy unpredictability. However, the patient is subjected to an additional operative procedure, and overall cosmetic result is often worse (especially with autologous tissue reconstruction).

Partial Breast Reconstruction

Over the last decade, many women have chosen breast conservation therapy (BCT) consisting of segmental mastectomy with sentinel lymph node biopsy and/or axillary lymph node dissection combined with postoperative whole-breast irradiation. Although this less invasive cancer treatment is quite beneficial to many women, significant breast deformity can result from the tissue removal and radiation-induced changes, especially in women with small breasts. Oncoplastic surgery refers to the set of techniques developed to lessen breast deformity from partial mastectomy, both in the delayed and the immediate settings. One of the most common methods of minimizing defect visibility in large-breasted women is to rearrange the breast parenchyma at the time of tumor extirpation using reduction mammoplasty techniques. Dermatoglandular pedicles supporting the nipple-areolar complex can be designed in any number of orientations to avoid the defect location. This procedure, combined with traditional contralateral breast reduction, can result in excellent cosmetic outcomes, often better than the preoperative appearance (Fig. 45-41). The lateral thoracodorsal flap, based on the lateral intercostal perforators at the inframammary fold, is particularly useful in correcting lateral breast defects⁴⁹

One drawback of these oncoplastic techniques when performed at the time of segmental mastectomy is the chance that, if the specimen margins are not clear, the reconstruction must be taken down to allow for reexcision. The oncologic implications of reusing the flap in this setting are unclear. Another shortcoming is the potential for fat necrosis, especially distally, in these nonaxial pattern flaps.

Implant-Based Reconstruction

By necessity or patient choice, many women undergo mastectomy for local control of breast cancer. In fact, recently in response to the increased recognition of multifocal disease and experience with poor aesthetic results after BCT in small-breasted patients, some women have chosen mastectomy despite being candidates for BCT. The simplest method of reconstructing the breast is placement of an implant into the mastectomy defect. Occasionally an implant may be placed at the time of mastectomy as a one-stage mound reconstruction. Usually, however, the first stage involves placement of a silicone shell tissue expander under the chest wall musculature (pectoralis major, serratus anterior, superior rectus sheath), followed by expansion of the skin and pocket regularly over the following few months. The patient then returns to the operating room for removal of the expander and placement of a saline or silicone breast implant (Figs. 45-42 and 45-43). After exhaustive investigation, silicone implants have been proven as safe and effective as saline implants in breast augmentation and reconstruction. After another few months, the nipple is reconstructed.

The advantages of the tissue expander/implant–based reconstruction are absence of donor site morbidity, short operative times, and short recovery periods. The disadvantages include the need for more reconstructive stages and longer cumulative time to completion of reconstruction. Implant breast reconstructions tend to lack the natural breast feel and ptotic appearance. This is particularly noticeable in unilateral reconstructions. Some of these disadvantages have been mitigated by the advent of nipple-sparing mastectomy and immediate, acellular dermal matrix-assisted implant reconstruction (Fig. 45-44). Complications related to prosthetic-based breast reconstruction include infection, malposition, hematoma, seroma, and rupture and deflation. Long term, the most common problem requiring reoperation is the formation of dense scarring around the implant (capsular contracture) causing firmness, visible deformity, and even discomfort. In addition, implants are medical devices that undergo mechanical wear, ultimately leading to leakage and deflation. All in all, the chance that a woman will need additional unanticipated surgery on her reconstructed breast within 5 years of prosthetic-based reconstruction is approximately 35%.⁵⁰ The cosmetic results worsen and the rate of complications increases when implants are placed in an irradiated chest wall, regardless of whether the radiation therapy occurs before or after reconstruction.

Total Autologous Tissue Reconstruction

An entirely different way to reconstruct the breast avoids the placement of implants in favor of using only the patient’s own redundant tissue. Indications for total autologous breast reconstruction are many and varied, including patient preference, previous or anticipated chest wall radiation treatment, a ptotic contralateral breast, and previous failed implant reconstruction. Contraindications are lack of a suitable donor site due to scarring or minimal adiposity, morbid obesity, and serious comorbidities that preclude a longer surgery and recovery period.

The most commonly used donor site is the abdomen. Most women in the breast cancer patient population have redundant skin and fat in the lower abdomen that may be transferred to the chest wall and fashioned into a breast mound. Many techniques have been developed to transfer this tissue, both as pedicled myocutaneous flaps and as free flaps. The workhorse abdominal flap for breast reconstruction is the pedicled transverse rectus abdominis myocutaneous (TRAM) flap. This flap is based on the superior epigastric vessels that run on the undersurface of the rectus abdominis muscle. A transversely oriented skin paddle with underlying fat is isolated based on its perforating vessels that course through the rectus muscle to join the main superior epigastric pedicle. The flap, along with the rectus muscle and blood supply, is tunneled under the anterior chest wall and delivered into the mastectomy defect, where it is then shaped into a breast mound. The donor site is closed in a manner similar to an abdominoplasty. The advantages of this and all total autologous reconstruction techniques are creation of a breast that looks and feels natural, that changes volume along with the patient’s weight (and the contralateral natural breast), and that avoids the potential complications of breast implants. In addition, patients are often pleased to have the incidental benefit of an abdominoplasty. The pedicled TRAM flap procedure is also relatively quick for a total autologous reconstruction. Downsides include the potential for partial or complete flap failure, fat necrosis, fullness in the upper abdomen from the tunneled pedicle, abdominal wall bulge or hernia, and abdominal wall weakness.

The free TRAM flap was introduced to improve on the sometimes limited volume of tissue that can be carried by the relatively indirect blood supply of the pedicled TRAM’s superior epigastric vessels. The free TRAM flap is similar to the pedicled TRAM flap but is based on the deep inferior epigastric vessels, which are the dominant blood supply to the lower abdomen. The flap is harvested as a free flap, and the deep inferior epigastric artery and vein are anastomosed to recipient vessels in the chest, usually the internal mammary or the thoracodorsal vessels. A refinement to this method is the muscle-sparing free TRAM flap procedure, in which less fascia and rectus abdominis muscle is harvested with the flap to minimize donor site morbidity. The ultimate muscle-sparing free TRAM flap is the deep inferior epigastric perforator flap (Fig. 45-45). In this case, the fascia is opened but no muscle is included with the flap, and the perforating vessels of the deep inferior epigastric system are dissected between the muscle fibers to join the main pedicle. When patients are carefully selected, muscle-sparing techniques decrease abdominal wall morbidity and increase useful pedicle length for microsurgery without significantly compromising flap perfusion⁵¹ (Fig. 45-46A,B). Finally, in some patients, the lower abdominal tissue may be transferred to the breast as a free flap without violating the abdominal wall fascia at all. The superficial inferior epigastric artery is often capable of supporting enough abdominal tissue volume to reconstruct the breast. Because this artery and its accompanying vein do not traverse the anterior rectus sheath, the flap can be harvested with no more abdominal wall ­morbidity than an abdominoplasty. Unfortunately, this artery is frequently absent or too diminutive in size to be used in the majority of patients. Despite the many advantages of microsurgical total autologous breast reconstruction, it is associated with longer operative times than pedicled TRAM procedures, requires expertise in microsurgery, and has the potential for complete flap failure due to microvascular thrombosis.

Implant and Autologous Tissue Reconstruction

The pedicled latissimus dorsi myocutaneous flap procedure is a straightforward, reliable method used for breast reconstruction. It is often reserved for reconstructing breasts when other methods have previously failed. The latissimus flap is relegated to second-choice status because it carries the major disadvantage of autologous tissue reconstruction (donor site morbidity) as well as all of the potential complications associated with breast implants. That aside, the latissimus flap/implant–based reconstruction can produce excellent cosmetic results with relatively low donor site morbidity (Fig. 45-47). The latissimus dorsi muscle with overlying skin paddle is elevated based on its thoracodorsal vessel pedicle, tunneled through the axilla, and delivered into the mastectomy site. After partial insetting, either a tissue expander or permanent implant is usually placed behind the muscle to give adequate volume to the reconstruction (Fig. 45-48). Drawbacks specific to this method include contour irregularity of the back, high rate of donor site seroma, and shoulder weakness (uncommon).

Accessory Procedures

After creation of the breast mound, refinements and accessory procedures are performed after approximately 3 months. These may include breast mound revision, scar revisions, fat grafting, and nipple-areola complex reconstruction. Scores of methods have been described for reconstructing the nipple. These include local flap techniques (e.g., star flap, skate flap, C-V flap), grafting techniques (contralateral nipple/areola sharing, groin skin, labia skin), and tattooing.

Radiation-Related Considerations

With some notable exceptions, most surgeons advocate avoidance of implant-based breast reconstruction in chest walls that have previously received radiation or are likely to receive radiation due to the relatively high rate of complications and disappointing results. Delayed total autologous reconstructions bring healthy nonirradiated tissue to replace the damaged fibrotic tissue and are the preferred mode of breast reconstruction in this setting. Similarly, latissimus dorsi/implant reconstructions replace much of the irradiated skin, which probably explains to some degree why, in the face of previous irradiation, implants fair better with an overlying latissimus flap than without.

The question of whether total autologous reconstructions should be done before or after anticipated radiation therapy is still controversial. Those in favor of delaying the reconstruction argue that an irradiated flap will exhibit shrinkage and fibrosis that subtracts from the overall aesthetic result. Those in favor of performing immediate reconstruction in this setting feel that, because immediate reconstructions have inherently better aesthetics, the imperfect result due to irradiation it is still comparable to the result of delayed reconstruction without the additional operation. To date, no prospective study has been performed comparing the two approaches.

Trunk and Abdominal Reconstruction

In the trunk, as in most areas of the body, choice of reconstructive method is determined by the location and size of the defect and the properties of the deficient tissue. A distinction is made between partial-thickness and full-thickness defects in deciding between grafts, flaps, synthetic materials, or a combination of techniques. Unlike the head and the lower leg, the trunk harbors a relative wealth of regional transposable axial pattern flaps that allow sturdy reconstruction, only rarely requiring distant free tissue transfer. Indeed, the trunk serves as the body’s arsenal, providing its most robust flaps to rebuild its largest defects.

Thoracic Wall

The chest wall is a rigid framework designed to resist both the negative pressure associated with respiration and the positive pressure from coughing and from transmitted intra-abdominal forces. Furthermore, it protects the heart, lungs, and great vessels from external trauma. Reconstructions of chest wall defects must emulate these functions.

The pectoralis major muscle is the workhorse pedicled flap for coverage of the sternum, upper chest, and neck. It is a Mathes and Nahai type V flap with one dominant pedicle (pectoral branch of the thoracoacromial artery) and several secondary segmental pedicles (intercostal perforators and the pectoral branch of the lateral thoracic artery).⁵² The muscle may be advanced or transposed on its dominant pedicle or used as a turnover flap based on its internal mammary perforators. Both methods are useful in covering the sternum after dehiscence or infection. Before the turnover flap is elevated, previous operative notes should be reviewed carefully to determine whether the internal mammary artery is still a viable perfusion source; the artery, especially the left, is frequently used for heart revascularization. The muscle may also be used for obliteration of intrathoracic dead space infections and as a myocutaneous flap for head and neck reconstruction. Although it is a reliable flap, the loss of the pectoralis major muscle results in upper extremity weakness and cosmetic deformity from loss of the anterior axillary fold.⁵³

The rectus abdominis muscle is a type III axial pattern flap that can be based on the superior epigastric vessels or the deep inferior epigastric vessels.⁵¹ When elevated as a myocutaneous flap it can be designed with a transverse (TRAM) or vertical rectus abdominis myocutaneous skin paddle. Although the vertical rectus abdominis muscle flap has better vascularized skin due to its multiple longitudinally oriented perforators, the TRAM flap provides a larger area of donor skin that can be primarily closed with an easily concealable scar. The rectus abdominis muscle is frequently used for lower sternum reconstruction when the pectoralis muscle is insufficient. It can also be used in pedicle or free flap configuration for repair of large chest wall defects from cancer resection (Fig. 45-49).

The latissimus dorsi myocutaneous flap is probably the most widely used flap in nonsternal chest wall reconstructions due to its broad size, location, reliability, and pedicle length. The flap is based on the thoracodorsal vessels arising from the subscapular system. Its secondary blood supply comes from the posterior intercostal and lumbar vessels.⁵² The arc of rotation of this flap can extend to most areas on the ipsilateral torso as well as to the abdomen, head and neck, and upper arm. The serratus anterior muscle can be included on the same vascular pedicle to further increase its surface area. Use of this donor site is relatively well tolerated, but shoulder weakness can be significant. The major drawbacks of the latissimus flap are its conspicuous scar and the high risk of seroma.⁵³

The trapezius muscle flap, based on the transverse cervical vessels, is generally used as a pedicled flap to cover the upper midback, base of neck, and shoulder. The superior portion of the muscle along with the acromial attachment and spinal accessory nerve are preserved to maintain shoulder elevation function. Other useful flaps of the thoracic region include the scapular/parascapular fasciocutaneous flap, the external oblique flap, the medially or laterally based thoracoepigastric skin flaps, and the omental flap.

When a full-thickness defect of the chest wall involves more than two adjacent ribs, the inherent rigidity of soft tissue flaps may provide insufficient chest wall integrity. Although cadaveric bone and autologous bone grafts have been used in the past to lend structural support, the availability of well-tolerated synthetic and biologic materials has become more common. These materials include polypropylene (Prolene), polyethylene (Marlex), and polytetrafluoroethylene (Gore-Tex) meshes, methyl methacrylate, and acellular dermal allograft. Even if these avascular foreign bodies must be removed due to chronic infection, often a thick fibrous layer of tissue will have formed that can maintain chest wall stability.⁵³

Abdominal Wall

The abdominal wall also protects the internal vital organs from trauma, but with layers of strong torso-supporting muscles and fascia rather than with osseous structures. The goals of reconstruction are restoration of structural integrity, prevention of visceral eventration, and provision of dynamic muscular support. Defects in the abdominal wall may arise from trauma, oncologic resection, congenital deformities, and infection. By far the most common reason for abdominal wall deficiency, however, is incisional fascial dehiscence and herniation after laparotomy. When a reconstruction plan is being formulated, careful physical examination and review of the medical history will help prevent selection of an otherwise sound strategy that, because of previous incisions and trauma, is destined for failure.

Partial Defects of the Abdominal Wall

Large defects of the abdominal skin and subcutaneous tissue are usually easily controlled with skin grafts, local advancement flaps, or tissue expansion. Myofascial defects are more difficult to manage. The abdominal wall fascia requires a minimal-tension closure to avoid dehiscence, recurrent incisional hernia formation, or abdominal compartment syndrome.⁵⁴ Prosthetic meshes are frequently used to replace the fascia in clean wounds and in operations that create myofascial defects. When the area of fascial deficiency is contaminated, as in infected mesh reconstructions, enterocutaneous fistulas, or viscus perforations, prosthetic mesh is avoided because of the risk of infection. A delayed reconstruction can be prefaced by insetting a resorbable polyglactin (Vicryl) mesh that will eventually granulate to allow skin grafting. The ensuing hernia is repaired later with prosthetics under cleaner conditions. The separation-of-components procedure has enjoyed much success in closing large midline defects without resorting to mesh. This procedure involves advancement of bilateral myofascial flaps consisting of the anterior rectus fascia/rectus abdominis/internal oblique/transversus abdominis muscle complex. Mobility of this myofascial unit is created by release of the external oblique muscle at the semilunate line. Midline defects measuring up to 10 cm superiorly, 18 cm centrally, and 8 cm inferiorly can be closed using separation of components.⁵⁵ This technique is less effective in closing lateral defects, for which regional muscle and fascial flaps are usually better suited (rectus abdominis flap, internal oblique flap, external oblique flap).⁵⁴

Full-thickness abdominal defects and large myofascial defects require large robust pedicled flaps or free flaps for closure. The tensor fasciae latae pedicled flap, based on the ascending branch of the lateral circumflex femoral vessels, is useful in reconstructing the lower two-thirds of the abdomen. Bilateral flaps can be used for very large defects, although the skin-grafted donor site is unsightly. The rectus femoris flap and the vastus lateralis flap can be used for smaller lower abdominal defects. The “mutton-chop” flap, which is an extended rectus femoris flap with fascia lata included distally, has been used successfully in closing massive defects.^56,57 Large defects of the upper abdominal wall may be repaired with pedicled extended latissimus dorsi flaps with attached pregluteal fascia. Very large full-thickness defects, especially superiorly, are best treated with free tissue transfer of large myofascial units such as the latissimus dorsi or the tensor fasciae latae. These can also be innervated flaps to reestablish contractile force and strength in the abdominal wall.

Extremity Reconstruction

Posttraumatic Reconstruction

With the beginnings of modern orthopedic and plastic surgery, improvements in the understanding of anesthesia, trauma resuscitation, infection, and the availability of early antibiotics, the requirement to amputate almost all open (compound) lower extremity fractures as a life-saving procedure gradually decreased while attempts at limb salvage became more realistic. The introduction and maturation of microsurgical techniques witnessed increasing successes in distal extremity replantations and free flap reconstructions. Soft tissue reconstruction thus advanced alongside evolving techniques of bone fixation, joint reconstruction, general vascular surgery, and acute multitrauma management. Current lower extremity reconstruction incorporates the use of vascularized bone, bone distraction techniques, composite tissue flaps, and functioning muscle transfers tailored to the given defect.⁵⁸ The future may behold the use of cadaveric vascularized composite allografts or even tissue-engineered vascularized composite tissue constructs.

Common causes of high-energy lower extremity trauma include road traffic accidents, falls from a height, direct blows, sports injuries, and gunshots. Understanding the anatomy of the lower limb compartments, nerve and vascular supplies, muscle functions, skeletal structure, and mechanics is essential for accurate bony and soft tissue restoration for function and appearance. Several limb-salvage scoring systems have been suggested to aid in the decision regarding whether to amputate or attempt limb salvage, but their routine use remains controversial; nevertheless, they can provide guidance during this life-altering decision process.⁵⁹ Compound fractures are often classified according to the system devised by Gustilo and colleagues (Table 45-12).⁶⁰

In addition to following standard multiple trauma evaluation and resuscitation guidelines, the multidisciplinary team must assess the injured limb for neurovascular status, soft tissue defects and degloving, configuration of fractures, and presence of compartment syndrome. Neurovascular status and evidence for compartment syndrome require frequent reassessment, particularly following interventions such as fracture reduction, splintage, and surgery. Bony stabilization may be critical to controlling fracture hemorrhage. Doppler ultrasound examination may help assess vascular integrity. Angiography is a lengthier procedure that provides more detailed information, but the team must be cognizant that delay to revascularization increases the risk of massive reperfusion injury and multiple organ failure.⁶¹ Compartment syndrome must be released with urgent fasciotomies when present. Its most critical early feature is increasingly severe pain especially on passive stretch of the compartment’s musculature; pulselessness, pallor, paresthesia, and paralysis are late signs. Compartment pressure monitors are useful in patients who are unconscious or have proximal nerve blocks in place. Antitetanus vaccine and antibiotics should be provided as soon as possible according to contemporary guidelines.⁶² An evaluation of the patient as a whole allows treatment to be planned within the context of comorbidities, socioeconomic considerations, and rehabilitative potential. The loss of plantar sensation historically favored below-knee amputation, but this is no longer an absolute recommendation.⁶¹

With the availability of microvascular free tissue transplantation, radical débridement (i.e., wound excision) can be adequate even for the largest wound. Early one-stage wound coverage and bony reconstruction is generally advocated and should be performed jointly by extremity trauma orthopedic and plastic surgical teams whenever possible.^61,62 It is reasonable for reconstruction to be deferred briefly if there remain tissues of questionable viability so that these can be reassessed and débrided as required. Placement of a temporary negative pressure dressing between débridements helps reduce bacterial ingress and the inflammatory response. If débridement produces an irregular dead space that cannot be completely obliterated, or if tissues remain questionable even after a second look, the resultant cavity may be filled with antibiotic-impregnated beads or available vascularized soft tissues to act as a spacer until definitive reconstruction is possible. This applies also to segmental bone losses within a soft tissue envelope of doubtful viability. In these situations, soft tissue coverage preferably is still achieved early; bony reconstruction can be completed at a later date, when both the bone and soft tissue envelope are stable and healthy. It remains debated whether fasciocutaneous or muscular flaps are superior for treating compound fractures. Dead space is critical to obliterate, and this is more readily achieved using muscle. Fasciocutaneous flaps may be superior for coverage of metaphyseal fractures, particularly around the ankle. Reviewed experimental data in animals suggest that diaphyseal tibial fractures with periosteal stripping are better covered by muscle instead of fasciocutaneous flaps.⁶³ Perforator-based chimeric flaps, such as the anterolateral thigh flap with a chimeric portion of vastus lateralis, can be designed to incorporate the best features of both tissue types for the given defect.

Once meticulous débridement is complete, the order of surgical repair is fracture stabilization followed by vascular repair and reconstruction of a stable soft tissue envelope. The choice of method for soft tissue coverage is determined by the location and extent of the injury (Table 45-13). Coverage for weight-bearing areas should be durable, stable (nonshearing), and sensate. Properly fitted footwear provides essential protection against pressure-related complications. Split-thickness skin grafts are reasonable for coverage of exposed healthy muscle or soft tissue. Local flaps may be used to cover smaller defects. Island pedicled perforator-based flaps are more versatile in design and inset, preserve viable muscles by excluding them from flap harvest, and can be a useful option when there is no significant degloving injury (Fig. 45-50). Using retrograde pedicle dissection, they can be harvested in freestyle fashion both to avoid the zone of injury and to suit the defect requirements.⁶⁴ Free tissue transplantation is preferred for larger or more complex defects, particularly in the middle and lower thirds of the leg where there are less soft tissues available for reconstruction. Free flaps need not be limited to providing only soft tissue coverage; incorporation of vascularized bone, such as of fibula or iliac crest, can aid in fracture management.⁶⁵ Chimeric flap configurations can improve flap insetting into composite defects. Flow-through designs, such as the anterolateral thigh flow-through free flap, can be used to bridge segmental vascular defects to revascularize the distal extremity.⁶⁶ Muscular flaps can be motor innervated to restore lost muscle functions at the recipient site.⁶⁷ Other techniques such as bone distraction and tissue expansion may be indicated in select circumstances. Traditional cross-leg flaps are almost never used now; they cause complete immobilization and increase the risk of deep vein thrombosis and contracture formation.

Osteomyelitis often complicates inadequately débrided compound leg fractures. Delayed coverage also appears to increase the risk of this dreaded complication. Generous irrigation, débridement, removal of dead bone (even in a segment), expedient antibiotic therapy, and healthy soft tissue coverage are important in both acute compound fracture and established posttraumatic osteomyelitis. Large segmental bone losses can be addressed with microvascular free transplantation of osseous flaps or distraction lengthening.^61,68

When limb salvage either is not possible or is not in the best interests of the patient, attention is directed to providing soft tissue stump coverage suitable for weight bearing and allowing ambulation with a properly fitted prosthesis. Ideally, local tissues are used; however, when they are unavailable or inadequate, the amputated part can be a useful source of skin grafts or tissues for microvascular free transfers to the stump, which preserves length and avoids a more proximal amputation.

Reconstruction after Oncologic Resection

The refinements in surgical ablation techniques, in adjuvant radiation therapy and chemotherapy, and in limb reconstruction methods have opened the possibility for curative limb-sparing treatments instead of amputation. Extensive soft tissue and segmental long bone defects from radical tumor resection and radiation-­compromised wound healing can often be reconstructed now by liberal importation of fresh tissues through microvascular free tissue transplantation tailored to the defect.

Diabetic Ulceration

The pathophysiology of primary diabetic lower limb complications has three main components: peripheral neuropathy (motor, sensory, and autonomic), peripheral vascular disease, and immunodeficiency. Altered foot ­biomechanics and gait caused by painless collapse of ligamentous support, foot joints, and foot arches change weight-bearing patterns. Blunted pain allows cutaneous fissuring and ulceration to progress. Multiflora infections are established amid local immunodeficiency and microvasculopathy. Frank neuroarthropathic Charcot’s foot deformities may ultimately result. Cutaneous ulcerations may chronically deteriorate relatively painlessly, involving deeper tissues, including bone. Persistent soft tissue infection and osteomyelitis, worsened by peripheral vascular compromise and immunodeficiency, traditionally ends in gangrene and amputation. More than 60% of nontraumatic lower extremity amputations occur in diabetics.⁶⁹ Indeed, the age-adjusted lower extremity amputation rate in diabetics (5.5 per 1000 diabetics) was approximately 28 times that of people without diabetes (0.2 per 1000 ­people).⁶⁹ Improved patient education and medical management, timelier detection of diabetic foot problems and referral for treatment, and the use of more refined techniques for wound management play important roles in improving the chances of limb preservation.⁷⁰

Diabetic patients with lower limb disease often have significant multisystemic comorbidities that must be optimized for surgery; strict perioperative control of blood glucose levels is mandatory. Clinical examination must include documentation of sensory deficits, vascular insufficiencies, and evidence of osteomyelitis. Plain radiographs, MRI, nuclear bone scans, and angiography or duplex imaging may be indicated. A patient with significant vascular disease may be a candidate for lower extremity endovascular revascularization or open bypass.⁷¹ Nerve conduction studies may diagnose surgically reversible neuropathies at compressive sites and aid in decisions about whether to perform sensory nerve transfers to restore plantar sensibility.⁷⁰ Antibiotic and fungal therapies should be guided by tissue culture results.

Plastic surgical management starts with thorough débridement of devitalized or infected tissues, purulent cavities, and osteomyelitic bone. Methods of wound closure are dictated by the extent and location of the postdébridement defect (Table 45-14). Vacuum-assisted closure may be appropriate for superficial defects. Skin grafts should be used cautiously and not in weight-bearing areas. Local and regional flaps can be used after careful evaluation of their vascularity given concurrent peripheral vascular disease and possible recent distal vascular bypass procedures. Microvascular free tissue transfers are appropriate when defects are large or when local flaps are not available. Combination lower extremity bypass and free flap coverage has proved beneficial for the treatment of the diabetic foot in terms of healing and reduction of disease progression.⁷² Orthopedic surgeons should be consulted to improve foot biomechanics and address bony prominences to reduce the risk of recurrent ulceration. Proper footwear (including orthotic devices and off-loading shoe inserts), hygiene, and toenail and skin care are essential.⁷⁰

Lymphedema

The lymphatic system provides a high-volume transport mechanism, clearing proteins and lipids from the interstitial space to the systemic vasculature by means of differential pressure gradients. Factors that contribute to circulatory lymphatic flow include segmental lymphangion contractility, skeletal muscle activity, and one-way valves that prevent backflow.^73,74 The lymphatics course throughout the body alongside the venous system, into which they eventually drain via the major thoracic and cervical ducts. With lymphatic obstruction, abnormal connections form between the superficial and deep lymphatics and between the lymphatic and venous systems. Lymphatic stagnation, hypertension, and valvular incompetence contribute to edema, inflammatory fibrovascular proliferation, and collagen deposition, causing firm, nonpitting swelling with peau d’orange cutaneous changes. Lymphoscintigraphy reveals the lymphatic anatomy and quantifies lymphatic flow. MRI provides anatomic information regarding lymphatic trunks, nodes, and obstructive lesions. It is essential to rule out neoplastic lymphatic invasion, especially after oncologic ablation, as a cause of secondary lymphedema. Lymphangiosarcoma is a rare cause of lymphedema that is deadly if diagnosed late.⁷⁵

Primary lymphatic obstruction may arise from congenital malformations of the lymphatic system such as lymphatic hypoplasia, functional insufficiency, or absence of lymphatic valves. Identified genetic causes include the autosomal dominant ­Milroy’s disease. Lymphedema praecox accounts for >90% of cases of primary lymphedema, generally appears during puberty but sometimes as late as the third decade, and occurs more commonly in females. It is usually unilateral and limited to the foot and calf. Lymphedema tarda appears after the age of 35 years and is relatively rare. Secondary (acquired) lymphedema is much more common, with filariasis being the leading cause worldwide.⁷⁶ In Western countries, secondary lymphedema is more commonly the result of neoplasms and their surgical treatments and radiotherapy.⁷⁶

The mainstays of management for lower extremity lymphedema are patient education and nonsurgical measures, including one or more of the following: use of external compressive garments and devices, limb elevation, administration of antibiotics for episodes of cellulitis, and specialized complex physical therapy.^77,78 Until recently, the efficacy of available surgical options was generally poor, so they were reserved for cases in which aggressive nonsurgical measures had failed. The classic Charles procedure involved radical excision of lymphedematous suprafascial tissues with skin grafting for coverage; cosmetic outcomes were often disastrous, and functional problems arose due to high rates of contracture, wound breakdown, and ulcerations. This method was later modified into multiple staged excisions of subcutaneous tissues. Other techniques include liposuction and bridging procedures.⁷⁸ Microsurgical lymphatic-lymphatic, lymphatic-venous, lymphatic-venous-lymphatic, and lymph node–venous anastomoses were all tried historically, with some techniques showing efficacy early on but long-term results showing high variability.⁷⁹ Recently, however, with an increased understanding of its pathophysiology and improved preoperative investigations, objective staging of lymphedema severity has become more accurate and allowed microsurgeons to tailor treatments for properly selected patients.^80,81 These factors, alongside improvements in microsurgical techniques, instrumentation, and long-term postoperative care, have provided better surgical results and a resurgence in interest in microsurgical treatment for lymphedema.⁷⁶ Nonsurgical techniques can be, and usually are, combined with any of the surgical methods.

Pressure Sore Treatment

A pressure ulcer is defined as tissue injury, usually over a bony prominence, due to pressure or a combination of pressure and shear forces. These wounds occur in patients debilitated by age, illness, immobilization from orthopedic injuries, or spinal cord injury. Prevention of pressure ulcers first requires identification of susceptible patients. Once such patients are identified, measures to prevent development of ulceration include frequent position changes (by both the patient and caretakers), use of pressure reduction equipment (low air loss mattresses and seat cushions, heel protectors), nutritional optimization, hygienic control of incontinence, and medical and/or surgical treatment of muscle spasm and joint contracture. Once an ulcer has developed, these same factors must be carefully evaluated and deficiencies corrected before embarking on a complex reconstructive treatment plan. Successful reconstruction also requires a medically stable, cooperative, motivated patient with adequate social support.

Pressure ulcers are described by their stage, based on depth of tissue injury (Table 45-15).⁸² Stage I and II ulcers are treated conservatively with dressing changes and basic pressure ulcer prevention strategies as already discussed. Patients with stage III or IV ulcers should be evaluated for surgery. The wound is examined for soft tissue infection or abscess, osteomyelitis, and involvement of deeper structures or spaces (e.g., joint space, urethra, spinal canal) to determine the urgency and specific requirements of the problem. Blood laboratory work and imaging studies are performed to help establish whether soft tissue or bone infection is present. Radiographs are usually adequate to rule out osteomyelitis; CT and MRI are helpful when plain films are equivocal. Wet gangrenous tissue and abscesses should be surgically débrided without delay to prevent or treat sepsis. In patients who do not meet the strict reconstruction criteria, débridement to healthy tissue without subsequent reconstruction may be the optimal treatment. If bone is present at the wound base, it should be débrided only to bleeding bone and left with a smooth contour. Complete ischiectomy should not be performed for ischial decubitus ulcers, because removal of one ischium only transfers subsequent pressure trauma to the contralateral ischium or the perineum. If osteomyelitis is present, which is best proven by culture of specimens obtained by intraoperative bone biopsy, long-term antibiotic therapy guided by microorganism sensitivity is indicated. A special note should be made regarding surgical treatment of spinal cord injury patients with T5 or higher injuries. In these patients, manipulation of a pressure ulcer and even simple urinary retention can trigger autonomic hyperreflexia. This dangerous condition is characterized by critically high blood pressure elevation and sympathetic discharge. Effective management is immediate recognition and reversal of trigger factors along with prompt administration of pharmacologic agents to prevent complications such as intracranial and retinal hemorrhage, seizure, cardiac irregularities, and death.

Direct closure of a pressure ulcer is rarely performed because it usually creates tension in the healing tissues already stressed by nonphysiologic external pressure, predisposing the closure to breakdown. Skin grafting is useful for shallow ulcers with well-vascularized beds that are not subjected to high mechanical shear. Unfortunately, these requirements remove most pressure ulcers from skin graft candidacy. The mainstay of deep pressure ulcer reconstruction is coverage with well-vascularized local flaps. There is debate over whether myocutaneous flaps are better than fasciocutaneous flaps for resurfacing regions prone to excess pressure and shear. Although myocutaneous flaps have excellent bulk and blood supply, muscle has low tolerance for ischemic injury. From an anatomic viewpoint, there is no pressure point on the human body where bone is padded by muscle. On the other hand, although fasciocutaneous flaps provide reasonable bulk and are teleologically appropriate, some argue that subcutaneous fat and fascia have low resistance to pressure and shear forces and have less robust perfusion than muscle.⁸³

The anatomic location of the pressure ulcer naturally has a profound impact on flap choice. Regardless of the wound site, however, the flap design should be very large, more than needed for closure, so that if the ulcer recurs the flap can be readvanced. In addition, care should be taken to place suture lines, the weakest part of the reconstruction, away from pressure points. Over the last few decades, patterns have developed in the selection of particular flaps for particular pressure sores. Sacral decubiti are well treated with gluteus maximus myocutaneous flaps (Fig. 45-51). In ambulatory patients, either the superior or the inferior gluteus muscle is spared to preserve hip extension function. The downside of using the gluteal muscle is the relatively bloody dissection. A common alternative is the gluteal fasciocutaneous advancement or rotational flap. Ischial pressure sores are generally due to sitting in a wheelchair with improper cushioning or insufficient position changes. A good first-choice flap for ischial wound reconstruction is the hamstring V-Y myocutaneous flap. The gluteus maximus flap may also be transposed inferiorly to cover this wound. A fasciocutaneous alternative is the posterior thigh flap, based on the continuation of the inferior gluteal artery. Trochanteric ulcers develop from prolonged positioning in the lateral decubitus position or from poorly fitting seat or wheelchair equipment. The tensor fasciae latae myocutaneous flap is an expendable muscle unit in ambulatory patients that has a reliable blood supply. It can be advanced superiorly or transposed on its long arc of rotation (see Fig. 45-51). Good second-choice flaps are the rectus femoris muscle flap and the vastus lateralis myocutaneous flap. When pressure sores are neglected, they can become confluent, forming large areas of deep tissue destruction. This dire situation may require hip disarticulation and use of the upper leg soft tissue as a total thigh flap for coverage.

The postoperative care after flap reconstruction of pressure ulcers is as important for success as the surgery itself. The authors recommend transfer of the patient from the operating room table onto an air-fluidized bed, where the patient will remain for the next 7 to 10 days in the hospital. Meticulous instructions must be given to the nursing staff and therapists regarding the positioning and rolling of the patient to prevent stressing the suture lines during these maneuvers. Nutrition and muscle spasm control are carefully maintained. The posthospitalization care plan, which should have been arranged preoperatively, is confirmed to avoid lapses in proper care. Patients with ischial sores are advised to abstain from sitting for 6 weeks to allow for sufficient healing. Care of the pressure ulcer patient is a labor-intensive process that requires attention to detail by the surgeon, nurses, therapists, caseworkers, and family. Unfortunately, small gaps in care inevitably lead to large gaps in the debilitated patient’s integument.

Reconstructive Transplant Surgery

Composite tissue allotransplantation (CTA), such as hand and face transplantation, has become a clinical reality and offers enormous potential for many reconstructive problems, including amputation of extremities. However, as with solid organ transplantation, there remains the issue of allograft rejection. In contrast to visceral organ transplantation, which involves homogeneous tissues, CTA may involve a combination of skin, subcutaneous tissue, nerve, blood vessels, muscle, tendon, and bone, and thus carry the antigenicities of all these tissue types. The basic principles of immunosuppression for solid organ transplantation have been applied to CTA and include therapy with a variety of combinations of T-cell–depleting agents, monoclonal antibodies, calcineurin inhibitors, antimetabolites, and rapamycin. The complications associated with immunosuppression are well known, including opportunistic infections, metabolic disturbances, and malignancies. Patients selected to undergo CTA, specifically hand transplantation, are young and healthy and therefore more resistant to immunosuppressive side effects than typically less robust solid organ recipients.

As with any surgical procedure, the benefits, success rate, and complications must be understood. Unlike solid organ transplantation, CTA is not a lifesaving procedure. There remains much debate over the risks associated with lifelong administration of potentially dangerous immunosuppressive agents to patients who have no life-threatening illness. The ultimate goal in CTA research is immune tolerance in which the recipient of the allograft remains fully immunocompetent yet does not mount an immunologic response to the transplanted allograft. Accomplishment of this goal would allow the decrease or possible elimination of immunosuppressive medications. If immune tolerance is achieved, CTA clinical applications will broaden dramatically as they become the next frontier in reconstructive surgery⁸⁴ (Fig. 45-52).

The American Medical Association defines cosmetic surgery as “surgery performed to reshape normal structures of the body to improve the patient’s appearance and self-esteem.” Reconstructive surgery is performed on structures of the body that are abnormal due to congenital defects, developmental abnormalities, trauma, infection, tumors, or disease. It is generally performed to improve function but may also be done to approximate a normal appearance.⁸⁵ In practical terms, there are both reconstructive and cosmetic elements to almost every plastic surgery case, and the definition of “normal” structure is sometimes unclear. Nevertheless, there are patients for whom it is a priority to make surgical changes to their bodies in the clear absence of a functional deformity. Aesthetic surgery patients present a unique challenge to the plastic surgeon, because the most important outcome parameter is not truly appearance, but patient satisfaction. Optimally, a good cosmetic outcome will be associated with a high level of patient satisfaction. For this to be the case, the plastic surgeon must do a careful analysis of the patient’s motivations for wanting surgery, along with the patient’s goals and expectations. The surgeon must make a reasonable assessment that the improvements that can be achieved through surgery will meet the patient’s expectations. The surgeon must appropriately counsel the patient about the magnitude of the recovery process, the exact location of scars, and potential complications. If complications do occur, the surgeon must manage these in a manner that preserves a positive doctor-patient relationship.

Assessment of Facial Aesthetics

A thorough evaluation of the patient who presents for facial aesthetic surgery should start with elicitation of the patient’s chief complaint, and the examination should be focused on that region. Physical examination of the entire face should note skin quality as well as the presence of redundant skin on the neck, jowls, and eyelids. Depth of the nasolabial folds and the presence of “marionette” lines on the chin should be noted. Brow position should be evaluated, along with the distance from brow to hairline. Bulging fat in the lower eyelid region and the presence of a “tear trough” deformity, or deep fold at the lid-cheek junction, should be evaluated. Facial fat atrophy and descent, a hallmark of facial aging, should be noted.

Blepharoplasty and Browlift

Excess skin and adipose deposits of the upper eyelid are approached through an incision based on the supratarsal crease. Careful attention to marking will avoid the complication of overresection. A strip of orbicularis muscle is often excised to accentuate the supratarsal fold. Fat deep to the orbital septum is resected selectively. In the lower lid, excess skin is removed through a subciliary incision. Lower eyelid fat may be either excised or repositioned. Complications can include hematoma, lower lid retraction, and injury to ocular muscles. If a hematoma forms in the retro-orbital region, a true surgical emergency exists. Permanent vision loss can occur if it is not immediately decompressed. Brow ptosis, judged relative to the superior orbital rim, can be corrected through a number of incisions (Fig. 45-53).⁸⁶

Facelift

Correction of jowls, nasolabial folds, and redundant neck skin can be accomplished with a facelift procedure that both removes skin and tightens the superficial musculoaponeurotic system (SMAS) layer. The SMAS lies deep to the subcutaneous tissue and contains the muscles of facial expression. The facial nerves are in a plane just deep to the SMAS. The SMAS can be simply plicated or a portion of it excised and closed. A sub-SMAS dissection technique can help to elevate and develop this layer in separate fashion, with care being taken to avoid injury to the underlying facial nerves. The incisions for most facelift techniques are preauricular with extension into the temporal hairline superiorly and into the retroauricular region posteriorly and inferiorly (Figs. 45-54 and 45-55). The platysmal layer is continuous with the SMAS layer and can be plicated through a small neck incision to eliminate the appearance of vertical bands along the muscle edge. The most common facelift complication is hematoma, which may require operative drainage to prevent skin flap necrosis. Injury to facial nerves, most often temporal branch and marginal mandibular branch, is seen in approximately 1% of cases.⁸⁷

Rhinoplasty

The key to understanding rhinoplasty is appreciating the complex nasal anatomy (Fig. 45-56) and the way in which altering this framework will impact the appearance of the nose. Evaluation of the rhinoplasty patient not only should include the aesthetic complaints, but also should consider the function of the nasal airways. Nasal airway obstruction can occur from several structural problems. A deviated septum can severely impede airflow, as can problems with the internal nasal valve. Obstruction at the internal nasal valve, which is the junction of the upper lateral cartilage and septum, can be identified by applying lateral traction on the cheek skin to open the valve and observing whether airflow improves (Cottle sign). Airway obstruction can be addressed surgically at the time of rhinoplasty. Aesthetic deformities of the dorsum of the nose are treated by a combination of osteotomies, which serve to reposition the nasal bones, and rasping of the bone. Aesthetic deformities of the tip of the nose are treated by reducing the width of the lower lateral cartilages and/or sewing the cartilages together to reduce tip width. Small tips can be augmented with cartilage grafts harvested from septum or auricle (Fig. 45-57). Complications of rhinoplasty include induction of new nasal airway obstruction and a variety of aesthetic deformities.⁸⁸

Suction Lipectomy

Liposuction involves the removal of adipose tissue through minimal incisions using a hollow suction cannula. Although the scarring is quite innocuous, a key principle of liposuction is that fat is being removed without skin tightening. Therefore, one relies on the patient’s inherent skin elasticity to provide retraction over the treated adipose depot. Assessment of skin tone is a vital part of the patient evaluation. If there is skin laxity in the area to be treated, it may worsen after liposuction. Importantly, liposuction should be used as a tool for contouring prominent adipose depots and is not considered a weight loss treatment. The best candidates for liposuction are individuals who are close to their goal weight and have focal adipose deposits that are resistant to diet and exercise (Fig. 45-58). The suction cannula removes fat by avulsing small parcels of adipose tissue into small holes at the cannula tip. With standard suction lipectomy, fat is removed only when the cannula is actively moved through the tissue planes. Minimal tissue effects are seen when the cannula is stationary. In general, larger-diameter cannulas remove adipose tissue at a faster rate but carry a higher risk of causing contour irregularities such as grooving and uneven removal of fat. Newer liposuction technology uses an ultrasonic probe to emulsify the fat via cavitation before suction. Advocates of ultrasonic liposuction report that the technique provides a more even and uniform removal of adipose tissue. Recognizing that no one technique is best for all patients and all anatomic regions, many surgeons use ultrasonic energy selectively.

A major advance in the field of liposuction was the development of tumescent local anesthesia. This method involves the infiltration of very dilute lidocaine and epinephrine (lidocaine 0.05% and epinephrine 1:1,000,000) in large volumes throughout the subcutaneous tissues. Tumescent volumes may range from one to three times the anticipated aspirate volume. The dilute lidocaine provides sufficient anesthesia to allow the liposuction to be performed without additional agents, although many surgeons prefer to use sedation or even general anesthetic when large volumes of fat are to be removed. When general anesthesia is used, the lidocaine dose may be reduced or even eliminated. With tumescent anesthesia, the absorption of the dilute lidocaine from the subcutaneous tissue is very slow, with peak plasma concentrations occurring approximately 10 hours after the procedure.⁸⁹ Therefore, the standard lidocaine dosing limit of 7 mg/kg may be safely exceeded. Current recommendations suggest a limit of 35 mg/kg of lidocaine with tumescent anesthesia.⁹⁰ A very important component of the tumescent anesthetic solution is the dilute epinephrine, which limits blood loss during the procedure.

Safety issues are paramount for liposuction because of potential fluid shifts postoperatively and hypothermia. If ≥5000 mL of aspirate is to be removed, the procedure should be performed in an accredited acute care hospital facility. After the procedure, vital signs and urinary output should be monitored overnight in an appropriate facility by qualified and competent staff who are familiar with perioperative care of the liposuction patient.⁹⁰

Autologous Fat Grafting

The concept of reinjecting fat tissue harvested by liposuction has been put into practice for decades. Key to the technique is a processing step in which the sterilely collected fat is separated from the aqueous (primarily tumescent fluid) and free lipid fractions. This can be done by centrifugation or filtering. The adipose grafts are then injected into the tissues using specially designed blunt-tipped cannulas. Small aliquots of graft material are injected with each cannula pass, and the fat is interposed within the vascularized tissues of the recipient bed in small channels. Autologous fat grafting has been used primarily for facial aesthetic augmentation of the midface, but has been gaining popularity for breast aesthetic applications, buttock augmentation, and breast reconstruction.

Excisional Body Contouring

When significant skin laxity is present, improvement in contour can be achieved only through skin excision. Therefore, all body-contouring surgery represents a trade of excess skin for scar, and this must be emphasized during patient consultation. The patient willing to accept scars in exchange for improved contour is likely to be satisfied with the procedures. With the increased number of bariatric surgery procedures over the past decade, body-contouring surgery has become very popular and is emerging as a new subspecialty of plastic surgery.

Abdominoplasty/Panniculectomy

Abdominoplasty/panniculectomy is the most common body-contouring procedure and can range from a limited-incision skin removal in the lower abdomen to a major skin excision with transposition of the umbilicus and placation of the rectus muscles to further enhance contour.⁹¹ Some patients may benefit from a concurrent vertical incision to remove skin in two vectors (Fig. 45-59). Possible complications include skin necrosis, persistent paresthesias of the abdominal wall, seroma, and wound separation. Necrosis of the umbilicus may complicate preservation of that structure if the stalk is excessively long or an umbilical hernia is repaired. Adding a vertical resection increases the incidence of skin necrosis, especially at the confluence of scars in the lower abdomen.

Brachioplasty (Arm Lift)

Brachioplasty, or arm lift, leaves a visible longitudinal scar on the upper arm. Therefore, it is reserved for patients with excessive skin in that region. The patient willing to accept the scar can be happy with the results. Complications include distal seroma and wound separation. Paresthesias in the upper arm and forearm may occur secondary to injury of sensory nerves passing through the resection area, although this rarely affects function. Scar contracture in the axilla may limit shoulder excursion in rare cases and require revision.

Thigh and Buttock Lift

Treatment of loose skin on the thighs and buttocks involves a spectrum of operations customized to the individual patient. The outer thighs can be lifted at the same time that an abdominoplasty is performed with one continuous scar along the belt line. The same scar can be continued all the way around the back to lift the buttocks as well. This combination of abdominoplasty, thigh lift, and buttock lift is commonly referred to as a circumferential lower body lift. The inner thighs can be contoured by lifting the skin and placing the incisions along the groin crease. Firmly anchoring the deep thigh fascia to Colles’ fascia is essential to help prevent spreading of the labia. In cases of severe excess skin on the inner thighs, a long vertical incision is necessary. Complications of thigh and buttock lift include seroma, wound separation, skin necrosis, and change in the shape of the genital region (with possible sexual dysfunction). Blood loss during the procedure may necessitate transfusion.

Reduction Mammaplasty

Breast reduction is performed to treat symptoms of macromastia, most commonly consisting of the triad of upper back pain, bra strap grooving, and rashes under the fold of the breasts. Although this procedure has reconstructive indications, the aesthetic outcome is of considerable importance. Fundamental to the success of the procedure is the establishment of symmetric and proper nipple position. Nipple ptosis is graded by the nipple position relative to the inframammary fold (IMF). Grade 1 ptosis describes a nipple ≤1 cm below the IMF. Grade 2 ptosis describes a nipple 1 to 3 cm below the IMF. Grade 3 ptosis describes a nipple position >3 cm below the IMF. Pseudoptosis or bottoming out is a term used to describe the descent of the breast tissue below the nipple and is a potential long-term complication of breast reduction. In addition to classification of nipple ptosis, a thorough preoperative evaluation also includes measurement of the distance from sternal notch to nipple bilaterally, as well as measurement of the distance from nipple to IMF. The base width of the breast should also be considered. Many patients are found to have significant baseline asymmetries in these measurements. Preoperative breast cancer screening consistent with current American Cancer Society guidelines should be performed for all patients undergoing elective breast reshaping surgery. The planned new nipple position should be symmetrical at the IMF along the breast meridian. There are many technical variations of the breast reduction procedure, but nearly all of them have common elements of reshaping the skin envelope in three dimensions and moving the nipple to a new location on a vascularized tissue pedicle. The pedicle is de-epithelialized to preserve the subdermal vascular plexus. Fig. 45-60 shows the classic “keyhole” Wise pattern reduction technique. The skin resection is designed to create a conical shape, and the nipple is transposed on an inferiorly based pedicle.⁹² This results in an inverted T-shaped scar. Fig. 45-61 shows a patient treated using this technique. All breast reduction techniques keep the scars on the lower half of the breast so they are covered by clothing. Techniques have been designed to minimize scar length and even eliminate the horizontal component in the IMF. Fig. 45-62 depicts a vertical scar skin resection pattern with the nipple preserved on a superior pedicle.^93,94 For excessively large breasts, the required pedicle length may be too long to provide adequate blood supply to the nipple. In such cases, the nipple is removed and replaced onto a viable tissue bed as a full-thickness skin graft. Complications of breast reduction include decreased nipple sensation, nipple loss (rare), skin necrosis, hematoma, and fat necrosis. This last complication can result in a firm mass of scar within the breast that may need careful evaluation and follow-up to distinguish it from a neoplastic mass. Long-term complications include inability to breastfeed and pseudoptosis, as mentioned earlier.

Mastopexy

In contradistinction to breast reduction, in which patients are treated for symptoms related to heavy breasts, mastopexy is a three-dimensional reshaping of the breast performed with no or minimal volume removal. The principles are the same, however. The skin envelope is contoured, and the nipple location is optimized. Because the degree of ptosis may be less severe than in breast reduction cases, the patterns of skin resection can vary widely. Minimal patterns may involve excision of just a crescent of skin from above the areola or a periareolar (“donut”) resection. The Wise keyhole pattern can be used for larger skin excisions.

Augmentation Mammaplasty

Although the use of prosthetic implants can successfully increase breast size, the surgeon must fully understand both the risks of the biomaterials and the way in which a specific implant of given shape and size can be surgically integrated into the existing breast mound to achieve the desired result.⁹⁵ To address the latter point, the surgeon must first consider the possible surgical approaches for implant placement. The three commonly used incisions for placement of cosmetic breast implants are inframammary, periareolar, and axillary (Fig. 45-63).⁹⁶ A transumbilical breast augmentation technique has been advocated by some surgeons more recently, but critics of this approach point out that there is poor control over the dissection of the implant pocket and that direct access to the tissues of the breast is inadequate to control bleeding vessels. In addition, only saline implants can be used with transumbilical breast augmentation because the prefilled silicone implants are too large to pass through the incision and narrow tunnel. The implants may be placed in a subglandular or subpectoral position (Fig. 45-64). Many surgeons prefer the subpectoral placement because it provides greater soft tissue coverage in the upper pole of the breast and can hide contour irregularities related to the implant. This soft tissue coverage is especially important with saline implants, because visible rippling can occur. The next issue to consider is existing nipple position. If a patient has mild ptosis, the sheer volume of the implant may raise the nipple to an acceptable level. For more severe ptosis, a concurrent mastopexy is necessary. Some surgeons advocate performing the mastopexy as a second stage after the implant has settled into position.

Potential complications related to the implant itself are numerous, and the patient must be fully informed of these possibilities before undergoing surgery. One important point is that there is a high likelihood that the patient will require a second operation to address an implant problem. The implant complications are essentially all local. Although there was concern in the past that implants might be associated with systemic connective tissue disorders, large epidemiologic studies have not supported such a link. The fears over implant safety were so strong that the Food and Drug Administration (FDA) declared a moratorium on the use of silicone gel implants in 1992. At that time, saline-filled implants were still allowed for general cosmetic use. Data were compiled on silicone gel implants, and these devices were approved by the FDA for general use in 2006.⁹⁷ A potential implant complication is rupture of the device. For saline implants, this results in rapid deflation. For silicone gel implants, the rupture may be not be obvious and can be confirmed by MRI. Another complication is capsular contracture, which results in a tight envelope of scar that can distort the shape of the implant and cause pain in severe cases. A complication more common to saline devices is the appearance of rippling in the upper pole of the device. Implant malposition can also distort the breast shape and require reoperation. Safety data printed on the official FDA-approved package insert from one of the device manufacturers show the incidence of reoperation to be 29.9% over 7 years in a study of 901 women undergoing primary breast augmentation with saline-filled implants (postapproval study). The rate of severe capsular contracture (grade 3 or 4 on a 4-point scale) was 15.7%, and the rate of implant rupture was 9.8%.⁹⁸ For silicone gel–filled implants, the reoperation rate was observed to be 23.5% over 4 years in a study of 455 women undergoing primary breast augmentation. The rate of severe capsular contracture (grade 3 or 4 on a 4-point scale) was 13.2%, and the rate of implant rupture (evaluated by MRI) was 2.7%. The three most common reasons for operation, in order, were capsular contracture (28.9%), implant malposition (15.6%), and ptosis (14.1%). For secondary augmentation, complication rates were much higher, with the reoperation rate over 4 years rising to 35.2%. The rate of capsular contracture was 17.0%, and the rate of implant rupture was 4.0%.⁹⁹

Another concern regarding breast implants is the issue of whether adequate mammography can be performed after augmentation. Displacement techniques can be used by the mammographer to view the breast tissue. Although patients are advised that implants may affect mammography, a study surveying women who did and did not undergo breast augmentation found no statistical difference in survival or detection of carcinoma between the two cohorts.¹⁰⁰

Gynecomastia

Male breast excess or gynecomastia can be caused by a host of medical diseases and pharmacologic agents. Medical conditions associated with gynecomastia include liver dysfunction, endocrine abnormalities, Klinefelter’s syndrome, renal disease, testicular tumors, adrenal or pituitary adenomas, secreting lung carcinomas, and male breast cancer. Causative pharmacologic agents include marijuana, digoxin, spironolactone, cimetidine, theophylline, diazepam, and reserpine. Although these numerous causes must be considered, a majority of patients present with either idiopathic enlargement of the breast parenchyma (more common in teenagers) or simple skin ptosis and excess adipose deposits on the chest wall (considered pseudogynecomastia; more common in adult males). To obtain a flat chest, both liposuction and/or skin excision techniques can be used.¹⁰¹