10-01 Skin Grafts, Substitutes and Principles of Flaps-1

HISTORY OF SKIN GRAFTSRatner 1 and Hauben and colleagues 2 give excel- lent overviews of the history of skin grafting. The following highlights are excerpted from these two sources. Grafting of skin originated among the tilemaker caste in India approximately 3000 years ago. 1 A common practice then was to punish a thief or adulterer by amputating the nose, and surgeons of their day took free grafts from the gluteal area to repair the deformity. From this modest beginning, skin grafting evolved into one of the basic clinical tools in plastic surgery. In 1804 an Italian surgeon named Boronio suc- cessfully autografted a full-thickness skin graft on a sheep. Sir Astley Cooper grafted a full-thickness piece of skin from a man’s amputated thumb onto the stump for coverage. Bunger in 1823 success- fully reconstructed a nose with a skin graft. In 1869 Reverdin rekinkled worldwide interest in skin graft- ing with his report of successful pinch grafts. Ollier in 1872 pointed out the importance of the dermis in skin grafts, and in 1886 Thiersch used thin split- thickness skin to cover large wounds. To this day the names Ollier and Thiersch are synonymous with thin (0.005–0.01-inch) split-thickness grafts. Lawson, Le Fort, and Wolfe used full-thickness grafts to successfully treat ectropion of the lower eyelid; nevertheless, it is Wolfe whose name is generally associated with the concept of full- thickness skin grafting. Krause popularized the use of full-thickness grafts in 1893, known today as Wolfe-Krause grafts. Brown and McDowell 3 reported using thick split- thickness grafts (0.01–0.022-inch) for the treatment of burns in 1942. In 1964 Tanner, Vandeput, and Olley 4 gave us the technology to expand skin grafts with a machine that would cut the graft into a lattice pattern, expanding it up to 12X its original surface area. In 1975 epithelial skin culture technology was published by Rheinwald and Green, 5 and in 1979 cultured human keratinocytes were grown to form an epithelial layer adequate for grafting wounds. 6 ANATOMY The character of the skin varies greatly among individuals, and within each person it varies with age, sun exposure, and area of the body. For the first decade of life the skin is quite thin, but from age 10 to 35 it thickens progressively. At some point during the fourth decade the thickening stops and the skin once again begins to decrease in sub- stance. From that time until the person dies there is gradual thinning of dermis, decreased skin elastic- ity, and progressive loss of sebaceous gland con- tent. The skin also varies greatly with body area. Skin from the eyelid, postauricular and supraclavicular areas, medial thigh, and upper extremity is thin, whereas skin from the back, buttocks, palms of the hands and soles of the feet is much thicker. Approximately 95% of the skin is dermis and the other 5% is epidermis. 7 The dermis contains seba- ceous glands and the subcutaneous fat beneath the dermis contains sweat glands and hair follicles. The skin vasculature is superficial to the superficial fas- cia and parallels the skin surface. The cutaneous vessels branch at right angles to penetrate subcuta- neous tissue and arborize in the dermis. The final destination of these blood vessels is a capillary tuft that terminates between the dermal papillae. TERMINOLOGY An autograft is a graft taken from one part of an individual’s body that is transferred to a different part of the body of that same individual. An isograft is a graft from genetically identical donor and recipient individuals, such as litter mates of inbred rats or identical human twins. An allograft (previ- ously homograft) is taken from another individual of the same species. A xenograft (heterograft) is a graft taken from an individual of one species that is grafted onto an individual of a different species. A split-thickness skin graft (STSG) contains epi- dermis and a variable amount of dermis. A full- thickness skin graft (FTSG) includes all of the der- mis as well as the epidermis 8 (Fig 1). The donor site SKIN GRAFTS AND SKIN SUBSTITUTES James F Thornton MD SRPS Volume 10, Number 1 2 of an FTSG must be closed by either direct suture approximation or skin graft. PROPERTIES OF SKIN GRAFTS Skin grafts have been used for over a century to resurface superficial defects of many kinds. Whether intended for temporary or permanent cover, the transplanted skin does not only protect the host bed from further trauma, but also provides an important barrier to infection. Thin split-thickness skin grafts have the best “take” and can be used under unfavorable conditions that would spell failure for thicker split-skin grafts or full- thickness grafts. Thin STSGs tend to shrink consid- erably, pigment abnormally, and are susceptible to trauma. 9 In contrast, full-thickness grafts require a well-vascularized recipient bed 9 until graft perfu- sion has been reestablished. FTSGs contract less upon healing, resist trauma better, and generally look more natural after healing than STSGs. Rudolph and Klein 9 review the biologic events that take place in a skin graft and its bed. An ungrafted wound bed is essentially a healing wound which, left alone, will undergo the typical processes of granulation, contraction, and reepithelialization to seal its surface. When a skin graft is placed on a wound bed, these processes are altered by the pres- ence of the graft. 10 Marckmann 11 studied biochemical changes in a skin graft after placement on a wound bed and noted similarities with normal skin in its response to physical or chemical injury and aging. The changes in wound healing brought about by the skin graft can also be described as a general adaptation of connective tissue to a diminished blood supply. 11 EPIDERMIS In the mid-1940s Medawar studied the behavior and fate of healing skin autografts. 12–14 His findings can be summarized as follows. Histologic Aspects During the first 4 days postgraft there is tremen- dous activity in the graft epithelium, which doubles in thickness and shows crusting and scaling of the graft surface. Three cellular processes may explain this thickening: 1) swelling of the nuclei and cyto- plasm of epithelial cells; 2) epithelial cell migra- tion toward the surface of the graft; and 3) accel- erated mitosis of follicular and glandular cells. 10 By the third day after grafting there is considerable mitotic activity in the epidermis of a split-thickness skin graft, whereas mitotic activity in full-thickness skin grafts is much less common and may be totally absent—a reflection of their less-efficient early cir- culation. Between the fourth and eighth days after graft- ing there is great proliferation and thickening of the graft epithelium associated with obvious desqua- mation. Epithelial thickness may increase up to sevenfold, with rapid cellular turnover. At the same time the surface layer of epithelium exfoliates and is replaced by upwardly migrating cells of follicular epithelium at an accelerated rate. This heightened mitosis does not begin to regress until after the first week postgrafting. By the end of the fourth week Fig 1. Split-thickness skin grafts include a variable amount of dermis. Full-thickness grafts are taken with all the dermis. (Reprinted with permission from Grabb WC: Basic Techniques of Plastic Surgery. In: Grabb WC and Smith JW: Plastic Surgery, 3rd Ed. Boston, Little Brown, 1979.) SRPS Volume 10, Number 1 3 postgraft the epidermal thickness has returned to its normal, pregraft state. Histochemical Aspects The RNA content of graft epithelial cells changes little in the first few days postgraft. 15 By the fourth day postgraft RNA content increases greatly in the basal layers of epithelium, paralleling the hyperac- tivity of epithelial cells caused by acceleration of protein synthesis during a period of rapid cellular replication. By the 10th day postgraft the RNA level returns to normal. 15 Over the first 2 to 3 days enzymatic activity pro- gressively decreases in split-thickness skin grafts, but as new blood vessels enter the dermis–epidermis junction, the enzyme levels rebound. DERMIS Cellular component The source of fibroblasts in a skin graft remains obscure. 16 Early investigators believed that these cells came from large mononuclear cells in the blood, while Grillo 17 theorized that they originated from local perivascular mesenchymal cells. Whatever their origin, most authors are convinced that active fibroblasts in a healing skin graft do not come from indigenous fibrocytes. Converse and Ballantyne 18 studied cell viability in rat skin grafts by assaying levels of diphosphopyri- dine nucleotide diaphorase, an indicator of active electron transport. The authors noted falling fibro- cyte numbers in the first 3 days after grafting. The remaining fibrocytes lay in two narrow layers, one beneath the dermis–epidermis junction and the other just above the host bed. After day 3 fibroblast-like cells began to appear, first in the graft bed and later in the graft itself. By the seventh to eighth day postgraft the fibroblast population and enzymatic activity were greater than in normal skin. After this early burst in fibroblastic activity, however, both fibroblast numbers and enzyme levels resumed their normal, pregraft states over the ensuing weeks. Fibrous component Medawar 12,13 stated that most of the collagen in an autograft persists through the 40th day after graft- ing. Hinshaw, Miller, and Cramer, 19,20 on the other hand, concluded that split-thickness and full- thickness skin autografts undergo considerable col- lagen turnover. In their experiments the dermal collagen became hyalinized by the third or fourth day postgraft, and by the seventh day all of the collagen was replaced by new small fibers. The replacement continued through the 21st postgraft day, and by the end of the sixth week postgraft all the old dermal collagen had been completely replaced. The rates of collagen turnover and epi- thelial hyperplasia peaked simultaneously in the first 2–3 weeks postgraft. Klein 21,22 and Peacock 23 used hydroxyproline to determine the collagen content of grafted wounds. Hydroxyproline is an amino acid found exclusively in collagen at a constant proportion of 14%. Changes in hydroxyproline and monosaccharide content of grafted beds paralleled those of other healing wounds. 24 Independent studies by Hilgert 25 and Marckmann 26 confirmed these findings and documented plunging levels of hydroxyproline soon after grafting. The hydroxyproline (collagen) level eventually rebounded and finally returned to the normal levels of unwounded skin. Although Hilgert’s cycle lasted 10 days and Marckmann’s 14–21 days, it is now well established that most of the collagen in a graft is ultimately replaced. On the basis of studies involving tritiated pro- line-labeled mature collagen, Udenfriend 27 and Rudolph and Klein 28 agreed that 85% of the origi- nal collagen in a graft is replaced within 5 months postgraft. The collagen turnover rate of grafts is 3X to 4X faster than that of unwounded skin. 29 In addi- tion, although equal amounts of collagen are lost from full- and split-thickness grafts, STSGs replace only half as much of their original collagen as do FTSGs of equal size. Elastin fibers in the dermis account for the resilience of skin. While the elastin content of the dermis is small, the elastin turnover rate in a healing graft is considerable, and most of the elas- tin in a graft is replaced within a short time. Elas- tin fiber integrity is maintained through the third postgraft day, but by postgraft day 7 the fibers are short, stubby, and have begun to fragment. 19 Elas- tin degeneration continues through the third postgraft week until new fibers can be seen beginning to grow at 4–6 weeks postgraft. This replacement process is the same in full- and split- thickness skin grafts. SRPS Volume 10, Number 1 4 Extracellular Matrix Far from simply supporting cells passively, the extracellular matrix (ECM) plays a vital role in cell- to-cell communication. 30 Through specific arrange- ments of protein sequences within, the ECM influ- ences cellular behavior in adjacent tissues with regard to proliferation, differentiation, migration, and attachment. The extracellular matrix in the skin consists of large insoluble proteins of fibroblast origin and smaller soluble proteins produced by either fibroblasts or keratinocytes. Both kinds of pro- teins appear to be involved in directing the behavior of keratinocytes and in promoting appropriate communication between keratino- cytes and fibroblasts. Epithelial Appendages The sweating capability of grafted skin is a func- tion of the number of sweat glands transplanted during grafting and of the extent of sympathetic reinnervation to the graft. A skin graft will sweat much like its recipient site due to ingrowing sym- pathetic nerve fibers from the graft bed. Thus a graft that is placed on the abdomen will sweat in response to physical activity, whereas an identical graft placed on the palm will sweat in response to emotional stimuli. Although both full- and split-thickness skin grafts demonstrate sebaceous gland activity, thin split- thickness grafts do not contain functional sebaceous glands and typically appear dry and brittle after take. Hair follicles are subjected to the same hyper- plastic stimuli as the rest of the graft. On the fourth day postgraft the original hair sloughs off and the graft becomes hairless. Soon after the graft follicles begin to produce new hair, and by the 14th postgraft day very fine, baby-like hair is seen growing out of the graft. 12 Full-thickness skin grafts produce hair while split- thickness skin grafts produce little or no hair. Full- thickness skin grafts that take well grow normal hair in terms of orientation, pigmentation, and follicular clustering. 13 Inadequate revascularization will dam- age the graft hair follicles and result in decreased hair density. Similarly, when graft take is inter- rupted for any reason, subsequent hair growth will be sparse, random, and lacking in pigment. 14 In summary, unlike STSGs, FTSGs contain sweat glands, sebaceous glands, and hair follicles. 8 Only full-thickness grafts, therefore, are capable of sweat- ing, oil secretion, and hair growth. GRAFT TAKE The large array of physiologic events usually seen in a healing skin wound are altered and modi- fied by placement of a graft. The graft becomes incorporated in the host bed through the process of graft “take”. The success of a graft depends primarily on the extent and speed at which vascu- lar perfusion is restored to this parasitic, ischemic tissue. Given equal clinical and technical conditions, two qualities of a skin graft influence its fate. The first determinant is the blood supply of the skin from which the graft was obtained. A graft har- vested from a highly vascular donor site will pre- dictably heal better than a graft taken from a poorly perfused area. The second factor in graft take is the metabolic activity of the skin graft at the time of application, which will dictate its tolerance to the inevitable period of ischemia. Skin graft take occurs in three phases. The first phase consists of plasmatic imbibition and lasts 24– 48 hours. This is followed by an inosculatory phase and a process of capillary ingrowth that occur essentially simultaneously until generalized blood flow has been established by the fifth or sixth postgraft day. Plasmatic Imbibition The exact significance of plasmatic imbibition to the healing of a skin graft is not clear. Hinshaw and Miller 19 and Pepper 31 believed that plasmatic imbibition is nutritionally important, while Clemmesen, 32,33 Converse, 34,35 and Peer 36,37 thought that it merely prevents the graft from drying out and keeps the graft vessels patent in the early postgraft period. Regardless of whose theory is correct, all concur in the following: • The graft is ischemic for an undetermined period of time that varies according to the wound bed: 24 hours for a graft placed on a bed that is already proliferative; 48 hours for a graft covering a fresh wound. SRPS Volume 10, Number 1 5 • Grafts placed on poorly vascularized beds will be ischemic for a longer time than those placed on wounds with good blood supply. Exactly how long a graft will tolerate this ischemic interval is unclear, but thick FTSGs seem to tolerate ischemia for up to 3 days while thin FTSGs sur- vive for up to 5 days. 32,37 Split-thickness grafts take well even after 4 days of ischemia. 37 • Plasmatic imbibition allows a graft to survive this immediate postgraft ischemic period until such time as graft vasculature is reestablished. 9 • Grafts gain weight during the phase of plasmatic imbibition, 33–35 adding as much as 40% to their pregraft weight through fluid movement from bed to graft. 35 The origin of graft edema is believed to be the same as that of inflammatory edema—ie, from disaggregation and depolymer- ization of proteoglycans, accumulation of osmoti- cally active metabolites, and increased vascular permeability. 38–41 Inosculation and Capillary Ingrowth At the end of 48 hours, a fine vascular network is established in the fibrin layer between the graft and its recipient bed. Capillary buds from the blood vessels in the recipient bed make contact with the graft vessels and open channels are formed. Blood flow is established and the skin graft becomes pink. Revascularization Three theories have been put forth to explain how a skin graft is revascularized. Connection of graft and host vessels. The first theory holds that after the inosculatory event, the definitive vasculature of a graft consists of the blood vessels originally present within the graft. Accord- ing to this theory, circulation is restored in a graft via the original skin graft vessels by anastomoses formed between the recipient bed and the skin graft through inosculation. Peer and Walker, 36 Clemmesen, 32,33 Haller and Billingham, 42 and Birch and Branemark, 38–40 among others, endorse this line of thinking. Clemmesen, 33 working on a porcine model, injected India ink into the host vessels of the autograft. No ink was seen within the graft on the first postgraft day, but on day 2 a number of graft vessels contained India ink, suggesting communi- cation between the host and graft vessels. After the second day many graft vessels contained India ink, indicating patent connections between ves- sels of the graft and its bed. Initially a fine fibrin mesh linked the graft to the bed, but over the first 4 days this meshwork became lined with endo- thelial cells and linked up with the vessels of the graft. Haller and Billingham 42 reached a similar con- clusion in a study involving the hamster cheek pouch model. They too noted that the pattern of vessels in the healed graft was the same as the pattern before grafting. Formation of new vascular channels. The sec- ond theory of graft revascularization holds that the graft is perfused through new vessels going from the recipient bed into the transplanted graft. Con- verse, 18,35,43–45 Zarem, 46 Ljungvist and Almgard, 47 and Wolff and Schellander 48 espouse this theory. Converse and Rapaport 43 studied skin grafts in humans and noted an early connection of graft and host vessels—the inosculatory event—after which there was active invasion of the graft by host vessels to produce the definitive vasculature of the graft. On the basis of a later study in a rat model involv- ing diaphorase, 18 Converse concluded that the final vasculature of a graft stemmed from ingrown ves- sels from the host bed. Degenerative changes in the original graft vasculature were apparent in the first 4 days postgraft, as evidenced by progressive loss of diaphorase activity during this time. With subsequent vessel ingrowth there was return of dia- phorase activity. Wolff and Schellander 48 measured cellular enzymes to evaluate return of circulation in por- cine skin grafts. ATP activity correlated well with the pattern of new vessel ingrowth, leading the authors to conclude that the new graft vasculature consisted entirely of ingrown vessels. Working on mice, Zarem et al 46 theorized that preexisting graft vessels served only as nonviable conduits through which the endothelium of the ingrowing vessels progressed. The rate of vessel ingrowth was measured at approximately 5 microns per hour. The original graft vessels degenerated concomitantly and at the same rate, leaving only those vessels growing from the recipient bed as the graft’s definitive vasculature. SRPS Volume 10, Number 1 6 Combined old and new vessels. Smahel 10 and Tsukada 49 proposed a third (and much less popular) hypothesis of graft revascularization: a compro- mise between the two above theories. The authors speculated that circulation in a graft is reestablished in various ways; that is, in any graft old vessels may be recycled and new ones may grow to variable degrees. These two pathways to restore circulation to ischemic tissue may occur simultaneously or as consecutive stages in the interaction between the graft and its bed. There are two methods of skin graft revas- cularization: primary and secondary. Primary revascularization. Under the scanning electron microscope it can be seen that no real circulation to the graft exists for the first 6 to 7 days postgrafting. Whatever flow there is within the graft is sluggish, shifting direction, and with atten- dant pooling and pendulum-like movement. 50 Clini- cally this manifests as cyanotic discoloration and is particularly noticeable in full-thickness skin grafts. 18,38,43 In the normal course of events circulation in a skin graft is reestablished through vascular anasto- moses between budding neovessels from the bed and those already present in the graft (inoscula- tion). Blood enters the graft via these newly formed vascular connections and the graft turns pink. A pink color is generally considered a sign of prob- able graft survival, although the intensity of colora- tion does not allow any conclusions regarding the graft’s circulatory status. Inside the graft the hemodynamic situation is complex. The old vessels of the graft are dilated and denervated and some of the circulatory routes are severed during graft harvest. Blood vessels from the recipient bed attach to both arteries and veins of the graft, yet all these connections are afferent with respect to the graft. Blood and tissue fluids moving into the graft are trapped there and unable to return to the bed because of inadequate reverse circulation. Sometime between days 4 and 7 postgraft, the newly formed vascular connections differentiate into afferent and efferent vessels, and other vessels retain their capillary-like character or simply disappear. 51 At this point the proper vascular system within the graft is reestablished and blood flow is restored. Secondary revascularization. When vascular con- nections between the bed and the graft are delayed, secondary revascularization occurs. Under normal graft conditions, the vasoactive agent directing the ingrowth of new blood vessels ceases to function and capillary proliferation stops as good blood flow is established by neovascularization. However, the longer a graft remains ischemic, the longer the vasoactive substance remains in the tissue. As a result, great numbers of new capillaries grow into the graft and granulation tissue accumulates under the graft. This phenomenon is known as secondary revascularization. The mechanism of secondary revascularization is as follows. Vascular connections between the graft bed and the graft inhibit the formation of cap- illary buds. If the graft is not well applied to the bed and vascular connections are not established early— eg, in the periphery of large grafts—the inhibiting effect does not take place. Within the graft itself the vessels may be functionally deficient or the vas- cular ingrowth may not reach the required level of biologic activity for the inosculatory event. If anas- tomoses fail to develop in time, the ischemic period is extended and capillary proliferation in the bed continues. Degenerative processes in the graft and exuberant granulation tissue in the host bed go hand in hand with prolonged ischemia. If blood vessels reach the graft in time, the graft will survive; if not, the graft will fail. In the host bed, insufficient vascular proliferation and wound contamination are the two common causes of delayed inosculation. Anastomoses may not form at the right time because of the increased distance between the graft and its bed from inter- posed necrotic material, a thick fibrin layer, hematoma, seroma, or air bubbles. Grafts that heal by secondary intention are smooth, fibrotic, tight, and have a slick, silvery sheen on the surface reflecting the large amount of cica- trix within the graft. Large grafts often heal both by primary and secondary revascularization, and cer- tain areas show the typical appearance and desqua- mation where the secondary process occurs. Histologically the epidermis and papillary dermis are destroyed by necrosis in the full-thickness graft that heals by secondary revascularization. The pap- illary dermis is replaced by a thin layer of connec- tive tissue, which in turn is covered by a flattened epidermis. The reticular dermis is normal histologi- SRPS Volume 10, Number 1 7 cally, but beneath the graft there is a layer of newly formed connective tissue that infiltrates the dermis, resulting in graft fibrosis. Hinshaw and Miller 19 noted accelerated collagen turnover in pig autografts that had healed by secondary revascularization. SKIN GRAFTING TECHNIQUES Donor Site Selection and Graft Harvest The selection of a graft donor site is based on three factors: 1) whether a full-thickness skin graft or a split-thickness skin graft is to be used; 2) whether the intended donor site matches the recipient bed in color; and 3) potential morbidity of graft harvest at that site. An appropriate color match is particularly impor- tant in head and neck reconstruction with skin grafts. Any skin graft taken below the clavicles and applied above the clavicle will result in a lifelong color mis- match that is extremely difficult, if not impossible, to correct. 52 Both full- and split-thickness skin grafts can be harvested above the clavicle; STSGs obtained from a shaved scalp, in particular, often yield very good results. Figure 2 illustrates two patterns of skin graft harvested from the submental, “turkey gob- bler” area, which is another good source of graft skin. 53 For large, full-thickness defects above the clavicle, tissue expansion is recommended to recruit an adequate volume of FTSG. Graft reconstruction of the nasal tip requires spe- cialized skin of similar thickness and pore size. The glabella provides just such skin. 54 Historically, donor sites for nasal tip grafting have included the concha, nasolabial fold, pre- and postauricular skin, the neck, and supraclavicular areas. 54 To minimize morbidity from graft harvest, donor sites should be carefully chosen to avoid hair-bearing skin and to camouflage the resulting scar. 52 Tiem 55 advocates a bilaminar harvest whereby an epithe- lial flap is raised, a dermal graft is taken, and the superficial layer is replaced in its original site. This is known as the trapdoor or dermatome technique. Tiem reports improved donor site management and fewer pigmentary changes with this method than with conventional harvest. Beck and colleagues 56 compared the trapdoor technique with standard elliptical excision in 52 patients (60 graft sites). Although both techniques were successful and had minimal complications, “the elliptical method [was associated with] less dis- comfort, texture change, numbness, and itching. The scars were concealed better and less notice- able.” 56 Common full-thickness graft donor sites are the groin, postauricular area, and clavicular region. 57 Yildirim and coworkers 57 also recommend the preputium as a source of graft skin in children. Split- skin grafts are usually harvested from the outer thigh because surgeons prefer this site for its technical ease and convenience of intraoperative position- ing and postoperative dressings. The public, on the Fig 2. The turkey gobbler deformity as a source of skin grafts. A U-shaped excision results in dogears that may be visible laterally. A triangular excision eliminates the dogear problem but yields less skin. (With permission from Shiffman MA: Re: Cervicomental “turkey gobbler”: a new source for full-thickness grafts (letter). Dermatol Surg 28:1099, 2002.) SRPS Volume 10, Number 1 8 other hand, would prefer that grafts be taken from their buttocks to avoid visible scars. 58 Graft Sizing and Expansion Techniques for sizing skin grafts usually involve preformed templates of easily available materials, such as cardboard and latex. 59,60 A simple and reproducible technique consists of placing card- board in the wound to develop a blotter pattern 61 (Fig 3). The cutout is then applied over the donor site, traced with a marking pen, and a graft of the outlined area is resected. 61 A wound is reepithelialized from the edges toward the center, therefore the perimeter of the graft is the only part that contributes to the epithe- lialization process. An expanded graft presents a larger perimeter through which epithelial outgrowth can proceed. With graft expansion, larger areas can be covered with smaller sections of skin. Various techniques to expand skin for grafting have been described, including pinch grafts, 62 relay transplantation, 63 meshing, 64–67 Meek island grafts, 68 microskin grafts, 69–74 and the Chinese technique of intermingling autografts and allografts. 75,76 A pinch graft breaks up a whole graft of skin into tiny pieces to increase the edge area. Pinch grafts are reported to be effective in treating small- to medium-size venous leg ulcers, 77,78 radiodermati- tis, pressure sores, and small burns. 62 Relay transplantation consists of cutting a graft into strips 3–6 mm wide and 5–10 mm apart. When the epithelial growth becomes clinically obvious 5 to 7 days later, the original strips are removed and transplanted, leaving the epithelial explants in place. This process may be repeated up to 4 times. 63 Meshing is the term used for cutting slits into a sheet graft and stretching it open prior to transplan- tation. Meshed grafts have a number of advantages over sheet grafts: (1) meshed grafts will cover a larger area with less morbidity than non-meshed grafts; (2) the contour of the meshed graft can be adapted to fit in a regular recipient bed; (3) blood and exudate can drain freely through the inter- stices of a meshed graft; (4) in the event of local- ized bacterial contamination, only a small area of meshed graft will be jeopardized; (5) a meshed graft offers multiple areas of potential reepi- thelialization. 64–66 The main disadvantages of meshed grafts are the considerable surface area Fig 3. A piece of cardboard is placed on the defect and the moisture blot is traced. The cutout pattern is then placed on the skin graft donor site and outlined. (With permission from Putterman AM: Blotter technique to determine the size of skin grafts (letter). Plast Reconstr Surg 112:335, 2003.) SRPS Volume 10, Number 1 9 that must heal by secondary intention and the less- than-ideal cosmetic result. A small ratio of expan- sion—1:1.5—and pulling the graft lengthwise to narrow the skin perforations to slits before trans- plantation lessens these problems. 65 Richard and colleagues 67 compared the Tanner and Bioplasty skin graft meshing systems with respect to their respective expansion ratios and predicted versus actual expansion. Both systems delivered approximately 50% of the anticipated skin expan- sion, leading the authors to recommend harvesting skin grafts larger than needed to compensate for the eventual shortage. Ingenious ways to mesh skin grafts when a mesher is not available have been reported. 79,80 Kirsner and associates conclude that meshed STSGs are safe and effective therapy for recalcitrant leg ulcers. 81 The Meek technique involves a special der- matome and prefolded gauzes for expanding small pieces of split skin. 68 The expansion ratio obtained with the Meek technique is almost 1:9. In contrast, the expansion ratio of allograft meshed with the Zimmer II dermatome set at 1:6 is actually 1:4. Meek grafts are useful alternatives to meshed grafts when donor sites are limited, and are particularly well suited for grafting granulating wounds and unstable beds. Several authors report successful coverage of burn wounds with microskin grafts. 69–74 These are sheet grafts that are minced with a Tanner-Vandeput der- matome to achieve an expansion ratio of 1:10. Graft take is said to be excellent even in difficult beds. Intermingled transplantation of autograft and allograft has been practiced successfully in China since at least 1973, 75,76 mostly in the treatment of large burns. Yeh and colleagues 82 compared this technique with the microskin method in a rat model, and noted significantly less scar contracture with the former. Other healing parameters were similar between the two groups. Graft Fixation Adherence of the graft to its bed is essential for skin graft take. A thin fibrin layer holds the graft to the bed and forms a barrier against potential infec- tion. 83 Factors such as bleeding, infection, and shear force tend to work against graft take. Two distinct phases of graft adherence occur. Phase 1 begins immediately after grafting and lasts about 72 hours. 84 During this time the graft remains adherent to the bed through the bond formed by the fibrin layer. Phase 2 coincides with the onset of fibrovascular ingrowth and vascular anastomoses between the graft and the host. Novel methods of graft fixation abound. When dealing with skin grafts to the penis and scrotum, which are particularly difficult to immobilize and dress, Netscher and associates 85 suggest wrapping the graft area in nonadherent gauze mesh over which Reston self-adhering foam is secured. The foam maintains penile length and gently but firmly compresses the skin graft during the crucial first week. The authors cite ease of application and removal, sterility, and effectiveness in wound cov- erage as advantages of this method. Saltz and Bowles 86 and Caldwell and col- leagues 87 also advocate the use of Reston foam applied over Xeroform gauze for securing skin grafts to wounds on the shoulder and face, respectively. Balakrishnan 88 prefers Lyofoam, a semipermeable, nonwoven polyurethane foam dressing. The foam is easy to apply directly on the graft and is biologically inert. Its hydropho- bic outer surface is said to retard bacterial colo- nization. Johnson, Fleming, and Avery 89 opt for a simple, versatile, and rapid technique consisting of staples and latex foam dressing to secure skin grafts. Wolf and coworkers 90 confirmed the effectiveness of rub- ber foam with staple fixation in various patterns to provide even pressure distribution on skin grafts. Smoot 91 uses a Xeroform sandwich filled with molded cotton balls stapled in place, while Amir et al 92 modify a cutoff disposable syringe to affix the silk threads of their graft dressings. Cheng and col- leagues 93 use a disk cut from the bottom of an IV infusion bottle on which multiple radial slits are made in the perimeter for tying the sutures holding the graft. Other suggested fixation methods for grafts include silicone rubber dressings 94 and silicone gel sheets, 95 rubber band stents, 96 transparent gasbag tie-over dressings, 97 Coban self-adherent wrap, 98 thin hydrocolloid dressings, 99 and assorted Silastic and foam dressings for grafts to the neck or hand. 100–102 SRPS Volume 10, Number 1 10 Dressings for specific applications include a dor- sal and ventral sandwich bolster for grafts on the tongue; 103 a cutout tie-over dressing of elastic tape with silk threads on which a bolster is placed; 104 and malleable ear dressings constructed of silicone- lined bandage with thin metal backing. 105 Modern bolster technologies of skin graft fixa- tion replace sutures and staples with either fibrin glue 106–111 or octyl-2-cyanoacrylate (“super glue”) on the edges of the graft. 112,113 Fibrin glue is strong, transparent, hemostatic, does not interfere with healing, and does not promote wound infection. Proponents of fibrin glue say that it improves graft survival, reduces blood loss, speeds reconstruc- tion by allowing large sheet-graft coverage, and produces better esthetic results. 111 Our experi- ence at The University of Texas Southwestern Medical Center bears out this assertion: A thin layer of fibrin glue improves graft take consider- ably, particularly in the head and neck and mobile body parts. Negative-pressure dressings (VAC device [KCI, San Antonio, Texas]) also enhance graft adherence and survival, 114–117 and are a good option in diffi- cult-to-bolster areas such as the hand and axilla. The total time of bolster application can be reduced from 5 to 3 days while the patient maintains mobil- ity of the extremity. Donor Site Management Open Wound Technique The open-wound technique of donor site man- agement is associated with prolonged healing time, more pain, and a higher risk of complications than if the wound is covered. Most authors recommend dressing the donor site of a skin graft to protect it from trauma and infection. Allen and coworkers 118 compared bacterial counts of wounds left open to granulate and of wounds covered by skin dressings. They found 12.5% of open wounds were sterile, but all the dressed wounds showed some microbial flora. When antibiotics were added, however, there was a dramatic decrease in bacterial colonization, lead- ing the authors to conclude that it was the antibi- otic, not the dressing, that had a sterilizing influ- ence. Skin grafts have no intrinsic bactericidal properties. 119 Biologic Dressings Autografts Feldman 120 recommends returning unused skin to the donor site as an autologous biologic dressing on the grounds that this is logical in terms of wound healing, tissue conservation, and expense. Wood 121 agrees that this is a good idea in immuno- compromised or steroid-dependent patients, but unnecessary in the general population. Careful plan- ning before surgery to harvest only the required amount of skin is the ultimate solution, in Wood’s opinion. Allografts Traditionally cadaver allografts have been the choice for resurfacing large denuded areas. Cadaver skin serves as temporary wound cover, reduces pain and fever, restores function, increases appetite, controls fluid loss, and promotes wound healing. As the grafts revascularize, they form a barrier against bacterial invasion and prevent further loss of water, electrolytes, and protein from the wound. Allografts decrease bacterial counts of underlying tissues and facilitate future grafting by promoting a sterile wound bed. 122 Glycerol-treated cryopreserved allografts have a number of applications such as in the treatment of scald burns in children, 123,124 extensive burns in both children and adults, 125 and deep burns down to muscle fascia or fat (when combined with alloge- neic cultured epithelial grafts). 126,127 The main draw- back of glycerol-preserved allografts is their expense. As discussed above, Chinese investigators have successfully used combinations of allografts and autografts for coverage of open wounds. 75–77 The autograft is cut into small pieces and placed in the slits of meshed allografts, or is laid down in alternat- ing strips of auto- and allograft. As rejection unfolds, epidermal cells in the autograft gradually replace the allograft. 128 Xenografts Xenografts (collagen–elastin prostheses) adhere to a wound bed via fibrin bonding. The advantages of xenografts are relatively low cost, ready availabil- ity, easy storage, and easy sterilization. Disadvan- tages are lack of antimicrobial activity, no proof that they promote reepithelialization, potential for absorption of toxic breakdown products, and poor SRPS Volume 10, Number 1 11 performance with respect to healing time and pain when measured against other donor site dressings. Synthetic Materials Feldman 120 lists methods for dressing the donor site of a skin graft (Table 1). TABLE 1 Dressings for Skin Graft Donor Sites (Annotated with permission from Feldman DL: Which dressing for split-thickness skin graft donor sites? Ann Plast Surg 27:288, 1991.) Synthetic wound dressings can be semiopen, semiocclusive, or occlusive. Semiopen dressings include Xeroform, Biobrane, and fine mesh gauze impregnated with Scarlet Red or Vaseline. Semiocclusive dressings include Op-Site, Tegaderm, and DuoDERM. Semiocclusive dressings are impermeable to bacteria and liquids, so fluid tends to collect beneath the dressing and must be drained frequently. Feldman and colleagues 129 evaluated the effec- tiveness of various donor site dressings in 30 patients with respect to healing, pain, infection, and expense. Xeroform had an average healing time of 10.46 days, no infections, and a low cost per patient ($1.16). The healing time for Biobrane was 19 days; for DuoDERM, it was 15.3 days. Biobrane was more comfortable than Xeroform, but was associated with 29% more infections and very high cost ($102.50/patient). In another study, donor site wounds dressed with Op-Site and Tegaderm showed rapid, relatively painless healing and low infection rates. 130 Brady et al 131 compared Op-Site, Vaseline gauze, Jelonet, Scarlet Red, and exposure in terms of healing time, pain, infection, and cost. (Pig skin was initially included in the study but was soon eliminated because of Pseudomonas infection and hyper- trophic scarring.) Wounds dressed with Jelonet healed quickly, followed closely by Vaseline gauze. The interval to healing was longest with the open method. Op-Site was the most comfortable dress- ing and the most expensive. Vaseline gauze was second to exposure in low cost. Recommendations from the authors were for Op-Site or Jelonet for dressing small donor areas and for Vaseline gauze to cover large wounds. 131 Barnett and coworkers 132 compared synthetic adhesive, moisture-vapor-permeable and fine mesh gauze dressings for STSG donor sites with respect to pain, rate of healing, adherence, and infection. Op-Site and Tegaderm promoted fast healing (mean 6.8 days) and were basically painless. Wounds cov- ered with fine mesh gauze healed in 10.5 days but were 3X as painful. In a study comparing Op-Site with simple polyvi- nyl film and tulle gauze, the authors note that Op- Site was associated with low discomfort, but PVC film was also well tolerated and was very inexpen- sive. 133 Dressings that promote a moist wound environ- ment are associated with faster healing. Zapata- Sirvent 134 compared Biobrane and Scarlet Red and found Biobrane to be better at controlling pain and exudate accumulation, with shorter healing times. Tavis et al 135 agree that Biobrane reduces pain, limits infection and desiccation, and optimizes heal- ing times, although its expense is considerable. Poulsen and colleagues 136 found Jelonet superior to Op-Site in the treatment of partial-thickness burns both in terms of speed of healing (7 vs 10 days) and residual scars (8% vs 21%). A large comparison study of STSG donor site healing under Xeroform and Jelonet dressings showed no difference in mean time from harvest to healing, similar cost and ease of use, and less discomfort with Xeroform, particu- larly with movement. 137 Nemeth et al 138 note much less discomfort and faster healing by nearly 4 days of shave biopsy sites treated with DuoDERM over SRPS Volume 10, Number 1 12 conventional therapy consisting of cleansing, baci- tracin, and band-aids. Lawrence and Blake 139 and Porter 140 evaluated Kaltostat, a calcium alginate dressing, in the healing of STSG donor sites. The rate of epithelialization, degree of pain, and convenience of use were mea- sured and compared with the same parameters in two other groups of patients treated with Scarlet Red and DuoDERM. The Kaltostat-treated patients had slower healing times (15.5 days) than other patients (10 days). On the other hand, the alginate was easier to apply and could be used on an outpatient basis. The topical application of anesthetic agents relieves the pain of skin donor sites. Goodacre et al 141 studied the effectiveness of topical local anes- thesia (EMLA) versus infiltrated anesthesia in an open parallel group comparison in 80 patients. During graft cutting and after harvest, patients who received EMLA reported no discomfort. Owen and Dye 142 report that topical application of 2% lignocaine gel to graft donor sites controlled discomfort during the first week postgrafting and did not impair healing. Azad and Sacks 143 recommend topical bupivacaine on graft donor sites under calcium alginate dress- ings to enhance comfort and improve hemostasis. Others recommend honey-impregnated gauze for dressing donor sites and report no significant difference in time of reepithelialization or patient comfort between this inexpensive material and the more costly hydrocolloid dressings. 144 GRAFT HEALING In his classic work on skin grafts in the mid-1940s, Medawar 12–14 described the appearance of healing grafts as follows: Immediately after removal from the donor area the skin graft is white, but once applied to the recipient area it becomes pink over the next few days. There is blanching on pressure with prompt capillary refill. At first the graft surface is depressed below the level of the surrounding skin, but by the 14th to 21st postgraft day it becomes level with the surrounding surface. 19 Collagen replacement begins by the seventh postgraft day and is complete in about 6 weeks. There is an abundance of polymorphonuclear lym- phocytes and monocytes. The mononuclear infil- trate persists in the dermis for an extended period of time. Vascular remodeling in the graft may take many months. 145 Host vessel ingrowth is perpendicular to the dermis–epidermis junction and forms a charac- teristic vascular pattern. The new vessels in the graft are more numerous and show greater arboriza- tion than those in normal skin. Lymphatic drainage is present through connec- tions between the graft and host lymphatics by the fifth or sixth postgraft day, and subsequently the graft loses weight until pregraft weight level is attained by the ninth day. 146 GRAFT CONTRACTION A skin graft begins to shrink immediately after harvest. Primary contraction is passive and prob- ably due to the recoil of the dermal elastic fibers. A full-thickness graft loses about 40% of its original area as a result of primary contraction; a medium- thickness graft, about 20%; and a thin split-thickness graft, about 10%. True Thiersch grafts do not undergo primary contraction. After transfer to a recipient site, the skin graft will shrink as it heals—secondary contraction. Full- thickness grafts tend to remain the same size (after primary contraction) and do not show secondary contraction. Split-thickness grafts, on the other hand, contract whenever circumstances allow. Unless split- thickness skin grafts are fixed to underlying rigid structures and cannot move, they will contract sec- ondarily. Once wound contraction ends, full- thickness grafts are able to grow, whereas split- thickness grafts remain fixed, contracted, and grow minimally, if at all. 147,148 Wound contraction is a critical part of wound healing and is clinically useful because it reduces wound size. A contracted wound is often tight and immobile and there is distortion of surrounding nor- mal tissue. The degree of graft contraction can be manipulated somewhat by adjusting the thickness and proportion of dermis in the graft. The contrac- tion-inhibiting effect of dermis depends more on the percentage of dermis included in the graft than in overall thickness of the graft: the greater the proportion of dermis, the greater the inhibition and the less the graft will contract. FTSGs therefore inhibit wound contraction better than STSGs; 147–149 thin FTSGs inhibit wound contraction better than thick STSGs, and thick STSGs contract less than thin STSGs. 8,150,151 SRPS Volume 10, Number 1 13 Brown, Garner, and Young 152 concluded that the capacity of a skin graft to inhibit wound con- traction is directly proportional to the amount of structurally intact dermal collagen present in the graft. The rate of wound contraction is not affected by graft orientation, amount of epidermis, or noncollagenous protein. Various hypotheses have been proposed to explain the mechanism of this inhibition, including a mass effect, cellular interactions between graft cells and host bed, epidermal interaction, mechani- cal restriction, etc. 152 Rudolph 153,154 explains the interaction between a graft and its bed in terms of the lifecycle of a myofibroblast. In this hypothesis a graft does not prevent the formation of myo- fibroblasts, but rather speeds up completion of their lifecycle and eventual disappearance. 155 Split- thickness grafts cause a rapid decline in the num- ber of myofibroblasts, and wounds contract less than comparable nongrafted sites. Full-thickness grafts trigger an even faster decrease in the myofibroblast population, and wounds show minimal contraction. Bertolami and Donoff 150,151 studied the effect of dermis on the actinomycin content of granulating wounds and suggest that the mechanism of wound contraction is not simply the result of myofibroblast activity; 155 the active role of collagen cannot be ignored. Substances that inhibit wound contrac- tion also inhibit prolyl hydroxylase activity (an indi- cator of collagen synthesis). Lower levels of this enzyme beneath a full-thickness graft may reflect decreased collagen synthesis, which in turn may be involved in preventing wound contraction. 150 Oliver and associates 156,157 highlight the impor- tance of the collagen matrix in inhibiting wound contraction. The matrix was prepared for grafting by adding azide to destroy the cells and trypsin to remove noncollagenous protein. These grafts, cell- free and noncollagenous-protein-free, resist wound contraction as well as full-thickness skin grafts, sug- gesting that dermal cells and noncollagenous pro- teins are not part of the inhibitory process. Grafts free of dermal cells but possessing a collagen matrix in fact behave much like FTSGs. It may be possible, therefore, to store nonantigenic dermal substitutes produced from banked cadaveric skin or xenoge- neic sources by adding trypsin or azide to remove noncollagenous protein and cells. This would increase dramatically the clinical availability of sub- stitute dermis as a potential source of grafts. In a porcine study, Walden and coworkers 158 report minimal contraction at 14 days when epi- dermal autografts were immediately placed over acellular dermis, presumably by reducing early inflammation. By day 30, however, these wounds had contracted more than conventional autografts. GRAFT REINNERVATION Nerves grow into skin grafts from wound margins and the graft bed. 159 The timing of neural invasion and disposition of nerves within a skin graft vary according to the graft thickness and recipient site. Human skin grafts begin to show sensory recovery at 4–5 weeks postgrafting, but occasionally sensa- tion is delayed for up to 5 months. The return of normal sensation is usually complete by 12–24 months. The extent of reinnervation depends on how accessible the neurilemmal sheaths are to the invading nerve fibers—ie, most accessible in full- thickness grafts and least accessible in thin split- thickness grafts. Skin grafts are initially hyperalgesic and slowly regain normal sensation. 8 If skin graft healing is uneventful, the results of two-point discrimination testing will be very close to those of normal skin. Other sensations do not recover so well. Waris and associates 159 measured the thermal sensitivity of 22 split skin grafts transplanted 1–4 years ear- lier. Cold sensitivity was present in 14, warmth in 6, and heat–pain in 8 grafts. If the warmth sensi- bility had recovered, the threshold was lower than for cold. Seven grafts showed no thermal sensibil- ity at all. Haro and colleagues 160 confirmed poor return of sensitivity in grafts by means of immunohistochemi- cal methods. Grafts less than 7 months old showed no sensitivity whatsoever, and pain sensation had developed only in the 15-month-old grafts. Although deep and superficial nerve plexuses regenerated, no sensory corpuscles were detected in grafted skin at any time. Stella et al 161 independently verified these find- ings and speculate that the failure of regeneration of sensory corpuscles may be related to the degen- eration of periaxonal corpuscular elements. Ponten 162 stated that grafts assume the sensory pattern of the host tissue, but Adeymo and Wyburn 163 and later Fitzgerald, Martin, and Paletta 164 noted that nerves entering the graft fol- SRPS Volume 10, Number 1 14 low the evacuated neurilemmal sheaths and rees- tablish the innervation pattern of the donor skin. Weis-Becker and coworkers 165 note better rein- nervation of split skin grafts placed on intact muscle fascia than if the fascia had been removed. Sen- sory functions on grafted skin were generally reduced. GRAFT PIGMENTATION Immediately after harvesting, a skin graft blanches from circulatory interruption. The con- sequent loss of melanoblast content causes pro- found alteration in the ratio of pigment-producing to nonpigment-producing cells in the graft. 166 After transplantation and graft revascularization there is inflow of erythrocytes and the normal equilibrium of the melanocyte population is restored. The graft resumes a pink color which over time fades to a normal skin tone. Mir y Mir 167 reviews mel- anogenesis, its peripheral nervous system control, the hyperpigmentation state that follows cutane- ous grafting, and the effects of ultraviolet radiation on the skin. Skin grafts change color during healing. 10 Grafts harvested from the abdomen, buttocks, and thigh become darker as they heal, while grafts taken from the palm tend to lighten. Grafts taken from brunettes progressively darken, while those from blondes usually lighten. Full-thickness grafts from the eyelid, postauricular and supraclavicular areas are usually good color match for the face, although they may remain red for many months. In gen- eral, grafts taken from below the clavicle assume a yellowish-brown hue, while grafts taken from above the clavicle provide a better color match for facial skin. Thin split-thickness skin grafts from the same donor site are usually darker than thick ones. 162 The best treatment for hyperpigmented grafts is dermabrasion. For dermabrasion to be effective, however, it must be done at the appropriate time. If it is performed too soon after skin graft, the blanching will not last and the dark pigment will reappear. The best results are seen when derm- abrasion follows biologic reinnervation of the graft. Generally, the later the dermabrasion is done after grafting, the more effective it is in removing unwanted pigment. Skin depigmentation states and their treatment are reviewed by Taki et al. 168 Vitiligo, senile leuko- derma, dyschromatosis symmetrica hereditaria, and second- or third-degree burns can produce signifi- cant cosmetic deformity, particularly in dark-skinned patients. Corticosteroids and oral psoralen may, with exposure to sunlight, be successful in the treat- ment of vitiligo provided that dopa-positive mel- anocytes are present in the skin. 169 Burns that invade the dermis (second- and third-degree) decrease the number of dopa-positive melanocytes, so that appropriate treatment consists of removing the depigmented skin and replacing it with very thin STSGs of normal color. This protocol is also successful in treating leukoderma. A number of authors report successful repig- mentation in leukoderma or vitiligo after treatment with ultra-thin, melanocyte-containing epidermal sheet grafts 170–177 or in-vitro cultured melanocytes. 178 Hosokawa and colleagues 179 report a novel method of tattoo elimination in which the pigment-contain- ing dermis is chemically removed and the epider- mis is replaced. Wound healing time was much shorter than for typical skin grafts. OVERGRAFTING Dermal overgrafting consists of applying a split- thickness skin graft to a recipient bed or dermis or denuded scar tissue. 180 Overgrafting preserves sub- cutaneous tissues, is a relatively simple procedure, and the tissue consequences of graft failure are minimal. Rees and Casson 181 offer technical details of skin removal and bed preparation and list the best donor sites. Their indications for overgrafting are as follows: • unstable, depressed, corrugated, or hypertrophic scars • unstable or hyperpigmented skin grafts • large pigmented nevi • radiation damage • tattoos Pigmented lesions should be excised deep enough to remove all the pigment before the graft is applied. A potential complication of the tech- nique is the formation of cysts and granulomas from retained epithelial remnants. 181 SRPS Volume 10, Number 1 15 GRAFT FAILURE A meticulous surgical technique contributes greatly to the survival of a skin graft. Particular attention should be paid to ensuring • atraumatic graft handling • a well-vascularized, scar-free bed • careful hemostasis and removal of accumulated blood before dressing the wound • postoperative immobilization of the graft recipi- ent site • use of a tourniquet during graft harvest and transfer • no proximal constricting bandages Flowers 182 reviews the usual complications asso- ciated with graft failure and recommends steps to avoid them. The graft bed should be as clean as possible, free of dead tissue, and have an appropri- ate substrate (eg, bone should have periosteum, tendon should have peritenon). A clean area with endothelium is all that is required in the bed of a successful skin graft. The most common cause of autologous skin graft failure is hematoma. The clot isolates the undersurface of the graft from the endothelial buds of the recipient site so that revascularization cannot take place. 182 The second most common cause of graft loss is infection. Infection can be avoided by carefully preparing the wound bed, using quilting sutures, meshing or pie-crusting the graft surface to allow free egress of subjacent fluids, and applying wet saline dressings that are changed every 4 hours. 182 Fluid beneath the graft can also cause graft necrosis. Areas rich in lymphatics such as the supraclavicular, inguinal, and axillary regions are particularly prone to develop seromas. Atraumatic tissue handling, cauterization of lymphatic vessels, limited use of electrocautery in the graft bed, and a light pressure dressing or VAC technique minimizes the risk of fluid accumulation under the graft. 182 Excessive pressure on a fresh graft may also cause it to die. The applied pressure should never exceed 30 mmHg. Tie-over dressings immobilize the graft, reduce dead space, and prevent hematoma forma- tion, but exert no significant pressure on the wound. 183 Other causes of graft failure include gravitational dependency, movement of the area, arterial insufficiency, venous congestion, lymphatic stasis, and surgeon error. Teh 184 studied 21 patients with stasis ulcers in an attempt to pinpoint the causes of graft failure. Wound exudates were assayed for fibrin degrada- tion products, fibrinogen, available plasminogen, and active plasmin. All wounds showed granulation tissue and were classified as clean or dirty. Clean wounds had low bacterial counts and showed no detectable plasmin activity. Dirty wounds had high bacterial counts and increased levels of active plas- min. High plasmin and proteolytic enzyme activity was generally seen in wounds contaminated with beta-hemolytic streptococci and various species of Pseudomonas. The presence of fibrin under autografts was associated with success in 17 of 21 ulcers, and the absence of fibrin was associated with graft failure. This finding suggested to the author that dissolution of fibrin by plasmin and pro- teolytic enzymes is the probable mechanism in graft failure secondary to microorganisms. 184 In conclusion, a grafted wound is rendered ster- ile through the blocking action of fibrin in the inter- face between graft and bed. Fibrin plays a central role in graft survival and is responsible for the anti- bacterial character of adherent dressings and autografts. This bacteriostatic effect of grafts has proved invaluable in the management of large burns. 184 Thourani and colleagues 185 assessed the effect of various recipient beds on the success of STSGs in a burn unit, and found it to be negligible at 14 days postgrafting. The exception were patients under 18 years of age, in whom STSG success was higher on granulation tissue than on fat. Hill 186 recommends a number of measures to enhance the survival of full-thickness grafts. Because streptococci produce streptokinase and other enzymes that break down the fibrin clot and decrease adherence of the graft to its bed, he pro- poses the administration of low-dose erythromycin for the first 5 days after grafting to combat potential strep and staph colonization. Patients should also take vitamin C and zinc for a week to 10 days to promote healing, and should abstain from using alcohol for at least 2 days before and 5 days after surgery. Ethanol in the bloodstream decreases the initial phase of wound healing (the PMN clean-up phase) and can result in infection and decreased graft adherence. 186 SRPS Volume 10, Number 1 16 Wolfort and colleagues, 187 working on rabbits, found that epinephrine added to local anesthetic solutions decreased inosculation in full-thickness grafts but had no effect on ultimate survival of split- thickness skin grafts. Subsequently Fazio and Zitelli 188 assessed the clinical effects of epinephrine in local anesthesia of the donor site. The authors found an increased risk of graft complications at 1 week and no effect on the 6-week cosmetic out- come. They do not recommend using plain lidocaine for harvesting full-thickness grafts unless the vascular supply of the donor area is compro- mised. Robson and Krizek 189 predict skin survival on the basis of successful homograft take prior to autografting. Perry 190 notes a direct correlation between skin graft survival and bacterial counts of <10 5 in the recipient bed. SKIN SUBSTITUTES Unlike temporary wound dressings, skin substi- tutes are designed to be left in place for long peri- ods of time. Fifteen years ago Pruitt and Levine 191 listed attributes of the ideal skin substitute which are still current today: • little or no antigenicity • tissue compatibility • lack of toxicity, either local or systemic • permeability to water vapor just like normal skin • impenetrability to microorganisms • rapid and persistent adherence to a wound sur- face • porosity for ingrowth of fibrovascular tissue from the wound bed • malleability to conform to an irregular wound surface • elasticity for motion of underlying tissues • structural stability to resist linear and shear stresses • a smooth surface to discourage bacterial prolif- eration • sufficient tensile strength to resist fragmentation • biodegradability • low cost • ease of storage • indefinite shelf life Classification Skin substitutes may be classified according to their origin—autologous, allogeneic, xenogeneic, or recombinant 192 —or whether they are used for wound cover or wound closure. 193 Materials used for wound cover are primarily indicated for superficial burns, where they provide a barrier against infection, control water loss, and create an environment suitable for epidermal regenera- tion. Examples of skin substitutes for wound cover are Biobrane, Transcyte (formerly Dermagraft- TC), cultured epidermal allogeneic keratinocytes, Dermagraft, and Apligraf (Graftskin). Materials intended for wound closure restore the epider- mal barrier and become incorporated into the healing wound. Skin substitutes for wound clo- sure include Alloderm, Integra, cloned autolo- gous keratinocytes (Epicel), and composites of epi dermal –dermal component s, al l ograf t – xenograft skin, or collagen–glycosaminoglycan matrix with a cultured epidermal autograft (CEA) surface (Table 2). Wound Cover Biobrane Biobrane is a bilaminar material consisting of nylon mesh bonded to thin, semipermeable silicone mem- brane. It provides a barrier function against fluid loss as well as protection from environmental bac- terial invasion. The product is often used as a tem- porary skin replacement for superficial partial- thickness burns as well as for skin graft donor sites. When applied to clean wounds, Biobrane elimi- nates the need for dressing changes and reduces the length of inpatient treatment. 192,193 Transcyte Transcyte is Biobrane with the addition of neo- natal fibroblasts seeded to the collagen-coated nylon mesh. The fibroblasts are nonviable at application and the nylon mesh is not biodegrad- able, so the material is designed for use as a tem- porary cover. Transcyte for preliminary coverage of partial thickness burns results in fewer dressing changes and less hypertrophic scarring than con- ventional treatment with topical silver sulfadiaz- ine. 194 Transcyte is considerably more expensive than Biobrane. 192,193 SRPS Volume 10, Number 1 17 TABLE 2 A Guide to Biological Skin Substitutes (Reprinted with permission from Jones I, Currie L, Martin R: A guide to biological skin substitutes. Br J Plast Surg 55:185, 2002.) SRPS Volume 10, Number 1 18 Cultured Allogeneic Keratinocytes The delay in growing sheets of confluent autolo- gous keratinocytes led to the deelopment of pregrown allogeneic keratinocytes. Epidermal grafts are obtained from neonatal foreskin or elective surgical skin specimens and are cultured. Cultured alloge- neic keratinocytes have been used to cover burn wounds, chronic ulcers, and as donor site dressings for split-thickness skin grafts. They will not in them- selves achieve wound closure, but may survive for up to 30 months. Allogeneic keratinocytes do pro- duce growth factors that facilitate the proliferation and differentiation of the host dermal and epidermal cells. The main disadvantage is that the cultured epithelial cell sheets are thin and fragile, requiring meticulous wound care if they are to survive. Apligraf/Dermagraft These are multilaminar materials designed to overcome the fragility of cultured allogeneic keratinocytes by improved ease of handling and healing characteristics. Apligraf is a type I bovine collagen gel with living neonatal allogeneic fibro- blasts overlaid by a cornified epidermal layer of neonatal allogeneic keratinocytes. Apligraf is avail- able in a ready-to-use form with a 5-day shelf life. It has wide application in treating chronic ulcers as well as in pediatric burn coverage, for coverage of widespread skin defects such as epidermolysis bullosa, and to cover full-thickness wounds result- ing from Mohs’ micrographic surgery pending definitive repair. 192,193,195–199 Apligraf is the most sophisticated tissue-engineered product available for wound coverage, and is also the most expen- sive. 193 Dermagraft is a cryopreserved dermal material consisting of neonatal allogeneic fibroblasts on a polymer (Dexon or Vicryl mesh) scaffold. Derma- graft stimulates the ingrowth of fibrovascular tissue from the wound bed and reepithelialization from the wound edges, and as such promotes the heal- ing of chronic lesions. 193 Dermagraft has been used to replace lost dermal tissue beneath meshed split- skin grafts on full-thickness wounds. 200 Wound Closure Alloderm Alloderm is processed human cadaveric skin from which the epidermis has been removed and the dermal cells extracted. Alloderm functions as a der- mal graft, but has no barrier function because it has no epidermal component. Alloderm is similar to Dermagraft in many respects. A split-thickness skin graft can be placed over Alloderm after tissue ingrowth, or an ultra-thin graft can be placed at the time of Alloderm application in a single-stage pro- cedure. The indications for Alloderm are as dermal replacement in full-thickness or deep partial- thickness wounds. 193,201 Integra Integra is a bilaminar skin substitute consisting of a cross-linked bovine collagen–glycosaminoglycan matrix coated on one side with silicone elastomer for a barrier function. Integra is applied in a two- stage procedure much like a split- or full-thickness skin graft. As the host tissue grows into the wound, the silicone “epidermis” separates and sloughs off in 3–4 weeks, after which the integrated matrix is covered with a thin STSG. Integra has widespread applications in burn and full-thickness wound closure. Its reliability is good on long clinical follow-up. Advantages of Integra include off-the-shelf availability; improved elastic- ity and cosmesis compared with thin STSG; and no risk of cross infection. Disadvantages are a some- what steep learning curve for application; the necessity for a two-stage procedure, and its high cost. 192,199,201 Cultured Epithelial Autografts Rheinwald and Green 5 pioneered a method to clone human epidermal cells in vitro in 1975. In 1979, Green et al 6 perfected a technique for grow- ing cultured epithelial keratinocytes into confluent sheets suitable for grafting. Clinical experience with epidermal cells grown in vitro include burns, chronic leg ulcers, giant pigmented nevi, epidermolysis bullosa, and large areas of skin necrosis. Like STSGs, cultured epithelial autografts must be applied on a wound bed with early granulation tissue or muscle fascia for proper take. 193 Sheets of cultured epithelial cells (Epicel) are expensive and require a fair degree of expertise for application. These sheets are fragile, often resulting in a friable, unstable epithelium that may spontaneously blister, break down, and contract long after application. 193 Cultured epithelial cells used for grafting have an expansion capability of 10,000X SRPS Volume 10, Number 1 19 the original surface area. 202–204 When cultured cells and allografts are combined, they tend to be more stable than either component alone, yet many pre- fer to use CEAs alone on large burns. 205,206 Many burn centers continue to use cultured epi- dermal autografts. The following conclusions regarding grafts of cultured keratinocytes derive from their combined experiences. • Tissue cultured grafts are commercially available. • CEAs are very expensive: a 2x2-inch graft cost approximately $550 in 1996. • Sheets of cultured keratinocytes are very fragile and must be handled with extreme care. • CEAs require well-vascularized beds. • Once the CEA takes, the cells will spread peripherally to join other grafts or surrounding skin. • CEAs are extremely sensitive to infection, toler- ating maximum bacterial counts of 10 2 to 10 3 / cm 3 (compared with 10 4 –10 5 /cm 3 for standard STSG). 207 BIBLIOGRAPHY 1. Ratner D: Skin grafting. From here to there. Dermatol Clin 16(1):75, 1998. 2. Hauben DJ, Baruchin A, Mahler D: On the history of the free skin graft. Ann Plast Surg 9:242, 1982. 3. Brown JB, McDowell F: Massive repairs with thick split- skin grafts; emergency “dressing” with homografts in burns. Ann Surg 115:658, 1942. 4. 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Hill TG: Enhancing the survival of full-thickness grafts. J Dermatol Surg Oncol 10:639, 1984. 187. Wolfort S, Rohrich RJ, Handren J, May JW Jr: The effect of epinephrine in local anesthesia on the survival of full- and split-thickness skin grafts: an experimental study. Plast Reconstr Surg 86:535, 1990. 188. Fazio MJ, Zitelli JA: Full-thickness skin grafts. Clinical observations on the impact of using epinephrine in local anesthesia of the donor site. Arch Dermatol 131:691, 1995. 189. Robson MC, Krizek TJ: Predicting skin graft survival. J Trauma 13:213, 1973. 190. Perry AW, Sutkin HS, Gottlieb LJ, et al: Skin graft survival— the bacterial answer. Ann Plast Surg 22:479, 1989. 191. Pruitt BA Jr, Levine NS: Characteristics and uses of biologic dressings and skin substitutes. Arch Surg 119:312, 1984. 192. Beele H: Artificial skin: past, present and future. Int J Artif Organs 25:163, 2002. 193. Jones I, Currie L, Martin R: A guide to biological skin substitutes. Br J Plast Surg 55:185, 2002. 194. Purdue GF, Hunt JL, Still JM Jr, et al: A multicenter clinical trial of a biosynthetic skin replacement, Dermagraft-TC, compared with cryopreserved human cadaver skin for temporary coverage of excised burn wounds. J Burn Care Rehabil 18:52, 1997. 195. Bello YM, Falabella AF: Use of skin substitutes in derma- tology. Dermatol Clin 19:555, 2001. 196. Nanchahal J, Dover R, Otto WR: Allogeneic skin substi- tutes applied to burn patients. Burns 28:254, 2002. 197. Carucci JA, Kolenik SA III, Leffell DJ: Human cadaveric allograft for repair of nasal defects after extirpation of basal cell carcinoma by Mohs micrographic surgery. Dermatol Surg 28:340, 2002. 198. Gohari S, Gambla C, Healey M, et al: Evaluation of tissue- engineered skin (human skin substitute) and secondary intention healing in the treatment of full thickness wounds after Mohs micrographic or excisional surgery. Dermatol Surg 28:1107, 2002. 199. Ozerdem OR, Wolfe SA, Marshall D: Use of skin substitutes in pediatric patients. J Craniofac Surg 14:517, 2003. 200. Hansbrough JF, Dore C, Hansbrough WB: Clinical trials of a living dermal tissue replacement placed beneath meshed, split-thickness skin grafts on excised burn wounds. J Burn Care Rehabil 13:519, 1992. 201. Ramos-e-Silva M, Ribeiro de Castro MC: New dressings, including tissue-engineered living skin. Clin Dermatol 20:715, 2002. 202. Donati L, Magliacani G, Bormioli M, et al: Clinical expe- riences with keratinocyte grafts. Burns (Suppl 1):S19, 1992. 203. Latarjet J, Gangolphe M, Hezez G, et al: The grafting of burns with cultured epidermis as autografts in man. Two case reports. Scand J Plast Reconstr Surg 21:241, 1987. 204. Thivolet J,Faure M, Demidem A, Mauduit G: Long-term survival and immunological tolerance of human epider- mal allografts produced in culture. Transplantation 42:274, 1986. 205. Still JM Jr, Orlet HK, Law EJ: Use of cultured epidermal autografts in the treatment of large burns. Burns 20:539, 1994. 206. Sheridan RL, Tompkins RG: Cultured autologous epithe- lium in patients with burns of ninety percent or more of the body surface. J Trauma 38:48, 1995. 207. Kumagi N, Nishina H, Tanabe H, et al: Clinical applications of autologous cultured epithelia for the treatment of burn wounds and burn scars. Plast Reconstr Surg 82:99, 1988. DEFINITIONS A llap ls a unlt ol tlssuo that malntalns lts ovn blood supply vhllo bolng translorrod lrom a donor to a roclplont slto. ln contrast, gralts aro translorrod unattachod to a vascular sourco and roly on tho blood supply at tho roclplont slto lor tholr survlval. llaps rango lrom slmplo advancomonts ol skln and subcutanoous tlssuo to composlto llaps that may contaln any comblnatlon ol skln, musclo, bono, lat, or lascla. HISTORY AND EVOLUTION 1ho orlgln ol tho torm llap orlglnatod lrom tho 16th contury Dutch vord ºllappo¨, moanlng somo- thlng that hung broad and looso, lastonod only on ono sldo. 1 1ho hlstory ol plastlc surglcal ropalr vlth llaps can bo documontod as lar back as 600 ßC, vhon Sushruta Samlta doscrlbod nasal roconstruc- tlon uslng a chook llap. 1ho orlglns ol lorohoad rhlnoplasty can bo tracod to lndla about 1440 AD, but probably vas practlcod long boloro tho blrth ol Chrlst. 2 1hoso surglcal procoduros lnvolvod tho uso ol rotatlon llaps, vhlch transport skln to an ad|acont aroa vhllo tvlstlng or rotatlng a podlclo. 1ho lronch aro crodltod vlth tho orlglnal doscrlp- tlon ol slldlng or advancomont typo llaps, vhlch translor skln lrom an ad|acont aroa vlthout torslon ol tho baso. Dlstant podlclod llaps, vhlch translor tlssuo to a romoto slto, voro lnltlally roportod ln tho ltallan lltoraturo durlng tho konalssanco. 3 Subsoquont llap ovolutlon happonod ln phasos. llrst thoro vas an oarly porlod durlng tho llrst and Socond World Wars vhon podlclod skln llaps voro usod oxtonslvoly. 1ho noxt porlod occurrod ln tho 1950s and 60s, vhon vhat vo nov rocognlzo as roglonal axlal pattorn llaps voro roportod. A thlrd porlod took placo malnly durlng tho 1970s, vhon a dlstlnctlon vas mado botvoon axlal and random llaps, musclo and musculocutanoous llaps voro olovatod and translorrod, and lroo tlssuo translor camo lnto bolng. 1ho 1980s sav tho dovolopmont ol lasclocutanoous llaps, ossoous and ossoocutanoous llaps, and spoclallzod lroo llaps. 1,4 ln 1984 Song ot al 5 lntroducod tho lroo thlgh llap basod on porloratlng soptocutanoous artorlos ln tho thlgh. 1hls vas tho llrst roportod doscrlptlon ol tho nov vory popular antorolatoral thlgh llap. loshlma and Sooda 6 colnod tho torm ºporlorator llap¨ ln 1989 vhllo roportlng on lnlorlor oplgas- trlc artory llaps basod on a slnglo musculocutano- ous porlorator vossol. 1ho orlglnal porlorator llaps voro translors ol skln torrltorlos basod on a namod vascular podlclo to a musclo vhllo prosorvlng tho musclo and lts lnnorvatlon. 610 1ho porlorator con- copt has ovolvod slnco tho dovolopmont ol supormlcrosurgory. 11 Skln llaps aro nov succoss- lully translorrod basod on tho small porloratlng vos- sol alono, vlthout dlssoctlon ol tho namod vascu- lar podlclo. Supormlcrosurglcal tochnlquos laclll- tato tho anastomosls ol vossols 0.5 mm ln dlam- otor. 1214 1ho rocont lnnovatlons ln porlorator llap surgory roprosont a shllt tovard osthotlc lroo llap rollno- monts and attompts to mlnlmlzo donor slto morbld- lty. 1hln, supor-thln, and mlcro-thln porlorator llaps havo lurthor advancod tho osthotlc roconstructlon (llg 1) ol dolocts roqulrlng covorago vlth llno pll- ablo tlssuo. 1519 1ho luturo ol porlorator llaps may llo ln tho cllnlcal appllcatlon ol anglosomos 20 and tho croatlon ol ºlroo-stylo lroo llaps¨ ln vhlch a porlorator locallzod by Dopplor slgnal can bo tho basls lor a skln llap ln any anatomlc roglon. 2125 VASCULAR ANATOMY OF THE SKIN Arterial Anatomy ln 1889 Manchot 26 doscrlbod cutanoous vascu- lar torrltorlos. 1n 1964 Soltchlk and lahn 27 stud- lod tho anatomy ol tho ºlntrlnslc clrculatlon¨ ol tho skln and obsorvod that artorlal branchos ponotrato tho suporllclal layor ol tho suporllclal lascla and |oln a subdormal ploxus ol artorlos tormlnatlng ln skln caplllarlos. 1ho vonous dralnago systom paral- lolod tho artorlal systom. Spaltoholz 28 ln 1893 dom- onstratod anatomlcally that tho clrculatlon to tho skln vla subdormal and dormal ploxusos could bo PRINCIPLES OF FLAPS Amanda A Gosman MD SRPS Volume 10, Number 1 2 lod by olthor dlroct or lndlroct branchos lrom an undorlylng sourco vossol 29 (llg 2). 1aylor and lalmor 20 proposo tvo thoorlos ol tho blood supply to tlssuos. 1ho llrst dollnos tho angiosome vhlch ls a composlto unlt ol skln and lts undorlylng doop tlssuo suppllod by a sourco artory. 1ho socond dollnos tho routos by vhlch tho lntogu- mont ls suppllod by that sourco artory. 1ho direct routo oncompassos vossols that aro prlmarlly dlroctod tovards tho skln, vhothor thoy lollov tho lntormuscular soptum or plorco tho musclo. 1ho indirect routo constltutos vossols vhoso maln sup- ply ls olthor to musclo or anothor doop tlssuo and only socondarlly supply tho skln. 1ho lollovlng romarks aro basod on tho rosults ol tholr study. 1. 1ho blood supply ol tho body coursos vlthln or ad|acont to tho connoctlvo tlssuo lramovork, vhothor lt ls bono, sopta or lascla. 2. 1ho vossols courso lrom llxod locl to mobllo aroas. 3. 1ho vascular outllov ls a contlnuous systom ol artorlos llnkod prodomlnantly by roducod callbor vossols, lo, tho choko artorlos and artorlolos. 4. 1ho body ls a throo-dlmonslonal |lgsav mado up ol composlto blocks ol tlssuo suppllod by namod sourco artorlos. 1ho artorlos supplylng thoso blocks ol tlssuo aro rosponslblo lor tho supply ol tho skln and tho undorlylng structuros. 1hoso composlto unlts vo havo namod ANGIOSOMES. 1aylor and lalmor (1987) 1aylor and lalmor 20 doscrlbod 40 anglosomos (llg 3) that aro llnkod to oach othor by ºtruo¨ anas- tomotlc artorlos ol slmllar callbor or roducod call- bor ºchoko¨ anastomotlc vossols. 30 1ho choko vos- sols can potontlally dllato to tho callbor ol a truo anastomosls altor surglcal dolay or vlth a docroaso ln sympathotlc tono. 1ho anglosomo thoory has moro rocontly boon appllod ln dotallod anatomlc lnvostlgatlons ol tho loroarm, lovor oxtromlty, and hoad and nock. 3133 Although many lmportant Fig 1. 1ho ovolutlon ol tho ultrathln porlorator-basod llap. (Reprinted with permission from Hallock GG: Discussion of “A microdissected thin tensor fasciae latae perforator flap” by N Kimura. Plast Reconstr Surg 109:78, 2002.) Fig 2. 1ho cutanoous clrculatlon. (Reprinted with permission from Daniel RK, Kerrigan CL: Principles and Physiology of Skin Flap Surgery. In: McCarthy JG (ed), Plastic Surgery. Philadelphia, Saunders, 1990. Vol 1, Ch 9.) SRPS Volume 10, Number 1 3 roglonal dllloroncos voro ldontlllod, tho authors conllrmod that ln most casos connoctlons botvoon ad|acont anglosomos occurrod vlthln tlssuos and not botvoon thom. McCrogor 34 acknovlodgos that 1aylor and lalmor´s llndlngs havo practlcal appllcatlon ln tho doslgn ol skln llaps, but stross tho llmltatlons ln tholr concluslons duo to tho statlc naturo ol tho spocl- mons usod. 1o dotormlno skln porluslon pattorns, McCrogor porlormod lntraartorlal lluoroscoln ln|octlon studlos on 23 patlonts undorgolng abdoml- nal roductlon. ln 78.3° ol patlonts tho dlstrlbutlon ol lluoroscoln vas ovor a much smallor roglon than vould bo oxpoctod lrom 1aylor and lalmor´s study. McCrogor notos that unllko tho 1aylor ln|octlons, vhlch voro porlormod ln lrosh cadavors, hls study vas porlormod ln llvlng patlonts vhoso vascular roslstanco ls physlologlc rathor than anatomlc. Ho also lound that ºtho vatorshod botvoon ad|acont torrltorlos doos not corrospond to tho choko artor- los doscrlbod at tho porlphory ol tho anglosomo,¨ and suggostod that tho torm ºchoko artory¨ bo aban- donod. Naka|lma 35 concoptuallzod tho vascular supply to tho skln as an opllasclal vascular notvork vhlch ls lod by dllloront conllguratlons ol lnllov vossols. 1ho notvork ls prosont throughout tho subcutan- oous layor botvoon tho subdormal ploxus and tho doop lascla. 1ho archltocturo ol thls notvork var- los accordlng to anatomlc roglon but, llko tho sub- dormal ploxus, lt oxtonds throughout tho body as a contlnuous systom. 1hls opllasclal vascular notvork ls prosont throughout tho suporllclal lascla and ls callod tho lasclocutanoous ploxus. Naka|lma 35 ldontlllod slx vossol typos that por- lorato tho doop lascla to supply tho lasclocutanoous ploxus. A) dlroct cutanoous, ß) dlroct sopto- cutanoous, C) dlroct cutanoous branch ol muscu- lar vossol, D) porloratlng cutanoous branch ol mus- cular vossol, L) soptocutanoous porlorator, l) mus- culocutanoous porlorator (llg 4). 1ypos A and ß arlso lrom tho sourco vossol and supply a largo axlal torrltory abovo tho doop lascla. 1ypos C and D arlso lrom tho muscular vossol and supply tho lasclocutanoous ploxus and skln axlally ovor tho musclo. 1ypos L and l arborlzo undor, ln, and abovo tho doop lascla. 1hoso porlorators supply a small vascular torrltory and cannot support axlal skln pattorns. Fig 3. 1ho anglosomos ol tho sourco artorlos ol tho body. 1hoy aro. (1) thyrold, (2) laclal, (3) buccal, (4) ophthalmlc, (5) suporllclal tomporal, (6) occlpltal, (7) doop corvlcal, (8) trans- vorso corvlcal, (9) acromlothoraclc, (10) suprascapular, (11) postorlor clrcumllox humoral, (12) clrcumllox scapular, (13) prolunda brachll, (14) brachlal, (15) ulnar, (16) radlal, (17) postorlor lntorcostals, (18) lumbar, (19) suporlor glutoal, (20) lnlorlor glutoal, (21) prolunda lomorls, (22) poplltoal, (22a) doscondln gonlculato (saphonous), (23) sural, (24) poronoal, (25) latoral plantar, (26) antorlor tlblal, (27) latoral lomoral clrcumllox, (28) adductor (prolunda), (29) modlal plantar, (30) postorlor tlblal, (31) suporllclal lomoral, (32) common lomoral, (33), doop clrcumllox lllac, (34) doop lnlorlor oplgastrlc, (35) lntornal thoraclc, (36) latoral thoraclc, (37) thoracodorsal, (38) postorlor lntorossoous, (39) antorlor lntorossoous, (40) lntornal pudondal. (Reprinted with permission from Taylor GI, Palmer JH: The vascular territories (angiosomes) of the body: experimental study and clinical applications. Br J Plast Surg 40:113, 1987.) SRPS Volume 10, Number 1 4 Naka|lma and coauthors 36 studlod tho 3- dlmonslonal structuro ol tho blood supply to tho skln and subcutanoous tlssuo. Computor lmagos ol anglograms porlormod on 28 sogmontal artorlos ol tho body voro analyzod accordlng to tho tlssuo layor ln vhlch thoy voro domlnant (vhothor dor- mal, suporllclal, or doop adlpolasclal layors), tholr axlallty, and tholr slzo. Altor porloratlng tho doop lascla, tho artorlos voro asslgnod to ono ol slx dll- loront typos (llg 5). 1ho artorlos voro locallzod on a vholo body map and tho rolatlonshlp botvoon tho typo ol artory and tho moblllty ol tho tlssuo lt suppllod vas consldorod. Naka|lma´s slx typos ol artorlal conllguratlon ovolvod lrom hls provlous porlorator classlllcatlon. 35 1ypos l and ll aro contlnuatlons ol dlroct cutanoous and dlroct soptocutanoous porlorators (1ypos A and ß), rospoctlvoly. 1ypos l and ll aro mobllo vascular typos that shov axlallty and aro locatod ln tho doop adlpolasclal layor. 1ypos lll and lV aro porlphoral contlnuatlons ol olthor tho dlroct cutanoous branch or porloratlng cutanoous branch ol a muscular vossol (1ypos C and D). 1ypos ll and lV aro ol modlum slzo and ol modorato axlallty, but havo dlvorglng branch polnts. 1ypo lll ls domlnant ln tho doop adlpolasclal layor and lV ls domlnant ln tho suporllclal layor, rosultlng ln a roclprocal rolatlonshlp. 1ypos V and Vl (1ypos L and l) aro llxod vascular typos ol llttlo axlal- lty and aro contlnuatlons ol small soptocutanoous and musculocutanoous porlorators, rospoctlvoly (llg 6). ln tho torso typos l, lll, and lV aro locallzod ln tho Fig 4. Slx pattorns ol blood supply to tho lasclocutanoous ploxus. A, dlroct cutanoous vossol, ß, dlroct soptocutanoous vossol, C, dlroct cutanoous branch ol muscular vossol, D, porloratlng cutanoous branch ol muscular vossol, L, soptocutanoous porlorator, l, musculocutanoous porlorator. (Reprinted with permission from Nakajima H, Fujino T, Adachi S: A new concept of vascular supply to the skin and classification of skin flaps according to their vascularization. Ann Plast Surg 16:1, 1986.) Fig 5. Slx typos ol 3-dlmonslonal artorlal structuro. Soo toxt lor dotalls. (Reprinted with permission from Nakajima H, Minabe T, Imanishi N: Three-dimensional analysis and classi- fication of arteries in the skin and subcutaneous adipofascial tissue by computer graphics imaging. Plast Reconstr Surg 102:748, 1998.) SRPS Volume 10, Number 1 5 mobllo tlssuo at or around |olnts. 1ypo Vl vossols aro moro common ln llxod skln aroas, such as tho contor ol tho back. 1ypos ll, V, and Vl aro domlnant ln tho oxtromltlos. 1ypo ll accompanlos cutanoous norvos and volns that run ln tho doop adlpolasclal layor. lt ls lmportant to knov tho subcutanoous dopth ol a podlclo´s ploxus vhon olovatlng thln llaps and adlpolasclal llaps. Zhong and covorkors 38 classlllod tho vonous archltocturo ol tho skln and subcutanoous tlssuo lnto lour suporlmposod layors that aro dralnod by tvo largo vonous trunks, a suporllclal and a doop (llg 8). 1ho suporllclal vonous trunks aro locatod ln tho subcutanoous tlssuo and do not accompany artorlos. 1ho doop vonous trunks aro tho vonao comltantos ol tho sourco artory. 1ho authors pro- poso that tho maln vonous dralnago ol an anatomlc roglon can bo prlmarlly vla tho doop vonous trunk, tho suporllclal vonous trunk, or both. lmanlshl and othors 3941 doscrlbod tho vonous dralnago ol tho skln and subcutanoous tlssuo ol tho loroarm, scapular roglon, and tomporal and parlotal roglons. A slmllar pathvay ol vonous dralnago vas ldontlllod ln oach anatomlc roglon. Small opldor- mal and dormal branchos voro colloctod lnto a suporllclal polygonal vonous notvork locatod ln tho doop dormls or suporllclal adlpolaclal layor. Cstoal valvos voro ldontlllod at tho anatomosls ol tho llrst dralnlng dormal branchos and tho polygonal vonous notvork to roslst rollux. Dormal blood can pool ln tho polygonal notvork, vhlch has a varlablo dlstrl- butlon ol valvos dopondlng on anatomlc roglon, Fig 6. Classlllcatlon ol lasclocutanoous llaps. A, 1ypo l ls suppllod by tho dlroct cutanoous vossol. ß, 1ypo ll ls suppllod by tho dlroct soptocutanoous vossol. C, 1ypo lll ls suppllod by tho dlroct cutanoous branch ol tho muscular vossol. D, 1ypo lV ls suppllod by tho porloratlng cutanoous branch ol tho muscular vossols. L, 1ypo V ls suppllod by tho soptocutanoous porlorator. l, 1ypo Vl ls suppllod by tho musculocutanoous porlorator. (Reprinted with permission from Nakajima H, Fujino T, Adachi S: A new concept of vascular supply to the skin and classification of skin flaps according to their vascularization. Ann Plast Surg 16:1, 1986.) Venous Anatomy 1horo aro tvo systoms ol vonous dralnago ol tho skln and subcutanoous tlssuo. 1aylor and col- loaguos 37 studlod tho vonous torrltorlos (vonosomos) ol tho body and shovod that tho cutanoous vonous ploxus ls composod ol valvular suporllclal and doop cutanoous volns that parallol tho courso ol ad|acont artorlos, and ol osclllatlng avalvular volns that por- mlt bldlroctlonal llov botvoon ad|acont vonous tor- rltorlos (llg 7). Fig 7. Above, 1ho suporllclal (S) and doop (D) vonous systoms ln an oxtromlty. A largo vona communlcans (C) connocts thoso systoms, and tho altornatlvo pathvays ol lour vonao comltantos aro shovn. Below, Cthor roglons vhoro tho prodomlnant vonous dralnago ls by moans ol tho vonao comltantos. (Reprinted with permission from Taylor GI, Caddy CM, Watterson PA, Crock JG: The venous territories (venosomes) of the human body: experimental study and clinical implications. Plast Reconstr Surg 86:185, 1990.) SRPS Volume 10, Number 1 6 and vhlch ovontually dralns lnto largo cutanoous volns. 1ho authors dlstlngulsh botvoon a superfi- cial vein that ls locatod abovo tho doop lascla and a cutaneous vein that ls suporllclal and doos not accompany an artory. 41 Cutanoous vonous trunks aro tho prlmary dralnago ol tho dormls and aro connoctod by varlous communlcatlng branchos to tho vonao comltantos ol tho sourco artory (llg 9). sourco artory (og, suporllclal tomporal artory and voln), thoso parallol branchos may actually bocomo tho vonao comtantos to tho sourco artory 41 and to tho small artorlos that supply tho cutanoous voln (og, lossor saphonous and copha- llc). 39,42 1ho small artorlos corrospond to tho Naka|lma typo ll and aro tho sourco ol vono- cutanoous porlorators to tho skln. 1hoy aro an lmportant bypass to tho unldlroctlonal valvos ol tho cutanoous volns and pormlt rotrogrado llov ln dlstally basod llaps. 42 llnal and 1aylor 43 doscrlbod macrovonous and mlcrovonous systoms that bypass tho valvos ol tho vonao comltantos and pormlt rovorsal ol llov. Mul tl pl o vonous anastomotl c connoctl ons adoquatoly draln most dormal roglons vla olthor tho cutanoous voln or tho vonao comltantos ol tho sourco artory. FLAP CLASSIFICATION llap classlllcatlons aro multlplo and vary accordlng to tho organlzlng prlnclplo. Classlllca- tlon schomos havo hlstorlcally boon vory conlus- lng bocauso thoy voro basod on an lncomploto undorstandlng ol llap vascularlty. As our knovl- odgo ol tho vascular anatomy ol skln, subcutano- ous tlssuo, and musclo lncroasod, nov llap typos voro dovolopod and classlllcatlons voro proposod that voro lroquontly lncongruont vlth provlous systoms and vlth ono anothor. llaps usod to bo classlllod accordlng to tholr mothod ol movo- mont. 44 Local skln llaps aro stlll doscrlbod by thls tormlnology. Whon dlstant podlclod llaps bocamo commonplaco, 3 thoy voro labolod as local or dls- tant dopondlng on tholr proxlmlty to tho donor Fig 8. 1ho vonous archltocturo ol skln llaps. (Reprinted with permission from Zhong SZ, Wang GY, Yuan L, Xu DC: Anatomic basis of venous drainage in donor flaps. Surg Radiol Anat 16:349, 1994.) Fig 9. lolygonal vonous notvork ol tho loroarm. (1) Largo ascondlng voln. (2) Small ascondlng voln that anastomosod vlth tho vonous notvork. (3) Small ascondlng voln that anastomosod vlth ascondlng vossols lrom tho vonous notvork. (4) Anastomosls ol tho long voln vlth tho cophallc voln. (5 and 6) ßranchos that anastomosod small ascondlng vossols lrom tho vonous notvork and vonao comltantos ol tho radlal artory. ACV, accossory cophallc voln, CV, cophallc voln, kV, radlal voln (vonao comltantos). (Reprinted with permission from Imanishi N, Nakajima H, Aiso S: Anatomical study of the venous drainage architecture of the scapular skin and subcutaneous tissue. Plast Reconstr Surg 108:656, 2001.) ßotvoon tho cutanoous volns and tho vonao comltantos aro thln parallol branchos ol tho cutanoous volns that play cllnlcally lmportant rolos. ln aroas such as tho laco, vhoro tho courso ol tho namod voln dlvorgos slgnlllcantly lrom tho namod SRPS Volume 10, Number 1 7 and roclplont sltos. Subsoquontly llaps voro cat- ogorlzod by tholr tlssuo composltlon. musclo, skl n, muscul ocut anoous, l ascl ocut anoous, soptocutanous, and compound llaps. 1hls classl- llcatlon systom can bo conluslng bocauso dlllor- ont llaps basod on dllloront blood suppllos but ol tho samo composltlon can bo harvostod lrom tho samo roglon. 1ho lntrlnslc blood supply ol a llap ls tho most crltlcal dotormlnant ol succosslul translor and ls thoroloro tho most cllnlcally valld mothod ol clas- slllcatlon. Numorous anatomlc studlos ol tho blood supply to tho skln and lascla havo contrlb- utod to our undorstandlng and lod to a slmplor classlllcatlon ol cutanoous llaps. 15,20,25,3133,3542,45,46 Unlortunatoly, tho slmpllllod tormlnology doos not oxtond to all llap typos. lor oxamplo, tho lasclocutanoous llap that vas orlglnally dollnod by tho prosonco ol doop lascla ls nov classlllod accordlng to tho pattorn ol cutanoous vascularlty through tho lasclocutanous ploxus, and lroquontly doos not lncludo lascla. A lasclocutanoous llap can bo any llap basod on tho lasclocutanoous ploxus and composod ol any or all ol tho compo- nont layors botvoon tho skln and doop lascla. 25 1ho nov tormlnology ol porlorator and vonous llaps also rollocts tho trond tovard vascularlty- basod nomonclaturo, and currontly a conluslng comblnatlon ol old and nov llap tormlnology cooxlsts. Danlol and lorrlgan 29 groupod llaps lnto throo catogorlos accordlng to tholr mothod ol movomont, composltlon, and vascularlty. ln our dlscusslon ol spoclllc llaps vo havo comblnod tho lattor tvo crl- torla bocauso thoy ovorlap vlth oldor tormlnology basod on composltlon tormlnology. Spoclllc classl- llcatlons vlthln oach ol thoso llap typos vlll also bo dlscussod. Method of Movement Skln llaps can bo groupod accordlng to tho tochnlquo usod to translor tho tlssuo and tho dls- tanco botvoon tho donor and roclplont sltos. Local skln llaps aro usod to closo dolocts ad|acont to tho donor slto, and aro ln turn classlllod basod on tholr mothod ol movomont lnto llaps that advanco lrom tho baso ln tho samo dlroctlon as tho long axls ol tho llap (V-¥, ¥-V, slnglo-podlclo, and blpodlclo llaps) and llaps that plvot on a polnt (rotatlon, transposltlon, and lntorpolatlon llaps). Dlstant llaps uso donor tlssuo lrom sltos that aro not ad|acont to tho roclplont bod, and can bo groupod lnto dlroct llaps, tubo llaps, and lroo llaps. 29,47,48 Advancement flaps aro slld dlroctly lorvard lnto a doloct slmply by strotchlng tho skln, vlthout any rotatlon or latoral movomont. 47 1ho slmplost oxamplo ol thls typo ol movomont ls dlroct vound closuro. Varlatlons aro tho slnglo- and doublo- podlclo advancomont, V-¥ advancomont (llg 10), and lts opposlto, tho ¥-V advancomont llap. Suzukl and colloaguos 49 proposo a varlatlon ol tho tradl- tlonal V-¥-plasty ln vhlch tho ßurov´s trlanglos aro advancod rathor than oxclsod. Fig 10. A, roctangular advancomont llap. ß, V-¥ advancomont llap. (Reprinted with permission from Smith JW, Aston SJ (eds), Grabb and Smith’s Plastic Surgery, 4th ed. Boston, Little Brown, 1991.) Rotation flaps aro somlclrcular ln doslgn and rotato about a plvot polnt lnto tho doloct to bo closod (llg 11). 1ho donor slto can bo closod by a skln gralt or by dlroct suturo ol tho vound. 1o lacllltato rotatlon ol tho llap along lts arc, tho baso can bo back-cut at tho plvot polnt or a trlanglo ol skln (ßurov´s trlanglo) can bo romovod oxtornal to tho plvot polnt. SRPS Volume 10, Number 1 8 Fig 11. kotatlon llap. (Reprinted with permission from Smith JW, Aston SJ (eds), Grabb and Smith’s Plastic Surgery, 4th ed. Boston, Little Brown, 1991.) A transposition flap ls a (usually roctangular) llap that ls rotatod (latorally) about a plvot polnt lnto an lmmodlatoly ad|acont doloct. ßocauso tho olloc- tlvo longth ol tho llap bocomos shortor tho larthor tho llap ls rotatod, tho llap must bo doslgnod longor than tho doloct to bo covorod, othorvlso a back- cut may bo nocossary (llg 12). 1ho llap donor slto can bo closod by skln gralt, dlroct suturo, or soc- ondary llapog, bllobod llap (llg 13). A varlatlon ol tho transposltlon llap ls tho Z-plasty tochnlquo ln vhlch tvo trlangular llaps aro rovorsod and rotatod 90. 1ho throo llmbs ol tho Z must bo ol oqual longth and tho latoral llmb to contral llmb anglos should bo oqulvalont. 1ho galn ln longth ls rolatod to tho anglo botvoon tho contral and latoral llmbs (1ablo 1). 50 1ho 60 Z-plasty ls most olloctlvo bocauso lt longthons tho contral llmb vlthout plac- lng too much tonslon latorally (llg 14). lurnas and llschor 51 ostlmato that tho actual galn ln contral llmb longth ls 55°84° ol prodlctod and varlos vlth local skln tonslon. Soyhan 52 oxploros tho goomotry ol Z-plastlos and romlnds us that a slnglo largo Z-plasty ls moro olloctlvo than multlplo smallor onos lor longthonlng tho skln ln a doslrod locatlon. Fig 12. 1ransposltlon llap. 1ho llap bocomos shortor as lt plvots and should bo doslgnod largor than tho doloct. A back-cut may bo noodod to oaso tonslon at tho baso. (Reprinted with permission from Smith JW, Aston SJ (eds), Grabb and Smith’s Plastic Surgery, 4th ed. Boston, Little Brown, 1991; and Lamberty BGH, Healy C: Flaps: physiology, principles of design, and pitfalls. In: Cohen M (ed), Mastery of Plastic and Reconstructive Surgery. Boston, Little Brown, 1994.) Fig 13. 1ho bllobod llap. (Reprinted with permission from Jackson IT: Local Flaps in Head and Neck Reconstruction. St Louis, Mosby, 1985.) SRPS Volume 10, Number 1 9 1ho rhombold (Llmborg) llap ls anothor trans- posltlon llap charactorlzod by lts goomotrlc pat- torn. 1ho longltudlnal axls ol tho rhombold oxcl- slon parallols tho llno ol mlnlmal skln tonslon. lour dllloront rhombold llaps can bo doslgnod vhon 60 anglos aro usod (llg 15). 1hls concopt can bo oxpandod to croato a doublo or ovon a trlplo rhombold llap, tho donor sltos ol tho llap aro closod by dlroct suturo. 53 1ho Dulourmontol llap ls slmllar to tho rhombold llap oxcopt that lt can bo dravn vlth anglos ol up to 90. losor and colloaguos 54 doscrlbod a curvlllnoar modlllcatlon ol tho classlcal transposltlon llap. 1holr varlant has doublo opposlng somlclrcular llaps and ls usod to closo clrcular dolocts (llg 16). TABLE 1 Theoretical gain in length of the central limb with various angles in Z-plasty. (Reprinted with permission from Rohrich RJ, Zbar RIS: A simplified algorithm for the use of Z-plasty. Plast Reconstr Surg 103:1513, 1999.) Fig 14. Z-plasty. (Reprinted with permission from Smith JW, Aston SJ (eds), Grabb and Smith’s Plastic Surgery, 4th ed. Boston, Little Brown, 1991.) Fig 15. 1ho rhombold (Llmborg) llap. (Reprinted with permission from Smith JW, Aston SJ (eds), Grabb and Smith’s Plastic Surgery, 4th ed. Boston, Little Brown, 1991.) Fig 16. Doublo opposlng somlclrcular llaps. Altor olovatlng tho llaps and undormlnlng tho ad|acont tlssuo, llap A ls transposod vlth llap ß and llap A´ vlth llap ß´. 1ho anglos ol A and A´ llaps aro suturod to tho marks at x and x´, and ß and ß´ llaps to D and D´, rospoctlvoly. (Reprinted with permission from Keser A, Sensoz O, Mengi AS: Double opposing semicircular flap: a modification of opposing Z- plasty for closing circular defects. Plast Reconstr Surg 102:1001, 1998.) SRPS Volume 10, Number 1 10 Interpolation flaps rotato on a plvot polnt lnto a doloct that ls noar but not ad|acont to tho donor slto, so that tho llap podlclo must pass ovor or undor tho lntorvonlng tlssuo. Lxamplos ol lntorpolatlon llaps aro tho doltopoctoral (ßakam|lan) llap, lsland llaps such as tho Llttlor nourovascular dlgltal pulp llap (llg 17), and subcutanoous-podlclo llaps. Fig 17. 1ho nourovascular lsland llap (Llttlor). (Reprinted with permission from Daniel RK, Kerrigan CL: Principles and physiology of skin flap surgery. In: McCarthy JG (ed), Plastic Surgery. Philadelphia, Saunders, 1990. Vol 1, Ch 9, p 305.) Distant flaps lmply that tho donor and roclplont sltos aro not ln closo proxlmlty to oach othor. Lxamplos lncludo dlroct llaps (not to bo conlusod vlth dlroct cutanoous) such as tho thonar, cross-log, and groln llaps. Whon tho tvo sltos cannot bo approxlmatod, tubo llaps 55 (llg 18) or mlcrovascu- lar lroo tlssuo translors aro lndlcatod. Free Tissue Transfer ln 1963 Coldvyn and colloaguos 56 roportod tho llrst succosslul lroo llap translor vhon thoy olovatod an lsland podlclod llap lrom tho groln ol dogs and subsoquontly dlvldod tho podlclo and roplacod tho llap ln lts orlglnal slto vlth mlcrovascular anasto- mosos. Sovoral roports ol lroo llap roconstructlon lollovod ln short ordor. Cllnlcal mlcrosurgory has oxporloncod a rapld oxpanslon slnco lts boglnnlng ln tho oarly 1970s. Succoss ratos ol mlcrovascular procoduros ls voll ovor 90° ln most sorlos. 57 lor a dotallod ovorvlov ol mlcrosurgory and lroo tlssuo translor, ploaso rolor to tho Selected Readings lssuo on thls toplc. Fig 18. 1ho clavlcular tubod llap. (Reprinted with permission from Mendelson BC, Masson JK: Cervical and clavicular tubed skin flaps. In: Strauch B, Vasconez LO, Hall-Findlay EJ (eds), Grabb’s Encyclopedia of Flaps. Boston, Little Brown, 1990. Vol 1, Ch 42.) SRPS Volume 10, Number 1 11 Tissue Composition and Vascularity Cutaneous Flaps McCrogor and Morgan 59 catogorlzod llaps as ran- dom or axlal. kandom llaps aro basod on tho sub- dormal ploxus vhlch ls suppllod by dlroct cutano- ous, musculocutanoous, or lasclocutanoous vossols. 1 kandom llaps aro tradltlonally llmltod to 3.1 longth- to-vldth ratlos, and may roqulro multlplo dolays to bo translorrod to a dlstant slto. Mllton 60 challongod tho rolovanco ol longth-to-vldth ratlos and accu- ratoly arguod that tho survlval ol a skln llap doponds ontlroly on lts moans ol vascularlzatlon. Axlal pattorn llaps contaln a spoclllc dlroct cuta- noous artory vlthln tho longltudlnal axls ol tho llap. An lsland llap ls an axlal pattorn llap that ls ralsod on a podlclo dovold ol skln to lacllltato dlstant translor. 61 Slnco tho vascular anatomy ol lasclocutanoous por- lorators vas dotallod, a classlllcatlon systom that can bo appllod to all cutanoous llaps has boon dovlsod. 35,62 Cormack and Lamborty 1,63 stato that skln llaps can bo classlllod as dlroct cutanoous, musculocuta- noous, or lasclocutanoous accordlng to tholr ana- tomlc systom ol vascularlzatlon, not tholr tlssuo com- pononts. All skln llaps aro basod on tho lasclo- cutanoous ploxus, vhlch lncludos tho lntorcon- noctod componont parts ol tho sublasclal, lntralasclal, and supralaclal vascular ploxusos oncompasslng tho dormal, subdormal, suporllclal, and doop adlposlasclal layors. 35,36,64 1ho lasclo- cutanoous ploxus ls suppllod lrom porloratlng vos- sols that ponotrato tho doop lascla olthor dlroctly, through musclo, or botvoon musclos. Hallock 25 dollnos a porlorator as any vossol that ontors tho supralasclal plano through a lonostratlon ln tho doop lascla, rogardloss ol orlgln. llaps basod on lsolatod porlorator(s) aro dollnod as porlorator llaps. 65,66 Naka|lma 35 classlllod skln llaps lnto llvo typos accordlng to tholr vascularlzatlon. cutanoous, lasclocutanoous, adlpolasclal, soptocutanoous, and musculocutanoous (1ablo 2). All skln llaps aro sup- pllod by porloratlng vossols to tho lasclocutanoous ploxus. lasclocutanoous llaps voro lurthor groupod lnto slx typos basod on tho slx pattorns ol doop lasclal porlorators (soo llg 6). Naka|lma´s dollnltlon ol a dlroct cutanoous porlorator ls oqulvalont to tho axlal vossol ol McCrogor and Morgan. 59 Mathos and Nahal 67 dollnod lasclocutanoous llaps as thoso suppllod by a dlroct cutanoous podlclo, sopto- cutanoous podlclo, or musculocutanoous podlclo. Naka|lma 36 analyzod and classlllod tho 3-dlmon- slonal structuro ol tho skln and adlpolasclal tlssuo lnto slx typos and doscrlbod tholr corrospondlng llap appllcatlons ln a study that ls bocomlng lncroaslngly rolovant lrom a cllnlcal standpolnt. 1aylor and lalmor 20 stato that cutanoous artorlos contrlbutlng to an anglosomo can arlso directly lrom tho undorlylng sourco vossol to provldo tho prlmary cutanoous supply, or indirectly lrom tho branchos ol tho sourco artory to doopor structuros. 20,30 Hallock 25 dlllorontlatos dlroct and lndlroct porlora- tors basod on tho structuros that thoy travorso prlor to plorclng tho doop lascla. Direct perforators plorco tho doop lascla vlthout havlng travorsod any doopor structuros. Indirect perforators pass through doopor tlssuos, usually musclo or soptum, boloro ontorlng tho doop lascla. Hallock 25 appllod thls concopt to tho classlllcatlon ol doop lasclal porlorators pro- posod by Naka|lma 35 vhoroby all cutanoous llaps could bo doslgnatod as olthor direct or indirect porlorator llaps (llg 19). Perforator Flaps ßy tho oarly 1980s, mlcrosurglcal tochnlquos had boon succosslully lntogratod lnto tho practlco ol roconstructlvo surgory and thoro vas a quost to dlscovor nov donor llaps that vould bo rollablo, thln, tochnlcally oasy to ralso and translor, and that vould produco mlnlmal donor slto morbldlty. lor- lorator llaps and tho loss-succosslul artorlallzod vonous llaps ovolvod lrom thoso ollorts. 23,68 ln Chlna and }apan tho llrst porlorator llaps voro dovolopod lor hoad and nock roconstructlon and burn scar contracturos. ln 1984 Song ot al 5 roportod tho ºlroo thlgh llap¨, vhlch lncludod a doscrlptlon ol tho antorolatoral thlgh llap, tho andromoda thlgh llap, and tho postorlor thlgh llap. Lach llap vas doslgnod ovor a soptocutanoous porlorator ol tho sourco vos- sol, vhlch vas dlssoctod rotrogrado. ln 1989 loshlma and Sooda 6 roportod tho succosslul trans- lor ol an lnlorlor oplgastrlc artory skln llap basod on a roctus abdomlnls porlorator to a groln vound (lsland) and to tho lloor ol mouth. Allon and 1rooco 7 and ßlondool 8 roportod tho ultlmato musclo-spar- lng 1kAM llap vhon thoy publlshod tholr succosslul sorlos ol broast roconstructlons vlth tho doop lnlo- rlor oplgastrlc porlorator llap. Clutoal artory porlo- rator llaps voro llrst ralsod as podlclod llaps by SRPS Volume 10, Number 1 12 loshlma 69 lor tho ropalr ol sacral vounds, and lator by Allon and 1uckor 10 as lroo llaps lor broast rocon- structlon. Angrlglanl ot al 9 dovolopod tho ºlatlssl- mus dorsl musculocutanoous llap vlthout tho musclo¨, a llap ol skln and subcutanoous tlssuo basod on a thoracodorsal artory porlorator. 1ho lntroductlon ol porlorator llaps ushorod ln an ora ol sophlstlcatlon and rollnomont ln roconstruc- tlvo mlcrosurgory. 1ho omphasls shlltod lrom trylng to onsuro lroo llap survlval to prosorvlng musclo lunc- tlon, produclng mlnlmal donor slto morbldlty, and doslgnlng llaps that aro hlghly vorsatllo and can bo tallorod to tho spoclllc doloct. Cur undorstandlng ol cutanoous vascularlty and porlorator anatomy has grovn tromondously ln tho past 10 yoars. lorlorator llaps aro typlcally composod ol skln and subcutan- oous tlssuo suppllod by a doop lasclal porloratlng vossol. lorlorator llaps allov tho surgoon to rocon- struct body parts vlth tho samo tlssuos that aro most lroquontly mlsslng. skln and subcutanoous lat. lotontlal llap donor sltos aro numorous, and many also havo tho capaclty to lncorporato musclo, lat, and bono lnto tho llap doslgn. (Reprinted with permission from Nakajima H, Fujino T, Adachi S: A new concept of vascular supply to the skin and classification of skin flaps according to their vascularization. Ann Plast Surg 16:1, 1986.) TABLE 2 Classification of Skin Flaps Fig 19. Modlllcatlon ol Naka|lma´s pattorn ol doop lascla porlorators. (Reprinted with permission from Hallock GG: Direct and indirect perforator flaps: the history and the controversy. Plast Reconstr Surg 111:855, 2003.) SRPS Volume 10, Number 1 13 1ho lllth (Cont, ßolglum, 2001) and Slxth lntor- natlonal Courso on lorlorator llaps (1alpol, 1al- van, 2002) voro hold ln rosponso to tho rapld ovolutlon ol porlorator llaps and conluslon rogard- lng tholr tormlnology. 65 1ho consonsus dollnltlon ol a porlorator llap ln 2002 vas ºa llap conslstlng ol skln or subcutanoous lat. 1ho vossols that supply blood to tho llap aro lsolatod porlorator(s). 1hoso porlorators may pass lrom tholr sourco vossol orlgln olthor through or ln botvoon tho doop tlssuos (mostly musclo).¨ 65 1hroo dllloront klnds ol porlo- rator vossols voro rocognlzod. 1) lndlroct musclo porlorators, 2) lndlroct soptal porlorators, and 3) dlroct cutanoous porlorators 65 (llg 20). 1ho lndl- roct musclo and soptal porlorators glvo rlso to mus- culocutanoous and soptocutanoous porlorator llaps, rospoctlvoly. Fig 20. Slmpllllod dollnltlons omorglng lrom tho 2002 Slxth lntornatlonal Courso on lorlorator llaps. (1) lndlroct musclo or musculocutanoous porlorators travorso musclo to plorco tho outor layor ol tho doop lascla and supply tho skln. (2) lndlroct soptal or soptocutanoous porlorators travorso through soptum and supply tho skln altor plorclng tho outor layor ol tho doop lascla. (3) Dlroct porlorators ponotrato tho doop lascla only. (Reprinted with permission from Blondeel PN, Van Landuyt K, Hamdi M, Monstrey SJ: Perforator flap terminology: update 2002. Clin Plast Surg 30:343, 2003.) Wol 21 and othor purlsts 70,71 contlnuo to arguo that a ºtruo porlorator¨ should only rolor to a mus- cular porlorator, vhlch roqulros lntramuscular dls- soctlon and vhlch should thoroloro havo a dlstlnct ldontlty lrom tho moro oaslly dlssoctod soptal por- lorator. 25,65,66 llaps such as tho groln llap that voro provlously classlllod as olthor axlal, artorlal, or cuta- noous aro nov moro accuratoly doscrlbod as dlroct cutanoous porlorator llaps. 72 1o losson conluslon ovor spoclllc porlorator llap nomonclaturo, a consonsus vas roachod at tho moot- lng to namo oach porlorator llap altor tho nutrlont vossol(s) and not tho undorlylng musclo. 65 ln aroas vhoro multlplo porlorator llaps can bo ralsod lrom a slnglo vossol, tho llap should bo namod altor lts anatomlc roglon or musclo. 65 lor oxamplo, llaps basod on tho latoral clrcumllox lomoral vossols aro namod tho antorolatoral thlgh llap, tonsor lasclao latao porlorator llap, and so on, accordlng to loca- tlon or undorlylng musculaturo. lorlorator llaps havo tho lollovlng advantagos. 73 • prosorvo musclo lunctlon • produco mlnlmal donor slto morbldlty • roduco postoporatlvo rocovory tlmo and paln modlcatlon roqulromonts • can bo doslgnod ol varylng slzos and thlcknossos to lmprovo tho osthotlc rosult Many studlos comparlng tho doop lnlorlor opl- gastrlc (DlLl) llap and tho 1kAM llap lor broast roconstructlon attost to tho postoporatlvo advan- tagos ol musclo-sparlng llap harvost. 7480 lorlorator llaps ovo tholr vorsatlllty to tho largo cutanoous torrltorlos, long podlclos that pormlt convontlonal and lroo translor, potontlal lor bolng harvostod as compound or sonsato llaps, and ablllty to bo thlnnod to tho subdormal ploxus. 14,16,18,19,71,8183 1hoso char- actorlstlcs mako porlorator llaps ldoal solt-tlssuo unlts lor roconstructlon ln aroas that roqulro thln, pllablo tlssuo, such as tho hoad and nock and tho lovor oxtromlty. 69,71,8287 1ho dlsadvantagos ol porlorator llaps aro 1) tho tlmo-consumlng, motlculous dlssoctlon ol tho podlclo, 2) varlatlon ln porlorator anatomy, slzo, and locatlon, and 3) a hlghor rlsk ol lat nocrosls comparod vlth musculocutanoous llaps. 80,82,83,8893 1hoorotlcally, a porlorator llap could bo doslgnod ln oach ol tho cutanoous torrltorlos ol tho 374 porlo- rators >0.5 mm ln dlamotor ldontlllod by 1aylor and lalmor. 20,94 1ho most commonly usod porlorator llaps aro tho doop lnlorlor oplgastrlc (DlLl) llap, tho antorolatoral thlgh (AL1l) llap, tho suporlor glutoal artory (SCAl) llap, and tho thoracodorsal artory (1Al) llap. Many othor llaps havo boon doscrlbod but havo not yot galnod tho popularlty ol tho DlLl and tho AL1l llaps. 1o quallly as a potontlal donor sourco ol porlorator llap, a slto must havo a rollablo blood supply, ono or moro largo (>0.5 mm dlam) porlora- tors, podlclos ol sulllclont longth, and (prolorably) bo ablo to bo closod prlmarlly altor llap harvost. 1ho dovolopmont ol supormlcrosurglcal toch- nlquos has lacllltatod tho harvost ol llaps basod on smallor and shortor porlorators, such as tho paraum- SRPS Volume 10, Number 1 14 blllcal porlorator llap. 11,18 1ho ºlroo-stylo lroo llap¨ ls tho ultlmato appllcatlon ol tho anglosomo thoory and supormlcrosurglcal tochnlquos. 2125 A cutan- oous porlorator ls ldontlllod by Dopplor probo and a llap ls doslgnod on tho skln torrltory. 1ho porlora- tor ls usod lor tho anatomosls, vhlch ls porlormod vlth supormlcrosurglcal tochnlquos that ollmlnato tho nood lor todlous dlssoctlon ol tho sourco vossol. 1ho roador ls oncouragod to rovlov tho rolor- oncos on porlorator llaps lndopondontly bocauso an ln-dopth doscrlptlon ol spoclllc llaps ls boyond tho scopo ol thls toxt. Fasciocutaneous Flaps ln 1981 lonton 95 doscrlbod a novol vay to ralso a skln llap basod on tho vascular ploxus ol tho doop lascla. Although lonton mado tho lnltlal cllnlcal obsorvatlons, tho lnvostlgatlons ol tho anatomlcal vascular basls lor tho succoss ol thoso ºsuporllaps¨ vas subsoquontly accompllshod by Haortsch 96 ln 1981 and ßarclay ot al 97 ln 1982. 1olhurst and colloaguos 98,99 conllrmod tho usolulnoss ol tho lasclocutanoous llap and oxpandod tho concopt to oncompass roconstructlon ln othor parts ol tho body. Larly lnvostlgatlons lnto tho blood supply ol tho las- cla 1,63,99103 roportod that tho lasclocutanoous sys- tom conslsts ol porloratlng vossols that arlso lrom roglonal artorlos and pass along tho llbrous sopta botvoon musclo bolllos or musclo compartmonts. 1hls vascular ploxus ls locallzod to tho lovol ol tho doop lascla, vhlch ln turn glvos oll branchos to tho skln. Cn tho basls ol anatomlc studlos, ln 1984 Cormack and Lamborty 63,100 classlllod lasclo- cutanoous llaps accordlng to tholr vascular pattorns (llg 21). Type A ls a podlclod llap suppllod by multiple lasclocutanoous porlorators at tho baso ol tho llap and orlontod vlth tho long axls ol tho llap ln tho prodomlnant dlroctlon ol tho artorlal ploxus at tho lovol ol tho doop lascla. 1ho llap can bo proxlmally or dlstally basod and tho skln can bo romovod to croato an lsland llap. Lxamplo. lonton´s llap. Type B ls basod on a single lasclocutanoous porlo- rator ol modorato slzo vhlch ls conslstont ln both lts prosonco and lts locatlon. lt may bo usod as olthor a podlclod or lroo llap. Lxamplo. modlal arm llap. Type B modified ls stlll lod by a single porlorator but dlllors ln that tho porlorator ls removed in con- tinuity with the major vessel lrom vhlch lt arlsos. lt ls lntondod lor uso as a lroo llap. Type C llap supports lts skln by multiple small por- lorators along lts longth ln a laddor typo conllgura- tlon. 1hoso porlorators roach lt lrom a doop artory by passlng along a lasclal soptum botvoon musclos. lts maln uso ls as a lroo llap. Lxamplo. radlal loroarm llap. Type D conslsts ol an osteomusculofasciocutaneous lroo tlssuo translor. 1ho lnvostlgatlon ol tho lasclal vascular anatomy to dovolop llap classlllcatlon systoms contrlbutod groatly to our undorstandlng ol porlorator and cuta- noous blood supply. Lvontually lt bocamo ovldont that lncluslon ol tho doop lascla vas not nocossary lor tho survlval ol lasclocutanoous llaps, 20,98 although somo authors advocatod lts prosorvatlon lor protoc- tlon ol tho lasclal ploxus. 104 Naka|lma 35 doscrlbod tho lasclocutanoous ploxus as a vascular notvork that oxtondod lrom bolov tho doop lascla to tho dormls and vas porlusod by doop lasclal porlorat- lng vossols. Any llap basod on thls vascular notvork rogardloss ol lts tlssuo compononts ls a lasclo- cutanoous llap. 25 llaps that voro provlously con- sldorod lasclocutanous and that aro basod on lso- latod porloratlng vossols can nov bo accuratoly clas- slllod as dlroct or lndlroct porlorator llaps. 25,35,36,65,72 ln 1992 Masquolot 105 doscrlbod tho concopt ol a nouroskln llap basod on tho artorlos accompanylng cutanoous norvos. Naka|lma and colloaguos 106 doscrlbod tho nourocutanoous and vonocutanoous vascular systoms and throo typos ol podlclod lasclocutanoous llap ln tho oxtromltlos. vono- adlpolasclal (VAl), nouroadlpolasclal (NAl), and vono-nouroadlpolasclal (V-NAl). 1hoso llaps aro all basod on typo ll vossols, lo, nourocutanoous and vonocutanoous porlorators runnlng long ln tho doop adlpolasclal layor ol tho skln. 1ho llaps aro ralsod on a podlclo ol adlpolasclal tlssuo and doslgnod ol approprlato vldth to lncludo tho rolovant vascular systom. Naka|lma 107 roportod 23 succosslul casos ol lovor oxtromlty roconstructlon vlth VAl and V- SRPS Volume 10, Number 1 15 Fig 21. A classlllcatlon ol lasclocutanoous llaps. (Reprinted with permission from Cormack GC, Lamberty BGH: The Arterial Anatomy of Skin Flaps. Edinburgh, Churchill Livingstone, 1986.) SRPS Volume 10, Number 1 16 NAl llaps basod on tho lossor saphonous voln and sural norvo. lour dlstally basod and lour proxlmally basod typos ol llap aro ldontlllod (llg 22). 1ho lossor saphonous-sural V-NAl llap lncludos tho norvo, tho voln, and tholr rospoctlvo vascular sys- toms, and vas rocommondod as tho most rollablo llap cholco. lmanlshl 42 ovaluatod tho vonous dralnago ol tho dlstally basod lossor saphonous-sural V-NAl podlclod lasclocutanoous llap ln cadavors. Ho ldontlllod small, long volns along tho courso ol tho lossor saphonous voln that lntormlttonly anastomosod vlth tho largor voln, and proposod that tho small volns bypass tho valvos ln tho lossor saphonous voln and aro tho vonao comltantos to tho artory that accompanlos tho largor voln. lraccalvlorl ot al 108 roportod a sorlos ol 18 patlonts troatod vlth tho dlstally basod ºsuporllclal sural llap¨ lor roconstructlon ol solt-tlssuo dolocts ol tho lovor log and loot. 1ho authors roportod suporll- clal nocrosls ln ono patlont vho roqulrod graltlng and dolayod hoallng ln 2 patlonts. ßaumolstor and assoclatos 109 publlshod a sorlos ol ºsural artory llap¨ roconstructlons ln 70 patlonts, 60° ol vhom had at loast ono ma|or systomlc lllnoss. 1ho compllcatlon rato vas 59°, llap nocrosls occurrod ln 36°. klsk lactors lor compllcatlons voro comorbldlty, ostoo- myolltls, and a tlght subcutanoous tunnol. Cavadas 110 translorrod largo rovorso-llov nou- rocutanoous saphonous lsland llaps lor lovor oxtromlty roconstructlon ln 5 patlonts. ln a lollov- up artlclo 6 yoars lator, Cavadas 111 roports translor- rlng a postorlor tlblal porloratorsaphonous subcu- tanoous llap ln 40 casos. 1ho llap modlllcatlon vas a rosponso to dllllcult transposltlon, poor podlclo covorago, and donor slto compllcatlons vlth tho provlous llap tochnlquo. Naka|lma 45 vas tho llrst to roport tho artorlal supply to tho lossor saphonous voln and tho rolatod llap. Chon 112 roportod a sorlos ol 21 patlonts vho had lovor oxtromlty roconstructlon vlth tho dlstally basod ºsaphonous vonolasclocutanoous llap¨ (llg 23). 46 Dlstal llap nocrosls vas troatod vlth skln graltlng ln 2 patlonts. Although lt can bo ralsod as an lnnorvatod llap lor covorago ol plantar hool vounds, tho sural norvo ls usually prosorvod and thoroloro tho donor morbldlty ls loss than that ol tho nourocutanoous llap. Venous Flaps 1ho lntroductlon ol vonous llaps ln tho 1980s vas a rosult ol tho quost to dovolop tho ldoal lroo llap. ono that vas oasy, rollablo, thln, and not morbld. Nakayama ot al 113 and lator }ll and col- loaguos 114 and Nlchtor and Halnos 115 roportod artorlallzlng a llap through a vonous podlclo. A vonous lsland llap vlth an AV llstula vas thus cro- Fig 22. 1hoorotlcal llaps vlth a proxlmal baso. 1ypo A contalns both tho lossor saphonous voln and sural norvo. 1ypo ß ls tho samo as typo A oxcopt tho sural norvo has boon romovod lrom tho uppor llap. 1ypo C ls tho samo as typo A oxcopt tho lossor saphonous voln has boon romovod lrom tho uppor llap. 1ypo D ls tho samo as typo A oxcopt tho sural norvo has boon romovod. 1o tho rlght ol oach llap a dlagram shovs vhlch porlorators aro rosponslblo lor tho blood supply ol oach llap. 1ho small N donotos voak vascularlty to tho skln. (Reprinted with permission from Nakajima H, Imanishi N, Fukuzumi S, et al: Accompanying arteries of the lesser saphenous vein and sural nerve: anatomic study and its clinical applications. Plast Reconstr Surg 103:104, 1999.) SRPS Volume 10, Number 1 17 atod and vas roportod to havo up to 95 ° llap survlval and hlgh patoncy ratos. 1ho survlval ol thoso llaps, hovovor, vas not conslstont. Cormann and assoclatos 116 shovod that although blood llov ln plg lsland llaps vas rovorsod, oxygon consump- tlon romalnod bolov basollno, oarly thrombosls vas a common occurronco, and no llap survlvod longor than 48 hours. 1ho llov through vonous llap ln vhlch both tho alloront and olloront podlclos aro suppllod by vonous blood vas doscrlbod ln 1985 by ßaok ot al, 117 vho usod tho saphonous voln ol a dog. ßaok 117 pro- posos a ºto-and-lro¨ osclllatlng mochanlsm ol llov ln tho voln, vonulos, and vonous caplllarlos. 1vo yoars lator, Chavoln 118 appllod thls ln a cllnlcal sot- tlng. ln 1987 a slnglo-podlclod vonous lsland llap uslng tho saphonous voln vas croatod ln a dog by 1hatto and 1hatto. 119 1hoso slnglo-podlclod lsland llaps can bo lurthor classlllod lnto olthor proxlmally basod or dlstally basod llaps. Amaranto and covorkors 120 concludod that slnglo-podlclod vonous llaps cannot survlvo vlthout llov-through, and Lonoblo ot al´s 121 llov-through vonous llaps all dlod dosplto blood llov vlthln tho vonous systom. 1hatto and 1hatto 122 classlly vonous llaps lnto throo groups, rovlov tho oxporlmontal and cllnlcal studlos on vonous llaps, and dlscuss tho varlous thoo- rlos ol llap survlval. Accordlng to thls classlllcatlon, typo l ls a unlpodlclod vonous llap, or puro vonous llap vlth a slnglo cophalad voln as tho only vascular condult. ¥uan, Shan, and Zhu 123 doscrlbo tvo pat- torns ol llov ln puro vonous llaps. a shaklng movo- mont rolatod to hoart rato and a pondulum-llko movomont that ls tho maln contrlbutor to llap por- luslon. Also obsorvod vas ongolng rovascularlzatlon, vhlch ultlmatoly suppllod tho llap and vhlch ls ossontlal lor llap survlval. 124 Noroldln and othors 125 attrlbutod survlval to a porlvonous aroolar notvork ol vossols arrangod longltudlnally along tho vholo longth ol tho podlclo. Shalaby and Saad 126 ldontl- llod an artorlal notvork ln tho porlvonous aroolar tlssuo on hlstologlal study ol tho saphonous and cophallc vonous lsland llaps. Naka|lma´s 45 anatomlc study and doscrlptlon ol tho lntrlnslc and oxtrlnslc vonocutanoous vascular systom conllrmod tho prosonco ol porlvonous art- orlal llov ol tho slnglo-podlclod vonous llap. 1ho typo l vonous llap vould bo classlllod by tho author as a vonocutanoous adlpolasclal llap. 1hatto and 1hatto 122 typo ll vonous llaps aro blpodlclod ºllov-through¨ llaps vlth alloront and olloront volns oxhlbltlng llov lrom caudal to coph- alad. \lu and Chon 127 roportod that tho porlvonous aroolar tlssuo ls ossontlal lor llov-through llap sur- vlval and concludo that lt ls both protoctlvo and nourlshlng. 1hoy dlvldo tho survlval procoss lnto an oarly (up to 72 hours) vonous nourlshlng stago and a socondary (day 4 to 6 vooks) stago ol noovascularlzatlon charactorlzod by artorlal nour- lshlng and vascular roconstructlon. lnada´s group 128 lsolatod tholr llaps lrom tho roclplont tlssuo bod and concludod that llov-through vonous llaps vlth only a slnglo voln cannot survlvo ll largor than 12 cm. lor largor llaps to survlvo, a donso vonous notvork ls ossontlal, vhlch suggosts that moro than ono voln vould probably bo bonoll- Fig 23. 1hoorotlcal llaps vlth a dlstal baso. 1ypos A´, ß´, C´, and D´ aro rovorso llaps ol tho proxlmally basod llaps. (Reprinted with permission from Nakajima H, Imanishi N, Fukuzumi S, et al: Accompanying arteries of the lesser saphenous vein and sural nerve: anatomic study and its clinical applications. Plast Reconstr Surg 103:104, 1999.) SRPS Volume 10, Number 1 18 clal. 129 1hoy surmlsod that thoso llaps bohavo not unllko a gralt vhoso survlval doponds largoly on tho surroundlng clrculatlon. 1ypo lll vonous llaps aro artorlallzod through a proxlmal artorlovonous anastomosls and dralnod by dlstal volns. Loo 130 rovlovs tho concopt ol vonous llaps and tho artorlallzatlon ol tho vonous systom and lllustratos throo klnds ol artorlallzod vonous llaps (llg 24). Ho polnts out that tho clrculatlon ol blood ln vonous llaps ls basod on spoculatlon, and crodlts a numbor ol authors lor varlous oxplana- tlons. losslblo pattorns ol blood llov ln tho artorlal- lzod vonous llap rango lrom puro rotrogrado (lrom a vonous to a vonous systom), through rovorso shunt- lng (lrom vonulos to artorlolos lollovod by normal orthogrado llov), to puro shuntlng (vhoro no por- luslon ol tho llap occurs but rathor blood llovs dlroctly lrom tho alloront to tho olloront channols). Fig 24. 1hroo typos ol artorlallzod vonous llaps. (Reprinted with permission from Lee WPA: Discussion of “Arterialized venous flap for treating multiple skin defects of the hand”, by G Inoue, K Suzuki. Plast Reconstr Surg 91:303, 1993.) ¥llmaz ot al 131 doscrlbo tho lour optlons ln hook- lng up tholr radlal loroarm vonous llap. 1hoso lncludo orthogrado lnllov/orthogrado outllov, rot- rogrado lnllov/rotrogrado outllov, orthogrado lnllov/rotrogrado outllov, and rotrogrado lnllov/ orthogrado outllov. 1hoy choso tho lourth systom bocauso tho valvos aro rondorod lncompotont by tho hlgh prossuro ol tho artorlal lnllov. Moshammor ot al 132 roportod ln an oxporlmontal study that tho clrculatlon at tho porlphory ol tho artorlallzod vonous llap can bo onhancod by rotrogrado artorlallzatlon. 1ho authors proposo that tho roslstanco to llov lrom tho voln´s valvos lorcos blood lnto tho llap´s porlph- ory. lrlshnan 133 conllrmod thoso concluslons and also roportod that accordlng to tholr oxporlmontal modol, vonous llaps artorlallzod agalnst tho valvos achlovod a largor porluslon aroa than llaps por- lusod ln tho dlroctlon ol tho valvos. 1ho largost aroa ol porluslon vas soon ln bldlroctlonally por- lusod llaps. 1ho mochanlsm ol porluslon ol vonous llaps ls stlll not complotoly undorstood and has boon attrlb- utod to a numbor ol lactors such as plasmatlc lmbl- bltlon, porluslon prossuro, sltos ol artorlovonous anastomosls, porlvonous artorlal notvorks, voln-to- voln lntorconnoctlons and othor vascular notvorks, and tho clrcumvontlon ol vonous valvos. Sovoral studlos havo domonstratod lmprovod survlval ol vonous llaps vlth proartorlallzatlon and dolay pro- coduros. 68,134137 Unlortunatoly, tho survlval ol vonous llaps contlnuous to bo lnconslstont. Chavoln ot al 118 doscrlbo a rovorso shunt lrom vonulos to artorlolos lollovod by orthogrado llov lrom artorlolos to caplllarlos and thon to normal vonous channols. lmanlshl and colloaguos 138 pro- poso tho prosonco ol artorlovonous shunts around tho olloront voln ol tholr artorlallzod cophallc vonous llaps. 1hoy doscrlbo tho routo ol llov as bolng lrom voln to porlvonous notvork, to porlvonous artorlal notvork, to tho artorlal systom, and thon back to tho vonous systom and tho orlgl- nal voln. Studlos by Chov, Chon, and Cu 139 notod bottor survlval ol truo artorlal llaps than artorlallzod vonous llaps. 1ho quallty ol tho survlvlng llap lmprovod vlth lncroasod porluslon prossuro and bottor oxy- gonatod blood. Uoda ot al 140 notod lncroasod sur- vlval ol llov-through vonous llaps vhon dolayod. Uslng lnlrarod thormography, Wolll ot al 141 oxam- lnod throo typos ol vonous llaps vlth rogard to tholr porluslon and long-torm rosults. At 4 months tho survlval rato lor artorlallzod vonous llaps vas 92.7°, SRPS Volume 10, Number 1 19 lor llov-through vonous llaps, 62.4°, and lor vonous lsland llaps, about 31°. 1hoy concludod that art- orlallzod vonous llaps aro tho salost typo ol vonous llaps. 1ho cllnlcal advantagos ol vonous llaps aro mlnl- mal donor slto morbldlty roqulrlng only tho sacrlllco ol a voln and no artory, a long and vory thln, ana- tomlcally constant podlclo (og, tho saphonous voln), and last and oxpodlont llap olovatlon. 130,132,142145 1ho poorly undorstood physlology and unprodlctablo survlval ol vonous llaps makos tho cllnlcal appllca- tlon ol thoso llaps contovorslal. 1ho maln dlsadvan- tagos ol vonous llaps aro llmltod slzo ol tho llap, varlablo rato ol tlssuo nocrosls, dolayod hoallng, vonous congostlon, suscoptlblllty to lnloctlon, po- tontlal (though unllkoly) homodynamlc compllca- tlons ol a surglcally croatod AV shunt, rostrlctod locatlon ol donor sltos to maxlmlzo tho vonous ploxus, and lroquont nood lor skln gralt covorago ol donor sltos. 68,129,132,143145 Cllnlcal trlals ol pro- artorlallzatlon and dolay procoduros roport lmprovod llap survlval 68,137 vlth thoso moasuros. Nlshl and colloaguos 146 and lnouo and Suzukl 142 roport uslng artorlallzod vonous skln llaps lor tho troatmont ol skln dolocts ln tho hand. Noordholl´s group 147 appllod vonous llaps ln 28 patlonts and catogorlzod tholr oporatlons lnto lour typos. 1hoy noto tho advantagos and dlsadvantagos ol oach typo and concludo that vonous llaps aro not lntondod to roplaco moro convontlonal llaps. Chla and colloaguos 148 doscrlbo tho succosslul rotransplantatlon ol a vonous-notvork-pattorn skln llap uslng a 12 x 12 cm skln paddlo lrom tho modlal aspoct ol tho rlght thlgh translorrod to tho dlstal lovor oxtromlty. Calumbock and lrooman 144 por- lormod human anatomlcal studlos tho rosults ol vhlch suggostod that only tho vonous trlbutarlos ol tho llap rocolvo blood. 1ho authors appllod an artorlallzod saphonous voln lasclocutanoous gralt to covor tlssuo dolocts on both tho uppor and lovor oxtromltlos. Stovart and luckott 149 rovlov tho saloty ol rovorso vonous llov ln lroo llap translors, spoclll- cally tho radlal loroarm llap. loshlma ot al 143 usod tho saphonous voln and lncorporatod an ossoous componont. 1hoy voro ablo to lncroaso tho lunc- tlonal slzo ol tho llap to 7 x 11 cm lrom tho 3 x 8 cm roportod by Nakashlma. 150 ¥llmaz and colloguos 151 roportod succosslul lroo llap translor ol an artorlal- lzod vonous llap moasurlng 8 x 12 cm lrom tho loroarm to tho laco. lloln ot at 152 roportod 4 casos ol partlal llap nocrosls and 8 casos ol total llap nocrosls ln a sorlos ol 29 lroo artorlallzod lorarm llaps lor lntraoral roconstructlon. lovacs 153 comparod tvo typos ol artorlallzod loroarm llaps lor oral roconstructlon. 1ypo l vas a slnglo voln artorlallzod llov-through llap. 1ypo ll vas an artorlallzod llap vlth tvo parallol volns on tho proxlmal llap. 1ho smallor voln vas lor artorlal lnllov and tho largor lor vonous outllov, thoorotl- cally to avold bypasslng tho llap tlssuo. lour ol tho 5 typo l llaps shovod total or subtotal succoss and ono vas lost. Cl tho 5 typo ll llaps, 3 voro lost, ono vas a partlal lalluro, and tho othor ono vas a total succoss. Do Loronzl and colloaguos 145 roportod 40 casos ol dlgltal solt-tlssuo roconstructlon vlth artorlallzod vonous lroo llaps. lostoporatlvo congostlon vas prosont ln all llaps and rosolvod vlthln 14 days. 1horo vas total llap survlval ln 57.5°, 17.5° had suporllclal opldormolysls, 17.5° had lull-thlcknoss nocrosls that roqulrod graltlng, and 7.5° had total llap nocrosls. Cho ot al 68 roportod a cllnlcal sorlos ol 13 dolayod artorlallzod vonous llaps. 1ho survlvlng surlaco ol tho llap vas 100° ln 10 patlonts, 70 ° ln ono patlont, 50° ln ono patlont, and 0° (total nocrosls) ln ono patlont. Wungcharoon and othors 137 roportod tho ropalr ol oxtromlty vounds vlth a proartorlallzod vonous llap ln 8 patlonts. Artorlovonous shunts voro cro- atod at tho donor slto 2 vooks boloro llap harvost. llap survlval vas roportod to bo 93°100° ol tho surlaco aroa. Muscle and Musculocutaneous Flaps 1ho lnltlal vork doscrlblng tho prlnclplos, opora- tlvo procoduros, and cllnlcal appllcatlons ol musclo llaps vas dono by Cor 154 ln tho lato 1960s. ln 1977 Cor 155 roportod succosslul closuro ol opon vounds ln 43 casos. Musculocutanoous llaps aro compos- ltos ol skln, subcutanoous tlssuo, and undorlylng musclo and lascla suppllod by a domlnant vascular podlclo. 1anslnl 156 vas tho llrst to mako uso ol musculocutanoous llaps ln 1906 vhon ho rocon- structod a broast vlth a comblnatlon ol skln and latlsslmus dorsl musclo ralsod as ono unlt. lor tho SRPS Volume 10, Number 1 20 noxt 50 yoars no ono took notlco ol thls ovont untll Cvons 157 ln 1955 roportod tho ropalr ol masslvo laclal dolocts vlth tho stornocloldomastold llap, a compound llap lrom tho nock. 1ho ldoa that llat musclos (og, poctoralls and latls- slmus musclos) could ºcarry¨ tholr ovorlylng skln as composlto llaps camo lndopondontly to Huoston 158 and Doslroz. 159 Crtlcochoa 160,161 subsoquontly appllod thls concopt cllnlcally, uslng tho gracllls mus- culocutanoous unlt ln ponllo roconstructlon and to ropalr an anklo doloct. ln 1977 McCrav, Dlbboll, and Carravay 162,163 doscrlbod tho vascular torrltorlos ol sovoral nov musculocutanoous unlts and dollnod llap dlmon- slons and usolul arcs ol rotatlon. 1ho authors omphaslzod tho concopt ol a domlnant vascular podlclo that suppllos blood to a musclo and lts ovor- lylng skln torrltory through porloratlng vossols. Although somo dotalls ol tho goomotry, rollablllty, and appllcatlon ol spoclllc llaps voro subsoquontly lound to bo lnaccurato, tholr papors aro stlll consld- orod to bo classlcs ln tho hlstory ol roconstructlvo plastlc surgory. ln lator artlclos McCrav 164,165 tracod tho ovolutlon ol musculocutanoous llaps, cltod sourcos ol orlglnal doscrlptlons ol yot moro such llaps, and rovlovod tho baslc prlnclplos ol muscu- locutanoous llap anatomy and physlology. 1ho prlmary advantagos ol musclo llaps aro tho potontlal to ablato doad spaco vlth vascularlzod tlssuo and an lncroasod roslstanco to lnloctlon. 166 ßy moans ol radlolabolod mlcrosphoros, Cosaln ot al 167 notod a markod lncroaso ln blood llov to all lovols ol tlssuo ln both musculocutanoous and lasclocutanoous llaps altor olovatlon. ßlood llov vas also slmllar botvoon oqulvalont tlssuo layors. Musculocutanoous llaps shovod a rapld rlso ln blood llov that lovolod by 24 hours. ln contrast, lasclocutanoous llaps shovod a gradual but stoady rlso ln llov. 1ho groatost docroaso ln bactorlal concontratlon also occurrod ln tho llrst 24 hours, but vas slgnlllcantly groator ln tho musculocutan- oous vound spaco (dropplng by a lactor ol 10 4 ) than ln lasclocutanoous llaps, vhlch only docroasod by 10 2 . 1ho authors concludod that blood llov ls not alloctod by tho prosonco ol bactorla, but mus- culocutanoous llaps shovod bottor tlssuo lngrovth lnto an lnoculatod vound spaco than lasclo- cutanoous llaps. Caldoron, Chang, and Mathos 168 lound that lasclocutanoous llaps voro loss roslstant to tho olloct ol bactorlal lnoculatlon and oxhlbltod loss collagon doposltlon than musculocutanoous llaps. 1ho cllnlcal appllcatlon ol musclo to lnloctod vounds has boon succosslul ln ostoomyolltls, 155,169 postthoracotomy modlastlnltls, 170 and prosthotlc gralts. 171,172 1ho bonollts ol musclo oxtond to lroo llaps. Chon, 173 Hammond, 174 and lorklns 175 suc- cosslully troatod chronlc lntrathoraclc sopsls vlth lroo latlsslmus and 1kAM llaps contalnlng musclo, lat, and skln. 1ho prlmary dlsadvantagos ol musclo and musculocutanoous llaps aro tho lunctlonal dollclt at tho donor slto and tho bulk ol tho llap. 1ho doslgn ol a musculocutanoous llap roqulros anatomlc knovlodgo ol tho vascular archltocturo ol tho musclo and tho dlstrlbutlon ol cutanoous porlorators that vlll supply tho skln paddlo. ln 1979 Mathos and Nahal 67 dovolopod a usolul classlllcatlon ol tho blood supply to lndlvldual musclos. 1ho authors doscrlbod llvo typos ol musclo on tho basls ol tholr clrculatory pattorns (llg 25 and 1ablo 3). 1ypo l slnglo vascular podlcloog, tonsor lascla lata 1ypo ll domlnant podlclo(s) and mlnor podlclo(s)og, gracllls 1ypo lll tvo domlnant podlclosog, glutous maxlmus 1ypo lV sogmontal vascular podlclosog, sartorlus 1ypo V slnglo domlnant podlclo and socondary sogmontal podlclosog, latlsslmus dorsl Compound and Prefabricated Flaps llaps can conslst ol any numbor ol tlssuos ln vlr- tually any comblnatlon. Compound llaps aro dollnod as dlvorso tlssuo compononts that aro lncorporatod lnto an lntorrolatod unlt. 176 Composlto llaps aro a typo ol compund llap that olton lncorporato skln, lat, lascla, musclo, and bono basod on a solltary vascular podlclo, vhlch allovs slnglo-stago rocon- structlon ol complox dolocts. Spoclallzod llaps can provldo sonsory and lunctlonal musclo to aroas roqulrlng spoclal noods. 29 Craham and Dollon 177 rovlov spoclallzod llaps ln roconstructlon ol tho hand, loot, oropharynx, broast, and gonltalla. Hallock 176 proposod a usolul classlllcatlon ol com- pound llaps basod on tholr vascularlzatlon. Com- pound llaps aro dollnod as dlvorso tlssuo compo- SRPS Volume 10, Number 1 21 nonts such as bono, skln, lascla, and musclo that lncorporatod lnto an lntorrolatod unlt. Hallock s classlllcatlon placos thoso complox llaps lnto tvo groups, thoso vlth solltary vascularlzatlon and thoso vlth comblnatlons ol vascularlzatlon. 1ho com- pound llap vlth solltary vascularlzatlon ls a com- poslto llap that lncorporatos multlplo tlssuo compo- nonts dopondont on a slnglo vascular supply. Com- pound llaps ol mlxod vascularlzatlon aro lurthor subdlvldod lnto Slamoso llaps, con|olnt llaps, and soquontlal llaps (llg 26). 1ho concopt ol llap prolabrlcatlon (or, moro accuratoly, prolamlnatlon 178 ) vas lntroducod cllnl- cally by Crtlcochoa 179 and Washlo 180 ln 1971. 1ho Fig 25. llvo pattorns ol vascular anatomy ol musclo. (Reprinted with permission from Mathes SJ, Nahai F: Classification of the vascular anatomy of muscles: experimental and clinical correlation. Plast Reconstr Surg 67:177, 1981.) TABLE 3 Examples of Common Muscle Flaps by Type (Reprinted with permission from Cormack GC, Lamberty BGH: The Arterial Anatomy of Skin Flaps. Edinburgh, Churchill Livingstone, 1986.) SRPS Volume 10, Number 1 22 tochnlquo allovs lor tho croatlon ol an ºunllmltod array ol composlto lroo llaps¨ 181 that vould othor- vlso not bo avallablo vlth standard llaps. Com- blnod vlth skln oxpanslon and a dolay procoduro, prolabrlcatod llaps aro ovon moro vorsatllo. lhourl, Upton, and Shav 182 rovlov tho prlnclplos ol llap prolabrlcatlon and llst spoclllc advantagos to tholr uso, lncludlng ºvascular lnductlon¨ ol spoclllc blocks ol tlssuo vhlch aro not naturally porlusod by anatomlcally voll-dollnod axlal vossolslo, prolamlnatlon, 178 croatlon ol a largor llap than vould othorvlso bo posslblo, roducod donor slto morbld- lty, and ovaluatlon ol lunctlonal status boloro tho translor ol tho llap. 1ho authors doscrlbo ºpro- translor graltlng¨, vhlch vas usod by ßarton 183 to lncorporato skln and cartllago ln a lorohoad llap lor nasal roconstructlon. Cthors havo usod lt to croato a llap lncorporatlng a prolabrlcatod vascularlzod porlostoal gralt vlth good ostoogonlc capaclty. 184 ln tho luturo, slmplo musclo llaps may bo trans- lormod lnto moldod vascularlzod bono gralts through prolabrlcatlon. 182 ln anothor artlclo, lhourl ot al 185 addross laclal roconstructlon vlth an oxpandod prolabrlcatod llap. 1ho authors doscrlbo croatlon ol tho prolabrlcatod, lnducod, oxpandod (llL) llap uslng both a podlclod tomporoparlotal and lroo radlal loroarm lasclo- cutanoous llaps. 1ho llaps voro placod undor an oxpandor ln tho supraclavlcular roglon, vhlch sub- soquontly producod a capsulolasclocutanoous llap altor oxpanslon vas complotod. Although thls llap ls not lntondod to roplaco tho lorohoad lor spoclllc llaps ln laclal roconstructlon, lt doos provldo cor- taln advantagos vhon noodod. Homma ot al 186 concludod that oxpandod musclo- vascularlzod prolabrlcatod llaps havo largor aroas ol survlval than oxpandod lascla-vascularlzod llaps. Maltz 187 obsorvod lncroasod survlval ol dolayod pro- labrlcatod llaps, vhllo lomuro ot al 188 noto no slg- nlllcant dllloronco ln survlval ol prolabrlcatod arto- rlallzod vonous llaps comparod vlth controls. Cthor authors suggost that bocauso noovascularlzatlon ls nocossary lor a succosslul llap, a dolay ol at loast 4 vooks 189 and ovon up to 8 vooks 190 should bo obsorvod. Maltz, lrlbaz, and Horgruotor 191 noto docroasod survlval ol prolabrlcatod llaps sub|octod to mochanlcal prossuros or rostralnts (og, loldlng or klnklng) comparod vlth axlal-pattorn llaps. FLAP PHYSIOLOGY Regulation of Blood Flow to the Skin llap physlology boglns at tho lovol ol tho mlcro- clrculatlon. 1ho mlcroclrculatlon ls also vhoro thor- morogulatlon ol blood llovtho skln´s prlmary lunctlonoccurs. A numbor ol lactors contrlbuto to tho rogulatlon ol blood llov, such as dlstontlon, ondothollum-modlatod vasoconstrlctlon, noural con- trol, tomporaturo, local ln|ury, and vlscoslty. 1 Danlol and lorrlgan 62 llnd tvo klnds ol rogula- tory lactors ol cutanoous blood llov, systomlc and local. Systemic control ls lacllltatod ln ono ol tvo vays. • Neural rogulatlon acts through sympathotlc adronorglc llbors. Alpha-adronorglc rocoptors lnduco vasoconstrlctlon and bota-adronorglc rocoptors lnduco vasodllatlon. Comblnod, thoy malntaln basal tono ol vascular smooth musclo at tho artorlovonous anastomosos, artorlolos, and artorlos. Slmultanoously chollnorglc llbors lnl- tlato bradyklnln roloaso, vhlch contrlbutos to vasodllatlon. • Humoral rogulatlon causos vasoconstrlctlon through tho actlon ol oplnophrlno and noropl- nophrlno on alpha-adronorglc rocoptors ln tho cutanoous vossols. Sorotonln, thromboxano A 2 , and prostaglandln l 2 -alpha may also produco vasoconstrlctlon, vhllo bradyklnln, hlstamlno, and prostaglandln-L 1 causo dlroct vasodllatlon (llg 27). Fig 26. Compound llaps may bo subdlvldod lnto olthor solltary or comblnod typos basod on tholr sourco ol vascularlzatlon. Comblnod llaps may bo Slamoso, con|olnt, or soquontlal. (Re- printed with permission from Hallock GG: Simplified nomencla- ture for compound flaps. Plast Reconstr Surg 105:1465, 2000.) SRPS Volume 10, Number 1 23 1ho ollocts ol local ln|ury to a part ol tho artorlal vall can complotoly ovorrldo basal vascular tono and causo spasm ovon ln tho absonco ol sympa- thotlc lnnorvatlon. 1 lor lnstanco, a pln prlck ollclts a porslstont lsolatod rlng contractlon locally, and oxtonslvo crushlng or toarlng can lnduco a vldo- sproad and prolongod spasm dlstantly (llg 28). Fig 28. ßlochomlcal agonts alloctlng tho clrculatlon. (Reprinted with permission from Cormack GC, Lamberty BGH: The Arterial Anatomy of Skin Flaps, 2nd ed. Edinburgh, Churchill Livingstone, 1994.) Local ollocts (autorogulatlon) aro modlatod by motabollc and physlcal lactors. • Metabolic lactors act prlmarlly as vasodllators and lncludo hyporcapnoa, hypoxla, acldosls, and hyporkalomla. 1hoso lactors aro not as slgnlll- cant ln tho skln as ln musclo, vhlch has hlghor motabollc roqulromonts. • Physical lactors that lnlluonco blood llov lncludo tho myogenic reflex, vhlch trlggors vasoconstrlc- tlon ln rosponso to dlstontlon ol lsolatod cutano- ous vossols and thoroby malntalns caplllary llov at a constant lovol lndopondont ol artorlal pros- suro. Local hypothormla (vhlch acts dlroctly on tho smooth musclo ln vossol valls) and lncroasod blood vlscoslty (homatocrlt >45°) may also docroaso llov. 1ho ollocts ol homatocrlt voro quostlonod by llm ot al, 192 vho concludod that normovolomlc anomla (hct 19°) had no slgnlll- cant olloct on tho survlval ol podlclod musculo- cutanoous llaps. 1hoso samo concopts ol blood llov rogulatlon can bo appllod to musclos. Wlth rogard to systomlc control, although musclo has a much hlghor capll- lary donslty than skln, artorlovonous shunts aro absont. And bocauso tho motabollc domand ol musclo ls groator than that ol tho skln, autorogula- tlon plays a moro lmportant rolo. Nouronal controls such as oxorclso and artorlal hypotonslon lnduco a rolloxlvo vasoconstrlctlon, vhllo hyportonslon rosults ln vasodllatlon. Humoral rogulatlon ls slmllar oxcopt that oplnophorlno causos vasodllatlon, ln dlroct con- trast to tho vasoconstrlctlon soon ln skln. ln tho schomo ol local control, motabollc autorogulatlon ls llmltod ln musclo but doos oxcood that ol skln, and blood llov ls mlnlmally changod ln rosponso to tom- poraturo lluctuatlons. ßurnstock and kalovlc 193 rovlov nov lnslghts lnto tho local rogulatlon ol blood llov. 1ho authors dlscuss tho concopt ol co-transmlsslon, vhoroby norvos synthoslzo, storo, and roloaso moro than ono transmlttor, and tho lmportanco ol tho ondo- thollum as a modlator ol vasodllatlon and constrlc- tlon. ln summary, tho mochanlsms ol blood llov rogu- latlon aro dllloront ln skln and musclo. Myogonlc tono ls lmportant ln musclo rogulatlon but has llttlo olloct on cutanoous vossols, vhoroas sympathotlc vasoconstrlctors aro tho prodomlnant moans ol rogu- latlng blood llov to tho skln. Flap Transfer 1ho olovatlon ol a skln llap rosults ln many pro- lound changos that drastlcally dlsrupt tho llnoly bal- Fig 27. lhyslologlc lactors that rogulato tho cutanoous mlcroclr- culatlon. (Reprinted with permission from Daniel RK, Kerrigan CL: Principles and physiology of skin flap surgery. In: McCarthy JG (ed), Plastic Surgery. Philadelphia, Saunders, 1990. Vol 1, Ch 9.) SRPS Volume 10, Number 1 24 ancod oqulllbrlum ol homoostasls. lrlmary changos lncludo tho loss ol sympathotlc lnnorvatlon and tho lnsult ol lschomla. Hoopos 194 glvos a dotallod account ol tho clrcu- latory ovonts that tako placo ln a podlclod llap altor lts blood supply ls partlally lntorruptod durlng ol- ovatlon and translor. 0–24 hrs. roductlon ln artorlal blood supply, pro- grosslvoly docroaslng clrculatory olllcloncy lor tho llrst 6 hours, platoau at 612 hours, lncroaso ln clrculatory olllcloncy boglnnlng at 12 hours, markod congostlon and odoma durlng tho lnltlal 24 hours, markod dllatatlon ol artorlolos and caplllarlos 1–3 days. lncroaslng lsotopo appoaranco, lmprovo- mont ln pulso amplltudo, llttlo or no lmprovomont ln clrculatlon durlng tho lnltlal 48 hours, lncroaso ln numbor and callbor ol longltudlnal anastomosos, lncroaso ln tho numbor ol small vossols ln tho podlclo 3–7 days. progrosslvo lncroaso ln clrculatory olll- cloncy untll lt roachos a platoau at about day 7, vascular anastomosos botvoon llap and roclplont bod prosont at 23 days, bocomo lunctlonally slg- nlllcant at 5 to 7 days, lncroaso ln slzo and numbor ol lunctlonlng vossols, roorlontatlon ol vossols along tho long axls ol tho llap 1 week. clrculatory lunctlon voll ostabllshod bo- tvoon llap and roclplont bod, pulsatllo blood llov approachos prooporatlvo lovols 7–14 days. no lurthor slgnlllcant lncroaso ln vas- cularlzatlon, artorlal pattorn bocomos normal, ra- dlolsotopo cloaranco lndlcatos clrculatory olllcloncy surpasslng normal valuos at 1021 days, roturnlng to normal altor 3 vooks 2 weeks. progrosslvo rogrosslon ol tho vascular systom, contlnuous maturatlon ol anastomosos bo- tvoon podlclod llap and roclplont slto 3 weeks. vascular pattorn approxlmatos proopora- tlvo stato, llap achlovos 90° ol lts llnal clrculatlon, vltal stalnlng occurs slmultanoously vlth roclplont llmb, lully dovolopod vascular connoctlons botvoon podlclo and roclplont slto 4 weeks. all vossols docroasod ln dlamotor, lov romalnlng novly lormod vossols Most lnvostlgators ondorso tho concopt ol venous insufficiency as tho prlmary causo ol nocrosls ln podlclod llap tlssuo. 194 As oarly as 1967, lu|lno 195 concludod that roductlon ln vonous outllov prob- ably rosults ln llap nocrosls dosplto tho prosonco ol adoquato artorlal lnllov. 1suzukl and colloaguos 196 lound that mlld vonous lnadoquacy dld not alloct survlval ol an oxporlmontal llap vhon tho artorlal lnllov vas malntalnod, but onco artorlal lnllov vas lmpalrod, ovon mlld vonous lnadoquacy roducod llap survlval. Angol and covorkors 197 studlod socondary ls- chomla tlmo ln a rodont modol, and notod that vonous obstructlon vas moro dolotorlous to llap survlval than socondary lschomla lrom comploto podlclo obstructlon. ln contrast, lorrlgan lound inadequate arterial inflow vas tho prlmary causo ol llap lalluro, 198 and proposod a comblnatlon ol ls- chomla, lnllammatlon, and sympathoctomy to ox- plaln tho vascular collapso that undorllos tho lalllng skln llap. 199 lurthormoro, damago to tho llap bo- comos lrrovorslblo ll adoquato nutrlont clrculatlon ls not provldod May 200 studlod clrculatory changos ln lroo opl- gastrlc llaps ln rabblts. 1hoy notod conslstont odoma and svolllng ol tho vascular paronchymal colls vhon lroo llaps voro sub|octod to a porlod ol lschomla. 1horo vas concomltant narrovlng ol tho caplllary lumon and trapplng ol lorolgn blood olomonts as voll as sludgo or thrombus lormatlon ln tho stag- nant blood vlthln tho vascular troo ol tho lschomlc tlssuo. All llaps survlvod up to 4 hours ol lschomla. ßotvoon 4 and 8 hours ol lschomla, tho typlcal homodynamlc and collular ovonts occurrlng ln llaps as a rosponso to lschomla voro rovorslblo. As tho porlod ol lschomla longthonod, tho clrculatory al- toratlons gradually vorsonod and vascular obstruc- tlon progrossod untll thoy bocamo lrrovorslblo, thls occurs altor 12 hours. 1ho polnt at vhlch lt ls not posslblo to roostabllsh nutrlont lnllov dosplto roporluslon ls knovn as tho no-reflow phonom- onon . 1ho no-rollov phonomonon ls tho rosult ol lschomla-lnducod roporluslon ln|ury and procodos llap doath. 1ho motabollc ollocts ol lschomla durlng llap olovatlon aro many. Wlth lnadoquato tlssuo oxy- gonatlon thoro ls a chango lrom aoroblc to anaoro- blc motabollsm, rosultlng ln hlghor lovols ol supor- oxldo radlcals. Clucoso consumptlon and lactato productlon both lncroaso, vlth concomltant doplo- SRPS Volume 10, Number 1 25 tlon ol glycogon. 1ho motabollc dorangomonts ol tlssuo lschomla also alloct physlcal proportlos ol blood such as vlscoslty and clottlng. Dlroct cyto- toxlc ln|ury rosults lrom tho accumulatlon ol oxy- gon-dorlvod lroo radlcals durlng llap lschomla. lm ot al 201 ln 1985 and lator Manson and col- loaguos 202,203 notod lncroasod productlon ol toxlc suporoxldo radlcals durlng anaoroblc motabollsm. 1ho authors suggostod a rolo lor oxygon-dorlvod lroo radlcals (CDlk) as modlators ol tlssuo nocrosls ln tho lschomlc transltlon zono botvoon tho proxl- mal, vlablo portlon ol a skln llap and lts dlstal, non- vlablo sogmont. Wlth ronovod llov comos an abun- dant supply ol calclum lons and a roloaso ol oxygon lroo radlcal spoclostho so-callod rosplratory burst. lroo radlcals aro not only dlroctly cytotoxlc but also trlggor tho synthosls ol numorous prolnllammatory llpld modlators (og, lAl and L1ß 4 ) as voll as pop- tldo modlators (og, C5a, 1Nl-α, and lL-1ß). 204 Altor roporluslon, tho lroo radlcals aro attackod by lroo radlcal scavongors, causlng lurthor ln|ury to tho colls. 1hls phonomonon has como to bo knovn as ischemia-induced reperfusion injury (llkl). 1ho tran- sltlon lrom normal roporluslon and roporluslon ln|ury dlllors accordlng to tlssuo typo. 205 Skln and bono can usually tolorato lschomla lor up to 3 hours but musclo and lntostlnal mucosa aro much loss tolor- ant. lorrlgan and Stotland 206 rovlov tho cllnlcal slg- nlllcanco, otlology, pathophyslology, rosoarch lnvostlgatlons, and curront managomont ol lschomla and llkl. ßlochomlcal changos occurrlng durlng lschomla ºactually prlmo tho tlssuo to rospond ln a pathologlcal lashlon upon oxposuro to ro-ostabllshod vascular supply.¨ 1ho authors dlscuss tho xanthine oxidase and NADPH oxidase systoms, vlth tholr productlon ol tho toxlc radlcals suporoxldo anlon (C 2 ), hydrogon poroxldo (H 2 C 2 ), and tho hydroxyl radlcal (CH). 1hoso roactlvo oxygon lntormodlatos load to a varloty ol mlcrovascular and lnllammatory dorangomonts such as ondothollal coll svolllng and lncroasod caplllary pormoablllty. Loukotrlonos (L1ß 4 ), thromboxanos (A 2 ), and prostaglandlns play a ma|or rolo ln thoso procossos. ln addltlon, nou- trophlls contrlbuto to tho acuto lmllammatory ln|ury ol roporluslon through tholr adhoslon, omlgratlon, and protoolytlc onzymo dogradatlon. Carroll and Lsclamado 205 rovlovod llap physlol- ogy, lschomla/roporluslon ln|ury, and tho uso ol pharmacothorapoutlc agonts ln mlcrovascular sur- gory. FLAP DELAY Dolay ls tho surglcal lntorruptlon ol a portlon ol tho blood supply to a llap at a prollmlnary stago boloro translor. 1ho purposo ol dolay ls to lncroaso tho survlvlng longth ol a llap or to lmprovo tho clrculatlon ol a llap to dlmlnlsh tho lnsult ol translor. Dosplto advancos ln our undorstandlng ol llap physl- ology tho oxact mochanlsm ol dolay ls lncomplotoly dollnod. 1vo schools ol thought oxlst rogardlng tho mocha- nlsm ol tho dolay phonomonon. Cno thoory holds that delay conditions tissue to ischemia, allovlng lt to survlvo on loss nutrlont blood llov than normally noodod. Cthors bollovo that delay improves or increases vascularity. 1ho procoss by vhlch dolay contrlbutos to llap survlval ls llkoly to bo a comblna- tlon ol both mochanlsms actlng to a groator or lossor oxtont at varlous tlmos durlng surglcal dolay ol a llap. Dollnltlvo lnvostlgatlons lnto llap rosponso to docroasod blood supply havo boon hamporod by lnconslstont rosults obtalnod ln dllloront laboratory modols and lack ol adoquato controls to ostabllsh truo lncroaso ln survlvlng longth lollovlng dolay procoduros. Hoopos 194 llsts tho lollovlng llvo mochanlsms ol dolay. • sympathoctomy • vascular roorganlzatlon • roactlvo hyporomla • accllmatlzatlon to hypoxla • nonspoclllc lnllammatory roactlon A numbor ol anatomlc and physlologlc lnvostlga- tlons lnto tho dolay ol llaps bogan durlng tho 1950s. ßralthvalto 207,208 proposod that tho llkoly mocha- nlsm ol dolay conslsts ol vascular roorganlzatlon and roactlvo hyporomla actlng through nonlothal lschomla to condltlon tho tlssuo to survlvo on loss blood llov, togothor vlth an lncroaso ln slzo ol tho vossols ln tho dormovonous ploxus. Ho postulatod that tho hyporomla obsorvod vhon a tubod podlclo ls translorrod arlsos lrom a vascular dobt as a rosult ol lncroasod roslstanco to vonous outllov. ßrovn and McDovoll 209 statod that tho purposo ol dolay ls SRPS Volume 10, Number 1 26 to pormlt gradual hyportrophy ol tho blood vossols ln tho podlclo and posslbly to accustom tho tlssuos ln tho llap to a lovor oxygon tonslon or poor clrcu- latlon. 1ho accllmatlzatlon to hypoxla lormod tho basls lor Danlol and lorrlgan´s 29 bollol that dolayod llaps havo adoquato blood llov to survlvo tho oarly stago ol vasoconstrlctlon vhoroas acuto llaps do not. Hynos 210 usod a varlatlon ol tho svoat tost to dotoct tho prosonco or absonco ol sympathotlc ac- tlvlty ln tubod podlclos. ln hls study, sympathoc- tomy vas tho mochanlsm ol dolay, and lts olloct vas to onhanco vascularlty. }uroll 211 analyzod lov- ols ol noroplnophrlno, A1l, and cycllc-AMl ln do- layod and nondolayod skln llaps to |udgo tho ollocts ol sympathotlc donorvatlon on tho dolay phonom- onon. Noroplnophrlno causos vasoconstrlctlon and motabollc stlmulatlon. Whon llaps aro dolayod, blood vossols and adronorglc norvos aro sovorod, causlng a spontanoous dlschargo ol nourotransmlt- tors, so that by tho tlmo ol llap lnsot thoro ls llttlo roloaso ol noroplnophrlno and consoquont dlml- nutlon ln vasoconstrlctlon ol tho llap. 1ho author conllrmod slgnlllcantly lovor lovols ol noroplnoph- rlno ln llaps at tho socond oporatlon. Soltchlk and lahn 27 rovlovod tho hlstologlc al- toratlons assoclatod vlth dolay and conllrmod tho llndlngs ol Cormann and assoclatos 212 lrom 1933. 1holr obsorvatlons can bo summarlzod as lollovs. • longltudlnal roorlontatlon ol small vossols paral- lol vlth tho long axls ol tubod podlclos at 1 to 7 days postdolay • lncroaso ln slzo ol vossols • lncroaso ln numbor ol small artorlos ln tho sub- dormal ploxus lang and colloaguos 213 monltorod skln caplllary blood llov and anglogonosls ln dolayod and nondolayod random skln llaps ln tho plg. Caplllary blood llov vas slgnlllcantly hlghor ln tho dolayod skln llaps and camo lrom tho podlclo only, not as noovascularlzatlon lrom tho vound bod or margln. 1ho lncroaso ln llov vas dotoctablo vlthln 2 days ol surglcal dolay, lncroasod 100° by day 4, and romalnod at thls platoau untll day 14. 1horo vas, hovovor, no slgnlllcant lncroaso ln tho donslty ol artorlos botvoon acuto and dolayod skln llaps. 1ho authors concludo that tho dolay phonomonon ls not dopondont on anglogonosls but probably modlatod through locally roloasod nourohumoral substancos. Hovovor, as roportod llrst by Soralln 214 and lator by Carcla, 215 both an lncroaso ln tho numbor and slzo and an lngrovth ol nov vossols lrom tho surround- lng tlssuo occurrod about 4 to 5 days postopora- tlvoly. }onsson and colloaguos 216 notod that surglcal do- lay lmprovod dollvory ol oxygon to tho llap. Altor dolay, blood vossols voro soon to roorganlzo paral- lol to tho lnclslon llno and blood llov vas lncroasod llrst by vasodllatlon and socondly by anglogonosls untll about day 14. koroutlng ol blood llov by ln|ury, lnllammatlon, and anglogonosls causod by tho ropalr sooms to account lor a slgnlllcant portlon ol tho dolay phonomonon. Cthors 217,218 conllrm thoso llndlngs and suggost that an lschomlc tlssuo gradlont provldos tho lmpotus lor anglogonosls and loads to groator vlablllty ol dolayod llaps. 1ho anglogonlc procoss ln acuto and dolayod llaps vas lnvostlgatod by Lopoz ot al 219 by moans ol lmmunohlstochomlcal mothods vlth monoclonal antlbodlos to ovaluato vascular ondothollum. Do- layod llaps oxhlblt an lncroaso ln caplllarlos lrom 48 hours, and thls contlnuos untll 7 days altor llap ol- ovatlon. 1holr thoory ol dolay holds that hypoxla accounts lor vasodllatlon and roloaso ol nourohu- moral substancos. Macrophagos subsoquontly ml- grato to tho skln and roloaso anglogonlc lactors that, along vlth othor lactors by platolots, damagod on- dothollum, and tho olastlc layor ol vossols, trlggor caplllary prollloratlon at tho socond surglcal stago. 1ho porlod ol dolay ollorlng maxlmum survlval ls about 1 vook, vhoroas tho mlnlmum olloctlvo tlmo ls 2 to 3 days. Callogarl and colloaguos 220 subsoquontly con- ductod a numbor ol oxporlmonts to dollno tho ana- tomlc changos ln llaps altor surglcal dolay. 1ho authors roachod tho lollovlng concluslons. • tho survlval longth ol llaps ls rolatod to tho dls- tanco botvoon porlorators • tho nocrosls llno ol a llap usually appoars ln tho zono ol choko vossols connoctlng ad|acont tor- rltorlos • a surglcal dolay rosults ln dllatatlon ol oxlstlng vossols vlth maxlmal olloct ln tho zono ol choko artorlos • tho most olloctlvo dolay ls obtalnod by olovatlng tho llap ln stagos lrom tho baso and not dotach- lng tho tlp untll last SRPS Volume 10, Number 1 27 • tlssuo oxpanslon ls a lorm ol surglcal dolay, par- tlcularly ln torms ol vossol hyportrophy • slmllar changos occur vhon a musclo ls dolayod. (Appllcatlon ol tho dolay phonomonon ln musclo ls lurthor dlscussod by ßarkor ot al. 221 ) Dhar and 1aylor 222 lnvostlgatod tho soquonco ol anatomlc changos vlth dolay ln a dog musclo and rabblt skln modol to support tholr provlous conclu- slon that llap dolay rosults ln dllatlon ol oxlstlng vossols, not lngrovth ol nov vossols. 1ho authors concludod that tho anatomlc olloct ol dolay ls locusod on tho choko anastomotlc vossols that llnk ad|acont torrltorlos and that tho tlmo soquonco ol dolay ls slmllar ln dllloront tlssuo typos and ln dll- loront spoclos. 1holr dolay soquonco ls dlvldod lnto lour phasos (llg 29). Fig 29. 1ho dolay soquoncosummary ol rosults. (Reprinted with permission from Dhar SC, Taylor GI: The delay phenomenon: the story unfolds. Plast Reconstr Surg 104:2079, 1999.) Phase 1. lnltlal spasm ol all llap vossols vhlch lasts up to 3 hours and ls lollovod by gradual dllatlon ol vossol up to 24 hours. Phase 2. ßotvoon 24 and 72 hours, an accoloratod lncroaso ln tho callbor ol llap artorlos, prlmarlly at tho choko vossol lovol. Phase 3. lrom 72 hours to 7 days, lurthor gradual dllatlon ol vossol lumon assoclatod vlth vossol vall thlckonlng. Phase 4. lrom 7 days on, tho choko vossols romaln pormanontly and lrrovorslbly dllatod. klbullo and colloaguos 223 soloctlvoly dolayod tho doop and suporllclal lnlorlor oplgastrlc artorlos dur- lng 1kAM llap roconstructlons. 1ho authors lound slgnlllcantly lncroasod callbor ol tho suporlor opl- gastrlc artory and docroasod artorlal roslstanco lol- lovlng dolay ol olthor vossol. kostllo ot al 224 com- parod tho dlamotor and llov ol tho suporlor oplgas- trlc artory altor a dolay porlod ol 1 or 2 vooks. 1ho dolay procoduro conslstod ol dlvlslon ol tho supor- llclal and doop lnlorlor oplgastrlc vossols bllatorally. 1ho authors dld not llnd a statlstlcally slgnlllcant dllloronco botvoon dolay altor 1 vook vorsus 2 vooks. ln vlov ol tho conlllctlng ovldonco rogardlng tho anatomy and physlology ol dolay, tho only unquos- tlonablo lact sooms to bo that ºsurglcal dolay rosults ln hyportrophy and roorganlzatlon ol vossols along tho axls ol a llap¨ 220 and somohov lmprovos llap survlval. Curront thoorlos attompt to oxplaln tho dolay phonomonon as • a dramatlc altoratlon ol blood llov socondary to closuro ol AV shunts, transoctlon ol sympathotlc norvos, and hyporsonsltlvlty to catocholamlnos, • a condltlonlng ol tlssuo to lschomla, or • an lmprovomont ln vascularlty and blood llov brought about through vasodllatlon, anglogon- osls, or both. Timing of Flap Division Much ol tho oxporlmontal and cllnlcal data rogardlng approprlato tlmlng ol llap dlvlslon ls basod on obsorvatlons ol tubod podlclo llaps, at loast somo ol vhlch may not havo roqulrod an lnltlal dolay procoduro. Corman and assoclatos 212 concludod that clrculatlon ln llaps vas roostabllshod consldor- ably oarllor than provlously thought. 1hoy bogan dlvldlng tholr llaps at 14 days posttranslor, and sub- soquontly shortonod tho lntorval to 10 days vlthout dolotorlous ollocts on llap survlval. Stark, Hong, and lutroll 225 studlod tho rolo ol lschomla lrom lov porluslon as tho trlggor ol noovascularlzatlon ln a rat modol. 1hoy lound that noovascularlzatlon vas onhancod by a porluslon gradlont across tho vound marglns. loorly por- lusod tlssuo brought lnto a hoalthy roclplont bod onhancod noovascularlzatlon, oxcoodlng tho nood ol tho lschomlc tlssuo ltsoll to oncompass tho vholo ad|acont llap. 1ho authors concludo that thls ls oxporlmontal ovldonco lor tho bonollclal olloct ol dolayod dlvlslon ol a dlstant llap. 1o summarlzo tho avallablo data, 194,214,226229 although llaps can bo dlvldod as oarly as tho thlrd SRPS Volume 10, Number 1 28 day ln anlmal modols, cllnlcally dolay should bo longthonod to sult spoclllc anatomy, oxpoctod llap vlablllty, and charactorlstlcs ol tho roclplont slto. Accordlng to Hausor ot al, 230 tho tradltlonal 3 vooks lor dlvlslon ol an lnsot llap ls probably accoptablo ln 85° ol patlonts, but ls promaturo ln somo and oxcosslvoly long ln most. 1ho cumulatlvo oxporl- onco ol many surgoons suggosts that most llaps can bo dlvldod saloly at 10 days to 3 vooks. FLAP SURVIVAL Physical Factors 1ho physlcal onvlronmont ol a llap can bo manlpulatod to try to lmprovo llap survlval. Sasakl and colloaguos 231 koop tho llap odgos moist and roport an lncroaso ln tho survlvlng portlon ol llaps. McCrath 232 statos that a molst onvlronmont dlmln- lshos tho dopth ol tlssuo loss and lncroasos llap sur- vlval, prosumably by mlnlmlzlng doslccatlon ol lschomlc tlssuo. Avvad ot al 233 ostabllshod a dlroct rolatlonshlp botvoon local temperature and blood llov ln lsland and lroo llaps. Hypothormla lod to vasoconstrlctlon and lncroasod blood vlscoslty, vlth rosultant docroaso ln skln blood llov, varmlng ol tho llap had tho opposlto olloct. Whon llaps voro coolod to 20C, Hussl and colloaguos 234 lound a roductlon ln blood llov to 65° ol basollno and ln oxygon consumptlon to 25° ol basollno. At 14C, blood llov coasod complotoly, probably as a rosult ol lncroasod plasma vlscoslty. Mounsoy, lang, and lorost 235 oxploro tho con- copt ol preconditioning, ln vhlch tho protoctlon lrom lschomlc damago lnducod ln cardlac musclo by brlol porlods ol coronary artory occluslon ls trans- latod to skolotal musclo. 1o onhanco musclo llap survlval and sustaln normothormlc lschomla, tho musclo llap ls sub|octod to lntormlttont porlods ol global lschomla lollovod by roporluslon. Mounsoy notod a 20° lncroaso ln llap survlval at 30-mlnuto lntorvals. lrocondltlonlng as a moans to onhanco llap sur- vlval has boon trlod on both skln and podlclod mus- culocutanoous llaps. 236 Musculocutanoous llaps larod slgnlllcantly bottor altor procondltlonlng, but not so skln llaps, and both llap typos shovod lmprovod survlval vhon usod as lroo llaps. 1ho mochanlsm ol actlon ln procondltlonlng ls unknovn. lroposod thoorlos lncludo altoratlons ln blood llov, docroasod tlssuo motabollsm, soloctlvo loss ol cortaln nonos- sontlal collular lunctlons, docroasod lovols ol oxy- gon-dorlvod-lroo radlcals, and tho roloaso ol ondothollum-dorlvod rolaxlng lactors, vhlch may causo vasodllatlon and lmprovod dlstal blood llov. 235,237 1an and othors 238 and kamon ot al 239 roport lncroasod survlval ln rat abdomlnal llaps troatod vlth hyporbarlc alr (21° C 2 ) and hyporbarlc 100° C 2 , but not hyporbarlc 8° C 2 . Nomlroll and col- loaguos 240 also shovod a bonollclal olloct ol hyper- baric oxygen (HßC) on acuto skln llaps, and notod that, to bo holplul, HßC must bo glvon as soon as posslblo altor surgory. 1hoso llndlngs aro slmllar to thoso ol Çulrlnla and Vlldlk 241 and Lsclamado ot al, 242 vho llnd that HßC thorapy doos lmprovo skln llap vlablllty. laolln ot al 243 lound that prolongod prooporatlvo and postoporatlvo hyporbarlc oxygon troatmont lmprovod survlval ln a rat skln llap modol. 1ho bonollclal olloct ol HßC thorapy vas thought to bo duo to lncroasod suporoxldo dlsmutaso actlv- lty. Not all lnvostlgators havo had posltlvo rosults vlth hyporbarlc oxygon. Stovart and assoclatos 244 ovalu- atod tho ollocts ol HßC vlth and vlthout lroo- radlcal scavongors, and notod no slgnlllcant lncroaso ln llap survlval vlth HßC unloss lt vas comblnod vlth olthor alpha-tocopherol or suporoxldo dlsmutaso and catalaso (CA1). Alpha-tocophorol ls ono ol lour tocophorols maklng up vltamln L, vhoso actlon ls to tormlnato lroo-radlcal roactlons by com- potlng lor poroxyradlcals, ospoclally at coll mom- brano surlacos. Catalaso ls an H 2 C 2 scavongor. Pharmacologic lang, lorrost, and Morrls 245 prosont a conclso ovorvlov ol tho pathophyslology ol skln llap nocro- sls and tho pharmacologlc manlpulatlon ol skln llaps to provont or rovorso thls procoss. Carroll and Lsclamado 205 rovlov tho uso ol pharmacothorapou- tlc agonts ln mlcrovascular surgory (1ablo 4). A numbor ol oxporlmontal studlos havo lookod lnto drugs to lncroaso llap survlval. As lorrlgan 29 polnts out, many ol thoso studlos contradlct ono anothor, aro porlormod by only ono rosoarchor on a numbor ol dllloront oxporlmontal modols, and olton uso an lnadoquato cohort that procludos sta- tlstlcal valldatlon ol tho rosults. 1hls soctlon vlll SRPS Volume 10, Number 1 29 locus only on thoso pharmacologlc agonts that aro commonly usod ln cllnlcal practlco. Anticoagulants Dextran, orlglnally doslgnod as a volumo oxpandor, has boon a tool ol tho mlcrovascular surgoon lor many yoars. kothkopl ot al 246 clto a rovlov ol tho ollocts ol doxtran, vhlch lncludo docroaso ln platolot adhoslvonoss and procoagulant actlvlty, lncroasod bloodlng tlmo, lnhlbltlon ol plato- lot aggrogatlon, and docroaso ln blood vlscoslty. Wlth doxtran 40 as a porlusato, tho patoncy ol arto- rlal lnvorslon gralts (slmllar to thoso ol Wollort´s 247 ) almost doublod ovor that ol controls. Worklng on a vonous modol, Zhang and Wloslandor 248 obsorvod lncroasod mlcroclrculatory patoncy vhon uslng doxtran 70. 1ho mlcro- porluslon vas lurthor onhancod vhon lov- molocular-volght hoparln vas addod. Lator Salomark, lnudson, and Dougan 249 notod lncroasod patoncy ol mlcroclrculatlon vlth doxtran 40, but only on a short term basis. Altor 1 vook ol uso, Doxtran 40 shovod llttlo olloct rogardloss ol modol. Dlsa ot al 250 conductod a prospoctlvo random- lzod analysls ol tho morbldlty assoclatod vlth doxt- ran and asplrln prophylaxls ln hoad and nock mlcrosurgory patlonts. 1ho lncldonco ol systom compllcatlons lor patlonts rocolvlng lov molocular volght doxtran lor 120 hours vas 51°, lor 48 hours, lt vas 29°, and lor asplrln, 7°. 1ho authors havo dlscontlnuod tho uso ol doxtran ln tholr patlonts. Doxtran ls assoclatod vlth slgnlllcant systomlc morbldlty lncludlng anaphylaxls, pulmonary odoma, cardlac compllcatlons, adult rosplratory dlstross syn- dromo, and ronal lalluro. 1ho routlno uso ol doxt- ran ln lroo tlssuo translor ls nov dlscouragod. 251,252 Heparin ls an olloctlvo antlcogulant that acts ln con|unctlon vlth antlthrombln lll to lnhlblt throm- bosls by lnactlvatlon lactor \. Hoparln ls moro olloctlvo at provontlng vonous thrombosls than artorlal thrombosls. Savada, Hatayama, and Sono 253 roport lmprovod llap survlval vhon hoparln vas contlnuously and toplcally admlnlstorod to spoclllc roglons ol tholr llaps. 1hoy attrlbutod tho bonoll- clal olloct to platolot dlsaggrogatlon and malnto- nanco ol vascular patoncy by hoparln, not to vasodllatatlon and lncroasod vascular llov. 1hoso llndlngs corrospond vlth thoso ol tho Cox group, 254 vho notod a doso-rolatod lncroaso ln llap patoncy vlth hoparln. 1ho olloct vas llrst notod at hoparln concontratlons ol 100 U/mL, a doso tho rosoarch- ors llnd to bo ldoal lrom a morbldlty standpolnt. lnvostlgators lrom Duko Unlvorslty Modlcal Con- tor 255 roport that both unlractlonatod and lov molocular volght hoparln (LMWH) lmprovod mlcroclrculatory porluslon, but only LMWH lmprovod anastomotlc patoncy vhllo mlnlmlzlng homorrhago. lroll ot al 256 rotrospoctlvoly rovlovod 517 lroo llaps and notod a lovor lncldonco ol llap loss vhon hoparln vas admlnlstorod (olthor as bolus or ln lov doso), but thls dllloronco vas not statlstl- cally slgnlllcant. Hudson ot al 257 roportod tho oxporlmontal and cllnlcal uso ol a cathotor placod proxlmal to tho vonous anastomosls lor tho dlroct lnluslon ol hoparln to provont voous thrombosls. 1ho local partlal thromboplastln tlmo vas olovatod but tho systomlc valuo ramlnod normal, thoroloro roduclng tho systomlc compllcatlons ol hoparln. Thrombolytic agents act by tho stlmulatlon ol plasmlnogon vhlch ls tho procursor ol plasmln vhlch acts to cloavo llbrln vlthln a thrombus. Strop- toklnaso and uroklnaso aro llrst-gonoratlon agonts and tlssuo plasmlnogon actlvator (t-lA) and acylatod TABLE 4 Classification of Common Pharmacotherapeutic Agents Used in Microvascular Surgery (Reprinted with permission from Carroll WR, Esclamado RM: Ischemia/reperfusion injury in microvascular surgery. Head Neck 22:700, 2000.) SRPS Volume 10, Number 1 30 plasmlnogon-stroptoklnaso actlvator complox (AlSAC) aro socond-gonoratlon agonts. 1hrombo- lytlcs havo boon olloctlvo ln anlmal modols lor tho salvago ol llaps altor mlcrovascular thrombosls. 258 Stroptoklnaso ls a nononzymatlc protoln dorlvod lrom group C bota-homolytlc stroptococcl. ln llap salvago lt ls ln|octod lnto tho artorlal sldo ol tho llap and dralnod through tho vonous sldo, usually avold- lng systomlc ollocts. Dosos ol 50,000 to 125,000 unlts havo boon usod cllnlcally. 205 ¥ll ot al 259 roportod 6 lroo llaps that voro sal- vagod and 2 that lallod altor tho cllnlcal uso ol thrombolytlcs (uroklnaso and t-lA) lor podlclo throm- bosls. Sorlottl ot al 260 roportod 5 casos ol vonous thrombosls that voro salvagod by rovlslon ol tho vonous anastomosls lollovod by lntraoporatlvo lnluslon ol 250,000 unlts ol uroklnaso. Leeches havo boon usod ln modlclno slnco anclont tlmos lor tho troatmont ol varlous all- monts. 261 kocontly thoro has boon ronovod lntor- ost ln modlclnal loochos, Hirudo medicinalis, lor tho rollol ol vonous congostlon altor lroo tlssuo trans- lors and roplantatlons. 262,263 Loochos oxort tholr olloct by ln|octlng hlrudln at tho slto ol blto. Hlru- dln ls a naturally occurrlng antlcoagulant that lnhlb- lts tho convorslon ol llbrln to llbrlnogon and that, unllko hoparln, doos not roqulro antlthrombln-lll lor actlvatlon. ln addltlon, loochos socroto hyalu- ronldaso, vhlch lacllltatos sproad ol tho antlcoagu- lant vlthln tho tlssuos, and a vasodllator, vhlch con- trlbutos to prolongod bloodlng (up to 48 hrs). 261,264,265 Moroovor, loochos havo a mochanlcal actlon by croatlng physlcal channols through vhlch vonous dralnago can occur. Novortholoss, accordlng to kodgors ot al, 264 ºno controllod study has provon tho olllcacy ol loochlng.¨ 1ho maln lndlcatlon lor tho uso ol loochos ls ln casos ol vonous congostlon vhoro outllov ls lnsul- llclont or vonous channols aro olthor absont or unsultablo lor anastomosls. 1ho prlmary contraln- dlcatlon to loochos ls artorlal lnsulllcloncy, ln vhlch caso tho loochos vlll slmply not attach thomsolvos to tho llap. Looch thorapy ls not vlthout potontlal compllca- tlons. 1ho most slgnlllcant rlsks aro bactorlal lnloc- tlon lrom tho gram-nogatlvo rod Aeromonas hydrophila (vhlch ls tho looch ontorlc organlsm rosposlblo lor rod coll dlgostlon), anaphylaxls, por- slstont bloodlng, and oxcosslvo scarrlng. Curront rocommondatlons lor troatmont vlth modlclnal loochos lncludo prophylaxls vlth an amlnoglycosldo and a thlrd-gonoratlon cophalosporln and cautlon vhon troatlng lmmunocompromlsod patlonts. 261,265 Vasodilators Many studlos 266270 shov lncroasod llap survlval ln rats troatod vlth calcium-channel blockers—og, dlltlazom, nllodlplno, nltrondlplno, vorapamll vhlch act on tho vascular smooth musclos to causo vasodllatlon and lmprovo clrculatlon ln tho llap. 1hoso agonts do not rostrlct tholr ollocts to smooth musclo, hovovor. lor lnstanco, dlltlazom has boon shovn to stlmulato tho roloaso ol prostacyclln (lCl 2 ), a potont vasodllator and antlplatolot aggrogator, lrom vascular ondothollal colls. 266 }ornbock and Dalsgaard 271 doscrlbo tho cllnlcal appllcatlon ol lntravonous calcitonin gene-related peptide ln tho troatmont ol llaps vlth compromlsod clrculatlon. 1oplcal nitroglycerin ls a potont vasodllator vlth a groator olloct on tho vonous clrculatlon than on artorlal vossols. kohrlch and colloaguos 272 roportod lmprovod survlval ol axlal llaps ln plgs and rats troatod vlth nltroglycorln olntmont, as dld lrlco and loarl, 273 vho appllod nltroglycorln trans- dormally. Nlchtor, 274 on tho othor hand, lound no lncroaso ln survlval ol random pattorn llaps ln rats troatod vlth nltroglycorln pasto. lchloka and othors 275 ovaluatod tho ollocts ol amrlnono, a soloctlvo phosphodlostoraso lll lnhlbl- tor, and lound onhancod mlcroclrculatory blood llov lrom lts posltlvo lnotroplc and vasodllatlng prop- ortlos, vlth a corrospondlng lncroaso ln vlablo aroa ol llaps. ln a lator cllnlcal study, lchloka ot al 276 domonstratod an lncroaso ln mlcroclrculatory blood llov ln llaps altor lntravonous admlnlstratlon and a docroaso ln vasospasm altor toplcal appllcatlon ol amrlnono to tho podlclo. 1ho rosults obtalnod vlth amrlnono voro comparablo to tho rosults obtalnod vlth prostaglandln L1 and lldocalno. Crossman and assoclatos 277 roport lncroasod llap survlval ln a rat modol vlth lntraporltonoal ln|oc- tlon ol dimethyl sulfoxide (DMSC) or hyaluronldaso, and postulato a docroaso ln tlssuo odoma vlth rosultant lmprovod blood llov. Hallor, 1rachy, and Cummlngs 278 noto lmprovod llap porluslon altor lntraporltonoal ln|octlon ol DMSC as moasurod by lasor Dopplor voloclmotry and porluslon llovmotry. kand-Luby and covorkors 279 dotormlnod that topl- SRPS Volume 10, Number 1 31 cal appllcatlon ol DMSC lncroasod llap vlablllty ln humans by controlllng skln lschomla through vasodllatlon, roductlon ol platolot aggrogatlon, or tho lroo-radlcal scavonglng proportlos ol DMSC. 1hoy llnd DMSC salo to uso ln a cllnlcal sottlng. 1ho ollocts ol toplcal lidocaine and pentobar- bital, vhlch aro bollovod to lnhlblt ondothollum- dopondont rolaxatlon on tho vascular smooth musclo, voro studlod by Wadstrom and Cordln. 280 1hoy concludo that although thoro ls an olloctlvo and prompt rosolutlon ol mochanlcally lnducod vasospasm, tho ollocts aro clrcumvontod by mlcrovascular thrombosls. Prostacyclin (lCl 2 ) ls a potont vasodllator vhlch also docroasos platolot actlvatlon and lmpalrs tho roloaso ol cytotoxlns lrom vhlto blood colls. 205 Lmorson and Sykos 281 shovod lmprovod survlval ol random skln llaps ln rats altor troatmont vlth prostacyclln. lCl 2 vas lound to bo olloctlvo only ll glvon at tho tlmo ol llap olovatlon and contlnuod postoporatlvoly. 1ho authors thoorlzo that porhaps lCl 2 also stlmulatos nov vossol lormatlon ln lschomlc tlssuo. Cthors 282,283 havo had slmllar oxporloncos vlth oxogonously admlnlstorod lCl 2 ln laboratory anlmals, but cautlon that hlgh-doso prostacyclln actually has a dotrlmontal olloct on skln llap survlval. 283 Catoloy, McAnulty, and Martln 284 roport tvo lnstancos ol lntravonous lnluslon ol prostacyclln lor lmpondlng lroo llap lalluro, vlth subsoquont plnklng up ol tho llaps and a succosslul outcomo to tho casos. A lCl 2 analog, iloprost, vas ovaluatod by Sondoroll ot al, 285 vho lound slgnlllcantly hlghor llap survlval ratos ln tho study group comparod vlth llaps porlusod vlth lactatod klngor´s or uroklnaso solutlons. 1ho authors noto that lloprost has tho samo actlon and potoncy as lCl 2, but vlth groator chomlcal stablllty and thorapoutlc potontlal. ln addltlon, lloprost sooms to havo a cytoprotoctlvo olloct that provonts lysosomal onzymo roloaso dur- lng tlssuo hypoxla. konaud and assoclatos 286 roport succosslul rosolutlon ol a lalllng lroo llap altor lntraartorlal lnluslon ol lloprost ln tho acuto sottlng and lntravonous admlnlstratlon postoporatlvoly. Suzukl and colloaguos 287 doscrlbod tho uso ol prostaglandin E 1 (lCL 1 ). lts ollocts voro vory slml- lar to prostacyclln ln causlng porlphoral vasodlla- tlon and platolot dlsaggrogatlon. lCL 2 may bo avall- ablo ln a moro stablo lorm and, llko lCl 1 , has boon notod to havo a blphaslc rosponsolo, hlghor dosos ol tho agont rosult ln hypotonslon and slgnlllcant docroaso ln blood llov to tho vholo skln llap. Free Radical Scavengers A numbor ol lnvostlgators 288292 havo shovn lncroasod llap survlval vlth allopurinol troatmont ln a rat skln modol. Allopurlnol lnhlblts xanthlno oxldaso and ln tho procoss loads to dlmlnlshod lroo radlcal productlon and rotards tho loss ol purlno substratos avallablo lor hlgh-onorgy motabollc syn- thosls. llcard-Aml and colloaguos 293 noto that xan- thlno oxldaso lovols ln human tlssuo aro 1/40th ol thoso ln rats, castlng doubt on \C as a ma|or sourco ol lroo radlcals rosponslblo lor tlssuo ln|ury and llap nocrosls ln human skln. 1roatmont ol skln llaps vlth superoxide dismutase, a scavongor ol lroo oxygon radlcals, has boon shovn to lmprovo llap survlval. 201 Manson and col- loaguos 203 roportod that a slnglo doso ol SCD lmprovod llap survlval lrom 38° to 76° ln rats. 1lssuo lovols ol SCD voro hlghor ln tho survlvlng portlons ol llaps. Suzukl and covorkors 294 con- llrmod tho bonollclal ollocts ol SCD ln provontlng llap nocrosls, and suggostod that roporluslon lol- lovlng lschomla, not contlnuous lncomploto lschomla, producos roactlvo oxygon spoclos and a gradual lncroaso ln blood llov ln tho dlstal llap. Havkos, ¥oung, and Cloland 295 noto anaphylactlc roactlons ln a plg modol assoclatod vlth tho uso ol suporoxldo dlsmutaso. Angol and colloaguos 296 also domonstratod lmprovod llap survlval vlth deferoxamine, an lron cholator and lroo radlcal scavongor. Doloroxamlno has boon shovn to dlmlnlsh llap nocrosls causod by undorlylng homatomas. lts bonollclal olloct on llaps probably rolatos to lts ablllty to scavongo lroo radl- cals, although Croon and assoclatos 297 stato that tho loglc bohlnd uslng cholators such as doloroxamlno ls to lnhlblt hydroxy radlcal lormatlon lrom supor- oxldo radlcals. Antiinflammatory Agents 1ho rolo ol storolds on llap survlval contlnuos to bo hotly dobatod. Nancarrov 298 domonstratod a 25° lncroaso ln survlval ol groln lsland llaps ln rats altor admlnlstratlon ol 1.5 mg/lg ol dexametha- sone 12 hours prooporatlvoly. Nakatsuka and oth- ors 299 studlod tho olloct ol methylprednisolone on SRPS Volume 10, Number 1 32 plg musculocutanoous, axlal, and random pattorn llaps. 1hoy lound no lncroaso ln aroa ol llap sur- vlval or lluoroscoln dyo ponotratlon. 1horo vas no lncroaso ln skln caplllary blood llov as moa- surod by ontrapmont ol radloactlvo mlcrosphoros. ln summary, thoro vas no ovldonco to support tho cllnlcal uso ol cortlcostorolds to onhanco llap vlablllty. 1hoso llndlngs voro ln contrast vlth thoso ol Lsclamado, Larraboo, and Zol, 242 vho obsorvod that porloporatlvo storolds dld lmprovo skln llap vlablllty. lorrlgan and Stotland 295 rovlov tho accumulatod data rogardlng attompts to modulato tho prolnllam- matory mochanlsm lnvolvod ln roporluslon ln|ury. Varlous studlos havo lnvolvod platolot actlvatlng lac- tor antagonlsm, soloctlvo lnhlbltlon ol loukotrlono synthosls to provont loukocytoondothollal coll adhoslon and macromolocular loakago, lnhlbltlon ol thromboxano and complomont, and antlbodlos dlroctod agalnst noutrophll toxlclty. 1hromboxano A 2 (1xA 2 ) ls a potont vasoconstrlc- tor and platolot aggrogator roloasod by platolots. lrostacyclln (lCl 2 ) ls a potont vasodllator and lnhlbltor ol platolot aggrogatlon producod by ondothollal colls. ßoth aro products ol arachldonlc acld motabollsm and havo strong ollocts at tho ondothollal coll lovol 285 (llg 30). Fig 30. 1ho motabollsm ol arachldonlc acld. (Reprinted with permission from Senderoff DM, Israeli D, Zhang WX, et al: Iloprost improves survival of ischemic experimental skin flaps. Ann Plast Surg 32:490, 1994.) Asplrln (ASA) acotylatos tho onzymo cyclo- oxygonaso, thoroby docroaslng tho synthosls ol 1\A 2 ln platolots and lCl 2 ln tho vossol valls. At lov dosos tho olloct ol asplrln ls soloctlvo and only tho cyclooxygonaso systom ln platlots ls lnhlbltod and tho lormatlon ol thromboxano ls blockod. ln tho laboratory, prooporatlvo asplrln docroasos throm- bus lormatlon at vonous anastomosls and lmprovos caplllary porluslon ln tho mlcroclrculatlon. 300 Cthor studlos domonstrato lncroasod oarly anastomotlc patoncy but no dllloronco lrom controls altor 24 hour to a vook. 205 Salomark and assoclatos 301 studlod tho posslblo rolo ol ASA as an antlthrombogonlc agont. 1holr rosults voro dlssapolntlng ln that ASA shovod both bonollclal and dotrlmontal ollocts dopondlng on vhon tho ln|octod drug vas oxposod to tho subon- dothollal layors ol tho damagod vossol vall. 1horo ls no omplrlc support ln tho lltoraturo lor tho uso ol asplrln postoporatlvoly. 205 ßuckloy, Davldson, and Das 302 oxplorod tho ollocts ol anothor NSAlD, kotorolac tromothamlno (1oradol). Dosplto slgnlllcantly prolongod moan bloodlng tlmos, mark- odly roducod platolot aggrogatlon, and consldor- ably hlghor patoncy ratos ln tho kotorolac group at 20 mln, all vossols thrombosod at 24 hours. Nicotine lorrost, lang, and Llndsay 303 doscrlbod tho ollocts ol nicotine on caplllary blood llov ln random pat- torn skln llaps olovatod ln rats. 1ho authors lound that nlcotlno slgnlllcantly docroasod caplllary blood llov, dlstal porluslon, and llap survlval ln a doso- and tlmo-dopondont lashlon, and proposod sovoral hypothosos to oxplaln tho mochanlsm ol actlon ol tho drug. ßlack ot al 304 noto that acuto oxposuro ol human skln vasculaturo to nlcotlno ls assoclatod vlth ampllllcatlon ol noroplnophrlno-lnducod skln vasoconstrlctlon and lmpalrmont ol ondothollum- dopondont skln vasorolaxatlon. MONITORING FLAP VASCULARITY Dosplto tho cllnlcal succoss ol lroo llaps, strlct ovaluatlon ol llap porluslon ls ossontlal to provont, rocognlzo, and troat compllcatlons. 1ho lalluro rato ol lroo tlssuo translor ls roportod to bo loss than 5°, hovovor, tho lncldonco ol podlclo thrombosls ls hlghor than tho lalluro rato vould rolloct duo to a SRPS Volume 10, Number 1 33 salvago rato altor podlclo thrombosls that rangos lrom 36°70°. 259 Sovoral tochnlquos havo boon suggostod to assoss porluslon ol llap tlssuos ln an attompt to prodlct llap survlval. 29,305,306 1hoso moth- ods aro rovlovod by lurnas and koson, 307 1ruolson, 308 ßradlord, 309 and Capany. 310 ßrovn ot al 311 rotrospocltvoly rovlovod succoss- lul lroo llap salvago at tholr lnstltutlon. Duo to moro succosslul salvago vlthln tho llrst 24 hours altor tho lnltlal surgory, thoy rocommondod hourly monltorlng lor tho llrst 24 hours and thon ovory 4 hours lor 48 hours . 1ablo 5 lrom Danlol and lorrlgan 29 summarlzos varlous monltorlng tools usod to assoss llap vlablllty. Accordlng to tho authors, tho ldoal monltorlng dovlco should • rolloct tho condltlon ol tho ontlro (burlod) llap • bo rollablo, roproduclblo, conslstont, and sonsl- tlvo • provldo contlnuous monltorlng • bo usor-lrlondly and oaslly lntorprotod • bo allordablo • bo rolatlvoly unalloctod by tho oxtornal onvl- ronmont Subjective/Physical Criteria ºCllnlcal obsorvatlon romalns tho gold standard agalnst vhlch monltorlng systoms aro gonorally moasurod...and lt...lullllls many ol tho crltorla ol tho ldoal monltorlng systom.¨ 306 Cllmo 312 survoyod varlous cllnlcal moasuromonts ol llap vascularlty as ol 1951 and notod that tho color of the blood ooz- ing from the dermis vas a rollablo lndlcator ol clr- culatory status. ßluo dormal bloodlng vas tho bost varnlng slgn ol lnadoquato porluslon. Hoopos, 194 hovovor, bollovos that ºlt ls a mlsconcoptlon to oquato blood supply vlth vlablllty, tho cruclal tost ol adoquacy ol clrculatlon ls survlval ol tho podlclod llap tlssuo.¨ Danlol and lorrlgan 29 rovlov varlous tochnlquos lor sub|octlvoly ovaluatlng llap vlablllty and noto that color, caplllary blanchlng, and varmth aro unrollablo and ol llmltod uso. Cl tho sub|octlvo tosts, bloodlng lrom a stab vound ls probably tho most accurato. 1ablo 6 outllnos tho cllnlcal slgns that can bo usod to dlllorontlato vonous lrom art- orlal maladlos ln llaps. Temperature monltorlng ls a slmplo tochnlquo to ovaluato llap vlablllty. lt can bo accompllshod ln a numbor ol vays, lncludlng surlaco tomporaturo and dlllorontlal thormomotry. ln gonoral, surlaco tom- poraturo can bo takon oaslly, roqulros rolatlvoly lnoxponslvo oqulpmont, and ls cllnlcally usolul ln monltorlng lor oxtrlnslc compllcatlons. As an lndl- cator ol lntrlnslc llap lalluro lt ls lnadoquato, hov- ovor. Dlllorontlal thormomotry ls a usolul tool to monltor vascular patoncy ln burlod lroo tlssuo trans- lors ln vhlch a tomporaturo gradlont oxcoodlng 3C ls consldorod slgnlllcant. 29 }onos, Dunscombo, and Croonhalgh 313 took sorlal tomporaturo moasuromonts ol llap skln and control skln slmultanoously ln ordor to nogato onvlronmontal and motabollc varlablos. 1hoy lound that skln tom- poraturo rospondod slovly to vascular occluslon and vas not a rollablo lndlcator ol llap lalluro ln tho lmmodlato postoporatlvo porlod. 1omporaturo roadlngs, hovovor, can bo usod olloctlvoly to track tho courso ol roplantod dlglts. lhourl and Shav 314 rovlov surlaco tomporaturo rocordlngs ol 600 lroo llaps and concludo that vhon proporly appllod and lntorprotod, lts sonsltlvlty and prodlctlvo valuo approach 98° and 75°, maklng lt a slmplo, lnoxponslvo, and hlghly rollablo tochnlquo ol lroo llap monltorlng. Cho ot al 315 and Akln and ßasut 316 croatod small monltorlng llaps that aro oxtorlorlzod to lacllltato monltorlng ol burlod lroo llaps. 1ho monltorlng llap ls basod on a porlorator lod by tho maln podlclo. 1ho authors voro ablo to prodlct podlclo compro- mlso lrom tho appoaranco ol tho monltorlng llap. Vital Dye Measurements Fluorescein has boon usod lor ovor 40 yoars to cllnlcally assoss llap vascularlty. 317 ln 1962 Myors 318 rovlovod tho hlstory ol lluoroscoln and usod lt to dotormlno tho vlablllty ol skln llaps altor radlcal mastoctomy. McCrav, Myors, and Shanklln 319 dollnoatod tho pharmacologlc charactorlstlcs ol lluo- roscoln that onablod lt to bo an lndlcator ol blood llov, omphaslzod lts morlts ln prodlctlng tho vlabll- lty ol artorlal llaps, and suggostod cllnlcal appllca- tlons. lluoroscoln ls bollovod to bo bottor than 70° accurato as an lndlcator ol tho clrculatory sta- tus ol a llap. lluoroscoln ls usually glvon ln a bolus ln|octlon ol 500 to 1000 mg (15 mg/lg). Altor a valtlng SRPS Volume 10, Number 1 34 porlod ol 2030 mln, tho oxtont ol dyo stalnlng ln thoso tlssuos vhlch aro adoquatoly porlusod can bo soon vlth a Wood´s lamp. ll nocossary tho tost can bo ropoatod ovory 8 hours, 29 although othors sug- gost valtlng 24 hrs. 320 lang and othors 321 roport that vhon tho lluoroscoln tost ls porlormod 1 hour altor llap olovatlon, tho longth ol llap that ls vlablo ls conslstontly undorostlmatod. Whon tho tost ls por- lormod at 18 hours postoporatlvoly, tho longth ol dyo stalnlng and skln vlablllty corrolatod vory voll. 1hoso rosults voro obtalnod ln random llaps, axlal pattorn llaps, and musculocutanoous llaps. TABLE 5 Techniques for Monitoring Flap Perfusion (Reprinted with permission from Daniel RK, Kerrigan CL: Principles and physiology of skin flap surgery. In: McCarthy JG (ed), Plastic Surgery. Philadelphia, Saunders, 1990. Vol 1, Ch 9.) SRPS Volume 10, Number 1 35 Myors and Donovan 322 noto that all tochnlquos lor ovaluatlng llap porluslon vlth lluoroscoln aro roasonably accurato, lncludlng tho tradltlonal Wood´s lamp mothod vhlch vas as rollablo as novor onos. ln tholr oplnlon, lnaccuraclos ln lluoroscoln tostlng aro probably lnhoront and unavoldablo, ln that lt only moasuros vascularlty at tho tlmo tho dyo ls glvon and blood supply can chango. Moro spo- clllcs aro glvon by Cdland ot al, 323 vho noto that slnco lluoroscoln ls a dorlvatlvo ol phthaloln, a pH lndlcator, and lschomlc tlssuos bocomo acldotlc, tho acldosls mlght quonch tho oxpoctod lluoros- conco ln tho dlstal skln llap. Sllvorman, Norton, and ßroussoau 324 doscrlbod tho uso ol perfusion fluorometry, a tochnlquo vhoro tho admlttod lluorosconco ol tho tlssuo ls moasurod uslng a llboroptlc llght guldo (dormolluoromotor) and an ob|octlvo valuo ol dyo-lluorosconco unlts ls obtalnod. Accurato roadlngs can bo mado as oarly as 2 mlnutos altor ln|octlon, and sorlal ln|octlons and moasuromonts aro posslblo bocauso tho dosos ol dyo aro small (0.15 mg/lg). 1ho mothod vas 96° accurato ln prodlctlng ultlmato llap vlablllty at lovor dosago and vlth lovor sldo-ollocts than lluo- roscoln tostlng. Dormolluoromotry has rocontly boon appllod to vonous llaps. Suzukl ot al 325 comparod artorlallzod to nonartorlallzod and random-pattorn llaps and notod that tho lnstrumont ls a rollablo lndlcator ol clrculatlon ln all typos ol llaps ovaluatod. 1homson and lorrlgan 326 doscrlbod tho lormula lor calculatlng tho dyo lluorosconco lndox (Dll) and documontod that lluorosconco varlos vlth blood supply. 1ho authors conllrmod tho accuracy ol dormolluoromotry ln prodlctlng skln llap survlval ln plgs. Cllnlcally, a Dll ol 30° or moro ls consldorod salo. lsslng and Naumann 327 usod computor-aldod dlgl- tal morphomotry (CADM) to comparo lluoroscoln stalnlng, skln pH, and skln tomporaturo ln tho ovalu- atlon ol skln llap porluslon. 1hoy concludo that lluoroscoln stalnlng ls tho most accurato prodlctor ol llap vlablllty. lndocyanlno groon (lCC) ls a socond-gonora- tlon dyo that can bo usod as a cllnlcal markor ol cutanoous blood llov. 1ho prlnclplo ol monltor- lng ls slmllar to that ol lluoroscoln, but tho choml- cal proportlos ol lndocyanlno groon aro moro sult- ablo to cllnlcal uso. 328 lCC has boon usod succoss- lully ln oxporlmontal and cllnlcal modols. 328331 lntraoporatlvo lasor-lnducod lluorosconco ol lCC shovod artorlal spasm, vonous congostlon, and roglonal hypoporluslon ln mlcrovascular llaps and corrolatod strongly vlth tho cllnlcal outcomo. 329 Photoelectric Assessment 1vo typos ol Dopplor lnstrumonts aro currontly ln cllnlcal uso. 1ho llrst ls tho ultrasound Dopplor, vhlch usos rolloctod sound to plck up pulsatllo vos- sols. 1ho socond ls tho laser Dopplor, vhlch moa- suros tho lroquoncy shllt ol llght and thoroloro has llmltod ponotratlon (1.5 mm). 29 Amorhausor and assoclatos 332 ovaluatod color flow ultrasound (ClUS) ln an oxporlmontal and cllnl- cal sottlng and notod that lt vas sonsltlvo to vonous and artolal lnsulllcloncy at llov ratos as lov as 3.0 mL/mln. 1hoy lound ClUS vas capablo ol dlllor- ontlatlng blood llov and vas prollclont at vlsuallz- lng lumlnal dlssoctlons, lntlmal llaps, thrombosos, and artorlolar constrlctlons. 1ho laser Doppler flowmeter glvos an output volt- ago proportlonal to tho total llux ol rod blood colls ln tho volumo ol tlssuo samplod (approxlmatoly 1 mm 3 ), and thus lncludos tho subcaplllary ploxus. 1ho tochnlquo ylolds tvo valuos. 333 a Dopplor llov moasuromont, vhlch ls a rolloctlon ol tho numbor and voloclty ol movlng rod blood colls and vhlch docroasos to lov lovols ln rosponso to artorlal or vonous occluslon, and a photomotry valuo, vhlch ls a photoplothysmographlc roadlng ol tho lntonslty ol tho back-scattorod llght. 1hls valuo doos not chango vlth artorlal occluslon but docroasos ln rosponso to vonous occluslon, holplng to dlstlngulsh TABLE 6 Signs of Arterial Occlusion and Venous Congestion (Reprinted with permission from Adams JF, Lassen LF: Leech therapy for venous congestion following myocutaneous pectoralis flap reconstruction. ORL-Head Neck Nurs 13:12, 1995.) SRPS Volume 10, Number 1 36 botvoon vonous and artorlal causos ol llap ombar- rassmont. Hallock 334 lnvostlgatod tho crltlcal throshold lor tlssuo vlablllty as dotormlnod by lasor Dopplor llovmotry, and lound that a basollno ol 30° ls gon- orally sulllclont to prodlct llap survlval. Hodon and assoclatos 335,336 lound that lasor Dopplor llovmotry corrolatod voll vlth actual skln vlablllty and nocro- sls ln tho lmmodlato postoporatlvo porlod. A sonsl- tlvlty ol 93° and spoclllclty ol 94° voro rocordod by tho Hovlus group. 337 ßlrchor ot al 338 provldo an ln-dopth ovorvlov ol guldollnos lor tho moasuromont ol cutanoous blood llov by lasor Dopplor llovmotry. Svonsson, Holmborg, and Svodman 339 rovlov tho propor lntorprotatlon ol lasor Dopplor rocordlngs lrom lroo llaps and suggost tho lollovlng guldollnos to lmprovo accuracy ol tho analysls. • a llxod probo • contlnuous rocordlngs • attontlon to physlologlc lluctuatlons and tronds Many lactors alloct tho cllnlcal usolulnoss ol thoso tochnlquos. Among thom aro oaso ol appllcatlon, oqulpmont cost, and oxportlso roqulrod to oporato. Sllvorman and covorkors 340 comparod tho lasor Dopplor, porluslon lluoromotry, and transcutano- ous oxygon assay mothods and concludod that lluo- romotry ls moro proclso and can bo usod to monl- tor sovoral aroas ln sorlal lashlon. 1ranscutanoous oxygon and Dopplor problng voro bottor sultod lor contlnuous monltorlng. Cummlngs and col- loaguos 341 roachod slmllar concluslons but ompha- slzo, as doos Marks, 342 that boglnnlng 24 hours post- oporatlvoly tho lasor Dopplor tochnlquo ls tho most sonsltlvo. llaco, Wltt, and Hondrlcks 343 agroo that Dopplor llovmotry ls a usolul tool lor assosslng llap vlablllty, but stross that slnco postoporatlvo blood llov ls a dynamlc procoss that poaks about 52 to 80 hours and roturns to basollno somo 120 hours postopora- tlvoly, no slnglo moasuromont ls lndlcatlvo ol any- thlng oxcopt tho status at that ono tlmo. ¥uon and long 344 roportod a 5-yoar oxporlonco vlth lasor Dopplor llovmotor monltorlng ol 232 mlcrovascular llaps. Vascular compromlso vas dotoctod ln all casos, vlth no lalso posltlvos or noga- tlvos. 1ho salvago rato vas 69° and tho ovorall succoss rato vas 98°. Advantagos ol Dopplor problng aro hlgh rollabll- lty (approachlng 100° 24 hrs altor llap translor) and tho ablllty to contlnuously monltor skln porlu- slon by a nonlnvaslvo tochnlquo. Dlsadvantagos aro that lt ls not quantltatlvo, lt obtalns lnlormatlon only lrom a slnglo slto, ls sonsltlvo to movomont ol tho sub|oct, and has llmltod accuracy bolov tho crltlcal throshold at vhlch tlssuo nocrosls ls guaran- tood. 345 1ho scannlng lasor Dopplor 346 and lasor llovgraph 347 may glvo a moro global plcturo ol tho llap than could bo obtalnod by Dopplor llovmotry. ln lorrlgan and Danlol´s vlov, hovovor, ºno slnglo tochnlquo ls unlvorsally appllcablo or suporlor to all othors.¨ 199 Metabolic 1sur and covorkors 348 moasurod transcutaneous oxygen tension ln dolayod axlal and random pat- torn skln llaps by moans ol an oxygon oloctrodo appllod to tho skln. 1hoy lound oxygon partlal- prossuro moasuromonts to bo an olloctlvo prodlc- tor ol tho olloctlvonoss ol tho dolay procoduro. Slmllarly, H|ortdal and colloaguos 349 lound moasuro- mont ol subcutanoous and lntramuscular oxygon tonslon ln plg lsland llaps to bo a sonsltlvo lndlcator ol acuto lmpalrmont ol tho supplylng vossols. lorrlgan and Danlol 350 ovaluatod caplllary blood samplos ln plg lsland llaps and notod that vhllo PC 2 and PCC 2 moasuromonts voro hlghly varlablo, changos ln homatocrlt and pH voro usolul prodlc- tors ol llap vlablllty. Cthor loss popular mothods ol ovaluatlng clrculatlon ln a llap lncludo moasuro- mont ol tho llbrlllatlon potontlal ln skolotal musclo, 351 magnotlc rosonanco lmaglng, 352 and magnotlc roso- nanco spoctroscopy. 353 Coldo and Mahonoy 354 doscrlbod an lmplant- ablo optochomlcal oxygon-sonslng oloctrodo dovlco or optode that allovs rapld and contlnuous monltorlng ol tlssuo PC 2 and vhlch vas lolt to rollably rolloct vascular occluslon. 1ho probo ls small, oaslly lmplantablo, and lndopondont ol anas- tomotlc proxlmlty, but tho authors dld not com- mont on tho ablllty ol tho optodo to dlllorontlato botvoon artorlal and vonous compromlso. 1ho lmplantablo PC 2 sonsor ln Holor´s 355 sorlos accu- ratoly lndlcatod llap lalluro ln all casos, yot tho authors´ doclslon to rooxploro a lalllng lroo llap vas stlll basod on cllnlcal obsorvatlon. SRPS Volume 10, Number 1 37 Photoplethysmography ls a tochnlquo that moa- suros lluld volumo by dotoctlng varlatlons ln lnlra- rod llght absorptlon by tho skln. lts curront uso ln cllnlcal practlco has sovoral llmltatlons. 29,305,307 ln addltlon to dlsplaylng tho vavolorms ol tho photoplothysmograph, tho pulse oximeter also moa- suros llght absorptlon to dorlvo oxygon saturatlon ol artorlal homoglobln. 1ho dovlco ls commonly usod ln anosthoslology and vas ovaluatod by Llndsoy ot al, 356 vho domonstratod lts usolulnoss but rocom- mondod lurthor study to dovolop spoclllc guldo- llnos boloro lt vas unlvorsally accoptod ln cllnlcal practlco. lrvln ot al 357 ovaluatod a novor and nonlnvaslvo tochnlquo lor assosslng llap clrculatlon that lnvolvos contlnuous monltorlng ol changos ln tho oxy-, dooxy-, and total homoglobln concontratlons ol llap blood. ln addltlon to doopor ovaluatlon (up to 10 cm) ol llaps than ls posslblo vlth tho lasor Dopplor, near infrared spectroscopy (NlkS) vas ablo to dollnoato tho dllloronco botvoon artorlal, vonous, and total vascular occluslon. Cthor moans ol ovaluatlng llaps lncludo quantl- tatlvo tosts, cloaranco tosts, radloactlvo mlcrosphoros, and oloctromagnotlc llovmotry. 1hoso aro osson- tlally rosorvod lor oxporlmontal puposos only, and vlll not bo dlscussod horo. SKIN EXPANSION James F Thornton MD HISTORY ßonnot and Hlrt 1 rovlov tho hlstory ol tlssuo oxpanslon and noto that lts orlglns dato to Colsus (25 ßC50 AD), vho ºdoscrlbod tho tochnlquo ol vound closuro by croatlng, strotchlng, and approxlmatlng skln llaps.¨ ln 1957 Noumann 2 roportod tho llrst cllnlcal uso ol controllod skln oxpanslon. Ho placod a rubbor balloon subcutanoously bonoath tho tom- poral scalp and postaurlcular skln. Cvor tho noxt 2 months tho balloon vas gradually oxpandod, lncroas- lng tho skln aroa by approxlmatoly 50° or onough to provldo sulllclont covor lor cartllago gralt roconstruc- tlon ol a traumatlc oar doloct. Not untll 1976, vhon kadovan 3 roportod hls vork vlth tlssuo oxpanslon lor broast roconstructlon, dld tho potontlal usolul- noss ol thls tochnlquo bocomo obvlous. Slnco thon, controllod tlssuo oxpanslon has boon usod lor tho roconstructlon ol all aroas ol tho body ln many dlvorso probloms. ßakor 4 summarlzos tho hlstory and dynamlcs ol tlssuo oxpanslon. TECHNIQUE Modorn oxpandors aro mado ol slllcon olastomors and como ln sovoral shapos and slzos or aro cus- tom-mado to llt lndlvldual noods. 1ho oxpandor ls usually connoctod to a subcutanoous valvo through vhlch lsotonlc sallno ls ln|octod lor lncromontal oxpanslon. }ackson and colloaguos 5 doscrlbod uslng an oxtornal rosorvolr that vas assoclatod vlth lov compllcatlons, but tho authors do not rocommond lt ln casos vhoro a pormanont prosthosls ls plannod, such as lor broast roconstructlon. 1ho tlmo lntorval botvoon ln|octlons ol sallno lor gradual oxpanslon doponds on tho naturo ol tho doloct and lts anatomlc locatlon as voll as host tls- suo charactorlstlcs. 1ho lntorval rangos lrom 3 to 10 days. Hallock and klco 6 advocato monltorlng tho oxpanslon procoss vlth a comblnatlon ol trans- cutanoous oloctrodos lor moasurlng oxygon lovols, lmplant prossuro, and local porluslon to gaugo tho ond-polnt ol oach oxpanslon sosslon. Comparlng slmultanoous lasor Dopplor llovmotry and transcu- tanoous oxygon monltorlng, 7 thoy noto that olthor tochnlquo rocords dlmlnlshod clrculatlon ln rosponso to lncroasod oxpanslon, but adoquato tls- suo clrculatlon stlll oxlsts at tho throshold ol paln. llotlla and colloaguos 8 rocommondod ovorlllllng tho oxpandor to lncroaso tho amount ol oxpanslon at oach sosslon and shorton tho total oxpanslon porlod, but Van ßook and Adson 9 cautlon that ll tho lntralu- mlnal prossuro oxcoods 500 mmHg, loakago at tho ln|octlon port ls llkoly, ospoclally vhon uslng largo- callbor noodlos. Although rapld oxpanslon ls pos- slblo ln somo clrcumstancos, prosorvlng tlssuo lntog- rlty takos procodonco ovor spood ol oxpanslon. Van kappard ot al 10 ovaluatod tho dllloroncos ln surlaco aroa ol oxpandod tlssuo ln rolatlon to shapo ol tho lndlvldual oxpandor. lor oxpandors vlth a round baso, a roctangular baso, or a croscontlc baso, tho rospoctlvo galns voro 25°, 38°, and 32°. 1ho authors concludod that an oxpandor ol appro- prlato slzo has a baso that ls 2.5 tlmos as largo as tho doloct to bo closod. Matton and assoclatos 11 doscrlbod a ºunlvorsal lnclslon¨ lor tlssuo oxpandor lnsortlon that has boon shovn to mlnlmlzo tho compllcatlons soon vlth SRPS Volume 10, Number 1 38 othor lnclslons. Austad and koso 12 doscrlbod a soll- lnllatlng oxpandor contalnlng hyportonlc sodlum chlorldo crystals vlthln a sholl that gradually lllls through osmosls. ßosldos tho protractod lnllatlon tlmos ol 8 to 14 vooks, tho dovlco vas plaguod by roports ol skln nocrosls and lmplant rupturo. 1ho concopt ol a soll-lnllatlng oxpandor vas oxplorod lurthor by Wloso, 13 vho lncorporatod a copolymor ol mothylmothacrylato and N-vlnyl-2-pyrrolldono ln a gol caslng capablo ol gonoratlng a maxlmum prossuro ol 235 mmHg. 1ho author notos that thls oxpandor ls ºblocompatlblo¨ and holds promlso ln tho aroa ol tlssuo oxpanslon vlthout tho dlsadvan- tagos notod abovo. ßorgé and colloaguos 14 roportod dlroct closuro vlth Hydrogol tlssuo oxpandors ln 9 ol 10 patlonts. 1ho dolocts closod voro tho rosult ol radlal loroarm llap harvost. At lmplantatlon tho lnltlal volumo ol tho oxpandors vas 10 mm, and ovor 20 days thoy voro lnllatod to 100 mm. HISTOLOGY OF EXPANDED SKIN }ohnson ot al 15 rovlov tho hlstology and physlol- ogy ol tlssuo oxpanslon. Austad and colloaguos 16,17 studlod changos ln tho opldormls, dormls, and sub- cutanoous tlssuo ol oxpandod gulnoa plg skln. Com- parod vlth normal skln, oxpandod skln shovod a slgnlllcantly thicker epidermis—vhlch thoy attrlb- utod olthor to lncroasod mltotlc rato or docroasod rato ol coll turnovorand a thinner dermis and pannlculus carnosus. 1horo vas mlnlmal lnllam- matory roactlon to tho oxpandor. 1holr conclu- slons slgnlllod that skln oxpanslon ls not slmply a mattor ol strotchlng skln but tho actual lormatlon ol addltlonal nov skln vlth all tho attrlbutos ol tho orlglnal tlssuo. Argonta and covorkors 18 summarlzo tho hlstomorphologlc changos occurrlng ln oxpandod skln. 1ho opldormls doos not chango ln thlcknoss, although thoro ls an undulatlon ol tho basal lamlna and a loss ol lntorcollular spacos. 1ho surroundlng dormls docroasos ln thlcknoss consldorably, and lncroasod numbors ol llbroblasts and myollbroblasts aro soon ln tho oxpandor capsulo. 1ho llbrous capsulo that lorms around tho lmplant conslsts ol thlck bundlos ol collagon llbors and olongatod llbroblasts and myollbroblasts. 1lssuo oxpanslon also trlggors an lncroaso ln vasculaturo, prlmarlly at tho |unctlon ol tho capsulo and host tlssuo and to a lossor dogroo ln tho dormls. Musclo and lat both dlmlnlsh ln mass ln rosponso to oxpanslon, and vhllo thoro ls no loss ol musclo lunctlon, tho loss ol lat appoars to bo pormanont. Llko Austad, lasyk ot al 19 notod slgnlllcant thlck- onlng ol tho opldormls altor 5 vooks ol oxpanslon, as voll as slgnlllcant thlnnlng ol tho dormls and subcutanoous tlssuos. Lolghton and assoclatos 20 lound dlllorontlal thlnnlng ol all tlssuo layors oxcopt tho opldormls, vhlch vas unchangod. Clonlus and }ohansson 21 also roport slgnlllcant lncroaso ln opl- dormal thlcknoss, but 6 months altor tho ond ol oxpanslon tho opldormls had roturnod to normal thlcknoss. Clonlus, Dalsgaard, and Wlckman 22 stud- lod tho mltotlc actlvlty ol human skln samplos altor tlssuo oxpanslon and notod a statlstlcally slgnlllcant rlso ln tho numbor ol labolod basal and suprabasal koratlnocytos. 1hls conllrmod oarllor llndlngs ol lncroasod mltosls 17 and suggostod a net gain ol tls- suo, not only by strotchlng tho oxlstlng aroa but through gonoratlon ol nov tlssuo. 1ho phonomonon ol tlssuo grovth ln rosponso to mochanlcal oxpanslon has boon lnvostlgatod by 1akol and colloaguos. 23 1ho authors stato. º1ho mocha- nlsm by vhlch straln causos an onhancomont ol col- lular grovth appoars to bo a notvork ol sovoral lnto- gratod cascados, lmpllcatlng grovth lactors, cytos- koloton, and tho protoln klnaso lamlly. . . . Addltlonal ovldonco has accumulatod that mochanlcal straln stlmulatos slgnal transductlon pathvays that could trlggor a sorlos ol cascados ovontually loadlng to a nov skln productlon.¨ 23 Normal human skln ls contlnually undorgolng strotchlng and rolaxatlon. Collagen llbors oxlst ln a convolutod lorm and, unllko llbors mado ol elastin, aro lncapablo ol roturnlng to tholr rolaxod stato altor bolng strotchod. ll tho llmlts ol tho olastlc llbors aro oxcoodod, pormanont dolormatlon ol collagon may rosult. 24 Molls and colloaguos 25 lound changos ln tho orlontatlon ol collagon llbors ln tho dormls as a rosult ol skln strotchlng. Altor 15 mln- utos ol strotchlng vlth a skln-strotchlng dovlco, tho llbors bocamo allgnod ln tho dlroctlon ol tho strotch- lng lorco, porpondlcular to tho vound margln. 1hls dynamlc roallgnmont ol collagon llbors oxplalns tho slgnlllcantly docroasod vound closlng tonslon rosultlng lrom skln strotchlng and oxplalns hov skln strotchos boyond lts lnhoront oxtonslblllty. Chang ot al 26 lound that tlssuo oxpanslon ln tho rat lnhlblts tho contractllo lunctlon ol dormal llbro- SRPS Volume 10, Number 1 39 blasts ln vltro. 1hls olloct vas moro pronouncod altor 5 vooks than ln tho llrst 1 or 2 vooks ol oxpanslon. Loo, Squlor, and ßardach 27 had provl- ously notod that antlcontractllo agonts lnstlllod lnto tho tlssuos surroundlng an oxpandor onhancod tho rato and oxtont ol skln oxpanslon, prosumably through rolaxatlon or lnactlvatlon ol contractllo llbroblasts ln tho porlprosthotlc capsulo. ßoauchonno 28 dotoctod hlghor lovols ol hydro- xyprollno and a not accumulatlon ol collagon ln oxpandod skln comparod vlth normal skln. }ohnson, lornahan, and ßauor 29 llkovlso notod lncroasod total collagon contont ln oxpandod skln, vhlch rosultod ln a thoorotlcal not galn ln tho dormal layor as voll as ln tho opldormal layor. lnlght and covorkors 30 conllrmod lncroasod collagon contont ln oxpandod dormls ol plgs, and spoculatod that lt could bo duo to tonsllo lactors durlng oxpanslon vhlch stlmulatod blosynthotlc actlvlty or mltosls ol llbroblasts. 1lmmonga and covorkors 31 notod thlckonod dormal collagon bundlos and collagon llbrlls that voro loosoly packod ln both oxpandod and sham- oporatod skln. 1ho mochanlsm ol actlon vas thought to bo tho normal procoss ol vound hoallng ln addl- tlon to a dolay phonomonon. Wlckman, Hodon, and }uroll 32 roport adronorglc suporsonsltlvlty ln oxpandod plg skln, suggostlng sympathotlc donor- vatlon as a rosult ol oxpanslon. lasyk, Austad, and Chorry 33 noto lormatlon ol a capsulo around ovory slllcono oxpandor. 1ho cap- sulo has lour hlstologlcal zonos. • lnnor zonoad|acont to tho oxpandor. Con- talns llbrln-llko lllamonts and a collular layor vlth macrophagos. • Contral zononoxt to tho lnnor zono. Con- talns olongatod llbroblasts and myollbroblasts orl- ontod parallol to tho surlaco ol tho lmplant. • 1ransltlonal zonoon tho outsldo ol tho contral zono. Has looso bundlos ol collago llbors. • Cutor zonomost suporllclal layor. Has ostab- llshod vossols loosoly lntorsporsod vlth collagon llbors. Cnco an oxpandor ls romovod, tho surroundlng llbrous capsulo rapldly thlns. Matturrl and colloaguos 34 blopslod provlously oxpandod skln at loast 1 yoar altor oxpandor romoval and lound normal-appoarlng opldormls vlth normal mltotlc actlvlty. 1ho dormls shovod only mlnlmal dogroo ol olastosls and zonal lragmontatlon ol olastlc llbors, vhllo tho hypodor- mls, vhlch vas ln contact vlth tho oxpandor cap- sulo, dld not manllost accontuatod llbrosls. Lxpanslon ol tho human scalp shortons tho tologon phaso ol halr lolllclos by actlvatlng and accoloratlng opldormal mltosls. 35 1ho hlstologlc olloct ol oxpanslon on musclo vas oxamlnod durlng broast roconstructlon vlth tlssuo oxpandors. 1ho undorlylng poctoralls ma|or musclo shovod consldorablo ultrastructural damago undor llght and oloctron mlcroscopy. 36 1lssuo oxpanslon ol lrradlatod plg skln shovs no lurthor hlstopathologlcal changos boyond thoso causod by lrradlatlon and ls lndlstlngulshablo lrom nonoxpandod lrradlatod skln ln tho porclno modol. 37,38 kadlatlon dld roduco tho ovorall aroa ol oxpandod skln by 23° ln ono study. 38 Worklng on a rabblt modol, Coodman and assoclatos 39 noto lncroasod opldormal thlcknoss but no dormal or capsular altoratlons ln lrradlatod skln postoxpanslon. BLOOD SUPPLY OF EXPANDED SKIN 1ho hlstologlc changos ovldont ln oxpandod skln lond support to tho concopt that skln oxpanslon ls a lorm ol dolay. Chorry, lasyk and othors 40 com- parod tho survlval ol oxpandod and dolayod llaps vlth acutoly ralsod random-pattorn skln llaps ln plgs. Lxpandod llaps shovod a 117° lncroaso ln survlv- lng longth ovor unoxpandod skln llaps. Dolayod llaps shovod a 73° lncroaso ovor tho controls. No slgnlllcant dllloronco vas notod botvoon oxpandod and dolayod skln llaps. Spoclmon anglograms ol oxpandod skln shovod ovldonco ol lncroasod vas- cularlty comparod vlth control skln. 1ho authors rocommondod lncludlng tho oxpandor capsulo ln tho llap at tho tlmo ol translor lor lts contrlbutlon to tho blood supply, and postulatod that mochanlcal lorcos aro ln somo vay rolatod to tho lncroasod vascularlty. ln a slmllar study, Sasakl and lang 41 locusod on tho vlablllty and caplllary blood llov ol oxpandod and dolayod skln llaps. Comparod vlth acutoly ralsod random-pattorn llaps, both oxpandod and dolayod skln oxhlbltod lncroasod total caplllary blood llov, and thls lncroaso parallolod llap sur- vlval. 1ho survlval longth ol random llaps ln skln ovorlylng tlssuo oxpandors vas also lncroasod, vhothor tho oxpandor vas lnllatod or not. SRPS Volume 10, Number 1 40 Saxby 42 also roportod 150° groator survlvlng longths ol oxpandod llaps ovor acutoly ralsod, nondolayod llaps and 50° groator survlvlng longths than nonoxpandod, dolayod llaps. Anglograms ol tho llap spoclmons rovoalod lncroasod callbor ol tho axlal vossols ln tho oxpandod llaps. Wlckman and assoclatos 32 lound ovldonco ol lncroasod suporllclal blood llov ln oxpandod skln by lasor Dopplor llovmotry and vonous outllov moa- suromonts, but no slgnlllcant dllloronco ln total blood llov botvoon llaps ralsod ln oxpandod and nonoxpandod skln. ßabovlc ot al 43 studlod tho ollocts ol tlssuo oxpanslon on lschomla ln lroo llaps. Comparod vlth tho control and sham groups, prooxpandod skln llaps domonstratod a statlstlcally slgnlllcant lncroaso (700°) ln porluslon as moasurod by lluoroscoln. 1ho lncroaso ln llap clrculatlon lnducod by tho oxpanslon lacllltatod an lncroaso ln llap toloranco to socondary lschomla. EXTENT OF EXPANSION Sovoral authors havo lnvostlgatod tho orlgln ol tho oxpandod tlssuo. Austad 12,16 documontod a truo tls- suo dlvldond lrom oxpanslon that vas thought to rosult lrom tho lncroasod mltotlc actlvlty ol tho strossod tlssuos. Vandor lolk and othors 44 roportod a 32° lncroaso ln mldhorlzontal longth and 44° lncroaso ln mldvortlcal longth ol oxpandod porclno skln. Altor llap olovatlon and lnsot, tho ovorall lncroaso ln sur- laco aroa avallablo lor covorago vas 30°. 1hroo months altor surgory thoro vas a sllght docroaso ln aroa vhlch vas not statlstlcally slgnlllcant. RATE OF EXPANSION 1radltlonally, tho oxpanslon procoss boglns 2 to 3 vooks altor lmplantatlon ol tho oxpandor and con- tlnuos at vookly lntorvals untll tho doslrod lnllatlon ls achlovod. 1ho skln adapts to stross ln tvo vays. llrst, ln tho ovont ol lmmodlato tlssuo oxpanslon, mochanlcal strotchlng changos tho olastlclty and allgn- mont ol collagon by a procoss callod creep. Croop ls tho ºtlmo-dopondont plastlc dolormatlon ol any matorlal or tlssuo ln rosponso to constant stross.¨ 45 Socond, tho procoss ol stress-relaxation occurs vhoro, ovor a porlod ol tlmo vhon skln ls strotchod to a glvon constant longth, tho lorco roqulrod to malntaln lt ls gradually docroasod. 24 As summarlzod by ßakor, 4 tho physlologlc changos ln skln durlng croop lncludo tho lollovlng. • dohydratlon ol tlssuo • mlcrolragmontatlon ol olastlc llbors • lncroaslngly parallol allgnmont ol randomly posltlonod collagon llbors • mlgratlon ol tlssuo ln tho dlroctlon ol tho lorco voctor ßakor 4 oxpands Clbson´s dollnltlon ol cyclic load- ing to moan strotchlng lollovod by rolaxatlon ol oxpandod tlssuo, as opposod to contlnuous oxpan- slon. lt appoars that cycllc loadlng ls tho most olloc- tlvo mothod ol rocrultlng oxtra tlssuo. Skln croop alono doos not account lor all tho oxtra skln durlng sorlal oxpanslon, and lactors such as rocrultmont, tlssuo comprosslon/thlnnlng, and nov grovth also play a rolo. ln 1987 Sasakl 46 doscrlbod lntraoporatlvo sus- talnod llmltod oxpanslon (lSLL) lor lmmodlato roconstructlon. 1ho author lator roportod lntraop- oratlvo oxpanslon ln closuro ol small skln dolocts on an omorgoncy basls. 47 Ho montlons dlsadvantagos ol tho slov oxpanslon mothod, namoly gradual lnllatlon ovor many vooks and months, tho rlsk ol lnloctlon and lmplant oxposuro lrom tho protractod prosonco ol tho oxpandor, partlcularly ln poorly vascularlzod aroas, and tho cosmotlc and lunctlonal dolormltlos ol burlod oxpandors and valvos. Sasakl statos that thoso shortcomlngs ol slov oxpanslon aro ollmlnatod by tho lntraoporatlvo oxpanslon toch- nlquo. Slogort ot al 45 ovaluatod lntormlttont lntraopora- tlvo short-torm tlssuo oxpanslon ln dogs and ln 30 patlonts vlth sovoro mlcrotla. Cyclod oxpanslons yloldod maxlmal lncroaso ln longth ol 15° to 20°. 1ho authors montlon mochanlsms that load to an lncroaso ln skln longth (llg 1)olastlclty, lntorstltlal dlsplacomont ol llulds, croop, and gonulno grovth yot lall to crodlt any ol thoso spoclllcally lor tholr llndlngs. lnstoad, thoy attrlbuto tho mochanlsm ol oxpanslon to anothor, undollnod lorm ol subcuta- noous moblllzatlon. Shaplro 48 comblnos acuto cyclod oxpanslons vlth roctangular skln llaps and notos a docroaso ln vound closlng tonslon comparod vlth slmplo llap undor- mlnlng. Novortholoss, tho author statos that ºun- dormlnlng must stlll bo consldorod tho most lmpor- tant olomont ln roduclng vound closlng tonslon.¨ SRPS Volume 10, Number 1 41 Woo, Logan, and Mustoo 49 doscrlbo a contlnu- ous lnluslon dovlco that malntalns a constant oxpandor prossuro and shortons tho tlmo to lull oxpanslon by tvo-thlrds. 1ho authors comparod tho olllcacy ol contlnuous vorsus lntraoporatlvo tls- suo oxpanslon ln a plg modol, and llnd throo tlmos moro tlssuo galn vlth tho lormor tochnlquo. lutran 50 dlscussos tho cllnlcal appllcatlons ol tho Suro-Closuro' skln-strotchlng dovlco orlglnally lntroducod by Hlrshovltz and colloaguos. 51 1ho dovlco ls sald to harnoss tho vlscoolastlc proportlos ol tho skln by applylng lncromontal tractlon to allov tho skln to rapldly strotch and oxtond vhllo mlnl- mlzlng lts tondoncy to rocoll. Wlckman and colloaguos 52 moasurod mochanlcal proportlos ol tho skln durlng rapld and slov tlssuo oxpanslon lor broast roconstructlon. Dlstonslblllty lossonod durlng oxpanslon, lncroasod altor tho oxpandor vas roplacod by a pormanont lmplant, and docroasod thoroaltor. Llastlclty dld not chango slg- nlllcantly and nolthor dld hystorosls (a moasuro ol tho skln turgor and plastlclty). ln summary, thoro voro mlnlmal dllloroncos ln skln proportlos botvoon rapldly and slovly oxpandod patlonts. APPLICATIONS OF EXPANDED SKIN 1ho maln advantagos ol tlssuo oxpanslon ln roconstructlvo surgory aro good color and toxturo match ol tho skln usod lor covorago, prosorvatlon ol sonsatlon and halr, absonco ol a donor doloct, slmpllclty, and rollablllty. 1o dato oxpandors havo boon usod to good olloct ln tho hoad and nock, tho oxtromltlos, tho trunk, and lor broast roconstruc- tlon. Lxpandors aro gonorally contralndlcatod ln aroas ol poorly vascularlzod tlssuo, vhoro thoro ls locallzod lnloctlon, or ll thoro ls a hlghor-than- avorago rlsk ol rocurront cancor. llshor and Hammond 53 rovlov tho lltoraturo ol oxpandors comblnod vlth llaps lor broast roconstructlon. Most roports ol roconstructlon by tlssuo oxpan- slon lmply movomont ol tlssuo as advancomont llaps. }oss and covorkors 54 noto that advancomont llap roconstructlon vastos tlssuo (ln dog-oars) at olthor ond ol tho doloct, and lnstoad rocommond trans- poslng tho oxpandod tlssuo lnto tho vound bod along a 90 arc (llg 2). 1ho oxpandor can bo ol any shapo but should bo tvlco as vldo as tho doloct to bo covorod. Wllmhurst and Sharpo 55 lnsort tlssuo oxpandors lmmodlatoly altor rosoctlon ol mallgnant skln loslons to comploto tho roconstructlon ln tvo oporatlons. 1ho oxclslonal bod ls tomporarlly covorod by a skln gralt. Austad 56 advocatos agalnst tlssuo oxpanslon ln acuto ln|urlos bocauso ol tho rlsk ol contamlnatlon and posslblo lnablllty to obtaln ratlonal lnlormod consont on an omorgoncy basls. Ho romlnds us that tlssuo oxpanslon rosults ln a dlstortlon ol body lmago that somo patlonts aro unablo to tolorato. COMPLICATIONS lotontlal compllcatlons ol tlssuo oxpanslon lncludo lnloctlon, homatoma, soroma, oxpandor oxtruslon, lmplant lalluro, skln nocrosls, paln, and nourapraxla. 1hoso probloms undoubtodly dolay tho roconstruc- Fig 2. Marklngs lor transposltlon llap and oxpandor placod bonoath llap and boyond. 1ho shapo ol tho ox- pandor ls lrrolovant. (Reprinted with permission from Joss GS, Zoltie N, Chapman P: Tissue expansion tech- nique and the transposition flap. Br J Plast Surg 43:328, 1990.) Fig 1. Skln oxpanslon mochanlsms. (Reprinted with permission from Siegert R, Weerda H, Hoffmann S, Mohadjer C: Clinical and experimental evaluation of intermittent intraoperative short- term expansion. Plast Reconstr Surg 92:248, 1993.) SRPS Volume 10, Number 1 42 tlvo procoss and may nocossltato lmplant romoval, but do not slgnal a catastropho vlth dlro conso- quoncos to tho patlont. Austad 56 notos a romark- ablo absonco ol dlsastors ln a survoy ol moro than 50,000 tlssuo oxpanslon procoduros, and polnts out that tho ovorall lncldonco ol compllcatlons assocl- atod vlth tlssuo oxpanslon has docroasod as sur- goons havo bocomo moro knovlodgoablo and oxporloncod ln tho routlno uso ol oxpandors. Austad rocounts lour casos ol partlal llap nocrosls altor tho oxpandor had boon romovod and tho llap advancod ovor tho doloct, and attrlbutos tho cyanosls to opl- nophrlno ln tho local anosthotlc solutlon knovn to bo dotrlmontal to tho survlval ol dolayodhonco oxpandodllaps. 57 Mandors and colloaguos 58 roport a 24° lncldonco ol ma|or compllcatlons that dolayod or compro- mlsod tho outcomo ol tholr casos ol tlssuo oxpan- slon. Mlnor compllcatlons voro notod ln 17° and lncludod paln on oxpanslon, soroma, and vldonlng ol scars. Argonta and assoclatos 18 also notod a 24° compllcatlon rato oarly ln tholr sorlos, but thls sub- soquontly loll to 7°. lnloctlon ls usually roportod ln 1° ol casos, and only ln patlonts vlth prodlsposlng lactors. 1ho most lroquont causo ol oxposuro ls an lnsulllclont pockot at tho lnltlal procoduro that lorcos tho prosthosls agalnst tho suturo llno. Sharp odgos or lrrogular lolds ln tho prosthosls should also bo smoothod out or rlsk thlnnlng ol tho sholl lrom lrlc- tlon and porhaps lmplant oxposuro. Argonta roc- ommonds valtlng lor 2 vooks altor lmplantatlon ol tho oxpandor boloro boglnnlng lnllatlon. Zoltlo and assoclatos 59 rovlov tholr oxporlonco vlth non-scalp, non-broast tlssuo oxpanslon ln 56 patlonts, and roport an ovorall lalluro ol 12°. lall- uros voro most common ln tho arm (31°) and rarost ln tho log (0°). 1hoy crodlt tholr lov lalluro rato to an oxpandor slzo tvlco as vldo as tho doloct, slov rato ol lnllatlon, aggrosslvo managomont ol any compllcatlon, and uso ol transposltlon llaps. ¥oum and covorkors 60 rovlovod rotrospoctlvoly 34 tlssuo oxpandors placod ln 30 patlonts at a Nov ¥ork Clty publlc hospltal ovor a 7-yoar porlod. Com- pllcatlons occurrod ln 22 ol 34 oxpandors (65°), nocossltatlng romoval ln 13 (38°). Cnly 12 ol 34 oxpandors (35°) voro lroo ol compllcatlons. 1ho paln assoclatod vlth tlssuo oxpanslon tonds to bo mlld and ol short duratlon, although an occa- slonal patlont may complaln ol dlsabllng paln. lntralumlnal lnstlllatlon ol lldocalno has boon sug- gostod to rollovo paln durlng oxpanslon, 61 but Slnov and Cunnlngham 62 roport no dllloronco ln paln altor oxpanslon botvoon patlonts rocolvlng lldocalno analgosla and placobo. McCulro and Calloo 63 noto that tho rato ol dllluslon ol lldocalno through an oxpandor mom- brano doponds on tho pH ol tho solutlon. Cnly by addlng sodlum blcarbonato to commorclally avallablo lldocalno to ralso lts pH to 8.0 vlll tho anosthotlc dllluso at a sulllclont rato to provldo analgosla durlng oxpanslon. Dorby and col- loaguos 64 slmllarly concludo that thls tochnlquo ol lldocalno dollvory by dllluslon across a tlssuo oxpandor sholl ºls unllkoly to provldo slgnlllcant salutary bonollt, and advlso agalnst lt bocauso ol tho potontlal lor progrosslvo lldocalno accumula- tlon¨ that could load to lldocalno ovordoso ln tho ovont ol lmplant lalluro. lnlroquont roports ol oroslon and dolormatlon ol bono undorlylng an oxpandor havo appoarod ln tho lltoraturo, spoclllcally rlb concavlty vlth tho- raclc skln oxpanslon and calvarlal dolormlty and romodollng vlth scalp oxpanslon ln chlldron. 65 lalotta 66 doscrlbos rupturo ol an oxpandor placod ln tho scalp ol a chlld causod by oroslon ol tho outor tablo ol tho skull and bono spur lormatlon lrom prossuro by tho oxpandor. CONCLUSIONS As summarlzod by ßakor, 4 tlssuo oxpanslon ls assoclatod vlth • lmprovod llap survlval • lncroaso ln vascularlty to tho skln or capsulo • probablo onhancomont ol tho blood supply ol rapldly oxpandod skln • croatlon ol addltlonal nov skln • thlnnlng ol tho dormls and subcutanoous tlssuo and corrospondlng docroaso ln tonsllo strongth • largor surlaco aroa galns vlth prolongod oxpan- slon • normallzatlon ol tho paramotors to tho proox- pandod stato vhon tho oxpanslon procoss ls dls- contlnuod SRPS Volume 10, Number 1 43 1. Cormack CC, Lamborty ßCH. The Arterial Anatomy of Skin Flaps. London, Churchill Livingstone, 1986. 2. Monlck l}. Aosthotlc rollnomonts ln uso ol lorohoad lor nasal roconstructlon. tho paramodlan lorohoad llap. Clin Plast Surg 17:4, 1990. 3. McDovoll l, Valono }A, ßrovn }ß. ßlbllography and hlstorlcal noto on plastlc surgory ol tho noso. Plast Reconstr Surg 10:149, 1952. 4. 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Am J Physiol Regulatory Integrative Comp Physiol 281:R1097, 2001. 305. Sloan CM, Sasakl CH. Nonlnvaslvo monltorlng ol tlssuo vlablllty. Clin Plast Surg 12(2):185, 1985. 306. Nollgan lC. Monltorlng tochnlquos lor tho dotoctlon ol llov lalluro ln tho postoporatlvo porlod. Microsurgery 14:162, 1993. 307. lurnas H, koson }M. Monltorlng ln mlcrovascular surgory. Ann Plast Surg 26(3):265, 1991. 308. 1ruolson }M. lorloporatlvo patlont managomont ol lroo llaps. Fac Plast Surg 12(1):13, 1996. 309. ßradlord Ck. llap monltorlng. Fac Plast Surg 12(1):19, 1996. 310. Capany M. lalllng llap. Fac Plast Surg 12(1):23, 1996. 311. ßrovn }S, Dovlno }C, Magonnls l, ot al. lactors that lnlluonco tho outcomo ol salvago ln lroo tlssuo translor. Br J Oral Maxillofac Surg 41:16, 2003. 312. Cllmo S. Dormal bloodlng and tho dolay oporatlon. Plast Reconstr Surg 8:59, 1951. 313. }onos ßM, Dunscombo lß, Croonhalgh kM. Dlllorontlal thormomotry as a monltor ol blood llov ln skln llaps. Br J Plast Surg 36:83, 1983. 314. lhourl kl, Shav WW. Monltorlng ol lroo llaps vlth surlaco-tomporaturo rocordlngs. ls lt rollablo: Plast Reconstr Surg 89(3):495, 1992. SRPS Volume 10, Number 1 51 315. Cho ßC, Shln Dl, ßyun }S, ot al. Monltorlng llap lor burlod lroo tlssuo translor. lts lmportanco and rollablllty. Plast Reconstr Surg 110:1249, 2002. 316. Akln S, ßasut C. A nov llap doslgn lor monltorlng tho clrculatlon ol a burlod lroo radlal loroarm llap ln pharyn- goosophagoal roconstructlon. J Reconstr Microsurg 18:591, 2002. 317. Lango l, ßoyd L. 1ho uso ol lluoroscoln to dotormlno tho adoquacy ol tho clrculatlon. Med Clin North Am 26:943, 1942. 318. Myors Mß. lrodlctlon ol skln sloughs at tho tlmo ol oporatlon vlth tho uso ol lluoroscoln dyo. Surgery 51:158, 1962. 319. McCrav }ß, Myors ß, Shanklln lD. 1ho valuo ol lluoros- coln ln prodlctlng tho vlablllty ol artorlallzod llaps. Plast Reconstr Surg 60:710, 1977. 320. lroldstoln ML, Lovlno kH, lnovlton k}, lang C¥. Sorlal lluoromotrlc assossmonts ol skln porluslon ln lsolatod porlusod human skln llaps. Br J Plast Surg 48:288, 1995. 321. lang C¥, ot al. Assossmont ol tho lluoroscoln dyo tost lor prodlctlon ol skln llap vlablllty ln plgs. J Surg Res 41:173, 1986. 322. Myors ß, Donovan W. An ovaluatlon ol olght mothods ol uslng lluoroscoln to prodlct tho vlablllty ol skln llaps ln tho plg. Plast Reconstr Surg 75:245, 1985. 323. Cdland kM, loolo DV, Lossard CM, ot al. lluoroscoln and acldosls. Arch Otolaryngol Head Neck Surg 118(7):712, 1992. 324. Sllvorman DC, Norton l}, ßroussoau DA. Sorlal lluoro- motrlc documontatlon ol lluoroscoln dyo dollvory. Sur- gery 97:185, 1985. 325. Suzukl ¥, lsshlkl N, lshlkava l, loyama H. Vlablllty and quantltatlvo dormolluoromotry ol oxporlmontal artorlallsod and non-artorlallsod vonous llaps. Br J Plast Surg 46:273, 1993. 326. 1homson }C, lorrlgan CL. Dormolluoromotry. 1hrosh- olds lor prodlctlng llap survlval. Plast Reconstr Surg 83:859, 1989. 327. lsslng W}, Naumann C. Lvaluatlon ol podlclod skln llap vlablllty by pH, tomporaturo and lluoroscoln. an oxporl- montal study. J Cranio-Maxillofac Surg 24:305, 1996. 328. Holm C, Mayr M, Holtor A, ot al. lntraoporatlvo ovaluatlon ol skln-llap vlablllty uslng lasor-lnducod lluorosconco ol lndocyanlno groon. Br J Plast Surg 55:635, 2002. 329. Holm C, 1ogolor }, Mayr M, ot al. Monltorlng lroo llaps uslng lasor-lnducod lluorosconco ol lndocyanlno groon. a prollmlnary oxporlonco. Microsurgery 22:278, 2002. 330. Lron S, kubbon A, lroln k, ot al. Assossmont ol mlcroclr- culatlon ol an axlal skln llap uslng lndocyanlno groon lluorosconco anglography. Plast Reconstr Surg 96:1636, 1995. 331. Stlll }, Lav L, Davson }, ot al. Lvaluatlon ol tho clrculatlon ol roconstructlvo llaps uslng lasor-lnducod lluorosconco ol lndocyanlno groon. Ann Plast Surg 42:266, 1999. 332. Amorhausor A, Moollokon ßkW, Mathos S}, ot al. 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Culdollnos lor moasuromont ol cutanoous blood llov by lasor dopplor llovmotry. Contact Dermatitis 30(2):65, 1994. 339. Svonsson H, Holmborg }, Svodman l. lntorprotlng lasor dopplor rocordlngs lrom lroo llaps. Scand J Plast Reconstr Hand Surg 27:81, 1993. 340. Sllvorman DC, ot al. Comparatlvo assossmont ol blood llov to canlno lsland llaps. Arch Otolaryngol 111:677, 1985. 341. Cummlngs CW, ot al. lrognostlcatlon ol myocutanoous llap vlablllty uslng lasor Dopplor voloclmotry and lluoros- coln mlcrolluoromotry. Otolaryngol Head Neck Surg 92:559, 1984. 342. Marks N}. Çuantltatlvo analysls ol skln llap blood llov ln tho rat uslng lasor Dopplor voloclmotry. J R Soc Med 78:308, 1985. 343. llaco M}, Wltt l, Hondrlcks D. Cutanoous blood-llov pattorns ln lroo llaps dotormlnod by lasor Dopplor llovmotry. J Reconstr Microsurg 12:355, 1996. 344. ¥uon }C, long Z. Monltorlng lroo llaps uslng tho lasor Dopplor llovmotor. llvo-yoar oxporlonco. Plast Reconstr Surg 105:55, 2000. 345. Hallock CC, Altobolll }A. Assossmont ol 1kAM llap porlu- slon uslng lasor dopplor llovmotry. an ad|unct to ml- crovascular augmontatlon. Ann Plast Surg 29(2):122, 1992. 346. Arnold l, Ho Cl, }la C¥, Chorry CW. lorluslon lmaglng ol skln lsland llap blood llov by a scannlng lasor-dopplor tochnlquo. Br J Plast Surg 48:289, 1995. 347. ¥amamoto ¥, Chura 1, Nohlra l, ot al. Lasorllovgraphy. a nov vlsual blood llov motor utlllzlng a dynamlc lasor spocklo olloct. Plast Reconstr Surg 91(5):884, 1993. 348. 1sur H, Cronstoln A, Mazkoroth k. 1ho uso ol transcuta- noous oxygon prossuro moasuromont ln llap surgory. Ann Plast Surg 8:510, 1982. 349. H|ortdal VL, Avvad AM, Cottrup l, ot al. 1lssuo oxygon tonslon moasuromont lor monltorlng musculocutanoous and cutanoous llaps. Scand J Plast Reconstr Hand Surg 24:27, 1990. 350. lorrlgan CL, Danlol kl. Monltorlng acuto skln-llap lalluro. Plast Reconstr Surg 71:519, 1983. SRPS Volume 10, Number 1 52 351. Larsson L. An oloctrophyslologlcal mothod lor monltorlng blood llov ln skolotal musclo. An oxporlmontal study ln tho rat. Scand J Plast Reconstr Surg 23:181, 1989. 352. Varnoll kM, ot al. Myocutanoous llap lalluro. oarly dotoctlon vlth Cd-D1lA-onhancod Mk lmaglng. Radiol- ogy 173:755, 1989. 353. lloln HW, Courloy lM. Uso ol magnotlc rosonanco spoctroscopy ln tho ovaluatlon ol skln llap clrculatlon. Ann Plast Surg 20:547, 1988. 354. Coldo Ak, Mahonoy }L. 1ho oxygon optodo. an lmprovod mothod ol assosslng llap blood llov and vlablllty. J Otolaryngol 23(2):138, 1994. 355. Holor SCl, 1lmmonga L}l, Chrlstlano k, ßos lL. An lntravascular oxygon tonslon monltorlng dovlco usod ln myocutanoous transplants. a prollmlnary roport. Micro- surgery 14:304, 1993. 356. Llndsoy LA, Watson }D, Çuabo AA. lulso oxlmotry ln postoporatlvo monltorlng ol lroo musclo llaps. Br J Plast Surg 44:27, 1991. 357. lrvln MS, 1hornlloy MS, Doro C}, Croon C}. Noar lnlra- rod spoctroscopy. a non-lnvaslvo monltor ol porluslon and oxygonatlon vlthln tho mlcroclrculatlon ol llmbs and llaps. Br J Plast Surg 48:14, 1995. Skin Expansion 1. ßonnott kC, Hlrt M. A hlstory ol tlssuo oxpanslon. Dermatol Surg Oncol 19:1066, 1993. 2. Noumann CC. 1ho oxpanslon ol an aroa ol skln by progrosslvo dlstontlon ol a subcutanoous balloon. Uso ol tho mothod lor socurlng skln lor subtotal roconstructlon ol tho oar. Plast Reconstr Surg 19:124, 1957. 3. kadovan C. Ad|acont llap dovolopmont uslng oxpandablo Sllastlc lmplant. Presented at the Annual Meeting of the American Society of Plastic and Reconstructive Surgeons, Boston, Mass., 1976. 4. ßakor Sk. lundamontals ol oxpandod tlssuo. Head Neck 13:327, 1991. 5. }ackson l1, Sharpo D1, lolloy }, ot al. Uso ol oxtornal rosorvolrs ln tlssuo oxpanslon. Plast Reconstr Surg 80:266, 1987. 6. Hallock CC, klco DC. Cb|octlvo monltorlng lor salo tlssuo oxpanslon. Plast Reconstr Surg 77:416, 1986. 7. Hallock CC, klco DC. lncroasod sonsltlvlty ln ob|octlvo monltorlng ol tlssuo oxpanslon. Plast Reconstr Surg 91(2):217, 1993. 8. llotllä }l, Nordström kLA, Vlrkkunon l}, ot al. Accoloratod tlssuo oxpanslon vlth tho ºovorlllllng¨ tochnlquo. Plast Reconstr Surg 81:204, 1988. 9. ßook AL, Adson MH. 1lssuo oxpanslon ln tho uppor oxtromlty. Clin Plast Surg 14:535, 1987. 10. kappard }HA, Molonaar }, Doorn D, ot al. Surlaco-aroa lncroaso ln tlssuo oxpanslon. Plast Reconstr Surg 83:733, 1988. 11. Matton CL, 1onnard lL, Monstroy S}, Landuyt lH. A unlvorsal lnclslon lor tlssuo oxpandor lnsortlon. Br J Plast Surg 48:172, 1995. 12. Austad LD, koso CL. A soll-lnllatlng tlssuo oxpandor. Plast Reconstr Surg 70:588, 1982. 13. Wloso lC. Csmotlcally lnducod tlssuo oxpanslon vlth hydrogols. a nov dlmonslon ln tlssuo oxpanslon: A prollmlnary roport. J Craniomaxillofac Surg 21:309, 1993. 14. ßorgé S}, Wloso lC, von Llndorn }-}, ot al. 1lssuo oxpanslon uslng osmotlcally actlvo hydrogol systoms lor dlroct clo- suro ol tho donor doloct ol tho radlal loroarm llap. Plast Reconstr Surg 108:1, 2001. 15. }ohnson 1M, Lovo L, ßrovn MD, ot al. Hlstology and physlology ol tlssuo oxpanslon. J Dermatol Surg Oncol 19:1074, 1993. 16. Austad LD, lasyk lA, McClatchoy lD, Chorry CW. Hlstomorphologlc ovaluatlon ol gulnoa plg skln and solt tlssuo altor controllod tlssuo oxpanslon. Plast Reconstr Surg 70:704, 1982. 17. Austad LD, 1homas Sß, lasyk l. 1lssuo oxpanslon. dlvldond or loan: Plast Reconstr Surg 78(1):63, 1986. 18. Argonta LC, Marks MW, lasyk lA. Advancos ln tlssuo oxpanslon. Clin Plast Surg 12:159, 1985. 19. lasyk lA, Argonta LC, Hassott C. Çuantltatlvo analysls ol tho thlcknoss ol human skln and subcutanoous tlssuo lollovlng controllod oxpanslon vlth a slllcono lmplant. Plast Reconstr Surg 81:516, 1988. 20. Lolghton WD, kussoll kC, lollor AM, ot al. Lxporlmontal protranslor oxpanslon ol lroo-llap donr sltos. ll. physlol- ogy, hlstology, and cllnlcal corrolatlon. Plast Reconstr Surg 82:76, 1988. 21. Clonlus M, }ohansson C. Varlatlons ln opldormal thlck- noss ln oxpandod human broast skln. Scand J Plast Reconstr Hand Surg 29(1):15, 1995. 22. Clonlus M, Dalsgaard C}, Wlckman M. Mltotlc actlvlty ln oxpandod human skln. Plast Reconstr Surg 91(2):213, 1993. 23. 1akol 1, Mllls l, Aral l, Sumplo ßL. Molocular basls lor tlssuo oxpanslon. cllnlcal lmpllcatlons lor tho surgoon. Plast Reconstr Surg 102:247, 1998. 24. kohrlch k}. lrlnclplos ol tlssuo oxpanslon. Presented at the PSEF symposium in Snowbird, Utah, Feb 16-21, 1988. 25. Molls l, Noorlandor ML, van dor Horst CM, van Noordon C}. kapld allgnmont ol collagon llbors ln tho dormls ol undormlnod and not undormlnod skln strotchod vlth a skln-strotchlng dovlco. Plast Reconstr Surg 109:674, 2002. 26. Chang ß, 1uchlor kL, Slobort }W, ot al. 1ho olloct ol tlssuo oxpanslon on dormal llbroblast contractlon. Ann Plast Surg 28:315, 1992. 27. Loo l, Squlor CA, ßardach }. Lnhancomont ol tlssuo oxpanslon by antlcontractllo agonts. Plast Reconstr Surg 76:604, 1985. 28. ßoauchono }C, ot al. ßlochomlcal, blomochanlcal, and physlcal changos ln tho skln ln an oxporlmontal anlmal modol ol thorapoutlc tlssuo oxpanslon. J Surg Res 47:507, 1989. 29. }ohnson lL, lornahan DA, ßauor ßS. Dormal and opldor- mal rosponso to solt-tlssuo oxpanslon ln tho plg. Plast Reconstr Surg 81:390, 1988. 30. lnlght lk, McCann }}, Vandorkolk CA, ot al. 1ho rodlstrl- butlon ol collagon ln oxpandod plg skln. Br J Plast Surg 43:565, 1990. 31. 1lmmonga L}l, Schoorl k, lloppor l}. ßlomochanlcal and hlstomorphologlcal changos ln oxpandod rabblt skln. Br J Plast Surg 43:101, 1990. SRPS Volume 10, Number 1 53 32. Wlckman M, Hodon l, }uroll C. Clrculatory and mota- bollc changos ln oxpandod plg skln llaps. Plast Reconstr Surg 88:650, 1991. 33. lasyk lA, Austod LD, Chorry CW. lntra-collular collagon llbors around slllcono oxpandor. J Surg Res 36(2):125, 1984. 34. Matturrl L, Azzollnl A, klbortl C, ot al. Long-torm hlsto- pathologlc ovaluatlon ol human oxpandod skln. Plast Reconstr Surg 90:636, 1992. 35. Loo ¥, Cll MS, Hong }}. Hlstomorphologlc changos ol halr lolllclos ln human oxpandod scalp. Plast Reconstr Surg 105:2361, 2000. 36. Cur L, Hanna W, Andrlghottl L, Somplo }L. Llght and oloctron mlcroscoplc ovaluatlon ol tho poctoralls ma|or musclo lollovlng tlssuo oxpanslon lor broast roconstruc- tlon. Plast Reconstr Surg 102:1046, 1998. 37. lao }1, Dagum Aß, Mahonoy }L, ot al. 1ho hlstopathologl- cal changos ln lrradlatod vs. nonradlatod tlssuo-oxpandod skln ln tho porclno modol. Ann Plast Surg 39:287, 1997. 38. Dvall L1, Dagum Aß, lang C¥, ot al. Llloct ol radlatlon on skln oxpanslon and skln llap vlablllty ln plgs. Plast Reconstr Surg 106:624, 2000. 39. Coodman CM, Mlllor k, latrlck CW }r, ot al. kadlo- thorapy. ollocts on oxpandod skln. Plast Reconstr Surg 110:1080, 2002. 40. Chorry CW, Austad L, lasyk l, ot al. lncroasod survlval and vascularlty ol random-pattorn skln llaps olovatod ln con- trollod, oxpandod skln. Plast Reconstr Surg 72:680, 1983. 41. Sasakl CH, lang C¥. lathophyslology ol skln llaps ralsod on oxpandod plg skln. Plast Reconstr Surg 74:59, 1984. 42. Saxby l}. Survlval ol lsland llaps altor tlssuo oxpanslon. a plg modol. Plast Reconstr Surg 81:30, 1988. 43. ßabovlc S, Angol Ml, lm M}, ot al. Lllocts ol tlssuo oxpanslon on socondary lschomlc toloranco ln oxporl- montal lroo llaps. Ann Plast Surg 34(6):593, 1995. 44. Vandor lolk CA, McCann }}, lnlght lk, C´ßrlon ßM. Somo lurthor charactorlstlcs ol oxpandod tlssuo. Clin Plast Surg 14:447, 1987. 45. Slogort k, Woorda H, Hollmann S, Mohad|or C. Cllnlcal and oxporlmontal ovaluatlon ol lntormlttont lntraopora- tlvo short-torm oxpanslon. Plast Reconstr Surg 92(2):248, 1993. 46. Sasakl CH. lntraoporatlvo sustalnod llmltod oxpanslon (lSLL) as an lmmodlato roconstructlvo tochnlquo. Clin Plast Surg 14(3):563, 1987. 47. Sasakl CH. lntraoporatlvo oxpanslon as an lmmodlato roconstructlvo tochnlquo. Facial Plast Surg 5:362, 1988. 48. Shaplro AL, Hochman M, 1homas }k, ßranham C. Lllocts ol lntraoporatlvo tlssuo oxpanslon and skln llaps on vound closlng tonslons. Arch Otolaryngol Head Neck Surg 122:1107, 1996. 49. Woo SS, Logan SL, Mustoo 1A. Contlnuous vorsus lntra- oporatlvo oxpanslon ln tho plg modol. Plast Reconstr Surg 90:808, 1992. 50. lutran ND. Closuro ol tho llbula lroo llap donor slto vlth tho Suro-Closuro' skln-strotchlng dovlco. Laryngoscope 106:1487, 1996. 51. Hlrshovltz ß, Llndonbaum L, Har-Shal ¥. A skln-strotchlng dovlco lor tho harnosslng ol tho vlscoolastlc proportlos ol skln. Plast Reconstr Surg 92:260, 1993. 52. Wlckman M, Clonlus M, Malm M, ot al. Altoratlons ln skln proportlos durlng rapld and slov tlssuo oxpanslon lor broast roconstructlon. Plast Reconstr Surg 90:945, 1992. 53. llshor }, Hammond DC. 1ho comblnatlon ol oxpandors vlth autogonous tlssuo ln broast roconstructlon. Clin Plast Surg 21(2):309, 1994. 54. }oss CS, Zoltlo N and Chapman l. 1lssuo oxpanslon tochnlquo and tho transposltlon llap. Br J Plast Surg 43:328, 1990. 55. Wllmshurst AD, Sharpo D1. lmmodlato placomont ol tlssuo oxpandors ln tho managomont ol largo oxclslonal dolocts on tho laco. Br J Plast Surg 43:150, 1990. 56. Austad LD. Compllcatlons ln tlssuo oxpanslon. Clin Plast Surg 14:549, 1987. 57. kolnlsch }, Myors ß. 1ho olloct ol local anosthosla vlth oplnophrlno on skln llap survlval. Plast Reconstr Surg 54:324, 1974. 58. Mandors Ll, Schondon M}, lurroy }A, ot al. Solt-tlssuo oxpanslon. Concopts and compllcatlons. Plast Reconstr Surg 74:493, 1984. 59. Zoltlo N, Chapman l, }oss C. 1lssuo oxpanslon. A unlt rovlov ol non-scalp, non-broast oxpanslon. Br J Plast Surg 43:325, 1990. 60. ¥oum 1, Marglotta M, lasablan A, larp N. Compllcatlons ol tlssuo oxpanslon ln a publlc hospltal. Ann Plast Surg 42:396, 1999. 61. Cohon ll, koborts C. Lldocalno rollovos paln vlth tlssuo oxpanslon ol tho broast (lottor). Plast Reconstr Surg 79:489, 1987. 62. Slnov }D, Cunnlngham ßL. lntralumlnal lldocalno lor analgosla altor tlssuo oxpanslon. A doublo-bllnd prospoc- tlvo trlal ln broast roconstructlon. Ann Plast Surg 28:320, 1992. 63. McCulro }}, Calloo HH. ln vlvo dllluslon ol lldocalno through tlssuo oxpandors. Plast Reconstr Surg 89:675, 1992. 64. Dorby LD, Slnov }D, ßovors LD, Cunnlngham ßL. Çuan- tltatlvo analysls ol lldocalno hydrochlorldo dollvory by dllluslon across tlssuo oxpandor mombranos. Plast Reconstr Surg 89:900, 1992. 65. Calobraco Mß, Dovnoy SL. Calvarlal dolormlty and romodollng lollovlng prolongod scalp oxpanslon ln a chlld. Ann Plast Surg 39:186, 1997. 66. lalotta CL, ßass }, Shohadl Sl. Cutor tablo skull oroslon causlng rupturo ol scalp oxpandor. Ann Plast Surg 23:538, 1989. SKIN GRAFTS AND SKIN SUBSTITUTES James F Thornton MD HISTORY OF SKIN GRAFTS Ratner1 and Hauben and colleagues2 give excellent overviews of the history of skin grafting. The following highlights are excerpted from these two sources. Grafting of skin originated among the tilemaker caste in India approximately 3000 years ago.1 A common practice then was to punish a thief or adulterer by amputating the nose, and surgeons of their day took free grafts from the gluteal area to repair the deformity. From this modest beginning, skin grafting evolved into one of the basic clinical tools in plastic surgery. In 1804 an Italian surgeon named Boronio successfully autografted a full-thickness skin graft on a sheep. Sir Astley Cooper grafted a full-thickness piece of skin from a man’’s amputated thumb onto the stump for coverage. Bunger in 1823 successfully reconstructed a nose with a skin graft. In 1869 Reverdin rekinkled worldwide interest in skin grafting with his report of successful pinch grafts. Ollier in 1872 pointed out the importance of the dermis in skin grafts, and in 1886 Thiersch used thin splitthickness skin to cover large wounds. To this day the names Ollier and Thiersch are synonymous with thin (0.005––0.01-inch) split-thickness grafts. Lawson, Le Fort, and Wolfe used full-thickness grafts to successfully treat ectropion of the lower eyelid; nevertheless, it is Wolfe whose name is generally associated with the concept of fullthickness skin grafting. Krause popularized the use of full-thickness grafts in 1893, known today as Wolfe-Krause grafts. Brown and McDowell3 reported using thick splitthickness grafts (0.01––0.022-inch) for the treatment of burns in 1942. In 1964 Tanner, Vandeput, and Olley4 gave us the technology to expand skin grafts with a machine that would cut the graft into a lattice pattern, expanding it up to 12X its original surface area. In 1975 epithelial skin culture technology was published by Rheinwald and Green,5 and in 1979 cultured human keratinocytes were grown to form an epithelial layer adequate for grafting wounds.6 ANATOMY The character of the skin varies greatly among individuals, and within each person it varies with age, sun exposure, and area of the body. For the first decade of life the skin is quite thin, but from age 10 to 35 it thickens progressively. At some point during the fourth decade the thickening stops and the skin once again begins to decrease in substance. From that time until the person dies there is gradual thinning of dermis, decreased skin elasticity, and progressive loss of sebaceous gland content. The skin also varies greatly with body area. Skin from the eyelid, postauricular and supraclavicular areas, medial thigh, and upper extremity is thin, whereas skin from the back, buttocks, palms of the hands and soles of the feet is much thicker. Approximately 95% of the skin is dermis and the other 5% is epidermis.7 The dermis contains sebaceous glands and the subcutaneous fat beneath the dermis contains sweat glands and hair follicles. The skin vasculature is superficial to the superficial fascia and parallels the skin surface. The cutaneous vessels branch at right angles to penetrate subcutaneous tissue and arborize in the dermis. The final destination of these blood vessels is a capillary tuft that terminates between the dermal papillae. TERMINOLOGY An autograft is a graft taken from one part of an individual’’s body that is transferred to a different part of the body of that same individual. An isograft is a graft from genetically identical donor and recipient individuals, such as litter mates of inbred rats or identical human twins. An allograft (previously homograft) is taken from another individual of the same species. A xenograft (heterograft) is a graft taken from an individual of one species that is grafted onto an individual of a different species. A split-thickness skin graft (STSG) contains epidermis and a variable amount of dermis. A fullthickness skin graft (FTSG) includes all of the dermis as well as the epidermis8 (Fig 1). The donor site SRPS Volume 10, Number 1 Fig 1. Split-thickness skin grafts include a variable amount of dermis. Full-thickness grafts are taken with all the dermis. (Reprinted with permission from Grabb WC: Basic Techniques of Plastic Surgery. In: Grabb WC and Smith JW: Plastic Surgery, 3rd Ed. Boston, Little Brown, 1979.) of an FTSG must be closed by either direct suture approximation or skin graft. PROPERTIES OF SKIN GRAFTS Skin grafts have been used for over a century to resurface superficial defects of many kinds. Whether intended for temporary or permanent cover, the transplanted skin does not only protect the host bed from further trauma, but also provides an important barrier to infection. Thin split-thickness skin grafts have the best ““take”” and can be used under unfavorable conditions that would spell failure for thicker split-skin grafts or fullthickness grafts. Thin STSGs tend to shrink considerably, pigment abnormally, and are susceptible to trauma.9 In contrast, full-thickness grafts require a well-vascularized recipient bed9 until graft perfusion has been reestablished. FTSGs contract less upon healing, resist trauma better, and generally look more natural after healing than STSGs. Rudolph and Klein9 review the biologic events that take place in a skin graft and its bed. An ungrafted wound bed is essentially a healing wound which, left alone, will undergo the typical processes of granulation, contraction, and reepithelialization to seal its surface. When a skin graft is placed on a wound bed, these processes are altered by the presence of the graft.10 Marckmann11 studied biochemical changes in a skin graft after placement on a wound bed and noted similarities with normal skin in its response to physical or chemical injury and aging. The changes in wound healing brought about by the skin graft can also be described as a general adaptation of connective tissue to a diminished blood supply.11 EPIDERMIS In the mid-1940s Medawar studied the behavior and fate of healing skin autografts.12––14 His findings can be summarized as follows. Histologic Aspects During the first 4 days postgraft there is tremendous activity in the graft epithelium, which doubles in thickness and shows crusting and scaling of the graft surface. Three cellular processes may explain this thickening: 1) swelling of the nuclei and cytoplasm of epithelial cells; 2) epithelial cell migration toward the surface of the graft; and 3) accelerated mitosis of follicular and glandular cells.10 By the third day after grafting there is considerable mitotic activity in the epidermis of a split-thickness skin graft, whereas mitotic activity in full-thickness skin grafts is much less common and may be totally absent——a reflection of their less-efficient early circulation. Between the fourth and eighth days after grafting there is great proliferation and thickening of the graft epithelium associated with obvious desquamation. Epithelial thickness may increase up to sevenfold, with rapid cellular turnover. At the same time the surface layer of epithelium exfoliates and is replaced by upwardly migrating cells of follicular epithelium at an accelerated rate. This heightened mitosis does not begin to regress until after the first week postgrafting. By the end of the fourth week 2 29 In addition. stubby. The authors noted falling fibrocyte numbers in the first 3 days after grafting. it is now well established that most of the collagen in a graft is ultimately replaced. pregraft states over the ensuing weeks. Fibrous component Medawar12. and have begun to fragment.19. first in the graft bed and later in the graft itself. STSGs replace only half as much of their original collagen as do FTSGs of equal size.16 Early investigators believed that these cells came from large mononuclear cells in the blood.15 By the fourth day postgraft RNA content increases greatly in the basal layers of epithelium. After this early burst in fibroblastic activity.20 on the other hand. and Cramer. After day 3 fibroblast-like cells began to appear. The remaining fibrocytes lay in two narrow layers. Klein21. On the basis of studies involving tritiated proline-labeled mature collagen. most authors are convinced that active fibroblasts in a healing skin graft do not come from indigenous fibrocytes. one beneath the dermis––epidermis junction and the other just above the host bed. Histochemical Aspects The RNA content of graft epithelial cells changes little in the first few days postgraft. Number 1 postgraft the epidermal thickness has returned to its normal.22 and Peacock23 used hydroxyproline to determine the collagen content of grafted wounds. Elastin fiber integrity is maintained through the third postgraft day. pregraft state. Udenfriend27 and Rudolph and Klein28 agreed that 85% of the original collagen in a graft is replaced within 5 months postgraft. The replacement continued through the 21st postgraft day. Although Hilgert’’s cycle lasted 10 days and Marckmann’’s 14––21 days.19 Elastin degeneration continues through the third postgraft week until new fibers can be seen beginning to grow at 4––6 weeks postgraft.24 Independent studies by Hilgert25 and Marckmann26 confirmed these findings and documented plunging levels of hydroxyproline soon after grafting. the elastin turnover rate in a healing graft is considerable. Hydroxyproline is an amino acid found exclusively in collagen at a constant proportion of 14%. The hydroxyproline (collagen) level eventually rebounded and finally returned to the normal levels of unwounded skin.13 stated that most of the collagen in an autograft persists through the 40th day after grafting. and by the seventh day all of the collagen was replaced by new small fibers. Whatever their origin. In their experiments the dermal collagen became hyalinized by the third or fourth day postgraft. Converse and Ballantyne18 studied cell viability in rat skin grafts by assaying levels of diphosphopyridine nucleotide diaphorase. paralleling the hyperactivity of epithelial cells caused by acceleration of protein synthesis during a period of rapid cellular replication. but by postgraft day 7 the fibers are short. the enzyme levels rebound. The rates of collagen turnover and epithelial hyperplasia peaked simultaneously in the first 2––3 weeks postgraft. The collagen turnover rate of grafts is 3X to 4X faster than that of unwounded skin. Hinshaw.and splitthickness skin grafts. an indicator of active electron transport. although equal amounts of collagen are lost from full.15 Over the first 2 to 3 days enzymatic activity progressively decreases in split-thickness skin grafts. both fibroblast numbers and enzyme levels resumed their normal. while Grillo17 theorized that they originated from local perivascular mesenchymal cells.SRPS Volume 10. but as new blood vessels enter the dermis––epidermis junction.and split-thickness grafts. and most of the elastin in a graft is replaced within a short time. This replacement process is the same in full. While the elastin content of the dermis is small. By the 10th day postgraft the RNA level returns to normal. and by the end of the sixth week postgraft all the old dermal collagen had been completely replaced. concluded that split-thickness and fullthickness skin autografts undergo considerable collagen turnover. Elastin fibers in the dermis account for the resilience of skin. however. By the seventh to eighth day postgraft the fibroblast population and enzymatic activity were greater than in normal skin. DERMIS Cellular component The source of fibroblasts in a skin graft remains obscure. Changes in hydroxyproline and monosaccharide content of grafted beds paralleled those of other healing wounds. 3 . Miller. migration. and hair follicles. subsequent hair growth will be sparse. when graft take is interrupted for any reason. oil secretion. Plasmatic Imbibition The exact significance of plasmatic imbibition to the healing of a skin graft is not clear. ischemic tissue. The first determinant is the blood supply of the skin from which the graft was obtained.8 Only full-thickness grafts. Hair follicles are subjected to the same hyperplastic stimuli as the rest of the graft.34.12 Full-thickness skin grafts produce hair while splitthickness skin grafts produce little or no hair. Both kinds of proteins appear to be involved in directing the behavior of keratinocytes and in promoting appropriate communication between keratinocytes and fibroblasts. random. FTSGs contain sweat glands. unlike STSGs. all concur in the following: • The graft is ischemic for an undetermined period of time that varies according to the wound bed: 24 hours for a graft placed on a bed that is already proliferative. The second factor in graft take is the metabolic activity of the skin graft at the time of application. The success of a graft depends primarily on the extent and speed at which vascular perfusion is restored to this parasitic. Skin graft take occurs in three phases. are capable of sweating.and split-thickness skin grafts demonstrate sebaceous gland activity. This is followed by an inosculatory phase and a process of capillary ingrowth that occur essentially simultaneously until generalized blood flow has been established by the fifth or sixth postgraft day. the ECM influences cellular behavior in adjacent tissues with regard to proliferation.37 thought that it merely prevents the graft from drying out and keeps the graft vessels patent in the early postgraft period. baby-like hair is seen growing out of the graft. two qualities of a skin graft influence its fate.30 Through specific arrangements of protein sequences within. therefore. Similarly. On the fourth day postgraft the original hair sloughs off and the graft becomes hairless.14 In summary. differentiation. Thus a graft that is placed on the abdomen will sweat in response to physical activity. A skin graft will sweat much like its recipient site due to ingrowing sympathetic nerve fibers from the graft bed. while Clemmesen. and follicular clustering. Soon after the graft follicles begin to produce new hair. A graft harvested from a highly vascular donor site will predictably heal better than a graft taken from a poorly perfused area. pigmentation. The first phase consists of plasmatic imbibition and lasts 24–– 48 hours. whereas an identical graft placed on the palm will sweat in response to emotional stimuli. Epithelial Appendages The sweating capability of grafted skin is a function of the number of sweat glands transplanted during grafting and of the extent of sympathetic reinnervation to the graft.33 Converse. and lacking in pigment. Although both full.SRPS Volume 10. GRAFT TAKE The large array of physiologic events usually seen in a healing skin wound are altered and modified by placement of a graft. the extracellular matrix (ECM) plays a vital role in cellto-cell communication. The extracellular matrix in the skin consists of large insoluble proteins of fibroblast origin and smaller soluble proteins produced by either fibroblasts or keratinocytes. 4 . The graft becomes incorporated in the host bed through the process of graft ““take””. and by the 14th postgraft day very fine. Given equal clinical and technical conditions. Number 1 Extracellular Matrix Far from simply supporting cells passively. Fullthickness skin grafts that take well grow normal hair in terms of orientation.13 Inadequate revascularization will damage the graft hair follicles and result in decreased hair density. which will dictate its tolerance to the inevitable period of ischemia. Hinshaw and Miller 19 and Pepper 31 believed that plasmatic imbibition is nutritionally important. and hair growth.32.35 and Peer36. thin splitthickness grafts do not contain functional sebaceous glands and typically appear dry and brittle after take. and attachment. 48 hours for a graft covering a fresh wound. sebaceous glands. Regardless of whose theory is correct. 35. Exactly how long a graft will tolerate this ischemic interval is unclear. Wolff and Schellander 48 measured cellular enzymes to evaluate return of circulation in porcine skin grafts. injected India ink into the host vessels of the autograft. Connection of graft and host vessels. but thick FTSGs seem to tolerate ischemia for up to 3 days while thin FTSGs survive for up to 5 days.46 Ljungvist and Almgard.35 The origin of graft edema is believed to be the same as that of inflammatory edema——ie.38––40 among others. as evidenced by progressive loss of diaphorase activity during this time. Converse and Rapaport43 studied skin grafts in humans and noted an early connection of graft and host vessels——the inosculatory event——after which there was active invasion of the graft by host vessels to produce the definitive vasculature of the graft. ATP activity correlated well with the pattern of new vessel ingrowth.42 and Birch and Branemark. Revascularization Three theories have been put forth to explain how a skin graft is revascularized. from disaggregation and depolymerization of proteoglycans.37 • Plasmatic imbibition allows a graft to survive this immediate postgraft ischemic period until such time as graft vasculature is reestablished. Zarem et al46 theorized that preexisting graft vessels served only as nonviable conduits through which the endothelium of the ingrowing vessels progressed. According to this theory. On the basis of a later study in a rat model involving diaphorase. The second theory of graft revascularization holds that the graft is perfused through new vessels going from the recipient bed into the transplanted graft. indicating patent connections between vessels of the graft and its bed. No ink was seen within the graft on the first postgraft day.33––35 adding as much as 40% to their pregraft weight through fluid movement from bed to graft. The first theory holds that after the inosculatory event.18. Peer and Walker.33 Haller and Billingham. leading the authors to conclude that the new graft vasculature consisted entirely of ingrown vessels. Blood flow is established and the skin graft becomes pink.47 and Wolff and Schellander48 espouse this theory.43––45 Zarem.37 Split-thickness grafts take well even after 4 days of ischemia. accumulation of osmotically active metabolites. a fine vascular network is established in the fibrin layer between the graft and its recipient bed.36 Clemmesen. the definitive vasculature of a graft consists of the blood vessels originally present within the graft. Working on mice.18 Converse concluded that the final vasculature of a graft stemmed from ingrown vessels from the host bed. Initially a fine fibrin mesh linked the graft to the bed. and increased vascular permeability. Converse.9 • Grafts gain weight during the phase of plasmatic imbibition. but over the first 4 days this meshwork became lined with endothelial cells and linked up with the vessels of the graft. leaving only those vessels growing from the recipient bed as the graft’’s definitive vasculature. With subsequent vessel ingrowth there was return of diaphorase activity. but on day 2 a number of graft vessels contained India ink. They too noted that the pattern of vessels in the healed graft was the same as the pattern before grafting. 5 . The original graft vessels degenerated concomitantly and at the same rate.32. Clemmesen.33 working on a porcine model. suggesting communication between the host and graft vessels. Formation of new vascular channels. The rate of vessel ingrowth was measured at approximately 5 microns per hour.32.38––41 Inosculation and Capillary Ingrowth At the end of 48 hours. Number 1 • Grafts placed on poorly vascularized beds will be ischemic for a longer time than those placed on wounds with good blood supply. Haller and Billingham42 reached a similar conclusion in a study involving the hamster cheek pouch model. endorse this line of thinking. Capillary buds from the blood vessels in the recipient bed make contact with the graft vessels and open channels are formed.SRPS Volume 10. Degenerative changes in the original graft vasculature were apparent in the first 4 days postgraft. circulation is restored in a graft via the original skin graft vessels by anastomoses formed between the recipient bed and the skin graft through inosculation. After the second day many graft vessels contained India ink. 38. There are two methods of skin graft revascularization: primary and secondary. Whatever flow there is within the graft is sluggish. the ischemic period is extended and capillary proliferation in the bed continues. The mechanism of secondary revascularization is as follows.51 At this point the proper vascular system within the graft is reestablished and blood flow is restored. in the periphery of large grafts——the inhibiting effect does not take place. Within the graft itself the vessels may be functionally deficient or the vascular ingrowth may not reach the required level of biologic activity for the inosculatory event. Sometime between days 4 and 7 postgraft. Blood vessels from the recipient bed attach to both arteries and veins of the graft. the vasoactive agent directing the ingrowth of new blood vessels ceases to function and capillary proliferation stops as good blood flow is established by neovascularization. tight. hematoma. silvery sheen on the surface reflecting the large amount of cicatrix within the graft. if not. The old vessels of the graft are dilated and denervated and some of the circulatory routes are severed during graft harvest. insufficient vascular proliferation and wound contamination are the two common causes of delayed inosculation. Anastomoses may not form at the right time because of the increased distance between the graft and its bed from interposed necrotic material. Vascular connections between the graft bed and the graft inhibit the formation of capillary buds. and certain areas show the typical appearance and desquamation where the secondary process occurs. in any graft old vessels may be recycled and new ones may grow to variable degrees. In the host bed. Large grafts often heal both by primary and secondary revascularization. secondary revascularization occurs. However. and other vessels retain their capillary-like character or simply disappear. This phenomenon is known as secondary revascularization.SRPS Volume 10. or air bubbles. a thick fibrin layer. and with attendant pooling and pendulum-like movement. Under the scanning electron microscope it can be seen that no real circulation to the graft exists for the first 6 to 7 days postgrafting. and have a slick. although the intensity of coloration does not allow any conclusions regarding the graft’’s circulatory status. great numbers of new capillaries grow into the graft and granulation tissue accumulates under the graft. Smahel10 and Tsukada49 proposed a third (and much less popular) hypothesis of graft revascularization: a compromise between the two above theories. A pink color is generally considered a sign of probable graft survival. the longer the vasoactive substance remains in the tissue. the newly formed vascular connections differentiate into afferent and efferent vessels. If the graft is not well applied to the bed and vascular connections are not established early—— eg. The papillary dermis is replaced by a thin layer of connective tissue. When vascular connections between the bed and the graft are delayed. Under normal graft conditions. the graft will survive. seroma. Degenerative processes in the graft and exuberant granulation tissue in the host bed go hand in hand with prolonged ischemia.50 Clinically this manifests as cyanotic discoloration and is particularly noticeable in full-thickness skin grafts. yet all these connections are afferent with respect to the graft. that is. fibrotic. Blood enters the graft via these newly formed vascular connections and the graft turns pink. The reticular dermis is normal histologi- 6 . Blood and tissue fluids moving into the graft are trapped there and unable to return to the bed because of inadequate reverse circulation. These two pathways to restore circulation to ischemic tissue may occur simultaneously or as consecutive stages in the interaction between the graft and its bed. Grafts that heal by secondary intention are smooth. The authors speculated that circulation in a graft is reestablished in various ways. the longer a graft remains ischemic. Secondary revascularization. which in turn is covered by a flattened epidermis. Primary revascularization. As a result.18. If blood vessels reach the graft in time. Number 1 Combined old and new vessels. Inside the graft the hemodynamic situation is complex. the graft will fail. shifting direction.43 In the normal course of events circulation in a skin graft is reestablished through vascular anastomoses between budding neovessels from the bed and those already present in the graft (inosculation). Histologically the epidermis and papillary dermis are destroyed by necrosis in the full-thickness graft that heals by secondary revascularization. If anastomoses fail to develop in time. on the 7 . numbness. donor sites for nasal tip grafting have included the concha. and the superficial layer is replaced in its original site.52 Tiem55 advocates a bilaminar harvest whereby an epithelial flap is raised. Tiem reports improved donor site management and fewer pigmentary changes with this method than with conventional harvest. 2) whether the intended donor site matches the recipient bed in color. and itching. postauricular area. (With permission from Shiffman MA: Re: Cervicomental ““turkey gobbler””: a new source for full-thickness grafts (letter). if not impossible.SRPS Volume 10. This is known as the trapdoor or dermatome technique. and clavicular region.) ““the elliptical method [was associated with] less discomfort. and supraclavicular areas. resulting in graft fibrosis. the neck.””56 Common full-thickness graft donor sites are the groin. Figure 2 illustrates two patterns of skin graft harvested from the submental.57 Yildirim and coworkers57 also recommend the preputium as a source of graft skin in children. Number 1 cally. Fig 2. STSGs obtained from a shaved scalp. Splitskin grafts are usually harvested from the outer thigh because surgeons prefer this site for its technical ease and convenience of intraoperative positioning and postoperative dressings. often yield very good results.54 Historically. The turkey gobbler deformity as a source of skin grafts. ““turkey gobbler”” area. Beck and colleagues56 compared the trapdoor technique with standard elliptical excision in 52 patients (60 graft sites). Any skin graft taken below the clavicles and applied above the clavicle will result in a lifelong color mismatch that is extremely difficult.53 For large. and 3) potential morbidity of graft harvest at that site. SKIN GRAFTING TECHNIQUES Donor Site Selection and Graft Harvest The selection of a graft donor site is based on three factors: 1) whether a full-thickness skin graft or a split-thickness skin graft is to be used. The public. in particular. The scars were concealed better and less noticeable. pre. donor sites should be carefully chosen to avoid hair-bearing skin and to camouflage the resulting scar. Although both techniques were successful and had minimal complications. texture change. to correct. Graft reconstruction of the nasal tip requires specialized skin of similar thickness and pore size.54 To minimize morbidity from graft harvest.52 Both full. Hinshaw and Miller19 noted accelerated collagen turnover in pig autografts that had healed by secondary revascularization. full-thickness defects above the clavicle. which is another good source of graft skin. Dermatol Surg 28:1099. A U-shaped excision results in dogears that may be visible laterally.and postauricular skin. tissue expansion is recommended to recruit an adequate volume of FTSG. 2002. The glabella provides just such skin. a dermal graft is taken. but beneath the graft there is a layer of newly formed connective tissue that infiltrates the dermis.and split-thickness skin grafts can be harvested above the clavicle. nasolabial fold. A triangular excision eliminates the dogear problem but yields less skin. An appropriate color match is particularly important in head and neck reconstruction with skin grafts. A piece of cardboard is placed on the defect and the moisture blot is traced. (2) the contour of the meshed graft can be adapted to fit in a regular recipient bed. including pinch grafts. The cutout pattern is then placed on the skin graft donor site and outlined.69––74 and the Chinese technique of intermingling autografts and allografts.62 relay transplantation. This process may be repeated up to 4 times.61 A wound is reepithelialized from the edges toward the center. (4) in the event of localized bacterial contamination. (3) blood and exudate can drain freely through the interstices of a meshed graft. traced with a marking pen. With graft expansion. Pinch grafts are reported to be effective in treating small.60 A simple and reproducible technique consists of placing cardboard in the wound to develop a blotter pattern61 (Fig 3).) 8 .64––67 Meek island grafts. larger areas can be covered with smaller sections of skin. Plast Reconstr Surg 112:335.58 Graft Sizing and Expansion Techniques for sizing skin grafts usually involve preformed templates of easily available materials. 64––66 The main disadvantages of meshed grafts are the considerable surface area Fig 3.62 Relay transplantation consists of cutting a graft into strips 3––6 mm wide and 5––10 mm apart. The cutout is then applied over the donor site.78 radiodermatitis.59. Number 1 other hand.63 meshing. the original strips are removed and transplanted.SRPS Volume 10.75.63 Meshing is the term used for cutting slits into a sheet graft and stretching it open prior to transplantation. (5) a meshed graft offers multiple areas of potential reepithelialization. An expanded graft presents a larger perimeter through which epithelial outgrowth can proceed. (With permission from Putterman AM: Blotter technique to determine the size of skin grafts (letter). leaving the epithelial explants in place. and small burns. such as cardboard and latex. therefore the perimeter of the graft is the only part that contributes to the epithelialization process. Meshed grafts have a number of advantages over sheet grafts: (1) meshed grafts will cover a larger area with less morbidity than non-meshed grafts. When the epithelial growth becomes clinically obvious 5 to 7 days later. 2003. pressure sores.68 microskin grafts. and a graft of the outlined area is resected. only a small area of meshed graft will be jeopardized.to medium-size venous leg ulcers. would prefer that grafts be taken from their buttocks to avoid visible scars.77. Various techniques to expand skin for grafting have been described.76 A pinch graft breaks up a whole graft of skin into tiny pieces to increase the edge area. Netscher and associates85 suggest wrapping the graft area in nonadherent gauze mesh over which Reston self-adhering foam is secured. Smoot91 uses a Xeroform sandwich filled with molded cotton balls stapled in place. The foam is easy to apply directly on the graft and is biologically inert. Fleming. Novel methods of graft fixation abound. Other suggested fixation methods for grafts include silicone rubber dressings94 and silicone gel sheets. and effectiveness in wound coverage as advantages of this method. and shear force tend to work against graft take. versatile.100––102 9 . and Avery89 opt for a simple. and are particularly well suited for grafting granulating wounds and unstable beds. and noted significantly less scar contracture with the former. Ingenious ways to mesh skin grafts when a mesher is not available have been reported.79. sterility. Cheng and colleagues93 use a disk cut from the bottom of an IV infusion bottle on which multiple radial slits are made in the perimeter for tying the sutures holding the graft. leading the authors to recommend harvesting skin grafts larger than needed to compensate for the eventual shortage. and rapid technique consisting of staples and latex foam dressing to secure skin grafts. infection. Number 1 that must heal by secondary intention and the lessthan-ideal cosmetic result. Several authors report successful coverage of burn wounds with microskin grafts. a semipermeable. Wolf and coworkers90 confirmed the effectiveness of rubber foam with staple fixation in various patterns to provide even pressure distribution on skin grafts. Graft Fixation Adherence of the graft to its bed is essential for skin graft take. Intermingled transplantation of autograft and allograft has been practiced successfully in China since at least 1973. nonwoven polyurethane foam dressing. The authors cite ease of application and removal. 96 transparent gasbag tie-over dressings. When dealing with skin grafts to the penis and scrotum.68 The expansion ratio obtained with the Meek technique is almost 1:9. Graft take is said to be excellent even in difficult beds. In contrast.5——and pulling the graft lengthwise to narrow the skin perforations to slits before transplantation lessens these problems.84 During this time the graft remains adherent to the bed through the bond formed by the fibrin layer.SRPS Volume 10.76 mostly in the treatment of large burns.81 The Meek technique involves a special dermatome and prefolded gauzes for expanding small pieces of split skin. Both systems delivered approximately 50% of the anticipated skin expansion.75.83 Factors such as bleeding. Meek grafts are useful alternatives to meshed grafts when donor sites are limited. Johnson. A thin fibrin layer holds the graft to the bed and forms a barrier against potential infection. A small ratio of expansion——1:1. The foam maintains penile length and gently but firmly compresses the skin graft during the crucial first week. the expansion ratio of allograft meshed with the Zimmer II dermatome set at 1:6 is actually 1:4. Its hydrophobic outer surface is said to retard bacterial colonization.97 Coban self-adherent wrap. Yeh and colleagues82 compared this technique with the microskin method in a rat model. Saltz and Bowles 86 and Caldwell and colleagues87 also advocate the use of Reston foam applied over Xeroform gauze for securing skin grafts to wounds on the shoulder and face.98 thin hydrocolloid dressings.99 and assorted Silastic and foam dressings for grafts to the neck or hand. which are particularly difficult to immobilize and dress.80 Kirsner and associates conclude that meshed STSGs are safe and effective therapy for recalcitrant leg ulcers. while Amir et al92 modify a cutoff disposable syringe to affix the silk threads of their graft dressings.69––74 These are sheet grafts that are minced with a Tanner-Vandeput dermatome to achieve an expansion ratio of 1:10. respectively. Other healing parameters were similar between the two groups. Phase 1 begins immediately after grafting and lasts about 72 hours. Balakrishnan88 prefers Lyofoam. Two distinct phases of graft adherence occur.95 rubber band stents.65 Richard and colleagues67 compared the Tanner and Bioplasty skin graft meshing systems with respect to their respective expansion ratios and predicted versus actual expansion. Phase 2 coincides with the onset of fibrovascular ingrowth and vascular anastomoses between the graft and the host. tissue conservation. electrolytes.125 and deep burns down to muscle fascia or fat (when combined with allogeneic cultured epithelial grafts). controls fluid loss. but all the dressed wounds showed some microbial flora. there was a dramatic decrease in bacterial colonization.123. reduces pain and fever. epidermal cells in the autograft gradually replace the allograft. they form a barrier against bacterial invasion and prevent further loss of water. As discussed above. Disadvantages are lack of antimicrobial activity. and does not promote wound infection. however. The total time of bolster application can be reduced from 5 to 3 days while the patient maintains mobility of the extremity. As rejection unfolds. and produces better esthetic results. and expense. in Wood’’s opinion.114––117 and are a good option in difficult-to-bolster areas such as the hand and axilla. reduces blood loss. leading the authors to conclude that it was the antibiotic. Allen and coworkers 118 compared bacterial counts of wounds left open to granulate and of wounds covered by skin dressings. 119 Biologic Dressings Autografts Feldman120 recommends returning unused skin to the donor site as an autologous biologic dressing on the grounds that this is logical in terms of wound healing. Cadaver skin serves as temporary wound cover. Number 1 Dressings for specific applications include a dorsal and ventral sandwich bolster for grafts on the tongue. Negative-pressure dressings (VAC device [KCI. potential for absorption of toxic breakdown products. Allografts decrease bacterial counts of underlying tissues and facilitate future grafting by promoting a sterile wound bed. transparent. When antibiotics were added.122 Glycerol-treated cryopreserved allografts have a number of applications such as in the treatment of scald burns in children. Proponents of fibrin glue say that it improves graft survival. hemostatic.127 The main drawback of glycerol-preserved allografts is their expense. Texas]) also enhance graft adherence and survival. Wood121 agrees that this is a good idea in immunocompromised or steroid-dependent patients. no proof that they promote reepithelialization. and promotes wound healing.126. Donor Site Management Open Wound Technique The open-wound technique of donor site management is associated with prolonged healing time.and allograft. and easy sterilization. Most authors recommend dressing the donor site of a skin graft to protect it from trauma and infection. that had a sterilizing influence. but unnecessary in the general population. more pain. They found 12.105 Modern bolster technologies of skin graft fixation replace sutures and staples with either fibrin glue106––111 or octyl-2-cyanoacrylate (““super glue””) on the edges of the graft.112. As the grafts revascularize. and a higher risk of complications than if the wound is covered. Chinese investigators have successfully used combinations of allografts and autografts for coverage of open wounds.103 a cutout tie-over dressing of elastic tape with silk threads on which a bolster is placed.124 extensive burns in both children and adults.5% of open wounds were sterile.75––77 The autograft is cut into small pieces and placed in the slits of meshed allografts.111 Our experience at The University of Texas Southwestern Medical Center bears out this assertion: A thin layer of fibrin glue improves graft take considerably.113 Fibrin glue is strong. Allografts Traditionally cadaver allografts have been the choice for resurfacing large denuded areas. speeds reconstruction by allowing large sheet-graft coverage. increases appetite. The advantages of xenografts are relatively low cost. particularly in the head and neck and mobile body parts. ready availability. or is laid down in alternating strips of auto.104 and malleable ear dressings constructed of siliconelined bandage with thin metal backing.SRPS Volume 10. restores function. and poor 10 . Careful planning before surgery to harvest only the required amount of skin is the ultimate solution. easy storage. not the dressing.128 Xenografts Xenografts (collagen––elastin prostheses) adhere to a wound bed via fibrin bonding. and protein from the wound. San Antonio. Skin grafts have no intrinsic bactericidal properties. does not interfere with healing. and DuoDERM. and less discomfort with Xeroform. and fine mesh gauze impregnated with Scarlet Red or Vaseline. Xeroform had an average healing time of 10. Tegaderm. for DuoDERM. Wounds covered with fine mesh gauze healed in 10. but was associated with 29% more infections and very high cost ($102.131 Barnett and coworkers132 compared synthetic adhesive. relatively painless healing and low infection rates. infection. particularly with movement. and cost. Poulsen and colleagues136 found Jelonet superior to Op-Site in the treatment of partial-thickness burns both in terms of speed of healing (7 vs 10 days) and residual scars (8% vs 21%).46 days. pain. no infections. it was 15. semiocclusive. and optimizes healing times. Op-Site was the most comfortable dressing and the most expensive. the authors note that OpSite was associated with low discomfort. Jelonet. donor site wounds dressed with Op-Site and Tegaderm showed rapid. Biobrane was more comfortable than Xeroform. infection.) Wounds dressed with Jelonet healed quickly. and exposure in terms of healing time.) Synthetic wound dressings can be semiopen. Semiocclusive dressings are impermeable to bacteria and liquids. although its expense is considerable. TABLE 1 Dressings for Skin Graft Donor Sites (Annotated with permission from Feldman DL: Which dressing for split-thickness skin graft donor sites? Ann Plast Surg 27:288. Recommendations from the authors were for Op-Site or Jelonet for dressing small donor areas and for Vaseline gauze to cover large wounds. Vaseline gauze was second to exposure in low cost. so fluid tends to collect beneath the dressing and must be drained frequently. and infection. ZapataSirvent134 compared Biobrane and Scarlet Red and found Biobrane to be better at controlling pain and exudate accumulation.16). and expense. with shorter healing times. A large comparison study of STSG donor site healing under Xeroform and Jelonet dressings showed no difference in mean time from harvest to healing.137 Nemeth et al138 note much less discomfort and faster healing by nearly 4 days of shave biopsy sites treated with DuoDERM over 11 . Tavis et al135 agree that Biobrane reduces pain. Biobrane.8 days) and were basically painless. Scarlet Red. 1991.130 Brady et al131 compared Op-Site. similar cost and ease of use. moisture-vapor-permeable and fine mesh gauze dressings for STSG donor sites with respect to pain. In another study. Semiopen dressings include Xeroform. Op-Site and Tegaderm promoted fast healing (mean 6. pain. adherence. Number 1 performance with respect to healing time and pain when measured against other donor site dressings. (Pig skin was initially included in the study but was soon eliminated because of Pseudomonas infection and hypertrophic scarring. The healing time for Biobrane was 19 days. The interval to healing was longest with the open method.133 Dressings that promote a moist wound environment are associated with faster healing. In a study comparing Op-Site with simple polyvinyl film and tulle gauze. and a low cost per patient ($1. but PVC film was also well tolerated and was very inexpensive. Synthetic Materials Feldman120 lists methods for dressing the donor site of a skin graft (Table 1). followed closely by Vaseline gauze.SRPS Volume 10.3 days.50/patient). limits infection and desiccation. rate of healing. or occlusive. Semiocclusive dressings include Op-Site.5 days but were 3X as painful. Vaseline gauze. Feldman and colleagues129 evaluated the effectiveness of various donor site dressings in 30 patients with respect to healing. but by the 14th to 21st postgraft day it becomes level with the surrounding surface. a mediumthickness graft. There is blanching on pressure with prompt capillary refill. degree of pain. After transfer to a recipient site. contracted. The contraction-inhibiting effect of dermis depends more on the percentage of dermis included in the graft than in overall thickness of the graft: the greater the proportion of dermis. fullthickness grafts are able to grow. The degree of graft contraction can be manipulated somewhat by adjusting the thickness and proportion of dermis in the graft.147. There is an abundance of polymorphonuclear lymphocytes and monocytes.150. Once wound contraction ends. in the healing of STSG donor sites. a calcium alginate dressing. Unless splitthickness skin grafts are fixed to underlying rigid structures and cannot move. on the other hand. Vascular remodeling in the graft may take many months. Lawrence and Blake139 and Porter140 evaluated Kaltostat. they will contract secondarily.19 Collagen replacement begins by the seventh postgraft day and is complete in about 6 weeks. and a thin split-thickness graft. if at all. At first the graft surface is depressed below the level of the surrounding skin. A full-thickness graft loses about 40% of its original area as a result of primary contraction. Number 1 conventional therapy consisting of cleansing. the skin graft will shrink as it heals——secondary contraction.SRPS Volume 10. bacitracin. and convenience of use were measured and compared with the same parameters in two other groups of patients treated with Scarlet Red and DuoDERM. Others recommend honey-impregnated gauze for dressing donor sites and report no significant difference in time of reepithelialization or patient comfort between this inexpensive material and the more costly hydrocolloid dressings. Primary contraction is passive and probably due to the recoil of the dermal elastic fibers. the alginate was easier to apply and could be used on an outpatient basis. whereas splitthickness grafts remain fixed. The Kaltostat-treated patients had slower healing times (15.5 days) than other patients (10 days).145 Host vessel ingrowth is perpendicular to the dermis––epidermis junction and forms a characteristic vascular pattern.147––149 thin FTSGs inhibit wound contraction better than thick STSGs. and grow minimally. Owen and Dye142 report that topical application of 2% lignocaine gel to graft donor sites controlled discomfort during the first week postgrafting and did not impair healing. about 10%. patients who received EMLA reported no discomfort. the greater the inhibition and the less the graft will contract.144 GRAFT HEALING In his classic work on skin grafts in the mid-1940s. Medawar12––14 described the appearance of healing grafts as follows: Immediately after removal from the donor area the skin graft is white. about 20%. Goodacre et al141 studied the effectiveness of topical local anesthesia (EMLA) versus infiltrated anesthesia in an open parallel group comparison in 80 patients. The mononuclear infiltrate persists in the dermis for an extended period of time. The new vessels in the graft are more numerous and show greater arborization than those in normal skin. Fullthickness grafts tend to remain the same size (after primary contraction) and do not show secondary contraction. and subsequently the graft loses weight until pregraft weight level is attained by the ninth day. contract whenever circumstances allow. but once applied to the recipient area it becomes pink over the next few days. Lymphatic drainage is present through connections between the graft and host lymphatics by the fifth or sixth postgraft day.8. True Thiersch grafts do not undergo primary contraction. On the other hand. and band-aids. FTSGs therefore inhibit wound contraction better than STSGs.151 12 . and thick STSGs contract less than thin STSGs.148 Wound contraction is a critical part of wound healing and is clinically useful because it reduces wound size. Azad and Sacks143 recommend topical bupivacaine on graft donor sites under calcium alginate dressings to enhance comfort and improve hemostasis. During graft cutting and after harvest. The rate of epithelialization. The topical application of anesthetic agents relieves the pain of skin donor sites. A contracted wound is often tight and immobile and there is distortion of surrounding normal tissue.146 GRAFT CONTRACTION A skin graft begins to shrink immediately after harvest. Split-thickness grafts. SRPS Volume 10. and wounds contract less than comparable nongrafted sites.8 If skin graft healing is uneventful. The rate of wound contraction is not affected by graft orientation.155 the active role of collagen cannot be ignored. Lower levels of this enzyme beneath a full-thickness graft may reflect decreased collagen synthesis.151 studied the effect of dermis on the actinomycin content of granulating wounds and suggest that the mechanism of wound contraction is not simply the result of myofibroblast activity. epidermal interaction. These grafts. Bertolami and Donoff150. warmth in 6. Substances that inhibit wound contraction also inhibit prolyl hydroxylase activity (an indicator of collagen synthesis). By day 30. amount of epidermis. Seven grafts showed no thermal sensibility at all.159 The timing of neural invasion and disposition of nerves within a skin graft vary according to the graft thickness and recipient site. no sensory corpuscles were detected in grafted skin at any time. The extent of reinnervation depends on how accessible the neurilemmal sheaths are to the invading nerve fibers——ie. presumably by reducing early inflammation. therefore. In this hypothesis a graft does not prevent the formation of myofibroblasts. Various hypotheses have been proposed to explain the mechanism of this inhibition. these wounds had contracted more than conventional autografts. and Paletta164 noted that nerves entering the graft fol- 13 . and Young152 concluded that the capacity of a skin graft to inhibit wound contraction is directly proportional to the amount of structurally intact dermal collagen present in the graft. and wounds show minimal contraction. GRAFT REINNERVATION Nerves grow into skin grafts from wound margins and the graft bed. Human skin grafts begin to show sensory recovery at 4––5 weeks postgrafting. and heat––pain in 8 grafts. Grafts less than 7 months old showed no sensitivity whatsoever. Waris and associates159 measured the thermal sensitivity of 22 split skin grafts transplanted 1––4 years earlier. cellular interactions between graft cells and host bed. suggesting that dermal cells and noncollagenous proteins are not part of the inhibitory process. The matrix was prepared for grafting by adding azide to destroy the cells and trypsin to remove noncollagenous protein. or noncollagenous protein. but occasionally sensation is delayed for up to 5 months. most accessible in fullthickness grafts and least accessible in thin splitthickness grafts. the threshold was lower than for cold. to store nonantigenic dermal substitutes produced from banked cadaveric skin or xenogeneic sources by adding trypsin or azide to remove noncollagenous protein and cells. Skin grafts are initially hyperalgesic and slowly regain normal sensation. cellfree and noncollagenous-protein-free. Garner. but rather speeds up completion of their lifecycle and eventual disappearance. etc. Stella et al161 independently verified these findings and speculate that the failure of regeneration of sensory corpuscles may be related to the degeneration of periaxonal corpuscular elements. mechanical restriction.155 Splitthickness grafts cause a rapid decline in the number of myofibroblasts. Walden and coworkers158 report minimal contraction at 14 days when epidermal autografts were immediately placed over acellular dermis. If the warmth sensibility had recovered. and pain sensation had developed only in the 15-month-old grafts. Although deep and superficial nerve plexuses regenerated.152 Rudolph153. including a mass effect. but Adeymo and Wyburn 163 and later Fitzgerald. Number 1 Brown. In a porcine study. resist wound contraction as well as full-thickness skin grafts. The return of normal sensation is usually complete by 12––24 months. Martin.157 highlight the importance of the collagen matrix in inhibiting wound contraction. It may be possible.154 explains the interaction between a graft and its bed in terms of the lifecycle of a myofibroblast. This would increase dramatically the clinical availability of substitute dermis as a potential source of grafts. Cold sensitivity was present in 14. Ponten162 stated that grafts assume the sensory pattern of the host tissue. which in turn may be involved in preventing wound contraction. Haro and colleagues160 confirmed poor return of sensitivity in grafts by means of immunohistochemical methods. however.150 Oliver and associates156. Full-thickness grafts trigger an even faster decrease in the myofibroblast population. Grafts free of dermal cells but possessing a collagen matrix in fact behave much like FTSGs. the results of two-point discrimination testing will be very close to those of normal skin. Other sensations do not recover so well. 162 The best treatment for hyperpigmented grafts is dermabrasion. corrugated. and second.169 Burns that invade the dermis (second. and the tissue consequences of graft failure are minimal. buttocks. This protocol is also successful in treating leukoderma. The consequent loss of melanoblast content causes profound alteration in the ratio of pigment-producing to nonpigment-producing cells in the graft. the hyperpigmentation state that follows cutaneous grafting. however. the blanching will not last and the dark pigment will reappear. OVERGRAFTING Dermal overgrafting consists of applying a splitthickness skin graft to a recipient bed or dermis or denuded scar tissue. or hypertrophic scars • • • • unstable or hyperpigmented skin grafts large pigmented nevi radiation damage tattoos Pigmented lesions should be excised deep enough to remove all the pigment before the graft is applied. For dermabrasion to be effective.and third-degree) decrease the number of dopa-positive melanocytes.or third-degree burns can produce significant cosmetic deformity.SRPS Volume 10. and thigh become darker as they heal. while grafts taken from the palm tend to lighten. Wound healing time was much shorter than for typical skin grafts. Number 1 low the evacuated neurilemmal sheaths and reestablish the innervation pattern of the donor skin. melanocyte-containing epidermal sheet grafts170––177 or in-vitro cultured melanocytes.10 Grafts harvested from the abdomen. A potential complication of the technique is the formation of cysts and granulomas from retained epithelial remnants. Weis-Becker and coworkers165 note better reinnervation of split skin grafts placed on intact muscle fascia than if the fascia had been removed.181 14 . The best results are seen when dermabrasion follows biologic reinnervation of the graft. while grafts taken from above the clavicle provide a better color match for facial skin. grafts taken from below the clavicle assume a yellowish-brown hue. depressed. Rees and Casson181 offer technical details of skin removal and bed preparation and list the best donor sites. the later the dermabrasion is done after grafting. Generally. A number of authors report successful repigmentation in leukoderma or vitiligo after treatment with ultra-thin. the more effective it is in removing unwanted pigment. If it is performed too soon after skin graft. In general. Their indications for overgrafting are as follows: • unstable. so that appropriate treatment consists of removing the depigmented skin and replacing it with very thin STSGs of normal color. be successful in the treatment of vitiligo provided that dopa-positive melanocytes are present in the skin. with exposure to sunlight. Full-thickness grafts from the eyelid. while those from blondes usually lighten.168 Vitiligo.180 Overgrafting preserves subcutaneous tissues. postauricular and supraclavicular areas are usually good color match for the face. and the effects of ultraviolet radiation on the skin. Grafts taken from brunettes progressively darken.166 After transplantation and graft revascularization there is inflow of erythrocytes and the normal equilibrium of the melanocyte population is restored. it must be done at the appropriate time. a skin graft blanches from circulatory interruption. Skin depigmentation states and their treatment are reviewed by Taki et al. dyschromatosis symmetrica hereditaria. Sensory functions on grafted skin were generally reduced. The graft resumes a pink color which over time fades to a normal skin tone. GRAFT PIGMENTATION Immediately after harvesting. its peripheral nervous system control. Mir y Mir167 reviews melanogenesis. is a relatively simple procedure. Corticosteroids and oral psoralen may. Skin grafts change color during healing.178 Hosokawa and colleagues179 report a novel method of tattoo elimination in which the pigment-containing dermis is chemically removed and the epidermis is replaced. Thin split-thickness skin grafts from the same donor site are usually darker than thick ones. particularly in dark-skinned patients. senile leukoderma. although they may remain red for many months. 182 Fluid beneath the graft can also cause graft necrosis. using quilting sutures. but exert no significant pressure on the wound. arterial insufficiency. Hill186 recommends a number of measures to enhance the survival of full-thickness grafts. The exception were patients under 18 years of age. Because streptococci produce streptokinase and other enzymes that break down the fibrin clot and decrease adherence of the graft to its bed. and found it to be negligible at 14 days postgrafting. and prevent hematoma formation. and have an appropriate substrate (eg. This finding suggested to the author that dissolution of fibrin by plasmin and proteolytic enzymes is the probable mechanism in graft failure secondary to microorganisms. meshing or pie-crusting the graft surface to allow free egress of subjacent fluids. and surgeon error. and applying wet saline dressings that are changed every 4 hours. movement of the area. Ethanol in the bloodstream decreases the initial phase of wound healing (the PMN clean-up phase) and can result in infection and decreased graft adherence.184 In conclusion. High plasmin and proteolytic enzyme activity was generally seen in wounds contaminated with beta-hemolytic streptococci and various species of Pseudomonas. Fibrin plays a central role in graft survival and is responsible for the antibacterial character of adherent dressings and autografts. free of dead tissue. in whom STSG success was higher on granulation tissue than on fat. Areas rich in lymphatics such as the supraclavicular. The applied pressure should never exceed 30 mmHg.184 Thourani and colleagues185 assessed the effect of various recipient beds on the success of STSGs in a burn unit. Atraumatic tissue handling.182 The second most common cause of graft loss is infection. The graft bed should be as clean as possible. scar-free bed • careful hemostasis and removal of accumulated blood before dressing the wound • postoperative immobilization of the graft recipient site • use of a tourniquet during graft harvest and transfer • no proximal constricting bandages Flowers182 reviews the usual complications associated with graft failure and recommends steps to avoid them. he proposes the administration of low-dose erythromycin for the first 5 days after grafting to combat potential strep and staph colonization. fibrinogen. and axillary regions are particularly prone to develop seromas. Patients should also take vitamin C and zinc for a week to 10 days to promote healing. lymphatic stasis. reduce dead space. Clean wounds had low bacterial counts and showed no detectable plasmin activity. and the absence of fibrin was associated with graft failure. This bacteriostatic effect of grafts has proved invaluable in the management of large burns. Wound exudates were assayed for fibrin degradation products. bone should have periosteum. Infection can be avoided by carefully preparing the wound bed.182 Excessive pressure on a fresh graft may also cause it to die. and active plasmin. tendon should have peritenon). All wounds showed granulation tissue and were classified as clean or dirty. a grafted wound is rendered sterile through the blocking action of fibrin in the interface between graft and bed. The clot isolates the undersurface of the graft from the endothelial buds of the recipient site so that revascularization cannot take place. venous congestion.SRPS Volume 10. The presence of fibrin under autografts was associated with success in 17 of 21 ulcers. limited use of electrocautery in the graft bed. and should abstain from using alcohol for at least 2 days before and 5 days after surgery. Number 1 GRAFT FAILURE A meticulous surgical technique contributes greatly to the survival of a skin graft. available plasminogen. Teh184 studied 21 patients with stasis ulcers in an attempt to pinpoint the causes of graft failure. and a light pressure dressing or VAC technique minimizes the risk of fluid accumulation under the graft. cauterization of lymphatic vessels. inguinal. The most common cause of autologous skin graft failure is hematoma. Tie-over dressings immobilize the graft.186 15 . Dirty wounds had high bacterial counts and increased levels of active plasmin.183 Other causes of graft failure include gravitational dependency. Particular attention should be paid to ensuring • atraumatic graft handling • a well-vascularized. A clean area with endothelium is all that is required in the bed of a successful skin graft. semipermeable silicone membrane.193 Transcyte Transcyte is Biobrane with the addition of neonatal fibroblasts seeded to the collagen-coated nylon mesh. They do not recommend using plain lidocaine for harvesting full-thickness grafts unless the vascular supply of the donor area is compromised. Skin substitutes for wound closure include Alloderm. found that epinephrine added to local anesthetic solutions decreased inosculation in full-thickness grafts but had no effect on ultimate survival of splitthickness skin grafts. and Apligraf (Graftskin). The authors found an increased risk of graft complications at 1 week and no effect on the 6-week cosmetic outcome. Integra.193 Materials used for wound cover are primarily indicated for superficial burns. allograft–– xenograft skin. The product is often used as a temporary skin replacement for superficial partialthickness burns as well as for skin graft donor sites. When applied to clean wounds. Perry190 notes a direct correlation between skin graft survival and bacterial counts of <105 in the recipient bed. SKIN SUBSTITUTES Unlike temporary wound dressings. or recombinant192——or whether they are used for wound cover or wound closure. xenogeneic. Materials intended for wound closure restore the epidermal barrier and become incorporated into the healing wound. so the material is designed for use as a temporary cover. Biobrane eliminates the need for dressing changes and reduces the length of inpatient treatment. and composites of epidermal––dermal components. Number 1 Wolfort and colleagues. Fifteen years ago Pruitt and Levine191 listed attributes of the ideal skin substitute which are still current today: • little or no antigenicity • tissue compatibility • lack of toxicity. where they provide a barrier against infection. either local or systemic • permeability to water vapor just like normal skin • impenetrability to microorganisms • rapid and persistent adherence to a wound surface • porosity for ingrowth of fibrovascular tissue from the wound bed • malleability to conform to an irregular wound surface • elasticity for motion of underlying tissues • structural stability to resist linear and shear stresses • a smooth surface to discourage bacterial proliferation • sufficient tensile strength to resist fragmentation • biodegradability • low cost • ease of storage Classification Skin substitutes may be classified according to their origin——autologous. cultured epidermal allogeneic keratinocytes.194 Transcyte is considerably more expensive than Biobrane. Transcyte (formerly DermagraftTC). or collagen––glycosaminoglycan matrix with a cultured epidermal autograft (CEA) surface (Table 2). Dermagraft. and create an environment suitable for epidermal regeneration. Examples of skin substitutes for wound cover are Biobrane.192. It provides a barrier function against fluid loss as well as protection from environmental bacterial invasion. Wound Cover Biobrane Biobrane is a bilaminar material consisting of nylon mesh bonded to thin. cloned autologous keratinocytes (Epicel). skin substitutes are designed to be left in place for long periods of time. Subsequently Fazio and Zitelli188 assessed the clinical effects of epinephrine in local anesthesia of the donor site.187 working on rabbits.SRPS Volume 10. The fibroblasts are nonviable at application and the nylon mesh is not biodegradable. Transcyte for preliminary coverage of partial thickness burns results in fewer dressing changes and less hypertrophic scarring than conventional treatment with topical silver sulfadiazine. control water loss. Robson and Krizek189 predict skin survival on the basis of successful homograft take prior to autografting.192.193 • indefinite shelf life 16 . allogeneic. 2002. Number 1 TABLE 2 A Guide to Biological Skin Substitutes (Reprinted with permission from Jones I. Currie L. Martin R: A guide to biological skin substitutes.SRPS Volume 10.) 17 . Br J Plast Surg 55:185. unstable epithelium that may spontaneously blister. but has no barrier function because it has no epidermal component. The indications for Alloderm are as dermal replacement in full-thickness or deep partialthickness wounds. These sheets are fragile. Number 1 Cultured Allogeneic Keratinocytes The delay in growing sheets of confluent autologous keratinocytes led to the deelopment of pregrown allogeneic keratinocytes. and as such promotes the healing of chronic lesions. and large areas of skin necrosis. Like STSGs. and no risk of cross infection. and its high cost. break down. A split-thickness skin graft can be placed over Alloderm after tissue ingrowth. and contract long after application. epidermolysis bullosa.193 Dermagraft has been used to replace lost dermal tissue beneath meshed splitskin grafts on full-thickness wounds. It has wide application in treating chronic ulcers as well as in pediatric burn coverage.199. improved elasticity and cosmesis compared with thin STSG.or full-thickness skin graft. giant pigmented nevi. They will not in themselves achieve wound closure. Apligraf/Dermagraft These are multilaminar materials designed to overcome the fragility of cultured allogeneic keratinocytes by improved ease of handling and healing characteristics. but may survive for up to 30 months. chronic ulcers.193 Cultured epithelial cells used for grafting have an expansion capability of 10. Integra is applied in a twostage procedure much like a split. the necessity for a two-stage procedure. The main disadvantage is that the cultured epithelial cell sheets are thin and fragile. and to cover full-thickness wounds resulting from Mohs’’ micrographic surgery pending definitive repair.200 Wound Closure Alloderm Alloderm is processed human cadaveric skin from which the epidermis has been removed and the dermal cells extracted.193.201 Cultured Epithelial Autografts Rheinwald and Green5 pioneered a method to clone human epidermal cells in vitro in 1975. and as donor site dressings for split-thickness skin grafts. chronic leg ulcers. Cultured allogeneic keratinocytes have been used to cover burn wounds. Allogeneic keratinocytes do produce growth factors that facilitate the proliferation and differentiation of the host dermal and epidermal cells. Its reliability is good on long clinical follow-up. In 1979.201 Integra Integra is a bilaminar skin substitute consisting of a cross-linked bovine collagen––glycosaminoglycan matrix coated on one side with silicone elastomer for a barrier function.SRPS Volume 10.193. Apligraf is a type I bovine collagen gel with living neonatal allogeneic fibroblasts overlaid by a cornified epidermal layer of neonatal allogeneic keratinocytes. As the host tissue grows into the wound. or an ultra-thin graft can be placed at the time of Alloderm application in a single-stage procedure. Green et al6 perfected a technique for growing cultured epithelial keratinocytes into confluent sheets suitable for grafting. Epidermal grafts are obtained from neonatal foreskin or elective surgical skin specimens and are cultured.192. requiring meticulous wound care if they are to survive. Dermagraft stimulates the ingrowth of fibrovascular tissue from the wound bed and reepithelialization from the wound edges. the silicone ““epidermis”” separates and sloughs off in 3––4 weeks.192.195––199 Apligraf is the most sophisticated tissue-engineered product available for wound coverage.000X 18 . Alloderm is similar to Dermagraft in many respects. Apligraf is available in a ready-to-use form with a 5-day shelf life. Integra has widespread applications in burn and full-thickness wound closure.193 Dermagraft is a cryopreserved dermal material consisting of neonatal allogeneic fibroblasts on a polymer (Dexon or Vicryl mesh) scaffold. after which the integrated matrix is covered with a thin STSG. Alloderm functions as a dermal graft. Advantages of Integra include off-the-shelf availability. Disadvantages are a somewhat steep learning curve for application.193 Sheets of cultured epithelial cells (Epicel) are expensive and require a fair degree of expertise for application. cultured epithelial autografts must be applied on a wound bed with early granulation tissue or muscle fascia for proper take. for coverage of widespread skin defects such as epidermolysis bullosa. often resulting in a friable. Clinical experience with epidermal cells grown in vitro include burns. and is also the most expensive. 1962. Br J Plast Surg 5:161. Munksgaard.202––204 When cultured cells and allografts are combined. 1965. 8. Science 152:1335. Copenhagen. Heiple KG: Quantification of 3-H collagen loss of rat allografted and isografted tendon. Pepper FJ: Studies on the viability of mammalian skin autografts after storage at different temperatures. 18. Plast Reconstr Surg 35:572. Ratner D: Skin grafting. 21. Proc Soc Exp Biol Med 119:557. J Surg Res 7:433. Surg Clin North Am 57:939. 23. 1977. N Engl J Med 253:847. 1954. Acta Chir Scand 124:11. From here to there. Vistnes LM: Grafting of skin. 1982. Medawar PB: The behaviour and fate of skin autografts and skin homografts in rabbits. the cells will spread peripherally to join other grafts or surrounding skin. Vessely JC. Hinshaw J: Autograft rejection induced by homografting. Dunphy JE.206 Many burn centers continue to use cultured epidermal autografts. 1979. Grillo HC: Derivation of fibroblasts in the healing wound. 27. Medawar PB: A second study in the behaviour and fate of skin homografts in rabbits. 13. PNAS 62:920. 7. 6. 1962. 1977. • CEAs are extremely sensitive to infection. 1945. 26.207 BIBLIOGRAPHY 1. 14. Plast Reconstr Surg 30:415. 32. 5. J Anat 79:157. • Sheets of cultured keratinocytes are very fragile and must be handled with extreme care. Klein L. Surg Forum 22:489. Hinshaw JR. 3rd ed. Little Brown. Miller ER: Histology of healing split-thickness. 1969. 19. 3. 1967. Tsurufugi F: Degradation and turnover of collagen in the moust skin and the effect of whole body x-irradiation. Tough JS: Histochemical studies of human skin autografts and homografts. 9. 1966. 22. Hilgert I: Changes in the hydroxyproline and hexosamine content of grafts after transplantation. Van Winkle W: The fibroblast in wound healing. Plast Reconstr Surg 34:287. Udupa KN: Chemical and histochemical sequences in the normal healing of wounds.SRPS Volume 10. Ann Plast Surg 9:242. they tend to be more stable than either component alone. 1994. Boston. In: Grabb and Smith’’s Plastic Surgery. 28. 2. yet many prefer to use CEAs alone on large burns. 1945. Thomas J: Growth of cultured epidermal cells into multiple epithelia suitable for grafting. Biochem Biophysiol Acta 208:475. 1966. Mac Neil S: What role does the extracellular matrix serve in skin grafting and wound healing? Burns 20:S67. 15. 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Otto WR: Allogeneic skin substitutes applied to burn patients. 182. Kolenik SA III. 2003. J Am Acad Dermatol 22:87. May JW Jr: The effect of epinephrine in local anesthesia on the survival of fulland split-thickness skin grafts: an experimental study. 2002. 163. 179. 1993. Dermatol Clin 19:555. J Trauma 54:562. Levine NS: Characteristics and uses of biologic dressings and skin substitutes. 192. Carucci JA. Fruhstorfer H. Plast Reconstr Surg 18:30. Acta Derm Venereol (Stockh) 78:136. J Dermatol Surg Oncol 10:136. Greiner D. Webster GV: Annual report to the American Society of Plastic and Reconstructive Surgeons. 1966. Law EJ: Use of cultured epidermal autografts in the treatment of large burns. Jarrett A. 162. Sheridan RL. 199.Faure M. Giele HP: Tie-overs under pressure. 1990. Marshall D: Use of skin substitutes in pediatric patients. Seymour FK. Beele H: Artificial skin: past. Ann Plast Surg 22:479. Kumagi N. 1994. Arch Dermatol 131:691. Orlet HK. Jones I. Wyburn G: Innervation of skin grafts. Dermatol Surg 24:365. et al: Sensory endings in skin grafts and scars after extensive burns. compared with cryopreserved human cadaver skin for temporary coverage of excised burn wounds. 1997. Yano K. including tissue-engineered living skin. 2002. Hansbrough WB: Clinical trials of a living dermal tissue replacement placed beneath meshed. 186. 193. Nanchahal J. Conway H. Bello YM. Gohari S. Dover R. et al: Surgical treatment of skin depigmentation caused by burn injuries. 1990. Tagami H: Therapeutic success of epidermal grafting in generalized vitiligo is limited by the Koebner phenomenon. 1998. Nishina H. Magliacani G. Gangolphe M. Plast Reconstr Surg 38:522. Purdue GF. 1956. Weis-Becker C. 180. 2002. et al: A multicenter clinical trial of a biosynthetic skin replacement. Dermatol Surg 28:340. Izawa Y. Ozerdem OR. Scand J Plast Reconstr Surg 21:241. Donati L. Ingram WL. 176. 197. 1960. Ann Plast Surg 24:53. 164. 191. 2002. Hansbrough JF. Hill TG: Enhancing the survival of full-thickness grafts. Clin Dermatol 20:715. 1992. Burns 20:539. 207. Int J Artif Organs 25:163. Casson PR: The indications for cutaneous dermal overgrafting. Adeymo O. Br J Plast Surg 55:185. Burns 28:254. Taki T. Still JM Jr. 187. Kato T. Acta Derm Venereol (Stockh) 77:463. 202. Hata Y. 1998. 178. J Burn Care Rehabil 18:52. Observations on innervation and other qualities. 1989. Ribeiro de Castro MC: New dressings. Feliciano DV: Factors affecting success of split-thickness skin grafts in the modern burn unit. 190. Hunt JL. Scand J Plast Reconstr Hand Surg 32:157. 2003. 194. 188. Rohrich RJ. Handren J. et al: Clinical applications of autologous cultured epithelia for the treatment of burn wounds and burn scars. 200. 174. Kahn AM. J Dermatol Surg Oncol 11:1218. Vander Kam VM: Treatment of vitiligo with melanocytic grafting. J Craniofac Surg 14:517. 1988. J Am Acad Dermatol 30:1044. 1985. Le Y. Teh BT: Why do skin grafts fail? Plast Reconstr Surg 63:323. Zitelli JA: Full-thickness skin grafts. 185. 195. Flowers R: Unexpected postoperative problems in skin grafting. Ann Plast Surg 33:644. 189. et al: The grafting of burns with cultured epidermis as autografts in man. Dermatol Surg 28:1107. 173. Cohen MJ: Vitiligo: treatment by dermabrasion and epithelial sheet grafting——a preliminary report. Tompkins RG: Cultured autologous epithelium in patients with burns of ninety percent or more of the body surface. Robson MC. 1994. Plast Reconstr Surg 86:535. J Trauma 13:213. 2002. 1990. Wolfe SA. Krizek TJ: Predicting skin graft survival. Winter H: Reinnervation of split skin grafts in humans: comparison of two different methods of operation. Healey M. Br J Plast Surg 14:303. split-thickness skin grafts on excised burn wounds. Gambla C. Dore C. Melanocyte transfer via ultra-thin grafts. 177. 15––19 The future of perforator flaps may lie in the clinical application of angiosomes20 and the creation of ““free-style free flaps”” in which a perforator localized by Doppler signal can be the basis for a skin flap in any anatomic region. when a distinction was made between axial and random flaps. Flaps range from simple advancements of skin and subcutaneous tissue to composite flaps that may contain any combination of skin.PRINCIPLES OF FLAPS Amanda A Gosman MD DEFINITIONS A flap is a unit of tissue that maintains its own blood supply while being transferred from a donor to a recipient site.11 Skin flaps are now successfully transferred based on the small perforating vessel alone. In contrast. without dissection of the named vascular pedicle.21––25 VASCULAR ANATOMY OF THE SKIN Arterial Anatomy In 1889 Manchot26 described cutaneous vascular territories. and micro-thin perforator flaps have further advanced the esthetic reconstruction (Fig 1) of defects requiring coverage with fine pliable tissue. were initially reported in the Italian literature during the Renaissance. Koshima and Soeda6 coined the term ““perforator flap”” in 1989 while reporting on inferior epigastric artery flaps based on a single musculocutaneous perforator vessel. and free tissue transfer came into being.6––10 The perforator concept has evolved since the development of supermicrosurgery.2 These surgical procedures involved the use of rotation flaps. Spalteholz28 in 1893 demonstrated anatomically that the circulation to the skin via subdermal and dermal plexuses could be . Thin. The 1980s saw the development of fasciocutaneous flaps. fat. The origins of forehead rhinoplasty can be traced to India about 1440 AD. First there was an early period during the First and Second World Wars when pedicled skin flaps were used extensively. but probably was practiced long before the birth of Christ. muscle. which transfer skin from an adjacent area without torsion of the base. The original perforator flaps were transfers of skin territories based on a named vascular pedicle to a muscle while preserving the muscle and its innervation. This was the first reported description of the now very popular anterolateral thigh flap. grafts are transferred unattached to a vascular source and rely on the blood supply at the recipient site for their survival. super-thin. and specialized free flaps. A third period took place mainly during the 1970s. 1n 1964 Seitchik and Kahn27 studied the anatomy of the ““intrinsic circulation”” of the skin and observed that arterial branches penetrate the superficial layer of the superficial fascia and join a subdermal plexus of arteries terminating in skin capillaries. fastened only on one side. bone. osseous and osseocutaneous flaps. when what we now recognize as regional axial pattern flaps were reported. meaning something that hung broad and loose. The French are credited with the original description of sliding or advancement type flaps. HISTORY AND EVOLUTION The origin of the term flap originated from the 16th century Dutch word ““flappe””. or fascia. Distant pedicled flaps.1. The next period occurred in the 1950s and ‘‘60s. The venous drainage system paralleled the arterial system.1 The history of plastic surgical repair with flaps can be documented as far back as 600 BC. 12––14 The recent innovations in perforator flap surgery represent a shift toward esthetic free flap refinements and attempts to minimize donor site morbidity. which transfer tissue to a remote site. when Sushruta Samita described nasal reconstruction using a cheek flap.4 In 1984 Song et al5 introduced the free thigh flap based on perforating septocutaneous arteries in the thigh. Supermicrosurgical techniques facilitate the anastomosis of vessels 0.3 Subsequent flap evolution happened in phases. which transport skin to an adjacent area while twisting or rotating a pedicle.5 mm in diameter. muscle and musculocutaneous flaps were elevated and transferred. The cutaneous circulation. 1990. Ch 9. The vessels course from fixed loci to mobile areas. 2002. Number 1 Fig 2. septa or fascia. and head and neck. The following remarks are based on the results of their study. The indirect route constitutes vessels whose main supply is either to muscle or another deep tissue and only secondarily supply the skin. Plast Reconstr Surg 109:78. The vascular outflow is a continuous system of arteries linked predominantly by reduced caliber vessels. The evolution of the ultrathin perforator-based flap. Plastic Surgery. Philadelphia. Taylor and Palmer (1987) Fig 1.SRPS Volume 10.) intermuscular septum or pierce the muscle. 4. 3. The direct route encompasses vessels that are primarily directed towards the skin. Saunders. 1. The arteries supplying these blocks of tissue are responsible for the supply of the skin and the underlying structures. (Reprinted with permission from Hallock GG: Discussion of ““A microdissected thin tensor fasciae latae perforator flap”” by N Kimura. These composite units we have named ANGIOSOMES. In: McCarthy JG (ed). The angiosome theory has more recently been applied in detailed anatomic investigations of the forearm. The first defines the angiosome which is a composite unit of skin and its underlying deep tissue supplied by a source artery. whether it is bone. (Reprinted with permission from Daniel RK.30 The choke vessels can potentially dilate to the caliber of a true anastomosis after surgical delay or with a decrease in sympathetic tone. whether they follow the Taylor and Palmer20 described 40 angiosomes (Fig 3) that are linked to each other by ““true”” anastomotic arteries of similar caliber or reduced caliber ““choke”” anastomotic vessels. Taylor and Palmer20 propose two theories of the blood supply to tissues. The body is a three-dimensional jigsaw made up of composite blocks of tissue supplied by named source arteries. Vol 1.) fed by either direct or indirect branches from an underlying source vessel29 (Fig 2). 2. lower extremity. Kerrigan CL: Principles and Physiology of Skin Flap Surgery. The second defines the routes by which the integument is supplied by that source artery. The blood supply of the body courses within or adjacent to the connective tissue framework. the choke arteries and arterioles.31––33 Although many important 2 . ie. The network is present throughout the subcutaneous layer between the subdermal plexus and the deep fascia. They are: (1) thyroid. (Reprinted with permission from Taylor GI. (20) inferior gluteal. F) musculocutaneous perforator (Fig 4). Nakajima35 identified six vessel types that perforate the deep fascia to supply the fasciocutaneous plexus: A) direct cutaneous. (29) medial plantar. like the subdermal plexus. (36) lateral thoracic. This epifascial vascular network is present throughout the superficial fascia and is called the fasciocutaneous plexus. Br J Plast Surg 40:113. D) perforating cutaneous branch of muscular vessel. (32) common femoral. These perforators supply a small vascular territory and cannot support axial skin patterns. (5) superficial temporal. Nakajima35 conceptualized the vascular supply to the skin as an epifascial vascular network which is fed by different configurations of inflow vessels. (24) peroneal. (13) profunda brachii. Types C and D arise from the muscular vessel and supply the fasciocutaneous plexus and skin axially over the muscle. but stress the limitations in their conclusions due to the static nature of the specimens used. (40) internal pudendal. (26) anterior tibial. (23) sural. (39) anterior interosseous. C) direct cutaneous branch of muscular vessel. E) septocutaneous perforator. Types A and B arise from the source vessel and supply a large axial territory above the deep fascia. (22a) descendin geniculate (saphenous). (27) lateral femoral circumflex. (35) internal thoracic. (6) occipital.”” and suggested that the term ““choke artery”” be abandoned. 3 . which were performed in fresh cadavers. in. (14) brachial. (10) suprascapular. The angiosomes of the source arteries of the body. Number 1 Fig 3. (18) lumbar.3% of patients the distribution of fluorescein was over a much smaller region than would be expected from Taylor and Palmer’’s study. (8) transverse cervical. the authors confirmed that in most cases connections between adjacent angiosomes occurred within tissues and not between them. (30) posterior tibial. (17) posterior intercostals. (16) radial. The architecture of this network varies according to anatomic region but. (31) superficial femoral. McGregor 34 acknowledges that Taylor and Palmer’’s findings have practical application in the design of skin flaps. (7) deep cervical. (15) ulnar. his study was performed in living patients whose vascular resistance is physiologic rather than anatomic. (34) deep inferior epigastric. (25) lateral plantar. (11) posterior circumflex humeral. (2) facial. (12) circumflex scapular. McGregor performed intraarterial fluorescein injection studies on 23 patients undergoing abdominal reduction. B) direct septocutaneous. (22) popliteal.) regional differences were identified. (9) acromiothoracic.SRPS Volume 10. (3) buccal. (33). (37) thoracodorsal. 1987. In 78. Palmer JH: The vascular territories (angiosomes) of the body: experimental study and clinical applications. (19) superior gluteal. it extends throughout the body as a continuous system. deep circumflex iliac. (28) adductor (profunda). (4) ophthalmic. To determine skin perfusion patterns. and above the deep fascia. (38) posterior interosseous. He also found that ““the watershed between adjacent territories does not correspond to the choke arteries described at the periphery of the angiosome. Types E and F arborize under. McGregor notes that unlike the Taylor injections. (21) profunda femoris. See text for details. After perforating the deep fascia. 1986. E. Adachi S: A new concept of vascular supply to the skin and classification of skin flaps according to their vascularization.SRPS Volume 10. (Reprinted with permission from Nakajima H. respectively. (Reprinted with permission from Nakajima H. In the torso types I. 1998. Number 1 Fig 4. Nakajima’’s six types of arterial configuration evolved from his previous perforator classification. and IV are localized in the Fig 5. but have diverging branch points. Types I and II are mobile vascular types that show axiality and are located in the deep adipofascial layer. The arteries were localized on a whole body map and the relationship between the type of artery and the mobility of the tissue it supplied was considered. Types V and VI (Types E and F) are fixed vascular types of little axiality and are continuations of small septocutaneous and musculocutaneous perforators. Types III and IV are peripheral continuations of either the direct cutaneous branch or perforating cutaneous branch of a muscular vessel (Types C and D). Six types of 3-dimensional arterial structure.35 Types I and II are continuations of direct cutaneous and direct septocutaneous perforators (Types A and B). Computer images of angiograms performed on 28 segmental arteries of the body were analyzed according to the tissue layer in which they were dominant (whether dermal. musculocutaneous perforator. and their size. direct septocutaneous vessel. their axiality. superficial. the arteries were assigned to one of six different types (Fig 5). perforating cutaneous branch of muscular vessel. Type III is dominant in the deep adipofascial layer and IV is dominant in the superficial layer.) Nakajima and coauthors 36 studied the 3dimensional structure of the blood supply to the skin and subcutaneous tissue. Imanishi N: Three-dimensional analysis and classification of arteries in the skin and subcutaneous adipofascial tissue by computer graphics imaging. B. resulting in a reciprocal relationship.) 4 . Ann Plast Surg 16:1. respectively (Fig 6). F. or deep adipofascial layers). Fujino T. Six patterns of blood supply to the fasciocutaneous plexus: A. direct cutaneous vessel. Minabe T. D. C. septocutaneous perforator. direct cutaneous branch of muscular vessel. Plast Reconstr Surg 102:748. III. Types II and IV are of medium size and of moderate axiality. Classification of fasciocutaneous flaps.) Venous Anatomy There are two systems of venous drainage of the skin and subcutaneous tissue. Type II accompanies cutaneous nerves and veins that run in the deep adipofascial layer. Type III is supplied by the direct cutaneous branch of the muscular vessel. 1990. a superficial and a deep (Fig 8). The deep venous trunks are the venae comitantes of the source artery. A similar pathway of venous drainage was identified in each anatomic region. D. Adachi S: A new concept of vascular supply to the skin and classification of skin flaps according to their vascularization. and temporal and parietal regions. (Reprinted with permission from Nakajima H. scapular region. A large vena communicans (C) connects these systems. Above. Type IV is supplied by the perforating cutaneous branch of the muscular vessels. and VI are dominant in the extremities. Fujino T. which has a variable distribution of valves depending on anatomic region. F. Types II. Dermal blood can pool in the polygonal network. Imanishi and others39––41 described the venous drainage of the skin and subcutaneous tissue of the forearm. Number 1 mobile tissue at or around joints. Watterson PA. Type VI is supplied by the musculocutaneous perforator. Other regions where the predominant venous drainage is by means of the venae comitantes. The superficial (S) and deep (D) venous systems in an extremity. Below. and the alternative pathways of four venae comitantes are shown. Type II is supplied by the direct septocutaneous vessel. A. Fig 7. Zhong and coworkers38 classified the venous architecture of the skin and subcutaneous tissue into four superimposed layers that are drained by two large venous trunks. Type I is supplied by the direct cutaneous vessel. Osteal valves were identified at the anatomosis of the first draining dermal branches and the polygonal venous network to resist reflux. It is important to know the subcutaneous depth of a pedicle’’s plexus when elevating thin flaps and adipofascial flaps. Taylor and colleagues37 studied the venous territories (venosomes) of the body and showed that the cutaneous venous plexus is composed of valvular superficial and deep cutaneous veins that parallel the course of adjacent arteries.SRPS Volume 10. V. Crock JG: The venous territories (venosomes) of the human body: experimental study and clinical implications. Small epidermal and dermal branches were collected into a superficial polygonal venous network located in the deep dermis or superficial adipofacial layer.) Fig 6. Type VI vessels are more common in fixed skin areas. or both. the superficial venous trunk. B. 5 . The authors propose that the main venous drainage of an anatomic region can be primarily via the deep venous trunk. such as the center of the back. and of oscillating avalvular veins that permit bidirectional flow between adjacent venous territories (Fig 7). C. E. The superficial venous trunks are located in the subcutaneous tissue and do not accompany arteries. (Reprinted with permission from Taylor GI. Type V is supplied by the septocutaneous perforator. Plast Reconstr Surg 86:185. Ann Plast Surg 16:1. Caddy CM. 1986. They are an important bypass to the unidirectional valves of the cutaneous veins and permit retrograde flow in distally based flaps.42 Pinal and Taylor43 described macrovenous and microvenous systems that bypass the valves of the venae comitantes and permit reversal of flow. subcutaneous tissue. accessory cephalic vein. The authors distinguish between a superficial vein that is located above the deep fascia and a cutaneous vein that is superficial and does not accompany an artery. ACV.) and which eventually drains into large cutaneous veins. As our knowledge of the vascular anatomy of skin. and muscle increased. new flap types were developed and classifications were proposed that were frequently incongruent with previous systems and with one another. lesser saphenous and cephalic).41 Cutaneous venous trunks are the primary drainage of the dermis and are connected by various communicating branches to the venae comitantes of the source artery (Fig 9). Wang GY. Nakajima H. 2001. Aiso S: Anatomical study of the venous drainage architecture of the scapular skin and subcutaneous tissue. (2) Small ascending vein that anastomosed with the venous network. where the course of the named vein diverges significantly from the named 6 .) Between the cutaneous veins and the venae comitantes are thin parallel branches of the cutaneous veins that play clinically important roles. Xu DC: Anatomic basis of venous drainage in donor flaps. Yuan L. RV. (Reprinted with permission from Zhong SZ. The venous architecture of skin flaps. (3) Small ascending vein that anastomosed with ascending vessels from the venous network. these parallel branches may actually become the venae comtantes to the source artery41 and to the small arteries that supply the cutaneous vein (eg. Flaps used to be classified according to their method of movement. (Reprinted with permission from Imanishi N. Number 1 Fig 8.SRPS Volume 10. Plast Reconstr Surg 108:656. (1) Large ascending vein. Surg Radiol Anat 16:349. FLAP CLASSIFICATION Flap classifications are multiple and vary according to the organizing principle. Multiple venous anastomotic connections adequately drain most dermal regions via either the cutaneous vein or the venae comitantes of the source artery. 1994. (5 and 6) Branches that anastomosed small ascending vessels from the venous network and venae comitantes of the radial artery. Polygonal venous network of the forearm.3 they were labeled as local or distant depending on their proximity to the donor Fig 9. Classification schemes have historically been very confusing because they were based on an incomplete understanding of flap vascularity.42 The small arteries correspond to the Nakajima type II and are the source of venocutaneous perforators to the skin. cephalic vein. (4) Anastomosis of the long vein with the cephalic vein. superficial temporal artery and vein). When distant pedicled flaps became commonplace. radial vein (venae comitantes).44 Local skin flaps are still described by this terminology. 39. In areas such as the face. CV. source artery (eg. For example.48 Advancement flaps are slid directly forward into a defect simply by stretching the skin.35––42.) Rotation flaps are semicircular in design and rotate about a pivot point into the defect to be closed (Fig 11). and interpolation flaps). This classification system can be confusing because different flaps based on different blood supplies but of the same composition can be harvested from the same region. The intrinsic blood supply of a flap is the most critical determinant of successful transfer and is therefore the most clinically valid method of classification. Subsequently flaps were categorized by their tissue composition: muscle. V-Y advancement flap. A. the Y-V advancement flap.25. Specific classifications within each of these flap types will also be discussed. Boston. To facilitate rotation of the flap along its arc. and vascularity.46 Unfortunately. and free flaps.31––33. Fig 10. Daniel and Kerrigan29 grouped flaps into three categories according to their method of movement. V-Y advancement (Fig 10). In our discussion of specific flaps we have combined the latter two criteria because they overlap with older terminology based on composition terminology. Number 1 and recipient sites. and its opposite. Method of Movement Skin flaps can be grouped according to the technique used to transfer the tissue and the distance between the donor and recipient sites. tube flaps. rectangular advancement flap. and currently a confusing combination of old and new flap terminology coexists. Variations are the single. and are in turn classified based on their method of movement into flaps that advance from the base in the same direction as the long axis of the flap (V-Y. the base can be back-cut at the pivot point or a triangle of skin (Burow’’s triangle) can be removed external to the pivot point. 1991.29. skin.47.15. The donor site can be closed by a skin graft or by direct suture of the wound.and doublepedicle advancement. B. and compound flaps.SRPS Volume 10. Distant flaps use donor tissue from sites that are not adjacent to the recipient bed. Numerous anatomic studies of the blood supply to the skin and fascia have contributed to our understanding and led to a simpler classification of cutaneous flaps. composition. Little Brown. Aston SJ (eds). fasciocutaneous. and can be grouped into direct flaps. 47 The simplest example of this type of movement is direct wound closure. the simplified terminology does not extend to all flap types.20. the fasciocutaneous flap that was originally defined by the presence of deep fascia is now classified according to the pattern of cutaneous vascularity through the fasciocutanous plexus.45. Suzuki and colleagues49 propose a variation of the traditional V-Y-plasty in which the Burow’’s triangles are advanced rather than excised. 4th ed. and frequently does not include fascia. single-pedicle. musculocutaneous. 7 . transposition. septocutanous. Y-V. Local skin flaps are used to close defects adjacent to the donor site. A fasciocutaneous flap can be any flap based on the fasciocutaneous plexus and composed of any or all of the component layers between the skin and deep fascia. and bipedicle flaps) and flaps that pivot on a point (rotation. without any rotation or lateral movement. (Reprinted with permission from Smith JW.25 The new terminology of perforator and venous flaps also reflects the trend toward vascularitybased nomenclature. Grabb and Smith’’s Plastic Surgery. Grabb and Smith’’s Plastic Surgery.) Fig 13. (Reprinted with permission from Jackson IT: Local Flaps in Head and Neck Reconstruction. Aston SJ (eds). Boston. the flap must be designed longer than the defect to be covered. Because the effective length of the flap becomes shorter the farther the flap is rotated. The flap becomes shorter as it pivots and should be designed larger than the defect. The three limbs of the Z must be of equal length and the lateral limb to central limb angles should be equivalent. Boston. Mosby. 1991. and pitfalls. Seyhan52 explores the geometry of Z-plasties and reminds us that a single large Z-plasty is more effective than multiple smaller ones for lengthening the skin in a desired location. and Lamberty BGH. A variation of the transposition flap is the Z-plasty technique in which two triangular flaps are reversed and rotated 90°. A back-cut may be needed to ease tension at the base. Rotation flap. principles of design. Little Brown. direct suture. 1991. Boston. Number 1 Fig 11. Little Brown.) A transposition flap is a (usually rectangular) flap that is rotated (laterally) about a pivot point into an immediately adjacent defect.50 The 60° Z-plasty is most effective because it lengthens the central limb without placing too much tension laterally (Fig 14). Little Brown. Fig 12. Furnas and Fischer51 estimate that the actual gain in central limb length is 55%––84% of predicted and varies with local skin tension. Mastery of Plastic and Reconstructive Surgery. The gain in length is related to the angle between the central and lateral limbs (Table 1).) 8 . Aston SJ (eds). bilobed flap (Fig 13). 1994. 1985. 4th ed. 4th ed. In: Cohen M (ed). The flap donor site can be closed by skin graft. The bilobed flap. Healy C: Flaps: physiology. (Reprinted with permission from Smith JW.SRPS Volume 10. St Louis. (Reprinted with permission from Smith JW. Grabb and Smith’’s Plastic Surgery. otherwise a backcut may be necessary (Fig 12). or secondary flap——eg. Transposition flap. (Reprinted with permission from Smith JW. 1999. The longitudinal axis of the rhomboid excision parallels the line of minimal skin tension. Aston SJ (eds). Keser and colleagues54 described a curvilinear modification of the classical transposition flap. the donor sites of the flap are closed by direct suture. Four different rhomboid flaps can be designed when 60° angles are used (Fig 15). After elevating the flaps and undermining the adjacent tissue. 1991. Grabb and Smith’’s Plastic Surgery.) The rhomboid (Limberg) flap is another transposition flap characterized by its geometric pattern.53 The Dufourmentel flap is similar to the rhomboid flap except that it can be drawn with angles of up to 90°. and B and B’’ flaps to D and D’’. Little Brown. (Reprinted with permission from Rohrich RJ. 1991.SRPS Volume 10. (Reprinted with permission from Keser A. 4th ed. Boston. Boston. Sensoz O.) 9 . 4th ed. Grabb and Smith’’s Plastic Surgery. respectively.) Fig 15. This concept can be expanded to create a double or even a triple rhomboid flap. Plast Reconstr Surg 102:1001. Fig 16. Their variant has double opposing semicircular flaps and is used to close circular defects (Fig 16). Double opposing semicircular flaps. Aston SJ (eds).) Fig 14. Zbar RIS: A simplified algorithm for the use of Z-plasty. flap A is transposed with flap B and flap A’’ with flap B’’. Plast Reconstr Surg 103:1513. Little Brown. Mengi AS: Double opposing semicircular flap: a modification of opposing Zplasty for closing circular defects. The angles of A and A’’ flaps are sutured to the marks at x and x’’. The rhomboid (Limberg) flap. (Reprinted with permission from Smith JW. 1998. Number 1 TABLE 1 Theoretical gain in length of the central limb with various angles in Z-plasty. Z-plasty. Vol 1. Vol 1. Saunders. 1990. Vasconez LO. Success rates of microvascular procedures is well over 90% in most series. Philadelphia. In: McCarthy JG (ed). Ch 42. cross-leg. Several reports of free flap reconstruction followed in short order. Clinical microsurgery has experienced a rapid expansion since its beginning in the early 1970s. The neurovascular island flap (Littler). (Reprinted with permission from Daniel RK. Grabb’’s Encyclopedia of Flaps. and groin flaps. In 1963 Goldwyn and colleagues56 reported the first successful free flap transfer when they elevated an island pedicled flap from the groin of dogs and subsequently divided the pedicle and replaced the flap in its original site with microvascular anastomoses. Ch 9. Boston. 1990. (Reprinted with permission from Mendelson BC. so that the flap pedicle must pass over or under the intervening tissue.) Free Tissue Transfer Fig 17.SRPS Volume 10. tube flaps55 (Fig 18) or microvascular free tissue transfers are indicated. The clavicular tubed flap. Plastic Surgery. In: Strauch B. Examples of interpolation flaps are the deltopectoral (Bakamjian) flap. When the two sites cannot be approximated. Fig 18. Hall-Findlay EJ (eds). and subcutaneous-pedicle flaps. p 305. Number 1 Interpolation flaps rotate on a pivot point into a defect that is near but not adjacent to the donor site. Examples include direct flaps (not to be confused with direct cutaneous) such as the thenar. Kerrigan CL: Principles and physiology of skin flap surgery. please refer to the Selected Readings issue on this topic. 10 . Masson JK: Cervical and clavicular tubed skin flaps.) Distant flaps imply that the donor and recipient sites are not in close proximity to each other.57 For a detailed overview of microsurgery and free tissue transfer. island flaps such as the Littler neurovascular digital pulp flap (Fig 17). Little Brown. the andromeda thigh flap. usually muscle or septum. technically easy to raise and transfer.62 Cormack and Lamberty1. Nakajima36 analyzed and classified the 3-dimensional structure of the skin and adipofascial tissue into six types and described their corresponding flap applications in a study that is becoming increasingly relevant from a clinical standpoint. intrafascial. Nakajima’’s definition of a direct cutaneous perforator is equivalent to the axial vessel of McGregor and Morgan. and that would produce minimal donor site morbidity. not their tissue components. adipofascial.SRPS Volume 10. musculocutaneous. Perforator Flaps By the early 1980s. Number 1 Tissue Composition and Vascularity Cutaneous Flaps McGregor and Morgan59 categorized flaps as random or axial. Allen and Treece7 and Blondeel8 reported the ultimate muscle-sparing TRAM flap when they published their successful series of breast reconstructions with the deep inferior epigastric perforator flap. and deep adiposfascial layers. subdermal. before entering the deep fascia. Taylor and Palmer20 state that cutaneous arteries contributing to an angiosome can arise directly from the underlying source vessel to provide the primary cutaneous supply. septo- cutaneous pedicle. and the posterior thigh flap.65.30 Hallock25 differentiates direct and indirect perforators based on the structures that they traverse prior to piercing the deep fascia.63 state that skin flaps can be classified as direct cutaneous. and suprafacial vascular plexuses encompassing the dermal. which was dissected retrograde. Milton60 challenged the relevance of length-to-width ratios and accurately argued that the survival of a skin flap depends entirely on its means of vascularization. Fasciocutaneous flaps were further grouped into six types based on the six patterns of deep fascial perforators (see Fig 6). or musculocutaneous pedicle.66 Nakajima35 classified skin flaps into five types according to their vascularization: cutaneous. or fasciocutaneous vessels. which included a description of the anterolateral thigh flap. 20.59 Mathes and Nahai67 defined fasciocutaneous flaps as those supplied by a direct cutaneous pedicle. or indirectly from the branches of the source artery to deeper structures. Indirect perforators pass through deeper tissues. thin. Each flap was designed over a septocutaneous perforator of the source vessel. septocutaneous. Axial pattern flaps contain a specific direct cutaneous artery within the longitudinal axis of the flap. and may require multiple delays to be transferred to a distant site. In 1989 Koshima and Soeda6 reported the successful transfer of an inferior epigastric artery skin flap based on a rectus abdominis perforator to a groin wound (island) and to the floor of mouth. a classification system that can be applied to all cutaneous flaps has been devised.35. which includes the interconnected component parts of the subfascial.23.68 In China and Japan the first perforator flaps were developed for head and neck reconstruction and burn scar contractures. Random flaps are based on the subdermal plexus which is supplied by direct cutaneous. microsurgical techniques had been successfully integrated into the practice of reconstructive surgery and there was a quest to discover new donor flaps that would be reliable. or between muscles. and musculocutaneous (Table 2). fasciocutaneous.36. Flaps based on isolated perforator(s) are defined as perforator flaps. regardless of origin. All skin flaps are supplied by perforating vessels to the fasciocutaneous plexus. Hallock25 defines a perforator as any vessel that enters the suprafascial plane through a fenestration in the deep fascia.64 The fasciocutaneous plexus is supplied from perforating vessels that penetrate the deep fascia either directly. All skin flaps are based on the fasciocutaneous plexus. or fasciocutaneous according to their anatomic system of vascularization. In 1984 Song et al5 reported the ““free thigh flap””. An island flap is an axial pattern flap that is raised on a pedicle devoid of skin to facilitate distant transfer.61 Since the vascular anatomy of fasciocutaneous perforators was detailed.1 Random flaps are traditionally limited to 3:1 lengthto-width ratios. Hallock25 applied this concept to the classification of deep fascial perforators proposed by Nakajima35 whereby all cutaneous flaps could be designated as either direct or indirect perforator flaps (Fig 19). superficial. through muscle. Direct perforators pierce the deep fascia without having traversed any deeper structures. Gluteal artery perforator flaps were first raised as pedicled flaps by 11 . Perforator flaps and the less-successful arterialized venous flaps evolved from these efforts.35. musculocutaneous. ) Fig 19. Ann Plast Surg 16:1. Perforator flaps are typically composed of skin and subcutaneous tissue supplied by a deep fascial perforating vessel. 1986. and many also have the capacity to incorporate muscle. Angrigiani et al9 developed the ““latissi- mus dorsi musculocutaneous flap without the muscle””. Plast Reconstr Surg 111:855. Adachi S: A new concept of vascular supply to the skin and classification of skin flaps according to their vascularization. and later by Allen and Tucker10 as free flaps for breast reconstruction. producing minimal donor site morbidity. Fujino T. 12 . The introduction of perforator flaps ushered in an era of sophistication and refinement in reconstructive microsurgery.) Koshima69 for the repair of sacral wounds. (Reprinted with permission from Hallock GG: Direct and indirect perforator flaps: the history and the controversy. Perforator flaps allow the surgeon to reconstruct body parts with the same tissues that are most frequently missing: skin and subcutaneous fat. Our understanding of cutaneous vascularity and perforator anatomy has grown tremendously in the past 10 years. Number 1 TABLE 2 Classification of Skin Flaps (Reprinted with permission from Nakajima H. The emphasis shifted from trying to ensure free flap survival to preserving muscle function. Potential flap donor sites are numerous. fat. Modification of Nakajima’’s pattern of deep fascia perforators. and bone into the flap design.SRPS Volume 10. a flap of skin and subcutaneous tissue based on a thoracodorsal artery perforator. and designing flaps that are highly versatile and can be tailored to the specific defect. 2003. potential for being harvested as compound or sensate flaps. meticulous dissection of the pedicle. flaps based on the lateral circumflex femoral vessels are named the anterolateral thigh flap. The vessels that supply blood to the flap are isolated perforator(s).20.80. and so on. To qualify as a potential donor source of perforator flap.25. The indirect muscle and septal perforators give rise to musculocutaneous and septocutaneous perforator flaps. a consensus was reached at the meeting to name each perforator flap after the nutrient vessel(s) and not the underlying muscle. 2002) were held in response to the rapid evolution of perforator flaps and confusion regarding their terminology.65 In areas where multiple perforator flaps can be raised from 13 .94 The most commonly used perforator flaps are the deep inferior epigastric (DIEP) flap. which requires intramuscular dissection and which should therefore have a distinct identity from the more easily dissected septal perforator.) Wei21 and other purists70. and 3) direct cutaneous perforators65 (Fig 20).81––83 These characteristics make perforator flaps ideal soft-tissue units for reconstruction in areas that require thin. The development of supermicrosurgical techniques has facilitated the harvest of flaps based on smaller and shorter perforators.5 mm diam) perforators. tensor fasciae latae perforator flap. such as the head and neck and the lower extremity. respectively.71 continue to argue that a ““true perforator”” should only refer to a muscular perforator.69. the anterolateral thigh (ALTP) flap.14. pliable tissue.18.82––87 The disadvantages of perforator flaps are 1) the time-consuming.19.88––93 Theoretically. Van Landuyt K. a single vessel. pedicles of sufficient length. Number 1 The Fifth (Gent. and ability to be thinned to the subdermal plexus.82. and location. (3) Direct perforators penetrate the deep fascia only.72 To lessen confusion over specific perforator flap nomenclature. and (preferably) be able to be closed primarily after flap harvest.65 The consensus definition of a perforator flap in 2002 was ““a flap consisting of skin or subcutaneous fat.65. (1) Indirect muscle or musculocutaneous perforators traverse muscle to pierce the outer layer of the deep fascia and supply the skin. a site must have a reliable blood supply.””65 Three different kinds of perforator vessels were recognized: 1) indirect muscle perforators.71.SRPS Volume 10. Many other flaps have been described but have not yet gained the popularity of the DIEP and the ALTP flaps. the superior gluteal artery (SGAP) flap. arterial.65 For example. size.74––80 Perforator flaps owe their versatility to the large cutaneous territories. such as the paraum- Fig 20. Taiwan.66 Flaps such as the groin flap that were previously classified as either axial.71.5 mm in diameter identified by Taylor and Palmer. (2) Indirect septal or septocutaneous perforators traverse through septum and supply the skin after piercing the outer layer of the deep fascia. Simplified definitions emerging from the 2002 Sixth International Course on Perforator Flaps. one or more large (>0. Belgium. 2001) and Sixth International Course on Perforator Flaps (Taipei. Clin Plast Surg 30:343. (Reprinted with permission from Blondeel PN. and the thoracodorsal artery (TAP) flap. the flap should be named after its anatomic region or muscle. 2) variation in perforator anatomy.83. Perforator flaps have the following advantages:73 • preserve muscle function • produce minimal donor site morbidity • reduce postoperative recovery time and pain medication requirements • can be designed of varying sizes and thicknesses to improve the esthetic result Many studies comparing the deep inferior epigastric (DIEP) flap and the TRAM flap for breast reconstruction attest to the postoperative advantages of muscle-sparing flap harvest. or cutaneous are now more accurately described as direct cutaneous perforator flaps. 2003. a perforator flap could be designed in each of the cutaneous territories of the 374 perforators >0. according to location or underlying musculature. and 3) a higher risk of fat necrosis compared with musculocutaneous flaps. Hamdi M.16. 2) indirect septal perforators. Monstrey SJ: Perforator flap terminology: update 2002. long pedicles that permit conventional and free transfer. These perforators may pass from their source vessel origin either through or in between the deep tissues (mostly muscle). Example: Ponten’’s flap. This vascular plexus is localized to the level of the deep fascia. which is performed with supermicrosurgical techniques that eliminate the need for tedious dissection of the source vessel. The reader is encouraged to review the references on perforator flaps independently because an in-depth description of specific flaps is beyond the scope of this text. These flaps are all based on type II vessels. The flaps are raised on a pedicle of adipofascial tissue and designed of appropriate width to include the relevant vascular system.72 In 1992 Masquelet105 described the concept of a neuroskin flap based on the arteries accompanying cutaneous nerves. neurocutaneous and venocutaneous perforators running long in the deep adipofascial layer of the skin. neuroadipofascial (NAF). Although Ponten made the initial clinical observations. Eventually it became evident that inclusion of the deep fascia was not necessary for the survival of fasciocutaneous flaps. and veno-neuroadipofascial (V-NAF). The perforator is used for the anatomosis.98 although some authors advocated its preservation for protection of the fascial plexus. Number 1 bilical perforator flap.65.SRPS Volume 10. Nakajima and colleagues106 described the neurocutaneous and venocutaneous vascular systems and three types of pedicled fasciocutaneous flap in the extremities: venoadipofascial (VAF).36. Type C flap supports its skin by multiple small perforators along its length in a ladder type configuration.99 confirmed the usefulness of the fasciocutaneous flap and expanded the concept to encompass reconstruction in other parts of the body. Fasciocutaneous Flaps In 1981 Ponten95 described a novel way to raise a skin flap based on the vascular plexus of the deep fascia.63. Type A is a pedicled flap supplied by multiple fasciocutaneous perforators at the base of the flap and oriented with the long axis of the flap in the predominant direction of the arterial plexus at the level of the deep fascia. It may be used as either a pedicled or free flap. Type B modified is still fed by a single perforator but differs in that the perforator is removed in continuity with the major vessel from which it arises.21––25 A cutaneous perforator is identified by Doppler probe and a flap is designed on the skin territory. which in turn gives off branches to the skin. These perforators reach it from a deep artery by passing along a fascial septum between muscles. It is intended for use as a free flap.11.100 classified fasciocutaneous flaps according to their vascular patterns (Fig 21). The flap can be proximally or distally based and the skin can be removed to create an island flap. The investigation of the fascial vascular anatomy to develop flap classification systems contributed greatly to our understanding of perforator and cutaneous blood supply. ie.99––103 reported that the fasciocutaneous system consists of perforating vessels that arise from regional arteries and pass along the fibrous septa between muscle bellies or muscle compartments.18 The ““free-style free flap”” is the ultimate application of the angiosome theory and supermicrosurgical techniques. Type B is based on a single fasciocutaneous perforator of moderate size which is consistent in both its presence and its location. Type D consists of an osteomusculofasciocutaneous free tissue transfer.25.25 Flaps that were previously considered fasciocutanous and that are based on isolated perforating vessels can now be accurately classified as direct or indirect perforator flaps. Any flap based on this vascular network regardless of its tissue components is a fasciocutaneous flap.35. in 1984 Cormack and Lamberty 63. Nakajima107 reported 23 successful cases of lower extremity reconstruction with VAF and V- 14 . Its main use is as a free flap.104 Nakajima35 described the fasciocutaneous plexus as a vascular network that extended from below the deep fascia to the dermis and was perfused by deep fascial perforating vessels. Tolhurst and colleagues98. Example: radial forearm flap. the investigations of the anatomical vascular basis for the success of these ““superflaps”” was subsequently accomplished by Haertsch96 in 1981 and Barclay et al97 in 1982.20. On the basis of anatomic studies. Example: medial arm flap. Early investigations into the blood supply of the fascia1. (Reprinted with permission from Cormack GC. Lamberty BGH: The Arterial Anatomy of Skin Flaps. A classification of fasciocutaneous flaps.) 15 . 1986.SRPS Volume 10. Edinburgh. Number 1 Fig 21. Churchill Livingstone. and proposed that the small veins bypass the valves in the lesser saphenous vein and are the venae comitantes to the artery that accompanies the larger vein. and not morbid. To the right of each flap a diagram shows which perforators are responsible for the blood supply of each flap. long veins along the course of the lesser saphenous vein that intermittenly anastomosed with the larger vein. Type D is the same as type A except the sural nerve has been removed. Risk factors for complications were comorbidity. The small N denotes weak vascularity to the skin. Imanishi42 evaluated the venous drainage of the distally based lesser saphenous-sural V-NAF pedicled fasciocutaneous flap in cadavers.46 Distal flap necrosis was treated with skin grafting in 2 patients. and donor site complications with the previous flap technique. Imanishi N. Fig 22. 60% of whom had at least one major systemic illness. Nakajima45 was the first to report the arterial supply to the lesser saphenous vein and the related flap. Cavadas110 transferred large reverse-flow neurocutaneous saphenous island flaps for lower extremity reconstruction in 5 patients. A venous island flap with an AV fistula was thus cre- 16 . Number 1 NAF flaps based on the lesser saphenous vein and sural nerve. He identified small. Fukuzumi S. Fraccalvieri et al108 reported a series of 18 patients treated with the distally based ““superficial sural flap”” for reconstruction of soft-tissue defects of the lower leg and foot. Although it can be raised as an innervated flap for coverage of plantar heel wounds. The flap modification was a response to difficult transposition. the vein. and was recommended as the most reliable flap choice. Cavadas111 reports transferring a posterior tibial perforator––saphenous subcutaneous flap in 40 cases. and their respective vascular systems. et al: Accompanying arteries of the lesser saphenous vein and sural nerve: anatomic study and its clinical applications. Baumeister and associates109 published a series of ““sural artery flap”” reconstructions in 70 patients. The complication rate was 59%. thin. The lesser saphenous-sural V-NAF flap includes the nerve. the sural nerve is usually preserved and therefore the donor morbidity is less than that of the neurocutaneous flap. 1999.) Venous Flaps The introduction of venous flaps in the 1980s was a result of the quest to develop the ideal free flap: one that was easy. Type B is the same as type A except the sural nerve has been removed from the upper flap. (Reprinted with permission from Nakajima H. poor pedicle coverage. osteomyelitis. Plast Reconstr Surg 103:104. Nakayama et al113 and later Jii and colleagues114 and Nichter and Haines115 reported arterializing a flap through a venous pedicle.SRPS Volume 10. Theoretical flaps with a proximal base. The authors reported superficial necrosis in one patient who required grafting and delayed healing in 2 patients. and a tight subcutaneous tunnel. In a followup article 6 years later. Type A contains both the lesser saphenous vein and sural nerve. reliable. Type C is the same as type A except the lesser saphenous vein has been removed from the upper flap. Chen112 reported a series of 21 patients who had lower extremity reconstruction with the distally based ““saphenous venofasciocutaneous flap”” (Fig 23). Four distally based and four proximally based types of flap are identified (Fig 22). flap necrosis occurred in 36%. and no flap survived longer than 48 hours. Yuan. Baek117 proposes a ““to-and-fro”” oscillating mechanism of flow in the vein. and venous capillaries. Theoretical flaps with a distal base. Thatte and Thatte122 classify venous flaps into three groups. Also observed was ongoing revascularization.119 These single-pedicled island flaps can be further classified into either proximally based or distally based flaps. (Reprinted with permission from Nakajima H. Plast Reconstr Surg 103:104. Number 1 Fig 23. They divide the survival process into an early (up to 72 hours) venous nourishing stage and a secondary (day 4 to 6 weeks) stage of neovascularization characterized by arterial nourishing and vascular reconstruction. Shalaby and Saad126 identified an arterial network in the perivenous areolar tissue on histologial study of the saphenous and cephalic venous island flaps. Xiu and Chen127 reported that the perivenous areolar tissue is essential for flow-through flap survival and conclude that it is both protective and nourishing.) ated and was reported to have up to 95 % flap survival and high patency rates. Types A’’. Germann and associates116 showed that although blood flow in pig island flaps was reversed. The flow through venous flap in which both the afferent and efferent pedicles are supplied by venous blood was described in 1985 by Baek et al. In 1987 a single-pedicled venous island flap using the saphenous vein was created in a dog by Thatte and Thatte. or pure venous flap with a single cephalad vein as the only vascular conduit.124 Noreldin and others125 attributed survival to a perivenous areolar network of vessels arranged longitudinally along the whole length of the pedicle. The survival of these flaps. According to this classification. venules. Amarante and coworkers120 concluded that single-pedicled venous flaps cannot survive without flow-through. review the experimental and clinical studies on venous flaps. C’’. Chavoin118 applied this in a clinical setting. For larger flaps to survive. Thatte and Thatte122 type II venous flaps are bipedicled ““flow-through”” flaps with afferent and efferent veins exhibiting flow from caudal to cephalad. The type I venous flap would be classified by the author as a venocutaneous adipofascial flap. a dense venous network is essential. early thrombosis was a common occurrence. 1999. B’’.117 who used the saphenous vein of a dog. Fukuzumi S. however. was not consistent. et al: Accompanying arteries of the lesser saphenous vein and sural nerve: anatomic study and its clinical applications. Imanishi N. and Lenoble et al’’s121 flow-through venous flaps all died despite blood flow within the venous system.SRPS Volume 10. type I is a unipedicled venous flap. Nakajima’’s45 anatomic study and description of the intrinsic and extrinsic venocutaneous vascular system confirmed the presence of perivenous arterial flow of the single-pedicled venous flap. Inada’’s group128 isolated their flaps from the recipient tissue bed and concluded that flow-through venous flaps with only a single vein cannot survive if larger than 1––2 cm. oxygen consumption remained below baseline. which ultimately supplied the flap and which is essential for flap survival. and discuss the various theories of flap survival. Shan. and D’’ are reverse flaps of the proximally based flaps. and Zhu123 describe two patterns of flow in pure venous flaps: a shaking movement related to heart rate and a pendulum-like movement that is the main contributor to flap perfusion. Two years later. which suggests that more than one vein would probably be benefi- 17 . and then back to the venous system and the original vein. He points out that the circulation of blood in venous flaps is based on speculation. Three types of arterialized venous flaps. Krishnan133 confirmed these conclusions and also reported that according to their experimental model. Plast Reconstr Surg 91:303. Imanishi and colleagues138 propose the presence of arteriovenous shunts around the efferent vein of their arterialized cephalic venous flaps. the survival of venous flaps continuous to be inconsistent. Ueda et al140 noted increased survival of flow-through venous flaps when delayed. to perivenous arterial network. by G Inoue. The quality of the surviving flap improved with increased perfusion pressure and better oxygenated blood. retrograde inflow/retrograde outflow. Several studies have demonstrated improved survival of venous flaps with prearterialization and delay procedures. Chen. and credits a number of authors for various explanations. The authors propose that the resistance to flow from the vein’’s valves forces blood into the flap’’s periphery. perfusion pressure. Using infrared thermography. Wolff et al141 examined three types of venous flaps with regard to their perfusion and long-term results. Fig 24. Lee130 reviews the concept of venous flaps and the arterialization of the venous system and illustrates three kinds of arterialized venous flaps (Fig 24). orthograde inflow/retrograde outflow.134––137 Unfortunately.SRPS Volume 10.68. At 4 months the survival rate for arterialized venous flaps was 92. Chavoin et al118 describe a reverse shunt from venules to arterioles followed by orthograde flow from arterioles to capillaries and then to normal venous channels. Moshammer et al132 reported in an experimental study that the circulation at the periphery of the arterialized venous flap can be enhanced by retrograde arterialization.129 They surmised that these flaps behave not unlike a graft whose survival depends largely on the surrounding circulation. The largest area of perfusion was seen in bidirectionally perfused flaps. K Suzuki. Studies by Chow. The mechanism of perfusion of venous flaps is still not completely understood and has been attributed to a number of factors such as plasmatic imbibition.7%. These include orthograde inflow/orthograde outflow. sites of arteriovenous anastomosis. (Reprinted with permission from Lee WPA: Discussion of ““Arterialized venous flap for treating multiple skin defects of the hand””. venous flaps arterialized against the valves achieved a larger perfusion area than flaps perfused in the direction of the valves. Number 1 cial. to pure shunting (where no perfusion of the flap occurs but rather blood flows directly from the afferent to the efferent channels). 1993. perivenous arterial networks. and Gu139 noted better survival of true arterial flaps than arterialized venous flaps. Possible patterns of blood flow in the arterialized venous flap range from pure retrograde (from a venous to a venous system). and retrograde inflow/ orthograde outflow. vein-tovein interconnections and other vascular networks. They chose the fourth system because the valves are rendered incompetent by the high pressure of the arterial inflow. through reverse shunting (from venules to arterioles followed by normal orthograde flow). They describe the route of flow as being from vein to perivenous network. Type III venous flaps are arterialized through a proximal arteriovenous anastomosis and drained by distal veins. and the circumvention of venous valves. to the arterial system. 18 .) Yilmaz et al131 describe the four options in hooking up their radial forearm venous flap. Cho et al68 reported a clinical series of 13 delayed arterialized venous flaps. They were able to increase the functional size of the flap to 7 x 11 cm from the 3 x 8 cm reported by Nakashima. and fast and expedient flap elevation. and 7. and frequent need for skin graft coverage of donor sites. Chia and colleagues148 describe the successful retransplantation of a venous-network-pattern skin flap using a 12 x 12 cm skin paddle from the medial aspect of the right thigh transferred to the distal lower extremity. De Lorenzi and colleagues145 reported 40 cases of digital soft-tissue reconstruction with arterialized venous free flaps. Number 1 for flow-through venous flaps. Klein et at152 reported 4 cases of partial flap necrosis and 8 cases of total flap necrosis in a series of 29 free arterialized forarm flaps for intraoral reconstruction. about 31%. The smaller vein was for arterial inflow and the larger for venous outflow.150 Yilmaz and collegues151 reported successful free flap transfer of an arterial- ized venous flap measuring 8 x 12 cm from the forearm to the face. venous congestion. delayed healing.SRPS Volume 10. They note the advantages and disadvantages of each type and conclude that venous flaps are not intended to replace more conventional flaps. one was a partial failure. the saphenous vein). Galumbeck and Freeman144 performed human anatomical studies the results of which suggested that only the venous tributaries of the flap receive blood.132.132. Wungcharoen and others137 reported the repair of extremity wounds with a prearterialized venous flap in 8 patients. Of the 5 type II flaps. restricted location of donor sites to maximize the venous plexus. For the 19 .143––145 Clinical trials of prearterialization and delay procedures report improved flap survival68.5% had superficial epidermolysis. variable rate of tissue necrosis. 50% in one patient. susceptibility to infection. Kovacs153 compared two types of arterialized forearm flaps for oral reconstruction. Flap survival was reported to be 93%––100% of the surface area. In 1977 Ger155 reported successful closure of open wounds in 43 cases. The main disadvantages of venous flaps are limited size of the flap. Muscle and Musculocutaneous Flaps The initial work describing the principles. Type II was an arterialized flap with two parallel veins on the proximal flap. They concluded that arterialized venous flaps are the safest type of venous flaps. subcutaneous tissue. There was total flap survival in 57. Musculocutaneous flaps are composites of skin. Koshima et al143 used the saphenous vein and incorporated an osseous component. 17.68. anatomically constant pedicle (eg.130.137 with these measures.5% had total flap necrosis. and clinical applications of muscle flaps was done by Ger154 in the late 1960s. Arteriovenous shunts were created at the donor site 2 weeks before flap harvest. 62.142––145 The poorly understood physiology and unpredictable survival of venous flaps makes the clinical application of these flaps contoversial. potential (though unlikely) hemodynamic complications of a surgically created AV shunt. The clinical advantages of venous flaps are minimal donor site morbidity requiring only the sacrifice of a vein and no artery. a long and very thin. Tansini156 was the first to make use of musculocutaneous flaps in 1906 when he reconstructed a breast with a combination of skin and latissimus dorsi muscle raised as one unit.129. Postoperative congestion was present in all flaps and resolved within 14 days. Four of the 5 type I flaps showed total or subtotal success and one was lost. The surviving surface of the flap was 100% in 10 patients. Type I was a single vein arterialized flow-through flap. specifically the radial forearm flap.4%. theoretically to avoid bypassing the flap tissue. 17.5%. Nishi and colleagues146 and Inoue and Suzuki142 report using arterialized venous skin flaps for the treatment of skin defects in the hand. The authors applied an arterialized saphenous vein fasciocutaneous graft to cover tissue defects on both the upper and lower extremities. 3 were lost.5% had full-thickness necrosis that required grafting. Noordhoff’’s group147 applied venous flaps in 28 patients and categorized their operations into four types. 70 % in one patient. and 0% (total necrosis) in one patient. and for venous island flaps. operative procedures. and the other one was a total success. and underlying muscle and fascia supplied by a dominant vascular pedicle. Stewart and Puckett149 review the safety of reverse venous flow in free flap transfers. The authors concluded that blood flow is not affected by the presence of bacteria. gracilis Type III —— two dominant pedicles——eg. fat. Specialized flaps can provide sensory and functional muscle to areas requiring special needs. In later articles McCraw164. sartorius Type V —— single dominant pedicle and secondary segmental pedicles——eg. Chen.SRPS Volume 10. Chang. but was significantly greater in the musculocutaneous wound space (dropping by a factor of 104) than in fasciocutaneous flaps.169 postthoracotomy mediastinitis.174 and Perkins175 successfully treated chronic intrathoracic sepsis with free latissimus and TRAM flaps containing muscle. but musculocutaneous flaps showed better tissue ingrowth into an inoculated wound space than fasciocutaneous flaps. fasciocutaneous flaps showed a gradual but steady rise in flow.166 By means of radiolabeled microspheres. Hallock176 proposed a useful classification of compound flaps based on their vascularization.161 subsequently applied this concept clinically.171. and Mathes168 found that fasciocutaneous flaps were less resistant to the effect of bacterial inoculation and exhibited less collagen deposition than musculocutaneous flaps. The authors emphasized the concept of a dominant vascular pedicle that supplies blood to a muscle and its overlying skin territory through perforating vessels. and bone based on a solitary vascular pedicle. The clinical application of muscle to infected wounds has been successful in osteomyelitis. reliability. fat. muscle. Blood flow was also similar between equivalent tissue layers. which allows single-stage reconstruction of complex defects. latissimus dorsi Compound and Prefabricated Flaps Flaps can consist of any number of tissues in virtually any combination. fascia. cited sources of original descriptions of yet more such flaps. The greatest decrease in bacterial concentration also occurred in the first 24 hours. and genitalia. Compound flaps are defined as diverse tissue compo- 20 . their papers are still considered to be classics in the history of reconstructive plastic surgery. gluteus maximus Type IV —— segmental vascular pedicles——eg. and Carraway162. foot.170 and prosthetic grafts. The idea that flat muscles (eg. pectoralis and latissimus muscles) could ““carry”” their overlying skin as composite flaps came independently to Hueston158 and DesPrez. The primary disadvantages of muscle and musculocutanoeus flaps are the functional deficit at the donor site and the bulk of the flap. using the gracilis musculocutaneous unit in penile reconstruction and to repair an ankle defect. which only decreased by 102. In 1979 Mathes and Nahai67 developed a useful classification of the blood supply to individual muscles.159 Orticochea160.165 traced the evolution of musculocutaneous flaps.29 Graham and Dellon177 review specialized flaps in reconstruction of the hand.155. tensor fascia lata Type II —— dominant pedicle(s) and minor pedicle(s)——eg. a compound flap from the neck.163 described the vascular territories of several new musculocutaneous units and defined flap dimensions and useful arcs of rotation. Dibbell. and reviewed the basic principles of musculocutaneous flap anatomy and physiology. and application of specific flaps were subsequently found to be inaccurate. and skin. The primary advantages of muscle flaps are the potential to ablate dead space with vascularized tissue and an increased resistance to infection. breast. Gosain et al167 noted a marked increase in blood flow to all levels of tissue in both musculocutaneous and fasciocutaneous flaps after elevation.173 Hammond.176 Composite flaps are a type of compund flap that often incorporate skin. In 1977 McCraw. Number 1 next 50 years no one took notice of this event until Owens157 in 1955 reported the repair of massive facial defects with the sternocleidomastoid flap. Musculocutaneous flaps showed a rapid rise in blood flow that leveled by 24 hours. The authors described five types of muscle on the basis of their circulatory patterns (Fig 25 and Table 3): Type I —— single vascular pedicle——eg.172 The benefits of muscle extend to free flaps. Calderon. oropharynx. In contrast. Compound flaps are defined as diverse tissue components that are incorporated into an interrelated unit. The design of a musculocutaneous flap requires anatomic knowledge of the vascular architecture of the muscle and the distribution of cutaneous perforators that will supply the skin paddle. Although some details of the geometry. more accurately. The concept of flap prefabrication (or. Hallock ‘‘s classification places these complex flaps into two groups. Lamberty BGH: The Arterial Anatomy of Skin Flaps. 1986. prelamination178) was introduced clinically by Orticochea179 and Washio180 in 1971.) TABLE 3 Examples of Common Muscle Flaps by Type (Reprinted with permission from Cormack GC. Edinburgh. Nahai F: Classification of the vascular anatomy of muscles: experimental and clinical correlation. and sequential flaps (Fig 26).SRPS Volume 10. Compound flaps of mixed vascularization are further subdivided into Siamese flaps. The compound flap with solitary vascularization is a composite flap that incorporates multiple tissue compo- nents dependent on a single vascular supply. (Reprinted with permission from Mathes SJ. 1981. those with solitary vascularization and those with combinations of vascularization.) nents such as bone. fascia. Churchill Livingstone. skin. and muscle that incorporated into an interrelated unit. Plast Reconstr Surg 67:177. The 21 . Number 1 Fig 25. Five patterns of vascular anatomy of muscle. conjoint flaps. histamine. such as distention. Khouri et al185 address facial reconstruction with an expanded prefabricated flap. 2000. or sequential.1 Daniel and Kerrigan62 find two kinds of regulatory factors of cutaneous blood flow. which contributes to vasodilation. Simultaneously cholinergic fibers initiate bradykinin release. folding or kinking) compared with axial-pattern flaps. while Komuro et al188 note no significant difference in survival of prefabricated arterialized venous flaps compared with controls. Homma et al186 concluded that expanded musclevascularized prefabricated flaps have larger areas of survival than expanded fascia-vascularized flaps. Other authors suggest that because neovascularization is necessary for a successful flap. including ““vascular induction”” of specific blocks of tissue which are not naturally perfused by anatomically well-defined axial vessels——ie. 22 . prefabricated flaps are even more versatile. and Shaw182 review the principles of flap prefabrication and list specific advantages to their use. Serotonin.178 creation of a larger flap than would otherwise be possible. temperature. The flaps were placed under an expander in the supraclavicular region. endothelium-mediated vasoconstriction. conjoint. Khouri. The microcirculation is also where thermoregulation of blood flow——the skin’’s primary function——occurs. local injury.) flaps in facial reconstruction. Combined with skin expansion and a delay procedure. A number of factors contribute to the regulation of blood flow. Upton. FLAP PHYSIOLOGY Regulation of Blood Flow to the Skin Flap physiology begins at the level of the microcirculation. Systemic control is facilitated in one of two ways: technique allows for the creation of an ““unlimited array of composite free flaps””181 that would otherwise not be available with standard flaps. thromboxane A2. Alpha-adrenergic receptors induce vasoconstriction and beta-adrenergic receptors induce vasodilation. and evaluation of functional status before the transfer of the flap. Combined flaps may be Siamese. • Humoral regulation causes vasoconstriction through the action of epinephrine and norepinephrine on alpha-adrenergic receptors in the cutaneous vessels. Others have used it to create a flap incorporating a prefabricated vascularized periosteal graft with good osteogenic capacity.182 In another article. they maintain basal tone of vascular smooth muscle at the arteriovenous anastomoses. reduced donor site morbidity. Maitz. and prostaglandin F2-alpha may also produce vasoconstriction.184 In the future. which subsequently produced a capsulofasciocutaneous flap after expansion was completed. simple muscle flaps may be transformed into molded vascularized bone grafts through prefabrication. systemic and local. neural control. Maitz187 observed increased survival of delayed prefabricated flaps. arterioles. prelamination. Although this flap is not intended to replace the forehead for specific • Neural regulation acts through sympathetic adrenergic fibers. Compound flaps may be subdivided into either solitary or combined types based on their source of vascularization. and prostaglandin-E1 cause direct vasodilation (Fig 27). and viscosity. and Hergrueter191 note decreased survival of prefabricated flaps subjected to mechanical pressures or restraints (eg. Plast Reconstr Surg 105:1465. Number 1 Fig 26. (Reprinted with permission from Hallock GG: Simplified nomenclature for compound flaps. induced. The authors describe creation of the prefabricated. a delay of at least 4 weeks189 and even up to 8 weeks190 should be observed. and arteries. which was used by Barton183 to incorporate skin and cartilage in a forehead flap for nasal reconstruction. while bradykinin. The authors describe ““pretransfer grafting””. expanded (PIE) flap using both a pedicled temporoparietal and free radial forearm fasciocutaneous flaps. Pribaz. Combined. it does provide certain advantages when needed.SRPS Volume 10. Lamberty BGH: The Arterial Anatomy of Skin Flaps. whereas sympathetic vasoconstrictors are the predominant means of regulating blood flow to the skin. Saunders. These same concepts of blood flow regulation can be applied to muscles. Biochemical agents affecting the circulation. In summary.SRPS Volume 10. In the scheme of local control. 1994. which has higher metabolic requirements. Fig 28. and blood flow is minimally changed in response to temperature fluctuations. metabolic autoregulation is limited in muscle but does exceed that of skin. although muscle has a much higher capillary density than skin. and the importance of the endothelium as a mediator of vasodilation and constriction. Philadelphia. hypoxia. (Reprinted with permission from Daniel RK. store. • Physical factors that influence blood flow include the myogenic reflex. With regard to systemic control. in direct contrast to the vasoconstriction seen in skin.) The effects of local injury to a part of the arterial wall can completely override basal vascular tone and cause spasm even in the absence of sympathetic innervation. And because the metabolic demand of muscle is greater than that of the skin. The authors discuss the concept of co-transmission. Number 1 hyperkalemia. Physiologic factors that regulate the cutaneous microcirculation. while hypertension results in vasodilation. • Metabolic factors act primarily as vasodilators and include hypercapnea. autoregulation plays a more important role. and extensive crushing or tearing can induce a widespread and prolonged spasm distantly (Fig 28). These factors are not as significant in the skin as in muscle. whereby nerves synthesize. Kerrigan CL: Principles and physiology of skin flap surgery. Humoral regulation is similar except that epinepherine causes vasodilation. Myogenic tone is important in muscle regulation but has little effect on cutaneous vessels. arteriovenous shunts are absent. Neuronal controls such as exercise and arterial hypotension induce a reflexive vasoconstriction. Churchill Livingstone. Ch 9. Edinburgh.1 For instance. and 23 . which triggers vasoconstriction in response to distention of isolated cutaneous vessels and thereby maintains capillary flow at a constant level independent of arterial pressure. The effects of hematocrit were questioned by Kim et al.) Local effects (autoregulation) are mediated by metabolic and physical factors. Burnstock and Ralevic193 review new insights into the local regulation of blood flow.192 who concluded that normovolemic anemia (hct 19%) had no significant effect on the survival of pedicled musculocutaneous flaps. Plastic Surgery. acidosis. 2nd ed. and release more than one transmitter. Local hypothermia (which acts directly on the smooth muscle in vessel walls) and increased blood viscosity (hematocrit >45%) may also decrease flow. In: McCarthy JG (ed). Vol 1. (Reprinted with permission from Cormack GC. a pin prick elicits a persistent isolated ring contraction locally. 1990. the mechanisms of blood flow regulation are different in skin and muscle. Flap Transfer The elevation of a skin flap results in many profound changes that drastically disrupt the finely bal- Fig 27. become functionally significant at 5 to 7 days. little or no improvement in circulation during the initial 48 hours. resulting in higher levels of superoxide radicals. inflammation. radioisotope clearance indicates circulatory efficiency surpassing normal values at 10––21 days.198 and proposed a combination of ischemia. In contrast. pulsatile blood flow approaches preoperative levels 7––14 days: no further significant increase in vascularization. the typical hemodynamic and cellular events occurring in flaps as a response to ischemia were reversible. this occurs after 12 hours. the circulatory alterations gradually worsened and vascular obstruction progressed until they became irreversible. vascular anastomoses between flap and recipient bed present at 2––3 days. increase in circulatory efficiency beginning at 12 hours.SRPS Volume 10. increase in size and number of functioning vessels. improvement in pulse amplitude. They noted consistent edema and swelling of the vascular parenchymal cells when free flaps were subjected to a period of ischemia. All flaps survived up to 4 hours of ischemia. Between 4 and 8 hours of ischemia. arterial pattern becomes normal. Number 1 anced equilibrium of homeostasis. Angel and coworkers197 studied secondary ischemia time in a rodent model. marked dilatation of arterioles and capillaries 1––3 days: increasing isotope appearance. returning to normal after 3 weeks 2 weeks: progressive regression of the vascular system. flap achieves 90% of its final circulation. few remaining newly formed vessels Most investigators endorse the concept of venous insufficiency as the primary cause of necrosis in pedicled flap tissue. There was concomitant narrowing of the capillary lumen and trapping of foreign blood elements as well as sludge or thrombus formation in the stagnant blood within the vascular tree of the ischemic tissue.194 As early as 1967. but once arterial inflow was impaired. increase in the number of small vessels in the pedicle 3––7 days: progressive increase in circulatory efficiency until it reaches a plateau at about day 7. continuous maturation of anastomoses between pedicled flap and recipient site 3 weeks: vascular pattern approximates preoperative state. with concomitant deple- 24 . and noted that venous obstruction was more deleterious to flap survival than secondary ischemia from complete pedicle obstruction. progressively decreasing circulatory efficiency for the first 6 hours. 0––24 hrs: reduction in arterial blood supply. fully developed vascular connections between pedicle and recipient site 4 weeks: all vessels decreased in diameter. damage to the flap becomes irreversible if adequate nutrient circulation is not provided May200 studied circulatory changes in free epigastric flaps in rabbits. Kerrigan found inadequate arterial inflow was the primary cause of flap failure. even mild venous inadequacy reduced flap survival. marked congestion and edema during the initial 24 hours. The metabolic effects of ischemia during flap elevation are many. plateau at 6––12 hours. As the period of ischemia lengthened. The point at which it is not possible to reestablish nutrient inflow despite reperfusion is known as the no-reflow phenomenon . increase in number and caliber of longitudinal anastomoses. The no-reflow phenomenon is the result of ischemia-induced reperfusion injury and precedes flap death.199 Furthermore. Tsuzuki and colleagues196 found that mild venous inadequacy did not affect survival of an experimental flap when the arterial inflow was maintained. Primary changes include the loss of sympathetic innervation and the insult of ischemia. vital staining occurs simultaneously with recipient limb. Glucose consumption and lactate production both increase. and sympathectomy to explain the vascular collapse that underlies the failing skin flap. reorientation of vessels along the long axis of the flap 1 week: circulatory function well established between flap and recipient bed. Hoopes194 gives a detailed account of the circulatory events that take place in a pedicled flap after its blood supply is partially interrupted during elevation and transfer. With inadequate tissue oxygenation there is a change from aerobic to anaerobic metabolism. Fujino195 concluded that reduction in venous outflow probably results in flap necrosis despite the presence of adequate arterial inflow. Despite advances in our understanding of flap physiology the exact mechanism of delay is incompletely defined.203 noted increased production of toxic superoxide radicals during anaerobic metabolism. viable portion of a skin flap and its distal. neutrophils contribute to the acute imflammatory injury of reperfusion through their adhesion. The authors suggested a role for oxygen-derived free radicals (ODFR) as mediators of tissue necrosis in the ischemic transition zone between the proximal. Carroll and Esclamado205 reviewed flap physiology. Biochemical changes occurring during ischemia ““actually prime the tissue to respond in a pathological fashion upon exposure to re-established vascular supply.204 After reperfusion. FLAP DELAY Delay is the surgical interruption of a portion of the blood supply to a flap at a preliminary stage before transfer. This phenomenon has come to be known as ischemia-induced reperfusion injury (IIRI). thromboxanes (A2). The purpose of delay is to increase the surviving length of a flap or to improve the circulation of a flap to diminish the insult of transfer. With renewed flow comes an abundant supply of calcium ions and a release of oxygen free radical species——the so-called respiratory burst. TNF-α.205 Skin and bone can usually tolerate ischemia for up to 3 hours but muscle and intestinal mucosa are much less tolerant. Two schools of thought exist regarding the mechanism of the delay phenomenon. pathophysiology. In addition. ischemia/reperfusion injury. nonviable segment. PAF and LTB4) as well as peptide mediators (eg. and IL-1ß). Number 1 tion of glycogen. Kerrigan and Stotland206 review the clinical significance. allowing it to survive on less nutrient blood flow than normally needed. the free radicals are attacked by free radical scavengers. Brown and McDowell209 stated that the purpose of delay is 25 . Im et al201 in 1985 and later Manson and colleagues202. He postulated that the hyperemia observed when a tubed pedicle is transferred arises from a vascular debt as a result of increased resistance to venous outflow. and the hydroxyl radical (OH).208 proposed that the likely mechanism of delay consists of vascular reorganization and reactive hyperemia acting through nonlethal ischemia to condition the tissue to survive on less blood flow. One theory holds that delay conditions tissue to ischemia. C5a. Direct cytotoxic injury results from the accumulation of oxygen-derived free radicals during flap ischemia. Definitive investigations into flap response to decreased blood supply have been hampered by inconsistent results obtained in different laboratory models and lack of adequate controls to establish true increase in surviving length following delay procedures. Leukotrienes (LTB4). research investigations. and prostaglandins play a major role in these processes.SRPS Volume 10. Free radicals are not only directly cytotoxic but also trigger the synthesis of numerous proinflammatory lipid mediators (eg. The metabolic derangements of tissue ischemia also affect physical properties of blood such as viscosity and clotting. with their production of the toxic radicals superoxide anion (O2). Hoopes194 lists the following five mechanisms of delay: • • • • • sympathectomy vascular reorganization reactive hyperemia acclimatization to hypoxia nonspecific inflammatory reaction A number of anatomic and physiologic investigations into the delay of flaps began during the 1950s. Others believe that delay improves or increases vascularity. and proteolytic enzyme degradation. These reactive oxygen intermediates lead to a variety of microvascular and inflammatory derangements such as endothelial cell swelling and increased capillary permeability. causing further injury to the cells. and current management of ischemia and IIRI. The process by which delay contributes to flap survival is likely to be a combination of both mechanisms acting to a greater or lesser extent at various times during surgical delay of a flap. and the use of pharmacotherapeutic agents in microvascular surgery. Braithwaite207. together with an increase in size of the vessels in the dermovenous plexus.”” The authors discuss the xanthine oxidase and NADPH oxidase systems. hydrogen peroxide (H2O2). The transition from normal reperfusion and reperfusion injury differs according to tissue type. etiology. emigration. However. In his study. Callegari and colleagues220 subsequently conducted a number of experiments to define the anatomic changes in flaps after surgical delay. When flaps are delayed. Delayed flaps exhibit an increase in capillaries from 48 hours. Macrophages subsequently migrate to the skin and release angiogenic factors that. causing a spontaneous discharge of neurotransmitters.218 confirm these findings and suggest that an ischemic tissue gradient provides the impetus for angiogenesis and leads to greater viability of delayed flaps. so that by the time of flap inset there is little release of norepinephrine and consequent diminution in vasoconstriction of the flap.SRPS Volume 10. Hynes210 used a variation of the sweat test to detect the presence or absence of sympathetic activity in tubed pedicles. along with other factors by platelets. and its effect was to enhance vascularity. Jurell211 analyzed levels of norepinephrine. inflammation. and the elastic layer of vessels. and cyclic-AMP in delayed and nondelayed skin flaps to judge the effects of sympathetic denervation on the delay phenomenon. trigger capillary proliferation at the second surgical stage. damaged endothelium. no significant increase in the density of arteries between acute and delayed skin flaps. and remained at this plateau until day 14. Their observations can be summarized as follows: • longitudinal reorientation of small vessels parallel with the long axis of tubed pedicles at 1 to 7 days postdelay • increase in size of vessels • increase in number of small arteries in the subdermal plexus Pang and colleagues213 monitored skin capillary blood flow and angiogenesis in delayed and nondelayed random skin flaps in the pig. as reported first by Serafin214 and later by Garcia. The authors reached the following conclusions: • the survival length of flaps is related to the distance between perforators • the necrosis line of a flap usually appears in the zone of choke vessels connecting adjacent territories • a surgical delay results in dilatation of existing vessels with maximal effect in the zone of choke arteries • the most effective delay is obtained by elevating the flap in stages from the base and not detaching the tip until last 26 . blood vessels and adrenergic nerves are severed. blood vessels were seen to reorganize parallel to the incision line and blood flow was increased first by vasodilation and secondly by angiogenesis until about day 14. and this continues until 7 days after flap elevation. whereas the minimum effective time is 2 to 3 days. Rerouting of blood flow by injury. The authors conclude that the delay phenomenon is not dependent on angiogenesis but probably mediated through locally released neurohumoral substances. sympathectomy was the mechanism of delay. and angiogenesis caused by the repair seems to account for a significant portion of the delay phenomenon. not as neovascularization from the wound bed or margin. however. Seitchik and Kahn27 reviewed the histologic alterations associated with delay and confirmed the findings of Germann and associates212 from 1933. Capillary blood flow was significantly higher in the delayed skin flaps and came from the pedicle only. Others217. There was. The period of delay offering maximum survival is about 1 week. The angiogenic process in acute and delayed flaps was investigated by Lopez et al219 by means of immunohistochemical methods with monoclonal antibodies to evaluate vascular endothelium.215 both an increase in the number and size and an ingrowth of new vessels from the surrounding tissue occurred about 4 to 5 days postoperatively. Their theory of delay holds that hypoxia accounts for vasodilation and release of neurohumoral substances. The author confirmed significantly lower levels of norepinephrine in flaps at the second operation. Norepinephrine causes vasoconstriction and metabolic stimulation. Jonsson and colleagues216 noted that surgical delay improved delivery of oxygen to the flap. increased 100% by day 4. After delay. The increase in flow was detectable within 2 days of surgical delay. ATP. The acclimatization to hypoxia formed the basis for Daniel and Kerrigan’’s29 belief that delayed flaps have adequate blood flow to survive the early stage of vasoconstriction whereas acute flaps do not. Number 1 to permit gradual hypertrophy of the blood vessels in the pedicle and possibly to accustom the tissues in the flap to a lower oxygen tension or poor circulation. Ribuffo and colleagues223 selectively delayed the deep and superficial inferior epigastric arteries during TRAM flap reconstructions.221) Dhar and Taylor222 investigated the sequence of anatomic changes with delay in a dog muscle and rabbit skin model to support their previous conclusion that flap delay results in dilation of existing vessels. an accelerated increase in the caliber of flap arteries. and Futrell225 studied the role of ischemia from low perfusion as the trigger of neovascularization in a rat model. Phase 2: Between 24 and 72 hours. The authors concluded that the anatomic effect of delay is focused on the choke anastomotic vessels that link adjacent territories and that the time sequence of delay is similar in different tissue types and in different species. 1999. exceeding the need of the ischemic tissue itself to encompass the whole adjacent flap. Poorly perfused tissue brought into a healthy recipient bed enhanced neovascularization. Taylor GI: The delay phenomenon: the story unfolds. at least some of which may not have required an initial delay procedure. Timing of Flap Division Much of the experimental and clinical data regarding appropriate timing of flap division is based on observations of tubed pedicle flaps. Hong. particularly in terms of vessel hypertrophy • similar changes occur when a muscle is delayed. Their delay sequence is divided into four phases (Fig 29): gastric artery and decreased arterial resistance following delay of either vessel. Current theories attempt to explain the delay phenomenon as • a dramatic alteration of blood flow secondary to closure of AV shunts. further gradual dilation of vessel lumen associated with vessel wall thickening. • a conditioning of tissue to ischemia. not ingrowth of new vessels. and subsequently shortened the interval to 10 days without deleterious effects on flap survival. They found that neovascularization was enhanced by a perfusion gradient across the wound margins. German and associates212 concluded that circulation in flaps was reestablished considerably earlier than previously thought. transection of sympathetic nerves. or both. The delay procedure consisted of division of the superficial and deep inferior epigastric vessels bilaterally. The authors found significantly increased caliber of the superior epi- 27 . primarily at the choke vessel level.214. They began dividing their flaps at 14 days posttransfer. Stark. The authors did not find a statistically significant difference between delay after 1 week versus 2 weeks. angiogenesis. To summarize the available data. the only unquestionable fact seems to be that ““surgical delay results in hypertrophy and reorganization of vessels along the axis of a flap””220 and somehow improves flap survival. (Application of the delay phenomenon in muscle is further discussed by Barker et al. The delay sequence——summary of results.) Phase 1: Initial spasm of all flap vessels which lasts up to 3 hours and is followed by gradual dilation of vessel up to 24 hours.226––229 although flaps can be divided as early as the third Fig 29. The authors conclude that this is experimental evidence for the beneficial effect of delayed division of a distant flap. Phase 3: From 72 hours to 7 days.SRPS Volume 10. In view of the conflicting evidence regarding the anatomy and physiology of delay. Number 1 • tissue expansion is a form of surgical delay. (Reprinted with permission from Dhar SC. Restifo et al224 compared the diameter and flow of the superior epigastric artery after a delay period of 1 or 2 weeks. Plast Reconstr Surg 104:2079. or • an improvement in vascularity and blood flow brought about through vasodilation. Phase 4: From 7 days on. the choke vessels remain permanently and irreversibly dilated. and hypersensitivity to catecholamines.194. presumably by minimizing desiccation of ischemic tissue.236 Musculocutaneous flaps fared significantly better after preconditioning. Kaelin et al243 found that prolonged preoperative and postoperative hyperbaric oxygen treatment improved survival in a rat skin flap model. The beneficial effect of HBO therapy was thought to be due to increased superoxide dismutase activity. Proposed theories include alterations in blood flow. Stewart and associates244 evaluated the effects of HBO with and without freeradical scavengers. and the release of endothelium-derived relaxing factors. selective loss of certain nonessential cellular functions. Mounsey noted a 20% increase in flap survival at 30-minute intervals. blood flow ceased completely. are performed by only one researcher on a number of different experimental models.237 Tan and others238 and Ramon et al239 report increased survival in rat abdominal flaps treated with hyperbaric air (21% O2) and hyperbaric 100% O2. As Kerrigan29 points out. Pang. many of these studies contradict one another. A number of experimental studies have looked into drugs to increase flap survival. Forrest. Alpha-tocopherol is one of four tocopherols making up vitamin E. but is premature in some and excessively long in most. To enhance muscle flap survival and sustain normothermic ischemia. When flaps were cooled to 20°C. to be helpful. Preconditioning as a means to enhance flap survival has been tried on both skin and pedicled musculocutaneous flaps. decreased tissue metabolism. According to Hauser et al. McGrath232 states that a moist environment diminishes the depth of tissue loss and increases flap survival. At 14°C. Mounsey. clinically delay should be lengthened to suit specific anatomy. whose action is to terminate free-radical reactions by competing for peroxyradicals. This section will 28 . in which the protection from ischemic damage induced in cardiac muscle by brief periods of coronary artery occlusion is translated to skeletal muscle.235. Awwad et al233 established a direct relationship between local temperature and blood flow in island and free flaps. Sasaki and colleagues231 keep the flap edges moist and report an increase in the surviving portion of flaps. Not all investigators have had positive results with hyperbaric oxygen. FLAP SURVIVAL Physical Factors The physical environment of a flap can be manipulated to try to improve flap survival. but not hyperbaric 8% O2. Carroll and Esclamado205 review the use of pharmacotherapeutic agents in microvascular surgery (Table 4). and noted no significant increase in flap survival with HBO unless it was combined with either alpha-tocopherol or superoxide dismutase and catalase (CAT). These findings are similar to those of Quirinia and Viidik241 and Esclamado et al. Number 1 day in animal models. and noted that. warming of the flap had the opposite effect. and both flap types showed improved survival when used as free flaps. and Forest235 explore the concept of preconditioning. probably as a result of increased plasma viscosity. Hussl and colleagues234 found a reduction in blood flow to 65% of baseline and in oxygen consumption to 25% of baseline. decreased levels of oxygen-derived-free radicals. but not so skin flaps. and often use an inadequate cohort that precludes statistical validation of the results.230 the traditional 3 weeks for division of an inset flap is probably acceptable in 85% of patients. The mechanism of action in preconditioning is unknown. and Morris245 present a concise overview of the pathophysiology of skin flap necrosis and the pharmacologic manipulation of skin flaps to prevent or reverse this process. and characteristics of the recipient site. with resultant decrease in skin blood flow. especially at cell membrane surfaces.SRPS Volume 10. The cumulative experience of many surgeons suggests that most flaps can be divided safely at 10 days to 3 weeks.242 who find that HBO therapy does improve skin flap viability. Hypothermia led to vasoconstriction and increased blood viscosity. which may cause vasodilation and improved distal blood flow. Pharmacologic Pang. HBO must be given as soon as possible after surgery. the muscle flap is subjected to intermittent periods of global ischemia followed by reperfusion. expected flap viability. Catalase is an H2O2 scavenger. Nemiroff and colleagues240 also showed a beneficial effect of hyperbaric oxygen (HBO) on acute skin flaps. Streptokinase and urokinase are first-generation agents and tissue plasminogen activator (t-PA) and acylated 29 . which include decrease in platelet adhesiveness and procoagulant activity.251. for 48 hours. Dextran 40 showed little effect regardless of model. increased bleeding time. The local partial thromboplastin time was elevated but the systemic value ramined normal. cardiac complications. a dose the researchers find to be ideal from a morbidity standpoint. not to vasodilatation and increased vascular flow. has been a tool of the microvascular surgeon for many years. The authors have discontinued the use of dextran in their patients. Anticoagulants Dextran. With dextran 40 as a perfusate.) focus only on those pharmacologic agents that are commonly used in clinical practice. Hudson et al257 reported the experimental and clinical use of a catheter placed proximal to the venous anastomosis for the direct infusion of heparin to prevent veous thrombosis.252 Heparin is an effective anticogulant that acts in conjunction with antithrombin III to inhibit thrombosis by inactivation factor X. but only on a short term basis. and Sone253 report improved flap survival when heparin was continuously and topically administered to specific regions of their flaps. Thrombolytic agents act by the stimulation of plasminogen which is the precursor of plasmin which acts to cleave fibrin within a thrombus. Esclamado RM: Ischemia/reperfusion injury in microvascular surgery. The microperfusion was further enhanced when lowmolecular-weight heparin was added. and decrease in blood viscosity. The incidence of system complications for patients receiving low molecular weight dextran for 120 hours was 51%. it was 29%. The routine use of dextran in free tissue transfer is now discouraged. Kroll et al256 retrospectively reviewed 517 free flaps and noted a lower incidence of flap loss when heparin was administered (either as bolus or in low dose). and for aspirin. Later Salemark. Disa et al250 conducted a prospective randomized analysis of the morbidity associated with dextran and aspirin prophylaxis in head and neck microsurgery patients. 7%. therefore reducing the systemic complications of heparin. Number 1 Classification of Common Pharmacotherapeutic Agents Used in Microvascular Surgery TABLE 4 (Reprinted with permission from Carroll WR. Investigators from Duke University Medical Center255 report that both unfractionated and low molecular weight heparin (LMWH) improved microcirculatory perfusion. After 1 week of use. but only LMWH improved anastomotic patency while minimizing hemorrhage. They attributed the beneficial effect to platelet disaggregation and maintenance of vascular patency by heparin. 2000. Working on a venous model. originally designed as a volume expander. and renal failure. adult respiratory distress syndrome. Head Neck 22:700.SRPS Volume 10. Heparin is more effective at preventing venous thrombosis than arterial thrombosis. Sawada. the patency of arterial inversion grafts (similar to those of Wolfort’’s247) almost doubled over that of controls. and Dougan249 noted increased patency of microcirculation with dextran 40.254 who noted a dose-related increase in flap patency with heparin. but this difference was not statistically significant. The effect was first noted at heparin concentrations of 100 U/mL. These findings correspond with those of the Cox group. inhibition of platelet aggregation. Knudsen. Dextran is associated with significant systemic morbidity including anaphylaxis. Hatayama. Zhang and Wieslander248 observed increased microcirculatory patency when using dextran 70. Rothkopf et al246 cite a review of the effects of dextran. pulmonary edema. 205 Yii et al259 reported 6 free flaps that were salvaged and 2 that failed after the clinical use of thrombolytics (urokinase and t-PA) for pedicle thrombosis.266 Jernbeck and Dalsgaard271 describe the clinical application of intravenous calcitonin gene-related peptide in the treatment of flaps with compromised circulation. Serletti et al260 reported 5 cases of venous thrombosis that were salvaged by revision of the venous anastomosis followed by intraoperative infusion of 250. and found enhanced microcirculatory blood flow from its positive inotropic and vasodilating properties. For instance. and a vasodilator. Current recommendations for treatment with medicinal leeches include prophylaxis with an aminoglycoside and a third-generation cephalosporin and caution when treating immunocompromised patients. a potent vasodilator and antiplatelet aggregator. 273 who applied nitroglycerin transdermally. The most significant risks are bacterial infection from the gram-negative rod Aeromonas hydrophila (which is the leech enteric organism resposible for red cell digestion). with a corresponding increase in viable area of flaps. Nevertheless.274 on the other hand.258 Streptokinase is a nonenzymatic protein derived from group C beta-hemolytic streptococci. and excessive scarring. does not require antithrombin-III for activation. Hirudin is a naturally occurring anticoagulant that inhibits the conversion of fibrin to fibrinogen and that. Ichioka and others275 evaluated the effects of amrinone. Ichioka et al276 demonstrated an increase in microcirculatory blood flow in flaps after intravenous administration and a decrease in vasospasm after topical application of amrinone to the pedicle. Doses of 50. verapamil—— which act on the vascular smooth muscles to cause vasodilation and improve circulation in the flap. in which case the leeches will simply not attach themselves to the flap. for the relief of venous congestion after free tissue transfers and replantations. In flap salvage it is injected into the arterial side of the flap and drained through the venous side. Nichter. however. Rohrich and colleagues272 reported improved survival of axial flaps in pigs and rats treated with nitroglycerin ointment. In addition.261.000 units of urokinase. according to Rodgers et al. nitrendipine. and Cummings278 note improved flap perfusion after intraperitoneal injection of DMSO as measured by laser Doppler velocimetry and perfusion flowmetry. unlike heparin.264 ““no controlled study has proven the efficacy of leeching.264. diltiazem has been shown to stimulate the release of prostacyclin (PGI2). persistent bleeding. and postulate a decrease in tissue edema with resultant improved blood flow. The results obtained with amrinone were comparable to the results obtained with prostaglandin E1 and lidocaine. Thrombolytics have been effective in animal models for the salvage of flaps after microvascular thrombosis. anaphylaxis. found no increase in survival of random pattern flaps in rats treated with nitroglycerin paste.261. Rand-Luby and coworkers279 determined that topi- 30 . Leech therapy is not without potential complications. as did Price and Pearl. nifedipine. These agents do not restrict their effects to smooth muscle. a selective phosphodiesterase III inhibitor. leeches secrete hyaluronidase. In a later clinical study.”” The main indication for the use of leeches is in cases of venous congestion where outflow is insufficient or venous channels are either absent or unsuitable for anastomosis. leeches have a mechanical action by creating physical channels through which venous drainage can occur. Grossman and associates277 report increased flap survival in a rat model with intraperitoneal injection of dimethyl sulfoxide (DMSO) or hyaluronidase.265 Vasodilators Many studies266––270 show increased flap survival in rats treated with calcium-channel blockers——eg. Haller. Leeches have been used in medicine since ancient times for the treatment of various ailments.261 Recently there has been renewed interest in medicinal leeches. diltiazem.265 Moreover. which facilitates spread of the anticoagulant within the tissues. Trachy. from vascular endothelial cells.262. Hirudo medicinalis.000 units have been used clinically. The primary contraindication to leeches is arterial insufficiency.263 Leeches exert their effect by injecting hirudin at the site of bite.SRPS Volume 10.000 to 125. usually avoiding systemic effects. which contributes to prolonged bleeding (up to 48 hrs). Topical nitroglycerin is a potent vasodilator with a greater effect on the venous circulation than on arterial vessels. Number 1 plasminogen-streptokinase activator complex (APSAC) are second-generation agents. 283 Gateley. Nakatsuka and others299 studied the effect of methylprednisolone on 31 . like PGI1. iloprost seems to have a cytoprotective effect that prevents lysosomal enzyme release during tissue hypoxia. Renaud and associates286 report successful resolution of a failing free flap after intraarterial infusion of iloprost in the acute setting and intravenous administration postoperatively. and Martin284 report two instances of intravenous infusion of prostacyclin for impending free flap failure. produces reactive oxygen species and a gradual increase in blood flow in the distal flap. A PGI 2 analog. Young. The authors note that iloprost has the same action and potency as PGI2.SRPS Volume 10.283 have had similar experiences with exogenously administered PGI2 in laboratory animals.201 Manson and colleagues203 reported that a single dose of SOD improved flap survival from 38% to 76% in rats. has been shown to improve flap survival. PGE2 may be available in a more stable form and. an iron chelator and free radical scavenger.205 Emerson and Sykes281 showed improved survival of random skin flaps in rats after treatment with prostacyclin. which are believed to inhibit endotheliumdependent relaxation on the vascular smooth muscle. although Green and associates297 state that the logic behind using chelators such as deferoxamine is to inhibit hydroxy radical formation from superoxide radicals. and suggested that reperfusion following ischemia. and Cleland295 note anaphylactic reactions in a pig model associated with the use of superoxide dismutase.285 who found significantly higher flap survival rates in the study group compared with flaps perfused with lactated Ringer’’s or urokinase solutions. with subsequent pinking up of the flaps and a successful outcome to the cases. but caution that high-dose prostacyclin actually has a detrimental effect on skin flap survival. In addition. a scavenger of free oxygen radicals. iloprost. Its beneficial effect on flaps probably relates to its ability to scavenge free radicals. Prostacyclin (PGI2) is a potent vasodilator which also decreases platelet activation and impairs the release of cytotoxins from white blood cells. PGI2 was found to be effective only if given at the time of flap elevation and continued postoperatively. Antiinflammatory Agents The role of steroids on flap survival continues to be hotly debated. casting doubt on XO as a major source of free radicals responsible for tissue injury and flap necrosis in human skin. not continuous incomplete ischemia. Others282. reduction of platelet aggregation. McAnulty. Hawkes. Suzuki and coworkers294 confirmed the beneficial effects of SOD in preventing flap necrosis. Suzuki and colleagues287 described the use of prostaglandin E1 (PGE1). Nancarrow298 demonstrated a 25% increase in survival of groin island flaps in rats after administration of 1. Its effects were very similar to prostacyclin in causing peripheral vasodilation and platelet disaggregation. Angel and colleagues 296 also demonstrated improved flap survival with deferoxamine.5 mg/Kg of dexamethasone 12 hours preoperatively. The effects of topical lidocaine and pentobarbital. Allopurinol inhibits xanthine oxidase and in the process leads to diminished free radical production and retards the loss of purine substrates available for high-energy metabolic synthesis. Treatment of skin flaps with superoxide dismutase. The authors theorize that perhaps PGI 2 also stimulates new vessel formation in ischemic tissue. were studied by Wadstrom and Gerdin. the effects are circumvented by microvascular thrombosis. was evaluated by Senderoff et al. They find DMSO safe to use in a clinical setting. but with greater chemical stability and therapeutic potential. Deferoxamine has been shown to diminish flap necrosis caused by underlying hematomas. Picard-Ami and colleagues293 note that xanthine oxidase levels in human tissue are 1/40th of those in rats. or the free-radical scavenging properties of DMSO. higher doses of the agent result in hypotension and significant decrease in blood flow to the whole skin flap. Free Radical Scavengers A number of investigators288––292 have shown increased flap survival with allopurinol treatment in a rat skin model. Tissue levels of SOD were higher in the surviving portions of flaps.280 They conclude that although there is an effective and prompt resolution of mechanically induced vasospasm. has been noted to have a biphasic response——ie. Number 1 cal application of DMSO increased flap viability in humans by controlling skin ischemia through vasodilation. and flap survival in a doseand time-dependent fashion. and Das302 explored the effects of another NSAID. and considerably higher patency rates in the ketorolac group at 20 min. Ann Plast Surg 32:490. The failure rate of free tissue transfer is reported to be less than 5%. distal perfusion. Despite significantly prolonged mean bleeding times.242 who observed that perioperative steroids did improve skin flap viability. and Zel. and Lindsay303 described the effects of nicotine on capillary blood flow in random pattern skin flaps elevated in rats.205 Buckley. The authors found that nicotine significantly decreased capillary blood flow. selective inhibition of leukotriene synthesis to prevent leukocyte––endothelial cell adhesion and macromolecular leakage. Number 1 pig musculocutaneous. Various studies have involved platelet activating factor antagonism. preoperative aspirin decreases thrombus formation at venous anastomosis and improves capillary perfusion in the microcirculation. Nicotine Forrest. Prostacyclin (PGI2) is a potent vasodilator and inhibitor of platelet aggregation produced by endothelial cells. In summary. and treat complications. and proposed several hypotheses to explain the mechanism of action of the drug. Larrabee. recognize. thereby decreasing the synthesis of TXA2 in platelets and PGI2 in the vessel walls. inhibition of thromboxane and complement. Thromboxane A2 (TxA2) is a potent vasoconstrictor and platelet aggregator released by platelets. markedly reduced platelet aggregation. all vessels thrombosed at 24 hours. At low doses the effect of aspirin is selective and only the cyclooxygenase system in platlets is inhibited and the formation of thromboxane is blocked. the incidence of pedicle thrombosis is higher than the failure rate would reflect due to a Fig 30. Their results were dissapointing in that ASA showed both beneficial and detrimental effects depending on when the injected drug was exposed to the subendothelial layers of the damaged vessel wall. Kerrigan and Stotland295 review the accumulated data regarding attempts to modulate the proinflammatory mechanism involved in reperfusion injury. axial. There was no increase in skin capillary blood flow as measured by entrapment of radioactive microspheres. 1994.SRPS Volume 10. There is no empiric support in the literature for the use of aspirin postoperatively.205 Salemark and associates301 studied the possible role of ASA as an antithrombogenic agent. They found no increase in area of flap survival or fluorescein dye penetration.300 Other studies demonstrate increased early anastomotic patency but no difference from controls after 24 hour to a week. et al: Iloprost improves survival of ischemic experimental skin flaps.) 32 . there was no evidence to support the clinical use of corticosteroids to enhance flap viability. (Reprinted with permission from Senderoff DM. Black et al304 note that acute exposure of human skin vasculature to nicotine is associated with amplification of norepinephrine-induced skin vasoconstriction and impairment of endotheliumdependent skin vasorelaxation. MONITORING FLAP VASCULARITY Despite the clinical success of free flaps. Zhang WX. Pang. These findings were in contrast with those of Esclamado. strict evaluation of flap perfusion is essential to prevent. however. The metabolism of arachidonic acid. Israeli D. In the laboratory. Davidson. and random pattern flaps. Both are products of arachidonic acid metabolism and have strong effects at the endothelial cell level285 (Fig 30). Aspirin (ASA) acetylates the enzyme cyclooxygenase. and antibodies directed against neutrophil toxicity. ketorolac tromethamine (Toradol). McCraw. the crucial test of adequacy of circulation is survival of the pedicled flap tissue.310 Brown et al311 retrospecitvely reviewed successful free flap salvage at their institution. According to the authors. Differential thermometry is a useful tool to monitor vascular patency in buried free tissue transfers in which a temperature gradient exceeding 3°C is considered significant. Fluorescein is believed to be better than 70% accurate as an indicator of the circulatory status of a flap..29. emphasized its merits in predicting the viability of arterial flaps. The monitoring flap is based on a perforator fed by the main pedicle.194 however. however. Fluorescein is usually given in a bolus injection of 500 to 1000 mg (15 mg/Kg). Khouri and Shaw314 review surface temperature recordings of 600 free flaps and conclude that when properly applied and interpreted.317 In 1962 Myers318 reviewed the history of fluorescein and used it to determine the viability of skin flaps after radical mastectomy.. and warmth are unreliable and of limited use. In general. 307 Truelson. and highly reliable technique of free flap monitoring. Dunscombe. and suggested clinical applications. Temperature readings. its sensitivity and predictive value approach 98% and 75%. and is clinically useful in monitoring for extrinsic complications. As an indicator of intrinsic flap failure it is inadequate. and sensitive • • • • provide continuous monitoring be user-friendly and easily interpreted be affordable be relatively unaffected by the external environment Subjective/Physical Criteria ““Clinical observation remains the gold standard against which monitoring systems are generally measured.. Of the subjective tests. and Greenhalgh313 took serial temperature measurements of flap skin and control skin simultaneously in order to negate environmental and metabolic variables. They found that skin temperature responded slowly to vascular occlusion and was not a reliable indicator of flap failure in the immediate postoperative period. Blue dermal bleeding was the best warning sign of inadequate perfusion. Hoopes. The authors were able to predict pedicle compromise from the appearance of the monitoring flap.309 and Gapany. Vital Dye Measurements Fluorescein has been used for over 40 years to clinically assess flap vascularity.SRPS Volume 10. the ideal monitoring device should • reflect the condition of the entire (buried) flap • be reliable. Due to more successful salvage within the first 24 hours after the initial surgery. bleeding from a stab wound is probably the most accurate. believes that ““it is a misconception to equate blood supply with viability. and Shanklin319 delineated the pharmacologic characteristics of fluorescein that enabled it to be an indicator of blood flow. Number 1 salvage rate after pedicle thrombosis that ranges from 36%––70%. surface temperature can be taken easily. can be used effectively to track the course of replanted digits. Temperature monitoring is a simple technique to evaluate flap viability. however. After a waiting 33 .29 Jones.””306 Climo312 surveyed various clinical measurements of flap vascularity as of 1951 and noted that the color of the blood oozing from the dermis was a reliable indicator of circulatory status. inexpensive. It can be accomplished in a number of ways.fulfills many of the criteria of the ideal monitoring system. Table 5 from Daniel and Kerrigan29 summarizes various monitoring tools used to assess flap viability.259 Several techniques have been suggested to assess perfusion of flap tissues in an attempt to predict flap survival.”” Daniel and Kerrigan29 review various techniques for subjectively evaluating flap viability and note that color. requires relatively inexpensive equipment. including surface temperature and differential thermometry. they recommended hourly monitoring for the first 24 hours and then every 4 hours for 48 hours . consistent.306 These methods are reviewed by Furnas and Rosen. Table 6 outlines the clinical signs that can be used to differentiate venous from arterial maladies in flaps. capillary blanching.308 Bradford. reproducible.. making it a simple. Myers.and it. Cho et al315 and Akin and Basut316 created small monitoring flaps that are exteriorized to facilitate monitoring of buried free flaps.305. axial pattern flaps. and musculocutaneous flaps. Philadelphia. Ch 9. Plastic Surgery. the length of flap that is viable is consistently underestimated. Saunders. Vol 1.) period of 20––30 min.320 Pang and others321 report that when the fluorescein test is performed 1 hour after flap elevation.SRPS Volume 10. These results were obtained in random flaps. Kerrigan CL: Principles and physiology of skin flap surgery.29 although others suggest waiting 24 hrs. Number 1 TABLE 5 Techniques for Monitoring Flap Perfusion (Reprinted with permission from Daniel RK. When the test is performed at 18 hours postoperatively. If necessary the test can be repeated every 8 hours. In: McCarthy JG (ed). 1990. 34 . the extent of dye staining in those tissues which are adequately perfused can be seen with a Wood’’s lamp. the length of dye staining and skin viability correlated very well. The principle of monitoring is similar to that of fluorescein. Indocyanine green (ICG) is a second-generation dye that can be used as a clinical marker of cutaneous blood flow.0 mL/min. which uses reflected sound to pick up pulsatile vessels. but the chemical properties of indocyanine green are more suitable to clinical use. which measures the frequency shift of light and therefore has limited penetration (1.328 ICG has been used successfully in experimental and clinical models. The laser Doppler flowmeter gives an output voltage proportional to the total flux of red blood cells in the volume of tissue sampled (approximately 1 mm3). ORL-Head Neck Nurs 13:12. and arteriolar constrictions. Clinically. intimal flaps. Dermofluorometry has recently been applied to venous flaps. which is a reflection of the number and velocity of moving red blood cells and which decreases to low levels in response to arterial or venous occlusion.329 Photoelectric Assessment Two types of Doppler instruments are currently in clinical use. Issing and Naumann327 used computer-aided digital morphometry (CADM) to compare fluorescein staining. Number 1 TABLE 6 Signs of Arterial Occlusion and Venous Congestion (Reprinted with permission from Adams JF. Norton. and Brousseau324 described the use of perfusion fluorometry. inaccuracies in fluorescein testing are probably inherent and unavoidable. and a photometry value. The method was 96% accurate in predicting ultimate flap viability at lower dosage and with fewer side-effects than fluorescein testing. More specifics are given by Odland et al. They conclude that fluorescein staining is the most accurate predictor of flap viability. and ischemic tissues become acidotic. Silverman. venous congestion.328––331 Intraoperative laser-induced fluorescence of ICG showed arterial spasm. The authors confirmed the accuracy of dermofluorometry in predicting skin flap survival in pigs. The second is the laser Doppler. and skin temperature in the evaluation of skin flap perfusion.) Myers and Donovan322 note that all techniques for evaluating flap perfusion with fluorescein are reasonably accurate. thromboses. in that it only measures vascularity at the time the dye is given and blood supply can change. a DFI of 30% or more is considered safe.323 who note that since fluorescein is a derivative of phthalein. This value does not change with arterial occlusion but decreases in response to venous occlusion. the acidosis might quench the expected fluorescence in the distal skin flap. In their opinion.5 mm). a technique where the admitted fluorescence of the tissue is measured using a fiberoptic light guide (dermofluorometer) and an objective value of dye-fluorescence units is obtained. Suzuki et al325 compared arterialized to nonarterialized and random-pattern flaps and noted that the instrument is a reliable indicator of circulation in all types of flaps evaluated. and thus includes the subcapillary plexus. helping to distinguish 35 . Lassen LF: Leech therapy for venous congestion following myocutaneous pectoralis flap reconstruction. They found CFUS was capable of differentiating blood flow and was proficient at visualizing luminal dissections. and serial injections and measurements are possible because the doses of dye are small (0. The first is the ultrasound Doppler.29 Amerhauser and associates332 evaluated color flow ultrasound (CFUS) in an experimental and clinical setting and noted that it was sensitive to venous and arteial insufficiency at flow rates as low as 3.15 mg/Kg). including the traditional Wood’’s lamp method which was as reliable as newer ones. Thomson and Kerrigan326 described the formula for calculating the dye fluorescence index (DFI) and documented that fluorescence varies with blood supply. which is a photoplethysmographic reading of the intensity of the back-scattered light. Accurate readings can be made as early as 2 minutes after injection.SRPS Volume 10. 1995. a pH indicator. skin pH. The technique yields two values:333 a Doppler flow measurement. and regional hypoperfusion in microvascular flaps and correlated strongly with the clinical outcome. ““no single technique is universally applicable or superior to all others. The implantable PO2 sensor in Hofer’’s355 series accurately indicated flap failure in all cases. Other less popular methods of evaluating circulation in a flap include measurement of the fibrillation potential in skeletal muscle.””199 Metabolic Tsur and coworkers348 measured transcutaneous oxygen tension in delayed axial and random pattern skin flaps by means of an oxygen electrode applied to the skin.345 The scanning laser Doppler346 and laser flowgraph347 may give a more global picture of the flap than could be obtained by Doppler flowmetry. and Hendricks343 agree that Doppler flowmetry is a useful tool for assessing flap viability. • a fixed probe • continuous recordings • attention to physiologic fluctuations and trends Many factors affect the clinical usefulness of these techniques.337 Bircher et al338 provide an in-depth overview of guidelines for the measurement of cutaneous blood flow by laser Doppler flowmetry. 36 . In Kerrigan and Daniel’’s view. Hallock334 investigated the critical threshold for tissue viability as determined by laser Doppler flowmetry. The probe is small. and transcutaneous oxygen assay methods and concluded that fluorometry is more precise and can be used to monitor several areas in serial fashion. Transcutaneous oxygen and Doppler probing were better suited for continuous monitoring. no single measurement is indicative of anything except the status at that one time. Holmberg.336 found that laser Doppler flowmetry correlated well with actual skin viability and necrosis in the immediate postoperative period. Kerrigan and Daniel350 evaluated capillary blood samples in pig island flaps and noted that while PO2 and PCO2 measurements were highly variable. Silverman and coworkers340 compared the laser Doppler. changes in hematocrit and pH were useful predictors of flap viability. and independent of anastomotic proximity. it obtains information only from a single site. is sensitive to movement of the subject. Hjortdal and colleagues349 found measurement of subcutaneous and intramuscular oxygen tension in pig island flaps to be a sensitive indicator of acute impairment of the supplying vessels. Svensson. They found oxygen partialpressure measurements to be an effective predictor of the effectiveness of the delay procedure. Disadvantages are that it is not quantitative. A sensitivity of 93% and specificity of 94% were recorded by the Hovius group. Heden and associates335. easily implantable.352 and magnetic resonance spectroscopy. however. and has limited accuracy below the critical threshold at which tissue necrosis is guaranteed. but the authors did not comment on the ability of the optode to differentiate between arterial and venous compromise. Yuen and Feng344 reported a 5-year experience with laser Doppler flowmeter monitoring of 232 microvascular flaps.342 that beginning 24 hours postoperatively the laser Doppler technique is the most sensitive. Place.353 Golde and Mahoney354 described an implantable optochemical oxygen-sensing electrode device or optode that allows rapid and continuous monitoring of tissue PO2 and which was felt to reliably reflect vascular occlusion.SRPS Volume 10. and Svedman 339 review the proper interpretation of laser Doppler recordings from free flaps and suggest the following guidelines to improve accuracy of the analysis: Advantages of Doppler probing are high reliability (approaching 100% 24 hrs after flap transfer) and the ability to continuously monitor skin perfusion by a noninvasive technique. with no false positives or negatives. as does Marks. Witt. The salvage rate was 69% and the overall success rate was 98%. Similarly. perfusion fluorometry. equipment cost. Cummings and colleagues341 reached similar conclusions but emphasize. yet the authors’’ decision to reexplore a failing free flap was still based on clinical observation. Among them are ease of application. and found that a baseline of 30% is generally sufficient to predict flap survival. but stress that since postoperative blood flow is a dynamic process that peaks about 52 to 80 hours and returns to baseline some 120 hours postoperatively. Number 1 between venous and arterial causes of flap embarrassment. Vascular compromise was detected in all cases. and expertise required to operate.351 magnetic resonance imaging. especially when using largecaliber needles. and local perfusion to gauge the end-point of each expansion session. and approximating skin flaps. Hallock and Rice6 advocate monitoring the expansion process with a combination of transcutaneous electrodes for measuring oxygen levels. stretching.29. clearance tests. Jackson and colleagues5 described using an external reservoir that was associated with few complications. or a crescentic base. who ““described the technique of wound closure by creating.SRPS Volume 10. 38%. but the authors do not recommend it in cases where a permanent prosthesis is planned. controlled tissue expansion has been used for the 37 .356 who demonstrated its usefulness but recommended further study to develop specific guidelines before it was universally accepted in clinical practice.5 times as large as the defect to be closed. Its current use in clinical practice has several limitations.7 they note that either technique records diminished circulation in response to increased expansion. Number 1 Photoplethysmography is a technique that measures fluid volume by detecting variations in infrared light absorption by the skin. reconstruction of all areas of the body in many diverse problems. and total vascular occlusion. did the potential usefulness of this technique become obvious. Pietila and colleagues8 recommended overfilling the expander to increase the amount of expansion at each session and shorten the total expansion period.307 In addition to displaying the waveforms of the photoplethysmograph. venous. and total hemoglobin concentrations of flap blood. but adequate tissue circulation still exists at the threshold of pain. Although rapid expansion is possible in some circumstances. Since then. preserving tissue integrity takes precedence over speed of expansion. Other means of evaluating flaps include quantitative tests. and will not be discussed here. The authors concluded that an expander of appropriate size has a base that is 2. but Van Beek and Adson9 caution that if the intraluminal pressure exceeds 500 mmHg. The device is commonly used in anesthesiology and was evaluated by Lindsey et al. Baker4 summarizes the history and dynamics of tissue expansion. TECHNIQUE Modern expanders are made of silicon elastomers and come in several shapes and sizes or are custom-made to fit individual needs. and 32%. In addition to deeper evaluation (up to 10 cm) of flaps than is possible with the laser Doppler. radioactive microspheres. a rectangular base. near infrared spectroscopy (NIRS) was able to delineate the difference between arterial. implant pressure. Van Rappard et al10 evaluated the differences in surface area of expanded tissue in relation to shape of the individual expander. deoxy-. Comparing simultaneous laser Doppler flowmetry and transcutaneous oxygen monitoring. such as for breast reconstruction. increasing the skin area by approximately 50% or enough to provide sufficient cover for cartilage graft reconstruction of a traumatic ear defect. The expander is usually connected to a subcutaneous valve through which isotonic saline is injected for incremental expansion. Matton and associates11 described a ““universal incision”” for tissue expander insertion that has been shown to minimize the complications seen with SKIN EXPANSION James F Thornton MD HISTORY Bennet and Hirt1 review the history of tissue expansion and note that its origins date to Celsus (25 BC––50 AD). and electromagnetic flowmetry. For expanders with a round base.”” In 1957 Neumann2 reported the first clinical use of controlled skin expansion. the pulse oximeter also measures light absorption to derive oxygen saturation of arterial hemoglobin. Irwin et al357 evaluated a newer and noninvasive technique for assessing flap circulation that involves continuous monitoring of changes in the oxy-. leakage at the injection port is likely. The time interval between injections of saline for gradual expansion depends on the nature of the defect and its anatomic location as well as host tissue characteristics. The interval ranges from 3 to 10 days. the respective gains were 25%. Over the next 2 months the balloon was gradually expanded.305. He placed a rubber balloon subcutaneously beneath the temporal scalp and postauricular skin. when Radovan3 reported his work with tissue expansion for breast reconstruction. These are essentially reserved for experimental puposes only. Not until 1976. The fibrous capsule that forms around the implant consists of thick bundles of collagen fibers and elongated fibroblasts and myofibroblasts. HISTOLOGY OF EXPANDED SKIN Johnson et al15 review the histology and physiology of tissue expansion. Like Austad. The surrounding dermis decreases in thickness considerably. are incapable of returning to their relaxed state after being stretched. expanded skin showed a significantly thicker epidermis——which they attributed either to increased mitotic rate or decreased rate of cell turnover——and a thinner dermis and panniculus carnosus. permanent deformation of collagen may result. Olenius. Austad and Rose12 described a selfinflating expander containing hypertonic sodium chloride crystals within a shell that gradually fills through osmosis. Muscle and fat both diminish in mass in response to expansion. which was unchanged. Collagen fibers exist in a convoluted form and. not only by stretching the existing area but through generation of new tissue. Their conclusions signified that skin expansion is not simply a matter of stretching skin but the actual formation of additional new skin with all the attributes of the original tissue.SRPS Volume 10. unlike fibers made of elastin. Bergé and colleagues14 reported direct closure with Hydrogel tissue expanders in 9 of 10 patients.23 The authors state: ““The mechanism by which strain causes an enhancement of cellular growth appears to be a network of several integrated cascades. the device was plagued by reports of skin necrosis and implant rupture. Additional evidence has accumulated that mechanical strain stimulates signal transduction pathways that could trigger a series of cascades eventually leading to a new skin production. Number 1 other incisions. but 6 months after the end of expansion the epidermis had returned to normal thickness. implicating growth factors. as well as significant thinning of the dermis and subcutaneous tissues. and Wickman22 studied the mitotic activity of human skin samples after tissue expansion and noted a statistically significant rise in the number of labeled basal and suprabasal keratinocytes. There was minimal inflammatory reaction to the expander. Pasyk et al19 noted significant thickening of the epidermis after 5 weeks of expansion. cytoskeleton. Austad and colleagues16. .17 studied changes in the epidermis. If the limits of the elastic fibers are exceeded. Dalsgaard. and increased numbers of fibroblasts and myofibroblasts are seen in the expander capsule. . . The concept of a self-inflating expander was explored further by Wiese. and over 20 days they were inflated to 100 mm. Argenta and coworkers 18 summarize the histomorphologic changes occurring in expanded skin. and while there is no loss of muscle function. although there is an undulation of the basal lamina and a loss of intercellular spaces. Chang et al26 found that tissue expansion in the rat inhibits the contractile function of dermal fibro- 38 . The author notes that this expander is ““biocompatible”” and holds promise in the area of tissue expansion without the disadvantages noted above. perpendicular to the wound margin. the loss of fat appears to be permanent. Leighton and associates20 found differential thinning of all tissue layers except the epidermis.13 who incorporated a copolymer of methylmethacrylate and N-vinyl-2-pyrrolidone in a gel casing capable of generating a maximum pressure of 235 mmHg. Compared with normal skin. primarily at the junction of the capsule and host tissue and to a lesser degree in the dermis.24 Melis and colleagues25 found changes in the orientation of collagen fibers in the dermis as a result of skin stretching. the fibers became aligned in the direction of the stretching force. The defects closed were the result of radial forearm flap harvest. dermis. After 15 minutes of stretching with a skin-stretching device.””23 Normal human skin is continually undergoing stretching and relaxation. The epidermis does not change in thickness. The phenomenon of tissue growth in response to mechanical expansion has been investigated by Takei and colleagues. Olenius and Johansson21 also report significant increase in epidermal thickness. This confirmed earlier findings of increased mitosis17 and suggested a net gain of tissue. Tissue expansion also triggers an increase in vasculature. At implantation the initial volume of the expanders was 10 mm. Besides the protracted inflation times of 8 to 14 weeks. and subcutaneous tissue of expanded guinea pig skin. This dynamic realignment of collagen fibers explains the significantly decreased wound closing tension resulting from skin stretching and explains how skin stretches beyond its inherent extensibility. and the protein kinase family. Squier. Pasyk and others40 compared the survival of expanded and delayed flaps with acutely raised random-pattern skin flaps in pigs. No significant difference was noted between expanded and delayed skin flaps. Knight and coworkers30 confirmed increased collagen content in expanded dermis of pigs. did not manifest accentuated fibrosis. The mechanism of action was thought to be the normal process of wound healing in addition to a delay phenomenon. Expanded flaps showed a 117% increase in surviving length over unexpanded skin flaps. and postulated that mechanical forces are in some way related to the increased vascularity. Specimen angiograms of expanded skin showed evidence of increased vascularity compared with control skin. This effect was more pronounced after 5 weeks than in the first 1 or 2 weeks of expansion. The dermis showed only minimal degree of elastosis and zonal 39 . Lee. while the hypodermis. which was in contact with the expander capsule. and this increase paralleled flap survival. Delayed flaps showed a 73% increase over the controls. Austad. and Bauer29 likewise noted increased total collagen content in expanded skin.38 Radiation did reduce the overall area of expanded skin by 23% in one study. presumably through relaxation or inactivation of contractile fibroblasts in the periprosthetic capsule. fragmentation of elastic fibers. Once an expander is removed. and Cherry33 note formation of a capsule around every silicone expander. Expansion of the human scalp shortens the telogen phase of hair follicles by activating and accelerating epidermal mitosis. BLOOD SUPPLY OF EXPANDED SKIN The histologic changes evident in expanded skin lend support to the concept that skin expansion is a form of delay. which resulted in a theoretical net gain in the dermal layer as well as in the epidermal layer. Timmenga and coworkers31 noted thickened dermal collagen bundles and collagen fibrils that were loosely packed in both expanded and shamoperated skin. and Bardach27 had previously noted that anticontractile agents instilled into the tissues surrounding an expander enhanced the rate and extent of skin expansion. The capsule has four histological zones. • Inner zone——adjacent to the expander. Has loose bundles of collage fibers. and speculated that it could be due to tensile factors during expansion which stimulated biosynthetic activity or mitosis of fibroblasts. whether the expander was inflated or not. Beauchenne28 detected higher levels of hydroxyproline and a net accumulation of collagen in expanded skin compared with normal skin. both expanded and delayed skin exhibited increased total capillary blood flow.36 Tissue expansion of irradiated pig skin shows no further histopathological changes beyond those caused by irradiation and is indistinguishable from nonexpanded irradiated skin in the porcine model. Wickman. suggesting sympathetic denervation as a result of expansion.38 Working on a rabbit model. The underlying pectoralis major muscle showed considerable ultrastructural damage under light and electron microscopy.SRPS Volume 10. The authors recommended including the expander capsule in the flap at the time of transfer for its contribution to the blood supply. Number 1 blasts in vitro. the surrounding fibrous capsule rapidly thins. Pasyk. The survival length of random flaps in skin overlying tissue expanders was also increased. Has estab- lished vessels loosely interspersed with collagen fibers. zone. Goodman and associates39 note increased epidermal thickness but no dermal or capsular alterations in irradiated skin postexpansion. and Jurell32 report adrenergic supersensitivity in expanded pig skin. Kernahan. In a similar study. Matturri and colleagues34 biopsied previously expanded skin at least 1 year after expander removal and found normal-appearing epidermis with normal mitotic activity. Heden. Johnson.35 The histologic effect of expansion on muscle was examined during breast reconstruction with tissue expanders.37. Compared with acutely raised random-pattern flaps. • Central zone——next to the inner zone. Sasaki and Pang41 focused on the viability and capillary blood flow of expanded and delayed skin flaps. tains elongated fibroblasts and myofibroblasts oriented parallel to the surface of the implant. Con- tains fibrin-like filaments and a cellular layer with macrophages. Con- • Transitional zone——on the outside of the central • Outer zone——most superficial layer. Cherry. After flap elevation and inset.SRPS Volume 10. the process of stress-relaxation occurs where.24 As summarized by Baker. Nevertheless. nondelayed flaps and 50% greater surviving lengths than nonexpanded. namely gradual inflation over many weeks and months. RATE OF EXPANSION Traditionally.16 documented a true tissue dividend from expansion that was thought to result from the increased mitotic activity of the stressed tissues. Austad12. Skin creep alone does not account for all the extra skin during serial expansion. It appears that cyclic loading is the most effective method of recruiting extra tissue.4 the physiologic changes in skin during creep include the following: • dehydration of tissue • microfragmentation of elastic fibers • increasingly parallel alignment of randomly positioned collagen fibers • migration of tissue in the direction of the force vector Baker4 expands Gibson’’s definition of cyclic loading to mean stretching followed by relaxation of expanded tissue. the risk of infection and implant exposure from the protracted presence of the expander. undefined form of subcutaneous mobilization. and genuine growth—— yet fail to credit any of these specifically for their findings. Compared with the control and sham groups. delayed flaps. Vander Kolk and others44 reported a 32% increase in midhorizontal length and 44% increase in midvertical length of expanded porcine skin. tissue compression/thinning. the overall increase in surface area available for coverage was 30%. preexpanded skin flaps demonstrated a statistically significant increase (700%) in perfusion as measured by fluorescein. Creep is the ““time-dependent plastic deformation of any material or tissue in response to constant stress. In 1987 Sasaki46 described intraoperative sustained limited expansion (ISLE) for immediate reconstruction. in the event of immediate tissue expansion. Wickman and associates32 found evidence of increased superficial blood flow in expanded skin by laser Doppler flowmetry and venous outflow measurements. the expansion process begins 2 to 3 weeks after implantation of the expander and continues at weekly intervals until the desired inflation is achieved. EXTENT OF EXPANSION Several authors have investigated the origin of the expanded tissue. and the cosmetic and functional deformities of buried expanders and valves. particularly in poorly vascularized areas. but no significant difference in total blood flow between flaps raised in expanded and nonexpanded skin. and factors such as recruitment. The author later reported intraoperative expansion in closure of small skin defects on an emergency basis. First. the author states that ““undermining must still be considered the most important element in reducing wound closing tension. Sasaki states that these shortcomings of slow expansion are eliminated by the intraoperative expansion technique. The skin adapts to stress in two ways. mechanical stretching changes the elasticity and alignment of collagen by a process called creep. Shapiro48 combines acute cycled expansions with rectangular skin flaps and notes a decrease in wound closing tension compared with simple flap undermining. Number 1 Saxby42 also reported 150% greater surviving lengths of expanded flaps over acutely raised. Angiograms of the flap specimens revealed increased caliber of the axial vessels in the expanded flaps. interstitial displacement of fluids. they attribute the mechanism of expansion to another. over a period of time when skin is stretched to a given constant length.””45 Second. Instead. and new growth also play a role. The increase in flap circulation induced by the expansion facilitated an increase in flap tolerance to secondary ischemia. Siegert et al45 evaluated intermittent intraoperative short-term tissue expansion in dogs and in 30 patients with severe microtia. Cycled expansions yielded maximal increase in length of 15% to 20%. The authors mention mechanisms that lead to an increase in skin length (Fig 1)——elasticity.”” 40 .47 He mentions disadvantages of the slow expansion method. creep. Babovic et al 43 studied the effects of tissue expansion on ischemia in free flaps. Three months after surgery there was a slight decrease in area which was not statistically significant. as opposed to continuous expansion. the force required to maintain it is gradually decreased. Joss and coworkers54 note that advancement flap reconstruction wastes tissue (in dog-ears) at either end of the defect.) 41 . and reliability. Fisher and Hammond53 review the literature of expanders combined with flaps for breast reconstruction.) Wee. simplicity. In summary. the extremities. skin necrosis. 1990. The authors compared the efficacy of continuous versus intraoperative tissue expansion in a pig model. The shape of the expander is irrelevant. Fig 2. 1993. hematoma.51 The device is said to harness the viscoelastic properties of the skin by applying incremental traction to allow the skin to rapidly stretch and extend while minimizing its tendency to recoil. where there is localized infection. Hoffmann S. Elasticity did not change significantly and neither did hysteresis (a measure of the skin turgor and plasticity). absence of a donor defect. COMPLICATIONS Potential complications of tissue expansion include infection. and Mustoe49 describe a continuous infusion device that maintains a constant expander pressure and shortens the time to full expansion by two-thirds. and find three times more tissue gain with the former technique. expander extrusion. To date expanders have been used to good effect in the head and neck. (Reprinted with permission from Siegert R. Weerda H. Wilmhurst and Sharpe55 insert tissue expanders immediately after resection of malignant skin lesions to complete the reconstruction in two operations. Expanders are generally contraindicated in areas of poorly vascularized tissue. or if there is a higher-thanaverage risk of recurrent cancer. Distensibility lessened during expansion. there were minimal differences in skin properties between rapidly and slowly expanded patients. and for breast reconstruction. pain. Mohadjer C: Clinical and experimental evaluation of intermittent intraoperative shortterm expansion.SRPS Volume 10. Zoltie N. and neurapraxia. Markings for transposition flap and expander placed beneath flap and beyond. These problems undoubtedly delay the reconstruc- Fig 1. He reminds us that tissue expansion results in a distortion of body image that some patients are unable to tolerate. Wickman and colleagues52 measured mechanical properties of the skin during rapid and slow tissue expansion for breast reconstruction. and decreased thereafter. increased after the expander was replaced by a permanent implant. Plast Reconstr Surg 92:248. (Reprinted with permission from Joss GS. Skin expansion mechanisms. Futran50 discusses the clinical applications of the Sure-Closure™™ skin-stretching device originally introduced by Hirshowitz and colleagues. preservation of sensation and hair. The excisional bed is temporarily covered by a skin graft. the trunk. and instead recommend transposing the expanded tissue into the wound bed along a 90° arc (Fig 2). Br J Plast Surg 43:328. The expander can be of any shape but should be twice as wide as the defect to be covered. Chapman P: Tissue expansion technique and the transposition flap. Austad56 advocates against tissue expansion in acute injuries because of the risk of contamination and possible inability to obtain rational informed consent on an emergency basis. Logan. Most reports of reconstruction by tissue expansion imply movement of tissue as advancement flaps. seroma. implant failure. Number 1 APPLICATIONS OF EXPANDED SKIN The main advantages of tissue expansion in reconstructive surgery are good color and texture match of the skin used for coverage. Austad recounts four cases of partial flap necrosis after the expander had been removed and the flap advanced over the defect. Only by adding sodium bicarbonate to commercially available lidocaine to raise its pH to 8. aggressive management of any complication.000 tissue expansion procedures. and attributes the cyanosis to epinephrine in the local anesthetic solution known to be detrimental to the survival of delayed——hence expanded——flaps. Sharp edges or irregular folds in the prosthesis should also be smoothed out or risk thinning of the shell from friction and perhaps implant exposure. Argenta recommends waiting for 2 weeks after implantation of the expander before beginning inflation. Failures were most common in the arm (31%) and rarest in the leg (0%). necessitating removal in 13 (38%). They credit their low failure rate to an expander size twice as wide as the defect. seroma. non-breast tissue expansion in 56 patients.57 Manders and colleagues58 report a 24% incidence of major complications that delayed or compromised the outcome of their cases of tissue expansion. Zoltie and associates59 review their experience with non-scalp. and only in patients with predisposing factors. but do not signal a catastrophe with dire consequences to the patient. slow rate of inflation. The pain associated with tissue expansion tends to be mild and of short duration. Austad56 notes a remarkable absence of disasters in a survey of more than 50. Youm and coworkers60 reviewed retrospectively 34 tissue expanders placed in 30 patients at a New York City public hospital over a 7-year period. CONCLUSIONS As summarized by Baker. Intraluminal instillation of lidocaine has been suggested to relieve pain during expansion. Infection is usually reported in 1% of cases. Derby and colleagues64 similarly conclude that this technique of lidocaine delivery by diffusion across a tissue expander shell ““is unlikely to provide significant salutary benefit.65 Paletta66 describes rupture of an expander placed in the scalp of a child caused by erosion of the outer table of the skull and bone spur formation from pressure by the expander. Argenta and associates18 also noted a 24% complication rate early in their series. The most frequent cause of exposure is an insufficient pocket at the initial procedure that forces the prosthesis against the suture line. and points out that the overall incidence of complications associated with tissue expansion has decreased as surgeons have become more knowledgeable and experienced in the routine use of expanders. Number 1 tive process and may necessitate implant removal.0 will the anesthetic diffuse at a sufficient rate to provide analgesia during expansion. Minor complications were noted in 17% and included pain on expansion. and advise against it because of the potential for progressive lidocaine accumulation”” that could lead to lidocaine overdose in the event of implant failure.61 but Sinow and Cunningham62 report no difference in pain after expansion between patients receiving lidocaine analgesia and placebo. Infrequent reports of erosion and deformation of bone underlying an expander have appeared in the literature. but this subsequently fell to 7%. although an occa- sional patient may complain of disabling pain. and widening of scars. McGuire and Caffee63 note that the rate of diffusion of lidocaine through an expander membrane depends on the pH of the solution. and report an overall failure of 12%.SRPS Volume 10. Complications occurred in 22 of 34 expanders (65%). and use of transposition flaps.4 tissue expansion is associated with • improved flap survival • increase in vascularity to the skin or capsule • probable enhancement of the blood supply of rapidly expanded skin • creation of additional new skin • thinning of the dermis and subcutaneous tissue and corresponding decrease in tensile strength • larger surface area gains with prolonged expansion • normalization of the parameters to the preexpanded state when the expansion process is discontinued 42 . specifically rib concavity with thoracic skin expansion and calvarial deformity and remodeling with scalp expansion in children. Only 12 of 34 expanders (35%) were free of complications. Treece P: Deep inferior epigastric perforator flap for breast reconstruction. 6. 1889. Taylor GI. Zhong SZ. Br J Plast Surg 47:457. Hallock GG: Discussion of ““A microdissected thin tensor fascia latae perforator flap. 35. Taylor GI: The blood supply to the skin. Urushibara K. Allen R. Valone JA. Fujino T. Takahashi Y. Gao JH: The ““super-thin”” flap. Nanba Y. Seventh Congress of the International Society of Reconstructive Microsurgery. Wang GY. 38. Imanishi N: Three-dimensional analysis and classification of arteries in the skin and subcutaneous adipofascial tissue by computer graphics imaging. Caddy CM. Seitchik MW. Number 1 BIBLIOGRAPHY 1. 30. J Reconstr Microsurg 7:313. Daniel RK. 2000. 1989. Churchill Livingstone. Br J Plast Surg 47:495. Plast Reconstr Surg 86:185. Song YL: The free thigh flap: a new free flap concept based on the septocutaneous artery. Moriguchi T: New microsurgical breast reconstruction using free paraumbilical perforator adiposal flaps. 1994. 2003. Allen RJ. Handchir Mikrochir Plast Chir 34:216. Heitmann C: Perforator flaps——The history of evolution. Plastic Surgery. Bogel. Mardini S. Taylor GI.SRPS Volume 10. Plast Reconstr Surg 33:16. 16. Allen R. Lamberty BGH. Taylor GI. 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Baik B-S: Clinical applications of the delayed arterialized venous flap. Imanishi N. Nakajima H. Matsuda K. 43. Mengi AS: Double opposing semicircular flap: a modification of opposing z-plasty for closing circular defects. Vasconez LO. 57. Vol 1. 1963. 2000. Aiso S: Venous drainage of the distally based lesser saphenous––sural veno-neuroadipofascial pedicled fasciocutaneous flap: a radiographic perfusion study. Number 1 39. White WL: An experimental study of large island flaps in dogs. 55. 2001. Minabe T. by PN Blondeel et al. Br J Plast Surg 26:202. 67. 70. 2nd Ed. Nakajima H. 1995. Yamamoto H. 1999. Aiso S: Anatomic study of the venous drainage architecture of the forearm skin and subcutaneous tissue. Hand Clin 13(2):175. Wei F-C. 68. Plast Reconstr Surg 101:870. 2003. et al: Have we found an ideal softtissue flap? An experience with 672 anterolateral thigh flaps. Nahai F: Clinical Applications of Muscle and Musculocutaneous Flaps. Plast Reconstr Surg 31:328. 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Williams HB: The free transfer of skin flaps by microvascular anastomoses: an experimental study and a reappraisal. Plast Reconstr Surg 103:104. Fischer GW: The Z-plasty: biomechanics and mathematics. Tittle BJ: Microsurgery: free tissue transfer and replantation. Masson JK. Plast Reconstr Surg 102:779. Plast Reconstr Surg 52:16. 77. 49. Moss ALH: The relationship between fasciocutaneous perforators and their fascial branches: an anatomic study in human cadaver lower legs. Taylor GI: The deep venous system and reverse flow flaps. Geddes CR. Blondeel PN. 1982. Lamb DL. Cervical and Clavicular Tubed Skin flaps. Ch 42. 64. Mendelson BC. Grabb’’s Encyclopedia of Flaps. classification. 1963. Fukuda H. et al: Free anterolateral thigh flaps for reconstruction of head and neck defects. 72. Sharma S. Selected Read Plast Surg 9(11). 1984. et al: The donor site morbidity of free DIEP flaps and free TRAM flaps for breast reconstruction. Zbar RIS: A simplified algorithm for the use of Z-plasty. Part I: the vascular supply of the skin. Morgan G: Axial and random pattern flaps. Lamberty BGH: A classification of fasciocutaneous flaps according to their patterns of vascularisation. 1994. et al: Accompanying arteries of the lesser saphenous vein and sural nerve: anatomic study and its clinical applications. Imanishi N. eds: Plastic Surgery. 51. Nakajima H. Koshima I. 66. 1970. Plast Reconstr Surg 103:1513. 41. Webster MHC. Clin Plast Surg 6:181. 1983. 112. Reece GP. Kroll SS. Barclay TC. Romana MC. Chen T-M. Urushibara K. Crockett DJ: Repair of lower led injuries with fasciocutaneous flaps. Costa MA. Lamberty BGH: Fasciocutaneous vessels. 94. Tolhurst DE. Plast Reconstr Surg 76:354. Verna G. 1982. Kuo Y-R. Marty F. 2003. Montandon D. Fukuzumi S. 2000. Plast Reconstr Surg 107:1766. Br J Plast Surg 35:127. Anat Clin 6:121. Chen S-L. 113. Ji SY. Plast Reconstr Surg 102:1517. Craigie JE. Patient selection. et al: Anterolateral thigh flap for abdominal wall reconstruction. Masquelet AC. Zbrodowski A: The subcutaneous tissue flap and the misconception of fasciocutaneous flaps. Cormack GC. Jeng S-F. 2002. 93. Sharpe DT. et al: The distally based lesser saphenous venofasciocutaneous flap for ankle and heel reconstruction. 106. Blondeel PN. Microsurgery 5:151. Tolhurst DE. Miller MJ. Lin C-H. Kuo Y-R. Br J Plast Surg. Mete D. 2000. Clin Plast Surg 30:331. et al: Free anterolateral thigh adipofascial perforator flap. 1975. 1982. Chen H-C. Lamberty BGH: Fasciocutaneous vessels in the upper arm: application to the design of new fasciocutaneous flaps. et al: Technique and strategy in anterolateral thigh perforator flap surgery. Kyo M-H. 85. Number 1 78. Plast Reconstr Surg 106:576. et al: Comparison of cost for DIEP and free TRAM flap breast reconstructions. Spierer R. 105. 79. DellaCroce FJ. 87. Imanishi N. Plast Reconstr Surg 103:494. Galdino G. 2002. Weiler-Mithoff EM. Wei F-C. 104. Marchetti C. Scand J Plast Reconstr Surg 20:61. 82. 101. 83. 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Tang Y-B: Anterolateral thigh flap: an ideal soft tissue flap. Baumeister SP. Sekido M. et al: Free anterolateral thigh flap for extremity reconstruction: clinical experience and functional assessment of donor site. 1981.SRPS Volume 10. et al: Sensory nerve repair in perforator flaps for autologous breast reconstruction: sensational or senseless? Br J Plast Surg 52:37. 103. Nakayama Y. Hamdi M. 2003. Plast Reconstr Surg 109:2211. Allen RJ. classification. 100. 2003. Imanishi N. Plast Reconstr Surg 110:466. 2002. et al: The distally based superficial sural flap: our experience in reconstructing the lower leg and foot. 1999. Yang C-C. Allen RJ: Cost-based comparison between perforator flaps and TRAM flaps for breast reconstruction. 2003. et al: Use of ““perforator flaps”” in skull base reconstruction after tumor resection. Kasai Y: Flaps nourished by arterial inflow through the venous system: an experimental investigation. 1981. their distribution on the trunk and limbs. Taylor GI: The angiosomes of the body and their supply to perforator flaps. et al: A realistic complication analysis of 70 sural artery flaps in a multimorbid patient group. Plast Reconstr Surg 99:1940. Momen B. and their clinical application in tissue transfer. Haertsch PA: The surgical plane in the leg. 1999. Nahabedian MY. Plast Reconstr Surg 106:10. 107. Sullivan SK: Autogenous breast reconstruction with the deep inferior epigastric perforator flap. Plast Reconstr Surg 103:1191. 1999. Br J Plast Surg 34:215. Plast Reconstr Surg 111:837. Uchiyama K. Hsieh C-H. Haeseker B. Dolcet M. Plast Reconstr Surg 112:976. 1981. 90. and outcome. Plast Reconstr Surg 102:779. 81. Cavadas PC: Reversed saphenous neurocutaneous island flap: clinical experience. 35:464. Koshima I. Webster MHC: Deep inferior epigastric perforator flap in breast reconstruction: experience with the first 50 flaps. 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Jackson IT: Role of perivenous areolar tussue in the viability of venous flaps: an experimental study on the inferior epigastric venous flap of the rat. 1985. J Reconstr Microsurg 14(3):147-152. Plast Reconstr Surg 82:892. Yilmaz M. Br J Plast Surg 45:18. 119. Thatte RL. 2002. 121. 116. Kovacs A. 122. Chow SP. J Craniomaxillofac Surg 26:249. 1993. Tamai S. Br J Plast Surg 48:61. Santidhananon Y. Barutcu A: Free arterialized venous forearm flap. Mizumoto S: The arterialised venous flap: experimental studies and a clinical case. Bachaud M. Baek SM. Lee WPA: Discussion of ““Arterialized venous flap for treating multiple skin defects of the hand””. Nichter LS. Chongchet V: Prearterialisation of an arterialised venous flap: clinical cases. Plast Reconstr Surg 97:408. et al: Arterialized venous free flaps for soft-tissue reconstruction of digits: a 40-case series. 134. Nagasaka S. 154. 1972. Plast Reconstr Surg 94:997. Br J Plast Surg 54:112. Plast Reconstr Surg 91:299. 133. 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