Basic Principles in Flap Reconstruction

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Chapter 2 Basic Principles in Flap Reconstruction

Reconstruction of wounds has long been a challenge to surgeons. Whereas some wounds may be closed in a simple linear fashion, others require complex movement of local or distant tissue to restore functional and anatomic relationships and to optimize the cosmetic outcome. Wound management considerations must always include healing by second intention, primary approximation, grafts, and flaps.

Surgeons have used skin flaps to repair wound defects for centuries. The term “flap” was derived from the Dutch word “flappe” during the sixteenth century. “Flappe” referred to something that was fastened by one side and hung broad and loose. As early as 700bce, Sushrata Samita first documented his technique of reconstructing a large nasal tip defect with a cheek flap.¹ Since that time, surgeons’ knowledge of biology, anatomy, and physiology has greatly increased. This understanding allows us to significantly decrease the likelihood of surgical complications such as flap failure. This chapter addresses some basic principles of flap reconstruction including flap design, construction, and classification. The authors’ experience with flap reconstruction of facial wounds will be utilized to emphasize the particular advantages of flap procedures.

BASIC TERMINOLOGY

A skin flap is a construct of skin and subcutaneous tissue with a partially intact vascular supply that is relocated or repositioned from a donor site to a recipient site. The recipient site is called the primary defect and, in dermatologic surgery, is usually the wound resulting from the removal of a tumor (Figure 2.1). The secondary defect is defined as the wound that is created by cutting, lifting, and sliding the flap to fill the primary defect (Figure 2.1). The base of the flap is that area that remains attached to the skin adjacent to the defect. It is this base, also known as the pedicle of the flap, which contains the vascular supply necessary for initial flap survival. The tip of the flap is the portion of the flap furthest from the flap’s base.

Figure 2.1 The wound resulting from the extirpation of the tumor is the primary defect. The secondary defect is defined as the wound created by cutting, lifting, and sliding the flap to fill the primary defect. Here, the secondary defect will be filled by the second lobe of the flap. The base of the flap is that area that remains attached to the contiguous skin adjacent to the defect.

FLAPS DEFINED BY BLOOD SUPPLY

There are many classification schemata for reconstructive flaps. One common method of defining flaps is to determine the flap’s perfusion sources. Flaps may be categorized based on vascular supply as arterial, musculocutaneous, fasciocutaneous, or random. Arterial flaps (also called axial flaps) have a relatively large-diameter, named artery in the pedicle of the flap, which directly provides nutrients to the full extent of the flap (including the tip). This named artery typically lies in the subcutaneous layer superficial to the muscle fascia. On the face, the most commonly used arterial flap is the paramedian forehead flap, which depends on the supratrochlear and/or supraorbital arteries for survival. A musculocutaneous flap includes muscle in the base of the flap, whereas a fasciocutaneous flap includes only the fascial covering of the muscle in the pedicle. The inclusion of deeper tissues in the flap’s base may increase the perfusion, and thus the reliability, of any flap. A random flap, the most commonly used flap design in reconstructive dermatologic surgery, depends on the small, unnamed perfusion plexus of highly anastomotic vessels in the dermis to provide nutrients to the flap tip. Because the arterial input of random pattern flaps is much less predictable, attention to proper flap design and delicate surgical technique is required to ensure surgical success.

Blood flow is obviously the most crucial factor for flap viability. Vascular perfusion pressure is a description of the force of blood flow through a vessel. Perfusion pressure and blood flow in the body’s vessels are analogous to water flowing from a faucet through a lawn hose. The greatest pressure and highest flow will be at the faucet head. As water travels away from the faucet, its pressure and flow decrease in strength. To maintain sufficient flow to the distal tip of the hose, the perfusion pressure within the hose must exceed the resistance of the hose. Similarly in the human body, the perfusion pressure of any vessels that supplies the skin must exceed the capillary resistance in order to maintain vessel patency and preserve continued blood flow. A critical pressure is required to maintain patency of capillaries. Below this certain pressure, the capillaries will close and insufficient blood will be supplied to the distal portions of the flap. The greater the distance from the feeding artery or arteriole, the lower the perfusion pressure will be (Figure 2.2). Thus, beyond a certain distance, the flap tip will no longer receive blood nutrients, and it will thus necrose.^2,⁵

Figure 2.2 Flap perfusion pressures necessary for flap survival.

The graph shows how perfusion pressure decreases the greater the distance that the blood must flow from the feeding artery or arteriole. (a) & (b) show that despite greater recruitment of random arterioles, there is a point where perfusion pressure is less than the capillary resistance. At this point of no flow, the flap will necrose.

Perfusion pressures have dictated that flaps should be designed with appropriate flap length to pedicle width ratios. Until 1970, it was widely believed that the viable length of a flap was directly proportional to the width of the base. Surgeons believed that in order to double the length of the flap one would simply need to double the width of the flap base, thereby including a sufficient number of vessels in the pedicle to sustain the flap tip. Many felt that there was no ultimate limit to flap length. In 1970, Milton disputed this conventional hypothesis by publishing his research on axial flaps in the pig model. He discovered that “flaps made under the same conditions of blood supply survive to the same length regardless of width.”³ Daniel and Williams confirmed Milton’s research on axial flaps and further studied survival of random pattern flaps. Although they concluded that “an increase in width did not result in an increased length of survival,”⁴ their data showed a trend toward wider pedicles allowing greater flap length survival. Clinical experience with random flap survival echoed this survival trend.

In 1979, Stell conducted further studies utilizing the pig model and extrapolated his findings to humans. His research supported the traditional hypothesis that the viable length of a flap is indeed dictated by its width, but there is an upper limit of length survival that cannot be increased by increasing the pedicle width.⁵ Also contrary to the hypothesis, viable flap length was not directly proportional to pedicle width. Instead, viable length appeared to be predicted with the formula [67.3 – (121.4/√Width)]. In his paper, Stell extrapolated his findings in the pig model to humans using a formula based on aorta size and surface area. By multiplying the maximum surviving random flap length on the pig abdomen by a factor of 2.25, he predicted a maximum random flap length of 12.5 cm on the human abdomen. Clinical experiences with random flaps on the human abdomen are similar to this predicted measurement. Beyond a certain pedicle width, greater recruitment of random vessels cannot support the flap tip (Figure 2.2). Overall, perfusion pressure limits the ultimate length of both axial and random flaps.

The greater the perfusion pressure in the flap’s pedicle, the longer the flap can be without undergoing necrosis. Moreover, the greater the perfusion pressure at the flap’s base, the more narrow the pedicle may be. Arteries always have greater perfusion pressures than distal arterioles and capillaries. Accordingly, the longest viable flaps with the narrowest bases (largest length-to-base ratios) are arterial flaps. Stell ⁵ found that the greatest length of a viable axial flap was approximately 60% greater than that of a random flap utilizing the same pedicle width. Since flap survival is based on blood supply,⁵^–⁷ it was apparent that axial flaps are better perfused. Therefore, a paramedian forehead flap that utilizes the supratrochlear artery may be at least four times as long as the flap’s pedicle width (at least a 4:1 ratio) (Figure 2.3). Musculocutaneous flaps have the next greatest blood supply in the pedicle, followed by fasciocutaneous and random flaps in descending order.

Figure 2.3 Measuring the flap length to width. By including a large bore artery (the supratrochlear artery) in the flap pedicle, the ratio may be at least as great as 4:1.

The commonly utilized random pattern flaps are largely supported by the redundant subdermal vascular plexus in the skin. Figure 2.4 highlights the innate vasculature of the skin upon which flap survival depends. The deeper, muscular-based arteries supply the subdermal plexus, which subsequently perfuses the intradermal plexus. The intradermal vasculature alone is usually unable to support tissue viability due to low perfusion pressures and blood flow within these distal capillaries.^2,⁸ However, the subdermal plexus, found in the mid to superficial subcutaneous fat, contains both arterioles and capillaries with sufficient perfusion pressure to sustain tissue viability following flap movement. This anatomy is critical to understand when undermining (dissecting under the flap and its surrounding area to allow tissue movement) a cutaneous flap. If undermining is performed superficial to the subdermal plexus (ie, within the dermis), the flap has a significantly increased chance of undergoing tissue ischemia.

Figure 2.4 The support of commonly utilized random pattern flaps by the redundant subdermal vascular plexus in the skin.

The deeper, muscular-based axial arteries (not shown) supply the subdermal plexus, which subsequently perfuses the intradermal plexus. The intradermal vasculature alone is usually unable to support tissue viability because of low perfusion pressures and blood flow within these distal capillaries. The subdermal plexus, found in the mid- to superficial subcutaneous fat, contains both arterioles and capillaries with sufficient perfusion pressure to sustain tissue viability following flap movement. Therefore, undermining of a random pattern flap must occur below the subdermal plexus.

The perfusion pressures of random cutaneous flaps vary with the flaps’ locations on the body.3–5,^7,⁹^–¹³ As soon as a random pattern flap is incised and raised, there is a significant decrease in the perfusion pressure to the distal, disrupted skin.^14,¹⁵ Fortunately at normal skin temperature, the amount of blood flowing through the facial skin is ten times greater than that needed to supply the skin’s basic metabolic needs.¹⁶^–¹⁹ Other areas of the body are not as well supplied with this redundancy of blood supply. A general rule is that the more distant the surgical flap is located from the heart, the less the perfusion pressure will be. Hence, a flap on the leg should be designed with a smaller flap length-to-pedicle width ratio when compared to a flap on the face.

There is typically a maximum length-to-width ratio for any random cutaneous flap that will generally allow adequate flap perfusion. In general, the longer the required flap, the wider the pedicle must be to ensure flap survival. With a wider flap base, there are a greater number of subdermal vessels employed to supply the most distal periphery of the flap. However, one must remember that these vessels at the pedicle of the random flap all share a common perfusion pressure. As previously discussed, there is a point at which no matter how many extra vessels are recruited at the base, the distal perfusion pressure will be less than the critical closing pressure of the arterioles and capillaries (Figure 2.2).^3,^5,^7,^15,²⁰ When the perfusion pressure is less than this intravascular resistance, the flap receives diminished nutrients and necrosis can ensue. Generally, random cutaneous flaps of the face with a maximum length-to-base ratio of 3:1 survive.²¹^–²³ On the trunk and legs, the maximum length-to-base ratio is considered to be 2:1.^12,^21,^22,^24,²⁵ An axial flap on the face may have a 4:1 or greater ratio depending on the arterial supply of the pedicle.^21,⁶⁰ Remember that these ratios are only guidelines. Patient factors such as tobacco abuse, medical comorbidities, and a history of radiation therapy or prior surgeries in the area will all influence local perfusion pressures and the maximum safe length-to-width ratios of the flaps.

FLAP PHYSIOLOGY

Flap survival is dependent on various factors including blood flow, angiogenesis and vascularization, edema, wound closure tension, and infection. Prior to the first incision, the flap skin is fully vascularized and viable using the definition of normal skin. Once the flap is raised, it is always ischemic since the normal vessels supplying that skin are cut and the flap now depends on decreased circulation from the collateral vessels. A flap is always initially viable since the skin can survive up to 12 to 13 hours of avascularity at 37°F.²⁶^–²⁸ An ischemic flap can survive even longer since the blood flow needed to sustain skin is only 2 to 8 cc per 100 gm per minute, and normal flow to the skin is ten times greater than this minimum.^16,²⁶ Thus, Meyers ²⁶ was correct when he commented that a fresh flap is always ischemic, but viable. Once incised and relocated, the nascent flap receives its nutrients from both the pedicle and the base of the primary defect. Sufficient blood flow through the base of the flap is essential in the initial 24 to 48 hours following the initial flap creation. In both axial and random flaps, blood flow immediately drops as the flap is elevated. For axial flaps, microvascular flow actually increases to a level greater than the preoperative state within 5 hours.^15,²⁹ Flow in random pattern flaps, however, starts to improve differen-tially for up to four weeks. Marks utilized the rat model to show that flow improved on a gradient; flow increased within 14–16 hours to the skin closest to the pedicle, within 24–48 hours to the skin 1 cm distal to the pedicle, and 96 hours 3 cm distal to the pedicle.¹⁵ All sites recovered approximately 30% of their blood flow per day, with the proximal most portion recovering full blood flow by the end of 7 days and the most distal tip by the end of 14 days. Until 14 days, recovery of blood flow occurred on a gradient that depended on the distance of the skin from the base of the flap. Microvascular flow grew to higher than preoperative levels from 14 to 21 days and then gradually returned to baseline during the fourth week. The opening of collateral vessels appears to allow this sequential recovery of blood flow. However, there appears to be a limit on how fast these collaterals can open.¹⁵

This time-dependent opening of collateral vessels may be partially explained by arteriovenous (AV) shunts. These shunts control blood supply to the capillary network that supplies the flap. There are pre-AV shunt sphincters under the control of the sympathetic nervous system. When the flap is incised and undermined, local sympathetic nerve fibers are disrupted and release catecholamines. As a result, there is local vasoconstriction for up to 48 hours, by which time the nerve’s supply of norepinephrine is exhausted.^26,³⁰ Once sympathetic tone is relaxed, the blood flow to the capillary collaterals is increased to help supply the flap with nutrients.¹⁴ However, this effective sympathectomy cannot fully explain why random flaps have a graded flow recovery. Upon incision, the entire flap should have equal catecholamine release and subsequent equal flow recovery.³¹ Other humoral factors such as prostaglandin release may come into play.³²

Local tissue conditions resulting from surgical trauma also decrease flap perfusion and subsequent survival. Following any local injury, the inflammatory cascade releases the powerful vasoconstrictor thromboxane A2.^33,³⁴ In addition, free radicals are released, causing direct injury to the flap.^35,³⁶ Finally, the edema inevitably associated with surgical trauma causes further capillary vessel resistance by increasing manual compression on the skin’s smaller caliber perfusion sources.³⁷ All of these negative factors decrease perfusion to the flap.

Conversely, the flap may also benefit from surgical trauma. Relative local hypoxemia and increased levels of metabolic by-products induce opening of pre-capillary sphincters, thereby promoting increased local blood flow.^26,^30,³⁸ Moreover, adhesion molecules, such as E-selectin, are activated following exposure to released coagulation cascade molecules such as endotoxin, interleukin-1, and tumor necrosis factor alpha.³⁹ These adhesion molecules recruit molecules including neutrophils to the flap to clear debris and anabolic waste products. Finally, ischemic tissue attracts endothelial progenitor cells, which allow for the ingrowth of new vascular channels to supply the flap.⁴³ Flap survival is dependent on the balance of all these factors ultimately influencing pedicle blood flow.

The nascent flap not only receives nutrients from the pedicle, but it also gains nutrition from the base of the primary defect through angiogenesis, revascularization, and neovascularization.⁴⁰^–⁴³ Within the first two days of flap placement, a fibrin layer develops below the flap and provides a suitable environment for angiogenesis.³⁵ Endothelial cells and macrophages release angiogenic cell factors important in neovascularization, the local growth of new blood vessels into the surgically manipulated skin.⁴³^–⁴⁶ Neovascularization is seen as early as 3 days in the rat model⁴⁷ and at 4 days in rabbit⁴⁸ and pig⁴⁹ models. In staged, pedicled flaps in humans, revascularization adequate for division of the flap pedicle has been demonstrated by the seventh postoperative day.⁴⁹^–⁵¹ This new vascular growth works in conjunction with the pre-existing collateral vessels to nourish the flap.

Tissue edema, wound closure tension, and infection also negatively affect flap blood supply and survival. Although none of these factors can solely lead to necrosis of a well-vascularized flap, each can contribute to further ischemia in a marginally perfused flap. Postoperative tissue edema places external force on small capillaries,³⁷ resulting in increased capillary resistance. Thus, there must be greater perfusion pressure at the pedicle to counter this resistance and ensure flap tip survival. Recent studies in the rat model revealed that significant postoperative edema will not solely cause flap necrosis.⁵² However, it can be an additive factor along with high wound closure tensions and/or infection.

Closing wounds under large amounts of tension can place undue vascular stress on the wound edges and tip of the flap. It is typically recommended that one undermine 2 to 4 cm,⁵³ or 50 to 100% of the defect width,¹⁰⁸ beyond the wound edge to decrease wound tension. Undermining beyond this distance may be detrimental since there may be unnecessary vascular compromise, more bleeding, and greater dead space, all of which can lead to surgical complications. High closure tension leads to dehiscence and wound edge necrosis, but it does not usually lead to entire flap necrosis.⁵⁴^–⁵⁶

Wound infection can cause partial or complete flap necrosis. With local infection, there is release of toxic free radicals and greater tissue edema.⁵⁷ Infection can also lead to vessel thrombosis.⁵⁸ In addition to local tissue destruction and vascular compromise, collagen production and deposition are hindered.⁵⁹ Therefore, flap adhesion to the wound bed and overall tensile strength are affected.

Clearly, there are many factors involved in the initial period of wound healing that are critical to the flap’s survival. Predictably acceptable flap results depend on proper flap design, gentle operative technique, and the avoidance of surgical complications.