Basic Principles in Flap Reconstruction

Basic Terminology

A skin flap is a construct typically consisting of skin and subcutaneous tissue with a partially intact vascular supply that is transferred or repositioned from an adjacent or more distant 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 cutaneous tumor ( Fig. 2.1 ). The secondary defect is defined as the wound that is created by cutting, lifting, or sliding the flap to fill the primary defect (see Fig. 2.1 ). The base of the flap is the area that remains attached to the skin adjacent to the defect. It is this base, also known as the pedicle of the flap, that 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.

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 musculocutaneous, fasciocutaneous, axial, or random. A musculocutaneous flap includes muscle tissue in the base of the flap, whereas a fasciocutaneous flap includes only the fascial covering of the muscle in the pedicle. An example of a musculocutaneous flap used in dermatologic surgery is the Keystone flap, which relies on musculocutaneous and fasciocutaneous vascular perforators taken together with venous and neural connections within the flap's base, which may increase the perfusion, and thus the reliability, of any flap.

The most common flaps used in dermatologic surgery, composed of primarily of subcutaneous tissue and skin (and sometimes superficial muscular fascia), are axial and random perfusion flaps. Axial flaps (also called arterial flaps) have a relatively large-diameter, named artery present within the pedicle of the flap, which directly provides nutrients to the full extent of the flap. This named artery typically lies in the subcutaneous layer superficial to the muscle fascia. On the face, the most commonly used axial flap is the paramedian forehead flap, which depends on the supratrochlear artery (and occasionally branches of the supraorbital artery) for survival. 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. 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 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 garden hose. The greatest pressure and highest flow will be at the faucet head. As water travels farther 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 vessel that supplies blood and nutrients to 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 ( Fig. 2.2 ). Thus beyond a certain distance, the flap tip will no longer receive blood nutrients, and it will thus necrose.

An understanding of perfusion pressures has dictated that flaps be designed with appropriate flap length to pedicle width ratio. 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.” 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,” their data showed a trend toward wider pedicles allowing greater flap length survival. Studies by Stell in a pig model and confirmed when extrapolated to humans suggested that viable flap length was not directly proportional to pedicle width, and that beyond a certain pedicle width, greater recruitment of random vessels cannot support the flap tip (see Fig. 2.2 ). Clinical experience with random flap survival has echoed this survival trend.

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. Therefore a paramedian forehead flap that uses the supratrochlear artery may be at least four times as long as the flap's pedicle width (at least a 4 : 1 ratio; Fig. 2.3 ). Musculocutaneous flaps have the next greatest blood supply in the pedicle, followed by fasciocutaneous and random flaps in descending order.

The commonly used random pattern flaps are largely supported by the redundant subdermal vascular plexus in the skin. Fig. 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. 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 (i.e., within the dermis), the flap has a significantly increased chance of undergoing tissue ischemia.

The perfusion pressures of random cutaneous flaps vary with the flaps' locations on the body. 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. Fortunately at normal skin temperature, the amount of blood flowing through the facial skin is 10 times greater than that needed to supply the skin's basic metabolic needs. 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 with a flap on the face.

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 (see Fig. 2.2 ). 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. On the trunk and legs, the maximum length-to-base ratio is considered to be 2 : 1. An axial flap on the face may have a 4 : 1 or greater ratio depending on the arterial supply of the pedicle. Remember that these ratios are only guidelines. Patient-related factors must be taken into account when contemplating the feasibility and design of a flap. In addition to location of the body, local perfusion pressures can be altered by a variety of factors such as tobacco use, history of radiation to the area, medical comorbidities (i.e., atherosclerosis, high or low blood pressure, arrhythmias), and use of vasoconstrictors. In addition, flap design must take into account variations in skin laxity based on location, age, and comorbid conditions.

Flap Physiology

Flap survival is dependent on various factors, including blood flow, angiogenesis and vascularization, edema, wound closure tension, postoperative complications such as hematoma/seromas, 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 immediately 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. An ischemic flap can survive even longer, since the blood flow needed to sustain skin is only 2 to 8 cc per 100 g per minute, and normal flow to the skin is 10 times greater than this minimum. Thus Meyers was correct when he commented that a fresh flap is always ischemic but viable.

Once incised and relocated, the flap receives its nutrients from both the cutaneous 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 after 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. Flow in random pattern flaps, however, starts to improve differentially for up to 4 weeks. Marks used 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 within 96 hours 3 cm distal to the pedicle. 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.

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. Once sympathetic tone is relaxed, the blood flow to the capillary collaterals is increased to help supply the flap with nutrients. 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. Other humoral factors such as prostaglandin release may come into play.

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. In addition, free radicals are released, causing direct injury to the flap. 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. In addition, fluid collection under the flap in the form of a postoperative hematoma or seroma can further decrease blood flow. All of these negative factors decrease perfusion to the flap and can threaten flap survival.

Conversely, the flap may also benefit from surgical trauma. Relative local hypoxemia and increased levels of metabolic by-products induce opening of precapillary sphincters, thereby promoting increased local blood flow. 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. 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. 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. Within the first two days of flap placement, a fibrin layer develops below the flap and provides a suitable environment for angiogenesis. Endothelial cells and macrophages release angiogenic cell factors important in neovascularization, the local growth of new blood vessels into the surgically manipulated skin. Neovascularization is seen as early as 3 days in the rat model, and at 4 days in rabbit and pig models. In staged, pedicled flaps in humans, revascularization adequate for division of the flap pedicle has been demonstrated by the seventh postoperative day. This new vascular growth works in conjunction with the preexisting 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, 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. 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, or 50% to 100% of the defect width, 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. Wound infection can cause partial or complete flap necrosis. With local infection, there is release of toxic free radicals and greater tissue edema. Infection can also lead to vessel thrombosis. In addition to local tissue destruction and vascular compromise, collagen production and deposition are hindered. Therefore flap adhesion to the wound bed and overall tensile strength are affected. Overall, 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.