Flap physiology
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A flap is a unit of tissue that is transferred from one site ( donor site ) to another site ( recipient site ) while maintaining its own blood supply.
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Flap physiology
- 1. Flap physiology Dr Himanshu Soni Fellow in Head and Neck Oncology- FHNO Fellow in CMF Trauma Surgery – AOMSI Oral and Maxillofacial Surgery
- 2. Introduction • The skin serves as a sensory and a protective organ. • The thick epidermal layers are largely impermeable to gases and most liquids.
- 3. • Epidermis of the skin - ectoderm • The glandular appendages of the skin (i.e., sebaceous glands and hair follicles) develop from tubes and solid cords that invaginate from the covering ectoderm. • The epidermis is a metabolically active, but avascular, stratified squamous epithelium. • The average epidermal thickness for most of the body is 0.1 mm.
- 4. • Dermis - mesoderm, consists primarily of noncellular connective tissue. The outer surface of the dermis has an uneven border contacting the epidermis that is known as the papillary layer.
- 5. Anatomy of Circulation • The blood reaching the skin originates from deep vessels • These then feed interconnecting perforator vessels which supply the vascular plexus • Thus skin fundamentally perfused by musculocutaneous or septocutaneous perforators
- 6. • Type A: Direct cutaneous pedicle.(temporoparietal fascia). • Type B: Septocutaneous pedicle.(deltoid, scapular) • Type C: Musculocutaneous pedicle. (nasolabial, Mathes and Nahai classification….
- 7. Anatomy of Circulation The vascular plexuses of the fascia, subcutaneous tissue and skin are divided into 6 layers -
- 8. Anatomy of Circulation 1)Subfascial plexus small plexus lying on the undersurface of the fascia
- 9. Anatomy of Circulation 2) Prefascial plexus -a larger plexus -particularly prominent on the limbs -fasciocutaneous vessels
- 10. Anatomy of Circulation 3)Subcutaneous Plexus -lies at the level of superficial fascia -Predominant on the torso -musculocutaneous vessels
- 11. Anatomy of Circulation 4)Subdermal Plexus -receives blood from underlying plexus -the main plexus supplying blood to the skin -represents the dermal bleed observed in incised skin
- 12. Anatomy of Circulation 5) Dermal Plexus -mainly arterioles -important in thermoregulation
- 13. Anatomy of Circulation 6)Subepidermal Plexus -contains small vessels without muscle in the walls -nutritive and thermoregulatory function
- 14. Angiosome • An important concept in skin vascular physiology as it applies to flaps is that of the angiosome. • In 1987, Taylor and Palmer1 coined the term angiosome to refer to the tissue supplied by a named artery. An angiosome is a composite block of tissue supplied by a main source vessel. The adjacent angiosomes are linked either by reduced caliber choke anastomotic vessels or vessels without reduction in caliber – the true anastomoses on the arterial side.
- 16. • When body temperature increases, the resulting decrease of norepinephrine leads to lesser sphincteric contraction, thus allowing greater blood flow to the skin; the opposite occurs with decreased body temperature. Vascular supply to the skin thermoregulation nutritional support capillary network precapillary sphincters vasodilation of the precapillary sphincters Local hypoxemia causes arteriovenous shunts sphincters of the arteriovenous shunts are under sympathetic control
- 17. Zones of Perfusion Macrocirculatory system Circulatory capillary Interstitial cellular levels. cell function and viability The importance of tissue vascularity is well recognized, but the complexity and diversity of tissue perfusion mechanisms require that the process be divided into components.
- 18. Each level of perfusion has unique physiologic characteristics, and optimal management is possible only if these differences are recognized. Johnson and Barker described two levels of risk zones for flap failure, making a distinction between thrombosis at the arterial and capillary levels.
- 19. Essential for flap survival. Delay phenomenon Free microvascular tissue transfer is also a zone I manipulation. The importance of the capillary circulation is shown by the “no-reflow phenomenon,” wherein a loss of nutritive blood flow occurs in the presence of an adequate vascular supply.4
- 20. Zone I: Macrocirculatory System • Blood vessels travel by one of two main routes to terminate in the cutaneous circulation. • Musculocutaneous arteries pass through the overlying muscle to which they provide nutrition • Septocutaneous arteries(also referred to as direct cutaneous arteries) travel through fascial septa that divide the muscular segments .
- 21. • The neural supply to the skin originates from sensory nerves and sympathetic nerves. The sensory nerves are distributed in segmental fashion, forming dermatomes, and participate in the skin’s protective function. The postganglionic terminals of cutaneous sympathetic nerves contain the neurotransmitter norepinephrine and are found in the area of cutaneous arterioles.
- 22. Zone II: Capillary System • The cutaneous capillary system, along with the arteriovenous shunts, serves the two important functions of nutritional support and thermoregulation.
- 23. Before entering the capillary bed, the arterioles branch into small vessels (e.g., terminal arterioles or metarterioles) that are surrounded by a discontinuous layer of smooth muscle. A simple ring of smooth muscle forms a sphincter at the point where the capillaries originate from the metarteriole. This sphincter can completely stop blood flow within the capillary. The capillary bed can be bypassed by arteriovenous shunts that allow the arterioles to empty directly into venules. During conditions of adequate systemic vascular pressure, preshunt and precapillary sphincters regulate the distribution of cutaneous blood flow.16
- 24. Zone III: Interstitial System • The interstitial space is filled with proteoglycans and collagen.13 In many tissues, hyaluronic acid filaments make up the interstitial ground substance. • These filaments are normally woven through the interstitium, producing a medium that exhibits high resistance to fluid movement unless the tissue is well hydrated. • In tissues with excess edema, the filaments do not overlap, producing shear planes of free fluid within the interstitium.5
- 25. Zone IV: Cellular Systems • The sodium-potassium pump is important in maintaining osmotic equilibrium across the cell membrane and has a requirement for energy in the form of adenosine triphosphate (ATP cell membrane extracellular and intracellular environments specific membrane proteins osmotic pressure The intracellular space is the endpoint for nutrient transport and the origin of metabolic waste. The cell wall is a fluid lipid bilayer 7.5 to 10.0 nm thick. The lipid bilayer is a major barrier to movement of solutes across the membrane.
- 26. Classification of Flaps Flaps are commonly classified according to their principal blood supply. They include •Random •Arterial cutaneous (i.e., axial), •Fasciocutaneous •Musculocutaneous • Venous flaps.
- 27. Random Cutaneous Flaps • Most common • Based on subdermal plexus • Unpredictable • Length : width of 3:1 or 4:1
- 28. • 1989 Pasyk • Demonstrated a significantly greater capillary density in the papillary and reticular dermis of the head, face, and neck than in the lower parts of the body. • Because of this increased density, it is possible to design and transfer longer random-pattern skin flaps in the face and neck than elsewhere in the body
- 29. • Limited by available vessels • Based on direct cutaneous vessels • Random flap at distal tip • Examples – nasolabial – midline forehead flaps Axial Flaps
- 30. Myocutaneous and Fasciocutaneous Flaps • The greater blood flow and higher tissue oxygen tensions available with myocutaneous flaps make this design superior in the management of contaminated or infected defects. • Improved phagocytotic and bactericidal activity of leukocytes is seen in myocutaneous flaps in comparison with random pattern flaps • These physiologic benefits contribute to the ability of myocutaneous flaps to resist bacterial inoculation more effectively than random pattern flaps.
- 31. On the amount of vascular inflow that is remaining after raising the flap • The efficiency of the venous drainage remaining • The amount of nutrition that is available • The relative ease and capability of the flap to develop collateral circulation from the recipient site • The prevention any kind of infection during the phase of reduced nutrition and vascularity. SURVIVAL OF A FLAP DEPENDS
- 32. • The primary insult affecting flap survival is impaired vascular supply and the resultant ischemia. In the presence of adequate blood flow, complete flap survival occurs. • Nerve section and inflammation influence flap survival primarily by affecting blood flow. Physiology of Acutely Raised Flaps
- 33. Impairment of Vascular Supply Elevation of flap Partial interruption of the vascular supply (zone I) to the skin local decrease in perfusion pressure Flap survival depends severity of ischemia and the amount of time before recovery of nutrient blood flow
- 35. • The venous outflow from the skin also is impaired with flap elevation. Venous flow can occur through the subdermal plexus or via venous channels that accompany the feeding artery in the pedicle. • Complete venous occlusion in the early post elevation period may be more damaging to flap survival than inadequate arterial supply. • Fortunately, the subdermal plexus alone is often able to provide adequate venous outflow. Care should be taken to preserve venous outflow in flaps pedicled solely on the feeding vessels
- 36. • Impairment of lymphatic drainage with flap elevation also occurs. Reduction of the cutaneous lymphatic drainage rise in interstitial fluid pressure increased leakage of intravascular protein associated with inflammation. increased interstitial pressure decreases capillary perfusion by raising the critical closing pressure
- 37. Microcirculatory Changes • Necrosis in flaps is caused by prolonged loss of nutritional blood flow. • There are several proposed mechanisms for loss of nutritional flow, each of which may play a role. • Erythrocyte sludging has frequently been noted in capillaries undergoing ischemia, often without thrombus formation. • The reason for the erythrocyte sludging is multifactorial.
- 38. The blood flow gradually increases in the flap A fibrin layer forms with in the first 2 days. Neovascularization of the flap begins 3 to 7 days after flap transposition. Revascularization adequate for division of the flap pedicle has been demonstrated by 7th day in animal models and man. STAGES OF FLAP HEALING Neovascularization
- 39. Nerve Section • Sensory and sympathetic nerves are severed in the process of flap elevation. Although loss of sensation may limit the usefulness of the flap after transfer, adrenergic denervation has implications for flap survival. • When a sympathetic nerve is divided, catecholamines are released from the nerve terminal, and the mechanism for catecholamine reuptake is eliminated. A local “hyperadrenergic state” exists, which produces vasoconstriction mediated by α- adrenergic receptors in the cutaneous vasculature. • The vasoconstricting effect of sympathectomy further reduces total flap blood flow. which has already been decreased by division of supplying vessels.
- 40. Inflammation and Prostaglandins Surgical trauma and ischemia Inflammatory response. Histamine, serotonin, and kinins are released into the extracellular Increasing the permeability of the microcirculation. Rise in the concentration of proteins and cells
- 41. The action of the primary mediators of the inflammatory response (histamine, serotonin, and kinins) is short- lived. After kinin formation and in the presence of complement, prostaglandins are synthesized by injured cells. Prostaglandins play an important role in the later stages of the inflammatory reaction while simultaneously initiating the early phases of injury repair. Vascular endothelium platelets
- 42. Reperfusion Injury • Both terms imply a period of ischemia, and both conditions result in microcirculatory failure. Controversy and, often, confusion surround the terms no-reflow and reperfusion injury No reflow phenomenon condition in which zone I perfusion has been reestablished but zone II or III failure prevails Reperfusion injury that tissues tolerate short periods of total ischemia fairly well but exhibit histologic injury after return of perfusion—thus, injury apparently caused by reperfusion
- 43. Free Radical Formation When oxygen becomes available with reperfusion, an additional menace to flap survival is produced—the free radical. This byproduct of reperfusion can cause damage at the cellular and subcellular levels, contributing to postischemic tissue necrosis. The neutrophil appears to play a major role in the mediation of reperfusion injury.99
- 44. Capillary Obstruction (No-Reflow Phenomenon) • Arterial and random flaps can tolerate several hours of total avascularity and remain viable. When the critical ischemia time for a flap is exceeded, an ischemia-related obstruction to blood flow, known as the no-reflow phenomenon, develops. Even though large vessels (zone I) have adequate flow, there is no perfusion in zone II or III. • The no-reflow phenomenon was described in skin flaps by May and colleagues.
- 45. Three pathogenic mechanisms have been suggested to play a central role in the development of no-reflow phenomenon : • (1) oxygen-derived free radicals causing damage in the endothelial and parenchymal cells; • (2) this cell membrane damage allowing Ca2+ influx, resulting in intracellular overload; • (3) change in arachidonic acid metabolism resulting in synthesis of less vasodilating and antithrombotic PGI2 by the endothelium and increased synthesis of vasoconstricting and thrombotic TXA2 by platelets.
- 46. Attempts to Alter Skin Flap Viability
- 47. • Delay • Three theories ▫ Delay improves blood flow Depletion of vasoconstricting substances Formation of collateral and reorientation of vascular channels Stimulation of inflammatory response Release of vasodilating substance ▫ Conditions tissue to ischemia ▫ Closure of arteriovenous shunts
- 48. Conclusion • An intimate knowledge of the vascular anatomy and basic physiology of skin allows to accurately predict and explain the physiologic changes that can affect the viability of local skin flaps used to repair facial defects
- 49. Thank you
Editor's Notes
- The majority of cells undergo keratinization and form the various epithelial layers.8 The superficial keratinized cells of the skin are continuously replaced by cells originating from the mitotic activity in the basal layer of the epidermis. Melanocytes derived from neural crest cells also are found in the epithelium of skin and constitute a second cell type.
- This relatively noncellular layer has metabolic requirements far less than those of the epidermis. Nerves, blood vessels, lymph vessels, and the base of the epidermal glandular appendages are found within the dermis. The dermis is 15 to 40 times thicker than the epidermis, with a maximum width of 4 mm on the back. The papillary dermis is characterized by an abundant ground substance, irregularly arranged collagen bundles, and a highly developed microcirculation. The reticular dermis is composed of thick bundles of collagen and coarse elastic fibers, and fibrocytes and blood vessels are proportionally less numerous. Deep to the reticular layer of the dermis, the subcutaneous layer consists of loose connective tissue and a varying amount of fat cells. It is a deeper continuation of the dermis and collagenous fibers continuous with those in the dermis. The density of the collagenous fibers is related to the degree of cutaneous mobility over the underlying structures. In the palms and soles, for example, these fibers are particularly numerous. The deep surface of the subcutaneous layer is attached to the superficial fascia of underlying muscle where it is present
- The head and neck region has several such angiosomes, including the important thyroid, facial, buccal, ophthalmic, superficial temporal, and occipital. Adjacent angiosomes are in communication with each other via choke vessels. This relationship becomes important in the design of various flaps. It has been demonstrated that axial pattern flaps (to be discussed in this chapter) are capable of supplying adequate blood flow to an adjacent angiosome. The incorporation of tissue on an additional angiosome beyond this adjacent angiosome, however, invites vascular compromise and likely flap failure. Techniques to extend this vascular supply, such as delay, may be necessary.
- The angiosome concept: an angiosome is a block of tissue (skin, muscle, bone, or a combination) supplied by an artery and the accompanying veins. It can survive when isolated on this pedicle. (a) The posterior tibial artery is an example of an axial artery along which a series of perforators arise to supply the overlying fascia and skin. Each perforator supplies an angiosome. (b) When the perforator to an angiosome is occluded, ‘choke’ or ‘variable resistance’ vessels, which connect to the adjacent angiosome, dilate to maintain the blood supply of the affected angiosome. (c) Usually, a perforator will only reliably perfuse one adjacent angiosome through opening of the intervening choke vessel. Therefore, it is possible to raise a fasciocutaneous flap comprising two angiosomes based on a single perforator to cover local defects. (d) However, attempts to capture more than a single adjacent angiosome risk necrosis of the distal part of the flap.
- Zones of perfusion. Zone I is the macrocirculatory system consisting of cardiopulmonary, neurovascular, and lymphatic function. Zone II is the capillary circulatory systems composed of arterioles, capillaries, venules, and arteriovenous shunts. The interstitial system is zone III and entails the capillary membranes and interstitial ground substance. The cell membrane, organelles, and intracellular space constitute zone IV, the cellular system. By extension of this concept, four zones of the circulatory system can be considered for all hazards. Proper function of each zone is crucial to tissue viability.
- Zone I consists of the cardiopulmonary system, the conduits for blood flow (arteries and veins), neural control of those conduits, and the lymphatic system. Zone I has historically been recognized as essential for flap survival. The delay phenomenon is primarily a zone I effect. The development of the pedicled flap3 underscores the importance of zone I in extending flap survival time. Free microvascular tissue transfer is also a zone I manipulation. Zone II comprises the capillary circulation. Zone III is the interstitial space and its mechanisms of nutrient delivery. The capillary wall is included in zone III because capillary permeability is a main determinant of interstitial space properties. Failure of metabolites to enter and traverse the interstitial space can result in loss of cell viability, even though there is adequate zone I and even zone II function. Interstitial systems are an important link in skin flap survival rate.5 The cell and its membranes constitute zone IV. Maintaining viable cells is the ultimate determinant of flap survival. Prolongation of cell survival through selective changes in cell permeability and uptake is a potential intervention that may improve flap survival rate
- The cutaneous portion of a septocutaneous artery typically runs parallel to the skin surface, providing nutrition to a large area of skin. Septocutaneous arteries are usually accompanied by pairs of veins and run above the superficial muscular fascia.11 The more common musculocutaneous arteries leave the muscle and enter the subcutaneous tissue to supply a smaller region of skin.
- Primarily because of its thermoregulatory function, the rate of blood flow through the skin is one of the most variable in the body. During ordinary skin temperatures, the amount of blood flowing through the skin (approximately 9 mL/min per 100 g of tissue) is greater than the flow required for nutritional support.13,14 Blood flow can increase to 20 times this value with maximal vasodilation. When the body is exposed to extreme cold, blood flow can be reduced to levels that are marginal for cutaneous nutrition.
- The primary regulation of blood flow to skin is at the arteriolar level. It is here that sympathetic tone regulates flow through the precapillary sphincters, arterioles, and arteriovenous anastomoses. When the precapillary sphincters constrict in response to either local or systemic sympathetic tone, blood flow is forced to bypass the Capillary bed through arteriovenous anastomoses. The preshunt sphincters are involved in regulating the changes in blood flow that affect thermoregulation and systemic blood pressure.16,17 Release of norepinephrine by the postganglionic sympathetic fibers results in contraction of the preshunt sphincters. This contraction diverts blood away from the skin surface, where heat loss could occur. With increased body temperature, the sympathetic vasoconstrictor impulses decrease, allowing for greater blood flow to the skin. Local production of bradykinin may play a role in regulating skin blood flow by causing vasodilation.15 The cutaneous circulation also is extremely sensitive to circulating norepinephrine and epinephrine. Even in areas of skin that have lost their sympathetic innervation, a mass discharge of the sympathetic system still results in intense vasoconstriction in the skin. The precapillary sphincter, which controls the amount of nutritive blood flow to the skin, responds to local hypoxemia and increased metabolic byproducts by dilating.16–18 Capillary blood flow is also affected by elevated interstitial pressure, which can compress the capillary and decrease transcapillary flow. Conversely, as pressure decreases in the interstitium, the capillary expands and flow increases.19 Acute rises in systemic blood pressure cause an immediate increase in local blood flow followed by return of flow to near normal levels in less than 1 minute. This normalization of capillary blood flow is called autoregulation.20 The metabolic theory for autoregulation proposes that an excess of oxygen and nutrients results in arteriolar constriction. This process is believed to be the primary functional mechanism of autoregulation. The myogenic theory suggests that stretching of the arteriolar muscle results in reflex contraction and may be a mechanism to protect capillaries from excessively high blood pressures. Reduction of blood flow may also occur as a result of increased interstitial pressure.
- Two processes by which substances can move across the interstitial space are diffusion and convection.21,22 Diffusion is the process wherein a molecule passively moves to a lower concentration. Molecular movement by diffusion is affected by many factors. An important characteristic is lipid solubility. Lipid-soluble molecules tend to traverse cell membranes more easily and quickly than non–lipid-soluble agents. Large molecules diffuse more slowly than small ones. As molecules diffuse away from the capillary, the concentration of that molecule decreases by the inverse square law. As edema occurs, diffusion distances increase.23 Convective flow, or bulk flow, is another way for molecules to move across the interstitium. Rather than diffusing to a lower concentration, an agent is swept along with the current of plasma that flows across the interstitial space in microchannels. The agent then diffuses the short distance from the microchannels to the cells. The relative importance of diffusion and convective flow is controversial. Some writers believe that diffusion is primarily responsible for cell nutrition. Convection becomes relatively more important for certain tissues, molecules, or pathologic states.
- The primary function of the cell membrane is to maintain or to vary in a controlled fashion the separation of the extracellular and intracellular environments. This separation is achieved by specific membrane proteins, which act as solute pumps and solute and solvent leaks. The osmotic pressure between the two environments also should be maintained to preserve normal cell volume. ).31 A loss of energy substrate (oxygen and consequently ATP) produces an intracellular movement of sodium and an increase in intracellular osmotic pressure.25 These changes occur quickly,32 within 10 minutes after arterial occlusion. Within seconds of hypoxia, levels of ATP begin to decrease, and cells begin to swell.29 Relatively brief periods of ischemia result in a reversible swelling of the cell and organelles. If the ischemic insult is severe and prolonged, cell lysis and flap necrosis occur.
- Venous flaps to this point have had no application in head and neck reconstruction. Flaps may also be described according to site of origin relative to the area to be reconstructed. Thus, flaps utilized in the head and neck are local, regional, or distant. Distant flaps may be pedicled or free flaps (microvascular free tissue transfer).
- Myocutaneous flaps represent an additional modification to improve flap survival. They are based on distal segmental vessels, leaving the local vasculature (perforators and cutaneous vessels) intact, which requires incorporation of muscle with the flap. Myocutaneous flaps are typically named for the donor muscle. Examples are the pectoralis myocutaneous flap, based on the pectoral branch of the thoracoacromial artery, and the latissimus dorsi myocutaneous flap, based on the thoracodorsal artery. As for arterial flaps, it often is desirable to extend the surface area of the flap in clinical situations. A random portion of the flap based on the subdermal plexus can be incorporated. This random extension is usually the portion of the flap most at risk for ischemic necrosis.
- It is imperative that a certain amount of damage to the vascularity occurs as soon as a flap is raised, primarily due to severing of some of the vessels supplying the region. Hence the
- Recovery from ischemia also can occur through the timely formation of new vascular channels between the transposed flap and the recipient bed.
- In arterial or myocutaneous flaps, the blood supply to the skin overlying the vascular pedicle is usually adequate.42 In random flaps or random extensions of flaps, the decrease in perfusion pressure becomes more pronounced with increasing distance from the base of the flap.43,44 When perfusion is reduced in one area of a random flap, the adjacent vascular territories supplied by a separate perforating vessel can provide a low-pressure blood supply through the subdermal plexus (Fig. 79-4). Because the nutritional requirements of skin are relatively low, a number of vascular territories can be compromised before necrosis results.
- Reduction of the cutaneous lymphatic drainage results in a rise in interstitial fluid pressure that is compounded by increased leakage of intravascular protein associated with inflammation. The resulting edema leads to increased interstitial pressure, which (Fig. 79-6).24,45 Alterations in the Starling forces result in further ischemic swelling of cells and the interstitial space, setting a positive feedback circle in motion.
- Erythrocyte sludging has frequently been noted in capillaries undergoing ischemia, often without thrombus formation. Therefore, sludging is not necessarily caused by platelet activation unless a microvascular anastomosis or other vessel injury is involved, such as tearing, stretching, laceration, or crushing. Microemboli are commonly generated from a microvascular anastomosis. The reason for the erythrocyte sludging is multifactorial. Erythrocytes become turgid and lose their flaccid, biconcave disk shape in the acidic environment of ischemia. Narrowing of the capillaries,presumably a result of external compression, also contributes to stacking of erythrocytes within the lumen of ischemic tissue capillaries. Sludging is seen less often if the hematocrit value is kept below 30%.
- Early neovascularization has been detected at 4 days in the pig and rabbit models The transient ischemia developed initially after development of the flap causes early release of angiogenic growth factors, leading to activation of the quiescent vascular endothelial cells, leading to the formation of new vessels.
- This further reduction negatively affects the ratio of perfusion pressure to the critical closing pressure of the arterioles in the subdermal plexus. A greater proportion of the distal flap is excluded from the blood supply, and necrosis becomes more likely. The stored transmitter is depleted within 24 to 48 hours, and blood flow increases as the concentration of norepinephrine declines. In critical areas of the flap, the time to recovery of nutrient blood flow may be delayed sufficiently to produce additional necrosis.
- Prostaglandins clearly play a role in the inflammatory response after flap surgery. Prostacyclin levels increase after flap elevation, with a peak concentration around 7 days, and then decrease to postoperative day 21.81 PGE2, PGF2α, and TxB2 levels also rise after the creation of a flap.86 The increase in PGE2, PGF2α, and TxB2 can be blunted by creation of a bipedicled flap. Conversion to a single-pedicle flap (“delay”) results in decreased levels of thromboxane and a higher level of PGE2, which remain elevated for at least 7 days.87 Whether these changes in prostaglandin levels represent a cause or a side effect of the observed phenomenon remains to be seen.
- All flaps experience some ischemia, and return of blood flow may result in microcirculatory impairment.53,93 Free radicals form during reperfusion and cause tissue injury, but other factors, such as hyperosmosis from lactic acid accumulation,94 have also been implicated.95,96
- A major source of free radicals in ischemic tissue is the enzyme xanthine oxidase (Fig. 79-10).100 With ischemia, high-energy phosphate compounds are converted to hypoxanthine, which accumulates in the tissues. When oxygen becomes available with reperfusion, xanthine oxidase catalyzes the conversion of hypoxanthine into uric acid, producing superoxide in the process. This reaction is believed to be an important mechanism in ischemic tissue injury in skin flaps.50 The role of xanthine oxidase has been brought into question by the fact that some investigators have found xanthine oxidase activity in ischemic skin27,101 but others have not.102 Xanthine oxidase activity has been found in normal rat skin and increases its activity after venous occlusion, reperfusion,27 and flap elevation, with the highest levels present distally.43 Tissue damage resulting from production of free radicals can occur through lipid peroxidation of the cellular membrane and denaturation of the intracellular matrix.98 Delayed neovascularization has been proposed as another consequence of free radical damage affecting proliferating endothelial cells.103
- Swelling of the endothelial and parenchymal cells, coupled with intravascular stasis and eventual thrombosis, leads to loss of nutritive flow. Interactions between polymorphonuclear cells and endothelial cells appear to play a fundamental role in the generation of a reperfusion injury.96 Both cell groups produce cytokine and proadhesive molecules that affect the inflammatory response.93 Polymorphonuclear cells adhere to the vascular wall and generate proteases and oxygen free radicals that injure the endothelial cells
- Increased Blood Supply Skin flap failure can occur from extrinsic and intrinsic causes.116 Extrinsic reasons for flap necrosis are reasons not resulting from the design of the raised flap. Examples are systemic hypotension, infection, and pedicle compression. These factors often can be overcome in the clinical situation. The primary intrinsic factor affecting flap survival is inadequate blood flow. Numerous experimental attempts have been made to influence flap microcirculation or decrease the deleterious effects of inadequate flap blood flow (Fig. 79-12). The most successful has been flap delay. Table 79-1 shows the zones of perfusion affected by various interventions to increase flap survival.
- Four facts are accepted about the delay phenomenon Surgical trauma to flap Large percentage of the neurovascular supply to the flap must be eliminated. Delay results in increased flap survival at the time of tissue transfer. Beneficial effects can last upto 6 weeks.