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4. Flap Physiology.pptx

  1. Flap physiology
  2. References • Mathes. Plastic surgery Vol 1 • Janis J. Essentials of Plastic Surgery 2007 • Peter C. Neligan. Plastic surgery third edition, volume one, 2013. 573-588 • Grabb & Smith’s Plastic surgery 6th Ed 2007 • Kayser M. Surgical Flaps. Selected Readings in Plastic Surgery • Carroll WR, Esclamado RM. Ischemia/reperfusion injury in microvascular surgery. Head Neck 22:700,2000 • Siemionow M, Arslan E. Ischaemia/reperfusion injury: a review in relation to free tissue transfers. Microsurgery. 2004;24(6):468-75 • Nguyen et al. Outcomes of flap salvage with medicinal leech therapy. Microsurgery. 2012 Jul; 32(5): 351-7 • Salgado CJ, Moran SL, Mardini S. Flap monitoring and patient management. Plast Reonstr Surg. 2009 Dec;124(6 suppl): e295-302
  3. References • Janis J, Kwon R The new reconstructive ladder: modifications to the traditional model. Plast. Reconstr. Surg. 127 (suppl.): 2055,2011 • Davis et al. The strength of microvascular anastomoses – an experimental evaluation in rats. J Microsurg. 1982 Spring; 3(3):156-61 • Chiu et al. Free flap monitoring using skin temperature strip indicators – adjunct to clinical examination. PRS 2008 122(5) pg 144e. • Lin et al. Tissue oximetry monitoring in microsurgical breast reconstruction decreases flap loss and improves rate of flap salvage. PRS 2011 127(3), 1080 • Giunta et al. Prediction of flap necrosis with laser induced indocyanine green fluorescence in rat model. BJPS 2005 58, 695 • Askari et al. Anti coagulation therapy in microsurgery – A review. J hand surg 2006;31A 836-846 • Machens et al. Flap perfusion after free musculocutaneous tissue transfer: the impact of postoperative complications. Plast Reconstr Surg. 2000 June; 105(7):2395-9
  4. Topic outlines 1. Introduction 2. Regulation of flap blood flow 3. Haemodynamic alterations on flap elevation 4. Metabolic changes in flap elevation 5. Ischaemic reperfusion injury 6. Ischaemic preconditioning & delay phenomenon 7. Timing of flap division 8. Flap failure or necrosis 9. Therapeutic interventions to improve flap survival 10. Flap monitoring
  5. What is a flap? • It is the essence of plastic surgery • Distinguished from graft in that it has an intrinsic vascular blood supply that is responsible for a flap viability o Graft relies on diffusion until its vascularity becomes re- established • Blood supply to flaps involves a continuous 3D network of vessels in all tissue layers following the angiosome concept – An angiosome: a block of composite tissue supplied by all the perforators of a source artery
  6. Vascular supply of flaps • Include both macrocirculation and microcirculation components • Both are subject to intrinsic and extrinsic factors that influence perfusions and thus viability Macrocirculation: • Anatomy of which is used to define and design a flap • Major arterial inflow and venous outflow of a flap constitutes the foundation of the microcirculatory function Microcirculation: • Consist of arterioles, capillaries, venules and arteriovenous anostomoses • Provides nutrition and oxygen • Carries away carbon dioxide and waste products • Therefore these form the basis of cellular metabolism throughout the flap • It is also where most of the control of the perfusion occurs
  7. Blood supply to skin
  8. Vascular structure of skin: Work of Manchot, Salmon and Taylor Manchot • Hamburg, 1889 • His work entitled ‘The Cuteneous Arteries of Human Body’ was published in English in 1983 • Describes 40 cutaneous vascular territories and assigned them to their underlying source vessels • Used ink injection studies on cadavers, WITHOUT the use of X-ray • His work excluded the head, neck, hands and feet • Limited to the cutaneous vasculature • Only a medical student, age 23, completing his thesis within 6 mos Salmon • French anatomist, 1936 • Describes 80 cutaneous vascular territories, each has its own source artery • Uses radiographic lead oxide injection studies
  9. 50 studies every plastic surgeon needs to know. CRC Press, 2015.
  10. Taylor and Palmer (1987) Proposed TWO theories of blood supply to skin 1. Angiosome concept 2. Direct or indirect route
  11. Angiosome • Angiosome derives from the Greek word Angeion, meaning vessel, and somite , meaning segment or sector of body. • Angiosome : A three-dimensional block of composite tissue, including skin and its underlying deep tissue supplied by a single source of artery and its branches • Proposed 40 angiosomes • Each angiosome is linked to its neighbour in each tissue by predominantly reduced calibre vessels called choke vessels, or similar calibre vessels called true anastomoses
  12. (Chapter 8. Handbook of Plastic Surgery 2014) intermuscular or intramuscular connective tissue to pierce the deep fascia. After emerging from the deep fascia, the cutaneous vessels follow the Figure 3 Schematic representation of choke anastomoses (A) and true anastomoses (B) between adjacent vascular territories. (From Taylor GI; Minabe T: The angiosomes of the mammals and other vertebrates. Plast. Reconstr. Surg. 89:181, 1992.)
  13. Principles of Flap, SRPS Volume 10, Number 1 (2004)
  14. Eg.: Angiosome of pedicled TRAM flap
  15. Blood supply to the skin 1. Primary: • Direct cutaneous arteries • Varies in calibres, number and density in different region of the body 2. Indirect vessels: • Reinforce primary supply • Terminal branches of arteries supplying the deep tissue
  16. • One of the primary functions of skin is thermoregulation o Accomplished through regulation of skin blood flow o ↑ skin blood flow = heat dissipation o ↓ skin blood flow = heat conserved • Primary regulation of skin blood flow is at arteriolar level o Sympathetic tone regulates flow through 1. Precapillary sphincters 2. Arterioles 3. Arteriovenous anastomoses • Normal blood flow to skin is approximately 20ml per 100g of tissues o Higher in muscles ( due to higher demand for oxygen and metabolites )
  17. • Effective microcirculatory perfusion is dependent on its proximity to the nearest nutrient vessel. o Flaps that are based on an axial nutrient vascular system is more reliable than random flaps • Random flaps are not based on dominant nutrient vascular system, but instead are supplied by flow through subdermal or subfascial plexus • Much less reliable than axial flaps • Their length is limited to a short distance from the pedicle origin • Therefore, the single most important factor in classifying flaps is whether they are axial or random in nature
  18. Random flap Vs Axial flap
  19. Regulation of cutaneous blood flow • Cutaneous flaps are regulated at the level of the microcirculation o This is where thermoregulation of blood flow occurs • Primary regulator of blood flow in arteriolar network is controlled by systemic and local mechanism • Systemic control • Neural regulation • Humoral regulation • Local control • Metabolic factors • Physical factors
  20. Systemic control Neural regulation Sympathetic adrenergic fibres maintain basal tone of vascular smooth muscle at the arteriovenous anastomoses, arterioles, and arteries Alpha adrenergic receptors Vasoconstriction Beta-adrenergic receptors Vasodilation Cholinergic fibres Bradykinin release  Vasodilation Humoral regulation Epinephrine, Norepinephrine, Serotonin, Thromboxane A2, Prostaglandin F2 Vasoconstriction Bradykinin, Histamine, Prostaglandin E1 Vasodilation
  21. Local control (autoregulation) • Local regulation are mediated by metabolic and physical factors. • Important especially in those with high metabolic rate e.g skeletal muscle • Metabolic factors – Act primarily as vasodilators, and include hypercapnia, hypoxia, acidosis, and hyperkalaemia • Physical factors – Local hypothermia has a direct effect on vascular smooth muscle to cause vasoconstriction  Local hyperthermia has opposite effect – Myogenic reflex – triggers vasoconstriction in response to distension of isolated cutaneous vessels, thereby maintaining capillary flow at a constant level independent of arterial pressure – Increased blood viscosity (Hct > 45%) may also decrease flow
  22. Rheologic factors • Rheology of blood in the microcirculation is determined by the cell concentration, plasma viscosity, red cell aggregation and deformability as well as the vessel characteristics • Flow in small vessel can be approximated by above formula which follows Poiseuille’s Law. • Flow is proportional to the fourth power of radius • Small decrease in vessel lumen results in big decrease in flow  Decrease in intraluminal pressure (hypovolaemia, hypotension)  Increase in extravascular pressure (oedema, haematoma)
  23. Other considerations Same concept of cutaneous blood flow can be applied to muscle but with the following differences: 1. Arteriovenous shunts are believed to be absent in muscle 2. Muscle has a much higher capillary density than skin 3. Metabolic demand of muscle is far greater than that of skin, thus autoregulation plays a more important role 4. Epinephrine causes vasodilation, in direct contrast to vasoconstriction seen in skin 5. Temperature has less effect on blood flow 6. Myogenic tone is very important in regulating blood flow in muscle • Cutaneous blood flow predominantly rely on sympathetic vasoconstrictors
  24. Haemodynamics of flap transfer • The elevation of skin flap produces profound changes which drastically disrupts the finely balanced equilibrium that regulates blood flow to the tissue • Immediate loss of sympathetic innervation that results in spontaneous discharge of vasoconstricting neurotransmitters • Combined with drop in perfusion pressure from physical removal of inflow vessels, the result is that the peripheral portions of the flap become acutely ischaemic
  25. Haemodynamics of flap transfer Hoopes’ circulatory events in a pedicled flap after its blood supply is partially interrupted during elevation and transfer 0-24 hours: • Reduction in arterial blood supply • Progressively decreasing circulatory efficiency for first 6 hours • Plateau at 6-12 hours • Increase in circulatory efficiency beginning at 12 hours • Marked congestion and oedema during the initial 24 hours • Marked dilatation of arterioles and capillaries
  26. Hoopes’ circulatory events in a pedicled flap during elevation and transfer 1-3 days: • Improvement in pulse amplitude • Little or no improvement in circulation during the initial 48 hours • Increase in number and calibre of longitudinal anastomoses • 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 • Vascular anastomoses between flap and recipient bed present at day 2-3, becomes functionally significant at day 5-7 • Increase in size and diameter of functioning vessels • Reorientation of vessels along the long axis of the flap
  27. Hoopes’ circulatory events in a pedicled flap during elevation and transfer 1 week: • Circulatory function well established between flap and recipient bed • Pulsatile blood flow approaches preoperative levels 7-14 days: • No further significant increase in vascularization • Arterial pattern becomes normal 2 weeks: • Progressive regression of the vascular system • Continuous maturation of anastomoses between pedicled flap and recipient site
  28. Hoopes’ circulatory events in a pedicled flap during elevation and transfer 3 weeks: • Vascular pattern approximates preoperative state • Flap achieves 90% of its final circulation • Fully developed vascular connections between pedicle and recipient site 4 weeks: • All vessels decreased in diameter, few remaining newly formed vessels
  29. • Ultimate outcome of flap following flap elevation is determined by haemodynamic, anatomic and metabolic changes • Palmer, Nathanson, and Kerrigan carried out studies using labelled microspheres to study the haemodynamic changes o Showed that although flow at the base of a pedicle is preserved after elevation, flow at the tip of the flap often drops to < 20% of normal within first 6-12 hours o Flow gradually returns to approximately 75% of normal within 1-2 weeks, and to 100% by 3-4 weeks • As gradual returning of flow to the ischaemic portion of flap occurs by longitudinal flow from pedicle, additional flow is also returning by inosculation, and neovascularization from the bed
  30. • Musculoutaneous flaps take on the perfusion benefits of underlying axial muscle flap • Gottrup et al, showed that they have an early and continuous increase in blood flow after elevation • Whereas random skin flaps have an early decrease but develop a subsequent lasting increase in flow • Tissue oxygen tension higher in musculocutaneous flaps up to 6 days after elevation, and are higher in proximal than distal portions in each flap type • This difference is greater in random-pattern flap than in axial muscle or musculocutaneous flap • Differences in patterns of oxygen delivery to random vs musculocutaneous flaps, may explain the greater reliability of musculocutaneous flaps when they are used in the presence of infection • Provides better bacterial killing function in the setting of an infection
  31. • Banbury et al described muscle flaps’ triphasic microcirculatory response to sympathectomy & denervation. • The genitofemoral nerve of 30 rats was divided and the proximal vessels were stripped of their adventitia. The muscle was not elevated. • Red blood cell velocity increased transiently, immediately after denervation • Main arterioles dilated at 24 hours • Capillary perfusion increased at 2 weeks • The microvessels had hyperactive responses to all vasoactive agents 2 weeks after denervation 1. Initial acute hyperadrenergic phase 2. Non adrenergic phase (with significant vasodilatation) 3. Sensitized phase (Increased capillary perfusion & hyperresponsiveness vasoactive substances)
  32. Metabolic changes following flap elevation 1. Ischaemic tissue undergoes anaerobic metabolism – Rapid depletion levels of oxygen, glucose and ATP – Concomitant increase of CO2 and lactic acid 2. Prostacyclin & thromboxane levels are elevated 3. Glucose & Glycogen consumption increased in ischaemic but viable portions of the flap, in proportion with the degree of ischaemia 4. Glucose consumption peaks around D3, and returns to normal by D7
  33. 5. Increased production of toxic superoxide radicals (a/w anaerobic metabolism) – Causes direct cytotoxic effects – Acts as trigger for local acute inflammation, adherence and accumulation of leukocytes, and subsequent endothelial injury – Subsequent cellular events leads to microvascular shutdown 6. Levels of superoxide dismutase decreased in distal portions of acute flaps as the enzyme is consumed in converting superoxide to oxygen in a tissue-protective mechanism Metabolic changes following flap elevation
  34. Reperfusion injury
  35. Reperfusion injury Ischaemic period • Cell energy level falls, disrupting ion gradients and allowing calcium to enter cytoplasm • Calcium activates a cytosolic enzyme that transforms xanthine dehydrogenase to xanthine oxidase which reduces molecular oxygen into oxygen free radicals
  36. • During reoxygenation after ischaemia, xanthine dehydrogenase is converted to xanthine oxidase – Catalyzes the conversion of Hypoxanthine + O2  Xanthine – With production of superoxide anion as byproduct – Superoxide anion then lead to formation of other oxygen radical species  direct cellular injury Reperfusion injury
  37. Pathogenesis of ischaemic reperfusion injury: • When O2 is reintroduced, superoxide anion, hydrogen peroxide and hydroxyl radical are produced. These metabolites causes injury via: 1. Direct reaction of superoxide radical with endothelial membrane – Causes lipid peroxidation, disruption of membrane proteins, increased cell permeability – Consequently cytoplasmic swelling & dysfunction 2. Chemotactic property of O2 metabolites, primarily superoxide anion – Causes neutrophil migration into the reperfused area, with the neutrophils actually causing tissue destruction
  38. Pathogenesis of ischaemic reperfusion injury: 3. Arachidonic acid metabolism pathways • Activated neutrophils produce leukotrienes and perpetuate inflammatory reaction • The activation of lipoxygenase that yields leukotriene B4 (a potent chemoattractant) further induce superoxide anion generation and degranulation in neutrophils, leading to further generation of free radicals & neutrophils recruitment • Similarly, cyclooxygenase, in the setting of ischaemia, results in the generation of thromboxane & prostaglandins – Thromboxane A2 is a potent vasoconstrictor & induces platelet aggregation – Prostacyclin (PGI2) is a potent vasodilator, inhibitor of platelet aggregation & increase capillary permeability • LTB4, TXA2 & PGs – all important in microvascular & inflammatory derangements
  39. • Free radicals also play an important role in hematoma- related flap necrosis – Hemoglobin and iron catalyse the chemical reactions that lead to the production of highly destructive free radicals, in particular the hydroxyl radical
  40. • The rapid intravascular accumulation of neutrophils can lead to progressively decreased perfusion and may represent the “no-reflow” phenomenon with ischaemia and reperfusion
  41. The role of neutrophils in ischaemic reperfusion injury Activated PMNs may cause injury through: – Direct endothelial injury, resulting in loss of vascular integrity, oedema, haemorrhage and thrombosis – Microvascular occlusion, and further ischaemia resulting from adherence and accumulation of aggregates of PMNs within the vessel lumen
  42. Regulation of neutrophil adhesion Two major adhesion molecules: 1. The selectins and their carbohydrate counterstructures 2. The leukocyte integrins and their ligands on endothelial cells that are members of the immunoglobin (Ig) superfamily
  43. • The selectin receptors are lectin-containing proteins that recognize specific carbohydrate counsterstructures, expressed on glycoproteins. – Responsible for the initial transient adhesion of neutrophils that occurs at sites of inflammation, manifested as “rolling” • Once slowed by selectin-carbohydrate interactions, local inflammatory stimuli subsequently activate the neutrophils to produce firm adhesion through the integrin-Immunoglobulin- like-ligand interaction – Mediates the steps of firm adhesion of neutrophils to endothelium at sites of inflammation, diapedesis & emigration
  44. • Many inflammatory mediators & vasoactive substances have been implicated in recruitment, adhesion, migration, & activation of neutrophils to further inflict tissue injury in ischaemic reperfusion phenomenon o Thrombin o Histamine o Oxidants o Interleukin-1 o TNF- o Platelet activating factor o Chemotactic peptides (eg C5a) o Chemokines (eg Interleukin-8)
  45. Ischaemic preconditioning & delay phenomenon (non-lethal ischaemia) • Ischaemic preconditioning is a process whereby tissue is subjected to a brief period of non lethal ischaemia • This process confers the tissue a resistance to damage by subsequent prolonged ischaemic events • This phenomenon was first described by Murry et al in a model of myocardial ischaemia-reperfusion, in which it was shown to reduce infarct size in rat myocardium
  46. • Surgically, flap survival can be extended by the strategic division of vascular pedicles at various time intervals along the length of the proposed flap – the “flap delay” procedure • Delay is the surgical interruption of a portion of the blood supply of a flap at a preliminary stage before transfer
  47. Purpose of flap delay procedure: • To increase the surviving dimension (length) of a skin flap • To improve the circulation of a flap • Diminish the insult of transfer Arteriogram of control (left) and delayed (right) rectus abdominis muscle of a dog 7 days post operatively. Note the dilated choke vessels in the delayed flap by ligation of the deep inferior epigastric artery (arrow)
  48. • Theories of flap delay concept: – Conditions tissue to ischaemia, allowing it to survive on less nutrient blood flow than normally needed – Improves or increases vascularity through o Dilation of choke vessels connecting adjacent vascular territories o Reorientation of vessels within the flap to a more longitudinal pattern o Angiogenesis & vasculogenesis • Five mechanisms of delay phenomenon (according to Hoopes): 1. Sympathectomy 2. Acclimatization to hypoxia 3. Vascular reorganization 4. Reactive hyperemia 5. Non specific inflammatory reaction (producing vasodilation) • Maximum survival of delayed flap achieved at 1 week & minimum effective time is 2-3 days
  49. Anatomic changes in flap delay • Sympathectomy causes depletion of cathecholamines from the initial procedure itself – Begins after incision and ending by 30 hours – Hence, enhanced vascularity from less vasoconstriction due to lack of cathecolamines • Gradual hypertrophy of blood vessels & acclimatization to hypoxia as a result of ischaemic tissue conditioning from exposure to lower O2 tension or poor circulation – Vessel enlargement is permanent & irreversible involving o Multiplication (hyperplasia) o Elongation o Hypertrophy of red cells in each layer of the vessel wall – Maximum effect between 48-72 hours after operation
  50. • Vascular reorganization – Longitudinal reorientation of small vessels parallel to the long axis of pedicles at 1-7 days post delay • Reactive hyperemia – Due to increase resistance to venous outflow, and increase in size & number of subdermal arterial & dermovenous plexuses – These vessels are toneless, dilated and unable to respond to local changes • Ingrowth of new vessels (neovascularization) – 4 to 5 days post operatively – Vasodilation & angiogenesis until about day 14
  51. Hemodynamic changes in flap delay • Overall blood flow increase reached 75 - 90% of normal by the second week o Vasodilation hypothesis – relaxation in precapillary arterioles of delayed flaps as a result of – Sympathectomy – Tissue ischaemia with local arterial dilation – Inflammation producing vasodilation – Formation of new collateral vessels or dilation of pre-existing channels • Significantly higher capillary blood flow in delayed random flap – Increase flow detectable within 2 days of surgical delay – Increased 100% by D4 – Remained plateau until D14 • AV shunts do not have significant role in the pathogenesis of distal skin flap necrosis – Tissue ischaemia due to vasoconstriction of small random arteries that supply blood to arterioles in AV shunts
  52. Metabolic changes in flap delay • Increase glucose consumption & lactate production, with concomitant depletion of glycogen • Inadequate tissue oxygenation leads to a change from aerobic to anaerobic metabolism, releasing higher levels of superoxide radicals • Metabolic derangements affect physical properties of blood such as viscosity and clotting
  53. • However, a critical minimal level of tissue glucose is necessary to accommodate metabolic adaptation in the ischaemic tissue – Glycolytic enzyme level highest in the first 3 days, supporting the theory that delay acclimatizes tissue to hypoxia – Metabolic changes reversible for up to 4 hours – Ischaemic periods of 12 hours and longer resulted in complete loss of energy reserves
  54. In summary: • Initial primary event is dilation of existing vessels within the flap, no ingrowth of new vessels – Initial period of vasoconstriction resolved within 3 hours post operatively • Active and progressive dilation of choke vessels is most dramatic between 48-72 hours • Choke vessels dilation is permanent & irreversible – Hyperplasia & hypertrophy of the cells in all layers of the choke artery wall • In clinical setting, the traditional delay period is 2-3 weeks
  55. Timing of flap division • Hoffmeister concluded that flap transfer is best done 2-4 weeks after delay • Arterial connections between the transferred flap and its bed begins at 4 to 5 days and venous drainage several days earlier • Although flap division can be performed safely as early as day 3 in many animal studies, clinically this interval must be lengthened according to - Regional anatomic differences - On-the-spot assessment of flap viability and “vigor” - Size and characteristics of the recipient site - Presence or absence of infection - Haematoma
  56. • Hauser et al proposed that the traditional mean of 3 weeks for division of an inset flap is probably acceptable in 85% of patients, but is premature in some and excessively long in most • On the basis of published reports as well as the cumulative anecdotal experience of many surgeons, it may be concluded that most flaps can safely be divided between 10 days and 3 weeks • For free flap, Berger and Machens showed that flap perfusion remained autonomous on its vascular pedicle even after 10 years of surgery
  57. Flap failure or necrosis • Multifactorial 1. Composition of the flap 2. Arterial or venous insufficiency 3. Presence of global ischaemia
  58. 1. Composition of the flap • Inherent blood flow o Proximal pedicled flap – reduced blood flow as a result of sympathectomy, cathecolamine release, & local response to injury o Distal portion - local ischaemia (even in maximal vasodilation) due to inadequate perfusion pressure from the proximal portion • Tolerance to ischaemia o Factors affecting ischaemic tolerance – Ischaemia time – Energy & metabolic requirements – Temperature: cold vs warm – Tissue composition  Gut  muscle  skin  Bone  Cartilage  Decreasing metabolic demand
  59. • Adipocutaneous flaps can tolerate ischaemia better than musculocutaneous flaps • Ischaemia time of up to 4 hours for a perforator flap may be well tolerated • Musculocutaneous flaps, on the other hand, do not tolerate prolonged ischaemia time because of the metabolic requirement of the muscle • In general, 2-3 hours of ischaemia is the maximum time tolerated
  60. Composition Skin flap Muscle flap Inherent blood flow Less blood flow More blood flow Response to ischaemia Marked decrease in flow rate Early hyperemic phase during reperfusion - Maintain significant blood flow to all region - Including area that is destined for necrosis Tolerance to ischaemia - Lower metabolic requirement - More tolerant to ischaemia - Higher metabolic demand - Less tolerant to ischaemia
  61. 2. Arterial or venous insufficiency • Sufficient reduction in venous outflow can produce flap necrosis despite adequate arterial inflow – In free tissue transfers, venous occlusion is more common than arterial occlusion – In most pedicle flaps, however, the two are closely linked and any venous insufficiency in the face of impaired arterial inflow will lead to significant tissue necrosis • Venous insufficiency causes more damage than equivalent arterial insufficiency • Hjortdal et al & Gurlek et al found significant stasis, hemoconcentration, and increased viscosity were associated with venous ischaemia
  62. 3. Presence of global ischaemia (the entire flap is ischaemic) due to • Flap design too large for its intrinsic blood supply • Arterial thrombosis – Platelet aggregation is the underlying cause • Venous thrombosis – Primarily the result of fibrin clotting • In random & axial pedicle flap – Thrombosis usually secondary to low-flow state in microcirculation level o Improper flap design o Ischaemia reperfusion injury o Systemic causes (eg hypotension, smoking, sepsis, vasoconstrictors) o Local physical compression of flap (eg Improper inset, kinking, hematoma)
  63. • In free flaps – Thrombosis at site of microvascular anastomosis o Due to poor technique (allowing prothrombotic adventitia or media to be exposed to the luminal blood flow, with subsequent platelet & fibrin deposition • Ischaemic changes are reversible up to 4-8 hours of ischaemia • Damage irreversible after 12 hours of ischaemia at which point, it is not possible to re-establish inflow – No reflow phenomenon (precedes flap death)
  64. Therapeutic interventions to improve flap survival • No consensus exists on the use of anticoagulation therapy after microsurgery • Many surgeons have their own particular protocols for perioperative anticoagulation that has been shaped by personal trials and errors 1. Physical factors & leeches therapy 2. Pharmacological factors 3. Increase tolerance to ischaemia 4. Modulating proinflammatory mechanism
  65. Physical factors Factors that have experimentally demonstrated a survival advantage include: • Maintenance of a moist environment along flap edges o Minimize desiccation of ischaemic tissue • Keep flap warm o Reduce vasoconstriction & decrease blood viscosity • Ischaemic preconditioning o Causes alterations in blood flow, decreased tissue metabolism, decreased level of oxygen-derived-free radicals o Release of endothelium-derived relaxing factors which may cause vasodilation and improved distal blood flow
  66. Physical factors • Hyperbaric oxygen therapy o Given as soon as possible after surgery in rat model improves skin flap viability o Due to increased superoxide dismutase activity & reduced xanthine oxidase activity, especially when coupled with prolonged cold ischaemia
  67. Physical factors • Leeches (Hirudo Medicinalis) o Provides relief of venous congestion after free tissue transfers and replantations o Saliva contains – Hirudin : a naturally occurring anticoagulant that inhibits thrombin & prevent the conversion of fibrinogen to fibrin – Hyaluronidase: facilitates spread of the hirudin within the tissues – Vasodilator histamine: Contributes to prolonged bleeding (up to 48 hours) – Mechanical effect by creating physical channels through which venous drainage can occur
  68. Physical factors • Leeches (Hirudo Medicinalis) cont. o Main indication is for venous congestion – Outflow insufficient – Venous channels either absent or unsuitable for anastomosis o Most significant risk of leeches are – Bacterial infection from the G-ve rod Aeromonas Hydrophilia – Anaphylaxis – Excessive bleeding – Scarring if infected o Prophylaxis with ciprofloxacin or an aminoglycoside, or a third- generation cephalosporin sufficient o Caution when treating immunocompromised patients
  69. Pharmacologic factors • Anticoagulants • Receptor & axon blocker • Direct smooth muscle relaxants • Rheologic agents • Anti-inflammatory agents
  70. Anticoagulants: 1. Dextran • A polysaccharide synthesized by bacteria from sucrose, originally designed as a volume expander • Has been shown to improve short-term microcirculatory patency • Mechanism of action: o Decrease in platelet adhesiveness & procoagulant activity o Inhibition of platelet aggregation o Increases bleeding time o Decrease in blood viscosity • Usually administered as a continuous IV infusion during the flap procedure and continuing for several days post operatively – 500 ml/day for 3-5 days
  71. Anticoagulants: 1. Dextran (cont) • Associated with significant systemic morbidity o Anaphylaxis o Pulmonary oedema o Cardiac complications o ARDS o Renal failure • Therefore, a small test dose is usually administered before infusion • Routine use in free tissue transfer is discouraged
  72. 2. Low molecular weight heparin (LMWH) • Acts in conjunction with antithrombin III to inhibit thrombosis by inactivation of factor X • More effective at preventing venous thrombosis than arterial thrombosis • Improves microcirculatory perfusion & anostomotic patency while minimizing haemorrhage 3. Heparin • Act by binding to antithrombin III, which then inactivates thrombin, factor Xa and other proteases • Used both systemically and as a topical irrigant at the time of anastomosis • Flap survival improvement only when administered continuously but clinically significant risk of hematoma formation • Systemic heparin usually reserved for microvascular applications when intraoperative thrombosis occurs and require mechanical clearing Anticoagulants:
  73. 3. Heparin (cont) • Topical irrigation with heparinized saline is a widely used technique in microsurgery in concentration of 100 units/mL • Beneficial effect attributed to platelet disaggregation & maintenance of vascular patency • A dose related increase in flap patency – target a 2 fold increase in APTT for 3-7 days 4. Thrombolytic agents • Stimulates the conversion of plasminogen to plasmin, which acts to cleave fibrin within a thrombus • Have been effective in salvaging flaps after microvascular thrombosis • First generation agents o Streptokinase, urokinase • Second generation agents o Tissue plasminogen activator (t-PA) o Acylated plasminogen-streptokinase activator complex (APSAC) Anticoagulants:
  74. Receptor & axon blocker: • Conflicting evidence in their benefits 1. Anti adrenergic drugs • Reserpine and guanethidine deplete norepinephrine stores in nerves and lessen the effects of alpha and beta agonists • Propanolol opposes beta-mediated metabolic stimulation • Phentolamine causes vasoconstriction mainly by blocking alpha-receptors 2. Topical nitroglycerin • A potent vasodilator • Greater effect on the venous circulation than on arterial vessels 3. Amrinone • Selective phosphodiesterase III inhibitor • Enhances microcirulatory blood flow due to its – Positive inotropic properties – Vasodilating properties
  75. Direct smooth muscle relaxants: 1. Calcium channel blockers • Diltiazem, verapamil, nifedipine • Act on the vascular smooth muscles to cause vasodilation • Improves circulation in the flap • Diltiazem also stimulates the release of prostacyclin (PGI2), a potent vasodilator and anti-platelet aggregator from the vascular endothelial cells 2. Dimethyl sulfoxide (DMSO) • Increases flap viability by o Vasodilation o Reduction of platelet aggregation o Reduction of free radical scavenging
  76. Direct smooth muscle relaxants: 3. Buflomedil • A vasoactive drug • Used clinically to treat claudication or symptoms of peripheral arterial disease • Protects flaps of poor design, ischaemic flaps, and flaps suffering from reperfusion injury • Mechanism of action: – Inhibitory effect on platelet aggregation – Improves the deformation capacity of red blood cells with abnormal flowability 4. Hydralazine • Affects arteriolar smooth muscle by increasing intracellular cAMP, which in turn causes relaxation and reduces peripheral resistance
  77. Rheologic agents: 1. Fluorocarbons • Lowers the viscosity of blood • Improves microcirculation & oxygen carrying capacity of blood 2. Pentoxifylline • Hemorrheologic agent • Improves the deformability of red blood cells, therefore improving its blood flow characteristics • Decreases fibrinogen levels – Decreases blood viscosity
  78. Anti inflammatory agents: 1. Steroids • Prednisolone & dexamethasone – controversial • Thought to act as vasodilator and membrane stabilizer • Also confers nonspecific anti-inflammatory effect – similar to anti-neutrophil strategies • Systemic steroid administration reduces flap oedema, but the risk of infection may outweigh its perceived benefit 2. Aspirin (ASA) • Acetylates enzyme cocylooxygenase (COX), thereby decreasing the synthesis of Thomboxane A2 (TxA2 ), a potent vasoconstrictor in platelets and Prostacyclin (PGI2), a potent vasodilator in vessel walls
  79. Anti inflammatory agents: 2. Aspirin (ASA) (cont) • At low doses, the effect of aspirin is selective – Only inhibits the cyclooxygenase system in platelets • Experimentally, preoperative aspirin decreases thrombus formation at venous anastomoses and improves capillary perfusion in the microcirculation • Carrol et al, demonstrate increased early anostomotic patency in their study, but there’s no difference from controls after 24 hours to 1 week • No empiric evidence in the literature for using aspirin postoperatively
  80. • In summary, there are many promising potential therapies currently bring investigated that may someday be employed clinically to improve flap physiology and flap viability, allowing expanded flap applications • Nevertheless, there is no substitute for proper flap selection and design, and technical execution
  81. No factors mentioned above should substitute: • Proper flap selection and design • Meticulous debridement & preparation of bed • Careful flap elevation & inset • Appropriate dressing application • Post operative positioning • Close post-operative clinical monitoring – Hematoma – Compression – Kinking – Anostomotic thrombosis – Bleeding
  82. Flap selection pre-op • Surgical reconstruction goal – Preservation & restoration of form & function while minimizing morbidity • In simple terms, “what is available, weighed against what can be spared”
  83. Flap selection pre-op • Optimal reconstructive plan follows careful analysis of flap selection based on: a) Defect analysis (recipient site) b) Patient factors (medical and functional status) c) Reconstructive options d) Cost of care e) The surgeon & his institution
  84. A) Defect analysis • Location • Size & surface area (after adequate debridement) • Quality of the surrounding tissue • Tissue missing or expose (eg hair, skin,mucosa, subcutaneous tissue, muscle, vessels, nerves, cartilage, bone) – Which component need to be repaired? – Which component can feasibly be replaced?
  85. • Vascular status of wound or surrounding tissue – Presence of vascular disease – Evaluation of zone of injury (trauma) – Adequate microcirculation to support grafts or local flaps – Suitable recipient vessels available for free tissue transfer – Previous radiation – Previous surgery or trauma • Infection & bacteriology of wound • Future management concerns (eg need for post op radiation, future surgical needs) A) Defect analysis
  86. B) Patient factors • History & causes of current defect o The need to treat the underlying cause • Patient co-morbidities (influence the safety and success of reconstructive options) – Diabetes – Tobacco use – Obesity – Advanced age – Hypertension & IHD – Pulmonary dysfunction – Peripheral vascular disease – Hematologic disorders – Immunosuppresion
  87. • Compliance – Functional status, lifestyle & rehabilitative capacity of the patient (eg neurological disorder) • Patient’s expectation – Meeting your own potential expectation? • Life expectancy – Complex reconstruction may be questionable • Remember that the sacrifice of specific muscles for flap coverage impacts individuals differently depending on other disabilities present (eg paraplegia) or their occupation & lifestyle (eg professional athlete vs accountant) B) Patient factors
  88. C) Reconstructive options • Helps to organize reconstructive solutions in order of complexity • From most simple solution to most complex
  89. • Factors related to the donor site selection include: – Appropriate tissue match o “Replace like with like” – Length of the vascular pedicle – Caliber of recipient vessels – Surface area – Volume – Thickness of the flap – Donor site morbidities o Functional & aesthetic implications C) Reconstructive options
  90. D) Cost of care • Both financial & psychological aspect • Cost of life? • Impact on quality of life
  91. E) The surgeon & his institution • Skill set • Network of support (eg Facilities, staff, etc)
  92. Flap monitoring • Early detection of compromised flap – Critical for early intervention, correction and salvage of flap • The ideal flap monitoring system should be o Simple o Reliable o Reproducible o Sensitive o Continuous o Representative of the entire flap o User friendly o Easily interpreted o Affordable o Relatively unaffected by external environment
  93. • Note that in certain situations, such as buried flaps or free flaps, the monitoring system itself may need to be buried, or the monitored area of the flap may need to be used as a small window to the overall flap status • Limited access to the flap may lead to faulty assessment
  94. Flap monitoring modality 1. Physical methods • Clinical monitoring • Doppler probe o Ultrasound Doppler probe o Laser Doppler probe • Temperature monitoring • Fluorescein 2. Metabolism monitoring methods • Transcutaneous oxygen tension • Skin punctures and blood glucose measurements • Continuous pH monitoring • Photoplethysmography • Microdialysis
  95. Physical method Clinical monitoring Direct observation o “Gold standard” of all monitoring systems – Skin colour (compared with the adjacent normal skin colour) – Warmth – Capillary refill  Healthy flap – pink color within 1-2 seconds capillary refill  Arterial insufficiency – pale colour without capillary refill  Venous congestion – dusky color with exceptionally brisk refill – Pin-prick bleed  Bright pink oozing reflects a healthy flap  Dark purplish oozing reflects compromised perfusion or venous insufficiency
  96. Physical method Doppler probe • The most widely accepted adjunct to clinical assessment • Uses Doppler effect o Measure the velocity of blood flow, as first described by Strandness • Two main types of Doppler instruments 1. Ultrasound Doppler probe – Uses reflected sound waves to measure the flow of blood cells within the larger arteries and veins of tissues 2. Laser Doppler probe – Measures the frequency shift of light rather than sound, and as such, has a limited penetration of only 1-2 mm • Advantages: Near 100% reliability, continuous & non invasive monitoring • Disadvantages: non quantitative, single site information, and sensitive to movement
  97. 1. Conventional Doppler ultrasonography • More than 40 years • One of the simplest, most direct, and most reproducible methods • Vessels several centimeters deep can easily be evaluated • Arterial signal – classic triphasic patterns – Compromised arterial inflow will lose its triphasic signal pattern and become more “watter-hammer” in nature or disappear
  98. • Venous signal – Lower pitched & continuous – Varying with respiratory cycle – Easily augmented with gentle pressure of the flap – Compromised venous outflow  Venous signal absent or muted  Lost of ability to augment venous flow by gentle compression of the flap • Limitation: o Difficult in separating the flap signal from signals coming from adjacent normal vessels deep to the flap 1. Conventional Doppler ultrasonography
  99. • Miniature implantable Doppler probes, surgically placed on the effluent vein of a free flap o Continously monitor venous outflow o No interference from adjacent vessels o Provide instant notification of either arterial or venous occlusion • Sensitivity 100%, false-negative rate 3% • Allowed early re-exploration & 100% flap salvage • Becoming the standard of monitoring of free flaps
  100. 2. Laser Doppler study • Measurement of skin blood flow • Provides continuous non invasive monitoring of flaps • A laser light prove is affixed to a specific area of the skin, and produces a voltage output proportional to the total flux of red blood cells in the small volume of tissue sampled
  101. • Flowmeter value 30% of baseline o Predicts flap survival • Sensitivity 93%, specificity 94% • Guidelines to improve accuracy: o A fixed probe o Continuous recordings o Attention to physiologic fluctuations and trends • Limitations: – Sensitivity to minor changes in the probe position & angle on the tissue surface with the patient’s movement – Sensitivity to temperature changes – Only a small amount of tissue is sampled at any one time 2. Laser Doppler study
  102. Temperature monitoring Physical method One of the oldest & simplest indirect methods A. Surface temperature  Affected by local external environment  Responds slowly to vascular compromise  Sensitivity > 90% B. Diferential thermometry  More reliable  Thermocouple probes are placed proximal and distal to a microvascular anastomosis, and the temperature differential is recorded o Temperature gradient exceeding 3˚C is significant  This is particularly applicable for muscle flaps or buried flaps  However, it is still affected by local environment variables
  103. Physical monitoring Fluorescein • Provide direct assessment of skin perfusion • Usually administered as an intravenous bolus (15mls/kg); then after 20 minutes, the tissue is examined with an ultraviolet lamp (wood’s lamp) – Adequately perfused tissue fluoresces – Inadequately perfused tissue, no fluorescence seen • Only useful 18H post operatively
  104. Perfusion fluorometry (dermofluorometry) with dermofluorometer • Provide quantitative measurement whereby a fibreoptic light is used to measure and quantify the dermal fluorescence • Continuous flap monitoring by serial fluorescein injections (0.15mg/kg dose) • Optimum dye fluorescence index (DFI) thresholds after flap elevation (generally 30% and above is acceptable) – 7% at 2 hours – 27% at 5 hours • Consistent, highly accurate and reproducible Fluorescein
  105. Metabolism monitoring methods 1. Transcutaneous oxygen tension 2. Skin puncture and blood glucose measurements 3. Photoplethysmography 4. Continuous pH monitoring 5. Microdialysis
  106. 1. Transcutaneous oxygen (PO2) tension • One of the oldest methods • Uses a heated oxygen electrode placed on the skin surface • Measures trends over time • Provides safe, reliable monitoring of peripheral oxygenation in the microcirculation that is rapid, continuous and non invansive
  107. • Limitation – Subject to many other systemic factors affecting oxygen transport and tissue oxygenation • A more refined method uses an implantable optochemical oxygen-sensing electrode (oxygen optode), inserted in the subcutaneous tissue of the flap 1. Transcutaneous oxygen (PO2) tension
  108. 2. Skin punctures and blood glucose measurements • Easy-to-use and efficient adjunct for monitoring postoperative blood flow in flaps • Blood glucose level reduced in congested flaps • A cutoff value for the blood glucose is 62mg/dL • Sensitivity 88% & specificity 82% • Limitations: – Not for ischaemic flaps because sufficient blood cannot be obtained to measure the glucose level in a pinprick test – Unreliable in diabetic patients
  109. 3. Photoplethysmography • Measures fluid volume by detecting variations in light absorption by the skin • Uses a light-emitting diode to transmit light into a tissue • Reflected light from haemoglobin in the dermal capillary red blood cells is received by a photo detector and is analysed as light intensity along a frequency spectrum, removing noise and allowing a means to distinguish between perfused and non perfused tissues.
  110. • Limitation: – Measures flow in tissues only to a depth of 1 to 2 mm • Provide a rapid, precise method to determine flap ischaemia • Differentiate venous compromise versus arterial compromise almost immediately after the onset of an ischaemic insult • However, its use has never achieved widespread acceptance 3. Photoplethysmography
  111. 4. Continuous pH monitoring • Uses a miniaturized glass pH probe that allows the continuous measurement of subcutaneous tissue pH – A rapid fall in tissue pH is seen in response to either arterial or venous occlusion • Reliable experimental tool but never reached widespread clinical application
  112. 5. Microdialysis • An invasive, intermittent, indirect monitoring technique • A sampling technique that studies the biochemistry of organs or tissues • A double-lumen microdialysis catheter or probe similar in size to an 18-gauge venous cannula is placed (using an open needle) under direct vision into the tissue • Connected to a small pump, which infuses physiologic fluid through the catheter
  113. • Across a dialysis membrane, this fluid equilibriates with the interstitial fluid surrounding the catheter, and therefore aliquots of the perfusate can be analysed on the tissue content of glucose, lactate, pyruvate, and glycerol metabolite concentrations. – A falling glucose and rising lactate-to-pyruvate ratio indicates indicates anaerobic metabolism (arterial compromise) – A rising glycerol level reflects cell membrane damage (venous congestion & arterial compromise) 5. Microdialysis
  114. Salvage procedure for the failing flap • When recognized early and managed promptly (<6h), compromised flaps have a 75% salvage rate when taken back to the operating room • If circulation cannot be re-established within 8 to 12 hours, salvage of a free-tissue transfer may become impossible because of the development of the no-reflow phenomenon • Studies have demonstrated that venous thrombosis alone is more common than either arterial or combined arterial and venous thrombosis
  115. Flap monitoring regime • Majority (>80%) of thrombi occurred within the first 2 post operative days • 95% circulatory compromise occurs within 72 hours after surgery • This decreases to 10% after postoperative day 3 • Most centres recommend a minimum of hourly monitoring for the first 24-48 hours
  116. Thank you

Hinweis der Redaktion

  2. Angiosome concept has now been augmented by perforasome theory Perforasome: 3 dimensional vascular territory supplied by a single perforator from a source artery.
  3. Neither work addressed the blood supply to deep tissue
  4. When the precapillary sphincters constrict in response to either local / systemic sympathetic tone, blood flow is forced to bypass the capillary bed through arteriovenous anastomoses. In addition, a number of other factors come into play in regulating flap blood flow. systemic central blood pressure, and cellular factors within the microcirculation involving the endothelium, platelets, and white blood cells
  5. Shows the importance of axial perfusion of a flap Panel A: Shows the reliable perfused area of a flap based on purely random perfusion from the vascular pedicle Panel B: Shows random flap designed beyond the limits of reliable random perfusion, resulting in distal flap necrosis Panel C: Shows the benefit of designing a flap based on an axial pedicle. The length of reliable flap perfusion includes the same length of reliable random perfusion PLUS the length of the axial pedicle
  6. Neural regulation: Occurs primarily through sympathetic adrenergic fibres Regarding humoral regulation: Important to realize that the effects of local injury to the artery can completely override basal vascular tone, and can cause vascular spasm even in the absence of sympathetic denervation. Epinephrine & norepinephrine acts on alpha-adrenergic receptors in the cutaneous vessels.
  7. The effect of haematocrit questioned by Kim and colleagues who found that normovolaemic anaemia with an (Hct 19%) had no significant effect on the survival of pedicled musculocutaneous flaps.
  8. P: pressure difference between two ends L: length of the vessel N: fluid viscosity Abnormally elevated rheologic factors as in polycythaemia / sickle cell disease can compromise perfusion and viability, especially at the marginal portions of a flap
  9. This study showed that with minimal access to the cremaster muscle flap neurovascular pedicle and without changing the blood supply to the flap, significant hemodynamic improvement can be made in the peripheral microcirculation. (Plast Reconstr. Surg. 104:730, 1999)
  10. Body’s key protective enzyme: superoxide dismutase
  11. Once oxygen is introduced, more free radicals produced : superoxide anion, hydrogen peroxide, hydroxyl radical Other mechanism of reperfusion injury involves arachidonic acid derivatives - Further activate the inflammatory process (activates neutrophil, production of leukotrienes B4, thromboxane A2, prostaglandin I2)
  12. Figure: Oxidant generation with ischaemia & reperfusion. During reoxygenation after ischaemia, xanthine dehydrogenase is converted to xanthine oxidase, which catalyzes the conversion of hypoxanthine (formed from degradation of ATP during ischaemia) plus oxygen to form xanthine, with the production of superoxide anion as a byproduct.
  13. Thromboxane A2 is a potent vasoconstrictor and induces platelet aggregation
  14. Figure: Molecular basis of leukocyte-endothelial adhesion. Diagrammatic representation of the known neutrophil-endothelial adhesion receptors. The B2 integrin receptors on neutrophils, LFA-1 (CD11a/CD18) and Mac-1 (CD11b/CD18; both represented as alpha-beta dimers), bind to intercellular adhesion molecules (ICAMs) Endothelial E-selectin (CD62E), and P-selectin (CD62P; represented with their N-terminal lectin domain, epidermal growth factor domain, multiple complement-regulatory repeat sequences, transmembrance domain, and cytoplasmic domain) bind to carbohydrate ligands, particularly sialyl Lewis X antigen, expressed on glycoproteins of neutrophils, with PSGL-1 being the primary ligand for P-selectin. L-selectin (CD62L) on neutrophils binds to carbohydrate ligands on endothelium in systemic vasculature and also presents Slex to E-selectin and P-selectin
  15. From Dhar SC, Taylor GI; The delay phenomenon: the story unfolds, Plastic Reconstructive Surgery 1999;104:2079
  16. Taylor and colleagues demonstrated the opening of existing blood vessels in vascular delay of skin flaps in the guinea pig, rabbit, dog, pig and human Yang and Morris also published similar findings in rat skin flaps These investigators labelled this phenomenon as angiosome territory expansion by opening of existing choke blood vessels
  17. Aeromonas Hydrophilia: leech enteric organism responsible for red cell digestion
  18. Hein KD, Wechsler M, Schwartzstein RM, et al. The adult respiratory distress syndrome after dextran infusion as an antithrombotic agent in free TRAM flap breast reconstruction. Plast Reconstr Surg 103:1706, 1999. Brooks D, Okeefe P, Buncke HJ. Dextran-induced acute renal failure after microvascular muscle transplantation. Plast Reconstr Surg 108:2057, 2001.
  19. Buflomedil hydrochloride has an inhibitory effect on platelet aggregation and improves the deformation capaciry of red blood cells with abnormal flowability. In vitro studies suggest that the drug has an wlspecific antagonist effect on the calcium ion and an unspecific alpha receptor blocking effect(5).
  20. Steroids Increased flap survival in some experimental models, but no evidence to support clinical use of corticosteroids to enhance flap viability
  21. Carroll WR, Esclamado RM. Ischemia/reperfusion injury in microvascular surgery. Head Neck 22:700,2000
  22. Hisako Hara et al, Blood glucose measurement for flap monitoring to salvage flaps from venous thrombosis. JPRAS December 09,2011