Fwd: Wound Healing


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Date: 2009/2/20
Subject: Wound Healing
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Fwd: Wound Healing

  1. 1. The Surgical Wound Cormac Joyce November 6 th 2008
  2. 2. Surgery <ul><li>It is the branch of medicine concerned with diseases and conditions which require or are amenable to operative procedures </li></ul><ul><li>It is derived from Greek “cheirourgia” </li></ul><ul><li>“ cheir” = the hand </li></ul><ul><li>“ ergon” = work </li></ul>
  3. 3. Surgery <ul><li>It is often said that it is “controlled trauma” </li></ul><ul><li>Carried out in a sterile environment </li></ul><ul><li>Under aseptic conditions </li></ul>
  4. 4. Surgery <ul><li>Many protocols are put in place to prevent infections in surgical wounds </li></ul><ul><li>Hand washing </li></ul><ul><li>Gowns and gloves </li></ul><ul><li>Painting and draping </li></ul><ul><li>Drains </li></ul><ul><li>Antibiotics </li></ul><ul><li>Laminar flow theatres </li></ul><ul><li>Sterile instruments </li></ul><ul><li>Sterile dressings </li></ul>
  5. 5. Mask does not come with beard attached!!
  6. 6. Operating Theatre
  7. 7. Surgery <ul><li>But wound infections can occur despite these measures causing: </li></ul><ul><li>Death </li></ul><ul><li>Morbidity </li></ul><ul><li>Longer hospital stays </li></ul><ul><li>Cosmetically displeasing wounds </li></ul>
  8. 8. Wound Infection
  9. 9. Wound Infection
  10. 10. Wound Dehiscence
  11. 11. Healthy Wound
  12. 12. Surgery <ul><li>Surgical wound infections are common </li></ul><ul><li>Comprising 12% of nosocomial infections </li></ul><ul><li>The rate of infection depends on the type of surgery undertaken </li></ul>
  13. 13. Operation Types <ul><li>The risk of a wound infection depends on the operation </li></ul><ul><li>For that reason, operations are classified into distinct types </li></ul><ul><li>Clean </li></ul><ul><li>Clean-Contaminated </li></ul><ul><li>Contaminated </li></ul><ul><li>Dirty </li></ul>
  14. 14. Class I :Clean wounds <ul><li>Elective operations (non emergency) </li></ul><ul><li>Non traumatic injury </li></ul><ul><li>Good surgical technique </li></ul><ul><li>Respiratory, gastrointestinal, biliary and genitourinary tracts not breached </li></ul><ul><li>Risk of infection < 2% </li></ul><ul><li>Eg: mastectomy, hernia repair </li></ul>
  15. 15. Class II: Clean - Contaminated <ul><li>Urgent or emergency case that is otherwise clean </li></ul><ul><li>GI, GU or respiratory tracts entered electively, no spillage or unusual contamination </li></ul><ul><li>Minor break in sterile technique occurred </li></ul><ul><li>Endogenous flora involved </li></ul><ul><li>Risk of infection: <10 % </li></ul><ul><li>Eg: appendicectomy, bowel resection </li></ul>
  16. 16. Class III: Contaminated <ul><li>Non-purulent inflammation </li></ul><ul><li>Gross spillage from GIT, entry into GU or biliary tract in the presence of infected bile/urine. </li></ul><ul><li>Major break in technique </li></ul><ul><li>Penetrating trauma < 4hrs old </li></ul><ul><li>Chronic open wounds </li></ul><ul><li>Risk of infection: 20% </li></ul><ul><li>Eg: GSW, rectal surgery </li></ul>
  17. 17. Class IV : Dirty <ul><li>Purulent inflammation (abscess) </li></ul><ul><li>Pre-operative perforation of GI, GU, biliary or respiratory tract </li></ul><ul><li>Penetrating trauma > 4 hrs </li></ul><ul><li>Existing acute bacterial infection or a perforated viscera is encountered (clean tissue is transected to gain access to pus). </li></ul><ul><li>Risk of infection: 40% </li></ul>
  18. 18. Signs of Infection <ul><li>The cardinal points of acute inflammation </li></ul><ul><li>Calor </li></ul><ul><li>Rubor </li></ul><ul><li>Dolor </li></ul><ul><li>Tumour </li></ul><ul><li>Functio Laesa </li></ul>
  19. 19. ? Wound infection
  20. 20. Signs of Infection <ul><li>Patient may be systemically unwell </li></ul><ul><li>↑ Temp </li></ul><ul><li>Tachycardic </li></ul><ul><li>Hypotension </li></ul><ul><li>Wound breakdown </li></ul><ul><li>Wound discharge </li></ul><ul><li>Warm peripheries </li></ul><ul><li>Septic shock </li></ul>
  21. 21. Prevention <ul><li>Aseptic technique </li></ul><ul><li>Good technique </li></ul><ul><li>Prophylactic antibiotics where appropriate </li></ul><ul><li>Microbiology input </li></ul><ul><li>Clean operating theatre </li></ul><ul><li>Elective surgery </li></ul><ul><li>Good post op care </li></ul>
  22. 22. Wound Healing <ul><li>Wound healing is a complex and dynamic process of restoring cellular structures and tissue layers </li></ul><ul><li>There are 3 distinct phases </li></ul><ul><li>There are various categories of wound healing </li></ul><ul><li>the ultimate outcome of any healing process is repair of a tissue defect </li></ul>
  23. 23. Wound Healing <ul><li>The types of wound healing: </li></ul><ul><li>1° healing </li></ul><ul><li>Delayed 1° healing </li></ul><ul><li>2° healing </li></ul><ul><li>(Epithelialisation) </li></ul><ul><li>Even though different categories exist, the interactions of cellular and extracellular constituents are similar. </li></ul>
  24. 24. Primary wound healing <ul><li>Also known as “healing by primary intention” </li></ul><ul><li>Think of a typical surgical wound: the wound eges are approximated </li></ul><ul><li>Minimal number of cellular constituents die </li></ul><ul><li>Results in a small line of scar tissue </li></ul><ul><li>Minimizes the need for granulation tissue so scarring is minimized </li></ul>
  25. 25. Primary wound healing
  26. 26. Primary Intention Keloid Scar
  27. 27. The importance of good… <ul><li>Technique </li></ul><ul><li>Choice of suture </li></ul><ul><li>Choice of needle </li></ul><ul><li>Training </li></ul><ul><li>Instruments </li></ul><ul><li>Antibiotics </li></ul><ul><li>Aftercare </li></ul>
  28. 28. Delayed Primary healing <ul><li>Occurs if wound egdes are not approximated immediately </li></ul><ul><li>May be desired in contaminated wounds </li></ul><ul><li>By day 4: phagocytosis of contaminated tissues has occurred </li></ul><ul><li>Usually wound is closed surgically at this stage </li></ul><ul><li>If contamination is present still : chronic inflammation ensues leading to prominent scar eventually </li></ul>
  29. 29. Delayed Primary healing
  30. 30. Delayed Primary healing
  31. 31. Secondary Healing <ul><li>Also called healing by secondary intention </li></ul><ul><li>A full thickness wound is allowed to heal by itself: there is no approximation of wound edges </li></ul><ul><li>Large amounts of granulation tissue formed </li></ul><ul><li>Wound eventually very contracted </li></ul><ul><li>Takes much longer to heal </li></ul>
  32. 32. Secondary Intention Healing Fungal sinusitis
  33. 33. Secondary Intention Healing Post Op
  34. 34. Secondary Intention Healing 2 weeks post op – healing by 2 ° intention
  35. 35. Epithelialization <ul><li>Epithelization is the process by which epithelial cells migrate and replicate via mitosis and traverse the wound </li></ul><ul><li>Occurs by one of 2 mechanisms </li></ul><ul><li>Common in the healing of ulcers and erosions </li></ul>
  36. 36. Epithelialization: Mechanisms <ul><li>Mechanism 1 </li></ul><ul><li>If basement membrane is intact ie some dermis or dermal appendages remain </li></ul><ul><li>Epithelialization occurs by epithelial cells migrating upwards </li></ul>
  37. 37. Epithelialization: Mechanisms <ul><li>Mechanism 2 </li></ul><ul><li>Occurs in a deeper wound </li></ul><ul><li>A single layer of epithelial cells advance from the wound edges to cover the wound </li></ul><ul><li>They then stratify so wound cover is complete </li></ul>
  38. 38. Normal Wound Healing <ul><li>There are 3 phases </li></ul><ul><li>Inflammatory phase: Days 0-4 </li></ul><ul><li>Proliferative phase : Days 5-21 </li></ul><ul><li>Remodelling phase: Days 22-60 </li></ul>
  39. 39. Wound Healing <ul><li>It can also be classified in 4 stages: </li></ul><ul><li>Haemostasis </li></ul><ul><li>Inflammation </li></ul><ul><li>Granulation </li></ul><ul><li>Remodelling </li></ul>
  40. 40. Haemostasis <ul><li>Injury causes local bleeding </li></ul><ul><li>Vasoconstriction is mediated by : </li></ul><ul><li>Adrenaline </li></ul><ul><li>Thrombaxane A2 </li></ul><ul><li>Prostaglandin 2 α </li></ul>
  41. 41. Haemostasis <ul><li>Platelets then adhere to damaged endothelium and discharge ADP </li></ul><ul><li>Which promotes thrombocyte clumping and “dams” the wound </li></ul><ul><li>Inflammation is initiated by cytokine release from platelets </li></ul>
  42. 42. Haemostasis <ul><li>α -granules from platelets release: </li></ul><ul><li>Platelet Derived Growth Factor (PDGF) </li></ul><ul><li>Platelet factor IV </li></ul><ul><li>Transforming Growth Factor β </li></ul><ul><li>Thrombocyte dense bodies release: </li></ul><ul><li>Histamine </li></ul><ul><li>Serotonin </li></ul>
  43. 43. Haemostasis <ul><li>PDGF attracts fibroblasts chemotactically </li></ul><ul><li>Leading to collagen deposition in later stages of wound healing </li></ul><ul><li>Fibrinogen -> Fibrin </li></ul><ul><li>Thus providing the structural support for the cellular components of inflammation </li></ul>
  44. 44. Inflammatory Phase <ul><li>Capillary dilatation occurs due to: </li></ul><ul><li>Histamine </li></ul><ul><li>Bradykinin </li></ul><ul><li>Prostaglandins </li></ul><ul><li>NO </li></ul><ul><li>This dilatation allows inflammatory cells to reach the wound site </li></ul>
  45. 45. Inflammatory Phase <ul><li>These PMNs or leukocytes have several functions: </li></ul><ul><li>Scavenge for debris </li></ul><ul><li>Debride the wound </li></ul><ul><li>Help to kill bacteria by: </li></ul><ul><li>-oxidative burst mechanisms </li></ul><ul><li>-opsonization </li></ul>
  46. 46. Inflammatory Phase <ul><li>Opsonin </li></ul><ul><li>“ factor which enhances the efficiency of phagocytosis because it is recognized by receptors on leucocytes </li></ul><ul><li>2 major opsonins are: </li></ul><ul><li>Fc fragment of IgG </li></ul><ul><li>A product of complement, C3b </li></ul>
  47. 47. Inflammatory Phase <ul><li>Monocytes now enter the wound and become macrophages </li></ul><ul><li>They have numerous functions </li></ul>
  48. 48. Macrophage functions in healing <ul><li>Secretion of numerous enzymes and cytokines </li></ul><ul><li>Collagenases and elastases </li></ul><ul><li>To break down injured tissues </li></ul><ul><li>PDGF, TGF β , IL, TNF </li></ul><ul><li>To stimulate proliferation of fibroblasts, endothelial and smooth muscle cells </li></ul>
  49. 49. Proliferative Phase <ul><li>Angiogenesis </li></ul><ul><li>The formation of new blood vessels </li></ul><ul><li>Formed by endothelial cells becoming new capillaries within the wound bed </li></ul><ul><li>Angiogenesis stimulated by TNF α </li></ul>
  50. 50. Proliferative Phase <ul><li>Collagen deposition </li></ul><ul><li>Type III collagen is laid down by fibroblasts </li></ul><ul><li>Fibroblasts are attracted by TGF β and PDGF </li></ul><ul><li>Total collagen content increases until day 21 </li></ul>
  51. 51. Proliferative Phase <ul><li>Granulation Tissue </li></ul><ul><li>Is the combination of collagen deposition and angiogenesis </li></ul>
  52. 52. Granulation Tissue <ul><li>Definition: </li></ul><ul><li>Newly formed connective tissue, often found at the edge or base of ulcers and wounds made up of : capillaries, fibroblasts, myofibroblasts, and inflammatory cells embedded in a mucin rich ground substance during healing </li></ul>
  53. 53. Granulation Tissue
  54. 54. Granulation Tissue
  55. 55. Granulation Tissue Occasionally overgranulation can occur (as above following a flexor tendon repair) Treatment is steroid topical cream (1% hydrocortisone cream)
  56. 56. Proliferative Phase <ul><li>Re-epithelialization occurs next: </li></ul><ul><li>By upward migration of epithelial cells if BM is intact </li></ul><ul><li>Or from wound edges </li></ul>
  57. 57. Remodelling Phase <ul><li>Fibroblasts become myofibroblasts </li></ul><ul><li>And wound begins to contract </li></ul><ul><li>Can contract 0.75mm per day </li></ul><ul><li>Can over contract however </li></ul><ul><li>Contraction allows wound to become smaller </li></ul><ul><li>A large wound can contract by up to 40-80% </li></ul>
  58. 58. Remodelling Phase <ul><li>Type III collagen is degraded </li></ul><ul><li>And replaced with Type I </li></ul><ul><li>Water is removed from the scar, allowing collagen to cross-link </li></ul><ul><li>Wound vascularity decreases </li></ul><ul><li>Collagen cross linkage allows: </li></ul><ul><li>Increased scar strength </li></ul><ul><li>Scar contracture </li></ul><ul><li>Decreased scar thickness </li></ul>
  59. 59. Microbiology: Dr. Lynda Fenelon
  60. 60. Wound Strength <ul><li>During phase 1 and 2 (inflammatory and proliferative phases) </li></ul><ul><li>Wounds have very little strength </li></ul><ul><li>During remodelling: </li></ul><ul><li>Wounds rapidly gain strength </li></ul><ul><li>@ 6 weeks: wound is 50% of final strength </li></ul><ul><li>@12 months: wound is maximal strength: but this is only 75% of pre-injury tissue strength </li></ul>
  61. 61. Abnormal Scars <ul><li>Hypertrophic Scars </li></ul><ul><li>Keloid Scars </li></ul>
  62. 62. Hypertrophic Scars <ul><li>Raised, red and thickened </li></ul><ul><li>Limited to boundaries of scar </li></ul><ul><li>Occurs shortly after injury </li></ul><ul><li>Common on anterior chest and deltoids </li></ul><ul><li>Regresses over time </li></ul><ul><li>Related to wound tension and prolonged inflammatory phase of healing </li></ul>
  63. 63. Hypertrophic Scars
  64. 64. Hypertrophic Scars
  65. 65. Hypertrophic Scars <ul><li>Treatment: </li></ul><ul><li>Surgical excision </li></ul><ul><li>Intralesional Triamcenelone acetate injection </li></ul>
  66. 66. Hypertrophic Scars <ul><li>No racial or familial preponderance </li></ul><ul><li>Electron microscopy: flattened collagen bundles parallel in orientation </li></ul>
  67. 67. Keloid Scars <ul><li>Raised, red and thickened scar </li></ul><ul><li>Extends beyond original scar boundary </li></ul><ul><li>Occurs months after injury </li></ul><ul><li>Does not regress </li></ul><ul><li>Commoner in darker skinned people </li></ul><ul><li>Familial tendency </li></ul><ul><li>? Autoimmune phenomenon </li></ul><ul><li>Worsened by surgery and in pregnancy </li></ul><ul><li>Regresses post menopause </li></ul>
  68. 68. Keloid scar
  69. 69. Keloid scar
  70. 70. Keloid scar <ul><li>Treatment: </li></ul><ul><li>Surgical excision : caveat- recurrence = 65% </li></ul><ul><li>Compression treatment </li></ul><ul><li>CO2 lasers </li></ul><ul><li>Cryotherapy </li></ul>
  71. 71. Factors influencing scarring <ul><li>These can be broken down into: </li></ul><ul><li>Patient factors </li></ul><ul><li>Surgical factors </li></ul>
  72. 72. Patient Factors <ul><li>Age </li></ul><ul><li>Elderly scar well </li></ul><ul><li>-? 2° wrinkles </li></ul><ul><li>Skin type </li></ul><ul><li>Celtics : hypertrophic scar tendency </li></ul><ul><li>Dark skinned: keloid scars </li></ul>
  73. 73. Patient Factors <ul><li>Anatomic region </li></ul><ul><li>Midline </li></ul><ul><li>Deltoid region </li></ul><ul><li>Sternotomy post CABG </li></ul>
  74. 74. Patient Factors <ul><li>Patient morbidity </li></ul><ul><li>Nutritional state </li></ul><ul><li>Diabetes </li></ul><ul><li>Wound infections </li></ul>
  75. 75. Patient Factors <ul><li>Local tissue </li></ul><ul><li>Oedema </li></ul><ul><li>Previous radiotherapy </li></ul><ul><li>Vascular insufficiency </li></ul>
  76. 76. Surgical factors <ul><li>Atraumatic skin handling </li></ul><ul><li>Eversion of wound edges </li></ul><ul><li>Inversion places keratinised epidermis between the healing surfaces = delayed healing </li></ul><ul><li>Tension free closure </li></ul><ul><li>Clean and healthy wound edges </li></ul>
  77. 77. Everted Edges
  78. 78. Inverted Edges
  79. 79. Surgical factors <ul><li>Scar orientation </li></ul><ul><li>Parallel to lines of relaxed skin tension </li></ul><ul><li>Langers lines </li></ul><ul><li>Suture tension </li></ul><ul><li>“ Thou shall not commit tension” </li></ul><ul><li>Over-tight: pressure necrosis </li></ul><ul><li>Under-tight: wound gaping and widened scar </li></ul>
  80. 80. Langers Lines
  81. 81. Langers Lines
  82. 82. Acute Inflammation <ul><li>Definition </li></ul><ul><li>The cellular and vascular response to injury </li></ul><ul><li>Short in duration </li></ul><ul><li>Has cellular and chemical components </li></ul>
  83. 83. Acute Inflammation: Causes <ul><li>Injury by: </li></ul><ul><li>Pathogens </li></ul><ul><li>Bacteria, viruses, parasites </li></ul><ul><li>Chemical agents </li></ul><ul><li>Acids, alkalis </li></ul><ul><li>Physical agents </li></ul><ul><li>Heat, trauma (surgery), radiation </li></ul><ul><li>Tissue death </li></ul><ul><li>Infarction </li></ul>
  84. 84. Stages of Acute Inflammation <ul><li>Dilatation of local capillaries </li></ul><ul><li> endothelial permeability </li></ul><ul><li>Leakage of protein-rich fluid into interstitial space – including fibrinogen </li></ul><ul><li>Fibrinogen -> fibrin </li></ul><ul><li>Margination of leukocytes to peripheries of capillaries </li></ul><ul><li>Mostly neutrophils </li></ul>
  85. 85. Stages of Acute Inflammation <ul><li>Acute Inflammation is mediated by: </li></ul><ul><li>Chemicals: interleukins and histamine </li></ul><ul><li>Proteins: complement cascade </li></ul>
  86. 86. Complement Cascade <ul><li>Component of innate immune system </li></ul><ul><li>Cascade of proteins </li></ul><ul><li>Resulting in formation of Membrane-Attack-Complex (MAC) which can </li></ul><ul><li>Destroy invading bacteria </li></ul><ul><li>Recruit other cells ie neutrophils </li></ul><ul><li>Can also act as opsonins: enhancing phagocytosis </li></ul>
  87. 87. Complement Cascade <ul><li>2 main activating arms of CC: </li></ul><ul><li>Classic pathway: consists of antigen-antibody complexes </li></ul><ul><li>Alternative pathway: activated directly by contact with micro-organisms </li></ul>
  88. 88. Acute Inflammation: Neutrophils <ul><li>The role of the Neutrophil </li></ul><ul><li>First cellular component to appear </li></ul><ul><li>Attracted by inflammatory mediators </li></ul><ul><li>By chemotaxis </li></ul><ul><li>They can move: margination in blood vessels – by adhering to vascular endothelium: roll between endothelial cells: emigrate to interstitium </li></ul>
  89. 89. Acute Inflammation: Neutrophils <ul><li>Function: </li></ul><ul><li>Phagocytosis of micro-organisms </li></ul><ul><li>With lysosomal free radical degradation of pathogens </li></ul>
  90. 90. Chemical messengers in AI <ul><li>These allow cells to communicate with each other and mediate the immune response </li></ul>
  91. 91. Chemical messengers in AI <ul><li>Chemokines </li></ul><ul><li>Cause direct migration of target cells to site of release </li></ul><ul><li>Cytokines </li></ul><ul><li>Soluble, biologically active molecules secreted by cells which have a variety of effects on the target cells </li></ul>
  92. 92. Cytokines: Examples <ul><li>IL-1: neutrophil adhesion and vascular adhesion molecules </li></ul><ul><li>IL-2: proliferation of B cells and NK cells </li></ul><ul><li>TNF: causes fever and promotes inflammation </li></ul><ul><li>IFN: activates macrophages </li></ul><ul><li>Histamine: vasodilation and  permeability </li></ul>
  93. 93. Effects of AI: beneficial <ul><li>Dilution of bacterial toxin </li></ul><ul><li>Defence mechanisms are brought to the pathogen </li></ul><ul><li>neutrophils;: phagocytosis </li></ul><ul><li>Complement: cell lysis </li></ul><ul><li>Antibodies </li></ul><ul><li>Drug delivery </li></ul>
  94. 94. Effects of AI: beneficial <ul><li>Drainage to LNs: immune response stimulated </li></ul><ul><li>Fibrin traps the pathogen in place so it can be attacked </li></ul>
  95. 95. Effects of AI: non beneficial <ul><li>Destruction of normal tissue: RA </li></ul><ul><li>Lethal swelling in certain parts of the body ie epiglottitis </li></ul><ul><li>Hypersensitivity reactions </li></ul><ul><li>Asthma </li></ul><ul><li>Anaphylaxis </li></ul>
  96. 96. Outcomes of Acute Inflammation <ul><li>Resolution </li></ul><ul><li>Tissues restored to normal </li></ul><ul><li>Pus/abscess </li></ul><ul><li>Organization </li></ul><ul><li>Tissues replaced by granulation tissues </li></ul><ul><li>Chronic Inflammation </li></ul><ul><li>If causative agent not removed </li></ul>
  97. 97. Ruptured Abscess
  98. 98. Chronic Inflammation <ul><li>Definition </li></ul><ul><li>Tissue response to persistent injury </li></ul><ul><li>Long in duration </li></ul><ul><li>Cellular components differ from acute inflammation </li></ul>
  99. 99. Chronic Inflammation <ul><li>Causes </li></ul><ul><li>Foreign bodies: ie sutures </li></ul><ul><li>Bacteria: ie TB </li></ul><ul><li>Chronic abscess: ie osteomyelitis </li></ul><ul><li>Transplant: ie chronic rejection </li></ul><ul><li>IBD </li></ul><ul><li>Progression from AI </li></ul>
  100. 100. Chronic Inflammation <ul><li>Key points </li></ul><ul><li>Histological pattern not as predictable as acute inflammation </li></ul><ul><li>There may be areas of acute inflammation occurring simultaneously </li></ul><ul><li>Granulation tissue and fibrosis may both be present: indicating the tissues attempts at repair </li></ul>
  101. 101. Chronic Inflammation <ul><li>Lymphocytes predominate </li></ul><ul><li>Macrophages present too </li></ul><ul><li>In granulomatous inflammation they fuse forming multinucleate Langhans giant cells </li></ul><ul><li>Plasma cells are also present </li></ul>
  102. 102. Chronic Inflammation <ul><li>Macrophages </li></ul><ul><li>Derived from monocytes </li></ul><ul><li>Phagocytosis and killing of pathogens by lysosomes </li></ul><ul><li>Antigen presentation </li></ul><ul><li>Langhans giant cell formation </li></ul>
  103. 103. Chronic Inflammation: Effects <ul><li>Secondary infection ie chronic epithelial injury </li></ul><ul><li>Scarring </li></ul><ul><li>Resolution: restoration of normality </li></ul><ul><li>Local lymphadenopathy </li></ul>
  104. 104. Surgical Incisions
  105. 105. Surgical Incisions
  106. 106. Surgical Incisions
  107. 107. Surgical Incisions
  108. 108. Surgical Incisions
  109. 109. Surgical Incisions
  110. 110. Surgical Incisions
  111. 111. Surgical Incisions
  112. 112. Surgical Incisions
  113. 113. Surgical Incisions
  114. 114. Thank You