Fwd: lecture

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From: cormac joyce <cjoyce78@hotmail.com&gt;
Date: 2009/2/28
Subject: lecture
To: ucdgrad09@gmail.com



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Fwd: lecture

  1. 1. The Surgical Wound Cormac Joyce Final Med 2009
  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. 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>
  6. 6. 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>
  7. 7. 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>
  8. 8. 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>
  9. 9. 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>
  10. 10. 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>
  11. 11. 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>
  12. 12. 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>
  13. 13. 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>
  14. 14. 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>
  15. 15. 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>
  16. 16. 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>
  17. 17. 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>
  18. 18. 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>
  19. 19. 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>
  20. 20. 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>
  21. 21. 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>
  22. 22. 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>
  23. 23. 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>
  24. 24. 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>
  25. 25. 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>
  26. 26. 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>
  27. 27. 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>
  28. 28. 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>
  29. 29. 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>
  30. 30. 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>
  31. 31. 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>
  32. 32. 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>
  33. 33. Inflammatory Phase <ul><li>Monocytes now enter the wound and become macrophages </li></ul><ul><li>They have numerous functions </li></ul>
  34. 34. 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>
  35. 35. 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>
  36. 36. 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>
  37. 37. Proliferative Phase <ul><li>Granulation Tissue </li></ul><ul><li>Is the combination of collagen deposition and angiogenesis </li></ul>
  38. 38. 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>
  39. 39. 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>
  40. 40. 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>
  41. 41. 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>
  42. 42. 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>
  43. 43. Abnormal Scars <ul><li>Hypertrophic Scars </li></ul><ul><li>Keloid Scars </li></ul>
  44. 44. 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>
  45. 45. Hypertrophic Scars <ul><li>Treatment: </li></ul><ul><li>Surgical excision </li></ul><ul><li>Intralesional Triamcenelone acetate injection </li></ul>
  46. 46. Hypertrophic Scars <ul><li>No racial or familial preponderance </li></ul><ul><li>Electron microscopy: flattened collagen bundles parallel in orientation </li></ul>
  47. 47. 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>
  48. 48. 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>
  49. 49. 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>
  50. 50. 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>
  51. 51. 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>
  52. 52. 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>
  53. 53. 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>
  54. 54. 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>
  55. 55. Everted Edges
  56. 56. Inverted Edges
  57. 57. 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>
  58. 58. Langers Lines
  59. 59. 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>
  60. 60. 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>
  61. 61. 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>
  62. 62. 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>
  63. 63. 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>
  64. 64. 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>
  65. 65. 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>
  66. 66. 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>
  67. 67. Chemical messengers in AI <ul><li>These allow cells to communicate with each other and mediate the immune response </li></ul>
  68. 68. 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>
  69. 69. 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>
  70. 70. 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>
  71. 71. 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>
  72. 72. 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>
  73. 73. 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>
  74. 74. 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>
  75. 75. 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>
  76. 76. 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>
  77. 77. 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>
  78. 78. 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>
  79. 79. 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>
  80. 80. Surgical Incisions Gridiron: appendix
  81. 81. Surgical Incisions Lanz: appendix
  82. 82. Surgical Incisions Nephrectomy/ loin
  83. 83. Surgical Incisions Kochers
  84. 84. Surgical Incisions Inguinal : hernia, orchidectomy (for Ca) not for torsion
  85. 85. Surgical Incisions Midline sternotomy
  86. 86. Surgical Incisions Mercedes Benz/Chevron
  87. 87. Surgical Incisions Midline laparotomy
  88. 88. Surgical Incisions Rutherford Morrison : renal transplant
  89. 89. Surgical Incisions Lap Chole
  90. 90. Surgical Incisions Lap appendix

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