Fwd: Wound Healing
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Fwd: Wound Healing

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---------- Forwarded message ----------

---------- Forwarded message ----------
From: UCD Graduate '09 None <ucdgrad09@gmail.com>
Date: 2009/2/20
Subject: Wound Healing
To: ucdgrad09@gmail.com

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Fwd: Wound Healing Fwd: Wound Healing Presentation Transcript

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