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Wound Healing PGY1 surgery resident presentatin
- 1. Wound Healing:Types,Assessment and EmergingTechnology ,Wound Care and Regeneration Sushanta Paudel MS 1st year resident Moderator Dr Sumod Koirala
- 2. Objectives • To describetypes of wound and assessment of wound. • To describe normal phases of wound healing. • To describe factors affecting wound healing. • To describe some abnormal forms of wound healing. • To describe Emerging Technology in wound Care.
- 3. • Wound :Break in the integrity of skin or tissue . • Wound Healing: Attempts to restore • Mechanical integrity • Barrier to fluid loss • Infection • Normal flow pattern
- 4. • Classification ofwound • Rank and Wakefield • Tidy Wounds • Untidy Wound • Type of wound • Abrasion • Contusion • Laceration • Incised wound • Hematoma • Puncture • Penetrating • Avulsion • Crush Injury Figure 1A. Tidy Wound 1B. Untidy Wound
- 5. • Thickness ofwound • Superficial • Partial thickness • Full thickness • Deep Wound • Complicated • Involved structure • Simple Wound • Complex Wound • Time Elapsed • Acute Wound • Chronic Wound • Atypical Chronic Wound
- 6. • Classification ofsurgical Wound • Clean Wound • Clean Contaminated Wound • Contaminated wound • Dirty Wound Figure 2. Clean Wound of Thyroidectomy Surgery Figure 3 . Appendectomy Clean Contaminated Wound Figure 5 . Bowel Perforation Dirty Wound Figure 4 Burst Appendix Contaminated Wound
- 7. Assessment of Wound WoundEtiology • Surgical wound • Traumatic wound • Pressure injury (pressure ulcer) • Diabetic foot ulcer • Venous leg ulcer • Arterial ulcer • Malignant/fungating wound • A shallow, irregular wound on the medial malleolus with hemosiderin deposits and edema suggests a venous ulcer.
- 8. Location • Precise anatomicallocation to monitor changes over time. • A 3x2 cm wound located on the lateral aspect of the right lower leg, 5 cm above the lateral malleolus. Wound Dimensions • Length, width, depth in cm or mm • Use a measuring guide or wound tracing • Use of 3D wound measurement apps/tools in advanced settings • A wound measuring 5 cm (length) × 3 cm (width) × 0.5 cm (depth).
- 9. Wound Bed Characteristics Percentageand type of tissue: • Granulation tissue (red, healthy) • Slough (yellow, fibrinous) • Necrotic tissue/eschar (black, devitalized) • Epithelial tissue (pink, new skin) • Wound bed has 70% red granulation tissue, 20% yellow slough, and 10% black eschar.
- 10. Wound Edges • Well-definedor irregular • Rolled (epibole) – may suggest chronicity • Undermining or tunneling • Wound edges are rolled and undermined at 6 o’clock for 2 cm, indicating stalled healing. Exudate (Drainage) • Amount: none, scant, moderate, copious • Type: serous, serosanguinous, sanguineous, purulent • Odor: present/absent • Moderate purulent discharge with foul odor—suggestive of infection.
- 11. Signs of Infectionor Inflammation • Erythema, warmth, swelling • Increased pain • Delayed healing • Pus or abscess • Systemic signs: fever, elevated WBC • The surrounding skin is erythematous and warm with purulent discharge and pain—suggestive of local infection. Periwound Skin • Integrity: maceration, dryness, eczema • Color changes: erythema, hyperpigmentation • Induration or edema • Periwound skin is macerated and white due to excess moisture from dressing.
- 12. • Assessment ofwound • TIME Framework Component Focus Area Clinical Goal T Tissue Remove non-viable, support viable I Infection Control bioburden, reduce inflammation M Moisture Maintain optimal moisture E Edge Stimulate epithelialization
- 13. • MEASURE Method LetterComponent Description M Measure Length × Width × Depth in cm E Exudate Type (serous, purulent), amount A Appearance Granulation, slough, necrosis S Suffering (Pain) Use pain scales (e.g., VAS) U Undermining Probe for undermining or tunneling R Re-evaluate Assess progress every 1–2 weeks E Edge Advancing, rolled, epithelializing
- 14. Laboratory/Imaging Support • Woundswab or tissue biopsy for culture • Doppler ultrasound for vascular status • X-ray/MRI if osteomyelitis is suspected • In a diabetic foot ulcer with exposed bone, MRI confirms underlying osteomyelitis.
- 15. Wound Healing • Typesof Wound Healing • Primary Healing: Clean incised wound or surgical wound , Scar linear ,smooth. • Secondary Healing :Soft tissue Loss , Hypertrophied and contracted scar. • Healing by third intention: Delayed Primary Closure .
- 16. Normal wound healing Threephases: a. Inflammatory phase b. Proliferative phase c. Remodeling phase
- 17. Inflammatory phase: • Earlyinflammatory phase (days 1-2): platelet activation causes influx of inflammatory cells (particularly neutrophils) minimize bacterial contamination of wound • Platelets and local injured tissue also release vasoactive amines such as histamine and serotonin increase vascular permeability • Late inflammatory phase (days 2-3): monocyte appear in wound and differentiate into macrophages phagocytic cells and release proteolytic enzymes to help debride the wound
- 18. • Figure 6. Diagrammatic Representation of Inflammatory Phase of Wound Healing.
- 19. • Figure 7. Time Course of appearance of different cells in wound healing.
- 20. Proliferative phase: • Startaround day 3 and lasts for 2-4 weeks. • consist mainly of fibroblast activity with production of: • Ground substance (glycosoaminoglycans and proteoglycans) • Collagen • Angiogenesis • Re- epithelization • Hallmark • Granulation tissue formation • Fibroblasts that have differentiated into myofibroblasts have contractile ability.
- 21. • Figure 8.Diagrammatic Representation of Proliferative Phase of Wound Healing.
- 22. Applied aspects Wounds exhibitingan extended inflammation, shows a high content of metalloproteinases (MMPs) MMPs are involved in the degradation of ECM components. Avoiding the formation of the granulation tissue and consequently delaying the healing.
- 23. Remodelling phase • Begins2-3 weeks and last for years • Hallmarks: • Wound Contraction • Collagen remodelling • Figure 9. Diagrammatic Representation of Remodeling Phase of Wound Healing.
- 24. Applied aspects • Innon-healing pressure ulcers, this efficient and orderly process is lost and the ulcers are locked into a state of chronic inflammation. • It is characterized by abundant neutrophil infiltration with associated reactive oxygen species and destructive enzymes. • Dictum: Healing proceeds only after the inflammation is controlled
- 25. • Figure 10.Schematic Diagram of Wound Healing.
- 26. Normal healing inspecific tissue Bone • Periosteal and endosteal proliferation leads to the formation of callus(immature bone consisting of osteoid) • In the remodelling phase cortical structure and medullary cavity restored. • In accurately opposed and rigidly fixed, callus formation is minimal and primary healing occurs.
- 27. Nerve • Distal tothe wound, Wallerian degeneration occurs. • Proximally, the nerve suffers traumatic degeneration as far as the last node of Ranvier. • Nerve regeneration is characterised by profuse growth of new nerve fibres which sprout from the cut proximal end.
- 28. Tendon • Nutrients, cellsand new vessels reach tendon by 2 mechanisms: • Intrinsic: vincular blood flow and synovial diffusion. • Extrinsic: which depends on the formation of fibrous adhesions between the tendon and the tendon sheath. • Active mobilisation prevents adhesions limiting range of motion. • But the tendon must be protected by splintage in order to avoid rupture of the repair.
- 29. Factor affecting woundhealing: Local factors Systemic factors Bacterial burden Age Ischaemia of wound Diabetes Mellitus Foreign body in wound Steroid use Edema Malnutrition Pressure Chemotherapy Uraemia Alcohol and tobacco use Irradiation Table 1 . Factors Affecting wound Healing.
- 30. Abnormal form ofwound healing 1. Keloid scars 2. Hypertrophic scars Figure 11. Keloid Scar Figure 12. Hypertrophic scars
- 31. Keloid Hypertrophic scar Extendbeyond the boundaries of the original incision or wound Do not extend beyond the boundary of the original incision or wound Do not spontaneously regress Eventually regress Poor response to treatment Good response to steroid Recurrence – high Recurrence – is uncommon Genetic predisposition implicated No genetic predisposition Often occur as result of minor trauma and mainly with darker skin pigmentation More common in areas of increased tension, deep dermal burns and wound left to heal by secondary intention Table 2 .Difference Between Keloid and Hypertrophic Scar.
- 32. Emerging technology inWound Care and regeneration
- 33. Smart Dressings (pH-sensitive,thermoresponsive) • Respond to wound microenvironment (e.g., pH or temperature) to release drugs or signal infection. • pH-sensitive dressings detect alkalinity from infection and release antibiotics. • Thermoresponsive dressings change structure with temperature to enhance healing or deliver therapeutics. • Advantages: • Early infection detection • Controlled drug release Example: pH-sensitive hydrogel that releases silver nanoparticles when infected.
- 34. Hydrogels • Water-rich, 3Dpolymer networks that maintain a moist wound environment. • Retain moisture • Deliver growth factors/antibiotics • Reduce pain and scarring • Advantages: • Non-adherent, soothing • Can incorporate bioactive molecules Example: Amorphous hydrogel with embedded insulin for diabetic foot ulcers.
- 35. Electrospun Nanofibers • Mimicnative ECM structure to support cellular migration and proliferation. • High surface-to-volume ratio allows better oxygen/gas exchange and drug loading. • Nanofibers can be functionalized with antibiotics or stem cells. • Advantages: • ECM mimicry • Customizable for drug release Example: PCL/gelatin nanofiber dressing with ciprofloxacin for burn wounds.
- 36. • . BiologicalAgents • Growth Factors • Stem Cell Therapy • Exosomes and Secretomes • Platelet-Rich Plasma (PRP)
- 37. Gene Therapy • Introducegenes that encode healing factors into wound cells. Genes Used: VEGF, PDGF, bFGF • Vectors: • Viral (adenovirus, lentivirus) • Non-viral (liposomes, electroporation) Sustained production of growth factors at wound site • Challenges: • Immunogenicity • Short-lived expression • Expensive Example: Plasmid-based VEGF gene therapy improved perfusion in ischemic ulcers in trials.
- 38. 3D Bioprinting &Tissue Engineering • Fabricate skin constructs using patient-derived cells and scaffolds. • Components: • Bioink: hydrogel + cells • Scaffold: collagen, gelatin, fibrin • Steps: • Imaging wound • Designing 3D construct • Printing layers of skin • Maturation before application Example: Bioprinted full-thickness graft used in burns with reduced hypertrophic scarring.
- 39. Nanotechnology Nanoparticles (Silver, ZincOxide, Titanium Dioxide) • Antibacterial, anti-inflammatory • Disrupt biofilm formation. Advantages: • Sustained drug delivery • Increased bioavailability Example: Silver nanoparticle gel used for surgical site infections. Nanocarriers: • Deliver growth factors, genes, or antimicrobials in a controlled way Example: Chitosan nanoparticles delivering VEGF to chronic ulcers in animal models
- 40. Electrical Stimulation &Electromagnetic Therapy • Electrical cues enhance cell migration and division. • Improves fibroblast activity, angiogenesis • Enhances TGF-β signaling Devices: Accel-Heal, BioElectric dressing • Example: Pulsed electromagnetic field therapy used for chronic venous leg ulcers with significant size reduction. • Limitations: Needs frequent application, therapy standardization lacking
- 41. Negative Pressure WoundTherapy (NPWT) Advances • Vacuum exerts negative pressure • Removes exudate, reduces edema • Increases perfusion and granulation NPWTi: Combines negative pressure with intermittent irrigation (e.g., with polyhexanide or saline) Advantages: • Promotes wound contraction • Reduces microbial load Example: NPWTi in diabetic foot ulcers shows faster healing than standard NPWT.
- 42. Figure 13. Negativepressure assisted wound closure sponge in place on a Patients abdomen.
- 43. Photobiomodulation and LaserTherapy • Low-level light stimulates cellular metabolism. Wavelengths: 600–1000 nm • Activates cytochrome c oxidase in mitochondria • ↑ ATP → ↑ Collagen & fibroblast activity Devices: Cold laser, LED Example: 660 nm LLLT used in burn wounds → faster epithelialization and less pain. Limitation: Dose-dependent, non-uniform penetration
- 44. AI & DigitalHealth in Wound Management AI Imaging • Analyzes wound dimensions, color, depth • Predicts infection or deterioration Example: WoundVision® system detects early-stage pressure injuries. Tele-wound Care • Remote monitoring of chronic wounds • Reduces need for frequent hospital visits Smart Sensors • Track wound moisture, pH, temperature • Give real-time alerts for infection Example: Flexible pH-monitoring sensor dressing connected to smartphone alerting caregivers
- 45. References • Bailey andLove’s short practice of Surgery 28th edition • Sabiston Textbook of Surgery 21th edition
Editor's Notes
- #11 The Bates-Jensen Wound Assessment Tool (BWAT) is a comprehensive, standardized tool used to assess and monitor wound status and healing progress over time. It is particularly useful for evaluating chronic wounds, Category Item Description Size 1. Size Measure L × W Depth 2. Depth Superficial → full thickness Edges 3. Edges Attached/unattached/rolled Undermining 4. Undermining None → extensive Necrotic Tissue 5. Necrotic Tissue Type None → black eschar 6. Necrotic Tissue Amount None → >75% Exudate 7. Exudate Type Serous → purulent 8. Exudate Amount None → heavy Tissue Type 9. Skin Color Surrounding Wound Normal → red/black/edematous 10. Peripheral Tissue Edema None → severe 11. Peripheral Tissue Induration None → severe Granulation Tissue 12. Granulation Tissue 100% → none Epithelialization 13. Epithelialization 100% → none
- #12 The T.I.M.E. framework was developed by the European Wound Management Association and the World Union of Wound Healing Societies to guide systematic wound bed preparation and healing. 🔹 T – Tissue Management Identify and remove non-viable tissue (necrotic, slough) Promote healthy granulation tissue Debridement may be needed (surgical, enzymatic, autolytic, biological) 📌 Example: A wound with 40% yellow slough and 10% black eschar needs debridement to convert it to a granulating wound. 🔹 I – Infection or Inflammation Control Look for signs of local infection (increased exudate, odor, erythema) In chronic wounds, biofilm may be present, delaying healing Use topical/systemic antibiotics as appropriate 📌 Example: Foul-smelling wound with purulent discharge and periwound erythema suggests local infection—start antibiotics and possibly antimicrobial dressings. 🔹 M – Moisture Balance Ensure optimal moisture to facilitate healing (not too dry or too wet) Manage exudate to prevent maceration Choose dressings based on moisture level (e.g., foam, alginate, hydrocolloid) 📌 Example: A wound with excessive exudate and macerated edges may require absorbent foam dressings. 🔹 E – Edge of Wound (Epithelial Advancement) Assess whether the wound edges are advancing or stagnant Look for rolled (epibole) edges, callus, or undermining If stalled, consider biologic therapies, growth factors, or reassess debridement 📌 Example: A chronic ulcer with rolled edges and no epithelialization over 2 weeks needs edge stimulation via sharp debridement.
- #13 🔹 Example of MEASURE Use: A patient with a venous leg ulcer: M: 4.2 × 3.1 × 0.4 cm E: Moderate serous exudate A: 70% granulation, 30% yellow slough S: Pain score 3/10, dull ache U: No undermining R: Re-assess in 7 days E: Edges irregular, early epithelialization noted 🧩 Integration in Practice Many clinicians use both: TIME to decide how to treat the wound. MEASURE to decide how the wound is responding. 📌 For example: Start with TIME: debride necrotic tissue, start antimicrobial dressing, manage moisture. Track with MEASURE weekly: wound size reduced, pain reduced, edges re-epithelializing.
- #17 Immediate phase occurring before inflammation Disruption of the vascular endothelium following injury causes vasoconstriction and exposure of sub endothelial matrix Encourage platelets to adhere , activate and aggregate , resulting in a platelet plug
- #23 Wound contraction Produced by wound myofibroblasts, which are fibroblasts with intracellular actin microfilaments capable of force generation and matrix contraction. Collagen remodeling Type III collagen is initially laid down by fibroblasts during the proliferative phase will be replaced by Type I collagen. This phase is largely mediated by a class of enzymes known as matrix metalloproteinases that are secreted in large part by macrophages, fibroblasts, and endothelial cells. Maturation of collagen leads to increased tensile strength in the wound, max 12 week post injury represents approx. 80% of initial strength.
- #27 Definition: Wallerian degeneration is the anterograde (distal) degeneration of the axon and myelin sheath that occurs after a nerve fiber is cut or crushed. 🧠 Steps in Wallerian Degeneration (as depicted in the image): Axonal Injury Trauma, transection, or ischemia causes axonal damage. The axon is disconnected from the neuronal cell body. Distal Segment Degeneration The portion of the axon distal to the injury degenerates because it is separated from the soma (cell body), which provides essential nutrients. Myelin sheath disintegrates around the axon. Macrophage Infiltration & Cleanup Macrophages and Schwann cells clear axonal and myelin debris. This process is vital to prepare for potential regeneration. Proximal Axon Response The proximal axon stump may form growth cones and attempt regeneration if the environment is favorable. In the peripheral nervous system (PNS), Schwann cells guide axon regrowth. In the central nervous system (CNS), regeneration is poor due to inhibitory factors like Nogo-A and lack of supportive glial cells. 🧪 Clinical Significance: Occurs in Peripheral Nerve Injuries (e.g., neurotmesis, axonotmesis). Electromyography (EMG) changes are typically seen 7–10 days after injury. Nerve regeneration in PNS is possible (~1–3 mm/day), guided by Schwann cells. In the CNS, recovery is limited due to glial scarring and lack of regenerative support. Let me know if you'd like a comparison chart between Wallerian degeneration in PNS vs CNS, or how it's related to nerve injury classification (Sunderland or Seddon). Ask ChatGPT
- #29 Local tissue hypoxia is a common characteristic of most chronic wounds. Tissue fibrosis commonly encountered in chronic wounds can create a significant barrier to oxygen diffusion. Persistent tissue hypoxia and further fibrosis. Edema of foot also hamper tissue oxygen delivery Presence of devitalized, necrotic tissue in wound hamper oxygenation. Biofilm formation creates barrier to wound healing. Through a persistent inflammatory response, they establish an environment of free radicals, secreted toxins, and proteases that act to degrade growth factors. It prevents ordered assembly of matrix proteins. It results in the creation of proteinaceous debris that constitutes a pseudoeschar.
- #33 What Are Thermoresponsive Dressings? Thermoresponsive dressings are smart wound dressings that change their physical or chemical properties in response to temperature changes. These are typically hydrogels or polymer-based materials that respond to body heat or external thermal stimuli, enabling controlled drug delivery, wound protection, or tissue interaction. 🧪 Key Mechanism: They often utilize temperature-sensitive polymers, such as: Poly(N-isopropylacrylamide) (PNIPAAm) Exhibits Lower Critical Solution Temperature (LCST) around 32°C. Below LCST → Hydrophilic and swollen (gel-like). Above LCST → Hydrophobic and collapsed (releases contents or changes form).
- #36 🔹 B. Biological Agents 1. Growth Factors Examples: PDGF, EGF, VEGF, bFGF Mechanism: Stimulate angiogenesis, epithelial cell migration, and ECM production FDA-approved: Becaplermin (Regranex, PDGF-BB) Limitations: Expensive, short half-life, potential for tumorigenesis in chronic use 2. Stem Cell Therapy Sources: Bone marrow, adipose, umbilical cord Mechanism: Paracrine signaling enhances healing Differentiation into endothelial/fibroblast lineages Promote angiogenesis and reduce inflammation Types: Mesenchymal stem cells (MSCs) are most studied Example: Adipose-derived MSCs in radiation ulcers → accelerated healing. 3. Exosomes and Secretomes Definition: Cell-derived vesicles with proteins, mRNA, and miRNAs Function: Modulate immune response Stimulate angiogenesis and fibroblast activity Advantage: Acellular therapy—lower rejection risk Example: MSC-derived exosome gel improved diabetic wound closure in preclinical studies. 4. Platelet-Rich Plasma (PRP) Mechanism: Contains PDGF, VEGF, TGF-β Enhances cell recruitment, angiogenesis, collagen deposition Autologous and simple to prepare bedside Example: PRP applied to pressure ulcers—faster granulation vs saline control.
- #41 NPWTi: Negative Pressure Wound Therapy with Instillation