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Wound healing

Wound healing

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Wound healing

  1. 1. WOUND HEALING
  2. 2. I dressed the wound; god healed It“ -Ambroise Pare, French Surgeon, 16th Century
  3. 3. LEARNING OBJECTIVES  WOUND  CLASSIFICATION OF WOUND  WOUND HEALING  CLASSIFICATION  PHASES AND STAGES  HEALING IN SPECIFIC TISSUE  FACTOR AFFECTING WOUND HEALING  MANAGEMENT OF WOUND  COMPLICATION OF WOUND
  4. 4. WOUND  Wound is a break in the integrity of skin or tissue often ,which may be associated with disruption of the structure and function.  Wound is an injury to the body that is usually associated with damage to underlying tissues.  Common causes are violence, accident or surgery that typically involves laceration or breaking of a membrane (as skin).
  5. 5. CLASSIFICATION OF WOUND (Rank &Wakefield)  Two Types:  1.TIDY-Incised,caused by sharp object, no tissue loss,heal by primary intention.  2.UNTIDY-Crushed,teared,devitalised,burn, tissue loss,heal by secondary intention.
  6. 6. TIDY UNTIDY
  7. 7. OTHER CLASSIFICATION 1.CLOSED WOUND -Contusion or bruising -Abrasion -Haematoma 2.OPENED WOUND -Incised -Lacerated -Penetrating -Crushed or contused wound
  8. 8.  Contusion:-Minor soft injury without break in skin and there is discolouration of skin.  Abrasion:-Shearing of skin,surface rubbed off and epidermis of skin scraped exposing dermis.Painful as dermal nerve exposed.  Haematoma:-Collection of blood following injury.It may be subcutaneous,intramuscular, subfascial and intra articular.  Incised wound:-Caused by sharp object,neat and clean scar,tidy  Lacerated wound:-Caused by blunt object like in RTA or fall on stone.Edges are irregular and ragged,devitalised tissue,untidy
  9. 9.  Penetrating wound:Like stab injury of abdomen .It look like small but may have been damage internal organ.Depth is more than length.  Crushed wound:Caused by blunt trauma like RTA,earthquakes,wall collapse.Dangerous as they cause severe haemorrhge,death of tissue and crushing blood vessel.More prone for gas gangrene, tetanus,muscle ischemia, etc.
  10. 10. CONTUSION-soft tissue injury without break in skin. collection of blood underneath
  11. 11. ABRASION-epidermis is scraped, exposing dermis
  12. 12. HEMATOMA-collection of blood following injury or spontaneously as in patients who have bleeding tendencies
  13. 13. INCISED WOUND-caused by sharp objects like knife,blade,glass etc,have sharp edges
  14. 14. LACERATED WOUND-caused by blunt objects,like fall on hard surface,road traffic accidents
  15. 15. PENETRATING WOUND-stab injuries, innocent injury with 1-2 cm cut, but internal organs might have been damaged
  16. 16. CRUSHED WOUND-caused by blunt traumadue to run over by vehicle, wall collapse, earth quakes or industrial accidents.severe haemorrhage,death of tissues and crushing of blood vessels
  17. 17. WOUND HEALING Wound healing is a mechanism where by the body attempts-  To restore the integrity and function of injured part  To reform barrier to fluid loss and infection  Limit further entry of foreign organism and material  Re-establish normal blood and lymphatic’s patterns
  18. 18. CLASSIFICATION OF WOUND HEALING 1.By Primary intention:Occurs in clean incised wound,edges opposed and minimal scar that is clean,neat and thin. 2.By Secondary intention:Occurs in infected wound,discharging pus and skin loss like in major trauma,burn or sepsis.Wound left open,increased inflammation and proliferation. it heals by granulation,contraction and epithelialisation.Poor,ugly and wide scar.
  19. 19. 3.ByTertiary intention:Wound initially left open,edges later opposed when healing condition favourable.
  20. 20. Wound Healing Features Primary union (First intention ) Secondary union (Second intention ) 1 ) Cleanliness Clean Unclean 2 )Infection Generally uninfected May be infected 3 )Margins Surgically clean Irregular 4 )Sutures Used Not used 5 ) Healing Scanty granulation tissue at the incised gap and along suture tracks Exuberant granulation tissue to fill the gap 6 )Outcome Neat linear scar Contracted irregular wound 7 ) Complications Infrequent, epidermal inclusion cyst formation Suppuration, may require debridement
  21. 21. PHASES OF WOUND HEALING  1.Inflammatory phase  2.Proliferative phase  3.Remodelling phase(maturation phase)  All these 3 phase involve: -stage of inflammation -stage of granulation tissue formation and organisation -stage of epithelialisation -stage of scar formation and resorption -stage of maturation
  22. 22.  Inflammatory phase/lag/substrate or exudative phase: Occasionally haemostatic phase is referred to occur before inflammatory phase consisting of formation of blood clot (vasoconstriction & thrombus formation ) Inflammatory phase begin immediately after wounding and last 2-3 days.  Features-Rubur(redness),Tumour(swelling), Calor(heat),Dolor(pain) and loss of function.
  23. 23. Inflammatory Phase (cont…)  Damaged epithelial Blood platelets Macrophages cell GROWTH FACTORS CYTOKINES ENZYMES EGF TNF Prostaglandins Collagenase Interleukin Histamine Elastase Serotonin PDGF Platelet factor I V TGFβ F GF
  24. 24. Platelets and local tissue release vasoactive amines like histamine,serotonin,prostaglandins.Vasoactive amines &Growth factors attract inflammatory cells Increase vascular permeability aiding inflammatory cell Polymorphonuclear cell+macrophages ,PMN cells appears after 48hrs which secretes inflammatory mediators & bactericidal oxygen derived free radicals These cells remove devitalised tissue, microorganism, foreign body Macrophages regulate fibroblast activity by secreting FGF which enhances angiogenesis Beginning of Proliferative phase
  25. 25.  Proliferative phase:Last from 3rd day to 3rd week.  As fibroblastic activity begin it give rise to protocollagen which is converted into collagen in presence of protocollagen hydroxylase by hydroxylation require O2,vit-c and ferrous ions.  Production of collagen and ground substance(proteoglycans help in binding collagen fiber).from 5th day PMN cell decrease and monocyte increase(specialised scavanger).  Start growth of new blood vessel as capillary loop(angiogenesis) and re-epithelisation of wound surface.
  26. 26.  In early stage-Intense proliferation of fibroblast and capillaries and granulation tissue formation which is tissue in wound compromising newly laid capillaries with fibroblast and ground substance along with inflammatory cells.Epithelium of each side continue to grow and eventually unites in the upper dermis.  In late stage- There is increase tensile strength of wound due to increase collagen,which is first deposited in random fashion and consist of type III collagen.  80-90 % of final strength (in postop period ) is achieved in 30 days.
  27. 27.  Remodelling phase(maturation phase)(3week to 2 year):Begins during the fibroblastic phase. Reorganisation of previously synthesized collagen. Maturation of collagen (type-I replacing type-III until 4:1 achieved).Balance between collagen synthesis and collagenolysis.Realignment of collagen fiber along line of tension and get cross linked for giving further tensile strength to scar. In latter decreased wound vascularity and wound contraction due to fibroblast and myofibroblast activity so redness of scar fades gradually.Scar may be hypertophic at first but flatten out eventually due to contraction of dermal collagen network and increase breakdown of collagen .
  28. 28. Remodelling (Cont..) Collagen production is not present after 42 days of wound healing.  Wound is strengthened by proliferation of Fibroblast and myofibroblast which get structural support from Extracellular matrix which has following components : A- Collagen (Fibrous tissue,Bone, Cartilage,Valves, Cornea etc ) Stimulated by GF. Defective collagen synthesis leads to Fibrosis, Hypertrophic scar, Organ dysfunction B-Adhesive Glycoproteins (Glue) C- Elastic Fibres (Elastic recoil) D- Proteoglycans eg Dermatan & chondroitin sulphate 
  29. 29. Healing in specific tissue 1. Bone:fracture of bone Ist stage-stage of haematoma: From injury to blood vessel to haematoma formation. .osteoblast synthesis .fracture end gap filled by blood .blood clot act as frame work formed by fibrin This stage last up to 7days.If gap exist, secondary healing lead to malunion,delayed union and nonunion.
  30. 30.  IInd stage-Stage of granulation tissue: Procallus formation(mass of tissue , disorganise tissue) Mineralisation of procallus Fracture is mobile Last up to 2-3week  IIIrd stag-stage of callus:Bony callus formed ,fracture clinically united.Last up to 4-12week.  IVth stage:stage of remodelling of callus,done by osteoclast.Out line of callus become dense and sharply defined.It takes 1-4years  Vth stage:stage of modelling of endosteal &periosteal,fracture site is indistinguishable.
  31. 31. 2.Cartilage:Injury lead to permanent defect due to less blood supply. In superficial injury healing power inadequate &regeneration is incomplete ,slow to heal result persistent structural defect. In deep injury healing is better as underlying bone and soft tissue involvement(vascular).
  32. 32. 3.Tendon:Due to mobility of underlying bone or muscle, damage ends usually separated. Healing process is similar as other area of body. Hypovascular tendon tends to heal with less motion and more scar formation than tendon with better blood supply.
  33. 33. 4.Nerve:Distal to wound ,wallerian degeneration occur.Proximally the nerve suffer traumatic degeneration as far as last node of Ranvier. Regenerating nerve fiber attracted to their receptors by neurotropism which is mediated by growth factor,hormone and other extracellular matrix trophins.Profuse growth of nerve fiber which sprout from the cut proximal wound . Overgrowth with poor approximation lead to neuroma formation.
  34. 34. FACTOR AFFECTING WOUND HEALING  GENERAL FACTOR: 1. Age (older) - healing delayed 2. Obesity and weight loss 3. Smoking 4. Malnutriton=vit-c and zinc deficency delay wound healing as vit-c is cofactor for hydroxylation and zinc is cofactor for collagen synthesis, protein depletion prolongs inflammatory phase, Copper - extracellular cofactor, required for collagen crosslinking,Magnesium -cofactor in glycolization Vit-A increase inflammatory response in membrane so deficiency delay wound healing. Vit E does not increase wound healing, in absence of steroids may reactivate disease for which steroids are given, it decreases collagen synthesis and inhibits wound healing.
  35. 35. 5.Trace Metals- Zinc, Copper, Mg 6 .Anemia 7.Diabetic patient :delayed healing due to microangiopathy , atherosclerosis and decrease phagocytic activity 8.Jaundice and uraemic patient :healing delayed due to fibroblastic repair delayed 9.Colonisation (gram-ve bact) and translocation in GI tract(failure of gut-associated with lymphoid tissue and villous atrophy)
  36. 36. 10.Drug-Steroids(early given delay, after healing no effect) inhibit macrophage function, decrease inflammatory response and its inhibitory effects reversed by VitA . Anti neoplastic agent - (cyclophosphamide,methotrexate) decreased WBC’s, decreased fibroblast proliferation, decreased woundcontraction, decreased protein synthesis NSAIDs - decrease collagen synthesis by 45% even at normal levels. Tamoxifen(antiestrogen) delay healing 11.Malignancy 12.HIV and immunosuppresive disease 13.Peripheral vascular diseases
  37. 37.  LOCAL FACTOR: 1. Local infection 2. Presence of necrotic tissue and foreign body 3. Poor blood supply and perfusion 4. Venous or lymph stasis 5. Tissue tension 6. Haematoma and dead space 7. Large defect or poor opposition 8. Recurrent trauma 9. X-ray irradiated area 10. Site of wound-eg.over joint and back has poor healing
  38. 38. 11.Type of wound 12.Hypoxia 13.Faulty technique of wound closure
  39. 39. INVESTIGATION  Investigate according to location and type of wound  Investigate to rule out cause of delayed healing  Hb gm%-to rule out anemia  Total leucocyte count-to rule out infection  Blood sugar-to rule out DM  Blood urea-to rule out uraemia  LFT-to rule out jaundice  Lipid profile and doppler study of arterial pressure to rule out any ischemic aetiology  X-ray of dependent part to rule out is bony pathology involve or fracture.
  40. 40. MANAGING THE WOUND  Careful history  Examination of wound and classified it: depth of wound involvement of underlying structure configuration nonviable tissue if vital area involve then - airway maintained,bleeding controlled,IV FLUID started,if require o2 given
  41. 41. Administration of tetnus prophylaxis Administration of pain killer With normal saline clean the wound and remove the foreign material.(Iodine,hydrogen peroxide and organically based antibacterial not used as they impair wound healing due to injury to neutrophil and macrophage at wound site)
  42. 42.  If exsessive bleeding is there, haemostasis maintained by pressure pad and start I.V line.  If there is non-viable or devitalised tissue debridement done until bleeding occur.  All hematoma present within wounds should be carefully evacuated and bleeding sources controlled with ligature or cautery.  Having ensured hemostasis and adequate debridement and removal of foreign body,irregular wound edge should be debride in order to provide fresh edge for reapproximation.
  43. 43.  Approximation of superficial layer by nonabsorable suture,staples,monofilament, octyl-cyanoacrylate tissue glues and deeper layer by absorble suture . - incised wound-primary suturing - lacerated wound-excison and primary suturing. - crushed-delayed primary suturing after debridement - deep devitalised tissue-after debridement and granulation if it is small then secondary suturing,if it is large then split skin grafting done. - in significant tissue loss require tissue mass for closure.
  44. 44.  Primary suturing: suturing wound within few hour following injury(ideal 6hr). DONE IN-Incised wound,no infection and foreign body,minimal injury to either side structure.  Wound excision and primary suturing of skin indicated when wound edge are jagged , contamination of wound by organism or foreign body,tissue are crushed or devitalised then wound is explored ,remove foreign body, wound irrigated with saline ,convert lacerated wound into incised then suturing done.
  45. 45.  Wound excision and delayed primary suturing done in lacerated wound with major crush injury so in such situation excision of dead tissue , irrigation of wound by antiseptic agent,dressing done and after 4-6 day wound re-examined if no infection then suturing done.  Suturing is avoided because of-gross oedema increase tissue tension haematoma contamination with bacteria
  46. 46. SECONDARY SUTURING Sometimes after operations sutures may give way because of severe infection with persistent discharge of pus IN SUCH SITUATIONS 7-14 Days later, after controlling infection,skin is free from the edge of the wound from granulation tissue and skin is approximated .This is called secondary suturing .
  47. 47.  If wound is associated with tension then fasciotomy done to prevent compartment syndrome.  Drain may be placed in area at risk of forming fluid collection(craniotomy,intrathoracic, intraabdominal)  Fascicular repair of nerve and vessel using 8/0 or 10/0 monofilament nylon  Tendon repair for acheiving mobilisation.  Removal of suture :4-5day of face and 7-10 day of other skin ,failure to remove result cosmetically inferior wound.
  48. 48.  Antibiotics :used when obvious wound infection. Systemic antibiotic used as topical antibiotic frequently causes contact dermatitis.  Wound dressing:it provide ideal environment for wound healing,comfortability,pain control,odour control and prevent from viral and bacterial contamination and further damage.  2type- primary:placed directly on wound and provide absorption of fluid and prevent from infection. secondary:placed on primary dressing for further protection .
  49. 49. 1. Absorbent-keep cotton or sponge 2. Non adherent dressing-paraffin,petroleumjelly,jelonet they maintain moist environment and allow exudate to pass through them.Secondary dressing must be kept 3. Semipermiable films(tegaderm)-Useful in superficial wound and dressing around catheter sites.Impermiable to bacteria and fluid but permeable to air and water vapour. 4. Hydrogel(actiform cool,sterigel)transluscent,jelly like having soothing,cooling and analgesic effect.They are able to donate water to wound surface to maintain moist environment.useful in superficial and deep wound,sinus and cavity.useful in burn treatment.
  50. 50. 5.Hydrocolloid(tegasorb)-adhere to dry or moist site and allow patient to bathe.useful in shallow or cavity wound especially in difficult area such as sacrum and heels. 6.Absorbent material:Used within wound as hemostat and include collagen,gelatin and oxidised cellulose. 7.Alginates(sorbsan,kaltostat):derived from brown algae.Use –skin loss,open surgical wound with medium exudation and full-thickness chronic wound 8.Medicated dressing: Used as drug delivery system.Agent delivered in dressing include benzoyal peroxide,zinc oxide,neomycin and bacitracin-zinc.They shown increase epithelisation by 28%.Used depends upon amount of wound drainage.
  51. 51. Complication of wound healing 1. Infection 2. Avoidable scar 3. Excess healing-keloid and Hypertrophic scar 4. Pigmentation of skin 5. Marjolin ulcer-occur due to scar tissue 6. Contractures 7. Incisional hernia and wound dehiscence
  52. 52. INFECTED WOUND-when wound is red, swollen, painful, it has discharging pus or smells bad
  53. 53. KELOID  LIKE CLAW:Excessive scar tissue that extend beyond the boundaries of original incision or wound.  Etiology is unknown usually associated with elevated level of growth factor ,deeply pigmented skin and inherited tendencey.  Growth after 3month to year  Area involve xiphisternum,shoulder tip ,upper back,ear lobe  Excess collagen and hyper vascularity
  54. 54.  Itching present,margin slight tender,vascular,red and erythematous.Burning sensation present.  Treatment:Excision alone of keloids is subject to high recurrence rate 45 to 100%.Fewer recurrence when surgical excision combined with other modalities such as-application of silicone sheet use of radiation or pressure  Intralesional corticosteroid injection  Topical retinods  Vit-E or palm oil massage
  55. 55. HYPERTROPHIC SCAR  Excessive scar tissue does not extend beyond the boundary of original incision or wound but rises above skin level.  Develop 4 week after trauma  Stocking ,armlet, elastic bandage(pressure garments)  Excision, if required skin grafting done
  56. 56. INCISIONAL HERNIA-bulge or protusion at or near the area of surgical incision
  57. 57. CONTRACTURES-excessive contraction during wound healing
  58. 58. THANK YOU

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