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1. WOUND HEALING

2. Wound Healing Process of overlapping phases initiated by an injury or wound Phases of normal wound healing ( Cellular population and biochemical activities ): Hemostasis Inflammation Proliferation Maturation and remodeling

3. HEMOSTASIS Wound ---> Disrupt tissue integrity ---> division of blood vessel ----> exposed extracellular matrix and subendothelial collagen to PLATELETS ----> platelet aggregation, degranulation and activation of coagulation cascade PLATELET α granules release wound active substances Platelet derived growth factor (PDGF) Transforming growth factor-β (TGF-β) Platelet activating factor (PAF) Fibronectin Serotinin

4. INFLAMMATION PHASE Injury – day 6 Cellular Infiltration in the wound: Neutrophil Macrophages Lymphocytes Fibroblast

5. INFLAMMATORY PHASE

6. Neutrophil migration to the wound Increase vascular permeability Local prostaglandin release Presence of chemotactic substances Complement factors Interleukin 1 (IL-1) Tumor necrotic factor α (TNF-α) TGF-β Platelet factor 4 Bacterial products

7. Role of Neutrophil in the wound: Phagocytosis of bacteria and debris Major source of cytokines (TNF-α) important in angiogenesis and collagen synthesis Release proteases (collagenases) degrade matrix and ground substances important in wound maturation Implicated in delaying epithelial closure of wound

8. Macrophages migration (48-96 hrs)

9. Lymphocyte migration to wound Peak 7 days post injury, which also time of bridge of transition between inflammation and proliferative phase Role in the wound not well defined Play an active role in modulation of wound environment It maintains wound strength and collagen content

10. Proliferative Phase (day 4-12) Tissue continuity is re-established Fibroblast and endothelial cells last to infiltrate the wound. ( PDGF is the strongest chemotactic factor) Fibroblast ----> proliferate ----> activated by cytokines and growth factor released by macrophages ---->matrix/collagen synthesis, remodeling/matrix contraction Lactate which accumulate in the wound can also activate collagen synthesis

11. Fibroblast

12. Proliferative Phase (day 4-12) Endothelial cells – proliferate and promotes angiogenesis TNF-α, TGF-β, & VEGF activates endothelial cells Macrophage major source of VEGF

13. Proliferation/Maturation (Matrix Synthesis) Collagen synthesis (I & III) highly dependent on: Adequate oxygen supply Presence of sufficient nutrients (CHO & CHON) Sufficient cofactors (minerals and vitamins) Good local wound environment (vascular supply and lack of infection)

14. Maturation (Matrix Synthesis) Proteoglycan synthesis: Glycosaminoglycans (proteoglycan) – comprise major portion of ground matrix: Dermatan Chondroitin sulfate proteoglycan interact with collagen forming collagen fibrils Gradually diminished during maturation and remodeling

15. Maturation and Remodeling Characterized as reorganization of previously synthesized collagen. Collagen broken down by matrix metalloproteinases (MMP) . Net wound collagen content is the result of balance between collagenolysis and collagen synthesis. There is a net shift toward collagen synthesis. Collagenolysis and collagen synthesis controlled by cytokines and growth factors Wound strength and mechanical integrity in the fresh wound are determined by both the quality and quantity of the newly deposited collagen

16. Maturation and Remodeling Deposition of matrix at the wound Early matrix scaffolding Fibronectin and collagen III Glycosaminoglycans and proteoglycans Collagen I (Final matrix) 6-8 weeks amount of collagen reach a plateau but tensile strength continuous up to 6-12 months Mechanical strength of the scar never achieve that of the uninjured tissue

17. Epithelialization Final steps in establishing tissue integrity Characterized as proliferation and migration of epithelial cells adjacent to the wound Begins on 1 st day of injury as thickening epidermis at wound edges

18. Epithelialization MARGINAL BASAL cells detached from dermis, enlarge, undergo fast mitosis and migrate across the surface of matrix in a leapfrog fashion until the defect is covered. Then the layers of epidermis is reestablished.

19. Re-epithelialization and Neovascularization

20. Epithelialization Incised wound – reepithelialization complete 48 hrs Superficial partial thickness lesion --> 2-3 weeks Deep partial thickness/Full thickness wound lesions---> 4-6 weeks (fibroplasia, granulation tissue form and wound contracture)

21. Epithelialization Stimuli for re-epithelialization: Loss of contact inhibition Exposure of extracellular matrix, like fibronectin Mediators ( Cytokines and growth factors - EGF, TGF-β, FGF, PDGF, IGF-1 ) released by immune cells.

22. Growth Factors Name for the cell from which they derived (FGF, PDGF) Extremely potent action and may act as autocrine, paracrine or endocrine fashion . Each has multiple action , could be chemotactic for some cell but stimulate replication for other cells

23. Growth Factors Act on cells via surface receptor binding, then reach nucleus by ion channel, G-protein linked or enzyme linked Phosphorylation of nuclear protein----> transcription of target genes

24. Wound Contraction Myofibroblast – major cell cause wound contraction for it has cytoskeletal structure in its cytoplasm Has α smooth muscle actin called stress fibers Usually detected 6 th day and extremely expressed up to 15 day. Expression fades after 4 weeks and undergo apoptosis

25. Wound Contracture

26. Healing in Specific Tissues Gastrointestinal tissue Cartilage Bone Tendon Nerve

27. Gastrointestinal tissue Normal GI tract --> absorptive, barrier and motor fuction Layers of GIT tract: ---> Submucosa has the greatest tensile strength (greatest suture holding capacity) ---> Serosal healing – watertight seal - hence leak are common in esophagus & lower rectum

28. Gastrointestinal tissue Full thickness GI wounds --> heals by surgical re-apposition of bowel ends (initial steps in repair process) Sutures and staples are used Failure to heal ---> dehiscence, leak, fistula Excessive healing ---> stricture and stenosis

29. Gastrointestinal tissue Significant decrease of marginal strength 1 st week due to release of collagenase (neutrophil, macrophage & intraluminal bacteria- P. aeruginosa) During first 3-5 days collagen break down > synthesis Integrity of anastomosis depends on equilibrium between collagen lysis and synthesis, which takes few days to initiate

30. Gastrointestinal tissue Collagenase expressed during injury in any GIT but much more marked in colon than small bowel. Collagen synthesis is carried both by fibroblast and smooth muscle cells in GIT. For anastomosis to heal: Tension free Good blood supply Received adequate nutrition Free of sepsis No distal obstruction

31. Bone Tissue Phases of bone healing: Hematoma formation bld at fracture site has devitalized soft tissue, dead bone & necrotic marrow . Liquifaction and degradation of nonviable products at the fracture site. Normal bone adjacent to injure site undergo revascularization.

32. Bone Tissue Phases of bone healing: Soft callus stage (3-4 days) soft tissue forms a bridge between fracture bone segments. Serve as an internal splint to prevent damage to new vessels and providing fibrocartilagenous union. Present both externally and within marrow cavity. Characterized as cessation of pain & inflammatory sign

33. Bone Tissue Phases of bone healing: Hard callus stage: - mineralization of soft callus and conversion to bone Remodeling stage: -excessive callus are reabsorbed and marrow cavity is re-canalized . Correct transmission of forces & restore contours of bone

34. Bone Tissue Phases of bone healing: Growth factors and cytokines that mediates bone healing are: bone morphogenic proteins (BMPs), TGFα, PDGF, TGF-β, TNF-α, and FGF

35. Cartilage Has chondrocyte and in its matrix has proteoglycans, collagen fibers and water Avascular tissue , nutrients diffuse along its matrix ---> permanent damage

36. Cartilage Healing depends on the depth of injury Superficial injury – disruption of proteoglycans and chondrocyte. No inflammatory response Increase synthesis of proteoglycan and collagen depends on chondrocyte ---> inadequate & regeneration is incomplete

37. Cartilage Healing depends on the depth of injury Deep injury – usually involved underlying soft tissue and bone ---> exposed to vascular channels ----> granulation ---> mediator activation ----> fibroblast migrate --> synthesize fibrous tissue ---> chondrification ----> cartilage restore better

38. Tendon/Ligaments Links muscle and bone, bone and bone Consist of parallel bundles of collagen, interspersed with spindle cells Type of injuries: laceration, rupture or contusion Healing process (hematoma formation, organization, laying down of reparative tissue and scar formation)

39. Tendon/Ligaments Matrix – glycogen I, III and glycosaminoglycan Hypovascular tendons heals with less motion and more scar formation Tenocyte – very active and retain a large regenerative potential, even in the absence of vascularity

40. Nerve injuries: Neuropraxia focal demyelenization Axonotmesis interruption of axonal continuity but preservation of Schwann cell basal lamina Neurotmesis complete transectio n

41. Nerve injuries: Crucial Steps for nerve to heal: Survival of axonal cell body Regeneration of axon across the transected nerve to reach the distal stump Connection of proximal regenerating nerve to the other end or target organ.

42. Nerve Wallerian degeneration – phagocytes remove degenerating axon and myelin sheath from the distal stump. Regeneration of axon from proximal stump and probe the distal stump Schwann cell enveloped and help remyelinating the regenerating axon Functional unit – when the regenerating axon connects with end targets.

43. Nerve Important Factors in Nerve healing: Growth factors – nerve growth factor (NGF), brain derived neurotrophic factors, basic and acidic fibroblastic growth factor, and neuroleukin Cell adhesion molecules – nerve adhesion molecule, neuron-glia adhesion molecule, myelin adhesion glycoprotein, and N-cadherin

44. Classification of Wound Healing Heal by primary intension – a clean incised wound closed with a suture Surgically closed wound

45. Classification of Wounds Healing by Secondary Intention - A contaminated wound with bacteria and with tissue lost, left it open to heal by granulation and contraction requires tissue contraction, connective tissue deposition and epithelialization for healing

46. Classification of Wounds Healing by tertiary Intention (delayed primary closure) - allowing the wound to stay open for few days then subsequently sutures

47. Healing spectrum of Wound The maximal wound strength is reach after 6 weeks of healing A fully healed wound achieves only 75-80% of a normal tissue Impaired healing is characterized as failure to achieve mechanical strength equivalent to a normal healed wound. Seen in compromised immune system (DM, chronic steroid usage and with tissue damaged by radiotherapy)

48. Factors Affecting Wound Healing AGE: Old patients have relatively poor wound healing such as dehiscence and incisional hernia due to underlying illnesses such as cardiovascular disease, metabolic disease (DM, malnutrition), cancer, and widespread use of drugs that impairs healing Generally in a healthy person AGE will cause a delay in healing rather than non-healing.

49. Factors Affecting Wound Healing Hypoxia, Anemia and Hypoperfusion: Low oxygen tension has deleterious effect in all aspect of wound healing. Optimal collagen synthesis requires oxygen as a cofactor, hence increasing subcutaneous oxygen tension level by increasing FIO 2 of inspired air enhanced collagen deposition and lower rate of wound infection .

50. Hypoxia, Anemia and Hypoperfusion: Factors affecting O 2 delivery: Systemic causes: Hypovolemia Cardiac failure Anemia (less than 15% Hct. interfere healing) Local causes: Arterial insufficiency Local vasoconstriction (fluid status, temp.) Excessive tension on tissues (compartment syndrome)

51. STEROIDS reduced collagen synthesis and wound strength Inhibits inflammatory phase (angiogenesis, neutrophil and macrophage migration and fibroblast proliferation) The stronger the anti-inflammatory effect of the steroid the greater the inhibitory effect of healing

52. STEROIDS Steroid inhibit epithelialization and wound contraction ---> increase wound infection Giving steroid 3-4 days after injury do not affect wound healing as severely as when it was given immediately postoperative period VITAMIN A topical administration – stimulate epithelialization and collagen synthesis

53. Chemotherapeuic - Antimetabolite drugs: Affect wound healing by: Inhibit early cell proliferation Inhibit wound DNA and protein synthesis Inhibit inflammatory phase Decrease fibrin/collagen deposition Delay wound contraction Delay use of the drug 2 weeks after surgery to lessen wound healing impairment.

54. Metabolic Disorder: Diabetes : Reduced inflammation (defect in granulocyte function), angiogenesis and collagen synthesis (defect in fibroblast proliferation) With arteriosclerosis of artery there is hypo-perfusion and local hypoxemia. Preoperative correction of blood sugar level and giving insulin during early phase of healing improves out come of wound healing

55. Metabolic Disorder: Uremia: Decrease collagen synthesis and breaking stre ngth ----> delayed healing In some uremic pt --> deposition of calcium and phosphate in the tissue leading uremic gangrene syndrome (calciphylaxis) extremely painful and difficult to heal Dialysis helps in wound healing

56. Metabolic Disorder: Obesity : Uncomplicated obesity has deleterious effect on wound healing 30% wound dehiscence 17% surgical site infection 30% incisional hernia 19% seroma 13% hematoma 10% fat necrosis.

57. Nutrition wound failure and wound infection is a reflection of poor nutrition (protein-energy). Arginine – single amino acid that enhanced wound healing (significantly studied) Enhanced wound fibroplasia Increased wound collagen and protein deposition if 30g arginine aspartate given orally. Hence, improved wound strength. Has no effect in rate of epithelialization

58. Nutrition Vitamin C – important in wound healing Scurvy – failure in collagen synthesis and cross-linking Vit C def .--> increase wound infection due to: Impaired neutrophil function Decreased complement activity decreased walling-off of bacteria due to insufficiency of collagen Tx – Vit C 2 gm daily needed; no toxicity in excess dose

59. Nutrition Vitamin A deficiency: Vit. A – increases inflammatory response by increasing influx of macrophage facilitate its lysosomal function. Increased collagen synthesis Given orally can reverse the the inhibitory effect of steroid and chemotherapy. In severe injury --> recommend 25,000 – 100,000 IU/day

60. Nutrition Trace elements: ZINC: Promotes fibroblast proliferation Promotes collagen synthesis Improved overall wound strength Promotes epithelialization

61. Factors Affecting Wound Healing Infection: Affects outcome of surgical procedure (SSI), prolonged hosp. stay and medical cost. Wound dehiscence, delayed closure, incisional hernia. Incidence of Wound Infection: (5-10%) Wound infection high = >10 5 micro-org/gm of tissue Main pathogen ----> normal flor a

62. Factors Affecting Wound Healing Infection: Most common organism causing wound infection: Staphylococcus sp. Coagulase (-) Streptococcus Enterococci Escherichia coli Prophylactic antibiotic – (1-2hrs before surgery) Adequate concentration in the tissue (dose and time) Usually given for surgical lesions class II-III

63. Factors Affecting Wound Healing Infection: Repeated dose intra-op: lengthy surgical time exceeding biochemical half-life of the antibiotic Large volume blood loss and fluid replacement Difficult surgery & using prosthetic implants Unexpected intra-op contamination Additional dose of antibiotic 24 hrs postoperatively

64. Classification of Wound Infection Based on Degree of Contamination: Class I – Clean wound (thyroid surgery) No entry to GIT, GUT nor Respiratory tract Infection rate < 2% Class II – Clean contaminated (biliary surgery) GIT, GUT and Resp. tract entered but contamination is controlled Infection rate < 3%

65. Classification of Wound Infection Based on Degree of Contamination: Class III – Contaminated wound Hollow viscous structured entered with major contaminaion. Infection rate 5-7% Class IV – Dirty wound Infection established before a wound is made Infection rate 48-50% Surgical wound infection manifest 7-10 days postop

66. Wound Infection Any wound that drains purulent material with bacteria identified on culture. Broader definition: - all wounds draining pus, whether or not bacteriologic studies are positive; wounds that are opened by the surgeons and wounds that the surgeon considers infected

67. Wound Infection Presence of bacteria in an open wound does not constitute an infection: Contamination – presence of bacteria without multiplication Colonization – multiplication of bacteria with out host response Infection – presence of host response in reaction to deposition and multiplication of bacteria

68. Host response to wound infection: Cellulitis: Pain, erythematous Abscess Abnormal discharge Delayed healing

69. Anatomical Classification of Wound Infection Superficial wound infection Deep wound infection Organ/space wound infection

70. Superficial Wound Infection 75% are superficial wound infection Manifestation: Postoperative wound is edematous, erythematous and tender Undue incisional pain Low grade fever Leukocytosis Mx: -Some sutures or staples are removed, wound open and drain the abscess -----> c/s -----> systemic antibiotic

71. Deep Wound Infection (DWI) Above or below the deep fascia Fever and leukocytosis Pus drains out passing through fascial sutures Can lead to wound dehiscence

72. Necrotizing fasciitis High mortality, elderly Secondary skin necrosis ---> hemorrhagic bullae, surrounded inflammation & edema Fascial necrosis is wider than skin Toxic – high fever, tachycardia, marked hypovolemia ---> cardiovascular collapse

73. Necrotizing fasciitis Mixed infection; grams stain with C/S --> aid Dx & Tx Start with high dose penicillin (20-40 million U/d IV) Resuscitate pt ---> multiple debridement (remove all necrosed skin and fascia) Wound covered with homo or xenografts ----> definitive reconstruction and autografting

74. CHRONIC WOUND Wound does not heal in 3 months Wound that does not heal in 4 weeks already indicate chronicity Etiology: (Presence of barriers) Arterial or venous insufficiency Nutritional insufficiency Excessive inflammation/infection Environmental barrier (repeated trauma)

75. CHRONIC WOUND

76. CHRONIC WOUND Marjolin’s ulcer – malignant transformation of a chronic wound Wound that does not heal for prolonged period of time and present an overturned wound edges Biopsy of wound edges Squamous and basal cell carcinomas

77. CHRONIC WOUND Ischemic Arterial Ulcer: Due to poor blood supply with symptoms of peripheral vascular disease: Intermittent claudication Rest pain Color or trophic changes (hair loss, dryness, scaling, pallor of skin, decreases pulses)

78. CHRONIC WOUND Ischemic Arterial Ulcer – Ulcer usually distal part of extremities, inter-digital cleft Diminished or absent pulses with decrease ankle-brachial index Poor formation of granulation tissue in the wound Shallow wound with smooth margin and pale base and surrounding skin Non-healing: - selective arteriogram ---> degree of arterial narrowing Mx: Revascularization and wound care

79. CHRONIC WOUND Venous Stasis Ulcer – Ulcer that fails to re-epithelialized despite the presence of adequate granulation tissue in a patient with skin color changes in the area of ulceration and signs of venous hypertension

80. CHRONIC WOUND Venous Stasis due to venous hypertension: caused by Venous insufficiency Combined deep, superficial and perforator vein valvular reflux Ulcer painless and common to occur sites of incompetent perforators Most common medial malleolus (Cockett’s perforator) shollow wound, irregular margins & pigmented surroundings

81. CHRONIC WOUND Venous Stasis Ulcer – Venous hypertension and capillary damage----> extravasation of hemoglobin, irritates the skin----> pruritus & skin damage, also cause brownish discoloration around the wound. Together with loss of subcutaneous fat ---> LIPODERMATOSCELROSIS

82. CHRONIC WOUND Venous Stasis Ulcer – Cause of ulceration impaired healing Venous stasis/Increase venous pressure --->Distention of dermal capillaries---> leak of fibrinogen---->perivasular cuffing----> impede oxygen exchange---> ulceration Neutrophil adheres to capillary endothelium---> plugging---> decrease dermal blood flow

83. CHRONIC WOUND Venous Stasis Ulcer – Management: Compression therapy – rigid or flexible means Rigid-zinc oxide –impregnated none lastic bandage Compressive stocking

84. CHRONIC WOUND Venous Stasis Ulcer – Management: Wound care: Clean wound and maintain moist environment using hydrocolloids adesive dressings

85. CHRONIC WOUND Diabetic Ulcers (10-25% DM) Major Contributors to form diabetic ulcers: Neuropathy (60-70%) Foot deformity Ischemia ( 15-20%) micro-macro vascular impairment Loss of sensory and motor Sensory – unrecognized injury Motor – Charcot’s foot collapse or dislocation of the inter-phalangeal or metatarsophalangeal joints – pressure on areas little protection ---> ULCER

86. CHRONIC WOUND Diabetic Ulcers: Management: Systemic – control bld. sugar level Local: Control infection – complete debridement of necrotic tissue. Give antibiotic adequate levels both in soft tissue and bone Off- loading of the ulcerated area – orthotic shoes or casts to allow to ambulate protecting fragile wounds PREVENTION & FOOT CARE

87. CHRONIC WOUND Decubitus or Pressure Ulcers: Seen in body prominence and external surface

88. CHRONIC WOUND Decubitus or Pressure Ulcers: Contributory factors : Excessive pressure --> capillary collapse ---> decrease delivery of nutrients and oxygen Immobility Altered activity levels/mental status Altered nutritional status

89. Decubitus or Pressure Ulcers:

90. Decubitus or Pressure Ulcers: Stage I Stage II

91. Decubitus or Pressure Ulcers: Stage III Stage IV

92. Decubitus or Pressure Ulcers: Treatment: Surgical debridement (enzymatic proteolytic & hydrotherapy) of all necrotic tissue Changing position of the pt. (Air mattress)

93. Decubitus or Pressure Ulcers: Treatment: Good antibiotic for soft tissue and bones Maintain a moist wound environment absorbed secretion but do not dessicate the wound Improve nutritional, metabolic and circulatory status

94. Decubitus or Pressure Ulcers: Treatment: Negative wound pressure therapy: Faster skin production and wound shrinkage and favors angiogenesis. Serous fluid is drained and reduce edema Stabilize a favorable wound environment.

95. Decubitus or Pressure Ulcers: Treatment: Operative repair – rotation flap

96. Excess Healing Skin - Hypertrophic scar, keloid, contracture GI tracts – strictures, stenosis Solid organs – cirrhosis, pulmonary fibrosis Peritoneal cavity – adhesive disease (adhesive bands)

97. Hypertrophic Scar(HTSs) Over abundance of fibroplasia Occurs 4 weeks after trauma of the skin Rise above the skin but within confines of origin May be tender, pruritic and burning sensation Regress spontaneously No predilection in race Male and female equal

98. Keloid Abundance of fibroplasia Results from surgery, burns, skin inflammation acne, chickenfox, injections, may arise spontaneously Occurs 3 months to years after the initial insult

99. Keloid Project above surrounding skin, but does not extend into underlying subcutaneous Body sites – ear lobe, deltoid, pre-sternal and upper back Rarely involute spontaneously, recur after surgery, often worse result

100. Mechanism causing HTSs and Keloid Unknown Possible IMMUNE SYSTEM: It’s keratinocytes has receptor Human Leukocyte Antigen Keloid has increased IgG, IgA and IgM HTSs higher T lymphocyte and Langerhans cell Both has more fibroblast differentiating from mononuclear, leading to high collagen synthesis. It also generates large number of cytokines, growth factors and extracellular matrix protein

101. Treatment for HTS and Keloid GOAL: Restore the function of the area Relief of symptoms Prevention of recurrence

102. Treatment HTS/Keloid: 45-100% recurrence after keloid excision: Fewer recurrence after surgical excision: Intra-lesional corticosteroid injection Topical application of silicon sheets Use of radiation or pressure

103. Treatment for HTS/Keloid Steroid: Intra-lesional corticosteroid injections decreases fibroblast proliferation, collagen synthesis, glycosaminoglycan synthesis, inflammatory process and TGF-β First line tx for keloid and second-line tx for HTS if topical therapy failed It soften, flatten and give symptomatic relief Success enhance if combined with surgery

104. Treatment for HTS/Keloid Radiotherapy: Destroy fibroblast Better combined with surgical excision Dose of 1500 – 2000 rads appears effective Risks – hyperpigmentation, pruritus, erythema, pain and secondary malignancy ---> reserved for adults

105. Pressure: Creates ischemic environment - Reduces number of inflammatory & proliferative cells, decrease metabolism and increase collagenase activity Tx begin early with pressure between 24-30mmhg to exceed capillary pressure Garments worn for 23-24/day for 1 year to avoid rebound hypertrophy Scars older than 6-12months respond poorly

106. Treatment for HTS/Keloids Silicone: Decrease capillary activity, inflammation and collagen deposition Painless, maintained for 24 hrs for 3 months to prevent rebound hypertrophy. Surgery: Debulk large lesion or as second-line therapy when other modalities failed

107. Peritoneal Adhesions Peritoneal injury [surgery (67%)/ intra-abdominal infection (28%)] – fibrous band between organs or between organ and internal body wall. Injury disrupt mesothelial cell layer --> inflammation--> release WBC/platelet--->inflammatory cytokines and growth factors--> fibrin deposition

108. Peritoneal Adhesions Postop adhesion most common cause of small bowel obstruction Adhesion also a leading cause of secondary infertility in female and abdominal and pelvic pain

109. Peritoneal Scarring Strategies to prevent adhesions: Minimized surgical trauma, careful handling of tissues, avoid ischemia, spare use of cautery, laser and retractors. Use of Barrier membranes and gels, separating damaged mesothelial surfaces, allowing adhesion free healing. Interceed – oxidized regenerated cellulose (only pelvic surgery) Seprafilm – hyaluronic acid and carboxymethylcellulose (applied below incision) Adept

110. Treatment of Wounds: LOCAL CARE:

111. Treatment of Wounds: ANTIBIOTICS: Signs of infection needing antibiotics; Erythema Cellulitis Swelling Purulent discharge Type of antibiotic is based on location of the wound and if single or multiple Usually delivered topically as part of irrigations or dressings

112. Treatment of Wounds: Wound Dressing:

113. Oxygen Therapy in Wound Healing Oxygen plays important role in healing, provide superoxide that is angiogenesis stimulators and are bacteriostatic Chronic wound have decreased oxygen supply caused delayed healing The most useful oxygen therapy for wound healing is hyperbaric oxygen therapy (HBOT) Breathing 100% O 2 under high pressure. 1.4 atmosphere absolute

114. Hyperbaric Oxygen Therapy Increasing O 2 helps angiogenesis in bone and soft tissue Increase O 2 level decrease swelling around the wound site ----> allows blood and O 2 flow more freely It increases the ability of WBC to kill offending bacteria, better chance for wound to heal. Use to treat bone infection Bacteria cannot survive at a high oxygen level (gas gangrene)

115. BIOFILM Bacterial growth on a chronic wound that is encapsulated by a protective layer made up of the host and bacterial proteins

116. BIOFILM 60% of chronic wound has biofilm Stages: Stage I – (reversible bacterial adhesion stage) adhesion of bacteria to the surface of the wound

117. Stage II – (permanent adhesion or maturation stage) the organism permanently attach, proliferate and mature in the wound surface Stage III – organism secrete a surrounding protective matrix -->EPS (extracellular polymeric substance)

118. Treatment for Biofilm Frequent debridement to mechanically removed the biofilm (best method of treatment). WEEKLY Wound cleansing formulas (Prontosan) Topical broad spectrum antimicrobial --- > silver, iodine, honey