Wounds
Healing
LEARNING OBJECTIVES
 Definition of wound.
 types of wounds.
 phases of wound healing.
 Healing in specific tissue.
 Factors affecting wound healing.
 Management of wound.
 Complications of wound.
DEFINITIONS OF WOUND
 A cut or break in the continuity of any tissue, caused
by injury or incision. bailliere (23rd Ed).
 A wound is a break in the integrity of skin or tissues
often which may be associated with disruption of
structure and function.
 (SRB 4th edition)
 It is circumscribed injury which is caused by external
force and it can involve any tissue and organ.
Classifications of wounds.
Rank and wakefield classification
 Tidy wounds.
 Untidy wounds.
Classification based on type wound
Clean incised wound.
Lacerated wound
Bruise and contusion
hematoma
 Puncture wound.
 Abrasion.
 Crush injury.
 Penetrating wound.
CLASSIFICATION BASED ONTHICKNESS OF WOUND
 Superficial wound.
 Partial thickness wound.
 Full thickness wound.
 Complicated wounds.
Classifications of wounds
 Clean wound.
 Clean contaminated wound.
 Contaminated wound.
 Dirty infected wound.
CLASSIFICATION ON BASIS OF DURATION
 Acute wounds heal in an orderly manner through the
four overlapping phases of healing.
 chronic wounds heal similarly but have prolonged
inflammatory, proliferative, or remodelling phases,
resulting in tissue fibrosis and in non-healing ulcers.
HEALING
 Healing is the body response to injury in an attempt to
restore normal structure and function.
 process of healing involves regeneration or repair.
PROCESS OF HEALING
 Regeneration
 When healing takes place by proliferation of
parenchymal cells and results in complete restoration
of original tissues.The goal all healings should be
regeneration.
 Repair. Healing in which normal tissue donot return
and healing occurs ny granulation tissue only.
TYPES OF HEALING
 Primary or First intention healing.
Wound edges are apposed to each other. e.g.
Surgical incised wounds.
 Secondary or second intention healing.
Wound edges are separated.
 tertiary or delayed primary healing.
PHASES OF WOUND HEALING
Hemostatic Phase
 Vasoconstriction.
 by contraction of vessels caused nerve and chemical
mediators.
 Platelets plug formation: alpha granules release fibrinogen,
fibronectin, thrombospondin, von Willebrand factor.
Clot formation : by fibrin plug using clotting factors.
INFLAMMATORY PHASE
 Neutrophils enter wound in 06 hr peaking in 24 to 48
hr and Key role of neutrophil is wound
decontamination by phagocytosis.their number drop
rapidly after third day.
 Macrophages reach at peak by 3-4th day and remain in
wound till healing.
 it can last up to 2 weeks in normal wounds.
Pro-inflammatory Cytokines
They are realesd by macrophages, platelets and
lymphocytes.
 IL- 1.
 IL2.
 IL6.
 IL8.
 IFN-γ.
 TNF alpha.
PROLIFERATIVE PHASE
 key cells of this phase are fibroblasts and endothelial
cells.they migrate wound on third day and peak on 7th
day.
 it is characterized by formation of granulation
tissue which is made of ECM and ground
substance endothelial cells, new capillaries which
is stimulated by cytokines..
 Endothelial cells. form capillaries which are more
leaky..
Epithelialization Phase
 First step toward epithelial phase is formation of
epithelial cells seal over surface of fibrin clot.
 Epithelial seal typically start after 21 to 28 hours of
injury.
 Epithelial cells stop growing after contact inhibition
with epithelial cells of opposite edge.
REMODELLING PHASE
 In this phase number of capillaries in granulation
tissue start to mature and reduce in number.
 There is also a decrease in the amount of
glycosaminoglycans and proteoglycans.
 The initial, disorganized scar tissue is slowly replaced
by organized ECM of normal skin.
REMODELLING PHASE
SCAR STRENGTH
3% in one eek
20% in 03 week.
80% in 12 week
.
HARD TISSUE HEALING
 Inflammatory and proliferative phases are same for
soft tissue wound healing.
 Maturation differs markly in hard tissues as compare
to soft tissue healing.
 In bone healing osteoclasts play role of macrophages
MANAGEMENT OFWOUND
Managing the acute wound
 Cleansing
 Exploration and diagnosis
 Debridement
 Repair of structures
 Replacement of lost tissues where indicated
 Skin cover if required
 Skin closure without tension
 All of the above with careful tissue handling and
meticulous
COMPLICATIONS OF WOUND
 INFECTION
 ULCERATION
 WOUND DEHISCENCE
 HEPERTROPHIC SCAR
 KELOID
 CONTRACTURES
 Pigmentation
 Marjolin ulcer
 Incisional hernias
FACTORS AFFECTING WOUND HEALING
LOCAL FACTORS
Site of the wound
● Structures involved
● Mechanism of wounding Incision Crush Crush avulsion
● Contamination (foreign bodies/bacteria)a
● Loss of tissue
● Other local factorsVascular insufficiency (arterial or
venous) Previous radiation Pressure
● Systemic factors Malnutrition or vitamin and mineral
deficiencies Disease (e.g. diabetes mellitus) Medications
(e.g. steroids) Immune deficiencies (e.g. chemotherapy,
acquired immunodeficiency syndrome [AIDS]) Smoking
General factors
 Age
 Obesity
 Smoking
 Malnutrition zinc, copper
 Vitamin deficiency vit A. vit C.
 ANEMIA
 JAUNDICE
 DIABETES MELLITUS
 Hiv AND IMMMUNOSUPRESSIVE DISEASES
 STEROIDAND CYTOTOXIC DRUGS,BISPHOSPHONATES,NSAID
 MALIGNANCY
Normal Duration of Healing
REFERENCES
 1.Bennett NT, Schultz GS. Growth factors and wound healing: Part II. Role in normal and chronic wound healing. Am J Surg 1993; 166: 74–81. [PubMed]
 2.Bennett NT, Schultz GS. Growth factors and wound healing: Biochemical properties of growth factors and their receptors. Am J Surg 1995; 165: 728–37. [PubMed]
 3.Lawrence WT. Physiology of the acute wound. Clin Plast Surg 1998; 25: 321–340. [PubMed]
 4.Mast BA, Schultz GS. Interactions of cytokines, growth factors, and proteases in acute and chronic wounds. Wound Rep Regen 1996; 4: 411–20. [PubMed]
 5.Schultz GS. Molecular Regulation of Wound Healing. In RA Bryant (ed.), Acute and Chronic Wounds: Nursing Management, 2nd ed, 413–29. Philadelphia: Mosby, 2000.
 6.Gailit J, Clark RAF. Wound repair in context of extracellular matrix. Curr Opin Cell Biol 1994; 6: 717–25. [PubMed]
 7.RumallaVK, Borah GL. Cytokines, growth factors, and plastic surgery. Plast Reconstr Surg. 2001; 108: 719–33. [PubMed]
 8.Luster AD. Chemokines–chemotactic cytokines that mediate inflammation. N Engl J Med 1998; 338: 436–45. [PubMed]
 9.Gillitzer R, Goebeler M. Chemokines in cutaneous wound healing. J Leukoc Biol 2001; 69: 513–21. [PubMed]
 10.Dinarello CA, Moldawer LL. chemokines and Their Receptors. Proinflammatory and Anti-inflammatory Cytokines in Rheumatoid Arthritis, 1st ed, pp. 99–110. Thousand Oaks, CA: Amgen Inc., 2000.
 11.Frenette PS, Wagner DD. Adhesion molecules, blood vessels and blood cells. N Eng J Med 1996; 335: 43–5. [PubMed]
 12.Frenette PS, Wagner DD. Molecular medicine, adhesion molecules. N Eng J Med 1996; 334: 1526–9. [PubMed]
 13.Diegelmann RF, Cohen IK, Kaplan AM. The role of macrophages in wound repair: a review. Plast Reconstr Surg 1981; 68: 107–13. [PubMed]
 14.Duncan MR, Frazier KS, Abramson S, WilliamsS, Klapper H, Huang X, Grotendorst GR. Connective tissue growth factor mediates transforming growth factor beta-induced collagen synthesis: down-
regulation by cAMP. FASEB J. 1999; 13: 1774–86. [PubMed]
 15.Bhushan M, Young HS, Brenchley PE, Griffiths CE. Recent advances in cutaneous angiogenesis. Br J Dermatol 2002; 147: 418–25. [PubMed]
 16.Semenza GL. HIF-1 and tumor progression: pathophysiology and therapeutics. Trends Mol Med. 2002; 8: S62–S7. [PubMed]
 17.O’Toole EA. Extracellular matrix and keratinocyte migration. Clin Exp Dermatol 2001; 26: 525–30. [PubMed]
 18.Bucalo B, Eaglstein WH, Falanga V. Inhibition of cell proliferation by chronic wound fluid. Wound Rep Reg 1993; 1: 181–86. [PubMed]
 19.Katz MH, Alvarez AF, Kirsner RS, Eaglstein WH, Falanga V. Human wound fluid from acute wounds stimulates fibroblast and endothelial cell growth. J Am Acad Dermatol 1991; 25: 1054–58. [PubMed]
 20.Harris IR, Yee KC, Walters CE, Cunliffe WJ, Kearney JN, Wood EJ, Ingham E. Cytokine and protease levels in healing and non-healing chronic venous leg ulcers. Exp Dermatol 1995; 4: 342–9. [PubMed]
 21.Trengove NJ, Bielefeldt-Ohmann H, Stacey MC. Mitogenic activity and cytokine levels in non-healing and healing chronic leg ulcers. Wound Rep Regen 2000; 8: 13–25. [PubMed]
 22.Yager DR, Nwomeh BC. The proteolytic environment of chronic wounds. Wound Rep Regen 1999; 7: 433–41. [PubMed]
 23.Nwomeh BC, Yager DR, Cohen IK. Physiology of the chronic wound. Clin Plast Surg 1998; 25: 341–56. [PubMed]
 24.Trengove NJ, Stacey MC, Macauley S, Bennett N, Gibson J, Burslem F, Murphy G, Schultz G. Analysis of the acute and chronic wound environments: the role of proteases and their inhibitors. Wound Rep
Regen 1999; 7: 442–52. [PubMed]
 25.Yager DR, Zhang LY, Liang HX, Diegelmann RF, Cohen IK. Wound fluids from human pressure ulcers contain elevated matrix metalloproteinase levels and activity compared to surgical wound fluids. J
Invest Dermatol 1996; 107: 743–8. [PubMed]
 26.Rogers AA, Burnett S, Moore JC, ShakespearePG, Chen WYJ. Involvement of proteolytic enzymesplasminogen activators and matrix metalloproteinases-in the pathophysiology of pressure
ulcers. Wound Rep Regen 1995; 3: 273–83. [PubMed]
 27.Bullen EC, Longaker MT, Updike DL, Benton R, Ladin D, Hou Z. Tissue inhibitor of metalloproteinases-1 is decreased and activated gelatinases are increased in chronic wounds. J Invest
Dermatol 1995; 104: 236–40. [PubMed]
 28.Ladwig G P, Robson MC, Liu R, Kuhn MA, Muir DF, Schultz GS. Ratios of activated matrix metalloproteinase-9 to tissue inhibitor of matrix metalloproteinase-1 in wound fluids are inversely correlated
with healing of pressure ulcers. Wound Rep Regen 2002; 10: 26–37. [PubMed]
Wound healing. final yr  24 nov 23pptx.pptx

Wound healing. final yr 24 nov 23pptx.pptx

  • 2.
  • 4.
    LEARNING OBJECTIVES  Definitionof wound.  types of wounds.  phases of wound healing.  Healing in specific tissue.  Factors affecting wound healing.  Management of wound.  Complications of wound.
  • 5.
    DEFINITIONS OF WOUND A cut or break in the continuity of any tissue, caused by injury or incision. bailliere (23rd Ed).  A wound is a break in the integrity of skin or tissues often which may be associated with disruption of structure and function.  (SRB 4th edition)  It is circumscribed injury which is caused by external force and it can involve any tissue and organ.
  • 6.
    Classifications of wounds. Rankand wakefield classification  Tidy wounds.  Untidy wounds. Classification based on type wound Clean incised wound. Lacerated wound Bruise and contusion hematoma
  • 7.
     Puncture wound. Abrasion.  Crush injury.  Penetrating wound. CLASSIFICATION BASED ONTHICKNESS OF WOUND  Superficial wound.  Partial thickness wound.  Full thickness wound.  Complicated wounds.
  • 8.
    Classifications of wounds Clean wound.  Clean contaminated wound.  Contaminated wound.  Dirty infected wound.
  • 9.
    CLASSIFICATION ON BASISOF DURATION  Acute wounds heal in an orderly manner through the four overlapping phases of healing.  chronic wounds heal similarly but have prolonged inflammatory, proliferative, or remodelling phases, resulting in tissue fibrosis and in non-healing ulcers.
  • 10.
    HEALING  Healing isthe body response to injury in an attempt to restore normal structure and function.  process of healing involves regeneration or repair.
  • 11.
    PROCESS OF HEALING Regeneration  When healing takes place by proliferation of parenchymal cells and results in complete restoration of original tissues.The goal all healings should be regeneration.  Repair. Healing in which normal tissue donot return and healing occurs ny granulation tissue only.
  • 12.
    TYPES OF HEALING Primary or First intention healing. Wound edges are apposed to each other. e.g. Surgical incised wounds.  Secondary or second intention healing. Wound edges are separated.  tertiary or delayed primary healing.
  • 14.
  • 15.
    Hemostatic Phase  Vasoconstriction. by contraction of vessels caused nerve and chemical mediators.  Platelets plug formation: alpha granules release fibrinogen, fibronectin, thrombospondin, von Willebrand factor. Clot formation : by fibrin plug using clotting factors.
  • 17.
    INFLAMMATORY PHASE  Neutrophilsenter wound in 06 hr peaking in 24 to 48 hr and Key role of neutrophil is wound decontamination by phagocytosis.their number drop rapidly after third day.  Macrophages reach at peak by 3-4th day and remain in wound till healing.  it can last up to 2 weeks in normal wounds.
  • 18.
    Pro-inflammatory Cytokines They arerealesd by macrophages, platelets and lymphocytes.  IL- 1.  IL2.  IL6.  IL8.  IFN-γ.  TNF alpha.
  • 21.
    PROLIFERATIVE PHASE  keycells of this phase are fibroblasts and endothelial cells.they migrate wound on third day and peak on 7th day.  it is characterized by formation of granulation tissue which is made of ECM and ground substance endothelial cells, new capillaries which is stimulated by cytokines..  Endothelial cells. form capillaries which are more leaky..
  • 23.
    Epithelialization Phase  Firststep toward epithelial phase is formation of epithelial cells seal over surface of fibrin clot.  Epithelial seal typically start after 21 to 28 hours of injury.  Epithelial cells stop growing after contact inhibition with epithelial cells of opposite edge.
  • 24.
    REMODELLING PHASE  Inthis phase number of capillaries in granulation tissue start to mature and reduce in number.  There is also a decrease in the amount of glycosaminoglycans and proteoglycans.  The initial, disorganized scar tissue is slowly replaced by organized ECM of normal skin.
  • 25.
  • 26.
    SCAR STRENGTH 3% inone eek 20% in 03 week. 80% in 12 week .
  • 27.
    HARD TISSUE HEALING Inflammatory and proliferative phases are same for soft tissue wound healing.  Maturation differs markly in hard tissues as compare to soft tissue healing.  In bone healing osteoclasts play role of macrophages
  • 28.
    MANAGEMENT OFWOUND Managing theacute wound  Cleansing  Exploration and diagnosis  Debridement  Repair of structures  Replacement of lost tissues where indicated  Skin cover if required  Skin closure without tension  All of the above with careful tissue handling and meticulous
  • 29.
    COMPLICATIONS OF WOUND INFECTION  ULCERATION  WOUND DEHISCENCE  HEPERTROPHIC SCAR  KELOID  CONTRACTURES  Pigmentation  Marjolin ulcer  Incisional hernias
  • 30.
    FACTORS AFFECTING WOUNDHEALING LOCAL FACTORS Site of the wound ● Structures involved ● Mechanism of wounding Incision Crush Crush avulsion ● Contamination (foreign bodies/bacteria)a ● Loss of tissue ● Other local factorsVascular insufficiency (arterial or venous) Previous radiation Pressure ● Systemic factors Malnutrition or vitamin and mineral deficiencies Disease (e.g. diabetes mellitus) Medications (e.g. steroids) Immune deficiencies (e.g. chemotherapy, acquired immunodeficiency syndrome [AIDS]) Smoking
  • 31.
    General factors  Age Obesity  Smoking  Malnutrition zinc, copper  Vitamin deficiency vit A. vit C.  ANEMIA  JAUNDICE  DIABETES MELLITUS  Hiv AND IMMMUNOSUPRESSIVE DISEASES  STEROIDAND CYTOTOXIC DRUGS,BISPHOSPHONATES,NSAID  MALIGNANCY
  • 32.
  • 33.
    REFERENCES  1.Bennett NT,Schultz GS. Growth factors and wound healing: Part II. Role in normal and chronic wound healing. Am J Surg 1993; 166: 74–81. [PubMed]  2.Bennett NT, Schultz GS. Growth factors and wound healing: Biochemical properties of growth factors and their receptors. Am J Surg 1995; 165: 728–37. [PubMed]  3.Lawrence WT. Physiology of the acute wound. Clin Plast Surg 1998; 25: 321–340. [PubMed]  4.Mast BA, Schultz GS. Interactions of cytokines, growth factors, and proteases in acute and chronic wounds. Wound Rep Regen 1996; 4: 411–20. [PubMed]  5.Schultz GS. Molecular Regulation of Wound Healing. In RA Bryant (ed.), Acute and Chronic Wounds: Nursing Management, 2nd ed, 413–29. Philadelphia: Mosby, 2000.  6.Gailit J, Clark RAF. Wound repair in context of extracellular matrix. Curr Opin Cell Biol 1994; 6: 717–25. [PubMed]  7.RumallaVK, Borah GL. Cytokines, growth factors, and plastic surgery. Plast Reconstr Surg. 2001; 108: 719–33. [PubMed]  8.Luster AD. Chemokines–chemotactic cytokines that mediate inflammation. N Engl J Med 1998; 338: 436–45. [PubMed]  9.Gillitzer R, Goebeler M. Chemokines in cutaneous wound healing. J Leukoc Biol 2001; 69: 513–21. [PubMed]  10.Dinarello CA, Moldawer LL. chemokines and Their Receptors. Proinflammatory and Anti-inflammatory Cytokines in Rheumatoid Arthritis, 1st ed, pp. 99–110. Thousand Oaks, CA: Amgen Inc., 2000.  11.Frenette PS, Wagner DD. Adhesion molecules, blood vessels and blood cells. N Eng J Med 1996; 335: 43–5. [PubMed]  12.Frenette PS, Wagner DD. Molecular medicine, adhesion molecules. N Eng J Med 1996; 334: 1526–9. [PubMed]  13.Diegelmann RF, Cohen IK, Kaplan AM. The role of macrophages in wound repair: a review. Plast Reconstr Surg 1981; 68: 107–13. [PubMed]  14.Duncan MR, Frazier KS, Abramson S, WilliamsS, Klapper H, Huang X, Grotendorst GR. Connective tissue growth factor mediates transforming growth factor beta-induced collagen synthesis: down- regulation by cAMP. FASEB J. 1999; 13: 1774–86. [PubMed]  15.Bhushan M, Young HS, Brenchley PE, Griffiths CE. Recent advances in cutaneous angiogenesis. Br J Dermatol 2002; 147: 418–25. [PubMed]  16.Semenza GL. HIF-1 and tumor progression: pathophysiology and therapeutics. Trends Mol Med. 2002; 8: S62–S7. [PubMed]  17.O’Toole EA. Extracellular matrix and keratinocyte migration. Clin Exp Dermatol 2001; 26: 525–30. [PubMed]  18.Bucalo B, Eaglstein WH, Falanga V. Inhibition of cell proliferation by chronic wound fluid. Wound Rep Reg 1993; 1: 181–86. [PubMed]  19.Katz MH, Alvarez AF, Kirsner RS, Eaglstein WH, Falanga V. Human wound fluid from acute wounds stimulates fibroblast and endothelial cell growth. J Am Acad Dermatol 1991; 25: 1054–58. [PubMed]  20.Harris IR, Yee KC, Walters CE, Cunliffe WJ, Kearney JN, Wood EJ, Ingham E. Cytokine and protease levels in healing and non-healing chronic venous leg ulcers. Exp Dermatol 1995; 4: 342–9. [PubMed]  21.Trengove NJ, Bielefeldt-Ohmann H, Stacey MC. Mitogenic activity and cytokine levels in non-healing and healing chronic leg ulcers. Wound Rep Regen 2000; 8: 13–25. [PubMed]  22.Yager DR, Nwomeh BC. The proteolytic environment of chronic wounds. Wound Rep Regen 1999; 7: 433–41. [PubMed]  23.Nwomeh BC, Yager DR, Cohen IK. Physiology of the chronic wound. Clin Plast Surg 1998; 25: 341–56. [PubMed]  24.Trengove NJ, Stacey MC, Macauley S, Bennett N, Gibson J, Burslem F, Murphy G, Schultz G. Analysis of the acute and chronic wound environments: the role of proteases and their inhibitors. Wound Rep Regen 1999; 7: 442–52. [PubMed]  25.Yager DR, Zhang LY, Liang HX, Diegelmann RF, Cohen IK. Wound fluids from human pressure ulcers contain elevated matrix metalloproteinase levels and activity compared to surgical wound fluids. J Invest Dermatol 1996; 107: 743–8. [PubMed]  26.Rogers AA, Burnett S, Moore JC, ShakespearePG, Chen WYJ. Involvement of proteolytic enzymesplasminogen activators and matrix metalloproteinases-in the pathophysiology of pressure ulcers. Wound Rep Regen 1995; 3: 273–83. [PubMed]  27.Bullen EC, Longaker MT, Updike DL, Benton R, Ladin D, Hou Z. Tissue inhibitor of metalloproteinases-1 is decreased and activated gelatinases are increased in chronic wounds. J Invest Dermatol 1995; 104: 236–40. [PubMed]  28.Ladwig G P, Robson MC, Liu R, Kuhn MA, Muir DF, Schultz GS. Ratios of activated matrix metalloproteinase-9 to tissue inhibitor of matrix metalloproteinase-1 in wound fluids are inversely correlated with healing of pressure ulcers. Wound Rep Regen 2002; 10: 26–37. [PubMed]