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WOUNDS
ARIHO INNOCENT MINANE “AIM”
&
NANSEREKO PATRICIA “NP”
1/22/2023
• Anatomy
• Wound
 Definition
 Classification
 Causes
• Wound Healing
 Definition
 Stages
 Factors affecting wound healing
• Wound Management
• Wound Complications
• Consultations & referrals
Outline
Anatomy of the Skin
• Epidermis:– composed of several thin layers:
stratum basale, stratum spinosum, stratum granulosum,
stratum lucidum, stratum corneum
The several thin layers of the epidermis contain the following:
a) melanocytes, which produce melanin, a pigment that
gives skin its color and protects it from the damaging
effects of ultraviolet radiation.
b) keratinocytes, which produce keratin, a water repellent
protein that gives the epidermis its tough, protective
quality.
Anatomy cont’d
• Dermis:
– composed of a thick layer of skin that contains collagen
and elastic fibers, nerve fibers, blood vessels, sweat and
sebaceous glands, and hair follicles.
• Subcutaneous Tissue:
– composed of a fatty layer of skin that contains blood
vessels, nerves, lymph, and loose connective tissue filled
with fat cells
Definition;
A wound refers to the disruption in the
continuity of a tissue usually as a result of a
physical force.
For deep or visceral wounds, the term injury is
normally used, e.g. liver or splenic injuries
Classification of wounds depends on:
• Risk of bacterial contamination
• Thickness of the wound
• Involvement of skin or other structures
• Time elapsing from trauma
• Morphology
• Rate of healing
• Rank & Wakefield classification
Classification
Classification of Wounds
1. (bacterial contamination)
1) Clean Wound:
Operative incisional wounds
2) Clean/Contaminated Wound:
uninfected wounds in which no inflammation is encountered but the
respiratory, GIT, genital, and/or urinary tract ve bn entered.
3) Contaminated Wound:
open, traumatic wounds or surgical wounds involving major break in
sterile technique that show evidence of inflammation.
4) Infected Wound:
old, traumatic wounds containing dead tissue and wounds with
evidence of a clinical infection (e.g., purulent drainage).
2. Thickness of the wound
• Superficial – epidermis & papillary dermis
• Partial thickness – up to the reticular dermis
but hair follicles & sweat glands are intact
• Full thickness - skin & subcutaneous tissue
• Deep wounds/ complicated wounds –
involving muscles, laceration of blood vessels
and nerves + wounds penetrating into natural
cavities or organs
3. Involvement of skin or other
structures
• Simple wounds – one organ/ tissue
• Combined wounds – mixed tissue trauma
4. Time elapsing from trauma
• Fresh wounds – up to 6hrs
• Old wounds - > 6hrs
• Remember this is a generalisation it depends
on the site i.e scalp wounds can still be fresh
24hrs after injury
5. Morphology
Open wounds Closed wounds
• Incised
• Abrasions
• Friction burns
• Laceration
• Avulsion
• Puncture wounds
• Penetrating wound
• Bite
• Crush
• Contusion
• Hematoma
• Ecchymoses
• Bruise
Morphology cont’d
• Bruise/ Contusion; tissue bleeding with
discoloration
• Hematoma; locally collection of blood in tissues
• Abrasion; shearing injury of skin
• Laceration; cut
• Avulsion; tearing away
• Crush; squeezed between 2 hard surfaces
• Puncture wounds and bites
6. Rate of healing
• Acute
• Chronic (fail to heal within expected time and
despite proper wound care, by 3 months the
wound has not healed)
7. Rank & Wakefield classification
Tidy Un-tidy
• Inflicted by sharp objects
• No devitalised tissues
• Closed immediately
• Heal by primary intension
• Eg: surgical incisions,
lacerations from clean glass
or knife, abrasions
• Irregular skin damage with
skin loss
• External contamination
• Damage to underlying tss
(bld vss, nn, mm, #s)
• Shd not be closed
immediately
• Eg: crush injuries, avulsion
injuries with skin loss,
burns, infected wounds
Classification of Wounds’ Closure
• Healing by Primary Intention:
All Layers are closed. Heals in a minimum amount
of time, with no separation of the wound edges,
and with minimal scar formation.
• Delayed primary closure 3-5 day
• Healing by Secondary Intention:
Heal from the inside out. Healing is appropriate in
cases of infection, excessive trauma, tissue loss,
or imprecise approximation of tissue.
Causes of wounds
Being immobile-pressure sores
Burn injury
Trauma to the skin
Surgery – incisions made during operations
Underlying medical conditions such as diabetes or
some types of vascular disease
Specific types of infection such as Buruli ulcers
Tropic ulcers due to sensory loss e.g. leprosy
Phases of wound healing
1) Haemostasis by: vasoconstriction, platelet plug,
clot
2) Inflammation involving cellular and vascular
events ; histamine, bradykinin, serotonin,
complement, interleukin
Cells
Platelets; release PDGF, TGF, Von Willebrands
factor, serotonin, elastase, collagenase,
thrombokinase
Neutrophils 30sec-2min, macrophages ( 3-5 ) days
Cells of wound healing cont’d
• Lymphocytes; release stimulating and inhibitory
factors to neutrophils and macrophages and
colony stimulating factor
• Epithelial cells From; wound edges, hair follicles,
sweat and sebaceous. Closure is complete in
72hrs in sutured wounds.
• Keratinocytes produce GM CSF, TGF, VEGF,
fibroblast growth factor, IL 1,3,6. IL 1 stimulates
fibroblast proliferation, collagen 1&3
3) Granulation tissues formation
• Starts about 4-21 days after wounding. Tissue contains;
fibrin, fibronectin, collagen, GAGs, microphages, blood
vessels
• Fibroplasia; starts 24hrs myofibroblasts secret GAGs,
elastin and collagen and contribute to wound
contraction. Proliferation of fibroblasts is by thrombin,
serotonin, IL 1
• Angiogenesis; starts from capillary loops of blood
vessels adjacent to the wound by FGF and fibronectin.
Hypoxia initially plays a role later much Oxygen is
needed for neovasculisation complete in 7/7. Takes 12-
16/7 in burns.
Re-epithelialisation
• Re-construction of epithelium- Cells at the free
edge migrate across matrix and become stationary
then those behind migrate ( leap-frog). Cessation of
migration generates a basement with laminin v
collagen iv deposition. Bacteria delay process by
release of proteolytic enzymes.
• Contraction; this occurs 8-10/7 after injury. Full
thickness freeze injuries don’t contract.
4) Remodeling/maturation
Starts from the 3rd wk - 9-12 months. This is where
collagen III is converted to collagen I, and the
tensile strength continues to increase up to 80%
of normal tissue
Extracellular matrix has GAGs, proteoglycans,
glycoptns, collagen, fibronectin, laminins
Synthesis of collagen is intracellular extracellular
(amino/ carboxy-propeptidase ) then cross
linkages which if abn give abn healing. Fibroblasts
play a role in collagen organization
Fetal wound healing
• No scar formation till early 3rd trimester
• High hyaluronic acid and rapid deposition of
collagen is responsible for no scar formation.
• The growth factor profile is reduced in the
fetus with low PDGF and high Epidermal GF
giving high rate of wound healing.
• Higher type III collagen has also been
attributed to lack of scar in fetus
Scar tissue and abnormalities
(weaker, brittle, abn contraction, kelloids, hypertrophy)
Hypertrophic scar kelloid
• Begin after surgery
• Limited boundary
• Size commensurate with
injury
• Predilection flexor surfaces
• Improve with surgery
• Usually subside with time
• Collagen I:III decreased
• May take months to begin
• Overgrow their boundary
• Minor injury may cause
large lesion
• Predilection ear lobes
• Worsened with surgery
• Progressive
• Collagen I >>III than normal
Factors that affect wound healing
local systemic
• Poor blood supply
• Infection
• Foreign body
• Radiotherapy
• Corticosteroids
• Trauma
• hematoma
• Peripheral vascular disease
• Malnutrition macro & micro
• Chemotherapy & irradiation
• DM, RA, jaundice, uremia
• Aging, obesity, mental
status, shock, smoking
• Anticoagulants,
corticosteroids,
immunosuppresion
Healing defects
• Chronic wounds; the wound remains same size
despite care up to 3 months with no signs of
epithelialisation.
• The factors that delay healing can be local or
systemic and these ve to be addressed. DM or
venous insufficiency that cannot be alleviated
may pose difficulty in mgt.
• Chronic wounds show high turnover pathology (
rapid cell proliferation and death or growth factor
composition alteration like high TGF β3 no β1 in
DM )
DM ulcers
• Caused by pressure over bonny prominences
in neuropathy.
• There are rigid RBCs with micro-thrombi
compromising micro-circulation.
• Glycosylated Hb has increased affinity for O2
reducing delivery to tissues
• Abnormal matrix proteins are synthesized in
DM
• Angiopathy in DM impaires wound healing
impaired healing
• Venous ulcers; valvular incompetence is implicated with
edema  tissue ischemia and are subject to reperfusion
injury plus abn growth factor composition in the matrix 
chronicity. Pressure stockings can abate the process.
• Pressure ulcers; tissue ischemia due to pressure. Patients
with spinal cord injury ve abn leukocyte response.
• Rheumatoid arthritis
 osteogenesis imperfecta ( collagen 1 gene mutation )
 Ehlers-Danlos syndrome ( amino-protease deficiency )
 Epidermolysis bullosa ( high synthesis of metalloproteinases )
 Marfan’s syndrome
About management
• Clean wounds-surgical toilet + suturing + abx
• Dirty wounds/old– debridement + toilet + abx + tt
delayed closure
• Gun shot wounds and human bites, animal bites
managed as very contaminated wounds
• Burns managed as per protocol
• Full thickness wounds may need grafting
• Chronic wounds- manage underlying cause plus
wound care(DM, venous stripping,
Principles of Management
• Assessment
• Clean the wound
• Moist environment
• Bacterial load
• Prevent further injury
• Nutrition
• Rehabilitation
Treatment options
• Social and Surgical Toilet (Debridement)
• Tetanus Toxoid
• Wound dressing-moist dressing.
• Wound closure
– Primary closure
– Delayed primary closure
– Secondary closure
• Relieving pain with medications.
Treatment options
• Antibiotics
• Support stockings for varicose veins
• Treating other medical conditions, such as
anaemia and reviewing other treatments
• Surgery
– Wide excision
– Skin grafts
– Venous striping
Wound cleaning solutions
• Saline (0.9% NaCl+) is usually suitable
• Most other antiseptics are harmful to normal
tissue.
• Other antiseptics may be indicated for heavily
contaminated/infected wounds.
• Antiseptics are inactivated rapidly in presence
of pus/serum.
Wound cleaning solutions
• Recommended also are Chlorhexidine (aq
0.05% Unisept), Povidone-iodine (10% aq
solution (Betadine).
• Cetrimide is a detergent for cleaning and
can be used in presence of dirty.
• Acetic acid 5% or Oxygen are effective
against Pseudomonas aeruginosa.
• Hydrogen peroxide 3% can remove particles
of debris by its effervesces.
Wound dressing
• Why dress wounds
– Faster healing-moist
– Reduce bacterial contamination (Still
Controversial)
– Pain relief
– Personal hygiene
Properties of a good dressing
• Permit gaseous exchange to maintain PO2
and pH at required levels.
• Maintain high humidity: epithelization best
in moist environment.
• Maintain wound temperature close to body
core temperature for optimum mitosis and
phagocytosis.
Properties of a good dressing
• Enable removal of dead tissue and bacterial
chemicals, physical contaminants.
• Be impermeable to bacteria.
• Protect healing tissue from disruption by
physical forces.
• Be non adherent, no allergenic and free form
contaminants
Types of dressings
Conventional- gauze, cotton
Paraffin gauze
Polyurethane films (Opsite, Tegaderm)
Hydrocolloid dressings (Granuflex, Tegasorb)
Hydrogels dressings (Intrasite, Geliperm)
Osmotic Agents Dressings (Honey, Sugar)
Alginates from a sea weed (Kaltostat, Sorbsan)
Foams dressings (Lyofoam, Allevyn)
References;Mayo
clinic:wounds and wound
management
Thank You

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WOUND HEALING AND MANAGEMENT.pptx

  • 1. WOUNDS ARIHO INNOCENT MINANE “AIM” & NANSEREKO PATRICIA “NP” 1/22/2023
  • 2. • Anatomy • Wound  Definition  Classification  Causes • Wound Healing  Definition  Stages  Factors affecting wound healing • Wound Management • Wound Complications • Consultations & referrals Outline
  • 3. Anatomy of the Skin • Epidermis:– composed of several thin layers: stratum basale, stratum spinosum, stratum granulosum, stratum lucidum, stratum corneum The several thin layers of the epidermis contain the following: a) melanocytes, which produce melanin, a pigment that gives skin its color and protects it from the damaging effects of ultraviolet radiation. b) keratinocytes, which produce keratin, a water repellent protein that gives the epidermis its tough, protective quality.
  • 4. Anatomy cont’d • Dermis: – composed of a thick layer of skin that contains collagen and elastic fibers, nerve fibers, blood vessels, sweat and sebaceous glands, and hair follicles. • Subcutaneous Tissue: – composed of a fatty layer of skin that contains blood vessels, nerves, lymph, and loose connective tissue filled with fat cells
  • 5.
  • 6. Definition; A wound refers to the disruption in the continuity of a tissue usually as a result of a physical force. For deep or visceral wounds, the term injury is normally used, e.g. liver or splenic injuries
  • 7. Classification of wounds depends on: • Risk of bacterial contamination • Thickness of the wound • Involvement of skin or other structures • Time elapsing from trauma • Morphology • Rate of healing • Rank & Wakefield classification Classification
  • 8. Classification of Wounds 1. (bacterial contamination) 1) Clean Wound: Operative incisional wounds 2) Clean/Contaminated Wound: uninfected wounds in which no inflammation is encountered but the respiratory, GIT, genital, and/or urinary tract ve bn entered. 3) Contaminated Wound: open, traumatic wounds or surgical wounds involving major break in sterile technique that show evidence of inflammation. 4) Infected Wound: old, traumatic wounds containing dead tissue and wounds with evidence of a clinical infection (e.g., purulent drainage).
  • 9. 2. Thickness of the wound • Superficial – epidermis & papillary dermis • Partial thickness – up to the reticular dermis but hair follicles & sweat glands are intact • Full thickness - skin & subcutaneous tissue • Deep wounds/ complicated wounds – involving muscles, laceration of blood vessels and nerves + wounds penetrating into natural cavities or organs
  • 10. 3. Involvement of skin or other structures • Simple wounds – one organ/ tissue • Combined wounds – mixed tissue trauma
  • 11. 4. Time elapsing from trauma • Fresh wounds – up to 6hrs • Old wounds - > 6hrs • Remember this is a generalisation it depends on the site i.e scalp wounds can still be fresh 24hrs after injury
  • 12. 5. Morphology Open wounds Closed wounds • Incised • Abrasions • Friction burns • Laceration • Avulsion • Puncture wounds • Penetrating wound • Bite • Crush • Contusion • Hematoma • Ecchymoses • Bruise
  • 13. Morphology cont’d • Bruise/ Contusion; tissue bleeding with discoloration • Hematoma; locally collection of blood in tissues • Abrasion; shearing injury of skin • Laceration; cut • Avulsion; tearing away • Crush; squeezed between 2 hard surfaces • Puncture wounds and bites
  • 14. 6. Rate of healing • Acute • Chronic (fail to heal within expected time and despite proper wound care, by 3 months the wound has not healed)
  • 15. 7. Rank & Wakefield classification Tidy Un-tidy • Inflicted by sharp objects • No devitalised tissues • Closed immediately • Heal by primary intension • Eg: surgical incisions, lacerations from clean glass or knife, abrasions • Irregular skin damage with skin loss • External contamination • Damage to underlying tss (bld vss, nn, mm, #s) • Shd not be closed immediately • Eg: crush injuries, avulsion injuries with skin loss, burns, infected wounds
  • 16. Classification of Wounds’ Closure • Healing by Primary Intention: All Layers are closed. Heals in a minimum amount of time, with no separation of the wound edges, and with minimal scar formation. • Delayed primary closure 3-5 day • Healing by Secondary Intention: Heal from the inside out. Healing is appropriate in cases of infection, excessive trauma, tissue loss, or imprecise approximation of tissue.
  • 17. Causes of wounds Being immobile-pressure sores Burn injury Trauma to the skin Surgery – incisions made during operations Underlying medical conditions such as diabetes or some types of vascular disease Specific types of infection such as Buruli ulcers Tropic ulcers due to sensory loss e.g. leprosy
  • 18. Phases of wound healing 1) Haemostasis by: vasoconstriction, platelet plug, clot 2) Inflammation involving cellular and vascular events ; histamine, bradykinin, serotonin, complement, interleukin Cells Platelets; release PDGF, TGF, Von Willebrands factor, serotonin, elastase, collagenase, thrombokinase Neutrophils 30sec-2min, macrophages ( 3-5 ) days
  • 19. Cells of wound healing cont’d • Lymphocytes; release stimulating and inhibitory factors to neutrophils and macrophages and colony stimulating factor • Epithelial cells From; wound edges, hair follicles, sweat and sebaceous. Closure is complete in 72hrs in sutured wounds. • Keratinocytes produce GM CSF, TGF, VEGF, fibroblast growth factor, IL 1,3,6. IL 1 stimulates fibroblast proliferation, collagen 1&3
  • 20. 3) Granulation tissues formation • Starts about 4-21 days after wounding. Tissue contains; fibrin, fibronectin, collagen, GAGs, microphages, blood vessels • Fibroplasia; starts 24hrs myofibroblasts secret GAGs, elastin and collagen and contribute to wound contraction. Proliferation of fibroblasts is by thrombin, serotonin, IL 1 • Angiogenesis; starts from capillary loops of blood vessels adjacent to the wound by FGF and fibronectin. Hypoxia initially plays a role later much Oxygen is needed for neovasculisation complete in 7/7. Takes 12- 16/7 in burns.
  • 21. Re-epithelialisation • Re-construction of epithelium- Cells at the free edge migrate across matrix and become stationary then those behind migrate ( leap-frog). Cessation of migration generates a basement with laminin v collagen iv deposition. Bacteria delay process by release of proteolytic enzymes. • Contraction; this occurs 8-10/7 after injury. Full thickness freeze injuries don’t contract.
  • 22. 4) Remodeling/maturation Starts from the 3rd wk - 9-12 months. This is where collagen III is converted to collagen I, and the tensile strength continues to increase up to 80% of normal tissue Extracellular matrix has GAGs, proteoglycans, glycoptns, collagen, fibronectin, laminins Synthesis of collagen is intracellular extracellular (amino/ carboxy-propeptidase ) then cross linkages which if abn give abn healing. Fibroblasts play a role in collagen organization
  • 23. Fetal wound healing • No scar formation till early 3rd trimester • High hyaluronic acid and rapid deposition of collagen is responsible for no scar formation. • The growth factor profile is reduced in the fetus with low PDGF and high Epidermal GF giving high rate of wound healing. • Higher type III collagen has also been attributed to lack of scar in fetus
  • 24. Scar tissue and abnormalities (weaker, brittle, abn contraction, kelloids, hypertrophy) Hypertrophic scar kelloid • Begin after surgery • Limited boundary • Size commensurate with injury • Predilection flexor surfaces • Improve with surgery • Usually subside with time • Collagen I:III decreased • May take months to begin • Overgrow their boundary • Minor injury may cause large lesion • Predilection ear lobes • Worsened with surgery • Progressive • Collagen I >>III than normal
  • 25. Factors that affect wound healing local systemic • Poor blood supply • Infection • Foreign body • Radiotherapy • Corticosteroids • Trauma • hematoma • Peripheral vascular disease • Malnutrition macro & micro • Chemotherapy & irradiation • DM, RA, jaundice, uremia • Aging, obesity, mental status, shock, smoking • Anticoagulants, corticosteroids, immunosuppresion
  • 26. Healing defects • Chronic wounds; the wound remains same size despite care up to 3 months with no signs of epithelialisation. • The factors that delay healing can be local or systemic and these ve to be addressed. DM or venous insufficiency that cannot be alleviated may pose difficulty in mgt. • Chronic wounds show high turnover pathology ( rapid cell proliferation and death or growth factor composition alteration like high TGF β3 no β1 in DM )
  • 27. DM ulcers • Caused by pressure over bonny prominences in neuropathy. • There are rigid RBCs with micro-thrombi compromising micro-circulation. • Glycosylated Hb has increased affinity for O2 reducing delivery to tissues • Abnormal matrix proteins are synthesized in DM • Angiopathy in DM impaires wound healing
  • 28. impaired healing • Venous ulcers; valvular incompetence is implicated with edema  tissue ischemia and are subject to reperfusion injury plus abn growth factor composition in the matrix  chronicity. Pressure stockings can abate the process. • Pressure ulcers; tissue ischemia due to pressure. Patients with spinal cord injury ve abn leukocyte response. • Rheumatoid arthritis  osteogenesis imperfecta ( collagen 1 gene mutation )  Ehlers-Danlos syndrome ( amino-protease deficiency )  Epidermolysis bullosa ( high synthesis of metalloproteinases )  Marfan’s syndrome
  • 29. About management • Clean wounds-surgical toilet + suturing + abx • Dirty wounds/old– debridement + toilet + abx + tt delayed closure • Gun shot wounds and human bites, animal bites managed as very contaminated wounds • Burns managed as per protocol • Full thickness wounds may need grafting • Chronic wounds- manage underlying cause plus wound care(DM, venous stripping,
  • 30. Principles of Management • Assessment • Clean the wound • Moist environment • Bacterial load • Prevent further injury • Nutrition • Rehabilitation
  • 31. Treatment options • Social and Surgical Toilet (Debridement) • Tetanus Toxoid • Wound dressing-moist dressing. • Wound closure – Primary closure – Delayed primary closure – Secondary closure • Relieving pain with medications.
  • 32. Treatment options • Antibiotics • Support stockings for varicose veins • Treating other medical conditions, such as anaemia and reviewing other treatments • Surgery – Wide excision – Skin grafts – Venous striping
  • 33. Wound cleaning solutions • Saline (0.9% NaCl+) is usually suitable • Most other antiseptics are harmful to normal tissue. • Other antiseptics may be indicated for heavily contaminated/infected wounds. • Antiseptics are inactivated rapidly in presence of pus/serum.
  • 34. Wound cleaning solutions • Recommended also are Chlorhexidine (aq 0.05% Unisept), Povidone-iodine (10% aq solution (Betadine). • Cetrimide is a detergent for cleaning and can be used in presence of dirty. • Acetic acid 5% or Oxygen are effective against Pseudomonas aeruginosa. • Hydrogen peroxide 3% can remove particles of debris by its effervesces.
  • 35. Wound dressing • Why dress wounds – Faster healing-moist – Reduce bacterial contamination (Still Controversial) – Pain relief – Personal hygiene
  • 36. Properties of a good dressing • Permit gaseous exchange to maintain PO2 and pH at required levels. • Maintain high humidity: epithelization best in moist environment. • Maintain wound temperature close to body core temperature for optimum mitosis and phagocytosis.
  • 37. Properties of a good dressing • Enable removal of dead tissue and bacterial chemicals, physical contaminants. • Be impermeable to bacteria. • Protect healing tissue from disruption by physical forces. • Be non adherent, no allergenic and free form contaminants
  • 38. Types of dressings Conventional- gauze, cotton Paraffin gauze Polyurethane films (Opsite, Tegaderm) Hydrocolloid dressings (Granuflex, Tegasorb) Hydrogels dressings (Intrasite, Geliperm) Osmotic Agents Dressings (Honey, Sugar) Alginates from a sea weed (Kaltostat, Sorbsan) Foams dressings (Lyofoam, Allevyn)
  • 39.