this a basic presentation which I got inspired to do after seeing some presentations made on slideshare. It basically covers types of wounds,wound healing process,factors affecting wound healing and wound care.

1. Dr D Mwale – Presenter
Prof Munkonge - Moderator

2. 1. Introduction
2. Skin structure and function
3. Definitions
4. Classification of wound healing
5. Cellular basis of wound healing
6. Factors influencing wound healing
7. Outcomes of wound healing
8. Wound Care

4. Type of injury in which skin/epithelium is
torn,cut or punctured (open wound), or
where blunt force causes a contusion (a
closed wound)

5. 1. According to the type of exposure to the
environment.
2. According to risk of sepsis.
3. Classification according to Velocity of
inflicting object.
4. Classification according to Inflicting
substance

6. wounds
open
incision
avulsion
abrasion
puncture
penetration
gunshot
laceration
closed
haematoma
contusion
Crush injury

7.  1) Lacerations – Injury where tissue is cut or torn. For treatment,
tissue is first cleansed of any blood clots and foreign material,
derided and irrigated. Local anesthetic is administered and a
traumatic technique of wound closure is employed, where wound
margins are realigned with careful regard to prevention of any further
crush injury to tissues. Sterile dressings are applied and
immobilization is recommended for complex extremity wounds.
 2.) Incision – wound cause by sharp edged instrument/object i.e
knife resulting in a clean, regular edges.
 3.) Contusions – Injuries resulting from a forceful blow to the skin
and soft tissue, however leaving the outer layer of skin intact. These
injuries generally require minimal care as there is no open wound.
However, contusions should be evaluated for possible hematoma
deep to the surface or other tissue injuries that may indicate more
severe morbidity.
 4.) Avulsions – Injuries where a section of tissue is torn off, either
partially or in total. In partial avulsions, the tissue is elevated but
remains attached to the body.
 5.) Abrasions – Injury where a superficial layer of tissue is
removed, as seen with 1st degree burns. The wound is cleansed of
any foreign material, sometimes employing a scrub brush to prevent
traumatic tattooing by dirt and gravel, and should be performed
within the first day of injury.

8.  6.)Puncture wounds - caused by an object puncturing the skin, such as
a splinter, nail or needle.
 7.)Penetration wounds - caused by an object such as a knife entering and
coming out from the skin.
 8.)Gunshot wounds - caused by a bullet or similar projectile driving into or
through the body. There may be two wounds, one at the site of entry and
one at the site of exit, generally referred to as a "through-and-through.
 9.)Hematomas - also called a blood tumor, caused by damage to a blood
vessel that in turn causes blood to collect under the skin.
• Hematomas that originate from internal blood vessel pathology are petechiae, purpura,
and ecchymosis.The different classifications are based on size.
• Hematomas that originate from an external source of trauma are contusions, also commonly
called bruises.
 10.)Crush injury - caused by a great or extreme amount of force applied
over a long period of time resulting in damage to overlying skin and
underlying tissue such as bone,cartilage,muscle.

14. wound
Clean wound
Clean
contaminated
wound
contaminated
wound
Dirty wound

15.  No viscus entry
 No septic area
 No break in aseptic technique
 Such wounds if get infected risk = 3%

16.  Operation enters a non infected area but
may encounter bacteria
 Careful control of the area should result in
minimal spillage of organisms
 E.g upper GIT surgery,Respiratory tract
infection
 Infection rates = 10%

17.  Gross spillaqge of organisms,where there
is infection already present but without pus
formation.
 There is major break of aseptic technique
 There is an open wound that has been
exposed for less than 4 hrs (i.e following
major trauma)
 Infection risk > 30%

18.  There is an operation in an infected area
(e.g peforated viscus,abscess or traumatic
wound) that has been exposed for over
4hrs.

19. Response of an organism to a physical
disruption of a tissue/organ with an aim to
repair or reconstitute the defect and to re-
establish homeostasis.
Can be achieved by 2 processes: scar
formation & tissue regeneration.
Dynamic balance between these 2 is
different in different tissues.

20. During healing, a complex cascade of
cellular events occur to achieve
resurfacing, reconstitution and restoration
of tensile strength of injured tissue.
4 classic but overlapping phases occur:
I. Haemostasis
II. Inflammation,
III. Proliferation
IV. Maturation/Remodeling..

21. 1. Primary healing
2. secondary healing

22. feature Primary healing Secondary healing
cleaness clean Unclean
Infection Generally uninfected May be infected
Margins Surgically clean Irregular
Healing Scanty granulation tissue Granulation tissue fills
the wound gap
Healing period short Long
Healing direction Direct healing From the bottom to the
top
outcome Neat linear scar Contracted irregular
wound

25.  Clot formation
 Initiates inflammatory response
 Transient vasoconstriction, platelet plugging,
fibrin clot formation
 Controls bleeding, provides a framework for
cellular infiltrate support
 Coagulation pathways activated leading to
fibrin formation
[ Please revisit lecture on Hemostasis]

26. Blood vessels are disrupted, resulting in
bleeding. Hemostasis is achieved by
formation of platelet plug & activation of
extrinsic & intrinsic clotting pathways.
Formation of a provisional fibrin matrix.
Recruitment of inflammatory cells into the
wound by potent chemoattractants.

28.  Fibrin and fibronectin form a lattice that provides
scaffold for migration of inflammatory,
endothelial, and mesenchymal cells.
 Neutrophilic infiltrate appears: removes dead
tissue & prevent infection.
 Monocytes/macrophages follow neutrophils:
orchestrated production of growth factors &
phagocytosis.

30. Entry of lymphocytes.
Appearance of mast cell: aberrant
scarring?

32. i. Angiogenesis
ii. Fibroblast migration
iii. Granulation tissue formation (composed
of fibroblasts, macrophages and
emdothelial cells).
iv. Re-epithelialization (begins immediately
after injury)

33.  Angiogenesis reconstructs vasculature in areas
damaged by wounding, stimulated by high
lactate levels, acidic pH, decreased O2 tension
in tissues.
 Recruitment & assembly of bone marrow derived
progenitor cells by cytokines is the central
theme.
 FGF-1 is most potent angiogenic stimulant
identified. Heparin important as cofactor, TGF-
alpha, beta, prostaglandins also stimulate.

34. Fibroblasts are the major mesenchymal
cells involved in wound healing, although
smooth muscle cells are also involved.
Macrophage products are chemotactic for
fibroblasts. PDGF, EGF, TGF, IL-1,
lymphocytes are as well.
Replacement of provisional fibrin matrix
with type III collagen.

36.  Basal cell layer thickening, elongation,
detachment & migration via interaction with ECM
proteins via integrin mediators.
 Generation of a provisional BM which includes
fibronectin, collagens type 1 and 5.
 Epithelial cells proliferation contributes new cells
to the monolayer. Contact inhibition when edges
come together.

39. i. Programmed regression of blood vessels
& granulation tissue.
ii. Wound contraction.
iii. Collagen remodeling.

41. Begins approximately 4-5 days after
wounding by action of myofibroblasts.
Represents centripetal movement of the
wound edge towards the center of the
wound.
Maximal contraction occurs for 12-15 days,
although it will continue longer if wound
remains open.

42. The wound edges move toward each other
at an average rate of 0.6 to .75 mm/day.
Wound contraction depends on laxity of
tissues, so a buttock wound will contract
faster than a wound on the scalp or
pretibial area.
Wound shape also a factor, square is
faster than circular.

43. Contraction of a wound across a joint can
cause contracture.
Can be limited by skin grafts, full better
than split thickness.
The earlier the graft the less contraction.
Splints temporarily slow contraction.
Physiotherapy will reduce wound
contraction

44. After 21 days, net accumulation of
collagen becomes stable. Bursting
strength is only 15% of normal at this
point. Remodeling dramatically increases
this.
3-6 weeks after wounding greatest rate of
increase, so at 6 weeks we are at 80% to
90% of eventual strength and at 6months
90% of skin breaking strength.

45.  The number of intra and intermolecular cross-
links between collagen fibers increases
dramatically.
 A major contributor to the increase in wound
breaking strength.
 Quantity of Type 3 collagen decreases replaced
by Type 1 collagen
 Remodeling continues for 12 mos, so scar
revision should not be done prematurely.

46. 19 types identified. Type 1(80-90%) most
common, found in all tissue. The primary
collagen in a healed wound.
Type 3(10-20%) seen in early phases of
wound healing. Type V smooth muscle,
Types 2,11 cartilage, Type 4 in BM.

48. Local factors
Systemic factors

49.  Infection: impairs healing.
 Surgical Technique : type of sutures, suturing
tecnique,placement of incision, careful
haemostasis
 Wound tension : the higher tension the more
difficult the healing – across Langer’s lines, near
joints.
 Radiation: endarteritis, abnormal fibroblasts.
 Foreign bodies – endogenous or exogenous
delay healing
 Blood supply: areas with poorer blood supply
healing is delayed i.e. pinna.
 Size

50.  Nutrition status - Malnutrition
 Age – poor healing in old age, best healing in pre
and adolescent ages.
 Chronic diseases – Diabetes Mellitus(impaired
neutrophil chemotaxis, phagocytosis),cancers.
 Therapeutic drugs -Steroids and
immunosuppressants suppresses macrophage
migration, fibroblast proliferation, collagen
accumulation, and angiogenesis. Reversed by
Vitamin A 25,000 IU per day.
 Recreational Substances i.e. Smoking: increased
platelet adhesiveness, decreased O2 carrying
capacity of blood, abnormal collagen

51. Vitamin A
- Fat soluble vitamin
- Maintains epithelial and cell membrane integrity
- Cofactor in collagen synthesis
- Deficiency results in decreased collagen synthesis and
decreased rates of epithelialisation
- Supplementation should be given in severe burns , major
trauma , oncotherapy , steroid therapy, stress ulcers, etc

52. Vitamin C
- Cofactor in collagen synthesis
- Deficiency leads to immature fibroblast and defective capillary
formation , increased susceptibility to wound infection and
reduced neutrophil function

53. Vitamin B complex
- Eg Folic acid , pyridoxine , pentotheric acid
- Cofactors in a variety of enzyme systems
- Deficiency leads to impaired antibody formation and
function
- Supplementation required severe injury and acute
illness
Vitamin D
- Deficiency results in reduced bone strength and
retarded bone healing

54. Vitamin K
- Used for synthesis of clotting factors and calcium building
proteins
Vitamin E
- Powerful antioxidant
- Important in membrane stabilization
- Has antitumor and antiaging effects
- High doses inhibit wound healing
- Supplements should be stopped 1-3 weeks before planned
surgery

55. Wound
healing
Normal
Incisional
Hernia
Hypertrophic
scar
Keloids
Inadequate
regeneration
Inadequate scar
formation
Infection
Dehiscence
Contractures

56. CNS injuries
Bone nonunion
Corneal ulcers

57.  Diabetic foot ulcers.
 Sacral pressure sores.
 Venous stasis ulcers.

58.  Excessive healing results in a
raised, thickened scar, with both
functional and cosmetic
complications.
 Hypertrophic scars develop soon
after injury,
 If it stays within margins of wound
it is hypertrophic.
 Hypertrophic scars more likely to
cause contracture over joint
surface also found in the
presternal or deltoid area, wounds
that cross langerhans lines.
 Hypertrophic scars may subside in
time

59.  Keloids more familial. Dark
skinned, ages of 2-40.
 Keloids scar tissue extends
beyond the confines of the
original injury due to
excessive fibroblasts and
collagen proliferation.
 Keloids continue forming up
to a year later.
 keloids rarely subside with
time.

60. Can occur in any wound
More common with delayed
(secondary)healing.
Contracture across a joint will cause
limited movement.
Avoid vertical incisions across joints.
Treatment : Skin grafting, Local flaps,
wound Z – plasty.

62. 1. Optimize systemic parameters
2. Debride nonviable tissue
3. Reduce wound bioburden
4. Optimize blood flow
5. Reduce edema
6. Use dressings appropriately
7. Use pharmacologic therapy
8. Close wounds with grafts/flaps as indicated

63. Age: cannot be reversed, usage of growth
factors, aggressive optimization of
systemic parameters & supplementation.
Avoidance of ischemia & malnutrition.
Correction of diabetes, removal of FB.
Avoidance of steroids, alcohol, smoking.
Avoidance of reperfusion injury: total
contact casting, compression therapy.

64.  Surface irrigation with saline.
 Debridement: surgical, enzymatic (papain with
urea, collagenase), mechanical (pressurized
water jet), autolytic, maggots.
 Antibiotics: cellulitis, decreased rate of healing,
increased pain, straw colored oozing from skin,
contaminated wounds, mechanical implants.
 Removal of FB.

65. Warmth
Hydration
Surgical revascularization
Hyperbaric O2 therapy: limb salvage.

66. Elevation
Compression
Negative pressure wound therapy:
removes pericellular transudate & wound
exudate as well as deleterious enzymes.
Cannot be used in ischemic, badly infected
or inadequately debrided wounds or in
malignancy.

67.  Absorption characteristics: none – films, low –
hydrogels, moderate - hydrocolloids, high –
foams, alginates, collagen.
 Hydrogels (eg. starch) rehydrate wounds (benefit
in small amounts of eschar, infected wounds).
 Hydrocolloids promote wound debridement by
autolysis.
 Antimicrobial dressings: silver, cadexomer
iodine, mupirocin, neomycin.

68.  Autologous keratinocyte sheets.
 Biobrane
 Oasis
 Alloderm
 Integra (sites prone to contracture, coverage of
tendons, bone, surgical hardware)
 TransCyte
 Dermagraft
 Orcel

69. Antimicrobials
PDGF
EGF
VEGF
Vit A: steroid use
Absolutely of no use in normally healing
wounds

70. Radiation wounds require flaps.
Chronic nonhealing ulcers.
Extensive areas of ulceration.
Major soft tissue loss.
Other therapies: electrical stimulation for
recalcitrant ulcers.

71. Manuka honey (apitherapy) in venous leg
ulcers.
Hyperbranched polyglycerol electrospun
nanofibers.
Androstenediol in steroid inhibited healing.
GM-CSF hydrogel in deep 2nd deg burns.
LASER therapy enhances tissue repair?
Nitric oxide containing nanoparticles.

72. MERRY CHRISTMAS AND A WONDERFUL
NEW YEAR !