WOUNDS AND WOUND HEALING

1. WOUNDS &
WOUND
HEALING
SUDESHNA BANERJEE DUTTA
ASSISTANT PROFESSOR
S.R.S.V.M B.SC(N) COLLEGE

3. WOUND
 It is a circumscribed injury which is caused by external
force & it can involve any tissue & organ
 A wound is a break in the skin integrity or tissues often
which may be associated with disruption of the
structure & function
 A cut or break in the skin continuity of any tissue,
caused by injury or operation

5. CLASSIFICATION OF WOUNDS
Rank & Wakefield classification:
1. Tidy wounds
2. Untidy wounds

6. CLASSIFICATION BASED ON THE TYPE OF
WOUND
Clean incised wound
Lacerated wound
Bruising or contusion
Hematoma
Puncture wound
Abrasion
Crush injury
Injuries to bone & joint (open/ closed)
Injuries to nerve (clean cut or crush)
Injuries to arteries & veins
Penetrating wounds

13. CLASSIFICATION BASED ON THICKNESS OF
WOUND
Superficial wound
Partial thickness
Full thickness
Deep wounds
Complicated wounds
Penetrating wounds

17. CLASSIFICATION OF SURGICAL WOUNDS

18. HEALING
 Healing is the body’s response to injury in an attempt to
restore normal structure & function.
 The process of healing involves 2 distinct processes:
Regeneration
Repair

19. REGENERATION
 Is when healing takes place by proliferation of
parenchymal cells & usually results in complete
restoration of the original tissues.
 The goal of all surgical procedures should be
regeneration which returns the tissues to their normal
microstructure & function.

20. REPAIR
 It is a healing outcome in which tissues do not return
to their normal architecture & function.
 Repair typically results in the formation of scar tissue.

21.  During healing, a complex cascade of cellular events
occur to achieve resurfacing, reconstitution and
restoration of tensile strength of injured tissue
 Wound healing occurs in 3 phases
1. Inflammatory phase
2. Proliferative phase
3. Remodeling phase

22. INFLAMMATORY PHASE
A. Immediate to 2-5 days
B. Hemostasis
✓ Vasoconstriction – damaged blood vessels constrict
✓ Hemostasis is achieved by formation of platelet plug &
activation of extrinsic & intrinsic clotting pathways.
✓ Formation of a provisional fibrin matrix
C. Recruitment of inflammatory cells into the wound by
potent chemoattractants

23. EARLY EVENTS IN INFLAMMATION
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.

24. LATE EVENTS IN INFLAMMATION
Entry of lymphocytes.
Appearance of mast cell

25. PROLIFERATIVE PHASE
2 days to 3 weeks
Granulation tissue formation (composed of
fibroblasts,macrophages and endothelial cell)
Angiogenesis
Contraction: Wound edges pull together to reduce the
defect
Epithelialization
Epithelial cells migrate across the new tissue to form a
barrier between the wound and the environment

26. MESENCHYMAL CELL PROLIFERATION
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.

27. ANGIOGENESIS
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.
EGF-1 is most potent angiogenic stimulant identified.
Heparin is also an important as cofactor, TGF- alpha,
beta, prostaglandins also stimulate.

28. EPITHELIALIZATION
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 3
Epithelial cells proliferation contributes new cells to the
monolayer. Contact inhibition when edges come
together.

29. REMODELING PHASE
3 weeks to 2 years
New collagen forms which increases the tensile strength
of the wound
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.

30. REMODELLING
The number of intra and intermolecular crosslinks
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 months, so scar revision
should not be done prematurely.

31. WOUND CONTRACTION
Begins approximately 4-5 days after wounding by action
of myofibroblasts.
Generally occurs in large surface wounds.
Represents centripetal movement of the wound edge
towards the centre of the wound.
Maximal contraction occurs for 12-15 days, although it
will continue longer if wound remains open.

32. WOUND CONTRACTION
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
wound on the soft area will contract faster than a wound
on the scalp or pretibial area.
Wound shape also a factor, square is faster than circular.

33. WOUND STRENGTH
Skin wounds
At the end of first week, wound strength is approximately
10% of unwounded skin
Wound strength increases rapidly over next 4 weeks and
then slows down at approximately at third month,
reaches a plateau at about 70- 80% of the tensile strength
of unwounded skin
Scar tissue is never as strong as the original tissue

34. IMPORTANT GROWTH FACTORS
RESPONSIBLE FOR WOUND HEALING
Platelet derived growth factor:
Promotes migration and proliferation of fibroblasts
Is chemotactic for monocytes
Epidermal growth factor
Promotes growth of endothelial, epithelial cells and
fibroblasts

35. GROWTH FACTORS IN WOUND HEALING
Fibroblast growth factor:
✓ Promotes synthesis of ECM proteins including
fibronectin.
✓ Chemotactic for fibroblasts and endothelial cells
✓ Promotes angiogenesis
Vascular Endothelial Growth Factor (VEGF)
✓ Angiogenesis
Macrophage derived growth factors
✓ IL-1 and TNF
✓ Promote proliferation of fibroblasts and endothelial cells.

36. WOUND HEALING
 Wound healing is accomplished in one of the following
two ways:
➢ Healing by first intention (primary union)
➢ Healing by second intention (secondary union)

37. HEALING BY FIRST INTENTION (PRIMARY
UNION)
❑ Occurs in clean, incised wounds with good apposition
of the edges – particularly planned surgical incisions
(clean wounds – no infections or foreign bodies)
❑ The incision causes only focal disruption of epithelial
basement membrane continuity and death of a
relatively few epithelial and connective tissue cells
❑ As a result, epithelial regeneration predominates over
fibrosis

38. SEQUENCE OF EVENTS
Immediate:
❖ The narrow incisional space rapidly fills with fibrin
clotted blood
❖ Dehydration at the surface produces a scab to cover and
protect the healing repair site
Within 24 hrs
❖ Movement and proliferation of epithelial cells across the
wound resulting in a thin, but continuous epithelial layer
❖ Early inflammation close to the edges (neutrophils)

39. SEQUENCE OF EVENTS CONT…
2-3 days
❖ Neutrophils replaced by macrophages
❖ Macrophages remove the blood clot
❖ Proliferation of epithelial cells
❖ Fibroblastic activity

40. SEQUENCE OF EVENTS CONT…
10-14 days
❖ Scab loose (aka dry clot)
❖ Epithelial covering complete
❖ Fibrous union of edges
❖ Wound still weak
❖ vascularization

41. BY THE END OF THE FIRST MONTH
❖ Scar comprises of a cellular connective tissue devoid of
inflammatory infiltrate, covered by intact epidermis
❖ Dermal appendages destroyed in the line of incision are
permanently lost
❖ Tensile strength of the wound increases and

42. HEALING BY SECOND INTENTION
(SECONDARY UNION)
 This occurs in open wounds, particularly when there has
been significant loss of tissue, necrosis or large wounds
with irregular margins
 Regeneration of parenchymal cells cannot completely
reconstitute the original architecture
 Abundant granulation tissue grows in from the margin to
complete the repair
Granulation tissues consists of:
✓ ECM fibroblasts
✓ Macrophages, neutrophils
✓ New blood vessels

43. SEQUENCE OF EVENTS
Early
➢ Cavity fills with blood & fibrin clot.
➢ Acute inflammation commences at junction of living tissue.
A few days
➢ Scab dries out
➢ A single sheet of epithelial cells is being pushed between
the surface debris & the underlying living tissue.
➢ New capillary loops bring macrophages, neutrophills &
fibroblasts

44. SEQUENCE OF EVENTS CONT…
1 week:
➢ Epithelial proliferation
➢ Capillary loops (granulation)
➢ Scab shed
➢ Loose connective tissue formed by fibroblasts
2 weeks onward:
➢ Epithelial covering complete
➢ Collagen arranged transversely

45. MONTHS
➢ Full thickness of epithelium restored
➢ Thick collagenous scar tissue becoming less vascular

46. FACTORS THAT INFLUENCE HEALING
➢ Systemic Factors that Delay/Retard Wound
Healing:
✓ Nutrition : Protein deficiency, Vitamin C deficiency, Zn
deficiency (inhibit collagen synthesis)
✓ Metabolic status: Diabetes Mellitus
✓ Circulatory status: Inadequate blood supply
(Atherosclerosis, Vascular defects)
✓ Hormones: Glucocorticoids inhibit collagen synthesis,
decrease inflammation

47. LOCAL FACTORS THAT DELAY/RETARD
WOUND HEALING
➢ Infection : Most important cause of delayed wound healing,
Persistent injury and inflammation
➢ Mechanical factors: Motion early in healing
➢ Foreign material - like suture material and foreign bodies
➢ Size, location & type of wound: wounds in ↑ vascularized
areas (face) heal faster than in poorly vasc areas (tendon,
feet)
➢ Small wounds heal faster than larger: incisions faster than
blunt trauma (contusions)

48. COMPLICATIONS OF WOUND HEALING
Deficient scar formation:
Can lead to two types of complications:
A. Wound Dehiscence (rupture of wound): Most common
after abdominal surgery (coughing, vomiting)
B. Ulceration - Defect in the continuity

49. WOUND DEHISCENCE
➢ Rupture of wound
EXCESSIVE FORMATION OF REPAIR
COMPONENTS
➢ Keloid / hypertrophic scar (excess collagen)
➢ Exuberant granulation or proud flesh (excessive
granulation tissue that protrudes above the level of the
surrounding skin and impairs the growth of epithelium)

50. WOUND DEHISCENCE

51. KELOID / HYPERTROPHIC SCAR
➢ Raised scars due to accumulation of excess amounts of
collagen ( type III – type I)
➢ Hypertrophic scars do not grow beyond the boundaries
of the original wound
➢ Keloids grow beyond the boundaries of the original
wound (more serious)

52. HYPERTROPHIC SCAR

53. KELOID

54. EXUBERANT GRANULATION (PROUD
FLESH)
➢ Excessive granulation tissue
➢ Protrudes above surrounding skin
➢ Prevents re –epithelialization

55. EXAGGERATED CONTRACTION
➢ Deformation of surrounding tissue or wound
➢ Can compromise the movement of joints
➢ Most common on palms, soles, anterior thorax
following severe burns