Presentation on normal wound healing and types of wounds.

1. Wound healing and factors
affecting healing
Dr Preetinder Brar

2. Wounds, healing and tissue repair
5.1
Describe normal wound healing and factors
affecting wound healing
5.2
Elicit, document and present a history in a patient
presenting with wounds
5.3
Differentiate various types of wounds, plan and
observe management of wounds

3. Wound healing
• Wound healing is a mechanism whereby the
body attempts to restore the integrity of the
injured part.
• However, this falls far short of the
regeneration of tissue by pluripotent cells,
seen in some amphibians.

6. Wound healing
It is often detrimental, as seen in the problems
created by scarring such as
• Adhesions,
• Keloids,
• Contractures and
• Cirrhosis of the liver.
However, a clean incised wound in a healthy
person where there is no skin loss will follow a set
pattern.

7. Wound healing
NORMAL WOUND HEALING
• This is variously described as taking place in 3
or 4 phases, the most commonly agreed
being:
1. The inflammatory phase;
2. The proliferative phase;
3. The remodelling phase (maturing phase).

9. Normal wound healing
• Occasionally, a haemostatic phase is referred
to as occurring before the inflammatory
phase, or a destructive phase following
inflammation consisting of the cellular
cleansing of the wound by macrophages.

10. Normal wound healing
• The inflammatory phase begins immediately
after wounding and lasts 2-3 days.
• Bleeding is followed by vasoconstriction and
thrombus formation to limit blood loss.
• Platelets stick to the damaged endothelial
lining of vessels, releasing adenosine
diphosphate (ADP), which causes
thrombocytic aggregates to fill the wound.

11. (a) Early inflammatory phase with platelet-enriched blood
clot and dilated vessels.

13. Normal wound healing
• When bleeding stops, the platelets then
release several cytokines from their alpha
granules.

14. Normal wound healing
1. Platelet derived growth factor (PDGF),
2. Platelet factor IV and
3. Transforming growth factor beta (TGFβ).
• These attract inflammatory cells such as
polymorphonuclear lymphocytes (PMN) and
macrophages.

15. Normal wound healing
• Platelets and the local injured tissue release
vasoactive amines such as
1. Histamine,
2. Serotonin and
3. Prostaglandins, which increase vascular
permeability, thereby aiding infiltration of
these inflammatory cells.

16. (b) Late inflammatory phase with increased vascularity
and increase in polymorphonuclear cells and lymphocytes
(round cells)

17. Normal wound healing
• Macrophages remove devitalised tissue and
micro-organisms while regulating fibroblast
activity in the proliferative phase of healing.
• The initial framework for structural support of
cells is provided by fibrin produced by
fibrinogen.
• A more historical (Latin) description of this
phase is described in 4 words: rubor (redness),
tumor (swelling), calor (heat) and dolor (pain).

19. Normal wound healing
The proliferative phase lasts from the 3rd day to
the 3rd week consists of
1. Fibroblastic activity with the production of
collagen and ground substance
(glycosaminoglycans and proteoglycans)
2. The growth of new blood vessels as capillary
loops (angioneogenesis)
3. Re-epithelialisation of the wound surface.

21. Normal wound healing
• Fibroblasts require vitamin C to produce
collagen.
• The wound tissue formed in the early part of
this phase is called granulation tissue.
• In the latter part of this phase, there is an
increase in the tensile strength of the wound
due to increased collagen, which is at first
deposited in a random fashion and consists of
type III collagen.

22. Normal wound healing
• This proliferative phase with its increase of
collagen deposition is associated with wound
contraction, which can considerably reduce
the surface area of a wound over the first 3
weeks of healing.

23. (c) Proliferative phase with capillary buds and
fibroblasts.

25. Normal wound healing
The remodelling phase is characterised by
maturation of collagen (type I replacing type
III until a ratio of 4:1 is achieved).
• There is realignment of collagen fibres along
the lines of tension, decreased wound
vascularity and wound contraction due to
fibroblast and myofibroblast activity.

26. Normal wound healing
• This maturation of collagen leads to increased
tensile strength in the wound which is
maximal at the 12th week post injury and
represents approximately 80% of the
uninjured skin strength.

27. (d) Mature contracted scar.

28. Wounds, healing and tissue repair
NORMAL HEALING IN SPECIFIC TISSUES
• Bone
• Nerve
• Tendon

29. Normal healing in specific tissues
Bone
• The phases are the same, but periosteal and
endosteal proliferation leads to callus
formation, which is immature bone consisting
of osteoid (mineralised by hydroxyapatite and
laid down by osteoblasts).
• In the remodelling phase, cortical structure
and the medullary cavity are restored.

30. Normal healing in specific tissues
• If fracture ends are accurately opposed and
rigidly fixed, callus formation is minimal and
primary healing occurs.
• If a gap exists, then secondary healing may
lead to delayed union, non-union or malunion.

31. Normal healing in specific tissues
Nerve
• Distal to the wound, Wallerian degeneration
occurs.
• Proximally, the traumatic degeneration
extends as far as the last node of Ranvier.
• The regenerating nerve fibres are attracted to
their receptors by neurotropism, which is
mediated by growth factors, hormones and
other extracellular matrix trophins.

32. Normal healing in specific tissues
• Nerve regeneration is characterised by
profuse growth of new nerve fibres which
sprout from the cut proximal end.
• Overgrowth of these, coupled with poor
approximation, may lead to neuroma
formation.

33. Normal healing in specific tissues
Tendon
• While following the normal pattern of wound
healing, there are two main mechanisms
whereby nutrients, cells and new vessels
reach the severed tendon.
1. Intrinsic, which consist of vincular blood flow
and synovial diffusion

34. Normal healing in specific tissues
2. Extrinsic, which depends on the formation of
fibrous adhesions between the tendon and
the tendon sheath.
• The random nature of the initial collagen
produced means that the tendon lacks tensile
strength for the first 3-6 weeks.

35. Normal healing in specific tissues
• Active mobilisation prevents adhesions
limiting range of motion, but the tendon must
be protected by splintage in order to avoid
rupture of the repair.

36. Wound healing
ABNORMAL HEALING
• Some of the adverse influences on wound
healing are listed below:

46. Factors influencing wound healing
• Site of wound
• Structures involved
• Mechanism of wounding
• Incision
• Crush
• Crush avulsion
• Contamination (foreign bodies/bacteria)
• Loss of tissue
• Other local factors
• Vascular 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, AIDS)
• smoking

47. Abnormal healing
• Delayed healing may result in loss of function
or poor cosmetic outcome.
• The aim of treatment is to achieve healing by
primary intention and so reduce the
inflammatory and proliferative responses.

48. Classification of wound closure and healing
• Primary intention
– Wound edges apposed
– Normal healing
– Minimal scar
• Secondary intention
– Wound left open
– Heals by granulation, contraction and epithelialisation
– Increased inflammation and proliferation
– Poor scar
• Tertiary intention (also called delayed primary intention)
– Wound initially left open
– Edges later opposed when healing conditions favourable

49. Abnormal healing
Healing by primary intention is also known as
healing by first intention.
• This occurs when there is apposition of the
wound edges and minimal tissue trauma that
causes least inflammation and leaves the best
scar.

50. Abnormal healing
• Delayed primary intention healing occurs
when the wound edges are not opposed
immediately, which may be necessary in
contaminated or untidy wounds.

51. Abnormal healing
• The inflammatory and proliferative phases of
healing have become well advanced when
closure of the wound is carried out.
• This is also called healing by tertiary intention
in some texts and will result in a less
satisfactory scar than after healing by primary
intention.

52. Abnormal healing
Secondary healing or healing by secondary
intention occurs in the wound that is left open
and allowed to heal by granulation, contraction
and epithelialisation.

69. THE END