The document discusses the stages of wound healing including hemostasis, inflammation, proliferation, and remodeling, and the factors that influence wound healing such as wound type, patient health, and environmental conditions. It also covers abnormal wound healing which can result in hypertrophic or keloid scarring, and treatments for scarring including pressure therapy, steroid injections, and surgery.

1. Moderator: Dr.Gaurav Kaushal
Consultant, Dept. of Gen. Surgery
Max super speciality Hospital,
Mohali, Punjab
Presenter : Dr.Asif Mian Ansari
DNB Resident
Dept. of General surgery
Max super speciality Hospital,
Mohali, Punjab

3.  Break/breach in the integrity of skin or tissues
 Mechanism whereby the body attempts to restore the
integrity of the injured part
Wound healing

4.  Hemostasis & Inflammatory phase
 Proliferative phase
 Remodelling & maturing phase

5.  Wound directly exposes the ECM to platelets  platelets
aggregation  degranulation  activation of coagulation
cascade  formation of clot
 Platelets α-granules  PDGF,TGF-β, PAF, fibronectin, vWF,
serotonin
 Other chemoattractants (complement factors, IL-1,TNF-α,
TGF-β, PF4)
 Fibrin clot assists influx of neutrophils first, then macrophages
and lymphocytes also recruited

6.  first to arrive, peak 24-48h
 Phagocytosis of bacteria & tissue debris
 SecreteTNF-α  Angiogenesis & collagen synthesis
 Release proteases (collagenases)  degrade matrix and
ground substance in early wound healing

7.  Second in sequence  peak 48-96h
 Phagocytosis, O2 radical & nitric oxide
 Activation & recruitment of other cells
 Regulate cell proliferation, matrix

8.  Peak in 1 week
 Bridging from inflammatory to proliferative phase
 Decrease strength &collagen & Down regulating effect on
fibroblast
 Stimulate collagan synthesis by IL-1,TNF-α, IFN-gamma
release
rubor (redness), tumour (swelling), calor (heat) and dolour (pain)

9.  Starts from Day 3 & remains up to 3rd week
 1. PDGF recruits fibroblasts which proliferate  collagen type
III and ground substance (glycosaminoglycans and
proteoglycans)
 2. Angiogenesis of capillaries
 3. Re-epithelization
Granulation tissue

10.  3rd week to several months
 Collagen realignment along tension lines
 Type I collagen replacesType III collagen up to 4:1 ratio
 Myofibroblast activity
 Wound contraction
 Decrease wound vascularity
 Scar formation

13.  Primary intention
 Secondary intention
 Tertiary intention or delayed primary healing

14.  Wound edges opposed
 Normal healing
 Minimal scar
 E.g. surgical incision

15.  Wound left open
 Heals by granulation, contraction and epithelialisation
 Increased inflammation and proliferation
 Poor scar
 E.g. wounds with infection, excessive trauma, tissue loss

16.  Wound initially left open
 Edges later opposed when healing conditions favourable

17.  Site of the wound
 Structures involved
 Mechanism of wounding
 Incision
 Crush
 Crush avulsion
 Contamination (foreign bodies/bacteria)
 Loss of tissue
 Vascular insufficiency (arterial or venous)

18.  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

19.  Maturation phase of wound healing to formation of scar
 Immature scar –
 Pink, hard, raised & itchy
 Disorganised collagen fibers
 Lasts for over one year
 Mature scar –
 Collagen fibers realignment along stress tine
 Become denser, less cellular, less vascular, paler, flat and decreased r
absent itchiness. Maturation takes 2 to 3 years
 Maximum tensile strength  80 per cent that of normal skin

20.  Atrophic scar
 Hypertrophic scar
 Keloid formation

21.  Atrophic scar:
 Pale, flat and stretched
 Often appearing on the back and areas of tension
 Easily traumatised as the epidermis and dermis are thinned
 Excision and resuturing may only rarely improve such a scar

22.  Usually develop within 4 weeks of trauma
 Stay within the original wound
 Elevated less than 4 mm
 Result of prolonged inflammatory phase
 Develop across the lines of skin tension
 Histology  Excess collagen with hypervascularity

23.  15 times more common in pts with darker skin
 Strong genetic predisposition
 Develop 3 months-years after trauma
 Expand beyond wound edges, can become large
 Common site - triangle whose points are the xiphisternum
and each shoulder tip
 Histology  Excess collagen with hypervascularity more than
hypertrophic scar

25.  Pressure – local moulds or elasticated garments
 Silicone gel sheeting
 Intralesional steroid injection (triamcinolone)
 Excision and steroid injections
 Excision and postoperative radiation
 Intralesional excision (keloids only)
 Laser – to reduce redness (which may resolve in any event)
 Vitamin E or palm oil massage
 Very high rate of recurrence (keloid > hypertrophic)