IMMEDIATE AND TRANSIENT RESPONSE ( low grade inflammation) Ex : Coffee spillage 10 mins IMMEDIATE AND SUSTAINED RESPONSE (moderate inflammation) Ex : cooking boil – 12 -24 hrs Delayed and prolonged response Ex : Radiotherapy 2 weeks
WOUND HEALING Dr.vinod kumar
What is wound healing ? The process of repair The process of wound healing has been defined by Davidson as succession of cellular events which are co-ordinated by the release and recognition of soluble mediators.
•2000 B.C. Spiritual methods Physical methods •Egyptians Infected Non infected • Ebers Papyrus(1550 B.C.) Honey, Lint, Grease HISTORY
HISTORY 1822-1895 LOUIS PASTEUR – theory of spontaneous generation JOSEPH LISTER – credited with the discovery of antisepsis 1876 ROBERT JOHNSON – antiseptic dressing in the form of cotton gauge impregnated with iodoform 1960s and 1970s led to the development of polymeric dressings
INTRODUCTION Wound healing is a mechanism where the body attempts to restore the integrity of injured part Regeneration – without scar Repair _ with scar Falls short as tissue regeneration is by pluripotent cells
Mainly depends on 1. Nature of cell 2. Severity of injury
FACTORS AFFECTING WOUND HEALING Site of wound Structure involved Mechanism of wound Loss of tissue Malnutrition Medications (steroids) Immune deficiencies
CLASSIFICATION Based on thickness of wound 1. Superficial wound 2. Partial thickness wound 3. Full thickness wound
CLASSIFICATION OF SURGICAL WOUNDS CLEAN SURGERY Surgeries of Heart, brain, joints, transplants Excisions herniorrhaphy
CLEAN CONTAMINATED WOUND Bowel surgeries without spillage of contents Gallbladder, biliary and pancreatic surgeries appendicectomy
Contaminated wound Open fresh accidental wounds Bowel injuries with spillage contents
PHASES OF WOUND HEALING 1. BLEEDING AND CLOT FORMATION 2. INFLAMMATORY PHASE 3. PROLIFERATIVE PHASE 4. REMODELLING PHASE
BLEEDING AND CLOT FORMATION When an injury occurs, TXA2 ADP VWD are relesed These factors activates platelets which forms the platelet plug which is temporory
permanent plug is formed by activation of clotting factors Extrinsic pathway Intrinsic pathway
INFLAMMATORY PHASE Starts immediately after an injury Lasts for 2-5 days 0-24 hrs neutrophils will enter in to the site Next 2-3 days macrophages enter in to the site
Macrophages engulf debris and neutrophils Macrophages gets activated and releases substances VEGF BETA-FGF PDGF TGF-BETA
PROLIFERATIVE PHASE 5days to 3 weeks Granulation tissue is formed Re-epitheliasation of wound surface Granulation tissue initially contains blood vessels and collagen type III
REMODELLING PHASE As the time progresses collagen typeIII is replaced by collagen type I Blood vessels will disappear Wound gets contracts due to fibroblasts and myofibroblasts Finally only collagen typeI is left which is called as scar
REMODELLING Continue-sly takes place to make the scar tissue strength as normal tissue But, it never attains It attains maximum of 70-80% by 3 months to 1 year
NORMAL HEALING IN BONE Phases of healing are similar But, endosteal and periosteum proliferation leads to formation of osteoid. In REMODELLING phase, cortical structure and medullary cavity are restored
NORMAL HEALING IN NERVE Distal to wound wallerian degeneration occurs Proximal to wound, traumatic degeneration occurs. Nerve regeneration occurs from proximal end
TYPES OF WOUND HEALING
Wound edges opposed with sutures There is more epithelial regeneration than fibrosis Normal healing Minimal scar PRIMARY INTENSION
SECONDARY INTENSION It occurs in a wound with extensive tissue loss (wound left open) It heals mainly by fibrosis Heals by granulation, contraction and epithelialisation leading to poor scar, often hypertrophied and contracted
TERTIARY INTENSION Also called as delayed primary closure After wound debridement and control of wound infection, wound is closed with sutures
ABNORMAL SCARS
Due to proliferation of mature fibroblasts and mature blood vessels Limited only to previous scar More commonly seen in flexor surfaces No family ,no genetic predisposition HYPERTROPHIC SCAR
KELOIDS Due to proliferation of immature fibroblasts and immature blood vessels It may happen from previous scar or any where in the body without scar It extends to normal skin genetic predisposition to negroes
CONTRACTURES Scar crossing joints or flexion creases may lead to formation of tight webs known as contractures This may lead to hyperextension or hyperflexion Treated by grafts or flaps or z plasties
SILVER Siliver helps both in prevention and for treatment of infection S ilver has broad spectrum antibiotic coverage Elemental silver require ionisation for its anti microbial activity
MECHANISM OF ACTION Ag + proteins,DNA,RNA, chloride ions Silver product will be more effective when it has more residual activy
Minimum concentration of silver should be 30-40mg/l Silver sulfadizine Silver nitrate Nano crystalline silver Basing on residual capacity nanocrystalline silver > silver nitrate > siliver sulphasalazine
ADVANCED DRESSING Occlusive type Tegaderm Duoderm These products are permeable to air and water vapour But not to fluids and micro organisms