wound (1).pptx basic of inflammation part 1

VinodKumar3832 17 views 56 slides Jun 14, 2024
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About This Presentation

Surgery


Slide Content

INFLAMMATION

CARDINAL SIGNS RUBOR CALOR DOL AR TUMOUR FUNCTION LAESA

TYPES OF INFLAMMATION 1. Acute inflammation 2. Chronic inflammation

ACUTE INFLAMMATION PHASES OF ACUTE INFLAMMATION Vascular phase Cellular phase

VASCULAR PHASE 1.vasoconstriction 2.vasodilation 3.increased vascular permeability 4. Stasis

CELLULAR PHASE 1. Margination 2. Rolling 3. Adhesion 4. Diapedesis 5. chemotaxis 6.phagocytosis

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

NATURE OF CELL LABILE CELL. STABLE CELL. PERMANENT CELL epithelial cells. Liver, Striated muscle Cardiac muscle Neuron

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

DIRTY WOUND Abscess drainage Pyocele Empyema gallbladder Faecal peritonitis

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

Absorptive dressings Hydrogels Hydro fibre Alginates

ABSORPTIVE DRESSING Hydrogel Hydrofibres Alginates These dressings absorbs fluids (exudates) 20 times their weight

GROWTH FACTORS PgE1 - chronic ulcers Interleukin 1. -pressure ulcers GM-CSF. - venous stasis ulcers rhPDGF. - diabetic venous ulcers (FDA Approved – becaplermin)

Hyperbaric oxygen collagen
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