Wound Healing Flashcards
Epidermis
External surface of skin consisting of keratinised squamous epithelium
Dermis
Dense fibroelastic connective tissue with rich vascular and sensory receptors
Hypodermis
Also subcutaneous layer containing adipose tissue
Pathophysiology of wound healing
1) Acute inflammatory phase
2) Proliferative phase
3) Maturation phase
1) Tissue injury
Platelet activation
Clot formation
Complement activation
ACUTE INFLAMMATORY PHASE
2) Acute inflammatory phase
Vasodilation Vascular permeability Influx of fibroblasts and neutrophils Release of cytokines and growth factor PROLIFERATION PHASE
3) Proliferation phase
Fibroblasts 4-5 days ECM deposition)
Endothelial cells (Angiogenesis is triggered simultaneously as fibroblast activation, matrix metalloproteinases require zinc and ia proteolysis allow endothelial cell passage)
Keratinocytes/epithelial cells (wound closure usually within 48hrs)
3b) Proliferation phase
Epithelialisation
Angiogenesis
Collagen synthesis
Wound healing, maturation phase and remodelling
Cell types and timing
Platelets....immeddaysiate Neutrophils...0-1 day Macrophages...1-2 days Fibroblasts...2-4 days myofibroblasts...2-4 days Endothelial cells...3-5 days
Maturation and remodelling phase
Reduced vasculature causing change in scar colour
Tensile strength change as triple alpha helix collagen forms fibrils and cross links become stronger (aided by vit C)
Wound strength
Strength initially increases vquickly first 7-10days
Wounds usually take up to 12-18months to regain full maturation
Bowel and muscle-1 month
Skin-6 months
Wound healing types
Primary intention
Secondary intention
Tertiary intention
Bone and callus Primary healing
Primary bone healing occurs if fracture gap is 1-2mm, stabilised and anatomically reduced with good stable blood supply. This allows Haversian remodelling to occur and no callus formation
Bone and callus Secondary healing: Haematoma
Haematoma formation: Rupture of blood vessels within the medullary cavity, haematoma fills the fracture gap and surrounding tissues
Haematoma walls off fracture site and fills it with an influx of inflammatory cells, fibroblasts and capillary vessels
Bone and callus Secondary healing: Inflammatory Phase
Necrotic areas of fracture release inflammatory markers promoting neutrophil chemotaxis
Neutrophils release cytokines including TGF-b and fibroblast growth factor activating osteoprogenitor cells
Bone and callus Secondary healing: Repair Phase
Post 1 week haematoma–>soft callus
Soft callus–>fibrous matrix
Fibrous matrix–>cartilaginous phase–>bony callus
Hard callus is formed by osteoblasts placing woven bone beneath periosteum
Bone and callus Secondary healing: Remodelling Phase
Remodelling takes place over months and years following a fracture.
Haversian remodelling replaces disordered callus with lamellar bone (more organised)
Wolff’s law dictates internal architecture of bone alters in response to the varying loads placed upon it
Wound healing in Tendon, Nerve
Upper limb fracture, Lower limb fracture
Tendon: 3-5 weeks partial mobility, 5-12 full mobility, >12 full strength
Nerve: 4-6 weeks cast immobilisation of joint above/below, >6 weeks to free mobility
Upper limb fracture: 3-4weeks in cast
Lower limb fracture: 6-8 weeks, 3/4wks protected weight bearing, 12-16wks full wt bearing
Nerve injury overview (III)
Neuropraxia (I)-No axonal injury
Axonotmesis (II)-Axonal injury but preservation of the support framework
Neurotmesis(III-V)-Support framework lost
Principles of nerve repair
1) Apposition of nerve ends
2) Healthy tissue surrounding
3) No tension
4) Minimal dissection
Neuropraxia
Mildest form of injury
Crush, contusion or stretch
The axon is preserved but there is a loss or reduction of signal along a segment of the nerve causing a temporary loss of function (hrs-months) average recovery is 6-8weeks.
Motor>Sensory>Autonomic
Axonotmesis
Axonal disruption with preservation of the epineurium and perineurium. Wallerian degeneration occurs at the distal axon (anterograde) with a degree of retrograde degeneration of the remaining proximal axon.
Recovery occurs along the preserved framework, the proximal axon regenerates 2-3mm with the distal recovering 1mm per day. Recovery is slow taking weeks-months
Neurotmesis
Grade 3-5 Severity ranges up to complete transection of the axon but often involves internal disruption of the epi-,peri- and endo-neurium. Neuroma occurs at the proximal stump of the nerve III-Endoneurium IV-Perineurium V-Epineurium
Hepatocyte Regeneration
Initiation-TNF-a and IL-6
Sustained-HGF and TGF-b
Termination-TGF-b1
Delayed wound healing (nutritional factors)
Protein-ECM and immune response
Vitamin A-Epithelial cell proliferation and differentiation
Vitamin B6-Collagen cross-linking
Vitamin C-Hydroxylation of proline and lysine. Hydroxyproline-transports collage out of cells. hydroxylysine allows collagen cross linking
Zinc-Metalloproteinases
Copper-Collagen to elastin cross linking
