CHAPTER 01: WOUND AND TISSUE EXPANSION Flashcards
Describe the stages of wound healing
Wound healing involves several overlapping stages 1. Haemostasis - immediate - vasoconstriction, platelet plug and fibrin clot formation - clotting cascade activated 2. Inflammation - injury to 3 days - mast cells degranulate and release histamine - PDGF, TGFb and cytokines released by platelets attract o Neutrophils - produce inflammatory mediators and cytokines (peak at 24hrs) o Monocytes - become macrophages (peak 2-3 days) o Macrophages – produce cytokines and growth factors PDGF & TGFb, remove debris, stimulate collagen production and attract fibroblasts o Lymphocytes – unknown significance, possibly fibroblast recruitment and activation 3. Proliferation - 3rd day to 3wks - Fibroblasts – attracted by PDGF and TGFb (are D3, peak D7) - Collagen synthesis - Type III mainly - Angiogenesis - induced by VEGF - Re-epithelialisation 4. Remodeling - 6mths - 1yr - Type III collagen replaced by type I until a ratio I:III of 3:1 reached as in normal tissue - Wound tensile strength increases as disorganised collagen becomes lamellar along tension lines and cross-links - Vascularity decreases - Fibroblasts mature into myofibroblasts and cause wound contraction by forming cell-cell contacts - Peak tensile strength reached at 60 days (80% pre-injury level)
How do you classify factors that affect wound healing?
Systemic factors - Acquired - Congenital Local
What are the factors that affect wound healing?
Systemic conditions - congenital Systemic conditions -acquired Nutrition Environmental Endocrine Pharmacological Age Smoking Local IIRBCTNM infection Iatrogenic Radiotherapy Blood supply Chemotherapy Trauma Neuropathy Mechanical stress Patient factors Age Nutrition Systemic illness Diabetes - (infection, vascular disease and reduced oxygenation, neuropathy) Drugs - steroids, NSAIDS, chemo Genetic - ehlers danlos, cutis laxa, EB, progeria Wound factors Infection Oedema Denervation Radiation
What are the congenital systemic factors affecting wound healing?
Systemic factors - Congenital Ehlers-Danlos (cutis hyperelastica) - heterogenous collection of connective tissue disorders - results from collagen synthesis, cross-linking or structural defects - characterised by fragile hyper elastic skin, - joint hypermobility, aortic aneurysm Pseudoxanthoma elasticum - increased collagen degradation - AR - angina, aneurysms, retinal detachment, angioid streaks Cutis Laxa - defective elastic tissues (non-functioning elastase inhibitor) - coarse drooping skin, aneurysm, pneumothorax, emphysema, congenital cardiac disease, hernias - no problems with wound healing Epidermolysis bullosa - skin v susceptible to mechanical stress - Nikolsky sign - blistering with minor trauma - severe form - extensive fibrosis, adduction contracture of thumbs, volar contactures of palms and digits, pseudosyndactyly Progeria
What are the acquired systemic factors of wound healing? NEEPAS
- Vit A - Vit C: essential cofactor for collagen synthesis - Vit E: membrane stabilizer, deficiency inhibits healing - Zinc: enzymes co-factor, accelerates healing - Albumin: indicator of nutritional status - Methionine: essential amino acid for inflammation Pharmacological - Steroids - ↓ inflammation, inhibit macrophages and wound healing, Vit A counteracts this - NSAIDs - ↓ collagen synthesis Environmental Temperature - ↑ healing > 30° C , ↓tensile strength < 12°C Endocrine - Diabetes - delayed wound healing, neuropathy, microangiopathy, low O2 delivery, impaired phagocytosis and bacterial killing. Age - ↓ cell multiplication - All stages of healing more protracted - ↓ tensile strength Smoking - Nicotine is sympathetic stimulant, causes vasoconstriction ↓ tissue perfusion - CO shifts the O2 dissociation curve to the left and reduces tissue oxygenation
What are the local factors affecting wound healing? Part 1
- Infection - Wounds over 100,000 organisms/g tissue are considered infected - Infection ↓ tissue PO2 , ↑ collagenase, prolongs inflammation - reduced leucocyte chemotaxis - Impaired angiogenesis and epithelialisation - Bacterial toxins and metabolites impair epithelialisation 2. Iatrogenic Manipulation - Surgery, rough handling and over diathermy, tension. 3. Radiation - Stasis and occlusion of small vessels. - Causes endothelial cell, capillary and arteriole damage. - Lymphatics damaged, oedema and ↑ risk of infection. 4. Chemotherapy - ↓ fibroblast proliferation and wound contraction. - Chemo best left until 10-14 days post op.
What are the local factors affecting wound healing? Part 2
- Blood supply - ↓ tissue perfusion = ↓ wound oxygenation - Fibroblast function ↓ in hypoxic tissue ↓ O2 delivery = ↓ collagen formation, ↓ extracellular matrix, ↓Angiogenesis, ↓ epithelialisation 6. Trauma - Disrupts the neo-epidermis 7. Neural Supply - Wound in denervated tissue heal slowly. (pressure sores, DM) - ↑ collagenase activity 8. Mechanical Stress - Affects quality, aggregation and orientation of collagen fibres - ↑Tension = blanching → necrosis and rupture → stretching
How does epithelialisation occur?
Epithelialisation = the process by which epithelial continuity is re-established across a wound. 1. Mobilisation → cells at wound edges enlarge and flatten, detach from neighbouring cells and basement membrane. Move away from adjoining cells. 2. Migration → ↓ contact inhibition promotes cell migration across wound (epithelial stream) until they meet other cells from opposite wound edge. Contact inhibition then reinstituted and migration stops. 3. Mitosis (Proliferation) → during migration cell numbers are maintained by mitosis of the fixed basal cells away from the wound edges. Epithelial cells begin to proliferate once they have covered the surface of the wound. 4. Cellular differentiation → Normal structure of the stratified squamous epithelium is re-established.
How do skin grafts take?
full thickness vs split thickness contraction (physiological), contracture (pathological) Stages of skin graft take 1. Adherence (fibrin) (48hrs) 2. serum imbibition (first 2-4 days) - surrounding fluid absorbed, SG swells 3. Revascularisation (4-5 days) - inosculation: vessels in graft and bed kiss - revascularisation: new vessels in bed grow into graft vessels - neovascularisation: new vessels grow into g 4. Remodelling
why do skin grafts fail?
HIS SHIT!! Haematoma Infection Seroma SHear Inappropriate bed (bare cartilage, bone, tendon) Technical error
Foetal Wound Healing
1st 3 mths of foetal life - tissue healing by regeneration and not scarring regenerative healing - no scars - less inflammation - rapid epithelialisation - less angiogenesis - foetal fibroblasts migrate faster - more type 3 than 1 collagen, more organised (other way round?) - wound contains more hylauronic acid - more TGF beta 3, less 1&2 - Tenascin (cytotactin)
Microvascular anastomosis healing
necrosis between sutures neo-intimal hyperplasia, loss of media remodelling endothelial migration
What are the layers of skin?
Epidermis - Colin Likes Grilled Spicy Beef - Stratum corneum - lucidum - granulosum - spinosum - basale Dermis - papillary - reticular
What are the functions of skin?
control of fluid loss thermoregulation barrier against micro-organisms sensation immunology and metabolism (e.g. vit D)
What is a pressure sore?
A wound acquired by prolonged unrelieved pressure over a bony prominence leads to ischaemic necrosis if the tissue pressure is greater than perfusion pressure. It results from extrinsic factors and is propagated by intrinsic factors. Muscle is more susceptible than skin. Necrosis begins near bone leading to cone shaped area of tissue necrosis with apex at the skin.
Where are pressure sores found?
ischium greater trochanter sacrum heel malleolus occiput
What is the pathogenesis of pressure sores?
initiated by extrinsic factors, propagated by intrinsic factors hyperaemia -> ischaemia -> necrosis -> ulceration -> (Marjolins) EXTRINSIC Pressure Shear Friction INTRINSIC General factors - Age - Malnutrition - protein, carb, Vit A,C, Zn, Fe - Incontinence - Immobilisation - Systemic disease: diabetes, vascular disease, smoking Wound factors - ischaemia - insensate - decreased autonomic control - infection
Can you summarise the Waterlow score?
10 - at risk 15 - high risk 20 - very high risk A - Appetite - Age,sex - Ambulation - Anaemia B - Build and weight C - Skin type - Steroids/NSAIDS - Smoking - Surgery (ortho / #below waist) - Sensory disturbance (DM, paraplegia, CVA)
Waterlow Score
Assesses pressure sore risk 1. build, weight 2. skin type 3. continence 4. mobility 5. age sex 6. malnutrition Special risks - Tissue malnutrition - Neurological deficit - Major surgery / trauma - Medication 10-14 risk 15-19 high risk 20+ v high risk OTHER SCORES Braden, Norton
EPUAP - Grading of pressure sores (European Pressure Sore Advisory Panel)
I non-blanchable erythema II partial skin loss III full thickness skin loss IV full thickness tissue loss (exposed tendon, muscle, bone)
How can pressure sores be prevented?
Conservative, medical, surgical Conservative - skin care (clean, dry, urinary faecal diversion) - pressure dispersion (low air loss mattress, Roho cushions) - pressure awareness - bed turn 2hrly, seated lift 10secs every 10mins Medical - positioning - baclofen, diazepam, botox Surgical - release of contractures, cordotomy
How do you manage pressure sores?
Grade 1-2 pressure relief - minimise risk factors - wound dressings - duoderm, opsite, mepilex, flamazine Grade 3-4 - as above - debride non-viable tissue Dressing types - wet - dry - debriding (collagenase) - antimicrobial (flamazine) - occlusive (alginate, hydrocolloid) - growth factors - maggot therapy - VAC
How do you diagnose and treat osteomyelitis in pressure sores?
bone biopsy bone scan MRI - 98% sensitive, 90% specific Treatment - aggressive debridement, 6wk Abx, reg dressings
What are the indications for surgery on pressure sores?
Emergency - if pt septic Non-emergency, then full investigation correct predisposing factors prevent recurrence postop do not op if deteriorating delay op if pt mobility improving VAC good adjunct motivated, young, clinically stable / improving, compliant postop physio, social support
What are the principles of surgery on pressure sores?
radical debridement obliterate dead space reconstruct with durable skin use readvanceable flaps, don’t burn bridges! design as large as poss suture lines away from pressure areas large drains 2wks
What postop care is needed for pressure sores?
Drains Antibiotics optimise nutritional status special mattress Skin care frequent turning, pressure relief from op site 4-6wks control of spasm urinary and faecal diversion gradual reintroduction of sitting over 2wks Patient education
What complications are associated with pressure sore surgery?
haematoma infection dehiscence recurrence marjolins ulcer
What flaps are available for pressure sore recon?
SACRAL buttock rotation gluteus maximus musculocutaneous (rotation / VY advancement) - sup and inf gluteal arteries gluteus maximus muscle (type III) & SSG SGAP lumbosacral, transverse back flaps ISCHIAL lower gluteal flaps FC/MC Hamstrings VY advancement flaps (long head of biceps femoris type II, profunda femoris) posterior (gluteal) thigh flap - medially or laterally based - descending branch of inferior gluteal artery gracilis (small) pedicled VRAM TFL - Transverse or descending branch of the lateral circumflex artery GREATER TROCHANTER TFL (VY / Hatchet) lat thigh FC - 1st lateral perforator of profunda femoris art rectus femoris vastus lateralis - transverse br of lateral circumflex femoral art, type I flap (free flaps)
What papers are there regarding longterm outcome of pressure sores?
Yamamoto PRS 1997 FRCS plast notes
What is the history of tissue expansion?
Neumann 1957 - air filled sub cut expander for postauricular skin & ear recon (not popular) Radovan 1975 - silicone expander for arm (1976) & breast (1982) Austad 1982 - histological changes
What histological changes are seen?
Epidermis thickens (cellular hyperplasia) Dermis thins Muscle thins Adipose tissue atrophies Nerves - altered conductivity
Can you define Mechanical creep Biological creep Stress-relaxation
- elongation of skin under a constant load over time - collagen fibres stretch out, become parallel - elastin microfragments - insterstitial fluid is displaced - e.g. stretching skin intraop 2. generation of new tissue secondary to persistent chronic stretching - e.g. pregnancy, tissue expansion 3. tendancy for resistance of skin to a stretching force to decrease when held at a given tension over time - e.g. initially tight when expanded, but not so tight after 1wk
What are the layers of a capsule?
Capsule - Microscopic appearance (Paysk) 1. Inner Zone → fibrin layer with macrophages 2. Central Zone → elongated fibroblasts and myofibroblasts 3. Transitional Zone → composed of loose collagen fibres 4. Outer Zone → blood vessels and collagen
What are the advantages and disadvantages of tissue expansion?
Adv - allows replacement of like with like tissue - best match, colour, texture, hairbearing quality, sensate Disadv - staged procedure, deformity during expansion, can only do on healed wounds - not good for SSG / radiotherapy skin
What are the complications?
extrusion and wound dehiscence infection rupture migration
What is the technique for tissue expansion?
- place expander remote and radial to scar / defect 2. make the largest pocket possible, and choose expander base to fill pocket 3. place port remote to expander (or integral / self-expanding) 4. usu. capsule is kept after expansion 5. over expander e.g. in breast for more natural look
What is the experience on tissue expansion in limbs?
Overall high risk of complications (infection, migration, port movement, Most literature quote 40-50% complication rate place above muscle fascia
When are tissue expanders contraindicated?
- Open wounds - Immature scar - Irradiation - Under skin graft
How are expanders classified?
- Saline filled bags - Shape → oval, rectangle, round, square, crescentric (shorter donor defect as most expansion over central area) - Size → base dimension, projection when inflated - Location of port → Integral or remote, subcut or external - Envelope → smooth or textured, uniform shell or variable thickness to allow preferential expansion in certain directions. May have stiff backing
How is expansion performed?
Intraoperative o Sustained traction o Tissue expansion with foley o Sureclosure devices Rapid Expansion - every 2-3 days o Most tissue creep and growth occurs in first 2 days after expansion Conventional Expansion o weekly o tissues to stabilise b/t expansions o Stop when gain sufficient (overexpand slightly)
What are the complications of tissue expansion?
Haematoma, Infection, exposure, extrusion, pain, neuropraxia, pressure effects
