CHAPTER 01: WOUND AND TISSUE EXPANSION

Question 1

Describe the stages of wound healing

Answer 1

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)

Question 2

How do you classify factors that affect wound healing?

Answer 2

Systemic factors - Acquired - Congenital Local

Question 2

What are the factors that affect wound healing?

Answer 2

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

Question 3

What are the congenital systemic factors affecting wound healing?

Answer 3

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

Question 4

What are the acquired systemic factors of wound healing? NEEPAS

Answer 4

• 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

Question 5

What are the local factors affecting wound healing? Part 1

Answer 5

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.

Question 6

What are the local factors affecting wound healing? Part 2

Answer 6

5. 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

Question 7

How does epithelialisation occur?

Answer 7

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.

Question 8

How do skin grafts take?

Answer 8

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

Question 9

why do skin grafts fail?

Answer 9

HIS SHIT!! Haematoma Infection Seroma SHear Inappropriate bed (bare cartilage, bone, tendon) Technical error

Question 10

Foetal Wound Healing

Answer 10

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)

Question 11

Microvascular anastomosis healing

Answer 11

necrosis between sutures neo-intimal hyperplasia, loss of media remodelling endothelial migration

Question 12

What are the layers of skin?

Answer 12

Epidermis - Colin Likes Grilled Spicy Beef - Stratum corneum - lucidum - granulosum - spinosum - basale Dermis - papillary - reticular

Question 13

What are the functions of skin?

Answer 13

control of fluid loss thermoregulation barrier against micro-organisms sensation immunology and metabolism (e.g. vit D)

Question 14

What is a pressure sore?

Answer 14

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.

Question 15

Where are pressure sores found?

Answer 15

ischium greater trochanter sacrum heel malleolus occiput

Question 16

What is the pathogenesis of pressure sores?

Answer 16

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

Question 17

Can you summarise the Waterlow score?

Answer 17

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)

Question 18

Waterlow Score

Answer 18

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

Question 19

EPUAP - Grading of pressure sores (European Pressure Sore Advisory Panel)

Answer 19

I non-blanchable erythema II partial skin loss III full thickness skin loss IV full thickness tissue loss (exposed tendon, muscle, bone)

Question 20

How can pressure sores be prevented?

Answer 20

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

Question 21

How do you manage pressure sores?

Answer 21

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

Question 22

How do you diagnose and treat osteomyelitis in pressure sores?

Answer 22

bone biopsy bone scan MRI - 98% sensitive, 90% specific Treatment - aggressive debridement, 6wk Abx, reg dressings

Question 23

What are the indications for surgery on pressure sores?

Answer 23

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

Question 24

What are the principles of surgery on pressure sores?

Answer 24

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

Question 25

What postop care is needed for pressure sores?

Answer 25

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

Question 26

What complications are associated with pressure sore surgery?

Answer 26

haematoma infection dehiscence recurrence marjolins ulcer

Question 27

What flaps are available for pressure sore recon?

Answer 27

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)

Question 28

What papers are there regarding longterm outcome of pressure sores?

Answer 28

Yamamoto PRS 1997 FRCS plast notes

Question 29

What is the history of tissue expansion?

Answer 29

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

Question 30

What histological changes are seen?

Answer 30

Epidermis thickens (cellular hyperplasia) Dermis thins Muscle thins Adipose tissue atrophies Nerves - altered conductivity

Question 31

Can you define Mechanical creep Biological creep Stress-relaxation

Answer 31

1. 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

Question 32

What are the layers of a capsule?

Answer 32

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

Question 33

What are the advantages and disadvantages of tissue expansion?

Answer 33

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

Question 34

What are the complications?

Answer 34

extrusion and wound dehiscence infection rupture migration

Question 35

What is the technique for tissue expansion?

Answer 35

1. 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

Question 36

What is the experience on tissue expansion in limbs?

Answer 36

Overall high risk of complications (infection, migration, port movement, Most literature quote 40-50% complication rate place above muscle fascia

Question 37

When are tissue expanders contraindicated?

Answer 37

- Open wounds - Immature scar - Irradiation - Under skin graft

Question 38

How are expanders classified?

Answer 38

- 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

Question 39

How is expansion performed?

Answer 39

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)

Question 40

What are the complications of tissue expansion?

Answer 40

Haematoma, Infection, exposure, extrusion, pain, neuropraxia, pressure effects

Question 41

What is transplantation?

Answer 41

= Movement of tissue from one body location to another - Orthotopic → transplant to an anatomically similar site - Heterotopic → different site

Question 42

What are the different types of transplants?

Answer 42

Autograft - from 1 location to another within the same individual o Includes all flaps and grafts o Flaps have some intrinsic blood supply grafts don’t Isograft - between genetically identical twins Allograft (Homograft) between same species Xenograft (Heterografts) - between different species

Question 43

What is the 2nd set phenomenon?

Answer 43

Gibson and Medawar (1940s) First set reaction → when skin allograft is applied to an individual for the first time Second set phenomenon → accelerated rejection of allogenic tissue due to presence of humoral antibodies from prior exposure to the same allogenic source

Question 44

Allograft - 1st and 2nd set phenomena

Answer 44

First set o Days 1–3 allograft behaves as autograft → develop dilated capillaries with no blood flow o Days 4–7 grafts infiltrated by leucocytes and thrombi, punctate haemorrhages appear within vessels o Days 7–8 blood flow ceases and skin graft necrose Second set → occurs if individual has already been exposed to same allograft material o Immediate → hyperacute rejection, graft never undergoes any revascularisation → ‘white graft’

Question 45

What happens when grafts are rejected?

Answer 45

 Rejection occurs when the host immune system recognizes foreign antigens  Direct destruction – Cell mediated → CD4 and CD8 cytotoxic T cells cause damage to the graft  Indirect destruction – Antibody mediated → humoral system (stimulated B cells) produce antibody that binds with antigen and stimulates tissue destruction via complement system

Question 46

What are the different types of immunosuppression?

Answer 46

Non-specific - Radiation (graft) ↓ antigenicity - Drugs - Biological agents Specific - monoclonal anti T- lymphocyte antibodies

Question 47

Another classification of immunosuppressive drugs

Answer 47

Antibody mediated (biologic) 1. Antilymphocyte - antilymphocyte Ig, antithymocyte Ig, OKT3 2. Anti IL2 Non-biologic 1. Calcineurin inhibitors - cyclosporin, tacrolimus 2. Antiproliferative agents - azathioprine 3. Corticosteroids 4. Macrolide Inhibitors - sirolimus

Question 48

What are the ideal properties of an implant?

Answer 48

- Impervious to tissue fluid - Chemically inert - Non irritant (causing no inflammatory or foreign body reaction) - Noncarcinogenic - Nonallergenic - Resistant to mechanical strains - Capable of being fabricated to the desired form - Sterilisable - Readily available, cheap - Radiolucent - Resistant to reabsorption, corrosion or deformation - Non-supportive of growth of micro-organisms

Question 49

How do you classify them?

Answer 49

Liquids → silicone , collagen preparations, hyaluronic acid preparations Solids → metals, polymers, ceramics

Question 50

What is silicone?

Answer 50

- Silicon = element, silica = silicone oxide (sand) - Silicone = polydimethyl siloxane - interlinked silicon and oxygen molecules with methyl, vinyl or phenol side groups - Short polymer chains → viscous liquid, long chains → firmer cohesive gel - Cross linking of chains → solid silicone. - biologically inert but elicits a mild foreign body reaction → capsule formation - Synovitis can occur in silicone joint arthroplasty

Question 51

What collagen preps do you know?

Answer 51

Zyderm 1 o sterilised fibrillar bovine collagen o Used to inject fine superficial wrinkles Zyderm 2 o coarser wrinkles. Both Zyderms will ↓ as loose water component so over do by 30% initially. Zyplast o Cross linked collagen with glutaraldehyde o Firmer than Zyderm 1 or 2 o Treat deep dermal defects and coarse wrinkles, little resorption so DON’T overcorrect

Question 52

What hyaluronic acid preps do you know?

Answer 52

Hyaluronic Acid Preparations - Restylane and Perlane (Nufill!) - Synthetic hyaluronic acid - Absorption 20-50% of original volume by 6 months - Injected superficially to treat wrinkles or ↑ lip definition - HIV lipoatrophy

Question 53

What metals are used ?

Answer 53

Stainless Steel - alloy of iron, chromium and nickel - corrosion, implant failure, galvanic currents Vittalium - alloy of chromium, cobalt and molybdenum - higher tensile strength than titanium Titanium - pure metal, more malleable, less corrosion - less artefact on MRI CT Gold - resistant to corrosion, low tensile strength - eyelid weight to facilitate eye closure in facial palsy

Question 54

What polymers are there?

Answer 54

Polyurethane - Produces an intense foreign body reaction then tissue adhesion - Breast implants covered with polyurethane foam have a low rate of capsule contracture, but breakdown products → toluene-diamine dimers → ?carcinogenesis → implants withdrawn Fluorocarbons - Gortex polytetrafluoroethylene (PTFE) Polyethylene - Low density - High density → Medpore (facial augment) Methylmethacrylate - bone cement Cyanoacrylate - Superglue

Question 55

What ceramics are available?

Answer 55

Hydroxyapatite - major inorganic constituent of bone (the major organic constituent is osteoid) - in corals, available in block, granule or cement - osseoconductive → allows creeping substitution - not Osseoinductive or osteogenic - calvarial remodelling (inlay and onlay), facial augmentation - Inlay = replacement of full thickness defect - Onlay = outer table replacement Other ceramics - Calcium sulphate (plaster of Paris) - Calcium phosphate

Question 56

Describe nerve anatomy

Answer 56

Endoneurium (nerve cell - neurone, cell body, efferent axon, afferent dendrite) Perineurium (fascicle) Epineureum (peripheral nerve)

Question 57

What nerve fibre groups are there?

Answer 57

A-C - heavily myelinated →non-myelinated, diameter 20-0.5 micrometres, conduction speed 120-1.2 m/sec Group A o α fibres - motor o β fibres - touch, pressure o γ fibres → proprioception and motor tone o δ fibres → pain, temperature Group B o Myelinated , preganglionic autonomic (sympathetic) nerves Group C o Non-myelinated, postganglionic autonomic nerves - pain, temp (Chronic Pain – Gate Theory)

Question 58

What are local anaesthetics? What is the mechanism of action? What are the clinical characteristics?

Answer 58

An aromatic moiety connected to a substituted amine through an ester or an amide linkage M of A: - impair propagation of APs in axons - Acts on specific receptor site e.g. Na channel - Stability enhanced by adjusting pH of solns Clinical characteristics - Myelinated and smaller nerves are most affected Sequence of clinical anaesthesia are: - Vasodilation (B) - Loss of pain and temp sens (A-δ & C) - Loss of pressure sens (A-β) - Loss of motor function (A-α)

Question 59

How are local anaesthetics classified?

Answer 59

Amino-esters - metabolized by pseudocholinesterase to PABA (para-aminobenzoic acid) - e.g. Procaine, cocaine Amino-amides - metabolized by liver - e.g. Lidocaine, bupivicaine, prilocaine

Question 60

What is LA toxicity?

Answer 60

Local hypersensitivity (not toxicity) - erythema, urticaria, oedema, dermatitis CNS Prodromal - light-headed, dizzy - metallic taste - circumoral numbness - tinnitus Severe - grand mal seizures - unconsciousness CVS - hypotension - tachy or bradyarrythmias - VF - CV collapse Idiosyncratic - pseudocholinesterase deficiency, PABA hypersensitivity (esters) - liver disease

Question 61

How do you treat LA toxicity?

Answer 61

Stop administering LA! CNS Airway, oxygen (hyperventilate - toxicity exacerbated by hypercarbia) IV diazepam, thiopental CVS Fluids Treat arrhythmias as per ALS protocols Anaphylaxis Airway, oxygen Diphenhydramine IV fluids Vasopressors Bronchodilators

Question 62

What is the MRC grading of nerve function?

Answer 62

Motor M0 = No contraction M1 = Flicker M2 = Movement with gravity eliminated M3 = Movement against gravity M4 = Movement against gravity and resistance M5 = Normal Sensory S0 = No sensation S1 = Pain sensation S2 = Pain and some touch sensation, possible hypersensitivity S3 = Pain and touch with over-reaction – S2PD \> 15mm S3+ = S2PD 7-15mm S4 = normal – S2PD 2-6mm

Question 63

What is the classification of nerve injury?

Answer 63

Sunderland (1951) = 5, Seddon (1947) = 3 Neuropraxia 1. 1st degree → Axon in continuity, conduction impaired, recovery complete Axonotmesis 2. 2nd degree → Axonal divided, distal wallerian degeneration, connective tissue intact, recovery good. 3. 3rd degree → axon and endoneurium divided. Perineurium and epineurium are intact. Recovery reasonable 4. 4th degree → Complete division of all intraneural structures, epineurium intact. Recovery expected, may → neuroma in continuity Neurotmesis 5. 5th degree → Nerve trunk completely divided

Question 64

What happens in neuropraxia?

Answer 64

Critical pressure for nerve dysfunction is 30mmHg \< diastolic Compression → oedema → breakdown of blood/nerve barrier → fibrosis → demyelination → Wallerian degeneration

Question 65

What nerve graft sites do you know?

Answer 65

Sural (30cm) - post to lat malleolus Lateral antebrachial cutaneous nerve (8cm) - cephalic vein, BR Medial antebrachial cutaneous nerve (20cm) - basilic vein, b/t triceps biceps Terminal br of PIN - radial side of 4th extensor compartment at wrist

Question 66

How do you perform a nerve repair?

Answer 66

- direct approximation of divided stumps - Ends trimmed, epineurial repair - fine sutures , magnification - align fascicles of nerve trunks - min tension (nerve graft / vein conduit if needed) - Knowledge of internal nerve topography → ulnar nerve = motor central bn the volar sensory from palm and dorsal sensory from dorsum.

Question 67

How does bone form?

Answer 67

1. Intramembranous ossification → Occurs by direct deposition of bone within a vascularized membranous template. Flat bones of face, calvarium, ribs. 2. Endochondral ossification. → cartilage laid down first at epiphysis followed by ossification. All long bones and iliac crest.

Question 68

What is the blood supply of bone?

Answer 68

1. Periosteal vessels at muscle attachments 2. Apophyseal vessels at tendon and ligament attachments 3. Nutrient arteries - medullary cavity 4. Epiphyseal vessels - growth plates

Question 69

How do bones heal?

Answer 69

Haematoma, Inflammation, Proliferation D1-7 Clotting cascade activated, fibrin coagulum b/t bone ends invaded by neutrophils, macrophages, fibroblasts to form granulation tissue Callus formation Soft callus stage D3-4 Capillaries invade fibrin clot Periosteal mesenchyme cells differentiate into chondrocytes. Bridging callus is formed. Chondrocytes further differentiate into osteoblasts and endochondral ossification of callus occurs Hard callus is formed wk 3 Remodelling - over years Woven bone is replaced by lamellar bone along lines of stress Primary Healing = apposition and rigid fixation, no callus (e.g. phalanges) Secondary Healing = callus and endochondral ossification

Question 70

What are the complications of fracture healing?

Answer 70

Delayed union, Non-union, Mal-union, Infection, Avascular Necrosis (AVN), Shortening, Damage to adjacent structures

Question 71

Healing of bone grafts What factors affect take?

Answer 71

Incorporation, Osteoinduction, Osteoconduction, Osteogenesis Osteoinduction - pluripotential precursor cells present and are 'induced' → osteoblasts Osteoconduction - bone graft acts as scaffold for ingrowth of cells and capillaries. Old bone is reabsorbed and new bone deposited by 'creeping substitution' Osteointegration - new bone formation by surviving cells within vascularised bone graft 1. Systemic 2. Graft factors - intact periosteum 3. Graft bed - orthotopic (Graft placed in position normally occupied by bone) vs heterotopic (not normally occupied by bone), quality of bed, graft fixation 4. Mechanical stress - Physiological loading speeds up union and creeping substitution

Question 72

Describe the anatomy of tendons

Answer 72

- dense, metabolically active connective tissue - Collagen bundles arranged in regular spiralling fashion - Most Type 1 small amount Type 3 - Few cells → Tenocytes, synovial cells, fibroblasts - Endotenon → surrounds tendon, lie in synovial sheaths - Paratenon → loose adventitial layer that surrounds tendons OUTSIDE synovial sheaths

Question 73

What are the zones of flexor tendon injury?

Answer 73

Verdan Zone 1 → distal to FDS insertion Zone 2 → proximal tendon sheath → FDS Zone 3 → flexor sheath → flexor retinaculum Zone 4 → under flexor retinaculum Zone 5 → proximal to retinaculum Zone 2 = ‘no mans land’ – Bunnell → poor results of repair

Question 74

What are the zones of extensor tendon injury?

Answer 74

Zone 1 DIPJ Zone 2 Middle phalanx Zone 3 PIPJ Zone 4 Prox phalanx Zone 5 MCPJ Zone 6 between MCPJ and ext retinaculum Zone 7 under ext ret Zone 8 between ext ret and musculotendinous junction

Question 75

How do tendons heal?

Answer 75

Extrinsic healing - By cells recruited from synovial sheaths and surrounding tissues forming adhesions - Depends on fibrous attachments forming between tendon sheath and tendon Intrinsic healing - by cells within tendon itself - Depends on blood flow through long and short vinculae + diffusion from synovial fluid - Lunborg → tendons heal if placed in semipermeable membrane to stop cells but allow passage of nutrients - Post op EAM allowed Tendons also heal by inflammation, cell proliferation (fibroplasia) and remodelling.

Question 76

What are the phases of tendon healing?

Answer 76

Inflammation → 2-3 days - inflammatory cells infiltrate wound, secrete growth factors which attract fibroblasts Proliferation → 3 days → 3 weeks - fibroblasts secrete collagen and GAGs - Collagen initially randomly arranged and lacks tensile strength Remodelling → 3 weeks+ - collagen organised Early mobilisation limits formation of fibrous attachments with sheath, promotes intrinsic not extrinsic healing. Tendons are stronger than extrinsically healed ones.

Question 77

What is an ideal dressing?

Answer 77

- Physical protection - Non-irritant - Remove necrotic material - Promote epithelialisation - Promote granulation - Be cheap and readily available

Question 78

How do you classify dressings?

Answer 78

Passive vs. interactive vs occlusive Alginates, Films, Foams, Hydrocolloids, Hydrogels, Hydrofibre

Question 79

What low adherent dressings do you know?

Answer 79

Low adherent - Melolin → gauze with polyethylene backing - Inadine → rayon mesh with povidone-iodine impregnation - Jelonet → parafin gauze - Bactigras → Paraffin gauze impregrated with chlorhexidine - Mepitel → silicone

Question 80

What semipermeable film dressings do you know?

Answer 80

- Permeable to gas and vapours but not to liquids and bacteria - Opsite and Tegaderm → films with adhesive

Question 81

What are hydrogels and hydrocolloids?

Answer 81

Hydrogels e.g. intrasite - Starch-polymer matrix which swells to absorb moisture - Promote autolysis of necrotic material and are used to debride wounds Hydrocolloids e.g. Granuflex and Duoderm - Hydrocolloid matrix backed with adhesive - protects the wound, absorbs fluid and maintains moist environment

Question 82

What are alginates?

Answer 82

- derived from seaweed. Contain calcium, activates the, clotting cascade very absorbent, gelatinous when wet e.g. Sorbisan and Kaltostat

Question 83

What synthetic foams are used?

Answer 83

- Usually used in concave wounds, conform to the cavity, obiterating dead space - Suitable for heavy exudate - Lyofoam, Mepilex

Question 84

What is topical negative pressure therapy?

Answer 84

Application of suction aids wound healing. Mechanism unclear o Direct suction pulls the wound inwards o ↑ rate of angiogenesis and granulation o ↓ conc of tissue metalloproteinases o ↓ bacterial contamination o ↓ interstitial fluid Nonadherent sponge → semipermeable film → intermittent or continuous suction - Acute wounds 125mmHg - Chronic wounds 50-75mmHg Contraindicated - active bleeding, cancer

Question 85

How do you classify suture materials?

Answer 85

- Absorbable or non-absorbable - Synthetic or natural - Braided or monofilament

Question 86

What types of sutures do you know?

Answer 86

Polyglycolic acid o Dexon → sythetic suture of polyglycolic acid, degraded by hydrolyzation o Loses strength 21 days and absorbed 90 days Polyglactin 910 o Vicryl → loses strength by 21 days absorbed by 90 days o May provoke significant inflam reaction so avoid on face Poliglecaprone 25 o Monocryl → monofilament synthetic, similar absorption to vicryl Polydioxanone o PDS → monofilament synthetic → Loses strength by 3 months and absorbed by 6 months.

Question 87

What are the symptoms and signs of lignocaine toxicity?

Answer 87

Levels (mg/ml) 3-6: subjective (circumoral numbness, tinnitus, drowsiness, lightheadedness, difficulty focusing) 5-9: objective (tremors, twitching, shivering 8-12: seizures, cardiac depression 12-14: unconscious, coma 20: respiratory arrest 25: cardiac arrest

Question 88

How do you treat a patient with lignocaine toxicity?

Answer 88

ALS Stabilise potential life threats - impending airway compromise - significant hypotension - treat dysrhythmias - treat seizures (benzodiazepines, barbiturates) Antidote: Intralipid 20% 1.5ml/kg bolus, then ivi 0.25ml/kg

Question 89

What is a keloid scar? What is a hypertrophic scar?

Answer 89

Keloid - extend beyond original wound borders Hypertrophic - scar elevated but within borders of original scar Both characterized by excessive accumulation of collagen type III in particular

Question 90

What is the difference between hypertrophic and keloid scars

Answer 90

Keloid - FHx - Blacks \> Caucasians - F\>M - appears months after injury, rarely upsides - common: earlobes, chest, deltoid - aetiology: possible autoimmune Hypertrophic - low FHx / racial / sex predilection - appears soon after injury, subsides with time - common - across tension / joints / infection, delayed healing areas - aetiology: tension, timing of closure

Question 91

What are the different treatments for adverse scarring?

Answer 91

intralesional steroids intralesional excision compression therapy silicone gel / sheets DXT 5FU bleomycin

Question 92

International clinical recommendations on scar management (Mustoe 2002)

Answer 92

Keloid Intralesional steroid (kenolog 40mg/ml) - reduce inflammation, decrease collagen synthesis, increase collagenase activity Silicone gel sheet - hydration Pressure therapy (24-30mmHg) - same as steroid Surgery - alone (45-100% recurrence rate) surgery + steroid (\<50%) Surgery + DXT (10%) but small risk of cancer induction Laser - Nd:YAG flattens, pulse dye for erythema Hypertrophic Silicone Steroid Pressure Others (case reports) - 5FU, IF, imiquimod, bleomycin

Question 93

How is collagen made?

Answer 93

Hydroxyprolene, hydroxylysine Procollagen x3 Tropocollagen Collagen filaments Fibrils Fibres

Question 94

What is the difference between contraction and contracture?

Answer 94

Contraction = physiological (due to myofibroblasts, specialized fibroblasts with contractile myofilaments and cellular adhesion structures Contracture = pathological (may cause shortening, distortion, deformity and limit mvmt) Primary contraction of skin graft = elastin Secondary = myofibroblast

Question 95

What is a cytokine? What is a growth factor?

Answer 95

Cytokines are proteins required for cell defence that are secreted predominantly by immune cells. They mediate in protective and reparative processes and also regulate cell growth and maturation. Growth factors are polypeptides whose primary role is in regulation of cell growth and maturation.

Question 96

What are the 4 components of clotting and haemostasis?

Answer 96

Vasoconstriction Activation of platelets Coagulation Fibrinolysis

Question 97

What are the disorders of coagulation?

Answer 97

Congenital Haemophilia A Von Willebrands disease Acquired Vit K and warfarin (II, VII, IX, X) Liver disease DIC

Question 98

What are the disorders of haemostasis?

Answer 98

Thrombocytopenia - aspirin, clopidogrel Blood vessel abnormalities

Question 99

What are the hypercoagulability states?

Answer 99

Activated protein C resistance Anti phospholipid antibody Homocysteinaemia Elevated FVIII and XI Inherited blood clotting disorders for DVT Mutated genes (such as factor V Leiden, factor II) Decreased protein C, protein S, and antithrombin III Increased levels of antiphospholipid or lupus anticoagulant

Question 100

What factors influence scarring?

Answer 100

Surgical - atraumatic technique - everted wound edges - scar placement within RSTL - u shaped scars tend to pincushion Suture - Braided more traumatic - Absorbable more tissue inflammation Patient factors - Age - Skin type and tendency to scar - Region on body

Question 101

What are the goals of GA?

Answer 101

Analgesia Amnesia Preservation of vital functions Muscle relaxation and suppression of undesirable reflexes Quiet, relaxed field for surgeons

Question 102

What types of GAs are used for balanced analgesia?

Answer 102

Nitrous oxide Halogenated agents - halothane, enflurane, isoflurane

Question 103

what is the ASA grading of patients?

Answer 103

I Healthy individual no systemic disease II One-system, well controlled disease III Multisystem or well-controlled major system disease IV Severe, incapacitating, poorly controlled or end-stage disease V Imminent danger or death with or without op 'e' emergency op qualifier