Musculoskeletal Flashcards
0
Q
What are the essentials of fracture healing?
A
Blood supply - osseous, extra osseous
Stability of fragments, proximity of fragments.
Fracture healing needs vascularisation of the fracture side - adequate reduction & stability of fracture site which protects the bone cells in the fracture gap, an absence of complicating factors eg infection, and sufficient time.
1
Q
What are the clinical signs of a fracture?
A
Loss of function, swelling, change in limb length, alignment or orientation, limb usually shorter, abnormal motility (reduced or increased), pain, crepitus.
2
Q
How does healing occur under limited motion?
A
some movement at the fracture gap, healing occurs via callus formation, progressive increase in stiffness of the fracture gap, remodelling phase restores normal architecture.
3
Q
What is primary bone union
A
Requires - complete stability, no or small fracture gap, interfragmentary compression. contact healing is direct apposition of the fracture ends which permits direct remodelling. new cutting cones are initiated in the region of the fracture. reduced radiographic density at bone ends adjacent to fracture site. Gap healing - small gaps between the fracture end, minimal movement. Lamellar bone forms directly in the fracture gap.Intracortical remodellnig through the fracture gap then restores bone integrity.
4
Q
What is the benefit of primary bone union over healing by calus?
A
There is no benefit from primary bone union over healing by calus - the speed of healing is slower, gains strength at a slower rate. most of the benefits arise from rigid stabilisation - early return to function and reduced risk of fracture disease.
5
Q
What forces cause fractures?
A
Most fractures arise following external trauma. some arise following normal loading - applied in an uncoordinated way, beware of pathological fracture. High energy trauma - causes severe comminution, significant damage to the soft tissue envelope, increased chance of open fracture.
6
Q
Describe the neutralising forces of fractures
A
Tension - lengthening Compression - shortening Bending - combines tension and compression, tension on convex surface, compression on concave surface, neutral axis results. Torsion Shear
7
Q
What are pathological fractures
A
Bone fractures secondary to an underlying pathological process that weakens the structure - infection, neoplasia, nutritional disease. Normal loading results in the fracture.
8
Q
Describe metaphyseal fractures
A
Beware of the potential for growth plate damage in skeletally immature animals. always warn owners to watch for angular deformity developing. salter harris fracture
9
Q
Describe epiphyseal fractures?
A
Potential for growth plate damage in skeletally immature animals. likely articular involvement.
10
Q
What can cause a greenstick fracture (incomplete)
A
In skeletally immature animals where bone is incompletely mineralised so less brittle than fully mineralised adult bone. or secondary to skeletal demineralisation eg secondary nutritional hyperparathyroidism.
11
Q
What are fissues?
A
(incomplete) hair line fractures. Undisplaced fissures are often seen running along the cortex from a major fracture line.
12
Q
What is avulsion?
A
Fragment distracted by muscle pull or ligament attachment eg tibial tuberosity, olecranon, elective osteotomy. Seen along Physis in skeletally immature animals. at muscular/ligament insertions in skeletally mature animals. need to neutralise distractive forces during fracture repair.
13
Q
Describe what radiography should be done for fractures?
A
Minimum - orthogonal views, include adjacent joints
Contralateral limb - juvenile animals, complex fractures, curved bones
Additional - stressed views, traction views, angled beam views.
Minimum baseline will be pre operative for fracture fixation planning, immediate post operative to assess repair. frequency governed by anticipated rate of healing, presence of complicating factors, finance, intention to remove implants.
14
Q
How can you recognise that a fracture is healing?
A
Clinical function - progressive improvement in function, consistent weight bearing, minimal muscular atrophy, radiographic signs vary depending on type of healing anticipated, may a bridging calus, loss of fracture lines.
15
Q
What is a compound fracture?
A
also known as an open fracture. graded 1-3 on severity of soft tissue injury. can be an emergency Cover open wounds with a sterile dressing for immediate first aid and control haemorrhage. stabilise fracture and manage soft tissue injuries. prevent contamination progressing to nfection. achieve rapid bone union and restore limb function. high energy fractures - greater soft tissue damage, less resistance to infection, slow to heal. Clip widely, lavage copoiously, debride all devitalised tissue, start open wound management, manage initial trauma, avoid corticosteroids, prevent further contamination (immobilise and cover bone ends) antibiotic therapy, swab for C&S, give ASAP. Debride surgically, lavage, discard small avascular fracture fragments, keep fragments that contribute to stability.
16
Q
What is biological osteosynthesis?
A
Aims to take full advantage of biological healing potential to maximise rate of fracture healing, maintain limb length and orientation, avoid creating further surgical trauma, provide an optimal biological and mechanical environment for fracture repair.
17
Q
What should be the emergency support of fractures?
A
Cage rest for upper limb fractures. robert jones dressing for lower limb fractures. fractures are in general painful, give appropriate analgesia. conservative management - immobilisation by forced rest; cage rest for pelvic fractures & some pathological fractures. support if feasible - lower limb fracture.
18
Q
What are the advantages and disadvantages of external copatation?
A
Often seen as cheap &easy means of fracture management. But - intensive methods for fracture management, regular revisits needed, cast changes as necessary, high rate of complications - soft tissue sores, muscular atrophy and joint stiffness, they are common and difficult to avoid. Must immobilise the joint above and below the fracture - limits use to below elbow and stifle. only resist bending/angulation so only useful for transverse of short oblique fractures that are stable once reduced. reduction must be adequate before application. More appropriate when rapid healing is expected. never use for an articular fracture. may be useful as an adjunctive support to an inadequate internal fixation. There is preservation of soft tissues and blood supply, quick, don’t need much stuff, disadvantages - heavy maintenance, fracture disease.
19
Q
What are splints used for
A
Short term/adjunctive support. ok for radius and ulna. limited to hock distal. apply over cast padding and conforming bandage. (spoon part at the bottom). Anatomical moulded splints are strips of fibreglass/resin casting material encased in cast padding. They mould to the contours of the limb. thermoplastic materials - stronger and lighter than POP, need to be quite hot before they are mouldable, difficult to use unless you have the gift. Plaster of paris casts - cheap, easy to apply, conform well, take 8+ hours to dry fully, heavy to wear, radiodense. Fibreglass resin - light and strong, dont soften when wet, conform well, set rapidly, radiolucent. ned an oscillating saw for removal.
20
Q
How do you score fracture patient assessment score?
A
Clinical factors - eg good client compliance (10 little risk), 1 poor client compliance (caution).
Biological aspects - little risk (10) - juvenile, excellent health, good soft tissue, cancellous bone, low energy, closed. 1 - geriatric, poor health, poor soft tissue, cortical bone, high energy, extensive approach.
Mechaniical aspects - 1 - caution- buttress, multiple limb injury, giant breed. Little risk - compression, single limb, toy breed.
21
Q
How is fracture reduction done?
A
Most fractures are over ridden caused by muscle contraction and spasm. slow steady traction needed, bends fracture to engage ends, straighten bone to achieve final reduction.
22
Q
How do you apply a cast?
A
Reduce fracture and maintaiin reduction during cast application. immobilise the joint above the fracture. immobilise the limb in a normal standig position, include the toes + pads. Stirrups - retain cast in positioin, help to maintain reduction of fracture during application. Padding - cotton wool, synthetic cast padding, stockinette, don’t over pad the limb. read the instructions with regards to water temperature, squeezing etc. apply with a 50% overlap. Dont allow the animal to walk untill the cast has cured. check limb alignment/reduction radiographically. bivalve cast if desired. apply a waterproof overwrap. regular checks daily by owner and weekly by Vet. Complication signs include rubbing/chewing at cast, swollen foot pads, bad smell, stops weight bearing, becomes ill, keep clean and dry. Casts often need to be changed before union is complete as swelling reduces because of cast damage or expected healing time .
23
Q
What are the potential cast complications?
A
Pressure sores, poor technique or loosening, ischaemia may progress to gangrene, fracture disease - muscle wasting, stiffness, osteoporosis, tissue adhesion, malunion, delayed union.
24
What is external skeletal fixation?
A series of percutaneous pins, pass into or through the bone. they are connected together externally with clamps and rods, acrylic bars or epoxy putty. they are versatile, easy to apply, compatible with the principles of biological osteosynthesis, maintain alignment and length of limb, disturb fracture fragments miminally, can be removed in a staged way, excellent for management of open fractures, not restricted to use below elbow and stifle.
25
What are the different ESF frame designs available?
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Unilateral, uniplanar
Bilateral, uniplanar
Bilatera, Biplanar
Ilizarov - ring fixator, cESF.
Connecting bars may be made of stainless steel, aluminium, titanium, carbon fibre, acrylic or epoxy resins. Frame stiffness depends on frame geometry, pin factors; number type and placement., clamp factors; type and orientation, fracture configuration; load sharing with frame.
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26
what are the different types of pins available?
smooth pin - friction only, NPT pin -good bone purchase, weak point must be protected.
PPT pin - excellent purchase, no weak point, must pre drill a pilothole.
27
How is an ESF frame applied?
Prepare as for routine aseptic surgery. position patient with hanging limb preparation aids in fracture reduction and frame application, fatigues muscles. pin selection must be 20-30% of cortical width of bone. place pins spread out along fracture fragment, near far far near configuration, place by hand or with power. recommended to predrill. mandatory for PPT pins to predril. insert pins with low speed power. Protect the soft tissues- use stab incisions, retract soft tissues to periosteu, beware of PPT pins, releasing incisions if required. allow enough clearance of pin,
28
What are the complications of ESF pins?
Persistent pin tract drainage - best avoided by attention to soft tissue management, have to accept it at some sites. pin loosening - promotes pin tract discharge, remove loose pins, revise frame if necessary.
29
What is an ESF/IM pin tie in?
IM pin resists bending and maintains alignment. ESF fixator resists compression and resists torsion. Anti rotational two pin fixator - Fracture - resists axial collapse, allows a simple frame to be applied. other uses for ESF include stabilisation of open fracture/dislocations eg transarticular frame, protection of tendon repair - transarticular frame.
30
What are the mechanics of IM pins?
Holds fragments in aligment. Resists bending but not rotation, shear or axial shortening. fracture fragments may interdigitate to resist rotation. otherwise combine with ESF or P&S to enhance stability. Aim to fill the medullary canal at the narrowest point - radiographs of contralateral limb are useful for assessment. remember to allow 10-15% for magnification. Length - seated in distal metaphysis. protrude slightly proximally - for easy removal after healing. cut to correct length pre operatively or post operatively.
31
What is normograde pinning?
Introduce pin away from fracture site. reduce fracture, advance pin. may be able to do this closed.
32
How is retrograde pinning done?
Introduce pin at fracture site. push/pull pin through bone to allow fracture reduction. reduce and drive pin across fracture line. cant be done for tibia or radius (radius cant be pinned normograde either)
33
What is an interlocking nail?
An IM pin, perforated to accept bone screws, neutralises all forces very effectively - pin resists bending, screws lock bone to pin resisting shortening, rotation, shear. Requires specialised instrumentation or fluoroscopic guidance. can be technically challenging.
34
What are rush pins?
Used in pairs, have a hooked end and a sledge runner tip at the opposite end. they cross over and bounce off the opposite inner cortex. They are best manufactured in house from 1.0-2.0mm K wires. useful for metaphyseal fractures especially of the distal femur. they may allow physeal growth to continue in skeletally immature animals.
35
How is cerclage wire used?
Commonly combined with IM pinning. Full cerclage - wire encircles the bone circumference. hemicerclage - wire passes through a tunnel drilled in one of the fragments. Monofilament orthopaedic wire 0.8-1.2mm in diameter. Not suture wire, fuse wire, PDS. Use a wire twister/cutter and a wire passer. For using cerclage wire the fracture must be fully reconstructable. only two fragments in any circumference, otherwise may collapse into a bundle of sticks. Sufficiently oblique fractures other wise fragments override as wire is tightened. >2 wires as a single wire acts as a fulcrum - concentrates bending forces on the fracture site.
36
What is tension band wiring used for?
Used to repair fractures or osteotomies which are subjected to distractive forces, eg olecranon osteotomy, tibial tuberosity avulsion, malleolar fracture. Reduce fracture and maintain with one or two K wires. Do a figure of eight wire anchored in a transverse bone tunnel and passed around the ends of the pin. wire anchored by twisting, ensuring even tension. ends of wire bent over and the ends are cut short. Figure of eight wire combined with small diameter wires. This converts distractive forces to compression at the fracture line.
37
What are self tapping and tapped screws?
self tapping - cut their own thread in the bone with a cutting tip.
Tapped - the thread must be cut in the bone. the thread conforms exactly to the screw profile. this maximises metal bone contact and holding power. To place screws - drill pilot hole, measure depth of hole (and add 2mm), (countersink), tap (unless using self tapping screws).
38
What is a lag screw used for?
When the screw crosses a fracture line that cannot be compressed. it provides inter fragmentary compression. Screw threads only grip in the trans cortex. Overdrill cis cortex to provide a gliding hole with a threaded hole in the transcortex. Countersink in cortical bone only. tightening of the screw provides inter fragmentary compression. Inserting lag screw at 90degress to fracture line provides optimal compression. inserting at 90 degrees to long axis of bone gives optimal resistance to axial compression. Compromise is to bisect these two angles. screws should be inserted in the middle of the fragment, equidistant from the fracture edges, at 90 degrees to the fracture plane. This gives Max interfragmentary compression. Screws placed at any other angle introduce shearing forces between the fragments, loss of reduction ensues. They may be the sole method of fixation e.g in articular fractures or may be used as an adjunctive fixation to reduce a complex fracture to a simple fracture, may be used through a plate hole.
39
What is a position screw used for?
Used when a lag screw would cause a fragment to collapse into the medullary cavity or when a fragment is too small to take a gliding hole. Fracture held in reduction, drilled, measured and both cortices tapped. screw inserted.
40
Describe the uses of a bone plate and screws
Very versatile. if used carefully can neutralise effectively all forces acting on a fracture. Use as long a plate as feasible. aim for six gripping cortices above and below the fracture line. all screws must be tight. avoid bone defects and use cancellous bone graft if complete reconstruction is not possible. Plate may be applied in one of three ways; tension band, neutralisation, buttress.
41
What is the use of a neutralisation plate?
Applied to protect a lag screw reconstruction. cannot take significant loads without faliure. load sharing between plate and bone. lag screws provide interfragmentary compression, plate resists torsion, bending and shear. Lag screws can also be inserted through the plate holes.
42
When is a buttress plate used?
When a fracture cannot be anatomically reconstructed. there is no load sharing between the bone and plate. the plate transmits the full force of loading across the fracture gap.
43
What is a tension band plate?
Most bones bend under load. this gives a tension and a compression cortex. the plate is placed in tension to apply compression across the fracture gap. Promotes primary bone union. used for transverse or short oblique fractures, articular fractures, osteotomy repair, treatment of non unions, arthrodesis.
44
What is a dynamic compression plate?
Plate hole design allows the DCP to be used as a compression, neutralisation or buttress plate. spherical screw head slides down the incline of the screw hole as the screw is tightened. This compresses the fracture site.
45
How are plates applied?
Surgical preparation - thorough, wide prep to account for plan B, remember to prep accessible sites for bone graft it any possibility that one may be needed. Free limb draping - avoid fenestrated rapes, better manipulation of the limb and assessment of angulation and alignment. Chose plate based on FPAS - patient size, age, fracture conformation, owner factors. Can pre contour plate - to radiograph of opposite limb, to bone specimen, reduces surgical time. Approach and reduce fracture - requires a wide approach to apply plate to bone surface, final plate selection and contouring, apply screws - drill screw hole, depth gauge, tap screw hole, place and tighten screw.
46
What is postoperative care after bone screws/plates have been inserted?
Controlled exercise - cage rest usually best avoided. aim for rapid return to normal weight bearing to avoid muscle wasting and joint stiffness especially important following articular fracture repair. consider owner compliance. physiotherapy - passive flexion-extension exercises. hydrotherapy.
47
What is osteomyelitis?
Inflammation/infection of the bone and associated bone marrow. Sources of infection. post surgery; open fracture, open reduction of closed fracture. penetrating injury; bite wounds, gunshot wounds, foreign body penetration. local extension, haematogenous spread eg after dental work (rare). Normal bone is relatively resistant to infection. establishment of infection requires sufficient numbers of pathogenic bacteria, avascular cortical bone, favourable environment for colonisation and multiplication. over 70% of cases occur secondary to orthopaedic procedures, especially where metallic implants are placed. Glycocalyx biofilm protects bacteria from normal host defences - phagocytosis and antibodies and antibacterials.
48
What are the signs of acute osteomyelitis?
E.g following extension of a deep SSI - localised pain, sweling, pyrexia, anorexia, lethargy, usually 2-3 days post surgery, drainage may not be immediately evident.
49
What are the signs of chronic osteomyelitis
Lamenes,s muscle atrophy, fibrosis, contracture, bone pain, swelling, heat, discharging sinus tracts, anorexia, pyrexia.
50
What are the radiographic signs of osteomyelitis?
Bone destruction, periosteal new bone formatin, sequestrum formation - isolated fragment of dead bone separated from normal bone. appears radiodense and angular since not remodelled. may become walled off by an involucrum. delayed or non union. +- soft tissue swelling.
51
What is the treatment of osteomyelitis?
For a stable healing fracture- maintain fixation, fractuers will heal in the presence of persistent infection provided they are stable.
Healed fracture - remove implants
Unstable fracture - revise fixation to provide stability
Remove sequestrae - may need to graft significant deficits - cancellous autograft.
Establish drainage
Lavage
52
What antibiotic therapy should be used for osteomyelitis?
Culture if possible. sample by FNA or open collection. give a prolonged course of appropriate ABs. 50-60% involve staph spp. B lactamase producers. 65% involve anaerobes especially bite wounds and chronic infections.
53
What is malunion?
Due to inadequate fixation or inaccurate reduction. May be clinically irrelevant if patient has good function. may require osteotomy and realignment to correct significant deformity.
54
What is a non union fracture?
Failure of bone healing. usually iatrogenic i.e your fault. poor fracture management or technical failure. often due to inadequate stabiliity. Continual motion leads to persistently high strains and healing cannot progress to the mineralisation phase. Viable non union - usually arise due to inadeuate stability of the fracture site. also from inadequate reduction. should heal following adequate stabilisation. May be hypertrophic or oligotrophic. Hypertrophic non union - highly vascular fracture site, significant callus (bone is attempting to heal), work out what is wrong - remove loose implants and stabilise fragments, swab tissues for c&s.
55
What are non viable non union fractures?
May be dystrophic - blood supply inadequate
NEcrotic - necrotic tissue in fracture site
Defect - bone defect at fracture gap
Atrophic - sequel to above - biologically inactive, no evidence of attempt to heal, bone ends sclerotic and atrophied, medullary cavity may seal over, fracture gap fills with fibrous tissue, pseudoarthrosis formation.
56
What is the treatment for non union non viable fractureS?
require aggressive treatment- open approach, debride fracture ends to viable bleeding bone. tissue sample for C&S. Open medullary cavity. rigid stabilisation - plate and screws, bone graft. Beware of atrophic non union fractures in distal radius and ulna in toy breed dogs.
57
What is quadriceps contracture?
Quadriceps m. becomes adherent to fracture site. progressive decrease in range of stifle jt mobility. stifle & hock overextended. Avoid penetrating muscle masses during ESF application wherever possible. Treatment - surgical release of adhesions, muscle/tendon lengthening if necessary to allow normal ROM at stifle joint, passive and active physiotherapy are vital following surgical correction.
58
Why may implant failure occur?
Innapropriate implant size, errors in implant pacement, biomechanical environment ignored - cyclical loading causes implant failure, large cortical defects not reconstructed or grafted, fracture of plates through unfilled holes.
59
What are the different types of bone graft?
Autograft - D& R is same individual
Allograft- D & R are different animals of the same species
Syngenesiograft - D & R are blood relatives
Isograft - D & R have identical genetic background
Xenograft - D & R are from different species.
60
What is the mode of action of a bone graft and what are the different uses?
Sources of osteoprogenitor cells - from within the graft - osteogenesis, from within the surrounding tissues - osteoinduction, from a mechanical support - scaffold for bone cell invasion - osteoconduction. They can be used for filling defects eg left by removal of non reconstructable fragments, or limb salvage (OSA), to encourage healing in a comminuted fracture, non union fracture or arthrodesis and spinal fusion.
61
Describe the advantages and disadvantages of a cancellous autograft
Highly cellular but mechanically weak. collect from - lateral tuberosity of humerus, medial proximal tibia, greater trochanter of femur, wing of ilium. Advantages - no immune response, greatest osteogenic effect (high celllularity), no risk of cross infection. Disadvantage - extra operating sites must be prepped and accessed. large quantities can be difficult to obtain.
62
What are the advantages of cortical allograft?
Can be banked, convenient, unlimited quantity
Disadvantages - immunogenic, slow incorporation into host bone, risk of cross infection. Need strict asepsis since implanting a dead piece of bone. osseointegration within 1-3 months but complete substitution may take years. complications are common. infection in 20-49%, rejection, fracture, plate fracture, seqestration. Main use is for limb salvage.
63
What is rickets?
Rickets in skeletally immature animals, osteomalacia in adult animals. Failure of Mineralisation of osteoid. Dogs and cats cannot synthesise Vitamin D - dependent on dietary sources and metabolic pathway and sunlight. Rickets is not a simple vit D deficiency. dogs on a Vit D deficient diet do not develop rickets if dietary Ca & P levels are adequate. Probably require a concurrent Ca:P imbalance. a degree of secondary nutritional hyperparathyroidism probably coexists in animals with rickets. A highly stable cartilage matrix is produced - uncalcifiable, difficult to resorb. In young animals condrocytes fail to degenerate so there is increased physeal thickness & poor skeletal mineralisation, metaphyseal capillaries cannot penetrate cartilage, bone trabeculae surrounded by unmineralised osteoid.
64
What are the clinical signs of rickets?
Young dogs, lameness due to bone pain or pathological fracture, limb bon bowing, angular limb deformity, flaring of metaphyses -distal R&U, CC junctions. hypocalcaemia, ligamentous laxity - palmigrade/plantigrade stance. On radiograph - poor skeletal mineralisation, increased growth plate width, 'cupping' of metaphyes, bowing of diaphyses, pathological fracture.
65
What is the treatment for rickets?
Correct diet and exposure to sunlight - balanced diet, Ca:P ratio approx 2:1, potential for permanent growth plate damage, if hereditary form more guarded. Treat fractures conservatively - pathological. bone stock not as good for repair.
66
What are the functions of the parathyroid glands?
They regulate serum Ca2+, secrete PTH in response to Decreased Ca2+, which causes increased Ca2+ uptake (bones/gut/kidney). hypercalcaemia prevented by negative feedback loop - calcitonin, vitamin D mediates this pathway.
67
What is primary hyperparathyroidism?
Rare - autonomous secretion of PTH causes hypercalcaemia, Parathyroid adenoma - also carcinoma or hyperplasia.
68
What is secondary nutritional hyperparathyroidism?
common in reptiles. puppies in kittens fed all meat or meat rich diets, inability to absorb dietary calcium, excessive dietary PO4, low calcium: P ratio leads to relative calcium deficiency. Increased parathyroid hormone to maintain calcium in a normal range. calcium withdrawn from the skeleton. The clinical signs are bone/joint/muscle pain - reluctance to stand/walk. pathological fracture in pelvic limbs/vertebrae, ligament laxity - palmigrade/plantigrade stance. On radiograph: difusely poor skeletal mineralisation, apparent increased density on metaphyseal side of growth plate -osteoid undergoing active minerlisation. Thin bone cortices, pathological fracture, folding or compression fracture.
69
What is the treatment for secondary nutritional hyperparathyroidism?
Balanced diet, Ca supplementation initially. Ca:P 2:1 then to normal ratio 1.2:1. Manage fractures conservatively - poor holding power for imlants. NSAIDS not corticosteroids. cage rest. Euthanasia if severe neurological impairment.
70
What is secondary renal hyperparathyroidism?
Occurs secondary to chronic renal insufficiency/uraemia. hyperphosphataemia leads to relative hypocalcaemia. Reduced vitamin D production - impaired intestinal absorption of Ca, impaired mineralisation of osteoid (rickets/osteomalacia). Calcium is withdrawn from the skeleton (PTH), all bones affected but primarily cancellous bone of mandible and maxilla. teeth appear to float in skull. fibrous osteodystrophy (rubber jaw). Clinical signs primarily due to renal disease - vomiting, PUPD, depression, osteopaenia/osteomalacia - loose teeth, pliable mandible, failure to close jaw properly - salivation and tongue protrusion, mandibular fractures. Treatment: optimise renal function, reduce phosphorus levels in diet - oral phosphate binders. Al (OH)3, CaCo2, Ca acetate. erythropoietin if anaemia present.
71
What is hypervitaminosis A?
Seen in cats from 2 yo. excess dietary vitamin A intake - liver rich diets. stiffness/lameness. irritability/hypersensitivity, scruffy unkempt appearance - cant groom. thoracic limb neurological deficits - c/t nerve root compression. Extensive periosteal bone formation in the vertebrae and major limb joints, cervical and thoracic vertebrae. often progresses to spinal fusion - ankylosis. Treatment - correct diet stops progression of diseas, established new bone does not regress. give analgesia - nsaids. lameness often mechanical rather than inflammatory. Removal of bony exostoses if causing a clinical problem.
72
What are the effects of excess dietary calcium?
High calcium diets have a deleterious effect on endochondral ossification. important in the pathogenesis of osteochondrosis. puppies less able to restrict excess dietary calcium than adults.
73
What are the effects of excess dietary energy/?
Encourages a rapid growth rate. implications for many orthopaedic conditions such as hip dysplasia, osteochondrosis. Final height of a dog is strongly influenced by genetics. better strategy to allow adequate quantities of a commercial balanced diet to allow an animal to achieve its full genetic potential but in a controlled manner. dogs achieve the same ultimate height but at a slightly older age. Commercially produced complete diets for young dogs DO NOT need supplementation with calcium, vitamins, other minerals or anything else.
74
What is metaphyseal osteophaty?
Affects young dogs 4-6mths. medium to giant breeds - Great Dane, boxer, GSD, weimeraner. probably not related to vitamin C deficiency. dogs and cats have no requirement for extrinsic vitamin C. Necrosis, inflammation and subsequent fracture of trabeculae - in Metaphysis parallel to physeal plate, physis, epiphysis usually normal. Clinical signs can be very mild to extremely severe. Severely affected animals may be unable to stand. pain, reluctance to move, shifting lameness, pyrexia, anorexia, lethargy, diarrhoea, vomiting, bronchopneumonia, gross swelling of distal metaphyses, commonly R&U, T, often hot and painful.
75
What are the radiographic signs of metaphyseal osteopathy?
Early signs - Usually bilaterally symmetrical, soft tissue swelilng, bands of sclerosis and lucency at the metaphysis - trummerfield zone, usually parallel to epiphyseal plate.
Late signs - extraperiosteal cuff of mineralisation at the metaphysis - mineralising sub periosteal haematomas. Extraperiosteal swellings regress at maturity leaving a thickened metaphysis. Disease probably improves regardless of treatment in 7-10days. relapses may occur. symptomatic treatment - analgesia, check diet is adequate, death has been reported.
76
What is panosteitis?
Seen in GSD, lab, dobermann, bassett hound, occ other breeds. age 5-18 months. can be older or younger. males predisposed. in females often related to first oestrus. Unknown aetiology - inflammatory. degeneration of medullary adipocytes. enhanced OBL and fibroblast activity - in the endosteum, periosteum and marrow. fibrosis & ossification & periosteal proliferation. signs - lameness, often acute and severe waxing & waning shifting, may be NWB, recurring. Localised bone pain, pain due to medullary hypertension. systemic illness may be present - anorexia, pyrexia.
77
What are the radiographic signs of panosteitis?
Signs depend on duration of disease, patchy, mottled, sclerotic areas within medullary cavity - especially around area of nutrient foramen. small or extensive regions of involvement. Blurring of cortico medullary contrast - endosteal thickening, loss of trabecular patterning. Periosteal involvement in 30% of cases, roughened and cortical thickening. remodelling in lateral phase - normal medullary density, coarse trabecular pattern remains. Self limiting -resolved within a few days but relapses common. fully resolved by 2 years of age. symptomatic therapy with analgesia, rest, weight reduction.
78
What is hypertrophic osteopathy?
A paraneoplastic syndome. associated with intra thoracic or intra abdominal space occupying lesion. usually a tumour. humans and dogs mainly affected, it is reported in cats. unknown - toxins associated with noplasia, hormones, AV shunting (local hypoxia), neurovascular reflex. Older animals, lameness, joint ROM may be reduced due to ST swelling, limb swelling - bilaterally symmetrical, warm but non oedematous, distal limb, pain, thoracic signs e.g dyspnoea, cough. thoracic tumour in >90% of patients
79
What are the radiographic signs of hypertrophic osteopathy?
Periosteal new bone deposited in palisades. 90 degrees to long axis of bone, often phalangeal diaphysis, 2nd and 5th MC/MT, abaxial border. starts distally in limbs - phalanges and metacarpals/tarsals. Investigate chest and abdomen - space occupying lesion, neoplasia most common; pulmonary primary or metastatic neoplasia, granulomatous diseases/abscess, chronic brochopneumonia, pulmonary tb, rib tumours, bacterial eendocarditis, abdominal, liver adenocarcinoma, adrenocortical adenocarcinoma, bladder neoplasia. Treat the underlying cause. Prognosis depends on underlying cause. bone will remodel if primary lesion can be successfully removed. lameness heat and pain diminish within few weeks. resolve after 3-4 months. prognosis grave.
80
What is an osteosarcoma?
Common neoplasm of appendicular skeleton, axial skeleton less common, primary extraskeletal sites are rare. In appendicular - large and giant breed dogs, males > females ? , median age 7 years. Bimodal peak 18-24 mo. Axial - medium to large breed dogs, females > males, middle aged (exception: rib OSA)). Small dogs - axial > appendicular.
81
What are the risk factors for osteosarcoma?
Ionizing radiation, chemical carcinogens, metallic implants, skeletal abnormalities, genetic mutations, early neutering?
82
What is the most common location of the osteosarcoma?
Metaphyses of the long bones - away from the elbow, toward the knee. Less commonly: ribs, vertebrae and skull. Extraskeletal OSA. Appendicular - micrometastasis in 90% at the time of initial presentation. Primarily via haematogenous routes > lung most common metastatic site. rarely via lymphatics. Other sites include liver, kidneys, amputation stump and rarely subcut tissues and adjacent bones. Axial - 25% of all OSA cases. seen in ribs, scapula skull, vertebrae. metastatic rate in oral and maxillofacial OSA lower than other sites.
83
What are the clinical signs of OSA?
Lameness, swelling, pain, mass at the primary site. pathologic fractures due to weakened cortical bone. neurological deficits, dyspnoea, nasal obstruction, bloody to purulent nasal discharge. Haem& biochem - commonly normal. may have ALP/azotaemia. Thoracic radiographs often noral. <10% present with gross etastatic disease. discrete soft tissue opacity nodules.
84
What is the radiographic appearance of OSA?
lytic, productive or mixed appearance at the Metaphysis of long bones. away from elbow towards the knee. does not cross joint spaces. Can be in sunburst pattern- the result of tumour extension, mineralization and formation of periosteal spicules in the surrounding tissue, codmans triangle - regular periosteal elevation on either side of the lesion that apperas irregular and discontinuous. irregular osteolysis. There is little correlation between the type of radiographic pattern and the biological age of the neoplasm or its degree of malignancy.
85
What are the DDx for osteosarcoma?
Other primary bone tumours e.g chondrosarcoma, fibrosarcoma and haemangiosarcoma account for 5-10% of all primary bone tumour diagnoses. Metastatic bone tumours can be suspected if the lesion occurs in the diaphyseal area> requires haematogneous spread and lesions often establish adjacent to nutrient foramina at the ends of diaphyses or in the bodies of vertebrae especially caudal lumbar sites. fungal osteomyelitis - usually more proliferative lesion but some lysis may occur. dogs living in endemic areas/travelled should have this as ddx. cytology and serology of draining lesions may be helpful. Round cell bony tumours such as multiple myeloma or lymphoma usually have a different appearance on radiographs > are purely lytic, usually multiple and appear to be punched out. 5. Bacterial osteomyelitis in mature dogs requires for an access route for bacteria to enter so a draining tract or history of puncture wound required.
86
What may be seen on FNA/cytology with OSA?
Aspirates contain mesenchymal cells that appear round, plump or fusiform. cells occur singly or in small clusters. may exhibit anisocytois and anisokaryosis with eccentrically located nuclei, large nucleoli and basophilic vacuolated cytoplasm. well differentiated osteoblasts may have a plasmacytoid apperance. osteoclasts are large cells that are multinucleate. islands of osteoid may be observed within some clusters of neoplastic cells or within the background of the smear.
87
How is bone biopsy/histoathology done for OSA?
Often necessary for definitive diagnosis of OSA. can be obtained with a jamshidi needle or michels trephine. removes a core of the osseous neoplasm. core biopsy taken from the centre of the lesion is preferred for diagnostic purposes. multiple core samples may be necessary for a definitive diagnosis. potential complications include increased pain/lameness, resultant pathologic fracture, non diagnostic sample. an open biopsy technique can be performed if the closed technique did not yield a diagnosis. OSA may have a heterogenous appearance and be classified as poorly differentiated, firboblastic, osteoblastic, telangectatic, giant cell or chondroblastic based on the characteristics of the cell population and the matrixproduced. may also have a mixed appearance.
88
Describe treatment of OSA with surgery plus chemotherapy.
This is considered the standard of care therapy for dogs with OSA. this treatment protocol is effective in controlling the patients local disease and alleviating pain and it helps control metastatic disease. surgical options include amputation (easier procedure), limb sparing surgery most commonly performed for distal radial lesions, for axial lesions consider mandibulectomy maxillectomy. essentially no differences in survival times between amputation and those undergoing limb spare. Chemotherapy options include platinum based chemotherapy (carboplatin or cisplatin) every 3 weeks, doxorubicin every 2 weeks, platinum doxorubicin combinations. reported medial survival time is 1 year.
89
Describe treatment of OSA with radiation therapy
If surgery is not an option, RT is effective for temporary relief f bone pain associated with OSA. this is palliative not curative. coarse fractionation appears to be useful in most cases. overall response rate is 75-90%. Median duration of response for dogs with appendicular tumours is 700-130 days. unfortunately tumours will progress.
90
What are bisphosphonates?
Inhibitors of normal and pathologic bone resorption (osteoclasts induced). commonly used in combination with palliative radiation therapy. have proven to be therapeutic in patients with primary bone tumours and boney metastases. has been demonstrated that pamidronate inhibits the growth of canine OSA in cells in vitro and therefore may be useful for the treatment of this disease.
91
Describe treatment of OSA with amputation alone
Median survival time 4-5 months. is palliative but rarely increases survival time. quality of life is greatly improved because the pain of primary disease is resolved. 90% of dogs have micrometastasis at the time of diagnosis progression of these lesions is to be expected.
92
Describe treating osteosarcoma with analgesics only
If no treatment is given, dogs usually live a median of 1-2 months because euthanasia is performed secondary to worsening pain or pathologic fracture. consider use of nsaids or narcotics.
93
Describe the prognostic factors of OSA?
Location - site associated with a worse prognosis are proximal humerus, rib, scapula, extraskeletal, mammary. Mandibular location associated with better prognosis. Young dogs appear to have shorter survival times but recent studies show opposite. sex and breed are not prognosis factors. Lymph node or pulmonary metastasis - worse prognosi, telangiectic histologic subtype, body weight dogs >40kg appear to have shorter survival times. ALP increased has been associated with shorter survival time. over grade III associated with a shorter ST.
94
Describe feline osteosarcoma
Primary bone tumours are rare in cats but OSA is most common. 67-90% are malignant. 55% occur in appendicular skeleton. 45% occur in axial skeleton. mean age at diagnosis is 8-10 years. history clinical signs and radiographic appearance are similar to those dogs with osa however occurs more frequently in hind limbs than foorelimbs. appears to b e far less metastatic than canine OSA. surgery is treatment of choice. no adjuvant therapy is known to be effective. with amputation alone MST is 24-44 months. prognosis for axial sites is dependent upon resectability.
95
What are soft tissue sarcomas?
A diverse group of tumours that are classified on the basis of similar pathologic appearance and clinical behaviour. soft tissue sarcomas comprise approximately 15% of cutaneous and subcutaneous cancers in dogs. Occur in animals of all ages, although more common in older pets. in dogs, STS has been associated with radiation therapy, trauma (inflammation, foreign bodies (orthopedic implants), parasites (spirocerca lupi), vaccine associated sarcomas in dogs.
96
What are the different types of soft tissue sarcomas? What is their biologic behaviour?
Fibrosrcoma, peripheral nerve sheath tumour, haemangiopercytoma, liposarcoa, rhabdomyosarcoma, leioyosarcoma, undifferentiated or anaplastic sarcoma. They have Indistinct tumour margins despite the Appearance of being encapsulated. a pseudocapsule exists that often contains both normal and tumour cells that form a compressed rim together with edema and newly formed blood vessels. they infiltrate along fascial planes and are extremely locally invasive. Local recurrence is common following conservative resection. the most common route of metastasis is via haematogenous spread rather than via the lymphatic system. Most common route of metastasis is via haematogenous spread rather than via the lymphatic system.
97
How can soft tissue sarcomas be graded?
Histolpathological grade is important for prognosis an treatment. Immunocytochemical staining and monoclonal antibodies to tissue markers has proved helpful in accurately diagnosing human STS and in some part in animal STS. some commonly used staining patterns to differentiate sarcomas from other tumours include vimentin - intermediate filament that indicates mesenchymal, cytokeratin - specific for epithelial cells, CD-18 - indicates histiocytic origin.
98
What is the typical history and clinical signs with soft tissue sarcoma
Any breed but large breed dogs are often over represented. median age 8-10 years but can occur ni any age animal . males and females equally represented. slow growing usually painless mass located anywhere on the body. occasionally present with rapid growhth. clinical signs are directly related to the location and invasiveness of the tumour. there may be no adverse clinical effects on the patient. as part of a thorough physical examination each tumour should be body mapped - so measure, aspirate and record whether fluctuant, firm, adherent, moveable, SQ vs cutaneous.
99
How do you obtain a diagnosis of STS?
cytology is of limited usefulness but may rule out other ddx for lipomas, seromas or abscesses. sarcomas do not often exfoliate well so false negatives are common. Cells often appear - spindle to elongate to ovoid in shape, nuclei tend to be elongate in shape, wispy appearance to the slide - pink staining material amongst the neoplastic cells. obtaining a biopsy provides a definitive diagnosis in most cases. An incisional or punch biopsy almost always appropriate. Excisional biopsy or appropriate for small masses although it is extremely important that one documents the location and size of the lesion. Always submit for histopathology. Grading system for STS evaluates differentiation, the number of mitotic figures/ 10 HPF (mitotic index) A final grade is given based on scores obtained by looking at the individual criteria. It is predictive of metastasis. Most are low or intermediate grade. incomplete margins indicate that a tumour is more likely to recur at the site compared to completely excised margins. Mitotic index also independently prognostic.
100
How do you stage a soft tissue sarcoma
routine blood work and urinalysis, thoracic radiographs overall metastatic rate <20%. metastatic rate is related to tumour grade. Regional lymph node cytology, lymph nodes rarely positive. regional radiographs of the mass - extent of disease and involvement of adjacent tissue. comoputed tomography or magnetc resonance imaging. advanced imaging can always air in defining the extent of the tumour. generally indicated if mass is large and surgical resectability is questionable, the mass s large and pre operative radiation therapy is anticipated. if critical structures are involved. Abdominal imaging is not necessary in most patients given low diagnostic yield but is indicated if any GI signs are present.
101
What is the treatment for soft tissue sarcoma?
Generally - treatment is determined on basis of location, grade and clinical stage, ability to surgically remove. surgery and radiation therapy are the most successful treatment options. chemotherapy plays a minimal role in definitive treatment. Surgery - aggressive surgical excision is necessary despite the appearance of a well encapsulated mass - pseudocapsule exists and tumour cell extend beyond this. If the tumour is adherent to underlying tissues, remove all en blocl. goal is 3cm margins around palpable mass and 1 fascial plane below the tumour. Dissect only through normal tissues and change gloves/instruments for closure. Avoid placing drains. submit excised portion for histopathology. If radiation therapy is anticipated, place hemoclips, plate the scar strategically such that additional therapy can be done if margins are not achieved (do not create a horizontal surgical scar across the distal limb).
102
What is the prognosis of STS with surgery?
potentially curative with low and intermediate grade soft tissue sarcomas in dogs. most dogs experience long term survival following surgery. Incomplete excision of low grade tumours may also achieve long term local control in some dogs. recurrence rate is variable and is approx 10-30% and occurs at 3mo-5yrs. generally speaking, narrowly excised tumours have a better prognosis than those sections with tumour cells at the edge of the histology section. The time to recurrence becomes shorter and shorter with each surgery that is performed. the metastatic rate also increases with each recurrence. best change at long term control is with first treatment.
103
What are the treatment options for incomplete surgical resection?
Revision surgery - scar is treated as the tumour and a subsequent surgery is performed - goal is 3cms margin and 1 fascial plane deep. Radiation therapy - excellent option for narrowly excised or incompletely excised soft tissue sarcomas in the dog, as radiation works best against microscopic disease. This effectively sterilises cells left behind at the surgical bed. Close monitoring is always an option, up to 70-90% of low grade narrowly excised tumours will not recur after surgery. typically check 1 month post surgery, 3 months and every 3 months thereafter followed for 18 months then every 6 months for 18 months.
104
What is the prognosis for STS with radiation thrapy
typically delivered daily for 4-5 weeks the intent is to cure the tumour. radiation works best on microscopic disease although it has been used relatively unsuccessfully in the macroscopic disease setting. it kills cells in a logarithmic manner - it kills the same percentage of cells with each dose so the smaller number of cells, the higher the overall tumour cell kill. location is prognostic - oral tumours are harder to control.
105
What is the prognosis for STS with chemotherapy only?
not very effective for STS and response rates of 15-20% expected. unclear if combining chemotherapy with other treatments is useful for soft tissue. typically considered for palliation, high grade soft tissue sarcoma in conjunction with local contorl, if distant metastasis or lymph node metastasis is present.
106
What is hip Luxation and the common clinical signs?
Common, usually traumatic, most are unilateral, craniodorsal. Signs are NWB lameness, limb adducted, hock rotated outward. Asymmetry - greater trochanter displaced dorsally, increased distance from ischial tuberosity to trochanter, shortening of the affected limb, extend limbs evenly backwards.
107
What are the radiographic signs of hip luxation?
Always take two orthogonal views - check for pelvic or avulsion fractures as they may stop reduction, assess for the presence of hip dysplasia - makes closed reduction less likely to succeed.
108
What are the management options of hip luxation?
Closed reduction + adjunctive support.
Open reduction + adjunctive stabilising procedures
Surgical salvage + total hip arthroplasty, femoral head and neck excision
Prompt attention to avoid damage to articular cartilage, reluxation is common.
109
Describe closed reduction of hip luxation
Success rates are generally poor. most likely to succeed if hip conformation normal, if unilateral luxation, if no other orthopaedic injuries exist that require immediate weight bearing on the damaged hip, reluxation is usually due to soft tissue trapped in the acetabulum from the joint capsule or a haematoma. convert to craniodorsal luxation then reduce the joint. Put through a full ROM, assess apparent stability, (apply ehmer sling)
110
What is the ehmer sling?
Prevents weight bearing, maintains internal rotation of the femur - enhances hip stability, correct application is critical to avoid vascular compromise, difficult to maintain on cats.
111
What is a devita pin?
Maintains reduction following craniodorsal luxation, IM pin ventral to tuber ischium, dorsal to femoral neck and through the ventral aspect of the ilium, will pass close to the sciatic nerve, possible complications include sciatic damage, reluxation, pin migration.
112
Describe open reduction of a hip luxation?
Indications: closed reduction fails, reluxation, acetabular fracture, significant HD or OA present, contralateral limb injury, failure rates lower than for closed reduction, Approach - craniolateral, dorsal. Protect articular cartilage, preserve the joint capsule, remove soft tissues from the acetabulum - LFH & organising haematoma. Always attempt to reconstruct the joint capsule if performing an open reduction.
113
What is an iliofemoral suture?
Craniolateral approach, bone tunnels prepared in femoral neck & ventral ilium just cranial to the hip, tie suture with hip abducted and stifle joint internally rotated,
114
What is a dorsal capsulorhaphy?
Requires a greater trochanter osteotomy to provide access to the dorsal acetabular rim. Suture anchor points in dorsal acetabular rim - screws & flat washers, suture anchors, must not penetrate acetabulum. L Hip 10 and 1 oclock positions, R hip 11 and 2 oclock positions. heavy suture material anchored, through a transverse tunnel in the femoral neck and around the screws. tighten suture with hip in slight internal rotation, normal standing angle, slight abduction, femoral head firmly reduced.
115
What is toggle pin fixation?
Replacement of LFH with a prosthetic ligament. ligament anchored on the medial aspect of the acetabulum with a toggle pin, passes through acetabulum at origin of LFt. Passes into femoral head at insertion of LFH. Exits on lateral aspect of femur. passes through a second transverse bone tunnel.
116
What is a transarticular pin?
replaces the LFT with a SS pin, drill a pilot hole retrograde from the fovea capitis, insert Im pin until tip just visible, reduce luxation. Drive pin 4-5mm further through the acetabular wall, not too deep otherwise damage pelvic organs. bend pin over and cut off. usually removed 4-6 weeks later.
117
What is greater trochanter transposition
After greater trochanter osteotomy - re attach trochanter distally and caudally. increases tension in gluteal mm group - improves medially directed forces.
118
What is avascular necrosis of the femoral head?
It has an inherited basis in some breeds. affects terrier breeds & other small dogs. aetiology unknown. there is an inadequate blood supply to the femoral head during development. avascular necrosis, trabecular collapse, inadequate cartilage support & collapse of the femoral head with weight bearing. Clinical signs are progressive hindlimb lameness from 5 months, shifting lameness if bilaterally 10-20% of cases, muscle atrophy may do handstands, crouched stance, bunny hopping gait, pain & crepitus on hip manipulation, reduced ROM. VD extended view most useful. there are focal areas of lucency within the femoral head and neck. Trabecular collapse leads to areas of increased density. Joint incongruity, secondary degenerative change. Treatment is with femoral head and neck excision which allow rapid and predictable return to function.
119
Describe a femoral head and neck excision?
Craniolateral approach to the hip joint - maintains gluteal integrity. Luxate femoral head. externally rotate stifle to 9 degrees. Remove entire femoral head and neck. Avoid leaving a bone spur. Must section LFH to allow adequate visualisation. Osteotomy with Oscillating saw or osteotome - beware of femoral fracture, gigli wire, bone cutters. Always take a post op radiograph. revise if unhappy. no indication to use muscle slings if the procedure is performed correctly. Bilateral FHNE can be staged or performed together. FHNE results are adequate to excellent - better in animals with low body mass. Fibrous pseudoarthrosis forms. limb length and ROM are reduced but movement is pain free. Rest for 7-10 days after op then encourage exercise with frequent lead walks, analgesia, swimming, hysiotherapy, stair climbing. expect good function to be returning by 4-6 weeks.
120
What is hip dysplasia?
A developmental disease of the coxofemoral joint -affected animals are born with normal hips. there is an inherited predisposition to develop HD. Polygenic dominant trait with incomplete penetrance, heritability index 0.2-0.6. Environmental influences - exercise, body mass, growth rate etc. Affects many breeds, primarily large breeds, some cats. There is a disparity between skeletal and muscular growth which leads to hip LAXITY. this hip laxity allows SUBLUXATION. Subluxation means forces are unevenly distributed over the acetabulum and femoral head & concentrated over a small area. There are altered distribution of forces which causes microfracture, tearing of sharpeys fibres, cartilage degeneration, synovitis, pain.
121
What is the ortolani test for hip subluxation?
Assess the quality of the clunk which gives information about the integrity of the dorsal acetabular rim. if there is a slide: there is a loss of DAR. if there is a grate: articular erosion and degenerative change. Clunk: Ideal.
122
What occurs in hip dysplasia in skeletally immature dogs?
Changes lead to altered modelling and remodelling in an attempt to stabilise the joint. microfractures heal, periarticular soft tissues heal, femoral head flattens, infilling of acetabulum, clinical signs will often improve at about a year of age. Clinical signs may recur as secondary degenerative change becomes established - often from middle age onwards.
123
What are the clinical signs of hip dysplasia?
In young dogs; Signs primarily associated with pain - poor h/q muscle development, difficulty rising after lying down, rolling gait, bunny hopping when running, audible noise associated with hip movement, pain and crepitus on hip manipulation. In adult dogs: signs primarily associated with secondary osteoarthritis - stiffness on rising, stiffness after exercise, lameness, exercise intolerance, muscular atrophy, crepitus and pain on hip manipuation, reduced ROM in affected joints.
124
Which radiographs should be taken of the hips? What radiographic change may you see?
Standard VD extended hip view, lateral
Additional views - VD frog legged view
Might see; joint incongruency, subluxation (check fremoral head cover, norberg angle) increased angle of inclination (normal 130-1450, coxa valga), rotation of femoral neck (normal: 12-40 degrees anteversion, anteversion or retroversion).
125
What is the norberg angle?
Gives an objective measure of coxofemoral subluxation. normal considered >105.
126
What secondary radiographic change may be seen with hip dysplasia?
New bone deposition - around femoral neck, in and around acetabular fossa.
Joint remodelling - femoral head, acetabulum.
Severity of radiographic signs and clinical signs are poorly correlated.
127
What are the treatment options for skeletally immature animals?
Conservative - clinical signs will improve in many dogs following the period of rapid growth. surgical - triple pelvic osteotomy, femoral head and neck excision, pectineal myotomy/myectomy, total hip arthroplasty. Conservative management is the first line response in all immature animals unless they are a TPO candidate, very effective, affordable, few complications. three point plan for osteoarthrosis management - weight control, exercise regulation, analgesia.
128
What is pectineal myotomy/myectomy?
The pectineus muscle is transected or resected - normal function is as a hip addctor. may provide transient benefit & relief of pain. does not alter progression of disease.
129
What is triple pelvic osteotomy
Three osteotomies isolate the acetabulum. The acetabulum is rotated 20-30 degrees laterally to increase femoral head cover. aim to improve hip joint congruity to slow or halt the development of osteoarthrosis. Patient selection for TPO - significant lameness, no/minimal degenerative change, intact DAR - ortolani test, usually animals <10mo. TPO complications are avoided by good owner/patient compliance - strict exercise restriction until healing is complete. Implant failure - screw pull-out, screw fracture, loss of alignment, sciatic paralysis, narrowed pelvic canal.
130
What is total hip arthroplasty?
Expensive salvage procedure - £4000 if uncomplicated, requires specialised instrumentation, technically demanding, unforgiving of errors, referral procedure, high standard of asepsis needed. Can use a Modular cemented or non cemented prosthesis. Case selection is vital; unresponsive to conservative management, systemic disease, Neuromuscular disease, other causes of lamness, sources of bacterial infection. Unilateral THA is the normal. seldom necessary to replace both hips even in bilaterally affected animals. Post operative care - strict rest for 8 weeks - short lead walks, radiograph at 3,6 then every 12 months. complications are bad news e.g pulmonary embolism, femoral fracture, luxation, sepsis, aseptic loosening.
131
What is the BVA-KC hip dysplasia scheme?
Dogs must be >12 months. ventrodorsal extended hip view assessed. pelvis straight - obturator foramina, wings of ilium, femora pparallel and adducted - to each other (adducted) and to the film. Patella centred over trochlear grove. Patellae do not need to be in film. KC number, microchip/tattoo number, L/R marker, date. X-rite tape or light marked onto filim. Nine anatomical features are scored - 2 relate to primary pathology, 7 assess secondary change. Maximum score is 106 - 53 on each hip. tables of breed averages are published. aim to reduce the incidence of HD by identifying animals free from or with less severe disease. recommendation is to breed from dogs that score significantly lower than the BMA.
132
Describe the process of wound healing
Inflammatory phase - Haemorrhage and clot formation -scaffold for repair. Increase blood flow - increase oxygenation, source of inflammatory cells, start to control bacterial infection.
Debridement phase - Neutrophils phagocytose bacteria and die, macrophages - phagocytosis of debris, protease, release cytokines driving cellular response. Exudate - sloughing tissue, cells + bacteria.
Repair phase - Granulation tissue forms, macrophages promote fibroplasia and angiogenesis, vessels migrate into fibrin clot. collagen matrix is laid down. Epithelialisation - migration between eschar and granulation tissue.
Maturation phase
133
What should granulation tissue look like?
Healthy granulation bed - highly resistant to infection, lattice for scar formation, nutrient and oxygen supply, red, flat, epithelialising.
Unhealthy granulation bed - pale, not progressing, usually due to necrotic debris or infection.
134
what factors promote epithelialisation?
Absence of infection, absence of necrotic debris, oxygen at wound surface (vessels), moist wound environment, healthy granulation bed.
135
What is the maturation phase?
Scar contracts. Collagen remodels increasing strength. continues for weeks or months.
wound strength - inflammatory phase 3%
Proliferative phase 20%
Maturation phase 80%.
136
What factors affect wound healing?
endpoint of initial wound management: granulation tissue with epithelialisation, free of infection, free of necrotic debris, healthy local environment promoting repair.
1. host factors; old age, hypoalbuminaemia, endocrine disease eg cushings, diabetes mellitus, metabolic disease e.g uraemia, exogenous steroids.
2. Local factors - local factors often delay healing - foreign material, infection, trauma, dessication, hypoxia.
Host factors have less measurable effect. combinations of host factors have more effect.
To promote wound healing - removal of non viable tissue, coontrol of infection, good tissue oxygenation, moist surface, no trauma.
137
What are the different types of wound closure?
Primary closure - immediate closure of healthy wounds e.g surgical wounds and some traumatic wounds <6hours old.
Delayed primary closure - closure after bacteria and debris have been eliminated but before granulation starts.
Secondary closure - closure once granulation tissue has formed. Healthy granulation implies no infection or necrotic debris.
second intention healing - granulation, epithelialisation and contraction. Most surgical wounds can be closed immediately as they have no significant contamination or devitalised tissue. most traumatic wounds require an initial period of management prior to closure because of contamination and presence of devitalised tissue.
138
Describe bandages
1. contact layer
2. intermediary layer.
3. tertiary layer
Can be adherent - debrides wound surface, used in initial stages, speeds debridement phase.
Non adherent - protects surface, promotes granulation, cover surgical wounds.
Many non adherent dressings have an adhesive backing to stick to skin. these adhesives are inactivated by moisture so that the dressing does not adhere to the wound surface. The contact layer may be SEMI occlusive - exudate can leave surface, for moderate to high exudate. or Occlusive - traps fluid at surface, promotes epithelialisation, repair phase. Intermediary layer - holds contact layer in place and absorbs exudate passing through contact layer. provides padding and support. Tertiary layer - holds intermediary layer in place, protects from environmental contamination, applys pressure to dressing.
139
Describe the use of antibiotics in wound management
All traumatic wounds are contaminated. contaminated wounds become colonised with bacteria within hours. Antibiotics are indicated in most traumatic or open wounds. Open ended courses promote resistance and are ineffective. give therapeutic course then STOP. All topical agents have the potential to impede granulation and epithelialisation, select cases carefully.
140
What is silver sulfadiazine?
Topical wound bactericidal broad spectrum antibiotic. apply early to prevent bacterial colonization. for burn therapy.
141
What are silver dressings used for?
They are topical wound treatments. They have Ag+ Ions. they are bactericidal, independent of culture and sensitivity.
142
What are honey dressing used for?
Antibacterial, encourage sloughing, create moist wound environment, have osmotic effect, accelerate wound healing.
143
Describe open wound management
Initial assessment and preparation. debridement phase 2. granulation phase 3. Use clean or aseptic technique. cover wound with sterile dressing. give wide clip. Prevent further contamination - pack wound with sterile k-y gel. clip widely, gel traps hair. lavage gel off. Lavage to remove contaminations with sterile saline/isotonic crystalloid in high volumes and moderate pressure. use a 19 guage needle and 35 ml syringe.
144
Why do you debride tissue in wound management?
Initial debridement with sharp dissection, scraping with blade, rub with dry swab - devitalised/contaminated/redundant compromised tissue.
Devitalised tissue - white, green, black, does not bleed when nicked, loss of skin pliability, thinning of skin.
Continuing debridement - adherent dressing, 48 to 72 hours, during period when wound is exudative.
145
What is a wet to dry dressing
for debridement - primary layer -sterile open weave, moist - soaked in saline, wrung out. debris adheres.
Secondary layer - dry, sterile absorbent, wicks fluid from contact layer.
Immobilise.
changing dressing - do not moisten, painful, causes trauma. Lavaging at dressing changes helps to remove debris from surface.
146
How often should you change a dressing?
minimum of every 24 hours. typically every 12-24 hours. before dressing is saturated, before strike through. Change non adherent dressings when all necrotic tissue is removed and exudate reduces & granulation starts - will not progress with a wet to dry dressing.
147
What are the aims of a non adherent dressing with granulation?
Non adherent dressing, moist wound environment, promote granulation: angiogenesis + fibroplasia, initiate epithelialisation. Foam dressing (hydrocellular) - polyurethane foam, absorbent, non adherent, semi occlusive. Hydrogel - carboxymethylated cellulose polymer. fits irregular wounds well. prevents adherence of secondary layer. Healthy granulation tissue is red, uniform, minimal exudate, progressing daily. End point of wound management: no significant bacterial infection, no foreign material, no devitalised tissue, good blood supply, can now progress to wound closure. Unhealthy - pale, static, exudate.
148
What are the different layers of the skin
Epidermis, dermis, hypodermis, panniculus muscle.
Direct cutaenous vessels > subdermal plexus > middle plexus > papillary plexus. Undermine below the panniculus muscle to preserve the subdermal plexus and direct cutaneous blood supply.
149
What type of sutures should you use for the skin?
Buried suture increases risk of infection. synthetic monofilament, small knot. swaged on reverse cutting needles, simple appositional patterns,
150
What are drains
Eliminate dead space, remove exudate, maintain contact between skin and wound (active drains), always exist via separate incision.
151
When can tourniquets be used?
Distal extremties, caution over possible vascular compromise, aim <45 mins.
152
How can you relieve tension in a wound?
Wounds must be closed without tension, tension leads to dehiscence, tension can be accommodated by attention to tension lines, tension relieving suture patterns, reconstructive techniques. Pull of tissues create tension lines. close wounds parallel to tension lines. Consider tension lines when planning excisions. Skin elasticity - limited around eye, anus, extremities. plentiful over thorax and abdomen. Use undermining and waking sutures - the main form of tension relief. undermine below paniculus muscle. undermine below subcutaneous tissue when panniculus is absent. Walking sutures follow undermining - this distributes tension through wound and relieves tension from skin apposition.
153
Describe the tension relieving suture patterns?
Subcuticular pattern - continuous patterns distribute tension along entire suture line
Walking sutures
Mattress sutures
Cruciate mattress
Vertical mattress
Horizontal mattress
Temporary mattress sutures- stented mattress, leave in for 72 hours, skin elasticity increase.
154
Should dog ears in sutures be removed?
They are healthy skin, purely cosmetic, flatten over time, removing compromises blood supply to skin flaps.
155
What are relaxing incisions?
Close one wound by creating a second wound adjacent to it. rarely utilised for this reason. used to shift wound away from pressure point or into an area where there is more available skin.
156
Describe the removal of skin tumours
Clip widely. resect primary mass, biopsy tract & margin of grossly normal tissue. elliptical wounds - long axis along tension line. Consider staging prior to exciison. 1cm margin to next facial plane deeply - for excisional biopsy or known benign skin lesions. 2cm to 3cm margin _ include next unaffected deep plane for infiltrative & aggressive skin tumours e.g mast cell tumour soft tissue sarcoma.
157
Describe mastectomy technique
elliptical incision around glands. minimum 1cm margin of healthy tissue. ligate vessels proximally & distally. Dissect down to body wall fascia. Close wound with a combination of undermining and walking sutures. If tumours extends to level of body wall fascia, resect outer layer to give adequate margin.
158
Describe the resection of an invasive mass eg fibrosarcoma
Include 3cm margin laterally & one unaffected fascial plane deeply.
159
What are pedicle flaps?
Subdermal plexus flap - common & simple , rely on subdermal plexus, blood supply dependent on length and width of flap.
Axial pattern flap - less common & more complex, rely on single large direct cutaneous vessel flap length limited only by angiosome of vessel.
Advancement flap - utilises excess skin adjacent to defect. blood supply relies on width, length. simple technique.
Transposition flap - shortens as rotates, utilises excess skin close by. blood supply relies on width and length. advanced technique.
160
Describe a free skin graft
It must be developing new vascular supply from the wound bed. takes 10 to 14 days to establish new blood supply. most applicable to distal extremity. may be meshed.
161
What is synovial fluid?
An ultrafiltrate of blood. It has hyaluronan added (type B synoviocytes) functions are nutrition of articular cartilage/menisci, lubrication. It is clear, colourless/pale yellow, viscous, small volume, low cell count (<3x10^9 cells/l), mononuclear cytology.
162
Describe the joint capsule and ligaments
Made of dense fibrous tissue. ligaments may be joint capsule thickening (collaterals) or distinct entities (CCL, meniscal ligaments). functions - maintain normal bony relations. limit movement of joints.
163
What are the clinical signs of joint disease? How is it diagnosed?
Lameness, pain, reduction in normal movement, effusion, instability, crepitus. Further investigation: diagnostic imaging, radiographs, magnetic resonance imaging, computed tomography. Arthrocentesis - gross evaluation, cytological evaluation. culture, synovial biopsy, arthroscopy.
164
What is arthritis?
Inflammatory joint diseases
| Polyarthrtiis - inflammation of >1 joint
165
What is akylosis?
Reduction in articular motion
166
What is arthrodesis?
Surgical fusion of a joint
167
What is osteoarthritis?
a form of degenerative joint disease affecting diarthrodial joints. It is a clinical syndrome in which low grade inflammation results in pain in the joints. OA is caused by abnormal wearing of the cartilage and destruction or decrease of synovial fluid that lubricates those joints. As the bone surfaces become less well protected by cartilage the patient experiences pain. due to decreased movement because of pain, regional muscles may atrophy and ligaments may become more lax. OA is characterised by degeneration of articular cartilage with concurrent peri articular new bone formation and fibrosis. OA is inflammatory. May be primary - genetic. or secondary - developmental, inflammation, instability/trauma, iatrogenic.
168
What is the pathogenesis of OA?
Abnormal motion on normal cartilage. normal motion on abnormal cartilage. Fibrillation of the superficial layer, roughening of articular surface. fissues. Inflammatory response to increased motion/cartilage fragments in synovium - pro inflammatory mediators, prostaglandins, cytokines (IL1, TNFa). Release of destructive enzymes - matrix metalloproteinases, aggrecanases. The balance between cartilage anabolism and catabolism is disrupted. multiple tissues involved- cartilage, synovium bone, fat pad.
169
How is diagnosis of osteoarthritis made?
History; acute or chronic, intermittent or continuous, previous injury/disease to joint, stiffness after rest.
Feline - reduced ability to jump, height of jump, stiffness, activity (general demeanour), lameness. Clinical findings; lameness, pain, reduction in normal movement, effusion, crepitus. Radiography: effusion, soft tissue thickening, osteophytosis, sclerosis, computed tomography, magnetic resonance imaging. On arthrocentesis there may be increased or decreased volume, reduced viscosity, increased WBC (up to 5x10^9) - predominantly mononuclear.
170
What is the treatment of OA?
Medical (non surgical) management or surgical management. Medical management - weight management, reduce weight, this can delay signs of OA, decrease requirement for analgesic. Exercise management - controlled lead exercise, avoid impact activities (playing,stairs etc), tailor to minimise/prevent clinical signs, physical therapy - increase mobility. Nutritional supplementation with omega 3 fatty acids - replace arachidonic acid AA with eicosapentanoeic acid, this reduces pain and inflammation, direct supplementation or preformed diet. Give slow acting disease modifying agents eg glucosamine, chondroitin sulphate, pentosan polysulphate (cartophen). NSAIDS - block COX2, many available, may cause GI ulceration, renal disease. corticosteroids - last line of treatment, do not combine with NSAIDS. Pain management - acetaminophen, opiates. Also may give PSGAGs, hyaluronan.
171
Describe the surgical management of OA?
Corrective osteotomies,
Arthroplasty - excision arthroplasty, joint replacement, hip, elbow, stifle.
Arthrodesis - any joint except hip.
No treatment curative. no treatment prevents progression, tailored to individuals.
172
What is bacterial infective arthritis?
Septic arthritis.
Direct: penetrating wound, surgery
Indirect: haematogenous spread from respiratory, GIT, UG. usually affects an abnormal OA joint. Massive inflammatory response. extravasation of PMNS. enzyme release, loss of nutrition and load bearing. Articular cartilage destruction. Severity depends on duration and infective agent.
173
How is diagnosis of infective arthritis made?
Arthrocentesis - large volume, abnormal appearance (cloudy, watery), increased cell count >>3 x10^9 cells/l, neutrophilia, bacteria. Bacterial culture - before antibiotsis, enrich e.g blood culture media.
174
How is bacterial infective arthritis treated
Antibiotics - broad spectrum initially, culture and sensitivity. 4-6 weeks (or 2 weeks after signs resolve). surgical flush - arthrotomy, arthroscopy. 50% return to normal function. weight/duration worsen prognosis. surgical management confers no advantage.
175
What is Lyme disease?
Caused by borrelia burgdorferi. transmitted by ixodes ticks. owners report finding ticks. clinical signs are seen weeks - months later. waxing and waning signs - polyarthropathy, lymphadenopathy, fever. Culture difficult. serology - cross reacts with leptospires. can use PCR to diagnose. treatment - tetracycline
176
what are the principles of biological osteosynthesis?
Aims to take full advantage of biologic healing potential to maximise rate of fracture healing - maintain limb length and orientation, avoid creating further surgical trauma, provide an optimal biological and mechanical environment for fracture repair.
177
Compare and contrast the merits/drawbacks of using a bone plate or an external skeletal fixator for a fracture of the femur.
ESF - a series of percutaneous pins pass into or through the bone, connected together externally, by clamps and rods/acrylic bars /epoxy putty. they are versatile, easy to apply, compatible with principles of biological osteosynthesis as they maintain alignment and length of limb, disturb fracture fragments minimally, can be removed in a staged way - to encourage callus maturation, excellent for management of open fractures, not restricted to use below elbow and stifle. Use of a bone plate and screws - very versatile, if used carefully can effectively neutralise all forces acting on a fracture, Use as long a plate as possible and aim for six gripping cortices above and below the fracture line, all screws must be tight, avoid bone defects and use cancellous bone graft if comlete reconstruction is not possible. May be applied as a tension band plate - which compresses the tension cortex, used for transverse or short oblique fractures, articular fractures or osteotomy repair an treatment of non unions, arthrodesis. A neutralisation plate is applied to protect a lag screw reconstruction - cannot atke significant loads without failure, load sharing is between plate and bone the plate resists torsion bending and shear. buttress plate used when the fracture cannot be anatomically reconstructed - no load sharing between bone and plate. Plate takes whole load. Dynamic compression plate - spherical screw head slides down the incline of the screw hole as the screw is tightened with compresses the fracture site. Chose plate based on patient size, age, fracture conformation, owner factors, controlled exercise.
178
What is the pathogenesis of immune mediated joint disease?
Innapropriate response in the synovium, pain and lameness. Genetic component in RA, toy breeds predisposed to RA, females predisposed to IMPA.
179
What are the clinical signs of immune mediated joint disease?
Pyrexia, stiffness after rest, lameness of multiple limbs/waxning and waning. acute or chronic. Joint effusion, multiple joints affected (2-5), distal joints, symmetrical joint swelling, overt joints pain.
180
Describe arthrocentesis to diagnose immune mediated joint disease
Use a 40mm x 21G sterile needle and a 5ml syringe/2ml syringe, place in EDTA tube, then on glass slides & blood culture media. Analyse synovial fluid for increased volume, reduced viscosity, turbidity, raised cell count, neutrophilic cytology. For the elbow joint - elbow in a neutral position, palpate lateral epicondyle and electranon, needle in parallel to ulna. For antebrachiocarpal joint - Flex maximally, insert needle dorsally, medial to common digital extensor tendon/cephalic vein. for stifle joint - slight flexion, palpate tibial tuberosity/patella,/straight patella ligament, needle between them at 45 degree angle.
181
What is the treatment of immune mediated joint disease?
Immunosuppression: prednisolone 2mg/kd, not anti inflammatory dose, check remission with repeated arthrocentesis, gradually taper dose over 4-6 wks. For poor responders; cyclophosphamide, azathioprine, chlorambucil, leflunomide/ciclosporin. monitor for side effects.
182
Describe the use of azathioprine for immune mediated joint disease
May be given concurrently with prednisolone, if remission is achieved, reduce dose to 1-2mg. monitor haematological profile weekly for bone marrow suppression. do not use in cats.
183
Describe the use of cyclophosphamide for immune mediated joint diseases
50mg/m2 eod or 4 consecutive days each week. monitor haematological and biochemistry profile weekly for bone marrow suppression and hepatic/nephro toxicity. monitor urine for haemorrhagic cystitis.
184
Describe the treatment of immune mediated joint diseases with chlorambucil
May be given concurrently with prednisolone. 2-6mg/m2 sid, po until remission. if remission achieved reduce dose. monitor haematological profile weekly for bone marrow suppression.
185
Describe the classifications of immune mediated arthritis
Erosive forms;
Rheumatoid arthritis,
Periosteal proliferative polyarthritis. Non erosive forms: SLE, idiopathic IMPA types I, II, II, IV.
186
What is the pathogenesis of rheumatoid arthritis?
rheumatoid factors IgM and IgG to Fc IgG - immune complex disease/type 2 hypersensitivity. Immune complexes deposited in the synovium> inflammatory response> pain/synovitis > pannus deposition. Most common erosive IMJD. Small/toy breed dogs/ 5-6 yo. erosive changes take time.
187
What are the clinical signs of rheumatoid arthritis?
Stiffness after rest, pain in at least one joint, swelling of at least one joint, swelling of at least one other joint in 3 months, symmetrical join swelling, subcutaneous nodules, erosive lesions on radiography, positive rheumatoid factor, poor synovial fluid mucinclot, characteristic synovial histpathology. 20-70% are rheumatoid factor +ve.
188
What is the treatment of rheumatoid arthritis?
Immunosuppresion, arthrodesis
189
What is periosteal proliferative polyarthritis
(feline chronic progressive polyarthritis) Aggressive erosion and new bone formation. FeLV 60% of cases associated but pathogenesis unknown. Signalment - males, usually 18m-5yo, treat with immunosuppression. poor prognosis.
190
What are the main 2 types of non erosive immune mediated arthritis?
Idiopathic immune mediated polyarthritis or systemic lupus erythematosus. Also occasionally see polyarthritis/polymyositis, polyarthritis/polymeningitis, arthritis of japanese akitas, amyloidosis of chinese sharpei.
191
What is idiopathic immune mediated polyarthritis?
There are four subgroups - type 1 - no association. type 2 - reactive. type 3 - enteropathic. type 4- neoplastic. No association with vaccination. prognosis depends on underlying disease but better than for other IMPA. Type 1 - 50% cured.
192
What is systemic lupus erythematosus?
A multi system disease - which causes any of : non erosive polyarthritis, renal disease, dermatological lesions, haemolytic anaemia, thrombocytopaenia. It is caused by autoantibodies to nuclear antigens, immune complex disease.
193
Which vaccinations may cause joint disease?
Vaccination reactions uncommon, after primary vaccination course. antigenic stimulus. cats: feline calicivirus antigens. dogs: canine distemper. Resolves rapidly within 7 days. Quantify antibody titre before future vaccination.
194
What is a drug induced polyarthritis?
Antibody -drug induced vasculitis. long term or previous therapy. most common causes include cephalosporins, penicillins, sulfa drugs. dobermans are susceptible to - sulphadiazine-trimethoprim. resolves 2-7 days after drug stopped. Also causes thrombocytopaenia, haemolytic anaemia, polymyositis, dermatological abnormalities.
195
what is plasmacytic- lymphocytic synovitis
Seen in stifle joint, uni or bilateral, often associated with CCL rupture. Arthrocentesis - markedly increased WBC count, mononuclear. treatment: surgery for CCL rupture, immunosuppression.
196
What is elbow dysplasia?
a group of developmental conditions: fragmented coronoid process, osteochondrosis of the medial part of the humeral condyle, ununited anconeal process.
197
Describe the BVA/KC scoring scheme
Grade 0 - no osteophytosis, grade 1 - osteophytes 5mm.
198
What is a fragmented coronoid process
Spectrum of pathology - complete fragmentation, partial fissuring, abnormal shape. Abrasion of Medial conoronoid process and humeral condyle, development of elbow OA. Clinical examination - elbow pain on extension and flexion/supination. medical management - most cases improve, Surgical management - arthrotomy or arthroscopy, fragment removal, coronoidectomy. OA will progress regardless.
199
Describe OCD of the medial part of the humeral condyle
Osteochondrosis -failure of endochondral ossification. Genetics, over nutrition, ischaemia. Pathophysiology - Failure of ossification - thickens > necrotic chondrocytes - trauma causes cleft/flap (OCD). Clinical signs when flap present. Moderate/marked lameness, elbow pain on extension, frequently bilateral. Surgical removal of the flap - arthroscopy or medial arthrotomy, prognosis usually improve but lameness may not be fully resolvable. OA progression inevitable.
200
What is an ununited anconeal process
The anconeal process has a separate centre of ossification at 3months, and fuses to the ulna at 5-6 months. pathophysiology - developmental incongruity, long radius, narrow trochlear notch of the ulna. signs; crepitus, marked effusion, pain on extension, 25% bilateral disease, must be >6months. Take radiographs - flexed mediolateral. Medical management if not painful. surgery - removal, simple but profound OA. surgery - fixation - lag screw and ulna osteotomy, best choice if dog is young.
201
What is incomplete ossification of the humeral condyle?
At the humeral physics - intercondylar cartilage plate. Ossifies at 12 weeks. Failure of ossification - results in tissue IOHC, seen in some immature dogs but also mature. spaniels predisposed. IOHC predisposes to fracture of humeral condyle - lateral part, medial part or Di condylar. Treatment IOHC with a position screw, Treat fracture with a lat or med lag screw or dicondylar - plate fixation or ESF.
202
What is traumatic elbow luxation
Rupture/avulsion of collateral ligaments. Usully lateral luxation. History of trauma, non weight bearing, radial head lateral, extremely painful, characteristic posture. Test of integrity of collateral ligaments with normal opposite limb. Always take 2 views. check for avulsion fragments. Treat with closed reduction or if unable to reduce closed - open reduction. Surgical repair - re attach avulsion, replace ligaments.
203
What is developmental elbow luxation/subluxation
Assynchronous growth of the radius and ulna. Premature closure of physics (Trauma/chondrodystrophy) results in elbow incongruity. Diagnose by signalment - age, length, rotation, varus/valgus deformity, below pain.
204
Describe a short ulna in developmental elbow luxation
Distal ulna growth plate - effects - radius curtis, valgus, shortening, humeroulna subluxation. Treat - lengthen ulna (osteotomy or ostectomy
205
Describe a short radius in developmental elbow luxation
Proximal or distal radial Growth plate. effects - shortening, rotation, varus, humeroradial subluxation. Treat - legnthen radius, shorten ulna (ostectomy)
206
What is congenital elbow lunation?
Type 1: humeroulna subluxation - seen in toy breeds, olecranon rotated lateral to distal humerus, marked lateral deviation of the antebrachium. Treatment - using limb well: nothing, non weight bearing : refer. Type 2: radial head luxation - medium - large breeds. displaced caudal and lateral, palpable radial head, often minimal/no lameness. painful/poor limb function - refer for surgery.
207
What are the salvage procedures for congenital elbow luxation
Elbow arthrodesis - For a severe intractable elbow joint, fused at 110 degrees, caudal plate. marked mechanical lameness.
total elbow replacement - indication, painful elbow, unable to manage medically - results 80% success at 1m po. complications common, luxation, infection, fracture, may require arthrodesis.
208
Describe the shoulder joint
It is an enarthrodial joint (ball and socket) made up of the scapular glenoid, humeral head, glenohumeral ligaments, joint capsule and muscular support of the spinatous muscles and biceps brachia.
209
What is shoulder osteochondrosis?
Failure of endochondral ossification - flap formation (osteochondritis dissecans) at the caudal humeral head. seen at 4-8 months, males > females. Mild/moderate lameness, pain on shoulder exam, especially flexion, pain on palpation of biceps tendon if detached flap in the bicipital groove. 50% bilateral. On radiography: radiolucent deficit in subchondral bone. rarely flap may be mineralised/detached. Positive contrast arthrogram - identify presence/location with non ionic iodine contrast media - arthrocentesis, remove SF then install media.
210
What is the treatment of shoulder osteochondrosis?
Medical - 50% improve, flap becomes detached. surgical - arthroscopy/arthrotomy. Flap removal, abrade the surface to facilitate vascularisation. 90% sound within 4-8 weeks of surgery. will develop mild DJD with time.
211
What is traumatic shoulder luxation?
Dislocation. Trauma to supporting structures - the biceps brachii and glenohumeral ligaments. monitor for concurrent thoracic trauma. Non weight bearing, if lateral luxation - foot internally rotated, if medial luxation - foot externally rotated. Take VD extended radiograph.
212
What is the treatment of a traumatic shoulder lunation?
Non surgical for luxation with no other injuries. Velpeau for medial lunation, spica splint for lateral luxation. Surgical for medial luxation - biceps transposition (medial), medial glenohumeral ligament reconstruction. Surgical treatment for lateral luxation - Biceps transposition laterally, suture techniques. Good - mild lameness, DJD develops with time. If lunation recurrent - guarded prognosis, salvage procedure.
213
What is congenital shoulder luxation
seen in toy breeds. surgery - reconstruction techniques fail, arthrodesis. prognosis extremely good.
214
What is shoulder instability?
A relatively newly recognised condition. Tear or stretch of the support structures - medial or lateral glenohumeral ligament, subscapularis, biceps brachii tendon of origin. Seen in medium/large breed, chronic mild to moderate lameness, moderate muscle atrophy. Arthroscopy - subjective laxity/tearing of ligaments/ tendons. Treatment is analgesia, controlled exercise, radiofrequency shrinkage, prosthetic stabilisation, subscapular tendon imbrication - sling dog post op. Prognosis 60-80% lameness resolves - but lameness can take a long time to resolve.
215
What is biceps tendon disease?
Tenosynovitis - repetitive injury, chronic inflammation. Partial/complete rupture - direct trauma. Diagnosis - medium to large breed, history of trauma, mild to severe lameness. marked pain on shoulder flexion, pain on direct palpation of the tendon, rupture. Osteophytes interubercular groove on radiography, ultrasound: mineralisation. Arthrocentesis - mild inflammatory. Diagnosis & treatment: arthroscopy then tenotomy, or tenodesis ( with screw/washer), prognosis for partial rupture excellent in >90%, for tenosynovitis excellent in 50%.
216
Describe other conditions of the shoulder that you may encounter
Luxation of biceps tendon from inter tubercular groove (ruptured transverse ligament), un united caudal glenoid, shoulder dysplasia, mineralisation of the SS.
217
What is carpal luxation?
Loss of palmar ligament support - trauma, chronic immune mediated polyarthritis. Or seen in prolonged immobilisation - puppy laxity. Presenting signs; palmagrade stance, mild -moderate lameness. Medical management only indicated for puppy laxity. laxity will spontaneously resolve with exercise. Treatment - pan carpal arthrodesis, partial carpal arthrodesis. Principles of arthrodesis - Remove all articular cartilage, cancellous bone graft, rigid internal fixation, postoperative coaptation. Mechanical lameness afterwards. complications - failure of arthrodesis, metacarpal fracture.
218
What is carpal collateral ligament injury
Normal stance slight valgus. In the carpal joint - short collateral ligaments, oblique collateral ligaments. Treatment - APL transposition, prosthetic - bone tunnels.
219
Describe flexoral deformities of the carpus
young large breed, resolves with exercise, rarely require transection of FCU.
220
What does the glasgow coma score assess?
Level of consciousness, motor activity, brainstem reflexes.
221
Describe how fractures of the skull can be treated
Fractures of the maxilla/premaxilla - rarely require fixation - kirshner wires and cerclage. fractures of the zygomatic arch - can be plated/removed if severe.
222
What is the medical management for spinal fractures?
Analgesia, support with neck brace, lumbar spinal board, cage rest 6-8 weeks.
223
What is the surgical treatment of spinal fractures?
Significant mortality - stabilise unstable segment - plate, pins, vertebral bod, pin/screw articular facets, L7-S1 luxation: transilial pin, shortens recoveyr period.
224
What is the management of mandibular fractures
Preserve teeth unless loose or marked periodontitis. avoid roots. consider how to feed patient post operatively. if in doubt place an oesophagostomy tube. - Interdental fixation or maxillomandibular fixation or external skeletal fixation. inter fragmentary wires NOT indicated. complications - esf pin loosening, malocclusions - remove teeth. non union - hemimandibulectoy.
225
Describe the signs of temperomandibular joint diseases
Difficulty closing mouth, reduce range of motion, pain. Seen in bassets, CKCS -
226
What is craniomandibular osteopathy?
Proliferation of new bone on mandibular rami. WHWT, ST, CT. seen 3-7 months old. TMJ ankylosis may occur. Painful - give analgesia. Prognosis with total ankylosis is poor.
227
Describe lunation of the temperomandibular joint
Unable to close the mouth, mouth deviated to one side. bilateral luxation - cranial deviation. Treatment - closed reduction of lunation, open reduction & loose muzzle for 4 weeks.
228
What is TMJ ankylosis
True ankylosis - TMJ fused. False - zygoma to coronoid process. aetiology - trauma, neoplasia, idiopathic. Treatment TMJ excision.
229
What is Mandibular neuropraxia ?
Paralysis prevents mouth closure. History - carrying heavy object. Treatment - tape muzzle. resolves <3 weeks. if no history carrying heavy objects - tumours can cause dysfunction of the nerve, not usually bilateral.
230
What is tympanic bulla disease?
Neoplasia can cause pain on jaw opening. osteomyelitis can spread to the TMJ
231
What is masticatory myositis -
An autoimmune condition - signs: pain, temporal muscle atrophy, reduce opening. treatment - immunosuppression.
232
What are the indications for surgery for pelvic fractures?
Uncontrollable pain, pelvic canal compromised, other orthopaedic injuries, earlier return to function. suitable for fixation - sacroiliac laxations, ace tabular fractures, ilial body fractures. unsuitable for fixation - fractures of the ischium, pubis and tuber sacral, highly comminuted fractures,old pelvic fractures. Conservative management - cage rest 4-6 weeks.
233
Describe the anatomy of the stifle joint
Complex hinge joint (ginglymus) collateral ligaments, cranial and caudal cruciate, medial and lateral menisci, intfrapatella fat pad, lon digital extensor, joint capsule/muscle
234
Describe cranial cruciate ligament rupture
There are two bands - the craniomedial and craniolateral they limit cranial translation, limit internal rotation, limit valgus/varus motion, limit stifle extension, and are for proprioception. Cranial cruciate ligament rupture frequently bilateral. Neutering and being female increases risk. Very rare in cats. Traumatic rupture rare. Degenerative more common - young medium/large breed, ageing, conformational abnormality, immune mediated disease. History - acute or chronic lameness. 'sit test'. On clinical exam - stifle effusion, stifle thickening (medially), muscle atrophy (may be bilateral), pain on full extension. Arthrocentesis - increased volume, normal/mild inflammatory profile. Treatment - NSAID, controlled exercise, DJD progresses regardless. Treatment - surgical- debride ligament, meniscus, stabilise - not repair. Mensici damaged >50% of cases. medial predisposed to injury - caudal meniscotibial ligament. Lateral - meniscifemoral ligament. Check meniscus - remove tears.
235
what is intracapsular stabilisation
Over the top - fascia lat a graft reconstructs the CrCL. outcome not as good as other techniques.
236
What is extra capsular stabilisation
Lateral fabella-tibial suture lateral imbrication. monofilament nylon or wire suture. tibial tunnel, under SPL, around fabella.
237
What is dynamic stabilisation?
Tibial plateau levelling osteotomy (TPLO). Tibial wedge osteotomy (TWO). aim to reduce tibial plateau angle. Costs & complications increased. function - no proven improvement over lateral TF suture. preferred technique in larger dogs. OA progresses with ALL regardless of treatment. complications of all - post op meniscal injury, sepsis.
238
Describe caudal cruciate ligament disease
The functions of the caudal cruciates - to prevent caudal translation of the tibia, rotation and valgus/varus restriction. Rare, traumatic, caudal draw. Effusion. Treatment - for small dogs/cats - non surgical. for medium large dogs - patella - fibular head suture. prognosis excellent.
239
Describe Collateral ligament injury
Limit - valgus (med) stifle motion. Varus (lat) stifle motion. limit internal rotation in extension. Laxity of LCL permits slight internal rotation during flexion. Injury is caused by trauma. diagnosis is with varus and valgus stress test - stifle in extension. check integrity of CrCL, CdCL. Treatment - primary repair if possible. reattach avulsions (rare). supplement with screws and figure of eight monofilament non absorbable suture.
240
Describe multiple ligament injury
Multiple ligament injury global knee or stifle luxation. includes MCL, LCL, CrCL, CdCL, menisci. Treatment is to repairreplace individual components. TransArticular stabilisation - TA PIn, TA ESF. Prognosis - for multiple ligament injuries - moderate, expect lameness, DJD, Reduced ROM.
241
What is medial patella luxation?
Misalignment of the quadriceps mechanism which includes the quadriceps, patella, straight patella ligament, tibial tuberosity. Complication of CrCLR, trauma. Lameness variable, note the position of the tibial tuberosity, stifle effusion, usually bilateral.
242
How do you grade medial patella luxation
Grade 1 - in sulcus and spontaneously returns in sulcus when manually luxated. 2= when in sulcus stays in, when out of sulcus stays out. 3 = out of sulcus, can be returned in, but spontaneously luxes out. 4= out of sulcus all the time, can't be put in.
243
What is the treatment for patella luxation
asymptomatic - no treatment, symptomatic - surgical treatment - realign the patella mechanism, note this does not prevent DJD. Surgery - lateral tibial crest transposition. Trochlear wedge/block recession, medial desmotomy, lat capsular overlap. Confirm relocation with post op radiographs Grade 4- guarded may require corrective femoral or tibial osteotomy.
244
Describe lateral patella luxation
Usually large breed dogs (FC retrievers) variable lameness, clinically grade 1-4. Treatment - medial tibial crest transposition, trochlear wedge/block sulcoplasty, lateral desmotomy, medial retinacular imbrication. Good prognosis, complications common. grade 4 - may require corrective femoral or tibial osteotomy.
245
What is stifle osteochondrosis
Usually large breed dogs - 5-7 mo. Male > female. chronic moderate lameness. clinical examination - marked effusion, pain on extension, slight draw is normal in immature animals. Treatment is with arthroscopy or arthrotomy. Curette lesion +- osteochondral transplant. Meniscal lesions often associated. Develop marked OA. CrCL disease/rupture often develop later.
246
What is patella ligament rupture
Trauma: forced flexion vs quadriceps m results in patella ligament rupture. unable to extend stifle, patella proximally displaced (palpate and radiographs). treatment is primary repair, support suture (through patella -tibia).
247
What is stifle joint arthroplasty?
Rarely required - end stage OA, non reconstructible fractures. Arthrodesis gives marked mechanical lameness, increases stress on the hock and hip. total knee replacement - no long term follow up.
248
How do ligament injuries of the hock occur?
Trauma - ligaments, avulsion fractures, shearing injuries.
| Immune mediated disease.
249
Describe talocrural subluxations/luxation
Occur with malleolar Fractures. TC collateral ligament injury can be treated with primary repair, prosthetic (screws and suture), temporary transarticular ESF.
250
What is proximal intertarsal subluxation or luxation?
Caused by degenerative changes of the plantar ligament (shetland sheepdogs) or traumatic ligament rupture. there is a characteristic posture. must differentiate from achilles mech. Treat with arthrodesis - calcaneoquartal screw, plate and screws, or pins and tension band wire.
251
What is tarsometatarsal joint luxation
Usually plantar ligament disruption - trauma or degeneration. requires arthrodesis. occasionally lateral/medial/dorsal. treat with screws and tension band or external support, or arthrodesis, or lateral plate.
252
How do you treat a TMT shearing injury?
Temporary transarticular ESF. may require arthrodesis.
253
Describe osteochondritis Dissecans of the Hock?
Breed, 5-7m/o, presenting signs; marked hind limb lameness, marked effusion/swelling of the affected joint. Take standard D-Pl and Flexed D-Pl. Treatment - fragment removal, arthrotomy/arthroscopy - technically challenging. Prognosis guarded. develop marked OA as joint is unstable. some dogs will require arthrodesis.
254
Describe other conditions of the hock that you may encounter
Torsion of the tarsus - large giant breeds. Hyperextension of the tarsus - large giant breeds related to HD. Pes valgus - shetland sheep dogs/collies. Pes varus - dachshunds. Treatment:corrective osteotomy.
255
What is pan tarsal arthrodesis?
Indications - end stage OA of the TC joint, failed achilles mech injury. Medial or lateral plate. mechanical lameness.
256
Describe Muscle injuries/strains
Muscle healing - regeneration if nuclei not destroyed and endomysium around individual fibres is intact. If extensive cell death and haemorrhage then healing through scar tissue. Treatment - for a contusion/strain - cold compress and immobilisation - occasionally require surgical decompression. For a laceration - horizontal mattress or N-F-F-N sutures. heal by fibrous tissue.
257
What is Infraspinatous m. contracture
Occurs after severe strain/trauma in working dogs often. acute lameness fully resolving 3-4 weeks before contracture. mild lameness/characteristic posture. lateral deviation of carpus when limb flexed. Treatment - transect the tendon of insertion. Prognosis - excellent.
258
What is quadriceps contracture
Congenital (rare), muscle (trauma), immobilisation. Effect of contracture - stifle hyperextension and fibrosis. bone and cartilage atrophy. Treatment - Muscle Release (Z platy), transarticular fixator. Prognosis - poor. Frequently require amputation as fail to improve/recur/poor limb function.
259
What is fibrotic myopathy
Muscle contracture. Aetiology unknown - trauma, IMD, neuro. Fibrous band of the gracillis. diagnosis - GSD, males, short stride, internal rotation. Pain on abduction of limb/palpation, muscle feels taught, treatment is medical physical therapy, surgery: always recurs, poor prognosis.
260
Describe tendon injury
May be caused by laceration, acute or chronic overload, contusion. Healing - paratenon covered tendons: granulation tissue between paratenon ends, slow remodel. Sheathed tendons - rely on ingrowths of connective tissue from the sheath. Treatment - careful tissue handling and haemostats, monofilament suture material. suture patterns - 3 loop pulley best, then SI in tendon ends. For flat tendons: krackrow pattern. Healing - immobilise for 3-6 weeks.
261
Describe achilles tendon injury
Complete rupture (trauma) - plantigrade stance. Partial rupture (A. tendinopathy) - lengthening of gastrocnemius, flexed digits. Tendinosis - thickening but no lengthening. Treatment - temporary immobilisation or primary repair. for complete rupture - primary repair. Remove support after 6 weeks. Achilles tendinopathy/tendinosis often bilateral.
262
What is mineralisation of the supraspinatous tendon
Aetiology - possible trauma or blood supply, may be asymptomatic, pain on palpation, radiography. Treatment - non surgical, extra corporeal shock wave therapy, surgical exploration and removal. ensure no other shoulder pathology. prognosis - moderate, recurs.
