0
Q
What does fracture healing need?
A
Vascularisation of the fracture site - adequate reduction & stability of the fracture site which protects the bone cells in the fracture gap. An absence of complicating factors such as infection & sufficient time.
1
Q
What are the clinical signs of fracture?
A
Loss of function, swelling, change in limb length, alignment or orientation, abnormal motility, pain, crepitus.
2
Q
Describe healing 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 v small fracture gap, interfragmentary compression. No benefit from primary bone union over healing by callus - speed of healing slower, gains strength at a slower rate, most of the benefits arise from rigid stabilisation so early rerturn to function and reduced risk of fracture disease.
4
Q
What forces cause fractures?
A
Most arise following external trauma. Some arise following normal loading - applied in an uncoordinated way, beware of pathological fracture. High energy trauma causes severe comminution and significant damage to the soft tissue envelope. There is an increased chance of open fracture.
5
Q
What are the forces acting on a fracture?
A
Tension - lengthening Compression - shortening Bending - combines tension and compression, tension on convex surface, compression on concave surface, neutral axis results. Torsion Shear
6
Q
What is a pathological fracture?
A
A bone fracture secondary to an underlying pathological process that weakens the structure - infection, neoplasia, nutritional disease. Normal loading results in fracture.
7
Q
What is an incomplete articular fracture?
A
Either greenstick: skeletally immature animals where bone is incompletely mineralised so less brittle than fully mineralised adult bone. or secondary to skeletal demineralisation e.g secondary nutritional hyperparathyroidism. Fissure - undisplaced fissures are often seen running along the cortex from a major fracture line.
8
Q
What is Avulsion?
A
A fragment distracted by muscle pull or ligament attachment e.g the tibial tuberosity, olecranon, elective osteotomy. Along the physis in skeletally immature animals, or at muscular ligament insertions in skeletally mature animals. Need to neutralise distractive forces during fracture repair.
9
Q
What radiography should be done with a fracture?
A
Minimumm - orthogonal views, include adjacent joints
Contralateral limb - for juvenile animals, complex fractures or curved bones.
Additional - stressed views, traction views, angled beam views.
Minimum frequency will e pre operative for fracture fixation planning and immediate post operative to assess repair.
10
Q
How is fracture healing recognised
A
Clinical function - progressive improvement in function, consistent weight bearing, minimal muscular atrophy
Radiographic signs -vary depending on type of healing anticipatd, bridging callus, loss of fracture lines.
11
Q
What is an open fracture?
A
Also known as a compound fracture, graded 1-3 on the severity of the soft tissue injury. Possibly considered an emergency. Immediate first aid aimed at preventing further contamination, cover open wounds - clean or sterile dressing, control haemorrhage. Stabilise fracture and manage soft tissue injuries. Prevent contamination progressing to infection. Achieve rapid bone union and restore limb function.
12
Q
How are open fractures managed?
A
Clip widely, lavage copiously, 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 CS before AB.
13
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.
14
Q
What is external coaptation?
A
Cast. Often seen as a cheap and easy means of fracture management. Intensive method for fracture management - requires regular revisissts, cast changes as necessary, cast complications - such as soft tissue sores, muscular atrophy and joint stiffness. Common complications difficult to avoid. Must immobilise the joint above and below the fracture. Limits use to below elbow and stifle. Only resist bending/angulation - only useful for transverse or short oblique fractures that are stable once reduced.
15
Q
What are splints useful for?
A
Short term/adjunctive support. OK for radius and ulna - limited to hock distal. Apply over cast padding and conforming bandage. Anatomical moulded splints are strips of fibreglass/resin casting material encased in cast padding. Moulds to the contours of the limb. They are thermoplastic materials - stronger and lighter than POP. Need to be quite hot before they are mouldable.
16
Q
What may casts be made out of?
A
Plaster of paris - cheap, easy to apply, conform weell, takes 8+ hours to dry, heavy to wear, radiodense.
Fibreglass/resin - light and strong, dont soften when set, conform well, set rapidly, radiolucent. Need an oscillating saw for removal.
17
Q
What is fracture rerduction?
A
Most fractures are over ridden - muscle contraction and spasm. Slow steady traction, bend fracture to engage ends, straighten bone to achieve final reduction.
18
Q
How is a cast applied?
A
Reduce fracture and maintain reduction during cast application. Immobilise the joint above the fracture, immobilise the limb in a normal standing position, include the toes. Stirrups - retain cast in position, help to maintain reduction of fracture during application. PAdding - cotton wool, synthetic cast padding, stockinette. Apply with a 50% overlap - 6 layers usually sufficient. Dont allow animal to walk untill cast has cured. Apply waterproof ooverwrap.
19
Q
What are cast complications?
A
Soft tissue - pressure sores due to poor technique or loosening, ischaemia - may progress to gangrene.
Fracture disease - muscle wasting, stiffness, osteoporosis, tissue adhesion, malunion, delayed union.
20
Q
What is External skeletal fixation?
A
a Series of percutaneous pins, pass into or through the bone, connected together externally by clamps and rods, acrylic bars or epoxy putty. Versatily, easy to apply, compatible with the principles of biological osteosynthesis, can be removed in a staged way, excellent for management of open fractures, not restricted to use below elbow and stifle.
21
Q
Describe the classificiation of ESF frame designs?
A
Type 1 to type 3 Unilateral frame uses half pins, bilateral frame uses full pins. Type 1 - unilateral uniplanar Type 2 - bilateral, uniplanar Type 3 - bilateral, biplanar Ilizarov - ring fixator, cESF
22
Q
Describe different fixation pins for ESF?
A
Smooth pin - friction only
NPT pin - good bone purchase, weak point must be protected
PPT - no weak point, excellent purchase, must pre drill a pilot hole.
Connecting bars may be stainless steel, aluminium, titanium, carbon fibre, acrylic or eopxy resins.
23
Q
What does frame stiffness depend on?
A
Frame geometry Pin factors - number, type, placement Clamp factors - type, orientation Fracture configuration - load sharing with frame, Combination fixations.
24
How is ESF frame applied?
Patient prep as for routine aseptic surgery
Positioning - hanging limb preparation aids in fracture reduction and frame application - fatigues muscles.
Pin selection - 20-30% of cortical width
Pin placement - spread out along fracture fragment, near far, far near configuration. Place by hand or with power. Recommended to predril. Mandatory for PPT pins. Insert pins with low speed power.
25
How is pin tract drainage avoided?
Best avoided by attention to soft tissue managment. It has to be accepted at some sites. Pin loosening promotes pin tract discharge . Remove loose pins and revise frame if necessary.
26
What are the advantages of an ESF/IM pin 'tie in'?
IM pin - resists bending, maintains alignment
| ESF - resists compression, resists torsion
27
What are the uses of an anti rotational two pin fixator?
IM Pin - maintains alignment, resists bending, ESF - resists torsion, resists axial collapse
Fracture - resists axial collapse, allows a simple frame to be applied.
28
What is intramedullary pin fixation?
Im pin - holds fragments in alignment. 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. Diameter must be able to fill the medullary canal at the narrowest point. Radiographs of contralateral limb useful for assessment. Length - should be seated in distal metaphysis, protrude slightly proximally. Allow 10-15% for magnification.
29
What is normograde pinning?
Introduce pin away from fracture site. Reduce fracture, advance pin, may be able to do this closed.
30
What is retrograde pinning?
Introduce pin at the fracture site. Push/pull pin through the bone to allow fracture reduction. Reduce fracture and drive pin across fracture line. I
31
Where can retrograde pinning not be performed?
Tibia, radius.
| Normograde cannot be performed on radius either.
32
What is an interlocking nail?
An IM pin, perforated to accept bone screws, neutralises all forces very effectively. The pin resists bending, screws lock bone to pin to resist shortening, rotation, shear. Requires specialised instrumentation or fluoroscopic guidance. Can be technically challenging.
33
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. Best manufactured in house from 1.0-2.0 K wires. Rush pins are useful for Metaphyseal fractures - especially distal femur. They may allow physeal growth to continue in skeletally immature animals.
34
What is cerclage wire Used for?
Common used in combination with IM pinning. Full cerclage - wire encircles the bone circumference. Hemicerclage - wire passes through a tunnel drilled in one of the fragments. It is monofilament, orthopaedic wire. 0.8-1.2mm. Not suture wire, fuse wire or PDS. It provides inter fragmentary compression - reduces the fracture gap, increases inter fragmentary friction and enhances fracture stability. It stops Undisplaced fissures opening up or propagating from the fracture site.
35
What are thee principles of cerclage?
IT stops undisplaced fissures opening up or propagating from the fracture site. It provides interfragmentary compression. Knots must be twisted accurately, strand around strand. Wire must be tight before wound closure otherwise continual micromovement disrupts establishment of new blood supply. Avoid trapping soft tisues. Dont bend ends of wire over. Cut at 3-4 twists.
36
What type of fracture can be repaired with cerclage?
Fracture must be fully reconstructable. Only two fragments in any circumference - otherwise may collapse into a bundle of sticks. The fractures must be sufficiently oblique otherwise fragments over ride as wire tightened. >2 wires - single wire acts as a fulcrum and concentrates bending forces on the fracture line.
37
What is tension band wiring?
Used to repair fractures or osteotomies which are subjected to distractive forces. e.g olecranon osteotomy, tibial tuberosity avulsion, malleolar fracture. Reduce fracture and maintain with one or two K wires. Figure of eight wire anchored in a transverse bone tunnel and passed around the ends of the pins. Wire anchored by twisting - ensuring even tension. Figure of eight wire combined with small diameter wires. Converts distractive forces to compression at the fracture line.
38
Describe the different types of bone screws?
Self tapping - cut their own thread in the bone, cutting tip
Tapped - thread must be cut in the bone, thread conforms exactly to screw profile, maximises metal bone contact and holding power. Drill pilot hole, measure depth of hole and add 2mm. Countersink, and tap unless using self tapping screws. Place screw and tighten.
39
What are the different uses of bone screws?
Lag screw - when the screw crosses a fracture line that can be compressed. PRovides interfragmentary compression.
Position screw - when the screw crosses a fracture line that cannot be compressed. When near fragment is too small to take a gliding hole.
40
What is the principle of the lag screw?
Screw threads only grip in the trans cortex. Part threaded screw or over drill cis cortex to provide a gliding hole with a threaded hole in the trans cortex. Tightening of the screw provides interfragmentary compression. Inserted at 90 degrees to fracture line provides optimal compression. At 90 degrees to long axis of bone gives optimal resistance to axial compression. Compromise is to bisect these two angles. Lag screws should be inserted in the middle of the fragment, equidistant from the fracture edges, at 90 degrees to the fracture plane.
41
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 too small to take a gliding hole. The fracture is held in reduction, drilled, measured and both cortices tapped. Screw inserted.
42
What are bone plate and screws used for?
Used 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 plate, neutralisation plate, buttress plate.
43
Describe the difference between the neutralisation plate and the buttress plate and the tension band plate?
Neutralisation plate - applied to protect a lag screw reconstruction. Cannot take significant loads without failure. Load sharing between plate and bone - lag screws provide inter fragmentary compression. Buttress plate - fracture cannot be anatomically reconstructed. Plate transmits the full force of loading across fracture gap. Tension band plate - plate is placed in tension to apply compression across the fracture gap. Used for transverse or short oblique fractures, articular fractures, osteotomy repair, non unions.
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
What is osteomyelitis?
Inflammation/infection of the bone and associated bone marrow.
46
What are the sources of infection in osteomyelitis?
Post surgery - open fracture, open reduction of closed fracture. Penetrating injury - bite wounds, gunshot wounds, foreign body penetration, local extension, haematogenous spread. Establishment of infection requires sufficient numbers of pathogenic bacteria, avascular cortical bone, favourable environment for colonisation and multiplication.
47
Why does osteomyelitis often occur when metallic implants are placed?
Glycocalyx biofilm protects bacteria from normal host defences - phagocytosis and antibiodies, and antibacterials.
48
What are the clinical signs of acute osteomyelitis?
Localised pain, swelling, pyrexia, anorexia, lethargy, usually 2-3 days post surgery.
49
What are the radiographic signs of bone destruction?
Periosteal new bone formation, soft tissue swelling,bone destruction, sequestrum formation (isolated fragment of dead bone separated from normal bone) appears radiodense and angular. May become walled off by an involucrum. Delayed or non union.
50
What is the treatment for osteomyelitis?
For a stable healing fracture - maintain fixation, fractures will heal in the presence of persistent infection. Provided they are stable. For a healed fracture - remove implants. For an unstable fracture - revise fixation to provide rigid stability. Remove sequestrae - may need to graft significant deficits - cancellous autograft. Establish drainage, lavage. Culture bacteria if possible, sample by FNA or open collection. Prolonged course of antibiotics - 50-60% involve staph spp, B lactamase producers. 65% involve anaerobes - especially bite wounds and chronic infections.
51
What is delayed union, malunion and non union?
Delayed union - Correct any problems e.g treat infection - irrelevant since the bone will heal eventually. Malunion - due to inadequate fixation or inadequate reduction. May be clinically irrelevant if patient has good function. May require osteotomy and realignment to correct significant deformity. Non union - failure of bone healing, usually iatrogenic. Poor fracture management or technical failure. Often due to inadequate stability. Continual motion leads persistently high strains and healing cannot progress to the mineralisation phase.
52
What is a viable non union fracture?
Usually arise due to inadequate stability at the fracture site. Also from inadequate reduction. Should heal following adequate stabilisation - hypertrophic/oligotrophic.
53
What is hypertrophic non union fracture?
A highly vascular fracture site. Significant callus. Bone is attempting to heal. Remove loose implants and stabilise fragments. Swab/tissues for C&S. Don't usually require bone graft.
54
What is a non viable non union fracture?
May b e dystrophic - blood supply inadequate, necrotic - necrotic tissue in fracture site, defect - bone defect at fracture gap, atrophic - sequel to the above.
55
Describe an atrophic non union fracture?
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. They require aggressive treatment - open approach. Debride fracture ends to viable bleeding bone. Use rigid stabilisation - plate and screws, bone graft may be needed. Atrophic non union - beware of distal radius and ulna fractures in toy breed dogs.
56
What is quadriceps contracture?
Quadriceps becomes adherent to fracture site. Progressive decrease in range of stifle joint mobility. Stifle and hock overextend. Avoid penetrating muscle masses during ESF application wherever possible.
57
What is the treatment for quadriceps contracture?
Surgical release of adhesions, muscle/tendon lengthening if necessary to allow normal ROM at stifle joint, passive and active physiotherapy vital following surgical correction.
58
What causes implant failure?
Inappropriate implant size, errors in implant placement, bio mechanical environment ignored - cyclical loading causes implant failure, large cortical defects not reconstructed or grafted, fracture of plates through unfilled holes.
59
What is bone grafting?
Autograft - D & R are same individual
Allograft - D& R are different animals of same species
Syngenesiograft - D & R are blood relatives
Isograft - D & R have identical genetic backgroud
Xenograft - D & R are from different species.
60
What is the mode of action of a bone graft?
Sources of osteoprogenitor cells- from within the graft - osteogenesis
From the surrounding tissues - osteoinduction
From a mechanical support - scaffold for bone cell invasion - osteoconduction.
61
What are the uses for a bone graft?
Filling defects, eg left by removal of non reconstructable fragments. Limb salvage - OSA. to encourage healing - comminuted fracture, Non union, arthrodesis and spinal fusion.
62
What is a cancellous autografT?
Highly cellular but mechanically weak. Collect from lateral tuberosity of humerus, greater trochanter of femur, wing of ilium. There is no immune response, greatest osteogenic effect, no risk of cross infection. BUT extra operating sites must be prepped and acesed. Large quantities can be difficult to obtain.
63
What is a cortical allograft?
Can be banked, convenient, unlimited quanttiy, BUT - 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, rejection, fracture, plate fracture, sequestration. Main use is for limb salvage.
64
What is rickets?
Rickets in skeletally immature animals, osteomalacia in adult aimals. It is the failure of mineralisation of osteoid. Dogs and cats cannot synthesis Vitamin D. dependent on dietary sources and metabolic pathway and sunlight. Probably require a concurrent Ca:P imbalance to develop rickets.
65
What is the pathology of ricketS?
Highly stable cartilage matrix produced. It is uncalcifiable, difficult to resorb. In young animals- chondrocytes fail to degenerate. Increased physeal thickness and poor skeletal mineralisation. Metaphyseal capillaries cannot penetrate cartilage. bone trabeculae surrounded by unmineralised osteoid.
66
What are the clinical signs of rickets?
Lameness due to bone pain or pathological fracture. Limb bone bowing, angular limb deformity, flaring of metaphysis - distal radius & ulca, CC junctions, hypocalcaemia, ligamentous laxity - dog has palmigrade and plantigrade stance.
67
What are the radiographic signs of Rickets?
Poor skeletal mineralisation. Failure of growth plate mineralisation - increased growth plate width - cupping of metaphyses, bowing of diaphyses, pathological fracture.
68
What is the treatment of rickets?
Correct diet and exposure to sunlight - balanced diet, Ca:P ratio approx 2:1. Potential for permanent growth plate damage. If hereditary for more guarded. Treat fractures conservatively - pathological , bone stock not as good for repair.
69
What are the functions of the parathyroid glands?
They regulate serum calcium. They secrete PTH in response to Decreased calcium. They increase calcium uptake from the b ones /gut/kidneys. Hypercalcaemia is prevented by a negative fed back loop - via calcitonin. Vitamin D mediated this pathway.
70
What is primary hyperparathyroidism?
rare - autonomous secretion of PTH causes hypercalcaemia. Parathyroid adenoma or carcinoma/hyperplasia.
71
What is secondary Nutritional hyperparathyroidism?
Common in reptiles. In puppies & kittens fed meat rich diets. Inability to absorb dietary calcium. Excessive dietary P04. Low Ca:P ratio Leads to relative calcium deficiency. Increased PTH to maintain ICa2+ in normal range. Calcium withdrawal from skeleton.
72
What are the clinical signs of secondary nutritional hyperparathyroidism?
bone/joint/muscle pain. Lameness, reluctance to stand/walk. Pathological fracture - pelvic limbs, vertebrae, neurological impairment. Ligament laxity - palmigrade/plantigrade stance. On radiograph - diffusely poor skeletal mineralisation. Apparent increased density on metaphyseal side of growth plate - osteoid undergoing active mineralisation, thin bone cortices, pathological fracture.
73
What is the treatment for secondary nutritional hyperparathyroidism?
Correct diet - balanced diet, ca2+ supplementation initially. Ca: 2:1 then to normal radio 1.2:1. Manage fractures conservatively - poor holding power for implants. NSAIDs not corticosteroids. Cage rest. Euthanasia if severe neurological impairment.
74
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 Ca2+, impaired mineralisation of osteoid (rickets/osteomalacia). Calcium is withdrawn from the skeleton. All bones affected but primarily cancellous bone of mandible and maxilla. Teeth appear to float in skull. Fibrous osteodystrophy - rubber jaw. Clinical signs - renal disease, loose teeth, pliable mandible, failure to close jaw properly, mandibular fractures.
75
How is renal hyerparathyroidism treated?
Optimise renal function, reduce phosphoros levels in diet, - renal diets, oral phosphate binders. (Al0h3, CaC03, Ca acetate) erythropoietin if anaemia present.
76
What is hypervitaminosis A?
Cats from 2 years old. Excess dietary vitamin A intake - liver rich diets. Stiffness/lameness, irratibility/hypersensitivity, scruffy, unkempt appearance - can't groom, thoracic limb neurological deficits. Extensive periosteal bone formation - vertebrae and major limb joints. Often progresses to spinal fusion (ankylosis).
77
What is the treatment of hypervitaminosis A?
Correct diet - stops progression, established new bone does not regress. Analgesia - NSAIDS, lameness often mechanical rather than inflamatory. Surgery - removal of bony exostoses if causing a clinical problem.
78
How does excess dietary calcium affect the bones?
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.
79
What effect may excess dietary energy have?
Encourages 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,
80
What is metaphyseal osteopathy?
Scurvy, hypertrophic osteodystrophy. Affects young dogs - 4-6 months. Medium to giant breeds - Great Dane, boxer, GSD, weimeraner. Probably not related to vit C. Necrosis, inflammation and subsequent fracture of trabeculae. In metaphysis parallel to physeal plate. The physis, epiphysis usually normal. Gross swelling of distal metaphysis - commonly r&u. Usually bilaterally symmetrical, soft tissue swelling, bands of sclerosis an lucency at the metaphysis.
81
What is the treatment of Metaphyseal osteopathy?
Disease probably improves regardless of treatment. Most dogs improve in 7-10 days. Relapses may occur. Symptomatic treatment - analgesia. Check diet is adequate. Death has been reported.
82
What is Panosteitis?
Breed - GSD, Lab, doberman, basset. Young 5-18months. Can be older or younger. Males predisposed. 4:1. Females - first oestrus. Degeneration of medullary adipocytes. Enhanced OBL and fibroblast activity - Endosteum, periosteum and marrow. Fibrosis & ossification and periosteal proliferation. Localised bone pain, pain due to medullary hypertension. Patchy, mottled sclerotic thumbprint areas within the medullary cavity. Especially around the area of nutrient foramen. Small or extensive regions of involvement. Blurring of cortico-medullary contrast. Self limiting, resolves within a few days.
83
What is hypertrophic osteopathy?
A paraneoplastic syndrome. Associated with an intrathoracic or intra abdominal space occupying lesion Usually a tumour. humans and dogs mainly affected. Unknown - toxins associated with neoplasia. Old animals, limb swelling - warm but non oedematous, distal limb, pain, dyspnoea, cough. Periosteal new bone deposited in palisades, 90 degrees to long axis of bone.
84
What is hip dysplasia?
A developmental disease of the coxofemoral joint. Affected animals are born with normal hips. Inherited predisposition to develop HD - polygenic dominance trait with incomplete penetrance. Heritability index 0.2-0.6. Environmental influences - excercise, body mass, growth rate etc. Affects many breeds - primarily large breeds. Disparity between skeletal and muscular growth leads to the primary lesion which is HIP LAXITY. This allows hip subluxation.
85
Describe hip dysplasia in skeletally immature dogs?
Subluxation means forces unevenly distributed over the acetabulum and femoral head - concentrated over a small area. Altered distribution of forces causes microfracture, tearing of sharpeys fibres, cartilage degeneration, synovitis.
86
What is the ortolani test for hip subluxation?
Assess the quality of the 'clunk'. Information about the integrity of the dorsal acetabular rim. Slide: loss of DAR. Grate: articular erosion and degenerative change. Clunk: ideal. DAR intact.
87
Describe what happens as skeletally immature dogs mature with hip dysplasia?
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. The clinical signs may recur as secondary degenerative change becomes established often from middle age onwards.
88
What are the clinical signs in young dogs and clinical signs in adult dogs of hip dysplasia?
Young dogs - poor h/q muscle development, lameness, difficulty rising, rolling gait, bunny hopping, audible noise, pain and crepitus on hip movement. Clinical signs in adult dogs - stiffness on rising,stiffness after excercise, lameness, Excercise intolerance, muscular atrophy,, crepitus and pain on hip manipulation, reduced ROM in affected joints.
89
What primary radiographic change may be seen in hip dysplasia?
Joint incongruency, subluxation, increased angle of inclination (normal 130-145), rotation of femoral neck - normal 12-40 degrees anteversion.
90
What is the norberg angle?
Gives an objective measure of coxofemoral subluxation. Normal is considered > 105.
91
What secondary radiographic change may be present in hip dysplasia?
New bone deposition around femoral neck, in and around actabular fossa. Joint remodelling - femoral head, acetabulum.
92
What are the treatment optiions of hip dysplasia?
Conservative - clinical signs will improve in many dogs following the period of rapid growth. Surgical - triple pelvic osteotmy, femoral head and neck excision, pectineal myotomy/myectomy. Conservative is first line response in all immature animals unless they are a TPO candidate. Weight control, excercise regulation, analgesia.
93
What is a pectineal myotomy/myectomy?
Pectineus muscle transected or resected. Normal function is as a hip adductor. May provide transient benefit - a relief of pain. Does not alter progression of the disease.
94
What is a triple pelvic osteotomy?
Three osteotomies isolate the acetabulum. The acetabulum is then rotated 20-30 degrees laterally to increase femoral head cover. Aim is to improve hip joint congruity, to slow or halt the development of osteoarthritis. The patient must have significant lameness, no/minial degenerative change, intact DAR, usually animals <10mnths. Strict excercise restriction untill healing complete. Complications - screw pullout, screw fracture, loss of alignment, sciatic paralysis, arrowed pelvic canal.
95
Describe the BVA/KC HD scheme?
Dogs must be > 12 months. Ventrodorsal extended hip view assesssed. Pelvis straight. Nine anatomical features are scored - 2 reelate to primary pathology, 7 assess secondary change. Maximum score is 106, 53 on each hip.
96
What are the clinical signs of a hip luxation?
NWB lameness, limb adducted, hock rotated outward, symmetry 0 greater trochanter displaced dorsally, increased distance from ischial tuberosity to trochanter, shortening of the affected limb.
97
What are the management options for hip luxation?
Closed reduction - adjunctive support. open reduction - adjunctive stabilising procedures. Surgical salvage - total hip arthroplasty and femoral head and neck exicison. Prompt attention to avoid damage to articular cartilage, reluxation is common.
98
Describe closed reduction
Success rates generally poor. Most likely to succeed if hip conformation normal, unilateral luxation, no other orthopaedic injuries exist that require immediate weight bearing on the damaged hip. Reluxation is usually due to soft tissue trapped in the aceetabulum. - either joint capsule or haematoma. Convert to craniodorsal luxation then reduce the joint.
99
What is an Ehmer sling?
Prevents weight bearing - maintains internal rotation of the femur, enhances hip stability. Correct application critical to avoid vascular compromise. Difficult to maintain on cats
100
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.
101
What is open reduction?
Indicated for if close reduction fails, reluxatin, acetabular fracture, significant HD or OA present, contralateral limb injury. Failure rates lower than for closed reduction. Open reduction - approach - craniolateral, dorsal (Greater trochanter osteotomy), protect articular cartilage, preserve the joint capsule, remove soft tissues from acetabulum.
102
What is an iliofemoral suture?
Craniolateral approach, bone tunnels prepared in femoral neck and ventral ilium just cranial to the hip. Tie suture with hip abducted and stifle joint internally rotated.
103
What is a dorsal Capsulorhaphy?
Requires a greater trochanter osteotomy, to provide access to the acetabular rim. Suture anchor points in dorsal acetabular rim. Heavy suture material anchored through a transverse tunnel in the femoral neck and around screws. Tighten suture with Hip in sl internal rotation, normal standing angle, slight abduction.
104
What is toggle pin fixation?
Replacement of LFH with a prosthetic ligament. The ligament anchored on the medial aspect of the acetabulum with a toggle pin. Passes through the acetabulum at origin of LFH. Passes into femoral head at insertion of LFH, exits on lateral aspect of femur. Passes through a second transverse bone tunnel.
105
What is a transarticular pin?
Replaces the LFH with an 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.
106
What is greater trochanter transpositioon?
After greater trochanter osteotomy, reattach trochanter distally and caudally, increases tension in gluteal mm group, improves medially directed forces.
107
What is avascular necrosis of the femoral head?
Affects terrier breeds & other small dogs. Aetiology unknown. Inadequate blood supply to the femoral head during development - avascular necrosis, trabecular collapse, inadequate cartilage support, collapse of the femoral head with weight bearing. Will have progressive H/L lameness from 5 months. Shifting lameness if bilateral. Muscle atrophy, may do hand stands, crouched stance, bunny hopping gaiit. Pain & crepitus on hip manipulation.
108
How is a femoral head and neck excision performed?
Craniolateral approach to the hip joint, maintains gluteal integrity. Luxate femoral head - externally rotate stifle to 90 degrees. Remove entire femoral head and neck. Avoid leaving a bone spur, must section LFH to allow adequate visualisation. Do osteotomy with oscillating saw or osteotome, gigli wires, bone cutters.
109
What is osteosarcoma?
Common neoplasm of appendicular skeleton, axial skeleton less common. Primary extraskeletal sites are rare. Seen in large and giant breed dogs. Appendicular: Males > females? median age: 7 years, bimodal peak. Axial: medium to large breed dogs, females> males, middle aged (exception: rib OSA), small dogs - axial > appendicular.
110
What are the common locations of osteosarcoma?
Metaphyses of the long bone, away from the elbow, toward the knee. Less commoly: ribs, vertebrae and skull. Micrometastasis in 90% at time of initial presentation. Primarily via haematogenous routes > lung most common metastatic site. Others include liver, kidneys, amputation stump and rarely subcutaenous tissues and adjacent bones.
111
What are the clinical signs of Osteosarcoma
Lameness, swelling, pain, mass at the primary site. Pathological fractures due to weakened cortical bone, neurological deficits, dyspnea, nasal obstruction, bloody to purulent discharge. ALP, sometimes azotaemia? Thoracic radiographs often normal, <10% present with gross metastatic disease. Discrete soft tissue opacity nodules.
112
What is the radiographic appearance of OSA?
Lytic, productive or mixed apperance, metaphysis of the long bones, away from the elbow, towards the knee, do not cross joint spaces, sunburst pattern codman's triangle, irregular osteolysis.
113
What are the DDx for osteosarcoma?
Other primary bone tumours, metastatic bone tumours, round cell tumours involving bone, osteomyelitis - fungal/bacterial.
114
How is a definitive diagnosis of osteosarcoma made?
Jamshidi needle, multiple samples, - may have pain, pathological fracture, non diagnostic.
115
What is the treatment and diagnosis for OSA?
Surgery and chemo.
Amputation vs limb spare, carboplatin, cisplatin, doxorubicin, Single agent vs combination, MST - 1 year, 25% alive at 2 years. Palliative therapy includes bisphonsphonates, samariu, amputation alone, NSAIDS/opioids/gabapentin.
116
Describe the worse prognostic factors for OSA?
Location - worse prognosis: proximal humerus, rib, scapula, extraskeletal, mammary.
Better prognosis: mandible.
Alp Elevated.
Histological subtype, grade, body weight.
117
Describe feline OSA
Rare, malignant, 55 apendicular skeleton, 45% axial skeleton, mean age 8-10 years, hindlimbs > forelimbs, lower metastatic rate. Surgery is the treatment of choice - use adjuvant therapy, MST is 24-44 months. Prognosis for axial sites dependent on resectability.
118
What are soft tissue sarcomas?
Diverse group of tumours, classified on basis of similar pathologic appearance and clinical behhaviour. 15% cutaneous and subcutaneous cancers. They arise from mesenchymal tissues - fibrous tissue, pericyte of blood vessel, adipose tissue, nerve, synovial cells, skeletal muscle. Often miclassified as skin or SQ tumours. Malignant and benign forms exist for each mesenchymal cell type. they are locally infiltrative, haematogenous route of metastasis. Large breed, 8-10 yr, slow growing non painful mass in any location.
119
What is the treatment for soft tissue sarcoma?
Surgery = the treatment of choice for almost all tumours. Definitive, marginal. Post operative radiation therapy effective at controlling incompletely excised tumours. Role of chemotherapy unclear but offered.
120
What is the synovial membrane made up of?
Intimal layer - type A synoviocytes (macrophages)
Type B synoviocytes (fibroblasts)
Sub intimal layer - blood vessels, lymphatics, connective tissue. Synovial fluid - ultrafiltrate of blood, hyaluronan added (type B synoviocytes), Functions - nutrition of articular cartilage/menisci, lubrication.
121
How many cells in synovial fluid?
Low cell count <3x10^9 cells.
| Mononuclear cytology, clear, colourless, viscous, small volume.
122
What are arthropathies?
Joint diseases
123
What is arthritis?
Inflammatory joint diseases
124
What is polyarthritis?
Inflammation of >1 joint
125
What is ankylosis?
Reduction in articular motion
126
What is arthrodesis?
Surgical fusion of a joint
127
What is osteoarthritis?
A form of degenerative joint disease affecting diarthrodial joints. 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 the pain, regional muscles may atrophy and ligaments become more lax.
128
What is osteoarthritis characterised by?
Degeneration of articular cartilage with concurrent peri articular new bone formation and fibrosis. May be primary - unknown aetiology, secondary - developmental, inflammation, instability/trauma, iatrogenic. There is abnormal motion or normal cartilage or normal motion on abnormal cartilage. Fibrillation of superficial layer, roughening of articular surface, fissures.
129
Describe the pathogenesis of Osteoarthritis?
Inflammatory response to increased motion/cartilage fragments in synovium Pro inflammatory mediiators, prostaglandins, cytokines (IL1, TnFa). They release destructive enzymes - matrix metalloproteinases, aggrecanases. The balance between cartilage anabolism and catabolism is disrupted. Multiple tissues involved - cartilage, synovium, bone, fat pad.
130
Describe OA medical management.
Weight management - body condition score, reduce weight, appropriate weight management can delay signs of OA, decrease requirement for analgesic medication. Avoid impact activities, controlled excercise, tailor to minimise/prevent clinical signs. Physiotherapy. Omega 3 fatty acids - replace Arachidonic acid with eicosapentanoic acid - reduces pain and inflammation. Also - glucosamine chondroitin sulphate, pentosan polysulphate, Nsaids, corticosteroids - do not combine. Pain management with acetaminophen (paracetamol - not in cats) or opiates. Other medical management with PSGAGs, hyaluronan.
131
Describe OA surgical management?
Corrective osteotomies, arthroplasy - excision arthroplasty, joint replacement of hip, elbow, stifle or arthrodesis. No treatment curative. no treatment prevents the progression. Tailored to individuals.
132
What is bacterial infective arthritis?
Septic arthritis -- direct penetrating wound, surgery. Indirect - haematogenous spread from respiratory, GIT, UG. Usually affects an abnormal 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.
133
What may arthrocentesis of joint fluid appear like with bacterial infective arthritis?
Large volume, abnormal appearance (cloudy, watery), increased cell count >3x10^9 cells, neutrophilia, bacteria. Treat with broad spectrum antibiotics initially then culture and sensitivity 4-6 weeks or 2 weeks after signs resolve.
134
What is Lyme disease?
Borrelia burgdorferi. Transmitter by ixodes ticks. Clinical signs - weeks months later. Waxing and waning signs. Polyarthropathy, lymphadenopathy, fever. Culture difficult. Serology - cross reacts with leptospires, PCR, Treatment - tetracyclines.
206
Which types of immune mediated joint disease are erosive and which are non erosive?
Erosive: rheumatoid, periosteal proliferative polyarthritis
| Non erosive: SLE, idiopathic IMPA types I, II, III, IV.
207
What is the pathogenesis of immune mediated joint disease?
Inappropriate immune response in the synovium, pain and lameness. Genetic component in RA, and toy breeds are predisposed in RA. Gender - females predisposed to idiopathic IMPA. May be joint effusion, multiple joints affected, symmetrical joint swelling, overt joint pain.
208
How will the synovial fluid appear with immune mediated joint disease?
Increased volume, reduced viscosity, turbid, raised cell count, neutrophilic cytology.
209
How is immune mediated joint disease treated?
Immuno suppression - prednisolone, check remission with repeated arthrocentesis, gradually taper dose. Poor responders - try cyclophosphamide, azathioprine, chlorambulcil, leflunomide/ciclosporin.
210
Describe the pathogenesis of rheumatoid arthritis?
Rheumatoid factors - IgM and IgG to Fc IgG. Immune complex disease/type 2 hypersensitivity. IC deposited in synovium, inflammatory response, pain/synovitis, pannus deposition. Small toy breeds, 5-6 y, erosive changes take time. Prognosis poor. Very rare in cats.
211
What is Periosteal proliferative polyarthritis?
Aggressive erosion and new bone formation. Can be erosive. FeLV associated with 60% of cases. Signalment - males, usually 18m-5 yr. Treatment - immuno suppression. Poor prognosis.
212
What are the two types of non erosive immune mediated arthritis?
Idiopathic immune mediated polyarthritis, systemic lupus erythematosus.
213
What is idiopathic Immune mediated polyarthritis?
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.
214
What is systemic lupus erythematosus?
A multi system disease. Non erosive polyarthritis, renal disease, dermatological lesions, haemolytic anaemia, thrombocytopaenia. Autoantibodies to nuclear antigens, immune complex disease. Three or more organ systems. Treat with immunosuppression. Guarded prognosis.
215
What is drug induced polyarthritis?
Antibody- drug induced vasculitis. Long term or previous therapy. Most common causes: cephalosporins, penicillins, sulfa drugs. Dobermans susceptible to sulphadiazine trimethoprim, resolves 2-7 days after drug is stopped.
216
What is plasmacytic-lymphocytic synovitis?
Stifle joint, often associated with CCL rupture. Arthrocentesis - markedly increased WBC count, mononuclear. Treatment - CCL rupture surgery, immunosuppresion.
217
What is elbow dysplasia?
A group of developmental conditions: fragmented coronoid process, osteochondrosis of the medial part of the humeral condyle, ununited anconeal process. Male predisposition to FCP.
218
Describe the KC scoring scheme for Elbow dysplasia?
Grade 0: no osteophytosis, grade 1: osteophytes 5mm. highest score for either elbow is reported. Dog scored once in their life.
219
What is a fragmented coronoid process?
Most common elbow dysplasia. Undetermined aetiology. Complete fragmentation, partial fissuring or abnormal shape. Pathophysiology - abrasion of MCP and humeral coondyle, development of elbow OA. Large/giant breed, age, acute or chronic, mild or severe lameness, clinical examination - elbow pain on extension and flexion/supination. Most cases improve with medical management - surgical management - arthrotomy or arhtroscopy. Fragment removal or coronoidectomy. Surgery - short term improvement in most. Medical vs surgical - no difference at 6 months. OA will progress regardless.
220
What is Osteochondrosis of the medial part of the humeral condyle?
Failure of endochondral ossification. Aetiology - genetics, over nutrition, ischaemia. Cartilage nutrition comes from subchondral bone and synovial fluid. Failure of ossification leads to thickens > necrotic chondrocytes. Trauma causes cleft/flap (OCD). Clinical signs appear when flap is present. Elbow pain on extension - frequently bilateral. Treat by surgical removal of the flap - usually improve but lameness may not fully resolve. OA inevitable.
221
What is an ununited anconeal process?
Anconeal process has a separate centre of ossification at 3mths. IT fuses to the ulna at 5-6 mths. there may be a developmental incongruity - long radius, narrow trochlear notch of the ulna. Signalment, clinical exam - crepitus, marked effusion, pain on extension,over 6 mths. Radiography in flexed mediolateral. Surgery - fixation - lag screw and ulna osteotomy best choice.
222
What is incomplete ossification of the humeral condyle?
Intercondylar cartilage plate - ossifies at 12 weeks, Failure of ossification results in fissure, seen in some immature dogs, but also mature. Spaniels predisposed. IOHC predisposes to fracture of the humeral condyle. Treat with Position screw. Fracture - treat with Lag screw or plate fixation or ESF.
223
What is traumatic elbow luxation?
Elbow dislocation - rupture/avulsion of collateral ligaments. Anconeal process. History of trauma, NWB, extremely painful, characteristic posture. Treat by closed reduction, open reduction. Re-attach avulsion (origin or insertion), replace ligaments.
224
What is developmental elbow luxation/subluxation?
Asynchronous growth of the radius or ulna, premature closure of physis, results in elbow incongruity. Appearance - may have varus/valgus deformity, elbow pain. Short ulna - Effects - radius curvis, valgus, shortening, humeroulna subluxation. Short radius - shortening, rotation, varus, humeroradial subluxation.
225
What is congenital elbow luxation?
Type 1: humeroulna subluxation - olecranon rotated lateral to distal humerus, marked lateral deviation of the antebrachium. (toy breeds). Type 2: radial head luxation - medium - large breeds. Displaced caudal and lateral, often minimal /no lameness.
226
What is an elbow arthrodesis?
salvage procedure. Indication - severe and intractable elbow joint, fused at 110 degrees, caudal plate, marked mechanical lameness.
227
Describe total elbow replacement
Indication - painful elbow, unable to manage medically, results - 80% success at 12m po, complications common - luxation, infection, fracture.
228
Describe ligamentous injuries of the hock
Trauma - ligaments, avulsion fractures, shear injuries, or immune mediated disease. Diagnosis - Valgus/varus deformity, dorsal and plantar ligament support.
229
What is proximal intertarsal joint subluxation?
Caused by degenerative changes of plantar ligament or traumatic ligament rupture, with a characteristic posture, differentiate from achilles mech.
230
Descrine tarsoometatarsal joint luxation?
Usually plantar ligament disruption, through trauma or degeneration. Requires arthrodesis. Occasionally lateral/medial/dors - treat with screws and tension band or ext support.
231
What is osteochondritis Dissecans of the hock?
Marked hind limb lamness, swelling of the affected joint, Treatment = fragment removal via arthrotoy/arthroscopy. Prognosis guarded, will develop marked OA as joint unstable. Whether treated surgically or conservatively, some dogs will require arthrodesis.
232
What is pantarsal arthrodesis?
Fusion of the tibiotarsal, proximal and distal intertarsal and tarsometatarsal joints. Indications - end staage OA of the TC joint, failed achilles mech injury, medial or lateral plate, will have mechanical lameness.
233
Describe muscle injuries of the hock
Muscle contusions/strains - muscle healing - regeneration if nuclei are not destroyed and endomysium around individual fibres is intact. If extensive cell death and haemorrhage then healing through scar tissue. Treatment: cold compress and immobilisation, Occassionally requires surgical decompression. Laceration - horizontal mattress or N-F-F-N sutures. Heal by fibrous scar tissue.
234
What is fibrotic contracture of the infraspinatous M?
Severe strain/trauma in working dogs. History - acute lameness fully resolving 3-4 weeks before contracture. Mild lameness - characteristic posture. Lateral deviation of the carpus when limb flexed. Treatment - - transect the tendon of insertion. Excellent prognosis.
235
What is quadriceps muscle contracture?
Congenital (rare), muscle trauma, immobilisation can all cause contracture. Stifle hyperextension and fibrosis - bone and cartilage atrophy. Treatment - muscle release (Z Plasty), transarticular fixator. Poor prognosis - frequently require amputation as fail to imrpove/recur/poor limb function.
236
What is fibrotic myopathy?
Muscle contracture - fibrosis of the muscle. Aetiology unknown. Fibrous band of the gracillis. Signalment - GSD, males. Characteristic gait, short stride. Pain on abduction of limb/palpation - muscle feels taught. Treatment is medical or physical therapy - surgery:always recurs.
237
Describe Achilles' tendon injury
Complete rupture - plantigrade stance.
Partial rupture - lengthening of gastrocnemius, flexed digits
Tendinosis - thickening but no lengthening
Treatment: lengthening - temporary immobilisation, primary repair. Remove support after 6 weeks. good prognosis.
238
What is Mineralisation of SS tendon injury?
May be trauma or blood, may be assymptomatic, Pain on palpation, radiography. Treatment: extra corporeal shock wave therapy, surgical exploration and removal. Prognosis - moderate, recurs.
239
What are signs of prostatic diseasE?
dysuria, dyschezia, haematuria, urethral obstruction. In Mature dogs with benign prostatic hyperplasia the prostate moves cranially into the abdomen. In young dogs it is intrapelvic, small walnut sized.
240
What is benign prostatic hyperplasia?
95% intact males over 9 years, androgen stimulation, reversible hyperplasia, non- painful, symmetrical prostatic enlargement, predisposes to prostatic infection. Treatment - anti androgen therapy, castration. Do not use oestrogens.
241
What is bacterial prostatitis?
Prostatitis is common: acute - chronic. Any prostatic disease predisposes to infection. Commonest site of infection in male UTI. Physical/phsyiological drug barriers: fluoroquinolones, castration. Chronic bacterial prostatitis: persistent signs of UTI, other signs of prostatic disease.
242
What is a prostatic abscess?
An extension of bacterial prostatitis? Abscessation of prostatic cyst, asymmetric, painful prostatomegaly, systemic illness. May present with acute abdomen - surgical emergency. Complications of prostatic abscess - urethral erosion, septic peritonitis, uroperitoneum.
243
What are prostatic cysts?
Non septic fluid filled cavity. Within the parenchyma: prostatic cysts. Attached to the prostate:paraprostatic cysts. Prostatic cysts may be acquired or congenital - blockage of ducts, follow BPH. Periprostatic cysts - paraprostatic cysts - congenital but enlarge as patient ages, abdominal or intrapelvic do not communicate with prostatic tissue. Both asymmetrical, turgid, non painful, prostatomegaly, abdominal or pelvic mass.
244
Describe prostatic neoplasia?
Usually adenocarcinoma, extremely painful, metastasise early, often PTS on diagnosis. Radiography - will be extravasation of contrast, periosteal reaction: lumbar spine + pelvis. Prostatic wash & biopsy to confirm.
245
How do you do a prostatic biopsy?
Place urethral catheter. Isolate from abdomen. Wedge from each lobe on the ventral surface.
246
What is prostatectomy?
Not recommended, high complication rate, incontinence, profuse haemorrhage
247
What is shoulder osteochondrosis?
Failure of endochondral ossification. flap formation - osteochondritis dissecans, on the caudal humeral head. Mild/moderate lameness, pain on shoulder exam, especially flexion, pain on palpation of the biceps tendon if detached flap in the bicipital grove. Radiolucent deficit in subchondral bone. Rarely flap may be mineralised +/- detatched. 90% sound within 4--8 weeks of surgery, develop mild DJD with time. Arthroscopy/arthrotomy to remove flap, abrade the surface to facilitate vascularisation.
248
Describe traumatic Shoulder luxation
Dislocation. Trauma to supporting structures - biceps brachii, glenohumeral ligaments, monitor for concurrent thoracic trauma. Presenting signs - NWB, lateral - foot internally rotated, medial - foot externally. Use a veelpeau for a medial luxation, or a spica splint for a lateral luxation. DJD with time.
249
What is congenital Shoulder luxation?
Toy breeds. Surgery if reconstruction techniques fail - arthrodesis. Prognosis good.
250
What is shoulder instability?
A tear or stretch of the support structures. Medial or lateral glenohumeral ligament, subscapularis, biceps brachii tendon of origin. Medium/large breed, chronic mild to moderate lameness, moderate muscle atrophy.Measure shoulder abduction angle. Diagnosis - arthroscopy, - subjective laxity/tearing of the ligaments/tendons. analgesia, controlled excercise or surgical - radiofrequency shrinkage, prosthetic stabilisation, subscapular tendon imbrication.
251
What Is biceps tendon disease?
Tenosynovitis - partial or complete rupture. May be due to repetitive injury or chronic inflammation. Marked pain on shoulder flexion, pain on direct palpation of the tendon, rupture. Radiography - oesteophytes intertubercular groove. Arthroscopy then tenotomy.
252
What is carpal luxation or subluxation?
Loss of palmar ligament support - trauma or chronic immune mediated polyarthritis. Trauma or shetland sheep dog. Palmargrade stance, mild - moderate lameness. Medical management only indicated for puppy laxity - laxity will spontaneously resolve with Excercise. Surgical - pancarpal arthrodesis or partial carpal arthrodesis.
Musculoskeletal
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