Musculoskeletal Flashcards
What are the essentials of fracture healing?
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.
What are the clinical signs of a fracture?
Loss of function, swelling, change in limb length, alignment or orientation, limb usually shorter, abnormal motility (reduced or increased), pain, crepitus.
How does healing occur under limited motion?
some movement at the fracture gap, healing occurs via callus formation, progressive increase in stiffness of the fracture gap, remodelling phase restores normal architecture.
What is primary bone union
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.
What is the benefit of primary bone union over healing by calus?
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.
What forces cause fractures?
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.
Describe the neutralising forces of fractures
Tension - lengthening Compression - shortening Bending - combines tension and compression, tension on convex surface, compression on concave surface, neutral axis results. Torsion Shear
What are pathological fractures
Bone fractures secondary to an underlying pathological process that weakens the structure - infection, neoplasia, nutritional disease. Normal loading results in the fracture.
Describe metaphyseal fractures
Beware of the potential for growth plate damage in skeletally immature animals. always warn owners to watch for angular deformity developing. salter harris fracture
Describe epiphyseal fractures?
Potential for growth plate damage in skeletally immature animals. likely articular involvement.
What can cause a greenstick fracture (incomplete)
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.
What are fissues?
(incomplete) hair line fractures. Undisplaced fissures are often seen running along the cortex from a major fracture line.
What is avulsion?
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.
Describe what radiography should be done for fractures?
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.
How can you recognise that a fracture is healing?
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.
What is a compound fracture?
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.
What is biological osteosynthesis?
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.
What should be the emergency support of fractures?
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.
What are the advantages and disadvantages of external copatation?
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.
What are splints used for
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.
How do you score fracture patient assessment score?
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.
How is fracture reduction done?
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.
How do you apply a cast?
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 .
What are the potential cast complications?
Pressure sores, poor technique or loosening, ischaemia may progress to gangrene, fracture disease - muscle wasting, stiffness, osteoporosis, tissue adhesion, malunion, delayed union.
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.
What are the different ESF frame designs available?
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.
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.
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,
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.
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.
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.
What is normograde pinning?
Introduce pin away from fracture site. reduce fracture, advance pin. may be able to do this closed.
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)
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.
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.
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.
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.
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).
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
What are the signs of chronic osteomyelitis
Lamenes,s muscle atrophy, fibrosis, contracture, bone pain, swelling, heat, discharging sinus tracts, anorexia, pyrexia.
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.
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
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
What is primary hyperparathyroidism?
Rare - autonomous secretion of PTH causes hypercalcaemia, Parathyroid adenoma - also carcinoma or hyperplasia.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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
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.
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.
What are the risk factors for osteosarcoma?
Ionizing radiation, chemical carcinogens, metallic implants, skeletal abnormalities, genetic mutations, early neutering?
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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).
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.
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.
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.
