Lameness Flashcards
Goals of lameness assessment
Investigating Lameness
Important parts of history in a SA lameness exam?
What are you looking for in a visual assessment in a SA lameness exam?
Gait assessment in a lameness exam
What might you see in a neurological condition with the gait assessment?
How can you differentiate between a neurological condition and an ortho condition?
Before an ortho exam, what should you ensure? What is your most valuable tool in assessing lameness? How long will they take? What do you do if you are unsure of your findings?
* not possible in all patients- sedation/ anaesthetized
* stoic patients (Labs)– cessation of panting, licking lips, pupillary dilation
* examine lame limb last & all limbs distal to proximal
* standing patient: muscle atrophy, joint effusion, conformation
* goniometer/ digital photographs– angles
* comparing sides
* long bones and joints
What should you examine on the manus and pes?
What should you examine on the carpus?
What should you examine on the elbow? normal ROM?
What should you examine in the shoulder? normal ROM?
Shoulder abduction angle?
What should you examine with the hock?
What should you examine with the stifle?
What should you look for with the hip?
How do you assess for coxofemoral luxation (2 ways)?
What tests could you use to assess hip dysplasia (2 ways)?
Cat ortho exam differences
When is arthroscopy used?
Where do you perform arthrocentesis on the different joints?
What test shows cranial cruciate ligament disease?
* Cranial tibial thrust
** rare to get caudal cruciate ligament disease
What should you do if blood appears in the syringe during arthocentesis? What percentage of arthocentesis cultures are negative? What type of tube? What else should you assess?
When would you FNA the bone?
What would you use for a bone biopsy? Tests? Risk?
When would you refer?
Exit pathways for lameness?
* NSAID trial/ Crate Rest
In a young dog, what are the most likely candidates for lameness?
What is the pathogenesis of osteochondrosis (OC)?
* A group of diseases affecting the normal process of endochondral ossifications– occurs in young and growing animals ** dysplasia of osteochondrosis really**
* in adult animals articular cartilage is avascular relying on diffusion of nutrients from synovial fluid, but the AEC in immature animals depends on the presence of viable blood vessels within cartilage canals… these vessels gradually disappear as the lumens of the cartilage canals become filled with hyaline cartilage in the process of chondrification.
* Focal disruption of vascular supply in growing animals is believed to be the initiating cause–> focal area of cartilage necrosis and chondrolysis–> primary lesions focal ISCHEMIC NECROSIS of growth cartilage initiated by necrosis of cartilage canal blood vessels
** Because the necrotic cartilage does not undergo mineralization or vascular penetration, a focal failure of endochondral ossification occurs when the ossifaction front approaches the lesion
What is sequelae to osteochondrosis?
* Healing– replaced by granulation tissue which is then converted to bone
* Formation of a subchondral bone cyst
* Fissure which extends to the joint surface which creates a flap OSTEOCHONDRITIS DISSECANS
* Release of inflammatory mediators leads to synovitis/effusion and clinical signs
* Flaps may become mineralized and remain in situ attached to a pedicle or break off and become free within the joint to create a joint mouse
OC aetiology and risk factors
Treatment of OC
Emerging treatments: osteochondral grafting, tissue engineering
Prognosis of shoulder/ humeral head OCD?
* Good prognosis, racing greyhounds can go back to the track
** if the dog is not lame at all, surgery is not indicated
When do puppies usually present with OCD? How do they present?
6-8 months
* typically lameness is unilateral
Conservative management in OCD?
Prognosis of OCD on the femoral condyle?
What is the most advanced type of surgery for OCD of the humeral condyle?
Synthetic cartilage plug
Who is predisposed for OCD of the hock? What part is normally affected? Prognosis?
Most common presentation of OCD
Usually medial, often rottweiler less than 12 months
What is elbow dysplasia?
AKA Ununited anconeal process (UAP)
* umbrella term to describe a series of conditions that lead to the development of osteoarthritis in the elbow joint
*** fragmentation of the medial coronoid process (FMCP or FCP)
* Elbow incongruity
* OCD (under the umbrella of elbow dysplasia)
What is ununited anconeal process?
* GSD over represented
* Clinically silent vs. late onset cases
What are the clinical signs of ununited anconeal process? How would you diagnose?
Treatment of Ununited Anconeal Process?
* Ulna osteotomy + screw + pin– goal is to allow proximal ulna to float proximally (fusion has been documented in some cases, results poorer if fusion achieved)– good prognosis generally
What is medial compartment disease?
* umbrella term referring to conditions which affect the medial aspect of the elbow joint:
- fragmentation of the medial coronoid process
- OC/OCD of the medial humeral condyle
- incongruity
* The lesions may or may not be interrelated
Presentation of medial compartment disease?
* 6-12 months first presentation
* Popular large breeds: GSD, Lb, Rotty, Newfoundland, St Bernard, GR, BMD
* Elbow incongruity can affect smaller dogs especially chondrodystrophoid breeds
* Male 2 x
* Frequently bilateral
* History: progressive/ intermittent weight bearing thoracic limb lameness; most respond to NSAID trial
* Cause? Hereditary component proven, OC vs. incongruency
* Treatment: juvenile patient (limited OA): arthroscopic fragment removal, ulnar osteostomy, subtotaly coronoidectomy, SHO
- Adult patients (established OA): medical, weight control, total elbow replacement
Early lesions of medial compartment disease
Late lesions of medial compartment disease
Pathogenesis of medial compartment disease
* fragmentation of the medial coronoid process
* OC/OCD of the medial humeral condyle
* Incongruity
What does fragmentation of the medial coronoid process (FMCP) lead to?
Clinical signs of medial compartment disease
With medial compartment disease, what is radiography good for? CT?
With medial compartment disease, how can diagnostic arthroscopy be used?
* Changes seen in OCD
* Evaluating congruity
- superior method for both sensitive and specific in comparison with radiographs and CT (w/o 3D modelling)
Treatment of medial compartment disease?
* Due to lack of studies with objective outcome measures, treatment is largely opinion based and therefore highly controversial
*Conservative management: rest, NSAIDs
* Surgery: arthroscopic fragment removal, debridement and curettage (arthroscopy or arthrotomy)– in some dogs a free fragment exists and is readily IDed and removed, in other dogs, only fissuring of the articular cartilage is present. Fissures can extend variable depths into the subchondral bone. Most surgeons excise the affected region as if it were a fragment
What is a subtotal coronoidectomy?
Treatment of OCD, incongruity
Removal of the tip of the medial coronoid process via osteotome or microsaggital saw
Possible treatment of FCP?
Possible treatment of FCP?
What is angular limb deformity (ALD)?
* Mainly affected paired bone systems especially radius and ulna
* Occurs due to injury to the growth plate leading to premature closure (symmetric or assymetric)
- trauma when dogs are young
- distal ulna growth plate is most vulnerable
- synostosis of the radius and ulna
- heritable?
- retained cartilage cores in the distal ulna growth plate
** Premature closure of growth plates can lead to–> reduced length of bone which often causes elbow incongruity
- radial shortening= humeroradial subluxation and increased load on the medial coronoid process by the humeral condyle, predisposing to FMCP
- ulna shortening= leads to humeroulnar subluxation and inc load on the radial head and anconeal process, predisposed to UAP
* angular limb deformity
* discrepancy in limb length: not really an issue for dgs.
* Abnormal load bearing although adjacent joints can lead to postural OA, stretching of the joint capsule/ collateral ligaments
How do you diagnose ALD?
How do you treat ALD?
* Immature dogs with premature closure of the distal ulna growth plate
- distal ulna ostectomy– well tolerated, will prevent deformity getting worse, 2nd procedure may be necessary when the patient stops growing
* Placing a staple across the distal radial growth plate to prevent ongoing growth
* Addressing elbow incongruity:
- due to short ulna: proximal osteotomy can be performed
- due to short radius: proximal ulna osteotomy, transverse radial osteotomy then gradual correction via circular ESF/distraction osteogenesis, saggital stairstep radial osteotomy acute correction
* Correcting angular limb deformity:
- acute correction/ stabilization
- gradual correction via circular ESF
** challenging and time consuming
Hip dysplasia Pathogenesis
* Changes start at 30 days
* Two theories for initiating event:
- Capsular laxity leading to subluxation
- Abnormality of endochondral ossification
** environmental factors:
- maternal milk: relaxin persists for longer in the milk of dysplastic bitches, induces matrix metalloproteinases
- testosterone only found in the milk of dysplastic bitches
- excessive food consumption/ rapid growth– shortens time to first appearance and worsens severity
* Genetics
Sequelae of hip dysplasia
*Subluxation leads to cartilage wear, wear of the dorsal acetabular rim, synovitis and initiation of OA
* Periarticular fibrosis can make the joint more stable, reducing subluxation and resolving the lameness
* Long term, progression of OA can lead to lameness/ poor hindlimb function
* Usually bilateral but can be unilateral
Signalment and clinical signs of hip dysplasia
How do you determine magnitude of hip laxity?
Ortho exam of juvenile hip dysplasia
* laxity is the primary abnormality in juvenile hip dysplasia
* Mediolateral translation of the proximal femure relative to osseous portions of the pelvis- positive Ortolani sign
* assessment of pain during forced extension
Conservative management of juvenile hip dysplasia
Surgical management of hip dysplasia
* Triple pelvic osteotomy (TPO): achieve functional hip joint stability also improves congruency and load distribution, increases the weight bearing area of the surfaces of teh acetabulum and femoral head which reduces the stress on the articular cartilage (can’t have OA** recommended for early stages before DJD**, angle of subluxation must be < 10 degrees and angle of reduction needs to be < 30 degrees, 5-11 months old)
* Pelvis osteotomised in three places: ischium, ilium and pubis; acetabular fragment rotated 20-40 degrees to imporve femoral head coverage, ilial osteotomy is stabilized with a custom stepping plate… very invasice and expensive but good results.
What is Juvenile Pubic Symphysiodesis?
What is a coxofemoral neurectomy?
What is avascular necrosis of the femoral head (AVFH)?
Signalment and clinical signs of AVFH?
Diagnosis and treatment of AVFH?
What is FHNE?
Indications for total hip replacement
The surgical procedure takes approximately 60-120 minutes
•
Requires a coordinated team of surgeons and theatre nurses
•
Preparation of the femur and acetabulum are followed by implantation of custom prosthetic components
Contraindications for THR
Hip dysplasia in cats
Patella luxation pathogenesis
* Usually associated with skeletal deformities e.g. for medial patella luxation: coxa vara, genu varum, external rotation of the distal femure, poorly developed medial ridge of the tibia,, internal rotation of the foot, etc.
* The opposite abnormalities are present with lateral patella luxation
* For both medial and lateral patella luxation the groove can be shallow
* Tend to get redundant soft tissue on the side of the luxation and stretched tissue on the side opposite the luxation
* these developmental abnormalities are present during the growing period, however 1st luxation may occur later
* often bilateral
* bony abnormalities are likely inherited
* medial patella luxation more common
* occurs in cats, mainly medial, weak association with hip dysplasia
Clinical signs and ortho exam with patella luxation
Grading system for patella luxation
Patella luxation treatment
•
Can be an incidental finding with no lameness noted by the owners
•
Mild intermittent lameness: consider conservative mangement
•
Hydro & physio useful for quads tone/mass
•
Large breed dogs and cases with grade 4 luxation should have surgery as quickly as possible after diagnosis.
•
Lots of different techniques described and often a combination required.
•
Most cases require tibial tuberosity transposition and groove deepening combined with soft tissue techniques
•
Soft tissue techniques ALONE tend to fail
•
Cases with grade 4 luxation usually require corrective osteotomies of the femur +/-the tibia.
TIBIAL TUBEROSITY TRANSPOSITION:
•
Tuberosity secured with 2 k wires +/-a TBW
•
If transposed too far can create the opposite type of patella luxation
ANTIROTATIONAL SUTURES
•
Placed from fabellato tibialtuberosity to counter internal or external rotation.
•
Placed from lateral fabellafor MPL
•
Heavy monofilament nonabsorbablesuture material typically used.
•
If concurrent MPL and CCLR, antirotationalsuture will also address craniocaudalinstability
Typical problem with over nutrition (excess ME)
What is important with nutrition during cartilage precursor, osteoblast infiltration, and osteoid production?
What is key during osteoid production, cartilage and osteoid mineralisation and cortical and trabecular bone remodelling in regards to nutrition?
What is a big problem with puppy nutrition? Why?
Too much energy is what is undesirable– too much protein protects against OCD
** Ad lib feeding of large and giant breeds should be avoided, does not happen in cats
What can happen if you underfeed puppies?
* Osteoporosis (not enough bone)- stunting, pathological fractures, subsequent hypocalcaemia crises
* Copper deficiency– weakened/ reduced osteoid
What can happen in a dog or cat fed an all meat diet?
Could miss out on the appropriate Ca:P diet, 1:1 (grains and meat have a Ca:P of 1:10+)
* Try to provide > 50% commercial diet
* Need dietary Ca = 1.2% of DM, P= 0.6-1.2%
* Don’t add extra supplements (e.g. Ca)
How can we assess secondary nutritional hyperparathyroidism?
* Urinary P excretion… compare urein: serum % of phosphorous and creatinine (baseline metabolite that the kidney doesn’t reabsorb)
Who has the higher Ca diet?
What can happen with low dietary vitamin D?
Vitamin D needed for active Ca & P absorption from gut–> low Ca &/0r P means bone can’t be mineralised–> Rickets in growing animals or Osteomalacia in adults (remodelled bone is soft)
How do you ensure adequate levels of vitamin D in the diet?
Good levels in organ meats, fish, fish oils, dairy (use as components of carnivore diets)
How much calcium do you need to add to a diet to fix Ca:P ratio?
Ideal diet of a dog and cat?
* Base on a complete commercial food
* Add fresh fruit and veges (dogs) if meat based– but mainly avoid meat based
* Avoid extra supplements
* Cook raw foods to reduce microbial risk
* Cats need extra: vit A, B, D
- all found in meats, organs, fish
- vitamins A and D both toxic if over-supplemented
If we want high contrast and high detail, how do we make that happen in a radiograph?
* Low KV–> improves contrast but need enough to get through
* High mAs–> consider building the image with lots of photons thus more detail
What does single emulsion and single screen give us?
What does double screen/film give us?
Single Emulsion and Single Screen
- Increased detail
- Increased exposure
- Depends on thickness
- Increased contrast
- No parallax error
- Less quantum mottle
-
Double screen/film
- Intensifies xrays thus can reduce mAs required for density therefore less dose
- Quicker therefore sharper image if motion
- Get parallax error
- Need for horses to reduce exposure time
- Need for larger animals > 10cm to reduce exposure times
What’s wrong with this?
Tibial Condyle obliterated
Which one is dog and which is a cat?
Think maybe tibial evulsion fracture– common in puppies… BUT it is not! It is normal– it is an open growth plate, compare the other leg and the other bones
* Right radiograph has a tibial fracture
Bilateral tibia evulsion fracture
* You can also see lysis– presented after weeks
If they are not closed by about 9 months, then wonder??
Skeletal Mature vs Immature?
Produced bone
Removed bone
ABCs Approach to Viewing Musculoskeletal X-Rays?
Describe abnormal bony findings in xrays? Interpretation?
* Interpret– normal vs. abnormal? Normal anatomic variant, projection artefact, true abnormality
** Unlikely to give a definitive diagnosis– likely to need a biopsy
How do you prioritise differentials?
how do you assess?
Size, shape, opacity, number and position of organs.
The presence of cortical destruction, periosteal reaction, and non distinct transition zone will be AGGRESSIVE!!!
Cortical destruction/ cortical integrity
Examples of non-aggressive bone disease
Examples of aggressive bone lesions
Parameters to Develop DDX list– aggressive vs. non-aggressive
Lesion location examples
What is meant by an aggressive lesions rate of progressive?
Progresses rapidly– changes appearance over a week
Description and interpretation of skeletal change
Findings with OA
enthesiophyte- Enthesiophytes are abnormal bony projections at the attachment of a tendon or ligament. They are not to be confused with osteophytes, which are abnormal bony projections in joint spaces. It has been noted that Enthesiophytes and osteophytes are bone responses for stress.
(Osteophyte
–Periosteal new bone formation that develop at the periarticular margin
•
•
•Enthesophyte
–Periosteal new bone formation that occurs at a point of traction. That is at ligament, tendons or joint capsule attachments)
Septic Arthritis- differentiate between this and OA by history etc.
Septic arthritis
OA
OA
Other non-key causes of lameness in older dogs
Primary and secondary?
Aetiology of OA
Pathogenesis of OA
Synovitis:
- get hypertrophy and hyperplasia and infiltration with lymphocytes
- proteolytic enzymes and inflammatory cytokines released from macrophages
* Subchondral bone
- sclerosis
- formation of osteophytes
* pain
- nociceptors in all structures in joint except articular cartilage
- can lead to central sensitisation which may drive the progression of OA pathology. COX enzymes may play an important role in this
History and clinical signs of OA
Diagnosis of OA
Non surgical management of OA
Conservative management of OA
NSAID mechanism of action? Side effects?
COX 2 specific NSAIDs have improved safety profiles e.g. Firocoxib, COX ratio 350
* most have central effects
When is tramadol C/I?
If on TCAs
Possible deleterious effect of corticosteroids on joints?
Intra- articular preparations may have deleterious effects on cartilage matrix synthesis
What are DMOADs/ Neutraceuticals?
What are salvage surgeries performed with OA?
Causes of infective arthritis
Pathogenesis of infective arthritis
Clinical signs of infective arthritis
Diagnosis of infective arthritis
Treatment of infective arthritis
** septic arthritis: culture synovium, remove implants, radical synovectomy, implantation of PMMA beads with ABs
* Joint irrigation/ surgery indicated if:
- gross contamination
- poor response to initial antibiotic therapy
- implant retrieval required
* ingress/ egress needles with lavage
* Arthroscopy
* Open arthrotomy indicated if
- no access to arthroscopy
- penetrating wound
- implant removal required
- radical synovectomy
- placement of local delivery devices required
Prognosis of septic arthritis
Pathogenesis of Immune Mediated Arthritis
Classifications of immune mediated arthritis
History and Clinical Signs of Immune Mediated Arthritis
Diagnosis of immune mediated arthritis
* Haematology
- leukocytosis or leukopaenia
- thrombocytopaenia (sec to IMTP)
- anaemia (sec to AIHA or chronic disease)
* Biochemistry
- increased globulins
- low albumin if protein losing nephropathy/glomerulopathy present
* Serum C reactive protein:
- markedly elevated initially
- used to guid therapy and prognosis
Treatment of immune mediated arthritis
Carpal hyperextension injury
Pathogenesis?
Clinical exam findings of coxofemoral luxation
Imaging of coxofemoral luxation
Conservative management of coxofemoral luxation
Surgical approach coxofemoral luxation
Toggle? Transarticular pin?
Prosthetic capsulorrhaphy? Iliofemoral suture?
Treatment?
Hip Arthritis
* Excision arthroplasty- FHNE remains an economical procedure for the treatment of severe hip pain
* Chronic rehabilitation required for optimal longterm function
* Unreliable outcomes in larger dogs
* Surgical technique, age, patient size, duration of clinical sign and postoperative physical therapy have an effect on long-term outcome
Indications for total hip replacement
What is this kind of surgery? What is the other option?
Cement THR
Pathogenesis of Cruciate Disease
History and Clinical signs of cruciate disease
What can happen at the same time as cruciate disease?
What are the manipulative tests for cruciate disease?
What will you see on diagnostic imaging of cruciate disease?
Conservative management of cruciate disease
What does arthrotomy or arthroscopy do for cranial cruciate disease?
How can you restore stability after cruciate disease?
What is a lateral febellotibial suture?
What are the geometry altering procedures that can be used in cruciate disease?
Advantages and disadvantages of a TTO?
By changing the geometry of the forces of gravity and muscle contractions that act on the stifle during weight-bearing, it aims to neutralise the shear force that causes the cranial movement of the tibia with respect to the femur.
This shear force develops because the canine tibial plateau – the weight-bearing aspect of the joint – is sloped caudally (downwards towards the back of the joint)and there is an acute angle between the tibial plateau slope and the patellar ligament. In the TTO procedure, the tibia has three osteotomies (cuts into the bone with a bone saw) performed upon it with the aim of realigning the tibial plateau slope so that it ultimately becomes aligned at right angles to the patellar ligament instead of sloping backwards. By achieving this, shear forces within the joint are neutralised and the joint is stable as the dog weight-bears.
The joint is not stable, however, when it is physically manipulated by attempting to move the tibia cranially.This contrasts with previous methods of CrCL repair which aimed to provide stability to the joint by replacing the ligament either with a fascial graft within the joint, or using a prosthesis made of nylon placed externally from the lateral fabella to a hole drilled in the tibial crest.
The TTO procedure has been developed as a hybrid of two previously available orthopaedic procedures, the tibial tuberosity advancement (TTA) and the tibial plateau leveling osteotomy (TPLO). The TTA neutralises shear force within the stifle by advancing the tibial tuberosity until the tibial plateau is at right angles to the patellar ligament. The TPLO neutralises shear force by rotating the tibial plateau so that it is approximately horizontal with respect to the long axis of the tibia. The TTO combines both of these procedures and as such less radical changes than either are required.
Explain how the cranial tibial thrust test works
Tibial plateau leveling osteotomy
In a TPLO procedure, the tibial plateau, the portion of the tibia adjoining the stifle, is cut and rotated so that its slope changes to approximately 5 degrees from the horizontal plane,.[3][4] This prevents the femur from sliding down the slope of the tibial plateau when the dog puts weight on its knee.[5] Thus surgery generally results in faster recovery times compared to other procedures to stabilize the knee. Most dogs (over 90%) are expected to regain a very active and athletic lifestyle with no post-operative complications and without the need for any long-term pain relieving medication.[6]
TTO
TPLO
Advantages to TPLO
* earlier return to weight bearing compared to intra and extra articular techniques
* low rates of subsequent meniscal tears
* Recent studies used objective outcome measures have documented quicker return to function and better long term function
What is a Tibial Tuberosity Advancement?
TTA is a surgical procedure designed to correct CrCL deficient stifles. The objective of the TTA is to advance the tibial tuberosity, which changes the angle of the patellar ligament to neutralize the tibiofemoral shear force during weight bearing. A microsaggital saw is used to cut the Tibial Tuberosity off then a special titanium cage is used to advance the tibial tuberosity. A titanium plate is used to hold the tibial tuberosity in position.[2] By neutralizing the shear forces in the stifle caused by a ruptured or weakened CrCL, the joint becomes more stable without compromising joint congruency.
Disadvantage of TTA?
Subsequent meniscal tears associated
What is a CBLO?
Longterm functional outcome of TTA v. TPLO and ECR in dogs?
Extracapsular repair (ECR)
CCLR treatment algorithm
TKR= total knee replacement
So what?
Meniscal blood supply
** partial meniscectomy of damaged tissue only
* preservation of capsular attachment & preservation of cranial and caudal meniscotibial ligaments
Prophylactic intervention to reduce incidence of meniscal tears?
Aftercare of meniscal release
Treatment?
CALCANEAN TENDON INJURY / DEGENERATION Treatment? Recovery?
Recovery
- immobilization mandatory- left on for 4-6 weeks
* Methods: splint, trans articular application of external skeletal fixation, calcaneotibial screw
* Pan tarsal arthrodesis
* Prognosis is generally good
Blood supply in normal bone? Blood supply in fractured bone?
What is direct bone healing?
What is indirect bone healing?
Possible fracture radiology
* general anaesthesia is often req’d to obtain good quality radiographs due to potentially painful positive
* minimum of two orthogonal views (at 90 degrees of each other)
* radiography of the contralateral limb may be useful (comparison)
What are the possible nature’s of fractures?
Traumatic, Stress, Pathologic (e.g. renal disease)
What are the energy levels of trauma?
Low energy (non-displaced fracture), high energy (comminuted fracture- displaced or even shattered), very high energy (gunshot- soft tissue overlying the bone important because that is where blood supply comes from to heal the bone).
* Healing will change depending on how much energy has gone into causing the break. AND affects the stability of the fracture and might influence how we treat the fracture.
Terms of each.
Simple= one fracture line
Oblique= longer than one bone diameter or not
Segmental= segment of diaphysis that has a complete cortical rim
Comminuted= MUSH- fragments- they are not complete- no complete diaphyseal there
Avulsion= normally occur at sites of muscle attachment
Depressed fractures= flat bones, typically of the skull
T and Y fractures= Fractures of the elbow- normal fossa- Straight across or Y pattern
Salter Harris Classification
Description of articular fractures. Is epiphysis involved or also some portion of the metaphysis?
Overridden
Pull of muscles resulted in fractures moving towards each other.
Luxation
Dislocate
Gustilo-Anderson Classification
With open fractures.
Type I- wound
Type II- wound > 1 cm but lots of soft tissue damage, flap or avulsion
Type III- more severe- extensive soft tissue injury. Is there adequate soft tissue for closure (3 different levels)
** Important because they introduce contamination. Bones and screws left for the rest of the animal’s life unless they cause a problem. Except bacteria can adhere to surface of the implant with a sludge that protects them from antibiotics and the body’s immune system. So typically we don’t give antibiotics for the rest of the animal’s life.
Planning for implants
* Bone stock- have we got enough bone for the particular implant (metal stabilizer)
* Bone size
* What fracture forces?
* Which type?
* What size?
Hole should not be greater than 30% of the bone.
Blood supply to the bone- what happens after a fracture?
Extraosseous supply of healing bone. Transient. Then normal system is reestablished. Preserve soft tissue attachments and blood supply as much as possible.
Why are nutrient foramen important for us to know their locations?
Can be mistaken for a fracture.
Direct Bone Union
v.
Indirect Bone union
Internal remodelling. No intermediate cartilage stage/ endochondral ossification
Inter-fragmentary Strain Theory
New gap size vs. what the original gap size was. New bone cannot form if strain between two fragments is > 2%. Strain is high when the change in length is high. If original length of the gap is small, strain is also high.
Think of
Strain= change in length (gap size)/ original length (gap size)
e.g. broken tibia, moving around, unstable, high strain. If you fix tibia but you still have a gap, then there is strain. As long as less than 2%, new bone can form.
Indirect Bone Union
Becasue intrafragmentary strain is too high this is what happens. So tissues that are tolerant of high strain form and are laid down further away from the central axis of the bone. They impart stability to the fracture. Therefore strain decreases and NOW BONE CAN FORM!
** callus deposition is a response to instability and results in increasing stability.
Bone is not very tolerant of strain (instability), but what tissues are tolerant?
Haematoma, Granulation Tissue- 100% for both
Cartilage not as tolerant- 15% but more so than bone (
Contact Healing
vs.
Gap Healing
Contact Healing- Bones are together and healing. Compressed together, rigidly stable then we get new bone forming. Occurs with osteoclasts and osteoblasts- oriented parallel to long axis of the bone. Dont see much callus.
CLINICALLY UNCOMMON. REALISTICALLY USUALLY A MIXTURE.
vs.
Gap healing- we still have bone ends close together less than I mm. But because of a gap- it is more disorganized- not parallel. WOVEN BONE deposited- DISORGANIZED. Subsequently has to be remodelled so it TAKES LONGER.
Anisotropic
Stronger when loaded longitudinally vs. transversely
Stronger in compression vs. tension
The forces acting on bone determine the conformation of the fracture.
Compression = oblique fractures 30-45 degrees angle to the direction of compressive force
Tensile force= transverse fractures- straight across- perpendicular to tensile load
Bending= transverse fractures (think of bone on a bar)
Bending and compression= butterfly fracture
Torsional forces= spiral crack (~45 degrees)
What is meant by bones are NOT pure cylinders? Using the femur as an example.
Differential loading
Tension band wire
Neutralizes tension caused by muscle contraction.
Can also use a plate to neutralize tension forces.
Pins with interlocking nails. Implant placed in the neutral axis of the bone. Neutralization of torsional forces and also bending forces.
Comminuted fracture- so it cannot withstand force therefore plate is necessary for healing.
Some type of plate fixation.
aims of a surgeon with a fracture
Preserve vascular supply of the healing bone, provide stability vs. forces acting at the fracture site.
FORCES MUST BE OVERCOME for the fracture to heal.
Thoracic Limbs 30% BW
Pelvic limbs 20% BW at slow walk
5 x this with running and jumping
Comminuted fracture of the tibia- what are we doing here?
Why? 2 reasons!
Using a plate, interlocking nail, and external skeletal fixation
WHY??
Always a race between implant failing- and healing. THEY ALWAYS FATIGUE AND WILL EVENTUALLY BREAK.
Visco-elastic
Amount of deformation to rate of loading
Energy stored during deformation is released at time of yield (fracture)
Amount of soft tissue damage is proportional to energy released
When the sum of forces acting on the bone > stiffness = fracture
Bone is anisotropic (fine architecture)
* stronger when loaded longitudinally vs. transversely
* stronger in compressive vs. tension
What are the three factors in the fracture assessment score when determining how robust our intervention needs to be? Explain a little on each.
What is a problem with a cast?
Generally poor at countering forces at the fracture site. Instability is still present. Must immobilize the joint above and below the fracture. Can cause rubbing. Sometimes can become more expensive than a bone plate if you charge properly for each change.
ONLY IN ANIMALS where rapid uncomplicated healing anticipated.
A small increase in the radius of our pin, does what to AMI (area moment of inertia)?
What does an increase in height do?
Radius ^ 4
vs.
AMI (area moment of inertia) of the plate Height^3
Gardiner’s Approach vs. Carpenter Approach
New approach is Gardiner’s Approach. Want to make sure joint surfaces and rotational alignment is the same BUT we dont’ care about the little bits of bone. We want to disturb the soft tissue and vascular supply as little as possible for healing.
What does it mean that bone is viscoelastic?
The amount of energy that bone can absorb before it fractures is dependent on the rate at which that load is applied. Whenever energy is stored in bone, it will be released when it fractures. More energy stored = more energy released = more fragments and more damage to surrounding Soft tissue structures
High energy v. low energy fractures
Physiological forces acting on the repair (the forces we need to overcome to repair– create favorable conditions of intra fragmentary strain)
rotational, axial, bending
What does it mean that bone is anisotropic?
What is the significance of bones not being true cylinders and loaded eccentrically?
What does the shape of the bone cause in regards to forces on the bone?
A compression
Where do we put our bone plates on long bones? Radius? Ulna? Femur, tibia, humerus?
What are we avoiding with bone plates? Why?
metal is better at resisting tensile forces vs. compressive forces so in a perfect world we always choose to put our bone plate on the tension surface of the bone
** Avoid transcortical defects away from the surface of the bone to which we are applying the plate otherwise = bending fault = cyclical metal fatigue= failure of our implant
What is rotation mainly caused by? Which fractures is rotation mainly a concern with? Why is this important?
Muscle forces
Particularly a concern with transverse fractures
** Orthopaedic fracture fixation must consider all of the forces acting on the bone to maximize healing of the site
Tension forces a result of?
* Muscle contraction
* Tibial tuberosity avulsion fracture common in well muscle juvenile dogs e.g. Staffy– lands with a massive quadriceps contraction which pulls off fragment… must overcome tension forces– can use plates or tension band principle and twist wire so it tightens– force exerted by tension band wire and force by quadriceps– net vector creates compressive force across the fracture site = stability
Interfragmentary strain equation
Change in length = how stable the fracture site is
Small number top fraction = small strain= what we want
Small intrafragmentary strain = bone can form
Why do almost all implants fail?
* Cyclical metal fatigue
* Race between bone healing and implant failure
* Implant failure first = reoperation
** e.g. IF strain too high + bone not forming + dog not restrained = implant failure
What is key about patient assessment for trauma that is in need of orthopaedic surgery?
What is the fracture assessment score?
Taking a fracture radiograph
What is meant by the radiological classification in regards to nature of fracture, energy level of trauma, and completeness?
* greenstick- skeletally immature with intact thick periosteum
* folding- nutritional def- cortex collapses on itself
* impacted- metaphyseal regions or vertebral bodies with dense metaphyseal bone
* penetration- result of external trauma that penetrates the skin
* stress
* intra-periosteal- uncommon as a result of tumours usually
Location of fracture? Relationship of fracture fragments?
What is the salter harris classification?
Classification of growth plate injuries
What will you see on a radiograph with an open fractures? Why is this important?
* might influence the type of repair we would use– considering biofilms protects from immune system and antibiotics– treatment would require removal of the implant
How would you describe?
C. Comminuted- more than 2 fragments
* closed complete comminuted mid-diaphyseal fracture of the left femur
What is the carpenter’s approach to fracture repair?
Advantage- protect implants from failure
Disadvantage- extensive ST resection therefore interfering with cytokines, stem cells – interfering with healing– as well as interfering with transient extraosseous blood supply
What is the current approach to fracture repair?
Gardener’s approach aka Biological osteosynthesis
* Preserve the fracture haematoma which sets up early recruitment of cells for healing, preserve limb length, rotational and angular alignment of the limb, preserve the relative spatial orientation of the joint surface above and below the fracture so that the limb is going to be functional
** try and do this without messing around with the soft tissues too much e.g. external skeletal fixation
** unless it is a simple fracture then it makes sense to do the carpentry approach
What are the AO principles?
What is external coaptation?
* aka casting, bandages, splints
* can use as the sole method of immobilisation with some important caveats
* fracture fragments traumatising ST is extremely painful–so external coaptation can be very helpful to alleviate pain
** they are only good at preventing BENDING forces (not shear, not rotational either, not axial compression tensional forces)
* one acceptable situation: young animal with a fractured radius but intact ulna
** you must immobilize the joint above and below e.g. for a fracture above the elbow and below the knee
** NEVER for a fracture in the HUMERUS OR FEMUR
* Significant muscle atrophy resulting in physical therapy after the limb is healed
Limitations to external coaptation?
Advantages to external coaptation?
Disadvantages to external coaptation
** vascular complications– toes and feet fall off– must communicate clearly with the owner if the animal becomes uncomfortable, smelly, if the bandage gets wet– if you delay severe consequences
Vascular obstruction with external coaptation
Clinical signs of complications in external coaptation?
Client eduation with external coaptation
Indications for external coaptation as primary support
External coaptation contraindications
What can be used for temporary/ adjunctive support for fractures?
* do not use cast material or only half…
What is fracture reduction?
* considering muscle contraction and effects on bone approximation for fracture ends– need to hold the bone together long enough for it to heal
** favorable environment mechanically and biologically at the fracture site
* humeral or femoral fracture are difficult because of muscles– difficult to overcome– so use the animals weight helps to initially start fatiguing the bone but isn’t normally enough– trying to prevent overridden fragments, need to put clamps on the bone to try to pull it apart. May not be enough, may need fracture distractors helps to fatigue the muscles– mechanical advantage– not just shear strength.
* other ways– put a lever in there to force the bone ends in correct apposition, traction device… can use fluoroscopy– real time radiographs to assess how apposition is going.
Advantages and Disadvantages to Internal Fixation
* Titanium- more flexible and more biologically inert
What is AMI?
What are intramedullary pins? When you place them alone, what are the considerations? What are the considerations when used with a plate?
Great at resisting bending but not at axial forces: tension, compression, shear and rotational forces
** e.g. if the fracture ends will interdigitate might consider only using IM pins SOLELY otherwise usually will not use them alone
* used to try and protect a plate from bending forces
How are IM pins placed?
* Normograde- placed from the end of the bone down to the fracture site
* Retrograde- placed from the fracture site
How does bone shape affect implant choice?
* e.g. Radius and femur bent in the dog- intramedullary implant (if using intramedullary implant: IM pin or interlocking nail) into femur need to use a smaller one or shorter or over reduce fracture to get a straight line through here
C
* useful in long oblique fractures
* consider does this cause damage to the bone?
Orthopaedic Wire applications
* Also cerclage– which is never used by itself!
Guidelines for using cerclage wiring?
D
What are the types of bone screws? What contributes to screws AMI?
* Core diameter contributes to screw AMI
* Cancellous bone screws are not strong enough to use in the cortex
** self taping screws– need to have all of the cutting threads out the other side of the bone– they need to be longer– in order to be stable
How can screws be used?
Never use by themselves! Need to protect them with a plate!
Advantages and disadvantages of bone plates?
What is conventional plating?
Different types of plates?
What is dynamic compression plating?
What are locking plates?
Significantly more expensive and can no longer angle the screws to maximize bone purchase– they have to be at 90 degrees to the plate for the rigid coupling to develop
Selecting bone plate size
weight of the patient, relative bone size, screws should not exceed 30% of the bone diameter or you might create a fracture
What are interlocking nails?
With external skeletal fixation (ESF)– what is teh frame? What is the construct? What are percutaneous transfixation elements? What are the transfixation elements attached to?
What is a positive profile pin in regards to ESF? Negative profile?
End threaded half pins? Centred threaded full pins?
Linear construct
What fracture forces can an ESF resist? What about bending?
Types of linear ESFs
What is a hybrid ESF? Free form ESF?
Advantages of ESFs
Disadvantages of ESFs
Principles of application of ESFs
* Can increase frame strength/ stiffness by:
- more pins: minimum of 2, ideally 3 per fragment, beyond 4 advantage is neglible
- bigger pins: stiffness proportional to radius^4– No > 20-30% of bone diameter
- decreasing pin working length (distance between clamp and bone) by getting clamp close to bone: stiffness inversely proportional to length^3
- span the fragment with pins (far, near, near, far principle). No > 0.5 x bone diameter from fracture line or joint through
- use stronger clamps and connecting bars
- use threaded pins rather than smooth
- adding more connecting bars: add a 2nd connecting bar or plate on the same side/plan; more complex frame configurations
- Ultrastructural bone damage is minimized by: predrilling pilot holes, using low speed insertion < 300 rpm for insertion of pins- avoids thermal necrosis of bone > 47C; pins should penetrate the trans cortex for optimal stability
- Soft tissue impingement/irritation is minimized by generous release incisions
Aftercare with ESF
What is the Gustilo Anderson Classification System?
What is the ideal fixation of an open fracture?
Essential properties of bone grafts
Where are autogenous cancellous bone grafts used? When are cortical grafts used?
* osteogenesis, osteoinduction, osteoconduction, osteopromotion, structural support
Postoperative management of fracture repair
* sometimes poor limb use can be a problem.
- walk slowly
- walking in tight figure of eight circles
- holding up the opposite leg
- physiotherapy
- hydrotherapy
What are the 4 A’s in radiological assessment of fracture repair & monitoring?
Monitoring of bone healing considerations
What is delayed union?
What is malunion?
Consequences of malunion
Treatment of malunion
What is non-union?
What is viable non-union?
Depends on the amount of activity there
What is nonviable non-union?
What are causes of malunion?
* Bone can still heal in the presence of bacteria but it will delay healing
Treatment of viable non-union
* cancellous bone graft- osteogenesis (ability to generate bone– bone graft may not survive but becomes the scaffold), osteoconduction (the bone graft acting as a scaffold), osteopromotion, osteoinduction
* cortical bone graft does not have osteogenesis ability (ONLY OSTEOCONDUCTION)
What is meant by stress protection?
* exception for interfragmentary strain would be comminuted fracture is bigger up to 10%–motion would encourage osteogenesis
What is this showing an example of ?
Staged destabilisation
** 6 weeks postop atrophic non union = melting
Treatment of nonviable non-union
What is osteomyelitis?
Why do open fractures often get infected?
Nosocomial infection most common
What is a biofilm?
Conditioning film- organic material attached to metal
* bacteria produce glycocalyx– mechanical barrier nothing can cross, inside the biofilm bacteria activity is low so some antibacterials that target RNA DNA or folic acid– so if bacteria is really static they are not effective; harsh environment– low pH, low tension of O2 and high tension of CO2
Signs & symptoms, diagnosis and treatment of surgical site infection after fracture repair?
Types of implant failure
Treatment when implants fail
Reasons for refracture?
Take home points for fracture repair
Why are physeal fractures unique and important?
Quick once over endochondral ossification
Microscopic anatomy of the growth plate
When can physeal fractures occur?
Why do fractures occur at the physis?
What is the salter harris scheme?
Shitzus about 4 to 6 months!! Great Dane pups will have a lot longer opportunity for their growth plates to fracture– may not mature until 18 months
Go through the joint as well damaging the articular cartilage (type III and IV)
Go through the joint as well damaging the articular cartilage (type III and IV)
Healing of physeal fractures
* if growing cells are damaged in the reserve and proliferative zones, growth of physeal cartilage does not occur and endochondral ossification proceeds
* Bone is formed in the fracture gap, resulting in premature closure of the growth plate
* malalignment of the physis leads to bridging of the physis with bone
Consequences of Premature Growth Plate Closure
Consequences of premature growth plate closure- left carpal valgus occurred because type V physeal injury to the distal ulnar physis
* important to take contralateral radiographs to look at both sides especially hard in a young animal to know what is normal and what is not
Physeal fracture repair advantages and disadvantages
Good blood supply because it is near the epiphysis
** but must consider– are you damaging the joint, you are so close
Dos and Don’ts of physeal fracture repair
Big things about intra-articular fractures
* if you delay– more muscle contraction and more fibrosis
* need to be able to use their leg as this is key to avoid fibrosis and difficulty in recovery due to lack of movement in the joint
Common in racing greyhounds
* particularly on their inside leg (as in North America run the opposite way)
* acts as the fulcrum– trying to prevent hyperextension but ends up fracturing
* type intra articular fractures– type III and IV avulsion fractures
* 95% go back to racing
Treatment for metacarpal/ metatarsal fractures?
When to treat metacarpal/metatarsal fractures surgically
Post operative care for metatarsal/metacarpal fractures?
* Tibial tuberosity has evulsed & tibial plateau has lifted off a bit
How would you repair?
* Physis is minimally deplaced so do not need to repair
* KY’s directed away from the joint & tension band counteracting displacement force of the patellar ligament
* 3-4 weeks to repair
* Femur fracture– type I Salter Harris Fracture (commonly Type I and Type II) – you can tell because the condyles have rotated
* Cross wiring for repair
* Potential complications– limb shortening, valgus or varus complication, patellar luxation can happen (not super common but worth knowing if it doesn’t heal well)
** repaired with rush pinning (cross wiring is commonly performed)
What is this called? Treatment?
Type I Salter Harris Capital Physeal Fracture (common, not necessarily a lot of trauma associated)
Treatment?
* Use KY’s running parallel running together better for growth
* Diverging– which is better for stability
* Other options: salvage procedure if you didn’t notice it occured– so either FHNE or arthroplasty
Lateral condylar fracture
* Must be repaired immediately
* Do not have to provide coaptation
* Repair: repair with a plate (lateral condyle and metaphysis) and screw as well
* Consequences: Arthritis
* Final function: should do well
Post op goals: early weight bearing, physiotherapy down the track
Important points on physeal fractures, intra-articular fractures, and small bone fractures?
What is this called?
Extended ventrodorsal view (extended reference to pelvis)
Ligament of the head of the femur laxity cannot be assess properly by extended VD
* Take 3 radiographs
* Femurs perpendicular to table top– tibias are parallel to table top
* You can’t see all of the femur because it is coming straight up at you
* Now acetabulum and femoral head nice and tight– distractor between the legs acting as a fulcrum– forcing the coxofemoral point slightly apart
** Gives a good assessment of the laxity of the hips
What are you assessing?
2 is the most important– eventually you will see new bone forming at this site– the non-articular surface of the anconeal process- cannot have kV too high! Need nice contrast
5–medial coronoid process– like a ski slope– if you have a rubbish X-ray you can’t see that!
3– important area for osteophyte formation (1 as well– the medial epidcondyle)
4– imp for looking at sclerosis– bone would go lighter
What is the Norberg angle? What makes it change?
If the laxity of the femoral head was increased– the angle would become closer to 90
Where is the dot?
Dot is the center of femoral head
Arrow- theseophyte– forming where there is a tendon, joint capsule or ligament attaching the bone (where an osteophyte is at the junction of articular cartilage)
Morgan line
Section B. Key subjective criteria become more evident with time;
- Dorsal acetabular edge – smooth or irregular?
- Cranial effective acetabular rim - Angular and well-defined or rounded with osteophyte formation?
- Acetabular fossa – flattened, widened, sclerotic margins?
- Caudal acetabular edge – osteophytes?
- Femoral head/neck exostoses - may be a thin line of enthesophytes on the caudal aspect of the femoral head (Morgan line or “caudolateral curvilinear osteophyte”…even though it’s really an enthesophyte)
- Femoral head recontouring- altered shape, subchondral sclerosis or lucency?
- Sclerosis of the cranial acetabular edge - Does it conform to the femoral head or does it diverge? Is the subchondral bone normal or sclerotic?
Older dog– lots of changes
Same dog 8 years apart
* Screenings Can’t pick all dogs that end up with hip dysplasia
Can you point out the radial head? Medial coronoid process? Subtrochlear region? Medial epidcondyle?
What images?
Normal elbows
* Right image is craniocaudal image
Moderate volume of smoothly contoured new bone Periosteal new bone on the non-articular surface of the anconeal process
* NAD subtrochlear region, the epicondyles of the medial process are smooth
Radial head osteophytes
Subtrochlear sclerosis
FCP: MCP contour altered + sclerosis
(Medial Coronoid Process)
* new bone growth on anconeal surface
Point on the radial head
Driving into fog on the ski slope of the medial coronoid process
Fluffiness on the non-articular surface of the anconeal process
Cranio caudal medial process has a beet sticking out
What can cause elbow dysplasia?
FCP abnormal Left image, normal comparison image
** what else can cause elbow dysplasia– fragmented coronoid process, osteochondrosis of medial or lateral humeral condyle, ununited anconeal process, elbow incongruity
RIGHT IMAGE– subchondral defect– sclerosis– OCD lesion…
* MCP– kissing lesion MCP rubbing up against lateral condyle causing cartilage erosion
Contour of the radius should follow the humerus and the ulna– not congruent
Cleavage line through the anconeal process
* Growth plate that fuses at 5 months of age… but if over 6 months– ununited anconeal process
Trauma, severity of lamenessn (weight bearing), recurrence? worse with exercise? duration? history of lameness in litter? any therapy provided?
** investigation: general exam + orthopaedic exam, watching the dog walk, muscle atrophy? pain response?
A ortho exam
B. radiograph both shoulders
Depression of humeral head
C Arthroscopy… then CT, contrast arthrogram if no access to other equip
Contrast Arthrogram
You could try medical management and NSAIDs but surgical treatment (D) really is the treatment
* Carprofen
Arthroscopy
* remove the flap, currette the flap to subchondral bone so fibrocartilage can grow back in there– nice sharp edges around the cartilage defect
* place a KY
* NSAIDs, opioids, tramadol
What would you do next?
* ortho exam
* Radiographs
A medial trochlear ridge– reverse of horses
What is the special view for hock OCD?
Skyline view
Other imaging options for hock OCD?
CT– good for bone imaging and for imaging where there are superimposed structures
Same for OCD
* Arthroscopy, open arthrotomy, remove the lesion
Likely sequel with hock OCD in a dog?
OA– can be severe longterm
Assess other joints
** Amputation is radical
* Arthrodesis is a big surgery– tolerate well in tarsus but better in carpus
Differentials?
Right forelimb
What would you do if you weren’t sure?
B. Sliding humeral osteotomy- relatively new technique– good improvement after that surgery ($4K)
(total elbow replacement has a high complication rate)
Yearling TB swelling over stifle… swears the horse isn’t lame.
Hard to do a flexion test on a yearling!! But might not be that easy!!
** D Radiograph stifle
a. U/S
b. Arthroscopy
c. Re RG in 4-6 weeks
Subtle changes on the x-ray, there is flattening of lateral trochlear ridge (most common site for OCD in the stifle but not convinved it needs surgery– indications– fragmentation, gets worse)
A. U/S– or C if no comfort with U/S…. Arthroscopy is a very expensive procedure so wouldn’t jump straight to it (risks with knocking horses out too)
Presentation
* 2 yo TB
* Has been in work 12 weeks
* sudden onset LH lameness
* no localising signs
Examination: subtle RH femoropatellar effusion, grade 2/5 lameness, positive spavin test
Scintigraphy– shows growth plate of course and caudal view shows right general increased uptake– might just be increased bloodflow the leg…. focal area on the medial condyle in the femur. BONE CYST!!! because medial condyle…. Don’t often see this type of untake.
* Nerve blocks– pastern ring block- nochange; low 4 point- no change, subtarsal- no change, tibial and peroneal- no change, intra-articular stifle (all 3 comparments)- 60 % improvement
** Jumped straight to RG– which you would end up doing to confirm anyway… BONE CYST
Bone cyst
C or D
* prosand cons– 2 yo horse– intra- art in 2 yo less likely to be successful than in a yearling because the cyst has been there a long time– mature cyst… so a one year old more potential for healign. If you go straight to arthroscopic debridement you have nowhere to go from there
TB yearling, pre-sale RG, no swelling or lameness
BUT OCD fragment
A. do nothing
B. Restrict exercise and diet
C. arthroscopic debridement
C. operate and take them out performance is just as good as a horse who has never had one
Debridement BECAUSE it is an osteochondral fragment– if they break off and start floating around– risk of OA
2 yo TB
in training 4 weeks
hindlimb lameness
Effusion of left femoropatellar joint
Lateral trochlear ridge– most common lesions– vague lucency and vague defect
** take more views– oblique view?? caudolateral cranial medial view
6 yo WB cross
- sudden onset left tarsocrural effusion
- mild LH lameness
- pain on hindlimb flexion
** lateral to the right, medial to the left
What is the most likely cause of this lesion?
A. Osteochondrosis
B. Direct trauma
C. sepsis
B. Direct Trauma
** more likely trauma and not OCD because lateral malleolous– more common in OCD medial malleolous (not so much trauma because medial side of the leg)
* also because it is an older horse
Start thinking flatbone fractures with what presentations?
General considerations in flat bone fractures
What is meant by the weightbearing axis (clinical relevance)? Indications for surgical repair of the pelvis?
Considerations/ indications for acute repair, delayed surgery, or conservative management?
What is meant by conservative management with flat bone fractures (generally with fractures)?
Assessing pelvic fractures
Imaging for pelvic fractures
Sacroiliac luxation considerations
Repairing ilial fractures
Repairing acetabular fractures
Sacral fracture repair
Repair of pelvic floor fractures? What is the pelvic floor?
* attach to hamstring muscles so if you do not repair, you could limit the animal’s motion
Causes of mandibular and maxilla fracture?
Diagnostic imaging for mandibular or maxillary fractures
General considerations of maxilla and mandibular fractures
Repair of maxilla fractures
Repair of mandible fractures
** implants on tension surface of the bone– but with mandible you may have to put implants on compression surface
Repair of mandibular symphysis
Classic run over by owner in the driveway or fall from heights
Repair of mandibular body fractures
Repair of caudal mandibular fractures
Important points of flat bone repair and general fracture repair
Considerations for foot problems in dogs and cats
* home remedy: if the pet smells of dettol– can cause chemical burns– look in the mouth
Diagnostic tests for foot problem
Common paw problems
* slipping, wetness- hair dryer, plastic bags on to go outside but don’t leave it on otherwise bandage sweats, chewing– can end up constricting the foot, smelly, causing necrosis
After care?
Grass seeds
** Any FB use BS antibiotics for a week as well
If the whole paw is swollen, what do you think? Hair loss on paws, white fluffly and brown stained? Hair loss +/- suppuration?
Pad problems
Cut pad- bleed profuses, friable material– use big bites– vertical suture, sometimes tissue glue as well, bandaged well with a few bandage changes
* Cracked and dry pads– especially working dogs, can get infected– moisturizing (paw paw)– or booties
* Swollen, worn pads– hot concrete
Spongy paws in a cat? Owner thinks their pet grew an extra nail?
* plasmacytic pododermatitis- if you leave them too long they ulcerate.. treatment of choice is Doxy 5-10 mg/kg BID
Nail disorders? Most common?
Torn nail- antibiotics, pain relief with new nail growing in
** As the dogs age the quicks get longer– avoid unless obviously long
Basics of MSk exam of the greyhound
Race vision- video of the greyhound racing
* flex, extend, and rotate every joint
* palpate the border and surface of every muscle
* follow the course of every tendon
* compare one side to the other– stance, range of motion, symmetry, swelling, soreness, bruising, withering or change of shape, muscle tears, tense bands of muscle or the presence of scar tissue
Common racing Greyhound injuries
Tearing or straining of the gracilis m. (“back muscle”), the origin of the
long head of triceps m. (“dropped monkey muscle”) or the tensor fascia
lata m. (“triangle muscle”)
• Flexion pain or swelling of the tarsus or carpus
• Metacarpal soreness especially of the left 5th and proximal right 2nd
metacarpal.
• Fractures of the fibula, metacarpals, metatarsals and phalanges.
• Sprains or ruptures of the phalangeal collateral ligaments.
• “Track Leg” (swelling on the medial surface of the mid tibia) due to poor
running style causing striking of the medial tibia on the lateral humeral
epicondyle.
• Lameness from the pad - puncture marks, foreign body penetration (e.g.
glass) and “corns”
Grade 1 injury
Grade 2 injury
Grade 3 injury
Treatment basics for racing Greyhounds
Conservative treatment doesn’t go as well, they are a large breed
* important to get them to gallop ASAP (early return to function) so muscle fibres stretch and tear through scar tissue otherwise you let it heal– chronically it can actually retear… need to catch scar tissue early
Head and neck examination of a racing Greyhound
Brachium and Shoulder examination of a racing Greyhound
Scapula examination of a racing Greyhound
The brachium and shoulder examination of a racing Greyhound
Thoracic and Lumbar Spine examination of a racing Greyhound
Muscles of the Trunk and Abdomen examination of a racing Greyhound
The Pelvis, Hip and Tail examination of a racing Greyhound
Hind Limbs examination of a racing Greyhound
Common sites of muscle injury:
- Tensor fascia latae m.– bottom third
- Vastus lateralis m.- proximal third
- origin of insertion of semimembranosus or semitendinosus mm.– lack of resistance upon cranial movement of the hind limb to the point of the shoulder… marked bruising and swelling
- Gastrocnemius tendon- thickening and usually painful on hock flexion
Stifle examination of a racing Greyhound
Step lesion after healing from avulsion of the tibial tuberosity– not lame as pets but won’t race again
Fibula examination of a racing Greyhound
Tibia examination of a racing Greyhound
Tarsus (Hock) examination of a racing Greyhound
Types?
Metatarsal examination of a racing Greyhound
Greyhounds have thin skin so easily tear
Paw examination of a racing Greyhound
Metacarpal examination of a racing Greyhound? Common injuries?
Carpus examination of a racing Greyhound
The forearm examination of a racing Greyhound
Misc causes of lameness in racing Greyhounds
Limitations of Radiography
Uses of Ultrasound
U/S uses in small animal tendon/ muscle injuries
On U/S how does normal synovial fluid show up? Synovial tissue? Articular cartilage? Bone surface?
- Normal synovial fluid: anechoic
- Synovial tissue: hyperechoic
- Articular cartilage: hypoechoic
- Bone surface hyperechoic with profound distal shadow
Meninscal injury
How does muscle show up on U/S
Limitations of U/S
Rhabdomyolysis
Limitations of Scintigraphy
Uses of CT
Elbow dysplasia complex
Pelvic fracture
FB
MRI uses
Limitations of MRI
How does MRI work?
What does the axial skeleton include? Diseases of the axial skeleton normally cause?
Diseases that affect the axial skeleton
frequently cause
dysfunction of the
bone
or
nervous system
(brain and spinal cord)
•
These
conditions include congenital
malformation, neoplasia, infection, and
trauma resulting in fracture / luxation.
Conditions of the axial skeleton
Multi lobular osteochondroma (MLO)
(not spondylosis– new bone formation)
* Discospondylytis specially the end plates (growth plates) on either end– lots of capillary ends there so if you have a source of infection, commonly UTI, spreads haematogenously– will localize in those small capillaries– lysis and loss of bone detail in the space– Lumbar sacral and thoracolumbar as well
** Loss of stability causes neurological signs
If you have impingement and you can reduce it, better outcomes
Move them minimally– using horizontal beams, as opposed to dorsoventral
Middle to large working dogs commonly
At this level– cauda equina, peripheral nerves– as they exit the foraminae– impingement on the nerves which causes pain
* Diagnose via lordosis test– hyperextend back legs with pressure on lumbosacral area
* Due to instability or type II disc protrusion where the disc is pushing up
Most common form of primary bone cancer? Other types of primary bone cancer?
Distribution of Osteosarcoma
Signalment Osteosarcoma
Prognosis of Osteosarcoma
Osteosarcoma risk factors
Diagnosis of Osteosarcoma
* Inside out disease– spreading towards cortices
** often go in through thin cortices– alkaline phosphatase staining on cytology- higher sensitivity for osteosarcoma
- Jamshidi needle core– larger with stillette– central part of the lesion, do not penetrate to far cortex
Staging of Osteosarcoma
Proximal humerus– tend to have a larger mass and pick it up later
** why they die so quickly the micrometastases that you cannot see radiographically
“cannon ball” metastases - round, discrete lesions
>1 cm= radiographs
CT can detect = 0.5-0.6 cm ** not specific for cancer e.g. infection or bone healing, osteoarthritis
Amputation of forelimb
A skin incision is made from the dorsal border of scapula over scapula spine to proximal 1/3 of humerus. Continue skin incision around forelimb at this level.
The important surgical landmarks for the skin incision are the scapula spine, acromion process and axillary skin fold.
The trapezius and omotransversarius muscles are transected at their insertions on the scapula spine
The rhomboideus muscle is then transected from it’s attachment to the dorsal border of the scapula and the scapula retracted laterally to expose the medial surface of the scapula.
The serratus ventralis is elevate from the medial surface of the scapula with the aid of a periosteal elevator and electrocautery
At this point you should be able to visualize the brachial plexus and axillary artery and vein
** Triple ligate axillary artery and vein separately
- Encircling ligature
- Transfixing ligature
- Encircling ligature
- Transect between transfixing and distal encircling ligature
** Sharply transect brachial plexus nerves– bupivicaine
* Transect muscle
- Brachiocephalicus
- Deep and superficial pectorals
- Latissimus dorsi
Considerations of forelimb amputation
There is a large dead space left after an amputation surgery. It is very important to ensure that you have achieved good hemostasis and lavage the area with saline.
Does anyone have any thoughts on why it is important to remove blood clots and ensure that bleeding has stopped? (infection, seroma)
A local analgesic soaker catheter is used by some surgeons to provide additional local analgesia for the first 24-48 hours after surgery. These are less than $20 per catheter and are placed in the deep layers of the wound over the brachial plexus. Bupivicaine is administered through the catheter every 4-6 hours. This allows decreased opioid dose to be given and therefore earlier ambulation of the patient.
A three layer closure is done with monofilament absorbable sutures in the deep and superficial muscles layers apposing the pectorals to the latisimuss dorsi. Subcutaneous sutures are placed and then either non absorbable skin sutures (like nylon) or skin staples are used for closure.
This is the final result. This picture was taken the day after surgery. You can see that the dog is comfortable and weight bearing on three legs. You can see the analgesic soaker catheter in place and the large surgical wound. Here is a video of this dog walking the day after surgery. We often place a T-shirt cover over the wound to prevent any self trauma and provide some superficial wound protection. It is important top have the owner examine the wound regularly for any signs of seroma formation or wound breakdown / infection.
Forelimb salvage procedure
There is a large dead space left after an amputation surgery. It is very important to ensure that you have achieved good hemostasis and lavage the area with saline.
Does anyone have any thoughts on why it is important to remove blood clots and ensure that bleeding has stopped? (infection, seroma)
A local analgesic soaker catheter is used by some surgeons to provide additional local analgesia for the first 24-48 hours after surgery. These are less than $20 per catheter and are placed in the deep layers of the wound over the brachial plexus. Bupivicaine is administered through the catheter every 4-6 hours. This allows decreased opioid dose to be given and therefore earlier ambulation of the patient.
A three layer closure is done with monofilament absorbable sutures in the deep and superficial muscles layers apposing the pectorals to the latisimuss dorsi. Subcutaneous sutures are placed and then either non absorbable skin sutures (like nylon) or skin staples are used for closure.
This is the final result. This picture was taken the day after surgery. You can see that the dog is comfortable and weight bearing on three legs. You can see the analgesic soaker catheter in place and the large surgical wound. Here is a video of this dog walking the day after surgery. We often place a T-shirt cover over the wound to prevent any self trauma and provide some superficial wound protection. It is important top have the owner examine the wound regularly for any signs of seroma formation or wound breakdown / infection.
Osteosarcoma Palliative Treatment
* Combination therapy- XRT + Chemo + biphosphonates
* Disease progression
- development of metastatic disease, pathologic fracture, MST > amputation alone but < curative intent– XRT + Chemo longest MST
** Bisphosphonates– prevent ongoing bone destruction used in women to prevent osteoporosis– inhibit the action of the osteoclasts, not directly anti-neoplastic
Other MS neoplasia aside from OSA
* With Chondrosarcoma– would not necessarily recommend chemotherapy
Metastatic Bone Neoplasia
Do presenting with a big swelling on its head, neuro signs, changing demeanour
•
Slow
-growing, locally invasive tumor
with
moderate
metastatic
potential
•
Histological grade prognostic
–
Higher grade more aggressive biological
behaviour
•
Good Px if complete
excision
•
Adjuvant therapy no proven benefit
General approach to the diagnosis and management of oral masses
* Tumour staging– thoracic radiographs or CT, regional LN evaluation
* Radical surgical excision- maxillectomy or mandibulectomy
* Adjunct therapy- radiation (XRT), Cryotherapy, tumour vaccine
Clinical signs of oral neoplasia
Oral Neoplasia in cats and dogs
Don’t have to be black
Malignant oral tumour- Fibrosarcoma
Benign oral tumours– Papillomas, Fibromas, Odontogenic tumours
Epulides- benign oral tumours
Amputation indications
Pre-op considerations to amputation
List of clients who have been through limb amputation– good and bad experiences
Amputation principles? Partial amputation?
Pets in motion– physiotherapy- work with a company called Orthopets
Limb amputation haemostasis
Ligation- separately for veins and arteries– think of metastases as well so veins before arteries
Identify large veins prior to transection:
•
Prevent air entrainment and
embolisation
Limb amputation principles with muscle transection and nerves?
Thoracic Limb amputation techniques
Pelvic limb amputation techniques
Thoracic limb amputation
Mid-femoral amputation of pelvic limb
electrocaudery really helps otherwise time intensive with point ligation
Coxofemoral disarticulation surgery
Mostly for neoplasia– esp. affecting the femur
Limb amputation complications
Prevent seroma formation:
Jackson pratt helps post operatively
Increased movement helps
Indications for arthrodesis
Arthrodesis principles
** fix the joint at the standing angle
** two most common joints carpus and tarsus
Gait abnormalities will persist:
- advise owners pre-operatively
- aim for pain free, functional result
- compensatory mechanisms:
– increased flexion/extension remaining joints of affected limb and contralteral limb
– circumduction
** Sites subject to large forces:
- long lever arm
- fixation spans
- adequate fixation– Bone plates, ESF (where bone plates undesirable)
* More proximal sites = greater disability:
- hip NOT arthrodesed
- shoulder- compensation from articulation with thoracic wall musculature
Arthrodesis complications
Arthodesis implants
* due to tendons and ligaments have to compromise biomechanics and place the implant on the compression side
Arthrodesis of the shoulder indications
Not routinely done!
Arthrodesis of the elbow indications
Indications for arthrodesis of the carpus? Concurrent injury?
Implants :
e.g. screw goes through radial carpal bone
** MC 3 and 4 divergent screws
Implants used for pancarpal arthrodesis?
DCP – dynamic compression plate
Castless PCA- allows staggered screws
** Goal- apply compression– eccentric holes place the screws out to the side so they compress in (remove cartilage, bone graft)
Eventually you will see bony union- leave implant in unless causing problems
Partial carpal arthrodesis
Indications for stifle arthrodesis
Arthrodesis
- Stifle
•
Indications:
•
Severe degenerative joint disease:
•
Intra
-articular fractures
•
OCD
•
Instability from collateral or multiple ligament injury
•
Technique:
•
Plate fixation (pin techniques in small animals)
•
Maximise bone contact area removal of intra-
articular structures:
•
Cranial & Caudal
Cruciates
•
Menisci
•
Long Lever arms
– bone fracture
•
Compression
Stifle arthrodesis complications
Indications for hock arthrodesis
Techniques for hock arthrodesis
•
Techniques:
•
Plate fixation (Cranial
vs
Medial)
•
ESF
•
Pin and Tension
Band Wire
•
Pantarsal
vs
Partial Tarsal Arthrodesis:
•
Calcaneoquartal
•
Tarso
-metatarsal
Total Joint Hip Replacement Indications
When medical +/- surgical therapy has failed
** hips are the most reliable and most successful as well studied
Cemented Total Joint Replacement Hip
* problems with breakdown between the implant and the cement– aseptic loosening (simply the bonding)
– can become painful… PMMA can break down as well
Uncemented Total Joint Replacement- Hip
Uncemented is more biological vs. cemented
Outcomes of the total joint replacement- hip
Indications for total joint replacement- elbow
Do not have good chronic OA treatment of this joint
* Chris shifted away from this… looking more at resurfacing options with the Q system
Total Joint Replacement- elbow complications
Total Joint Replacement- Stifle
Total Joint Replacement- Stifle complications and outcomes?
Femoral Head and Neck Excision Indications and case selection
FHNE Technique
Sagittal plane – otherwise you’ll end up leaving a bone spur– palpate cut surface of the femur to feel for the spur
Complications of FHNE
Outcomes of FHNE?
What is ITAP?
ITAP
– Intraosseous
Transcutaneous
Amputation Prosthesis
•
Inspired by deer antler
•
Osseous and dermal integration of
implants
– robust prosthetic integration
•
Partial amputation
•
Complications:
•
Infection
•
Epidermal ingrowth (skin healing to the implant)
•
Marsupialisation
•
Peri-
prosthetic fracture
•
Indications?
Depth gauge, screwdriver, bending irons, pointed reduction forceps, 2.0mm, 2.5mm
and 3.5mm drills, 3.5mm tap, 2.5/3.5mm neutral drill guide, 2.5/3.5mm eccentric drill
guide, T handle countersink, handle with quick couple for tap
Different types of bone screws
* cancellous or cortical
* non- self tapping or self tapping (with cutting flutes)
* cancellous designed for implantation in regions of bone with thin cortices and abundant cancellous bone (e.g. the expanded metaphyses of long bones such as the proximal tibia, proximal humerus and distal femur)
- designed to engage in the softer cancellous bone with a relatively small core diameter, deep threads, and decreased pitch to provide increased resistance to pull out
- cancellous screws may be designed with threads along their full length of only on the end of the screw
* Cortical screws– implantation in regions of bone with a relatively thick cortex and little cancellous bone such as the diaphyses of long bones
- designed with increased pitch (e.g. more threads per unit length of screw) then cancellous screws and less thread depth so that the SA of contact between the screw threads and cortical bone is maximized
- cortical screws have a greater core diameter than cancellous screws which provides greater resistance to bendings
* Locking screws have a thread in the screw head that matches and engages into an identical thread profile in the plate hole. They have a wider core shaft diameter than equivalent sized non-locking cortical screws, which means they are significantly stronger. The locking system is fixed angle, e.g. screws can only be placed at one angle (90 degrees) relative to the plate which is an important consideration when placing screws close to a joint on the flared metaphyseal area.
What is the lag screw technique?
Used to compress bony surfaces together
What is the positional screw technique?
How do you place a positional screw?
How do you place a screw with the lag technique?
How do you apply a DCP?
Application of a lag screw and DCP in neutralization mode for an oblique fracture of the femur
What are interlocking nails?
Advantages and disadvantages of internal fixation with bone plates or interlocking nails
