Locomotor Flashcards
Clinical exam
Observation from a distance
Symmetry, posture, conformation (poor conformation doesn’t necessarily mean lameness)
Significant variations are usually obvious
Clinical exam
Gait observation
Patient moving away, towards and across you
Possibility of circling and turning to exaggerate abnormalities
Which limb? Characterise and score problem
Clinical Exam
Manipulation of joints
Moving the joint and limb in a controlled fashion to determine:
- Range of movement/abnormal movement
- Pain related to movement
- Load or unload specific structures in the limb
Safety factor
Maximum stress a structure withstand until breakage
OVER
Stress it is most likely to undergo during its lifetime
Factors of failure
Force/stress: magnitude, frequency, speed of loading, duration of loading
Influenced by: body mass, speed, gait
Constraints during locomotion
Need to support against gravity, force only produced when limb in contact with ground
Increase in speed - shorter stance, higher force
Ligaments in equine distal limb
Superficial digital flexor tendon SDFT
Deep digital flexor tendon DDFT
Distal accessory ligament DAL
Suspensory ligament SL
Flexor tendon muscles
Highly pennate
Muscle fibres about 1cm
Limited capacity for length change
Tendons
7% energy release as heat (horses)
Gallop tendons about 45 degrees C
Kills some cells but not tendon cells
Predilection for tendon core injuries
Joints - function
Relative movement of limb segments
Shock absorbers
Joints - horse
Reduction of phalanges, fusion of bones -> movement in sagittal plane only Interlocking configuration (ridges/grooves) - collateral ligaments -> restriction of movement without muscular control -> decrease in metabolic cost
Hoof (equine)
Horn capsule - protection but no expansion
Mechanical function - shock absorption, support and grip, propulsion
Constraints - resistance to abrasion, protection of senstive structures
Hoof (equine) - protective mechanisms
Shape of solar surface allows heel movement
Suspension of distal phalanx: forces transferred via distal border of hoof wall
Digital cushion: shock absorption and frog movement
Hoof sliding
Rotation and translation of the DIP joint
Duty factor
Ratio of stance and stride time
All stance phases critical to injury
1st impact: large accelerations, low forces
- likely to result in bruising to the soft tissues
- ‘vibrations’ good for bones??
2nd impact: low acceleration, high forces
- important to allow for a natural braking action
Support: large vertical force
- up to 2.5x body weight per limb
- excessive dorsiflexion of the fetlock means tendon stress
Force usually acts parallel to the long bones
Very tight safety factors in equine limb
High speed exercise
Increase tendon strain:
- reduced fatigue life
- potent stimulus for changes in structural properties
Trade off:
- providing stimulus and exceeding the mechanical capacity
- estimated fatigue life of around 10,000 cycles
Shifting of the PZM (point of zero movement)
Increase of moment around DIP
Increase in stress by the DDFT on navicular bone
Compensatory decrease in fetlock extension - unloading of the DDFT
Hindlimb: also point of force laterally in late stance -> shortening of moment arm around DIP
Mediolateral imbalance
Mediolateral wedge (6mm wide) moves PZM towards elevated side of the foot
Lateral extensions, trailer shoes in bone spavin:
- horses attempt to unload the dorsomedial aspect of small tarsal joints by redistributing weight to plantarolateral aspect of the foot
Assumed mechanism: redistribution of weight by rotating the foot or by helping the horse weight-bear on the lateral side of the foot
Alternate explanation: horse forced to move ‘normally,’ no unloading of painful tissues - eliciting the repair process
Heel wedges
Move PZM towards the heels
Reduce DIP moment arm, unloading DDFT and navicular bone (NB)
Give longer support through stance
Increase DIP joint pressure
Shift articular contact area dorsally
Increase in pressure may directly result in pain, can cause damage by changing vascularisation to the synovium and cartilage function triggering a cascade of detrimental pathways
Collapsed/underrun heels
Tubules start bending when grown distal to the distal phalanx
Impairment of natural hoof deformation and blood flow
Application of carbon fibre patches beneficial
Cow Lameness
History questions
Which lactation? How long calved? Previous (foot) problems? How long has she been lame? Treatment? Is she pregnant? Is she milking?
Cow Lameness
Score 0
Walks with even weight bearing and rhythm on all four feet with a flat back
Long fluid strides possible
Cow Lameness
Score 1
Steps uneven (rhythm or weigh bearing) or stride shortened affected limb(s) not identifiable immediately
Cow Lameness
Score 2
Uneven weight bearing on a limb that is immediately identifiable and/or obviously shortened strides (usually with an arch to the centre of the back)
Cow lameness
Score 3
Unable to walk as fast as a brisk human pace
Cannot keep up with healthy herd
Dutch 5 step foot trimming
1 Create a foot angle of 52 degrees 2 Create balance between claws 3 Transfer weight from sole on to the wall, toe and heel 4 Remove weight from painful claw 5 Remove loose or sharp horn
Examination of lame foot - cow
Visible lesions on sole, wall, heel and skin
Heat
Pain with hoof testers and finger pressure on soft tissues
Feel and look between claws
Softening above coronary band or in heel
Redness (skin)
Smell
Sole ulcers
Treat early - how early?
Dutch 5 step method
Antibacterial treatment
NSAIDs
Nursing and clean yard
Promote wound healing - nothing that cauterises
Prognosis - generally ok, recurrence next lactation, reduced fertility and life span in herd, milk should recover in several weeks
Effective herd interventions - sole ulcers
Increase straw bedding to 1 bale/10 cows/d in cubicles
Heifer comfort group 16 weeks vs cubicles
White line - treatment
Drain pus, pare out to allow good drainage, cut away dead horn (can be done 2 weeks later), apply a block, NSAIDs especially if local swelling of corium, apply antibacterial product
Generally good prognosis unless infected with Treponemes
White line presentation
Diseased horn affecting the junction between the sole and wall, including bruising (haemorrhage), separation (fissure), abscessation and ulceration
These are generally considered to be stages of a disease process
The last stage - wall ulcer - is usually recorded separately due to the severe and chronic pain associated with it
Digital dermatitis - treatment
M1: clean, dry (paper towel), topical oxytetracycline spray (3d)
M2: as above but debride with gauze/paper towel ad consider bandaging with antibacterial agent
M3 and M4: clean, debride/debulk (under local as necessary) bandage with antibacterial agent
Herd: Footbathing, Slurry management, Biosecurity
Foul (in-the-foot)
An acute bacterial infection of the SC tissues characterised by symmetrical swelling, separation of the claws and interdigital skin necrosis yielding pungent odour
Often associated with FB or sand between the claws
Super foul is a severe per-acute form, possibly involving mixed bacterial infections
Clean/debride interdigital space
Disinfect
Licensed inj antibiotic
Corkscrew claw
Bony swelling deep to abaxial coronary band is diagnostic
Not to be confused with gross claw overgrowth
Reshape foot as best as possible
Claw amputation
Parenteral antibiotics
NSAIDs and IVRA
Prep
Incise into interdigital space - 2-3cm, skin fold
Embryotomy wire - out then obliquely upwards
Curette and remove any excess tissue
Melolin and pressure dressing
Redress at 48 hour, 96 hour, 7d then leave open
Block on unaffected digit
Arthritis in piglets
Rare in outdoor pigs
Sporadic opportunist infection in individuals - strep, staph, E.coli - through wounds (tail, teeth, skin wounds, navel)
Group outbreaks - Strep suis type 14 via tonsils
2d - weaning
Can’t stand, dog sitting, enlarged joints, death
Diagnosis: Bacteriology
Treatment: penicillin, ampicillin, lincomycin, ketoprofen, or euthanasia
Lameness in growers - pigs
Injury - fractures, osteochondrosis dessicans, pantothenic acid def. (rare), Ionophore toxicity (rare)
Infectious:
- Mycoplasma hyosynoviae
- Mycoplasma hyopneumonia or hyorhinis polyarthritis (and pneumonia)
- Erysipelas (zoonosis, note skin lesions)
Diagnosis: history, exam, PM, paired serology
Treatment for infectious: tiamulin, tylosin, lincomysin
Lameness in adult pigs
30% sow culls due to lameness
Physical lameness:
- Cartilaginous pathology (osteochondrosis, osteochondritis, dyschondroplasia or degenerative joint disease (DJD))
- Bony path leading to weakness and fracture (osteomalacia)
Infectious arthritis:
- Erysipelas, Mycoplasma spp.
Septic laminitis: bush foot due to bacterial infection - lincomycin, NSAIDs
Scald - sheep
(70%)
Primarily caused by Fusobacterium necrophorum - in faeces
Can progress to foot-rot
Foot-rot - sheep
(30%) Dichelobacter nodosus - Present on 90% of farms - Lives for 7-10d on pasture - Lives up to 6 weeks in hoof trimmings - Infected sheep = reservoir
CODD - sheep
(25%)
Caused by Treponemes
Treatment of footrot
Oxytetracycline spray a clean foot Long acting parenteral antibiotics (Oxytetracycline, amoxicillin) Allow sheep to stand on clean concrete Ideally isolate sheep 14d Prognosis: 90% recover in 5d Scald treatment v similar
Foot bathing - sheep
Use chemicals at correct concentrations:
- 10% zinc sulphate - stand sheep for >2min
- 3% Formulin
Stand sheep for 1 hr after and then turn in field for >14d of rest
Footbvax - sheep
Vaccinate before high risk periods (usually Autumn/Spring)
Primary - twice, 6wks apart
Boost 6 monthly
Include all sheep (and rams)
Contagious ovine digital dermatitis (CODD)
Same treponemes as bovine digi
Use Tilmicosin
Footbath with lincomysin or tylosin
What is laminitis?
Failure of the attachment of the epidermal cells to the epidermal (insensitive) laminae to the underlying basement membrane of the dermal (sensitive) laminae
May occur following a failure of epithelial adhesion molecules (hemidesmosomes) which attach the epidermal cells to the basement membrane
Dysregulation of cell adhesion is most likely caused by inflammatory and/or hypoxic cellular injury
Laminitis: risk factors
Can arise in association with disease characterised by sepsis and systemic inflammation (GS disease, pneumonia and septic metritis), endocrine disorders, mechanical overload, access to pasture (can be predisposed individuals)
- Pony vs horse
- Spring and Summer
- Female
- Older
- Obesity
- Recent increase in body weight
- Recent new access to grass
- Increasing time since worming and insulin resistance
3 stages of laminitis
Developmental: contact with trigger, last about 72h, damage occurs but no clinical signs, can’t see it (may suspect)
Acute laminitis: clinical signs
Resolution or chronic laminitis: depends on diagnosis speed, treatment and response
Inflammation and laminitis
It is thought that a systemic inflammatory response that accompanies hindgut carbohydrate overload somehow initiates lamellar inflammatory response
Vascular and endothelial dysfunction - laminitis
Early stages: vascular events include digital venoconstriction and consequent laminar oedema
Venoconstriction may be caused by platelet activation and platelet-neutrophil activation resulting in the release of the vasoactive mediator 5-HT
Amines from hindgut fermentation of CHO are vasoactive
Laminitis - diagnosis
Clinical signs +/- radiography +/- endocrine tests
Clinical signs: lameness affecting two or more limbs, characteristic stance of leaning back on heels, bounding digital pulses, increased hoof wall temp, pain on hoof tester pressure of the region of the frog, palpable depression at the coronary band
Laminitis - radiographs
If concerned that P3 moved
Can be difficult is painful - nerve block, take xray machine to horses
Latero-medial xrays of feet following good foot prep - need to markers on the feet inc one on the dorsal hoof wall, starting at coronary band and one at the point of the frog
Can assess pedal bone rotation and founder distance (sinking)
Laminitis - endocrine tests
Basal ACTH
Dex suppression (not Autumn)
TRH stimulation test
Laminitis - treatment
Medical emergency
Analgesia:
- NSAIDs, such as PBZ, flunixin, carprofen etc IV/oral
- Opiates - morphine, pethadine, fentanyl (hospital)
Foot support:
- Increase bedding esp at front of stable
- Bed rest
- Frog support - bandages, lilypads, NFS etc.
- Frog and sole support - caudal 2/3
Vasoconstriction?? ACP/ice
Change diet - no grass, 1.5-2% poor quality hay, no or minimal concentrates
Prognosis of laminitis
After 8 weeks - 95% alive
Depression extending round the whole coronary band suggests sinker = 20% survival
Evidence of previous attacks = success rate decreased by 20%
Rotation >11.5 degrees = prognosis sig reduced
Founder distance >15mm = 40% chance of return to soundness
Prevention of laminitis
Number 1 priority for pasture associated laminitis - overconsumption NSC (fructan + starch + sugar) - lower in growing plants.
Pasture should be managed to encourage growth
Diet should be based on forage/fibre, not sugar/starch
Extra energy can be added with oil or unmollassed beet pulp
Various supplements recommended
Osteomyelitis
Infection of the cortical bone and medullary cavity
Technically means all three layers are affected
Osteitis
Inflammation of the cortex without involvement of the red or yellow bone marrow
Septic or aseptic
Osteomyelitis - acute
Single limb lameness, rapid onset, short duration
Often history of laceration or surgery
Clinical exam: heat, pain, swelling on palpation of bones, joint structure may be normal, febrile
Plan:
- Sedation and analgesia, flush, broad spectrum antibiotics (endomycin and tetracyclins penetrate bone well), swab, bandage
Osteomyelitis - chronic
Moderate? Intermittant? Lameness of days/weeks duration Often history of laceration or surgery Clinical exam: - Possibly heat, pain, swelling on palpation - Joint structures may be normal - Pain, discharge, sinus tract formation - Pathological fracture - becomes acute Radiography important
Bone biopsy
Jamshidi needle (like a corer) or Michelle trephine (rarely used)
Through centre of lesion, both cortex and medulla sampled
Multiple samples through same skin incision
Cytology and culture
Osteosarcome treatment options
Amputation (4 months) - doesn't treat metastases Amputation and chemo (12-14 months) Limb sparing and chemo (12-14 months) Radiotherapy (palliative only) NSAIDs/Biphosphonates (palliative only) Euthanasia (common)
Calcium deficient animal
Essential for neuro-muscular function
Serum levels highly protected
Ca10(PO4)6(OH)2 robbed to protect serum calcium
Secondary nutritional
Hyperparathyroidism
Low dietary calcium drive high PTH levels Serum calcium is often protected Bones are malformed or poorly formed Normally a problem in growing animal Usually in exotics
Secondary renal
Hyperparathyroidism
Chronic renal failure (normally adult) Decreased activation of vitamin D Lowered phosphate excretion - Phosphate binds to calcium - Serum calcium is lowered Increased PTH drive and effects on bones (soft jaw)
Metabolic bone disease of reptiles and chelonians
Low dietary availability of calcium
Decreased activation or availability of vitamin D
Esp green iguana
Diagnosis:
- Lethargy, Movement/lameness (joint swelling, limb swelling, muscular tone and atrophy)
- Radiography: joints, limbs and spine, egg binding, spontaneous fractures, swollen bones poor density, misshapen, often pliant mandibles
- Blood sample: low Ca
Treatment: Ca gluconate, dietary adjustment (2% Ca diet), UV light and/or direct sunlight - not through glass, Monitor blood Ca
Equine Rhabdomyolysis Syndrome
Muscle cramping/pain that occurs usually during or following exercise
Also called: Monday morning disease, set-fast, azoluria, myoglobinuria, tying-up
Rhabdomyolysis - lysis of muscle fibres
Clinical signs: stiff movements, pain, sweating, tachycardia, myoglobinuria, plasma CK and AST activities
Treatment of acute exertional rhabdomyolysis
Analgesics (NSAIDs, opiates)
IV or oral fluids
Diuretics - fluids and diuretics are used to maintain urine output in attempts to prevent or minimise the nephrotoxic effects of myoglobin
Aetiology of exertional rhabdomyolysis
Acquired:
- Overexertion (eccentric contraction, metabolic exhaustion, oxidative injury)
- Electrolyte imbalance
- Hormonal influence
- Infectious causes
Inherited:
- Recurrent exertional rhabdomyolysis due to defective calcium regulation
- Polysaccharide storage myopathy
Overexertion and exertional rhabdomyolysis
Probably a common cause
- Eccentric contraction (contraction during muscle lengthening)
- Metabolic exhaustion: hyperthermia, deficiency of ATP leads to inability to maintain ion homeostasis
- Oxidative injury: free radical induced damage
Horses that undergo repeated episodes of tying up
Certain ‘acquired causes’ may precipitate an attack ina genetically-susceptible animal
2 forms of genetic disorder are recognised:
- Recurrent exertional rhabdomyolysis of Tbs - defect calcium regulation, young nervous fillies (5% of Tbs)
- Polysaccharide storage myopathy
Prevention of RER
Oral dantrolene - a calcium release channel blocker, for Tbs with presumed calcium homeostasis
High fat/low carb diet
Regular exercise
PSSM1
Affects QH, warmbloods and draft horses, cobs and many others
Heritable (autosomal dominant)
Cause exertional rhabdomyolysis
Occasionally muscle atrophy/weakness in draft breeds
High prevalence in some draft breeds (>50%)
Abnormality of glucose metabolism
Mutation in glycogen synthase gene in skeletal muscle
DNA test: submit blood in EDTA or hair pluck
Treatment and management of PSSM1
High fat, low carb diet
Regular, daily exercise
The exhausted horse
Glycogen depletion from muscles, electrolyte loss from sweat, hypovolaemia
Clinical signs: depression, dehydration, anorexia, decreased thirst, increase rr and hr, pyrexia, poor sweating response, poor jugular distension, increased CRT, decreased pulse pressure, decreased gut sounds, laminitis, synchronous diaphragmatic flutter, muscle pain and stiffness
Treatment: IV or oral fluids, supplemented with additional electrolytes if required, rapid cooling, NSAIDs, check for evidence of rhabdomyolysis (CK and AST)
Prevention: training, heat acclimatisation, free acces to water and administer electrolytes during the ride, freq vet checks
Coccygeal muscle injury
‘Limber talk, cold tail, rudder tail’
Working breeds - labradors, pointers
- Pain at tail base, mild elevation in CK
- Recovery over several days
- Cold, exercise, swimming and prolonged caged transportation seem to predispose
Treatment: rest, NSAIDs
Muscle strain injury
Overstretching of muscle - disruption to fibres - inflammation, healing with fibrosis
Mild to sever (complete rupture)
Recovery is rapid with low grade injuries but fibrous tissue may predispose to re-injury or contracture
- Palpation and US may be helpful in diagnosis
Fibrotic myopathy
Common in QH: usually semitendinosus, usually semimembranous or gracilis
Causes: muscle tear, IM injection, neuropathy
Treatment: rest, NSAIDs, surgical resection of fibrous tissue or tenotomy
Atypical myopathy
Acute onset severe myopathy in horses at pasture
CK and AST massively increased
Muscle biopsy pre or post mortem
Triceps/intercostal/diaphragm
Osteochondrosis
Group of conditions of developing cartilage and its supporting bones
Initiated by a vascular problem in the epiphysis
Failure of the normal cartilage to bone succession
Examples of osteochondrosis
Osteochondritis dissecans (OCD): detachment of a chrondal or osteochondral fragment from the articular surface
Subchondral bone cysts (SBC)
Peri-articular fragmentation/fracture:
- Detachment of a chondral or osteochondral fragment from the peri-articular area
- e.g. Fragmentation/fracture of medial coronoid process of the canine elbow
Osteochondrosis - presentation
You, fast growing, large, pure breed Joint effusion - inconsistent Often bilateral Lameness - variable Sub-clinical disease is possible
Osteochondrosis - treatment
Symptomatic and conservative Surgical - open or arthroscopy - Fragment removal - Encourage repair Prognosis guarded specific to joint - depends on formation of OA
Canine elbow dysplasia (ED)
Osteochondrosis (OC) is the primary disease in this syndrome
ED includes:
- Humeral osteochondritis dissecans (OCD)
- Fragmented coronoid process (FCP/FCMP)
- United anconeal process (UAP)
- Secondary osteoarthritis
Combo of some or all of these is ED
Osteochondrosis and osteoarthritis
Irritation Direct cartilage damage Incongruency, mechanical incompetence Cycle of reaction Often temporarily stabilises in young adults
Genetics of hip and elbow dysplasia
Genetic component - high heritability
- Genetically vulnerable animals are predisposed
- Other factors (diet, exercise may affect signs)
Heritiability - proportion of a disease that can be proved due to genetics
- Totally due to genetically. Heritability = 100%
- Not due to genetics. Heritability = 0%
Elbow dysplasia - 50-70%
Hip dysplasia - 20-30%
Hip dysplasia
Ligament hypertrophy - slack ligaments Subluxation - ball and socket not together Destruction of cartilage Change of shape of joint surface Leads to .... Secondary osteoarthritis - bony fibrous
Hip dysplasia - clinical exam
Observation of gait: abnormality hindlimb gait, lame leg
Physical exam:
- Hindlimb muscle wastage
- Foot, tarsus, stifle, lumbo-sacral spine WNL
- Hip ROM normal, bilateral pain at full extension
Analysis:
- Problem appears to be in area of hip
- Young, medium-large pure-bred dog with persistent lameness
-Possible developmental problem
Hip dysplasia timeline
0-6 months
- Subluxation, abnormal gait
- Conservative treatment, diet, exercise
6-16 months
- Subluxation, abnormal gait
- Subluxation, damage and inflammation, pain, lameness
- Conservative treatment, diet, exercise (drugs)
- Surgical anatomical correction (>15-20kg)
- Ex. arthroplasty
16 months onwards
- Abnormal joint, secondary OA, pain, lameness
- Muscular/fibrous stabilisation - pain-free, restricted range
- Conservative treatment, diet, exercise (drugs)
- Surgical hip replacement (>15-20kg)
- Ex. arthroplasty
Hip dysplasia
Clinical vs subclinical
Subclinical
- Anatomical changes exist can be documented by radiographs
- Dogs shows no clinical signs e.g. pain or lameness
Clinical
- Anatomical changes lead to pain, lameness, restricted movement, exercise intolerance
Ageing
Progressive loss of physiological functions (fitness and reproduction) that increase the probability of death
Theories of ageing
Disposable soma theory
Natural selection tunes the life history of an organism so that sufficient resources are invested in maintaining the repair mechanisms that prevent ageing until the organism has reproduced
Organism needs to balance between repair and energy resources
Theories of ageing
Stochastic theory of ageing (Error catastrophe)
Random events at the cellular and molecular level drive the ageing process
- Protein with errors will be degraded and replaced
- But if protein is needed for genetic components this will lead to further errors and so on
Damage is the inevitable consequence of the interaction between organism and its environment
Cellular defense network evolved to protect
General characteristics of cartilage
Chondrocytes: Few, synthesise ECM
Avascular: no stem cells, poor capacity to repair, nutrient supply via vascularised subchondral bone and the synovial surface
Aneural
ECM: Collagen type I and II, proteoglycans, water and other components (collagens and proteins) for function etc.
Osteoarthritis
Often secondary disease - trauma or genetic condition
Progression influenced by ageing
Musculoskeletal injuries major cause of wastage
Common in greyhounds, large dog breeds (chondrodysplasia, OCD)
Pig (OCD - osteochondrosis or osteochondritis dissecans)
Ageing
Junk accumulation
Proteolytic mediated processing of proteoglycans:
- Increasing polydisperse population
Consequences:
- Decrease in fixed charge density due to loss of proteoglycans
- Accumulation of ‘junk’ degraded products
- Altered activity of cells in response to ‘junk’ proteins, ‘matrikine’ activity
Ageing
Reduced growth factor response
Anabolic responses of chondrocytes (human and equine) are diminished to TGF beta, bFGF, IGF-1
Consequences:
- Can drive an homeostatic imbalance - catabolic activity . anabolic activity
- Altered cell signalling pathways and receptor levels
Cells - depletion and molecular alterations
Cellularity decrease with advance age:
- Fewer cells to maintain ECM
- Fewer stem cells for endogenous repair
Calcification of the ECM increased - dead chondrocyte debris seems to enhance this
Proliferation of chondrocytes reduced - chondrocytes from older patients proliferate less well
Why is ageing of articular cartilage considered to be a risk factor for the onset of osteoarthritis?
Theory of ageing, disposable soma
Cells (senescence, responses to growth factor responses, cytokine susceptibility, junk product accumulate, proteolytic enzymes)
Thinning
Advanced glycation end products (AGEs
Limitations placed on homeostatic mechanisms
Functional consequences:
- Altered cellular activity
- Altered ECM
- Leads to increased mechanical stress to the cells
- Increase susceptibility by other risk factors
Tendon injuries
Traumatic - lacerations
Strains - breaking or dehiscence of fibres, mechanically induced or the result of weakening by degeneration
Muscular injuries
Injuries are similar but are less commonly specifically diagnoses
Tendon/muscular injuries
Presentation
Lameness - acute with trauma, chronic
Swelling - diffuse, painful, oedema in acute cases
- Organised and established in chronic cases
Specific functional disability e.g. unable to extend a specific joint
Tendon muscle injuries
Diagnosis
Clinical signs of dysfunction
Radiography - swelling, gap
Ultrasound - gap, loss of linear orientation of fibres
Tendon injury - repair
Pathophysiology:
- Fibroblasts and collagen fibres lining up along the line of action
- Sheathed tendons have poorer blood supply and heal slower
Time to heal:
- 6 weeks to regain 50% normal strength
- 1 year to regain 80% normal strength
Treatment:
- Rest
- Specific support to protect tendon from loading (dressings, casts, trans-articular fixator
- Primary surgical repair for lacerations (tendon sutures to manage load (locking loop, 3 loop pulley), direct contact of edges, suture of epi-tendon to promote healing)
-Ultrasound for monitoring
Sprain - ligamentous injury
Presentation and examination
Acute and chronic presentation similar to strains PE especial ROM Radiography and stress views Ultrasound Manipulation under anaesthesia Always check for ancillary damage
Sprain - ligamentous injury
Treatment
Rest, reduce swelling (drugs and cooling) External coaptation - support Ligament repair Internal ligament splintage Arthrodesis (salvage) Degree of Tx depends on instability, pain and potential for healing Not always acceptable function: - Repair mechanics not perfect - Extra chronic capsular tissue formed - Secondary osteoarthritis Many require arthrodesis at second stage
Canine cruciate disease
Normally related to degeneration - can be acute presentation (trauma or degenerative ligament ‘giving way’)
Associated with MPL
Causes a debilitating cranio-caudal instability at the stifle
60% cases involve the medial meniscus
Canine cruciate disease - presentation
Middle-aged dogs (2-10y)
Overweight dogs, neutered dogs
medium to large breed dogs ( Labrador, Rottweiler, Spaniel, Bull breeds, not sighthounds - greyhounds, lurchers etc.)
History:
- Typically insidious onset pelvic limb lameness
- May be bilateral
- Acute onset lameness can occur
Canine cruciate disease - physical examination
Pelvic limb lameness - distinguish from hip and LS disease
Muscle atrophy (quadriceps and hamstrings)
Stifle effusion
Medial buttress - soft tissue thickening medial aspect of joint
Craniocaudal stifle instability
Pain on manipulation, sit test
Canine cruciate disease - conservative (non-surgical) treatment
Appropriate if: - Minimal lameness - Low grade pain - Weight (<15kg) - Reason to avoid surgery - medical, age, financial Type of recovery: - Very slow return to to function - Continuous stimulation of OA change - No control of meniscal damage
Canine cruciate disease - surgical treatment
Advantages: - Should improve joint stability - Should speed up recovery - Allows meniscal lesions to be treated Features of recovery: - Joint will never be 100% stable - DJD will always be present = residual lameness - Limb function can be very good but is not 100%
Canine cruciate disease - surgical options
- Using an implant in a position analogous to the cranial cruciate (CCL) - lateral tibio-fabella suture
- Restores joint stability (temporarily)
- Allows fibrous tissue to stabilise stifle - Changing the mechanics of the stifle to negate the need for CCL support - tibial plateau levelling osteotomy (TPLO) or Tibial tuberosity advancement (TTA)
Any surgery to involved inspection of the meniscus and removal of damaged areas
Lateral tibio-fabella suture
Canine cruciate disease
Placed in the same line as the cruciate ligament but is extracapsular
The meniscus is normally inspected first via an arthrotomy then the joint is closed and the suture placed
Tibial Plateau Levelling Osteotomy
Changes the angle that the tibia meets the femur allowing the articular surface to bear more of the caudal shear force from tibial thrust
Tibial Tuberosity Advancement
The line of the patella tendon is advanced making it parallel to the line of force transfer across the joint
The tension in the tendon cancels out the compression across the joint negating the caudal movement of the femur
(CWTO - Closed wedge tibial osteotomy. Similar to TTA but distal displacement of tibial tuberosity)
(TTO - triple tibial osteotomy - mix of TTA/CWTO)
Canine cruciate surgery - post op care
Fast weight bearing Rest 6-8 weeks (lead walks) increase 5min/2 weeks Cold packs 48-72 hours Warm packs and PROM 2-3 times/day Reds 6-8 weeks No hydrotherapy
Rehabilitation
Look for the fastest return to reasonable exercise
Depends on condition and treatment
Graduated increase in exercise
Physiotherapy techniques
Fracture forces
Compression/shear are difficult to neutralise with a cast
Distraction forces are caused by muscle tension and are poorly neutralised by external coaptation e.g. olecranon fractures or fractures of greater trochanter
Sling to decrease weight beraing
Reduces tension force
Basic guidelines for coaptation
1. Reduction
Best suited for minimally displaced, stable fractures
Repeat radiographs to ensure that apposition remains adequate for healing
Adequate reduction varies between patients
Basic guidelines for coaptation
2. Alignment
Proper joint alignment must be maintained
failure to align major bone fragments to the joints of the limb results in rotational or angular malunion
Cause functional gait abnormality
Also cause painful lameness from secondary OA
Basic guidelines for coaptation
3. Standing position
External coaptation should be applied to maintain the limb in a normal standing position
Allows animal to bear weight when splint is in place and after removal
Basic guidelines for coaptation
4. Joint above and below
Must be immobilised
Therefore most conventional splints and cats cannot be used above the the stifle/elbow
Spica splints can be constructed to immobilise the hip or shoulder joint
Most are severely displaced
Advantages and disadvantages of external coaptation
Advantages:
- Relatively inexpensive (as long as no complications)
- Avoids surgery
Disadvantages:
- Only appropriate for stable, minimally displaced fractures
- May result in bone/limb malalignment
- Can cause serious complications
- Complications are more expensive/difficult to treat than original fracture
Difficult to manage (cast slip, casts get wet, animal pulls cast off)
External coaptation - complications
Distal limb soft tissue swelling Distal limb oedema Skin rubs Skin ulceration Skin necrosis Soft tissue necrosis Slippage of cast With severe complications, amputation could be the only option
Several different types of external coaptation
Robert Jones bandage
Modified RJ bandage - less cotton padding used
Reinforced RJ bandage
Spica splint
Full leg cast - extends to mid femur/humerus
Half-cast - does not extend above elbow/stifle
Bivalved cast - allows freq changes without new casting material
Walking bar - aluminium bar at end of cast
External coaptation
Primary layer
To cover and protect skin
To absorb discharge
Variety available
External coaptation
Secondary layer
Absorption
Provides support, pressure
Keeps primary layer in place
Roll cotton: do not allow this to contact wounds, very difficult to remove
Cast padding: less bulky and conforms better
Conforming gauze is wrapped over this padding layer to provide stability and occasionally compression
External coaptation
Casting tape
Applied over a light secondary layer
Fine balance:
- Too little padding may contribute to cast rubs/sores
- Too much padding will allow movement of bone fragments and delay healing
External coaptation
Tetiary layer
Holds inner layers together
Fixes inner layers to bandaged part
Barrier against physical abrasion
Barrier against environmental contaminants
Several types but elastic conforming bandage most common - allows application of consistent pressure to outer layer
Arthroplasty
Replacement or excision - both allow movement
Replacement: removes pain and restore/maintain normal movement
Excision: removes pain and has altered movement
Elective orthopaedic procedure where the joint is either commonly excised or replaced
Dogs, cats, (small ponies), other small animals, alpacas
Indications: dysplasia, intractable arthritis/joint pain, articular fracture, persistent luxation, avascular necrosis
Arthrodesis
Irreversible surgical fusion of two or more joints
Creation of osseous bridging that prevents joint motion and allows the joint to withstand weight bearing forces
All species depending on joint e.g. pancarpal/partial carpal and pantarsal/partial tarsal
Amputation
Normally considered as a fallback after other treatment
Has proved ineffective but may be used if finance is a problem
Dogs, cats (limbs, digits, tails) (limbs in small caged pets), occasionally in LA
Excision arthroplasty
Hip - most common joint treated this way
Also: TMJ, radial head, shoulder, MT/MC phalangeal joint
Femoral head and neck excision (FHNE)
Hip dysplasia - juvenile pain
Intractable osteoarthritis/DJD
Femoral head and neck fracture/acetabular fractures
Persistent luxation
Legg-Calve-Perthes disease (avascular necrosis of the femoral head)
Suitable for all sizes of dog but good results easier to achieve in animals up to 30kg (20kg better)
Some restriction in ROM will affect good (full) athletic performance
Total hip arthroplasty
Can be done in any dog
Typically large, active, working dogs (>20kg)
Anytime after skeletal maturity
Outcome influenced by obesity and other orthopaedic problems
Expensive - produces excellent results
‘Gold standard’
Ideal patient: painful hip, large breed dog, previously active lifestyle, sensible and well-trained, compliant, committed (insured) owners
Total hip replacement vs FHNE
Total hip replacent vs FHNE
£4000 COST £400-1400
10% risk COMPLICATIONS Very low risk
6 weeks cage rest AFTERCARE Activity encourages asap
Excellent/normal FUNCTION Reduced but acceptable
Arthrodesis - Indications
Intractable arthrtitis/joint pain Articular fracture - un-reconstructable Persistent luxation or instability Low grade pain interfering with performance Revision of failed joint surgery
Arthrodesis - Principles
Absolute stability, ideally through compression
Remove cartilage from contact areas
Contour opposing joint surfaces
Bone graft (osteogenesis, osteoinduction and osteoconduction)
Fuse at functional angle
External support
Amputation - indications
Neoplasia - malignant or locally invasive
Trauma - excessive tissue damage or ichaemia
Paralysis - brachial plexus avulsion
Unmanageable joint conditions, intractable pain, congenital deformity
Client finances
Considerations: temperament, concurrent orthopaedic disease, owner, mechanically to lose a pelvis rather than thoracic limb
Amputation - sites
Forelimb: Mid-humerus Hindlimb: - Mid/high femur - Trans articular (coxofemoral) - Hemipelvectomy Digit: - Proximal interphalangeal joint with cartilage removal in cattle - Distal P1 or P2 in small animals Tail: normally related to trauma, leave enough to cover perineum if possible
Amputation - General principles
Choose suitable margin of excision
Local block and fresh scalpel for neurectomies
Make sure it’s not possible for stump to get traumatised post-op and leave sufficient tissue (muscle, skin) to cover it
Careful reconstruction of tissue to eliminate dead space +/- drain
Inflammatory arthritis - clinical presentation
Can be stilted/crouched Arthralgia (subtle -> severe) May present as ataxia Painful, swollen joints Stiffness, lameness
Causes of septic arthritis
Haematogenous: from a focus elsewhere e.g. foal umbilicus, intestines, traumatic (esp horses) Lacerations, puncture wounds Iatrogenic - often 'aseptic' procedures - Intra-articular injections (PSGAG) - Surgery
Septic arthritis - Treatment, small animals
Amoxicillin/clavulanic acid 20mg/kg IV
No difference between surgical and medical treatment
94% infections will resolve
May need to remove implants if infections associated with them
6 week course of Abx based on culture results
Septic artritis - Treatment, horses
Acute infection - emergency
Eliminate organisms from joint
Eliminate enzymes and mediators that cause cartilage destruction
Abx/through and through lavage/arthroscopy and arthrotomy
Intra-articular antibiotics, IV antibiotics (penicillin and gentamycin)
Resample joint fluid every 48h
Oral Abx
Septic arthritis - Management
Antibiotics on basis of sensitivity
- IV to start with (amoxicillin and clavulanic acid 20mg/kg)
- Possibility of local delivery (gentamycin impregnated sponge) introsynovial catheters
Daily changed dressings for wounds
Early stages rest
Px excellent if treated rapidly
Physio/hydrotherapy to reduce adhesions and prevent peri-articular fibrosis
IMPA - aetiology
Immune mediated poly arthritis
Ag/Ab complex -> formation of inflammatory products
Host IgG and M to altered autologous IgG
Ag/Ab complex deposited on synovium -> neutrophil/macrophage chemotaxis
Erosive IMPA:
- Cellular or humoral immunopathogenic factors
- Release of chondrodestructive collagenases/proteases
- Failure of self tolerance or production of immunogenic immunoglobulins
Risk factors for autoimmune disease
Hereditory component e.g. Beagles Certain infections - GpA streptococcal pharyngitis -> acute rheumatic fever Bacterial endocarditis Discospondylitis Immune mediated bowel disease Neoplasia Chronic hepatitis
Type I Hypersensitivity reaction
Immediate/anaphylactic
IgE -> mast cells, basophils
Type II Hypersensitivity reaction
Ab-dependent cytotoxic r^n
IgG or IgG against a cell-surface component
Type III Hyper sensitivity reaction
Immune complex mediated r^n
Large amounts of IgG or IgM plus Ag -> microprecipitates
Clinical manifestations depend upon where complexes are formed or lodge
Type IV
Cell-mediated/delayed type r^n
Intra cellular organism
Immune-mediated arthritis
Immune complexes generated locally (joint) or systemically or both
Polyarticular disease (6+ joints) occasionaly pauciarticular (2-5), rarely monoarticular
Chronic disease due to:
- Continual or recurrent presence of inciting antigens
- Failure or normal down-regulation when inciting antigens gone
- Initial damage to host tissues resulting in exposure of altered self-antigens
Non-erosive polyarthritis
Type 1: uncomplicated idiopathic 50% (early RA?)
Type 2: associated with remote infections (reactive arthritis) 25%, endocarditis, urogenital etc.
Type 3: associated with GI disease/hepatic 15%
Type 4: associated with remote neoplasia <10%
Other non-erosive polyarthritis:
- Systemic lupus erythematous (SLE)
- Lyme disease (Borrelia burgdorfen)
- Drug associated e.g. Dobies and sulphonamides
- Caliciviral in kittens
- Associated with steroid-responsive meningitis-arteritis in adolescent dogs
- IBD
- Vaccine
Erosive joint disease
Rheumatoid arthrtitis
Periosteal proliferative polyarthritis in cats
Polyarthritis of Greyhounds (Felty’s syndrome)
Felty’s syndrome - RA, splenomegaly (splenectomy may help) and neutropaenia
Radiographic changes in erosive joint disease
Sub-chondral bone erosions
Destructive symmetric multi-joint arthropathy
Early: may be only soft tissue changes
Chronic: collapse of joint spaces, joint deformity or subluxation, peri-articular new bone formation, calcification of peri-articular soft tissues
Arthritis - general principles of therapy
Identify inciting factor - remove/treat
Modify life-style to decrease joint stress (controlled exercise, weight loss, physio/hydrotherapy)
Suppression of immune response/control of inflammation
Pain relief
Prenisolone:
- Immunosuppressive doses initially (2-4mg/kg/day divided doses)
- Gradually taper dosage - 25% decrease every 2-3 weeks
+/- cytotoxic drugs (-> bone marrow suppression)
- Cyclophosphamide (-> haemorrhagic cystitis, use for <3m)
- Azathioprine (not cats)
Disease-modifying antirheumatic drugs (DMARDs) - leflunomide, methotrexate
Biological agents (anti-TNFa, IL-1 blockers)
Arthritis - surgery
Management of pain in chronic disease
- Persistent inflammation may cause joint subluxation
- Synovectomy
- Arthrodesis/excision arthroplasty/total joint replacement
Crystal-based arthritis
True gout occurs in species that do not have enzyme uricase = humans, birds and reptiles
Reptiles: renal damage -> decreased excretion of urate
White periarticular deposits (urate crystals) -> inflammatory reaction
Renal failure the most common cause in reptiles
Failure to excrete uric acid
Tx - Fluid therapy, avoid meds that increase renal excretion
Transfixation casting - equine
Repaired or conservatively treated sital limb fracture that is unstable under axial loading
Fetlock breakdown injuries
Preparation for Fracture emergencies - equine
Bandage material: wound dressing, conforming gauze, sheet cotton, casting tape, duct tape
Splints: 2”x4” slats, boards, light metal rods, PVC pipes, Kimzey Leg saver splint
Chemical restraint: Xylazine HCl, Detomidine HCl, Romifidine HCl, Butorphanol tartrate
Antibiotics: Procaine penicillin G, K-Penicillin, Gentamicin sulfate
Other: Flunixin meglumine, Phenylbutazone, Tetanus toxoid vaccine, IV fluids
The ideal splint - equine
Neutralising damaging forces
Not too cumbersome: pendulum effect
Applicable under difficult circumstances: minimal assistance, no anaesthesia/recovery
Economical and accessible: Boards/slats, light metal rods, PVC pipes, casting material
Therapeutic basis for physiotherapy
Physical techniques that have a direct impact on healing tissues
Exercises that promote ‘proprioceptive learning’
Massage
Relaxation
Pain relief - lowered stress and the possibility of endorphin release
Decreased mobility - mechanical restriction, post surgery, disease
Preventative against injury in athletes and prep for performances
Relaxation
Cryotherapy
Affect vasculature (constriction) and nerves (analgesia) directly
Can be used even when patient is not ambulatory
Most effective in the management of acute inflammation
About 20min treatments
Thermotherapy
Affect vasculature (constriction) and nerves (analgesia) directly
Can be used even when patient is not ambulatory
Heat will make swelling, heart and pain worse
Once initial swelling has decreased, heat help vasodilation
Ultrasound physiotherapy
Primarily works through a heating effect and has the capacity to heat deeper tissues
Direct effect is difficult to monitor
Need good transducer ‘coupling’
Short treatment 10 min
Electrical stimulation
NMES - neuromuscular electrical stimulation (an electrical current applied to the patient that depolarises a motor nerve and causes muscle fibre contraction)
Increases muscle mass, strength and oxidative capacity
Provides a time efficient method of restoring muscle function in a protected environment
May also have an analgesic effect
Laser therapy
Claims to work on vasodilation, pain and tissue regeneration by a combination of heating and direct photostimulation effects
Very difficult to monitor how far the effect penetrates through the skin
Hydrotherapy
In the water, viscosity, friction and turbulences are the resistant forces but the loads are spread so its less detrimental
Animals work harder in the water than on the land and have a higher metabolic demand
