Locomotor Flashcards

1
Q

Clinical exam

Observation from a distance

A

Symmetry, posture, conformation (poor conformation doesn’t necessarily mean lameness)
Significant variations are usually obvious

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Clinical exam

Gait observation

A

Patient moving away, towards and across you
Possibility of circling and turning to exaggerate abnormalities
Which limb? Characterise and score problem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Clinical Exam

Manipulation of joints

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Safety factor

A

Maximum stress a structure withstand until breakage
OVER
Stress it is most likely to undergo during its lifetime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Factors of failure

A

Force/stress: magnitude, frequency, speed of loading, duration of loading
Influenced by: body mass, speed, gait

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Constraints during locomotion

A

Need to support against gravity, force only produced when limb in contact with ground
Increase in speed - shorter stance, higher force

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Ligaments in equine distal limb

A

Superficial digital flexor tendon SDFT
Deep digital flexor tendon DDFT
Distal accessory ligament DAL
Suspensory ligament SL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Flexor tendon muscles

A

Highly pennate
Muscle fibres about 1cm
Limited capacity for length change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Tendons

A

7% energy release as heat (horses)
Gallop tendons about 45 degrees C
Kills some cells but not tendon cells
Predilection for tendon core injuries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Joints - function

A

Relative movement of limb segments

Shock absorbers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Joints - horse

A
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Hoof (equine)

A

Horn capsule - protection but no expansion
Mechanical function - shock absorption, support and grip, propulsion
Constraints - resistance to abrasion, protection of senstive structures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Hoof (equine) - protective mechanisms

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Duty factor

A

Ratio of stance and stride time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

All stance phases critical to injury

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

High speed exercise

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Shifting of the PZM (point of zero movement)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Mediolateral imbalance

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Heel wedges

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Collapsed/underrun heels

A

Tubules start bending when grown distal to the distal phalanx
Impairment of natural hoof deformation and blood flow
Application of carbon fibre patches beneficial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Cow Lameness

History questions

A
Which lactation? 
How long calved?
Previous (foot) problems?
How long has she been lame?
Treatment?
Is she pregnant? Is she milking?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Cow Lameness

Score 0

A

Walks with even weight bearing and rhythm on all four feet with a flat back
Long fluid strides possible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Cow Lameness

Score 1

A
Steps uneven (rhythm or weigh bearing) or stride shortened
affected limb(s) not identifiable immediately
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Cow Lameness

Score 2

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Cow lameness | Score 3
Unable to walk as fast as a brisk human pace | Cannot keep up with healthy herd
26
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 ```
27
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
28
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
29
Effective herd interventions - sole ulcers
Increase straw bedding to 1 bale/10 cows/d in cubicles | Heifer comfort group 16 weeks vs cubicles
30
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
31
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
32
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
33
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
34
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
35
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
36
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
37
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
38
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
39
Scald - sheep
(70%) Primarily caused by Fusobacterium necrophorum - in faeces Can progress to foot-rot
40
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 ```
41
CODD - sheep
(25%) | Caused by Treponemes
42
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 ```
43
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
44
Footbvax - sheep
Vaccinate before high risk periods (usually Autumn/Spring) Primary - twice, 6wks apart Boost 6 monthly Include all sheep (and rams)
45
Contagious ovine digital dermatitis (CODD)
Same treponemes as bovine digi Use Tilmicosin Footbath with lincomysin or tylosin
46
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
47
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
48
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
49
Inflammation and laminitis
It is thought that a systemic inflammatory response that accompanies hindgut carbohydrate overload somehow initiates lamellar inflammatory response
50
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
51
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
52
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)
53
Laminitis - endocrine tests
Basal ACTH Dex suppression (not Autumn) TRH stimulation test
54
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
55
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
56
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
57
Osteomyelitis
Infection of the cortical bone and medullary cavity | Technically means all three layers are affected
58
Osteitis
Inflammation of the cortex without involvement of the red or yellow bone marrow Septic or aseptic
59
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
60
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 ```
61
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
62
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) ```
63
Calcium deficient animal
Essential for neuro-muscular function Serum levels highly protected Ca10(PO4)6(OH)2 robbed to protect serum calcium
64
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 ```
65
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) ```
66
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
67
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
68
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
69
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
70
Overexertion and exertional rhabdomyolysis
Probably a common cause 1. Eccentric contraction (contraction during muscle lengthening) 2. Metabolic exhaustion: hyperthermia, deficiency of ATP leads to inability to maintain ion homeostasis 3. Oxidative injury: free radical induced damage
71
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
72
Prevention of RER
Oral dantrolene - a calcium release channel blocker, for Tbs with presumed calcium homeostasis High fat/low carb diet Regular exercise
73
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
74
Treatment and management of PSSM1
High fat, low carb diet | Regular, daily exercise
75
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
76
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
77
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
78
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
79
Atypical myopathy
Acute onset severe myopathy in horses at pasture CK and AST massively increased Muscle biopsy pre or post mortem Triceps/intercostal/diaphragm
80
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
81
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
82
Osteochondrosis - presentation
``` You, fast growing, large, pure breed Joint effusion - inconsistent Often bilateral Lameness - variable Sub-clinical disease is possible ```
83
Osteochondrosis - treatment
``` Symptomatic and conservative Surgical - open or arthroscopy - Fragment removal - Encourage repair Prognosis guarded specific to joint - depends on formation of OA ```
84
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
85
Osteochondrosis and osteoarthritis
``` Irritation Direct cartilage damage Incongruency, mechanical incompetence Cycle of reaction Often temporarily stabilises in young adults ```
86
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%
87
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 ```
88
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
89
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
90
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
91
Ageing
Progressive loss of physiological functions (fitness and reproduction) that increase the probability of death
92
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
93
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
94
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.
95
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)
96
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
97
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
98
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
99
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
100
Tendon injuries
Traumatic - lacerations | Strains - breaking or dehiscence of fibres, mechanically induced or the result of weakening by degeneration
101
Muscular injuries
Injuries are similar but are less commonly specifically diagnoses
102
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
103
Tendon muscle injuries | Diagnosis
Clinical signs of dysfunction Radiography - swelling, gap Ultrasound - gap, loss of linear orientation of fibres
104
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
105
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 ```
106
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 ```
107
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
108
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
109
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
110
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 ```
111
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% ```
112
Canine cruciate disease - surgical options
1. 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 2. 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
113
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
114
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
115
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)
116
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 ```
117
Rehabilitation
Look for the fastest return to reasonable exercise Depends on condition and treatment Graduated increase in exercise Physiotherapy techniques
118
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
119
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
120
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
121
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
122
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
123
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)
124
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 ```
125
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
126
External coaptation | Primary layer
To cover and protect skin To absorb discharge Variety available
127
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
128
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
129
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
130
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
131
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
132
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
133
Excision arthroplasty
Hip - most common joint treated this way | Also: TMJ, radial head, shoulder, MT/MC phalangeal joint
134
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
135
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
136
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
137
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 ```
138
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
139
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
140
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 ```
141
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
142
Inflammatory arthritis - clinical presentation
``` Can be stilted/crouched Arthralgia (subtle -> severe) May present as ataxia Painful, swollen joints Stiffness, lameness ```
143
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 ```
144
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
145
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
146
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
147
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
148
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 ```
149
Type I Hypersensitivity reaction
Immediate/anaphylactic | IgE -> mast cells, basophils
150
Type II Hypersensitivity reaction
Ab-dependent cytotoxic r^n | IgG or IgG against a cell-surface component
151
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
152
Type IV
Cell-mediated/delayed type r^n | Intra cellular organism
153
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
154
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
155
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
156
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
157
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)
158
Arthritis - surgery
Management of pain in chronic disease - Persistent inflammation may cause joint subluxation - Synovectomy - Arthrodesis/excision arthroplasty/total joint replacement
159
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
160
Transfixation casting - equine
Repaired or conservatively treated sital limb fracture that is unstable under axial loading Fetlock breakdown injuries
161
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
162
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
163
Therapeutic basis for physiotherapy
Physical techniques that have a direct impact on healing tissues Exercises that promote 'proprioceptive learning'
164
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
165
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
166
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
167
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
168
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
169
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
170
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