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Veterinary Medicine > Locomotor > Flashcards

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

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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

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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
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4
Q

Safety factor

A

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

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5
Q

Factors of failure

A

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

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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

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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

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8
Q

Flexor tendon muscles

A

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

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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

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10
Q

Joints - function

A

Relative movement of limb segments

Shock absorbers

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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
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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

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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

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14
Q

Duty factor

A

Ratio of stance and stride time

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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

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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

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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

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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

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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

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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

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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?
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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

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23
Q

Cow Lameness

Score 1

A 
Steps uneven (rhythm or weigh bearing) or stride shortened
affected limb(s) not identifiable immediately
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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)

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25
Q

Cow lameness

Score 3

A

Unable to walk as fast as a brisk human pace

Cannot keep up with healthy herd

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26
Q

Dutch 5 step foot trimming

A 
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
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27
Q

Examination of lame foot - cow

A

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

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28
Q

Sole ulcers

A

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

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29
Q

Effective herd interventions - sole ulcers

A

Increase straw bedding to 1 bale/10 cows/d in cubicles

Heifer comfort group 16 weeks vs cubicles

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30
Q

White line - treatment

A

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

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31
Q

White line presentation

A

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

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32
Q

Digital dermatitis - treatment

A

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

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33
Q

Foul (in-the-foot)

A

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

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34
Q

Corkscrew claw

A

Bony swelling deep to abaxial coronary band is diagnostic
Not to be confused with gross claw overgrowth
Reshape foot as best as possible

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35
Q

Claw amputation

A

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

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36
Q

Arthritis in piglets

A

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

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37
Q

Lameness in growers - pigs

A

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

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38
Q

Lameness in adult pigs

A

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

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39
Q

Scald - sheep

A

(70%)
Primarily caused by Fusobacterium necrophorum - in faeces
Can progress to foot-rot

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40
Q

Foot-rot - sheep

A 
(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
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41
Q

CODD - sheep

A

(25%)

Caused by Treponemes

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42
Q

Treatment of footrot

A 
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
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43
Q

Foot bathing - sheep

A

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

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44
Q

Footbvax - sheep

A

Vaccinate before high risk periods (usually Autumn/Spring)
Primary - twice, 6wks apart
Boost 6 monthly
Include all sheep (and rams)

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45
Q

Contagious ovine digital dermatitis (CODD)

A

Same treponemes as bovine digi
Use Tilmicosin
Footbath with lincomysin or tylosin

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46
Q

What is laminitis?

A

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

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47
Q

Laminitis: risk factors

A

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
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48
Q

3 stages of laminitis

A

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

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49
Q

Inflammation and laminitis

A

It is thought that a systemic inflammatory response that accompanies hindgut carbohydrate overload somehow initiates lamellar inflammatory response

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50
Q

Vascular and endothelial dysfunction - laminitis

A

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

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51
Q

Laminitis - diagnosis

A

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

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52
Q

Laminitis - radiographs

A

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)

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53
Q

Laminitis - endocrine tests

A

Basal ACTH
Dex suppression (not Autumn)
TRH stimulation test

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54
Q

Laminitis - treatment

A

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

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55
Q

Prognosis of laminitis

After 8 weeks - 95% alive

A

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

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56
Q

Prevention of laminitis

A

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

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57
Q

Osteomyelitis

A

Infection of the cortical bone and medullary cavity

Technically means all three layers are affected

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58
Q

Osteitis

A

Inflammation of the cortex without involvement of the red or yellow bone marrow
Septic or aseptic

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59
Q

Osteomyelitis - acute

A

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

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60
Q

Osteomyelitis - chronic

A 
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
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61
Q

Bone biopsy

A

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

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62
Q

Osteosarcome treatment options

A 
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)
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63
Q

Calcium deficient animal

A

Essential for neuro-muscular function
Serum levels highly protected
Ca10(PO4)6(OH)2 robbed to protect serum calcium

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64
Q

Secondary nutritional

Hyperparathyroidism

A 
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
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65
Q

Secondary renal

Hyperparathyroidism

A 
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)
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66
Q

Metabolic bone disease of reptiles and chelonians

A

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

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67
Q

Equine Rhabdomyolysis Syndrome

A

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

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68
Q

Treatment of acute exertional rhabdomyolysis

A

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

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69
Q

Aetiology of exertional rhabdomyolysis

A

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
Q

Overexertion and exertional rhabdomyolysis

A

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
Q

Horses that undergo repeated episodes of tying up

A

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
Q

Prevention of RER

A

Oral dantrolene - a calcium release channel blocker, for Tbs with presumed calcium homeostasis
High fat/low carb diet
Regular exercise

73
Q

PSSM1

A

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
Q

Treatment and management of PSSM1

A

High fat, low carb diet

Regular, daily exercise

75
Q

The exhausted horse

A

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
Q

Coccygeal muscle injury

A

‘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
Q

Muscle strain injury

A

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
Q

Fibrotic myopathy

A

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
Q

Atypical myopathy

A

Acute onset severe myopathy in horses at pasture
CK and AST massively increased
Muscle biopsy pre or post mortem
Triceps/intercostal/diaphragm

80
Q

Osteochondrosis

A

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
Q

Examples of osteochondrosis

A

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
Q

Osteochondrosis - presentation

A 
You, fast growing, large, pure breed
Joint effusion - inconsistent
Often bilateral
Lameness - variable
Sub-clinical disease is possible
83
Q

Osteochondrosis - treatment

A 
Symptomatic and conservative
Surgical - open or arthroscopy
- Fragment removal
- Encourage repair
Prognosis guarded specific to joint - depends on formation of OA
84
Q

Canine elbow dysplasia (ED)

A

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
Q

Osteochondrosis and osteoarthritis

A 
Irritation
Direct cartilage damage
Incongruency, mechanical incompetence
Cycle of reaction
Often temporarily stabilises in young adults
86
Q

Genetics of hip and elbow dysplasia

A

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
Q

Hip dysplasia

A 
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
Q

Hip dysplasia - clinical exam

A

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
Q

Hip dysplasia timeline

A

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
Q

Hip dysplasia

Clinical vs subclinical

A

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
Q

Ageing

A

Progressive loss of physiological functions (fitness and reproduction) that increase the probability of death

92
Q

Theories of ageing

Disposable soma theory

A

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
Q

Theories of ageing

Stochastic theory of ageing (Error catastrophe)

A

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
Q

General characteristics of cartilage

A

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
Q

Osteoarthritis

A

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
Q

Ageing

Junk accumulation

A

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
Q

Ageing

Reduced growth factor response

A

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
Q

Cells - depletion and molecular alterations

A

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
Q

Why is ageing of articular cartilage considered to be a risk factor for the onset of osteoarthritis?

A

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
Q

Tendon injuries

A

Traumatic - lacerations

Strains - breaking or dehiscence of fibres, mechanically induced or the result of weakening by degeneration

101
Q

Muscular injuries

A

Injuries are similar but are less commonly specifically diagnoses

102
Q

Tendon/muscular injuries

Presentation

A

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
Q

Tendon muscle injuries

Diagnosis

A

Clinical signs of dysfunction
Radiography - swelling, gap
Ultrasound - gap, loss of linear orientation of fibres

104
Q

Tendon injury - repair

A

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
Q

Sprain - ligamentous injury

Presentation and examination

A 
Acute and chronic presentation similar to strains
PE especial ROM
Radiography and stress views
Ultrasound
Manipulation under anaesthesia
Always check for ancillary damage
106
Q

Sprain - ligamentous injury

Treatment

A 
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
Q

Canine cruciate disease

A

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
Q

Canine cruciate disease - presentation

A

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
Q

Canine cruciate disease - physical examination

A

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
Q

Canine cruciate disease - conservative (non-surgical) treatment

A 
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
Q

Canine cruciate disease - surgical treatment

A 
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
Q

Canine cruciate disease - surgical options

A
  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
Q

Lateral tibio-fabella suture

A

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
Q

Tibial Plateau Levelling Osteotomy

A

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
Q

Tibial Tuberosity Advancement

A

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
Q

Canine cruciate surgery - post op care

A 
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
Q

Rehabilitation

A

Look for the fastest return to reasonable exercise
Depends on condition and treatment
Graduated increase in exercise
Physiotherapy techniques

118
Q

Fracture forces

A

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
Q

Basic guidelines for coaptation

1. Reduction

A

Best suited for minimally displaced, stable fractures
Repeat radiographs to ensure that apposition remains adequate for healing
Adequate reduction varies between patients

120
Q

Basic guidelines for coaptation

2. Alignment

A

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
Q

Basic guidelines for coaptation

3. Standing position

A

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
Q

Basic guidelines for coaptation

4. Joint above and below

A

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
Q

Advantages and disadvantages of external coaptation

A

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
Q

External coaptation - complications

A 
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
Q

Several different types of external coaptation

A

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
Q

External coaptation

Primary layer

A

To cover and protect skin
To absorb discharge
Variety available

127
Q

External coaptation

Secondary layer

A

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
Q

External coaptation

Casting tape

A

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
Q

External coaptation

Tetiary layer

A

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
Q

Arthroplasty

A

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
Q

Arthrodesis

A

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
Q

Amputation

A

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
Q

Excision arthroplasty

A

Hip - most common joint treated this way

Also: TMJ, radial head, shoulder, MT/MC phalangeal joint

134
Q

Femoral head and neck excision (FHNE)

A

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
Q

Total hip arthroplasty

A

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
Q

Total hip replacement vs FHNE

A

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
Q

Arthrodesis - Indications

A 
Intractable arthrtitis/joint pain
Articular fracture - un-reconstructable
Persistent luxation or instability
Low grade pain interfering with performance
Revision of failed joint surgery
138
Q

Arthrodesis - Principles

A

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
Q

Amputation - indications

A

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
Q

Amputation - sites

A 
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
Q

Amputation - General principles

A

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
Q

Inflammatory arthritis - clinical presentation

A 
Can be stilted/crouched
Arthralgia (subtle -> severe)
May present as ataxia
Painful, swollen joints
Stiffness, lameness
143
Q

Causes of septic arthritis

A 
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
Q

Septic arthritis - Treatment, small animals

A

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
Q

Septic artritis - Treatment, horses

A

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
Q

Septic arthritis - Management

A

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
Q

IMPA - aetiology

Immune mediated poly arthritis

A

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
Q

Risk factors for autoimmune disease

A 
Hereditory component e.g. Beagles
Certain infections - GpA streptococcal pharyngitis -> acute rheumatic fever
Bacterial endocarditis
Discospondylitis
Immune mediated bowel disease
Neoplasia
Chronic hepatitis
149
Q

Type I Hypersensitivity reaction

A

Immediate/anaphylactic

IgE -> mast cells, basophils

150
Q

Type II Hypersensitivity reaction

A

Ab-dependent cytotoxic r^n

IgG or IgG against a cell-surface component

151
Q

Type III Hyper sensitivity reaction

A

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
Q

Type IV

A

Cell-mediated/delayed type r^n

Intra cellular organism

153
Q

Immune-mediated arthritis

A

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
Q

Non-erosive polyarthritis

A

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
Q

Erosive joint disease

A

Rheumatoid arthrtitis
Periosteal proliferative polyarthritis in cats
Polyarthritis of Greyhounds (Felty’s syndrome)
Felty’s syndrome - RA, splenomegaly (splenectomy may help) and neutropaenia

156
Q

Radiographic changes in erosive joint disease

A

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
Q

Arthritis - general principles of therapy

A

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
Q

Arthritis - surgery

A

Management of pain in chronic disease

  • Persistent inflammation may cause joint subluxation
  • Synovectomy
  • Arthrodesis/excision arthroplasty/total joint replacement
159
Q

Crystal-based arthritis

A

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
Q

Transfixation casting - equine

A

Repaired or conservatively treated sital limb fracture that is unstable under axial loading
Fetlock breakdown injuries

161
Q

Preparation for Fracture emergencies - equine

A

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
Q

The ideal splint - equine

A

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
Q

Therapeutic basis for physiotherapy

A

Physical techniques that have a direct impact on healing tissues
Exercises that promote ‘proprioceptive learning’

164
Q

Massage

A

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
Q

Cryotherapy

A

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
Q

Thermotherapy

A

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
Q

Ultrasound physiotherapy

A

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
Q

Electrical stimulation

A

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
Q

Laser therapy

A

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
Q

Hydrotherapy

A

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

Veterinary Medicine (15 decks)

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