Orthopaedics: Cattle Lameness, Arthritides, Tendons, Ligaments and Muscle Flashcards
What is lameness commonly mistaken for?
Disease
Lameness is a sign not a disease
Why is lameness on farms important to monitor and aim to reduce?
Animal welfare- painful
High yielding animals more susceptible and reduced lactation yield
Cows have delayed cyclicity
Increased ovarian cycts
Lower oestrus intensity
Prolonged calving intervals
Increased culling
Reduced eating/DMI
Low BCS
Costs- treatment, labour, reduced yields, culling
How can lameness be monitored?
Mobility scoring and lesion recording
How is mobility scored?
Different ways- fortnightly
Video analytics
Scale 0-3
0- even weight baring, rhythm, long strides, flat back
action- none needed, routine trimming
1- steps uneven, strides shortened, affected limb not identifiable
action- could benefit from routine foot trimming, further observation
2- Uneven weight baring on an identifiable limb, shortened stride usually with an arch
action- lame, likely to benefit from treatment, identify the cause, attend ASAP
3- unable to walk as fast as brisk human pace, signs of score 2
actions- very lame, treatm urgent attention, don’t make walk, cull?
What are the different foot lesions?
Sole bruising
Sole ulcer
White line disease
Digital dermatitis
Heel erosion
Interdigital growths
Heel ulcer
Foul
Axial wall fissure
Toe necrosis
Foreign body
Toe ulcer
How are hocks assessed?
Score 1- no swelling, no hair missing
Score 2- not swelling, bald area
Score 3- swelling, lesion through the hide
Score the rear hock
Define the following terms:
Foot
Claw
Claw capsule
Cannon bone
Axial Surface
Abaxial surface
Dorsal surface
Flexor surface
Solear surface
Dewclaw
Wall
Exostosis
foot- the region from hock to apex of claw
Claw- end of the digit
Claw capsule- structure composed of horn- pedal bone fit
Cannon bone- bone between the hock and fetlock (metatarsal)
Axial surface- the surface of the claw facing the space between the claws
Abaxial surface- the surface of the claw facing away from the claws
Flexor surface- back of the limb
Dorsal flexure- transition from axial to abaxial
Solear- sole
Dewclaw- miniature editions of claw
Wall- coronary segment of claw
Exostosis- bony growth protruding the surface
Label the following bones
Hind limb
What are the different labels?
What are lamellae and laminae?
Lamellae- these are leaflets of horn lining the inside of the wall
Laminae- leaflets of connective tissue, collagen fibres blood vessels and nerves that fit between lamellae
What attaches the pedal bone to the dermal lamellae?
Collagen fibres
What are the biomechanics of the cows foot?
Continuous growth
Continuous wear
Forelimbs attached to the body by more elastic componsnet
Lateral claws outgrow mdeial
Solar dermis is under pressure between the pedal bone and the sole
How should a foot be ideally trimmed?
What angle?
What is the dutch method to functional claw trimming?
- Start with medial hind claw
- Trim dorsal wall length to 7, 5-8cm
- Reduce sole depth at the toe to approx 5 to 7 mm
- Spare the heel
- Correct wall length
- Model- dish out
- Deeper and wider modelling of the lateral hind/medial foreclaw
What are the infectious and non-infectious lesions that cause lameness?
Infectious- digital dermatitis, foul, interdigital dermatitis, heel horn erosion
Non- infectious- sole haemorrhages/bruising, sole ulcers, white line lesions
What are arthritides?
What is arthritis?
Conditions causing pain and dysfunction related to joints
Arthritis- inflammation/degeneration of the joint including osteoarthritis, inflammation, infective
What is a diarthrodial joint?
A specialised joint consisting of a synovial cavity allowing articulation between two or more bones
Common examples- bone and socket
What is osteoarthritis?
Why is it important?
the degenerative condition ultimately leading to cartilage breakdown and loss of function
Importance-
Cause of pain and suffering- welfare
Cost to clients- drugs, milk loss
Loss of function- joint diseases most common cause of euthanasia with horses
What is synovial fluid?
What is in the fibrous joint capsule of synovial joints?
Synovial fluid- ultra filtrate of the plasma plus protein- hyaluronic acid
Fibrous joint capsule- synovial membrane, nerves and blood vessels- proprioception, supportive ligaments/tendons- collateral
What is articular cartilage?
Highly specialised- predominantly extracellular matrix with a low density of articular chondrocytes
Chondrocytes are responsible for the maintenance of the matrix
Matrix mainly- collagens, proteoglycans and water-
collagens confer shear resistance, hydrates proteoglycans provide compression
Limited repair
Dynamic loading/unloading- loading important for health of joint
What is osteoarthritis?
What are predisposing factors?
Classically thought of as articular cartilage disease
Number of tissues- contributing to progression- articular cartilage, subchondral bone, synovial membrane, joint capsule, ligaments, fat pad
Predisposing factors-
Excercise, trauma, biomechanics- normal joint, abnormal forces
sclerosis, intra-articular fracture, soft-tissue surgery
DOD- normal forces, abnormal joints-
hip and elbow dysplasia, osteochondrosis
Obesity- weight stress
Sepsis
Repeat medication- corticosteroids
Ageing- wear and tear
What history needs to be taken for osteoarthritis?
Describe the clinical exam for a dog with potential osteoarthritis?
History-
age, signalment, use
level of excercise
determine onset and progression of disease
response to medication
Clinical examination-
general physical examination
TPR, thoracic auscultation
Assessment of body condition, confirmation, muscling
Lamenss examination- observation, palpation, manipulation, movement
Diagnostic imaging
What are the radiographic signs of osteoarthritis?
- Soft tissue swelling
- Oestoephysis- new bone formation around the joint- extensions along margins- painful and restrictive
- Enthesiophytosis- new bone formation in soft tissues
- Subchondral bone sclerosis- increased bone density
- Intra-articular mineralisation- meniscus
- Fragmentation/joint mice
- Collapsed joint space
- Subchondral bone cysts
How does immune-mediated joint disease often present?
What is the cause?
Describe the pathophysiology
How is it diagnosed?
Usually, polyarthritis and can be erosive or non-erosive
Predominantly idiopathic- may be related to extra-articular disease- genetic
Most relate to abnormal activity of immune cells and antigen presentation
Path- early changes occur in the synovium
Chronic antigenic stimulation
Antibodies to infective agents or macromolecule modification leading to inappropriate immune response
Development of immune complexes
Diagnosis-
Multiple limb joint pain/swelling, generalised stiffness, shifting lameness, neck pain
Variable and intermittent, secondary to OA and fibrosis
How is immune-mediated joint disease managed and treated?
Managment-
Synoviocentesis- cell count, protein smear, differentiate from sepsis
Full clinical exam- characterise the involvement of other body systems, haematology
Diagnostic imaging- early non-specific effusion
Treatment- corticosteroids
What causes infective arthritis?
What are common causes?
Inflammatory arthropathy is due to an infective organism- usually bacteria arthropathy but occasionally fungi, mycoplasma, protozoa
Haematogenous-
often the separate focus of infection
More common in neonates- failure of passive transfer
Trauma/wound-
often seen in horses, cat bites- Pasteurella multicoda
adjacent infection
Iatrogenic-
Post joint/fracture surgery or following intra-articular injection
Describe the pathophysiology of infective arthritis?
Marked inflammatory response-
vasodilation and influx of neutrophils, the release of inflammatory cytokines/enzymes
Fibrin clots trap bacteria- protects bacteria, reduced synovial nutrient exchange
Cartilage destruction and extension of subchondral bone
How is infective arthritis diagnosed?
What are the DDXs?
History- a wound, FPT, recent injection
clinical signs-
acute onset, severe lameness- stiffness
wound near/over joint
pain on palpation
Ultrasound/radiography-
check for concurrent injury of bone infection
systemic disease- resp, umbilical
Synoviocentesis
DDXs-
Traumatic joint injury- ligament/fracture
Osteochondrosis
Bursitis, hygroma, cellulitis
How does normal and septic fluid appear from synoviocentesis?
How does it appear on smear?
Normal-
pale yellow, high viscosity
WBC <1x10^9
<10% neutrophils
Septic-
serosanguinous/turbid/reduced viscosity
WBV >1x10^9 and total protein >30-40g/l
>90% neutrophils
Smear-
PMNs
Free or intracellular bacteria
Distended joint with sterile saline
What are the aims for oesteoarthritis?
Provide analgesia
Control articular inflammation
Limit damage to articular tissues
Promote healing- holy grail
What considerations are the for the efficacy of treatments?
Heterogenicity of the disease
Poor correlation between imaging and disease process
In vivo versus in vitro
Inter-animal variation
High expectations/demands of owners
Shotgun approach- several drugs
How can osteoarthritis be conservatively and medically managed?
Conservative-
rest/restricted activity-
acute flare-ups, cold therapy, support
Weight loss- reduce strain and adipokines
Excercise- beneficial effects of exercise on cartilage/bone
Medical management-
most common- anti-inflam, anti-pyretic, analgesic
Cox inhibition-
Small animal- carprofen, firocoxib, meloxicam, paracetamol/codeine
Equine- phenylbutazone, flunixin, firocoxib, carprofen
What is hyaluronic acid?
What are its actions?
Hyaluronic acid- large unbranched nonsulphated glycosaminoglycan- important component of synovial fluid and articular cartilage
Action-
Chondroprotection
anti-inflam
stimulate proteoglycan synthesis
mechanical effect- improves viscosity
Analgesia- binds to stretch receptors
Often used with corticosteroids
What is pentosan polysulphate?
What is its action?
Marked as DMOAD
Action-
enhances proteoglycan synthesis
reduction in articular cartilage fibrillation
fibrinolytic- improves joint
Improves SF viscosity
Increase release of free radical scavengers
Licensed in dogs
What are bisphosphates?
Potent inhibitors of bone resorption
Inhibit osteoclasts
May inhibit collagenase release in chondrocytes/synovial cells
Clodronate and tiludronate- licensed in horses
What are biologics?
What surgical treatments can be done for osteoarthritis?
Biologics- autologous conditioned serum
Autologous- AKA IRAP or orthokine
Mesenchymal stem cells- bind to fibrillated cartilage, reduced progression of OA
Nutraceuticals- highly popular with owners
Surgical
Arthroscopy- assess damage, debride cartilage defects, flushing inflam mediators
Joints replacement
Arthrodesis- destruction of cartilage, bone-bone primary healing (horse pastern, DIPJ, carpus, tarsus)
What are the principles for treatment of infectious arthritis?
Treat underlying cause/infective agent
Systemic and local antimicrobials
Remove inflammatory mediators- joint lavage
What is the carrier of Lyme disease?
What does Lyme disease cause?
How is it diagnosed and treated?
Tick borne spirochaete borrelia burgdorferi
Multisystemic inflammatory disorder- dogs present with inflammatory, non-errosive arthropathy with shifting lameness and swollen joints
Diagnosis-
Synoviocentesis- increased cell counts- PMNs
Treat with doxycycline for 30 days
What do tendons and ligaments do?
Tendons-
passively transfer force generated by muscle to bony attachments
support joints
store energy
Ligaments-
attach/stabilise joints and bones
Protect tendons
Proprioception
What is the ultrastructure of tendons and ligaments and how are they different?
What is responsible for synthesis, maintenance and degradation?
Hierarchical structure which is adapted based on function
Differences in content and organisation of ECM
Tenocytes/ligamentocytes responsible for synthesis maintenance and degradation of ECM
What are the types of injuries of tendons/ligaments?
Extrinsic- external trauma
Intrinsic- overload/degenerative
How are tendon/ligament injuries diagnosed?
History-
age, type, previous injury, recent excercise, wound/laceration
Clinical exam- stance/gait, palpation
Diagnostic imaging- ultrasound, radiography
How can ultrasound be used for tendon/ligament disorders?
Change in cross sectional area
Fibre echogenicity- anechoic/hypoechoic/hyperechoic/mineralised
Margination
Position- rupture
Focal lesion versus generalised changes
Acute versus chronic changes
Blood flow- assess neovascularisation
What are the repair phases of tendon/ligaments?
Inflammatory response- chemokines, cytokines
Proliferative phase-
Cell migration, macrophages, monocytes
Angiogenesis
Tissue remodelling phase-
ECM and collagen deposition
What are the clinical signs, pathology and treatment principles of the acute inflammatory phase of tendon/ligament injuries?
CS- lameness, pain, heat, swelling
Pathology-
haemorrhage, inflammation- neutrophils, macrophages, increased blood flow, oedema
Treatment principles-
limit inflammation- cold therapy
Protect limb- supportive bandage
What are the clinical signs, pathology and treatment principles of the proliferative phase of tendon/ligament injuries?
CS-
reduction or absence of lameness
resolution of signs or inflammation
tendon enlarged and soft
signs of re-injury if exercised too early
Pathology-
angiogenesis
fibroplasia
Treatment principles-
promote angiogenesis
minimise formation of excessive scar tissue
early exercise
What are the clinical signs, pathology and treatment principles of the tissue modelling phase after ligament/tendon injury?
CS- stiffer, thicker
Pathology- fibrosis, gradual change from collagen III to I
Treatment-
increased loading and exercise programme
improve fitness
monitor progress by repeat ultrasound exam
With the following injuries to tendons/ligaments
What are options for surgery?
Laceratoin
Avulsion fracture
Intra-synovial tendon/ligament tear
Joint instability
Laceration- repair ends, cast if feasible
Avulsion fracture- re-attach avulsed bone fragment
Intrasynovial tendon/ligament tear- debire torn tendon/ligament
Joint instability- TPLO
How are skeletal muscles diagnosed?
History-
injury/trauma
breed, feeding management
frequency/severity
Clinical examination
acute: swelling/pain
chronic: stiffness, cramping, pain, fasciculations, weakness
Biochemistry- serum muscle enzymes, urine samples
Ultrasound- acute- haematoma, chronic- fibrosis/calcification
Muscle biopsy
How can muscles react to myopathies?
Atrophy
Hypertrophy
Degeneration
Regeneration
Calcification and ossification
Pigmentation
Circulatory disturbances
What is atrophy and what can cause it?
Reduction in size of muscle
Disure- reversible
Denervation-
irreversible- when cells degenerate or de-differentiate
trauma
myasthenia gravis
Cachexia-
1-5% muscle protein
What are the types of degeneration of muscle?
Cellular swelling-
minor chemical imbalances within the muscle, exhaustion leading to Ca2+ overload in mitochondria, moderate swelling but nuclei remain normal
Hyaline degeneration-
affects the sarcoplasm but spares the sarcolemma
often seen with nutritional myopathies
Granular degeneration-
severe damage with large basophilic granules of coagulated protein
stain positive for calcium
fibrosis or fat replacement
What is the regeneration and repair of muscle?
What commonly causes it?
Reconstruction of normal function to the fibre without complication
Calcification and ossification-
calcification due to irreversibly damages tissue
What circulatory disturbances can happen in muscles?
Collateral circulatory- compensates in local injury
Blockage of main arteries-
Arterial- partial blockage of distal aorta/iliacs can cause an ischaemic paralysis
Venous- blockage of large veins leading to congetsion with leakage of blood to muscles with eventual muscle necrosis and fibrosis
What causes white muscle disease?
What are the clinical signs and treatment?
Selenium/Vitamin E deficiency
most commonly in calves less than 6mo
degeneration of muscle
Clinical signs-
Muscle weakness/stiffness, recumbency, dyspnoea
Arrhythmias/murmurs when the myocardium is affected
Myoglobinuria
Serum- selenium
Treatment-
parenteral administration of selenium/vitamin E
What causes stiff lamb disease?
How is it treated?
2-4 week old
Similar aetiologies to white muscle- poor ewe rations
Neck and tongue muscles or shoulder, thigh, back and intercostal muscles
Similar appearance to calves but calcification
Treatment- vit E/Se supplementation
What are the clinical signs of acute exercise that induces exertional rhabdomyolysis in the horse?
How is it diagnosed?
What is the treatment?
Unfit horses- tying up, colic signs
Stiffness to severe pain
Commonly gluteals, semitendinosus, semimembranosus
Diagnosis- clinical exam, muscle enzymes- myoglobulinaemia
Treatment-
pain relief, fluid therapy, acepromazine
What are the clinical signs of chronic exercise induced exertional rhabdomyolysis in the horse?
How is it diagnosed and treated?
What is polysaccharide storage myopathy?
Chronic- stress/nervous, poor performance/stiffness/cramps
Diagnosis- history, muscle enzymes, biopsy
Treatment- warm up, avoid stress and high energy feeds
PSSM-
accumulation of glycogen
Dx- semimembranous muscle biopsy
Tx- diet
What are the clinical signs of inflammatory eosinophilic myositis?
How does histology appear?
What is the treatment?
Large breed dogs
Acute recurrent pain and mandibular immobility
Bilateral enlarged temporal/masticatory muscles
High percentage of eosinophils in the blood
Histology- central necrotic area with dead eosinophils and sarcoplasmic clumping, numerous eosinophils in periphery
Tx- corticosteroids
What are the parasitic and bacterial infectious conditions that affect muscles?
Bacterial-
blackles- Clostridium chauveoid
Malignant oedmema- Cl septicum, perfringens
Patasitic-
Trcihonellosis
Cysticercosis
Toxoplasmal myostisis
Sarcocysts
What are the clinical signs of toxic myoglobunlinuria?
What is the TXs?
CS-
acure onset, rapid and frequently fatal
muscle weakness/recumbancy
increased CK/AST
TXs- supportive therapy if survive
