Lameness and orthopaedic disease Flashcards
What to do first for lameness
- History
- Physical examination
- observation from a distance
- direct palpation
- ancillary tests
- Lameness examination
- basic examination
- additional movements/surfaces
- evocative tests
- “A clinical sign, [manifesting] signs of inflammation
including pain, or a mechanical defect that results in a
gait abnormality
Five “types” of lameness
* supporting limb (stance phase) lameness
* swinging limb lameness
* mixed lameness
* compensatory lameness
* induced/artefactual lameness
Almost never shoulder lameness – most common foot and less common more
proximally
Breeds of horse and levels of activity
Septic synovitis – hunting or jumping – hedges and thorns
Dressage – strains on ligaments – repetitive
Shetlands – more common shoulder – OCD shoulder
Forelimb much more common
Signalment clues for lameness
- Specific age groups often suffer from specific conditions:
- foals: haematological septic arthritis, lateral luxation of the patella
- young, skeletally immature animals: developmental orthopaedic diseases including OCD, stress related injuries (esp TB horses)
- older horses: chronic progressive OA, navicular disease
- … but these are not necessarily exclusive
There are very few sex related conditions; however, breeding potential may be important for treatment
* may also see behavioural changes associated with oestrus
* RER has been shown to be more common in female TB and event horses (recurrent equine rhabdomyolitis)
* anecdotally lameness has been implicated in cryptorchid animals
History: signalment
* Knowledge of the discipline and breed of the animal is extremely important
* certain disciplines will place unique strains on animals
* some manifestations of lameness are seen in all groups of animals
What history questions to ask for lameness
Conformation
Posture
Symmetry
Palpation
Cervical
- When did the owner first notice the problem? Is there a history of trauma?
- Have any treatments been attempted?
- What is the nature of the lameness?
- Does it improve with exercise? Is it worse on different surfaces/with different tack?
- Have there been any recent changes in management/exercise level/paraprofessional
involvement? - Is there any previous history of lameness?
- Understanding how conformation affects lameness is very important
- severe conformational abnormalities are easy to appreciate
- asymmetry of conformation is often particularly important
- there may be important breed characteristics that lead to lameness e.g. long toe/low heeled TBs
Hock conformation - hind limb suspensory desmopathy - poor prognosis with straight hocks
Posture - Careful observation from a distance is extremely important
* laminitis or severe skeletal injuries might be readily obvious
* pointing or reduced weight-bearing
* “dropped elbow” indicates failure of the triceps apparatus - olecranon fracture
* cervical pain
* upward fixation of the patella
* (neurological conditions)
- Asymmetry is often very important in lameness evaluation
- muscle atrophy (disuse or neurogenic)
- foot size
- fetlock height/angle
- localised swelling (synovitis, cellulitis, exostosis/callus formation)
- bony asymmetry (e.g. scapular height, tuber coxae/sacrale)
Looking for muscle atrophy – looking front or side – undeveloped – not using or
neurogenic
Foot size – chronic lameness
Fetlock – more weight – hyperextension – or failure of suspensory apparatus
Swelling – effusion of synovial structures, exosthosis – bone spurs
A good and systematic routine is vitally important
* always use the same system every time
* this will vary amongst individuals but choose a system that suits you
* examine limbs during weight-bearing and elevated from the ground
* ideally perform static examination before dynamic examination
- This should include assessment of:
- asymmetry
- signs of inflammation
- pain (by both deep palpation and induced movement)
- loss of function e.g. range of movement
- crepitus
- peripheral pulses
- Examination of the poll including wings of the atlas
- Palpation of the para-spinal musculature
- Palpation of the brachiocephalicus muscle
- If indicated assessment of the range of cervical movement using food
What are we assessing with forelimb lameness assessment
Shoulder and bicipital region
* Elbow and antebrachium
* Carpus
* Metacarpal region
* Fetlock
* Pastern
* Foot
* should include use of hoof testers
How to test thoracolumbar spine
- Use digital pressure to assess dorsal contour
- Deep digital pressure of the epaxial muscles is resented by many horses and is not pathognomomic for back pain
- pressure over the thoracic and cranial lumbar region usually results on lordosis
- pressure over the caudal lumbar and sacral region results in kyphosis
- often lack of these actions more indicative of back pain
- Often back pain is secondary to hindlimb lameness
What structures are we assessing for hindlimb lameness assessment
- Femoral region
- Stifle
- Tibia
- Tarsus
- capped hock, bog spavin, bone spavin, curb and thoroughpin
- Metatarsophalangeal region
- Fetlock
- Pastern
- Foot
Capped hock –
Bog spavin – swelling of tarsocrurual joint
Spavin – OA of small tarsal joints
Curb – swelling of plantar ligament
Thoroughpin – effusion of dft tarsal sheath
How to assess pelvis
- Often externally palpable abnormalities of the pelvis appreciated during observation
- include gentle rocking of the pelvis to detect crepitus
- generally performed last due to inherent risks
- include basic neurological assessment (tail tone, lower motor neurone function)
General clinical exam for lameness
- This should not be overlooked
- pyrexia may be concurrent with septic arthritis especially in the foal
- Lameness and gait abnormalities may also result from other conditions
- peritonitis/pleuritis, abscessation, genito-urinary disease
- One should never forget that “common things are common”
- however, good and systematic examination will help identify those uncommon cases
How to do dynamic exam
- Select an appropriate environment and surface
- safety of the horse and handler are paramount
- select an even, straight, firm surface free from distractions; however, alternate surfaces can be useful
- explain to inexperienced handlers exactly what you require
- Examination should attempt to assess:
- baseline lameness (i.e. before provocative tests) or lamenesses
- attempt to identify multiple limb lameness, and also establish whether these are primary or secondary problems, or if they are artefactual
- any lameness identified should be graded and immediately recorded to attempt to create a degree of objectivity
Lameness grading
- Several systems exist
- Ten point grading system (more commonly adopted in
Europe) - Five point systems usually attempt to be more objective
- care as different systems exist
- especially in the UK clinicians will refer to a 5 point system
without appreciating any objective nature
1 - Lameness difficult to observe and not consistently apparent regardless of circumstances (such as weight carrying, circling, inclines, hard surfaces)
2 - Lameness difficult to observe at a walk or trotting a straight line but is consistently apparent under certain circumstances (such as weight carrying, circling, inclines, hard surfaces)
3 - Lameness consistently observable at a trot under all circumstances
4 - Obvious lameness with marked nodding, hitching, or shortened stride
5 - Lameness characterized by minimal weight bearing in motion or at rest and the inability to move
Assessment at walk
- The horse should be walked at a steady pace away from and towards the observer
- observe horses carefully during the turn
- Careful attention should be placed upon
- foot placement
- gait abnormalities (e.g. “dishing”, “plaiting”)
- Include lateral observation to assess:
- foot flight
- “tracking up”
- cranial and caudal phases of the stride
Dishing – moving feet outwards
Plaiting – moving feet inwards towards straight line
Tracking up – hindlimb placement should be in footprints of forelimbs
Caudal how far back before picking limb up, cranial how far forward placing foot
Mechanical and neurological lameness
- Alternative/mechanical causes of lameness:
- “stringhalt”
- fibrotic myopathy
- upward fixation of the patella
- “shivers” syndrome
- Always remember to assess neurological function especially in young horses
- ataxia is difficult to define but important to remember that the etymology is from Greek (without order/regular arrangement i.e. inconsistent)
Stringhalt – hyperflexion of hind – uni or bi. No lack of performance – plant toxin in
Aus and UK
Fibrotic myopathy – scarring of muscles of hindlimb
Upwards fixation of patella – locking
Ataxia is not lameness
Examination at trot
Examination at trot
* Horse should again be moved at a steady pace away from and towards the observer
* ensure that the handler does not constrain the horse’s natural movement
* pace can sometimes mask or complicate assessment so different speeds can be useful
* assessment now focuses less on the foot placement and more on other alterations in gait
Forelimb lameness
- “Head nodding” is the most useful method of forelimb lameness assessment
- head elevation begins just before the stance phase of the lame limb
- results in reduced ground reaction force (GRF) due to upwards acceleration of the head and neck, and caudal movement of the centre of gravity
- consequently the horse appears to nod when the “good” leg is in contact with the ground
Hindlimb lameness
- Relative excursion of the tuber coxae is generally the accepted visual method of assessing hindlimb lameness
- often given terms like hip or pelvic “hike”
- the limb with the greater degree of movement is the lame limb
- visual cues can be improved by placing tape on each hindlimb running between the tuber coxae and tuber sacrale
- Hind limb lameness is harder to appreciate than forelimb lameness
Hindlimb lameness can mimic forelimb lameness at trot
* when the lame limb hits the ground the horse moves it centre of gravity cranially to help unload the limb
* the two-beat gait means that there will be a head nod during the stance phase of the contralateral forelimb
* therefore the horse appears to be lame on the ipsilateral forelimb to the lame hindlimb
* It should be noted that this is generally apparent only if moderate lameness is present
Additional assessments
* There are many other visual (and audible) clues which may help with lameness
* Unless riders are very experienced try to avoid their advice
* it is very difficult to differentiate forelimb and hindlimb lameness from the saddle
* owners are also more likely to be biased following diagnostic anaesthesia
* this does not, however, suggest that riders input is not valuable during lameness assessment
Additional assessments
Sound
* excluding all visual clues and listening to syncopation can be extremely useful (remembering the beats of the four standard gaits)
Fetlock drop
* at trot because there is a higher GRF in the sound (less lame limb) the fetlock will drop further
* structural disruption of the suspensory apparatus and flexor tendons will typically result in over-extension of the affected limb at walk
- Most lameness results from pain during limb loading
- therefore horses will attempt to reduce the duration of the stance phase
- can be especially useful in the assessment of hindlimb lameness during lunging exercise
Lunging
- Helpful in ascertaining there might be a bilateral component to lameness
- Lunging on different surfaces can also be extremely
useful - Beware of over interpretation
- “soft tissue lameness is worse with the limb on the outside/when lunged on soft ground”
- very tight circles on hard ground can evoke forelimb lameness of questionable significance, especially in heavier horses
At canter
Three beat gait
* L lead: LF, RF and LH, RH
* although RH contacts the ground on its own, stance phase, GRF and degree of flexion in the proximal joints is greater in the LH
* therefore a horse with a RH lameness may possibly prefer to canter on a left lead
* R lead: RF, LF and RH, LH
Ridden
The additional weight of the rider can elicit lameness in either the forelimbs or the hindlimbs
* subtle changes in weight can also mask signs of lameness
* having an experienced rider can be extremely useful especially when evaluating subtle poor performance issues
Flexion tests
Important to remember that these are not specific to one particular structure
* Different clinicians will also apply different forces
* consequently you need to be familiar with the normal responses to flexion
* it is possible to induce lameness
* studies show that 100-150N is optimal (????)
* aim to flex the limb to a point slightly before a withdrawal response is elicited
* No clear guidelines as to how long flexion should be applied
* most clinicians use 60 seconds
* however, it has been shown that 5 seconds of flexion generally produces similar results to 60 seconds in many cases
Horse temperament in lameness exam
- Safety of the horse and handler should be the first consideration
- acepromazine can be useful in calming fractious horses without providing analgesia
- some clinicians advocate low doses of xylazine; however, this will be analgesic and may result in ataxia
- more frequently xylazine is used to facilitate local anaesthesia in which case it is important to allow sufficient time for the effects to wear off
Forelimb static exam
Restrain and calm to examine
Palpate both legs
Look for heat, pain and swelling - synovial effusion
Dont jump to conclusions - may be old or insignificant - good records, history, dynamic and diagnostic tests
Principles of forelimb diagnostic anaesthesia
Aseptic, new bottle, sterile needle/syringe, prep (dont need to clip unless very hairy)
Mepivicaine - least tissue reaction. Bupivicaine slightly longer action but expensive
Place down leg
Needle seperate
VAN - nerve more palmar
DO NOT if
Suspect fracture of severe soft tissue injruy - DDFT rupture as will weight bear and catastrophic
Risk of infection - existing skin disease or cannot clean
Cannot perform safely
Start distally and work proximally
Palmar digital
Abaxial sesamoid
Low four point - fetlock and below
High four - metacarpal and below
Lateral palmar nerve - proximal suspensory
Static hindlimb examination
Stand square, both sides, conformation, asymmetry, muscle wastage, swelling - from side
Scoliosis - sway back or roach back
Hock conformation - straight hocks
Flexural conformation distal limb - hyperflexed fetlock
Symmetry of gluteal muscles
Tuber sacrum top
Tuber coxae
Tuber ischii
Bow legged (valgus - hocks out) or cow hocked (varus - hocks in)
Palpate for heat, pain, swelling
Stifle - will feel femoropatellar - patella ligament - effusion
Medial - feel effusion in medial femorotibial joint - lateral much harder
Hock - tibiotarsal most motion joint
Distal intertarsal and tarsometatasal
Fetlock - plantar pouch effusion, DFT sheath effusion,
is it dorsal or plantar to suspensory branch - plantar is flexor tendon, dorsal is fetlock joint
Remember with limb elevation - hock and stifle move together - suspensory apparatus
Hoof exam
How to make hindlimb regional anaesthesia safer?
Restraint of patient - handler, nose twitch, chemical restraint, lift ipsilateral forelimb
Personal safety - hat, case by case
Clipping - may well increase skin contamination - only clip if makes identifying landmarks easier
When is low 6 point used in hind limb over a low four point
Dorsal metatarsal nerves are the 5th and 6th point - important for skin sensitivity
What is main difference between perineural blocks and synovial blocks?
Synovial -into synovial structure - much more specific to structure injected - can return to block more distal structures
Perineural - need to work sequentially distal to proximal - each block adds additional areas of desensitisation
Where to start with hindlimb anaesthesia
Acute lameness, positive to proximal limb flexion (unilateral), effusion of medial femorotibial joint
Stifle
Where to start hindlimb anaesthesia
Chronic bilateral lameness in sports horse - mild to moderate positive to proximal flexion
Tarsal region - small tarsal joints or proximal suspensory ligaments
Where to start hindlimb anaesthesia
Acute unilateral lameness in native pony with marked digital flexor tendon sheath effusion
DFTS
What perineural nerve blocks can we do in hindlimb?
Plantar digital
Abaxial sesamoid
Low 4 point
Deep branch of lateral palmar
Tibial and peroneal
Deep branch of lateral palmar nerve - DBLPN
How to do
Fairly specific block for proximal suspensory ligament
- Limb is held flexed and rested on the vets knee
- The flexor tendons are pulled medially to open up injection site
- Needle is advanced along the axial surface of the lateral splint bone
- 3ml of local anaesthetic solution is injected (resistance should be low)
- The horse is re-examined after 10 minutes
What factors classify a fracture in horse
Location - which bone and where
Structures involved - articular vs non articular - synovial sepsis or not
Contamination - open or closed - bone contamination or skin barier
Extent of damage - complete vs incomplete, simple vs comminuted, complete both sides of bone or multiple pieces
Size of fragment - chip vs slab vs shaft fracture - shape or direction, chips
Fracture configuration - transverse, oblique, spiral, avulsion, growth plate
Displacement, fragments, margins
What are the different fracture types for pedal (p3) bone
Type 1 - wing fracture
Type 2 - articular wing fracture
3 - straight down middle - articular
4 - extensor process fracture
5 - comminuted fracture
6 - chip fracture
7 - foal - chip
Causes of fracture in the horse
Trauma - most common cuase, can be acute (kick, fall), or chronic repetative (stress in racehorses, general wear and tear)
Developmental - msot commonly due to OCD or other developmental orthopaedic disease
Secondary to other disease conditions - neoplasia or infection - uncommon but important
Common fracture sites - kick
splint bones, stifle bones (tibia, patella), olecranon, head
Common trauma/fall fracture sites
Head, vertebrae, long bones - femoral or cannon in anaesthetic recovery, joints during competitions - patella from hitting fence
Common repetative wear fracture sites
Distal phalangeal (pedal, p3), middle phalangeal (p2, pastern), distal sesamoidean (navicular bone)
Navicular disease and remodelling - secondary to wear and tear with mechanical changes
Common stress fracture sites
In racehorses - anywhere
Carpal bones - radius, radiocarpal, third carpal
Third metacarpal bone (cannon), middle phalangeal (pastern), proximal sesamoidean bones, radius, tibia, pelvis, vertebrae
Clinical signs of fracture
Range from mild / subtle to marked / severe!
Acute, severe or displaced fractures will have obvious conformational abnormalities, severe lameness, pain and crepitus at the fracture site
Non-displaced fractures (including stress fractures) and small chip fractures may have
minimal lameness and localising signs
Articular fractures normally have joint effusion
Know your anatomy, palpate carefully!
Diagnostic approach to fractures - history
Physical exam
Major red flags for fractures are history of trauma (e.g. kick or fall), acute onset severe lameness, acute onset joint effusion, heat, pain, swelling and palpable crepitus
Non-displaced stress fractures may present as acute onset lameness following exercise, which resolves over a few days
Non-displaced, repairable fractures can progress to catastrophic irreparable fractures if not recognised and treated appropriately
Physical exam
Careful and detailed palpation for heat, pain, swelling and crepitus.
Crepitus due to air/gas under skin is usually diffuse and non painful. Crepitus due to bone fragments is painful and localised.
Administer sedation and analgesia as needed until horse is calm and can be examined thoroughly
If attending event / accident and examine immediately, then consider re-examining later.
Exhausted or excited horses may mask some of the signs initially. Swelling and heat can take a few hours to appear.
Consider what underlying / associated structures may be affected
Diagnostic tests for fracture
Nerve or joint blocks – avoid if possible, only use is in chronic, mild, small fractures
Radiography – first line approach for most fractures
Minimum of two views
Some regions may not be accessible for radiography
Non-displaced fractures may not show any radiographic changes
Ultrasound – main use is in pelvic fractures in racehorses#
Gamma scintigraphy - valuable for non displaced stress fractures or areas which cannot be accessed with radioraphy - vertebrae, ribs, scapula, pelvis
CT - gold standard but availability of facilities and cost
Possible fracture complications
Articular involvement –> degenerative joint disease
Contamination -> osteomyelitis, synovial sepsis, soft tissue infection
Soft tissue involvement -> tendon, ligament, muscle or neurovascular damage
Unstable -> non-healing or malunion
Damage to periosteal vascular supply -> sequestrum formation
Mechanical overload of contralateral limb -> laminitis
Avoided by
- Recognise fracture promptly, adequate stabilisation
Do NOT nerve block or exercise if risk of fracture
Provide adequate support, splinting to prevent further damage - if travelling or moving as well
Cover and protect open wounds
Assess carefully for involvement of other structures - radiography for articular involvement, US to assess soft tissue, neuro for suspect nerve damage
Articular fractures
- Remove small unstable articular fractures which are non an integral part of articular surface and will cause trauma if left
- Stabilise large fragments which are an integral part of articular surface - screw, plate
- Arthrodesis is viable option for low motion joints - pastern, carpometacarpal, distal tarsal joints
Contamination
Internal fixation of open fractures is rarely successful
Open contamination / infection of a major fracture is a major complication
Identify, flush and protect and any wounds
Administer systemic antibiotics
Soft tissue involement may be limiting factor
- Complete tendon rupture - will drastically change prognosis of simple fracture
Which fractures to euthanase
Open, comminuted long bone fractures
Complete fractures of scapula, humerus, radius, femur and tibia in horses over 500kg
Consult insurance where possible
Seek advice from senior partner or referral surgeon as needed
If fracture is irreperable
Cannot be stabilised, transported for appropriate treatment
Quality of life long term will be poor - articular damage to arthritis
Owner cannot affort
Horse will not tolerate box rest, rehabilitation - preexisting conditions, temperament, behaviour
Horse will not return to previous work
Needs to be dialogue with owner - human factors and owner circumstances
Equine welfare long and short term
4 levels of triage
1 - immediate action or might die - head or spinal traima, internal injury, haemorrhage
2 - do not move or come become unfixable - fracture, tendon rupture, laceration, joint instability, vascular or neurological damage
3 - Urgent attention or prognosis wil be compromised - synovial or bony involvement, contaminated wounds
4 - delayed action - does not need urgent emergency visit
What to look for to triage on physical exam
Crepitus - fracture or emphysema
Degree of contamination
Soft tissue involvement
Bony involvement
Swellings and effusions
Principles of equine first aid
Restraint - consider will ataxia/weight bearing make this worse?
Control haemorrhage
Control pain
Reduce contamination
Close wounds
Bandage for wound protection
Splint fractures and tendon injuries
Avoid ACP in blood loss/hypovolaemic/exhaustion - also has no analgesic effects
Start low dose alpha 2 agonist - on duration required - xylazine, detomidine, romifidine
Combine IV and IM - IM less ataxia - better for travelling
Always include opioids
Haemorrhage - pressure bandage, tourniquet, ligatures
NSAIDS, Opioids, sedation, local
Splints - below fetlock - just dorsal
above fetlock below carpus/tarsus - laterally and caudally
above carpus/tarsus below elbow/stifle - laterally and medially
above elbow/stifle - stabilise carpus - all you can do
Decision making in first aid
Client considerations
- Prognosis for athletic function
- Pasture soundness
- Cost
- Duration of box rest
- Time out of work
- Amount of nursing required
Poor prognosis injury
Compound, open fractures with significant contamination or soft tissue damage
Complete fractures of femur, humerus and tibia
Complete laceration of SDFT, DDFT, and SL
Complete laceration of SDFT, DDFT and distal sesamoidean ligaments
Suspensory ligament above fetlock, distal sesamoidean ligament below fetlock
Long term analgesia considerations
NSAIDs
Phenylbutazone (Oral doses: Day 1 4.4 mg/kg BID, Day 2 2.2mg/kg BID, then reduce to 2.2mg/kg SID or every other day)
Licensed for long term use, but warn client about possible complications
Side effects include: right dorsal colitis, gastric ulceration, renal disease, blood dyscrasias
Safety threshold is low - work doses out correctly
Horses cannot compete on medication for most regulatory organisations
Do not use in foals <6 weeks
Oral flunixin, oral suxibuzone, oral meloxicam
Oral paracetamol (not licensed)
Intra-synovial corticosteroids – triamcinolone, methylprednisolone
Can be very effective for relatively long periods of time post injection, think carefully about loading and use of joints after medication
PsGAGs – intra-articular or IM administration – some anti-inflammatory action as well as effect on joint biology
Weight loss
Mobilisation and controlled exercise
Handwalking
ACP - anxiolytic
High fat low starch diet should calm down
Principles of fracture repair
1.Fracture reduction and fixation to restore anatomical relationships
2.Fracture fixation providing absolute or relative stability as the “personality” of the fracture, the patient, and the injury requires
3.Preservation of the blood supply to soft tissues and bone by gentle reduction techniques and careful handling
4.Early and safe mobilization and rehabilitation of the injured part and the patient as a whole
Lag screws, position screws, plate screws
Lag screws - achieve compression - essential for direct healing
Drill, countersink, measure, tap screw - drill far hole narrower than near - so when tapped it will engage with far bone not bone fragment - use countersink as compression
How to prep for emergency field radiography
Restraint
Anaglesia - NSAIDs and opiates
Sedation - alpha 2 agonist and ACP
Remove bandages
Tail bandage
Owner prep - stay calm - send away to get more assistants
Flat firm surface, out of direct sun, enclosed, private, electricity supply
Lead gown, thyroid protector, lead gloves, dosimeter, radiation warning signs
Pedal bone xrays
65 degree dorsoproximal palamar digital
Complications of fracture repair
Osteomyolitis
Screw loosening
Implant failure - race between fracture healing and implant failure
Delayed / non union
Ring sequestrum
Support limb laminitis
Clinically important points of soft tissue injury
COMP and crimp reduce with age - tendons become less elastic - affects injury rates
Tendons consist of large amounts of extracellular matrix (ECM) and relatively few cells - implications of healing and remodelling
Blood supply is poor - particularly within sheaths and bursae - poor recruitment of inflammatory cells
Where do most SDFT injuries occur?
Mid metacarpal region of forelimb
Occaisonally hindlimb seen and occaisonally disease of branches close to insertion onto second phalanx
Where do most DDFT injuries occur?
Distal flexor tendon sheath, pastern or within hoof
Occaisonally in mid metacarpal in forelimb alongside severe check ligament injury
Where do most suspensory injuries occur?
At proximal origin or at branches of insertion onto proximal sesamoid bones
seen in suspensory body sometimes but as rare solitary lesions
Where do most inferior check ligament injuries occur?
ALDDFT
Easily palpated in proximal third of forelimb metacarpus usually larger on lateral side
Hindlimb VERY rare - some dont even have hind check
Stifle soft tissue pathology
Cruciate ligaments and medial meniscus are a common site of pathology –
usually accompanied by effusion
Patellar ligaments can also be injured and very occasionally the lateral
meniscus
How does microdamage lead to injury?
Increasing age, working in non-elastic region of loading curve, repetitive loading, poor reparative and adaptive processes in tendon tissue, matrix degeneration, reduction in crimp, reduction in comp, increases in type 2 and 3 collagen, poor vascularity, tendon heating
Use of solid boots?
Will reduce risk of direct trauma from overreach
BUT - physiological effects - HEating
Clinical diagnosis of SDFT
An easy diagnosis by palpation/visual inspection
Characteristic “palmar bow” seen to the profile of the tendon
Heat, pain, swelling, resentment of palpation
Immediate events – Inflammatory Phase (Days)
Clinical signs
*Lameness
*Pain on palpation
*Heat
*Swelling
Pathology
*Haemorrhage
*Inflammation
*neutrophils
*macrophages and monocytes
*increased blood flow
*edema
*proteolytic enzymes
Reparative/proliferative phase – fibrosis (Weeks)
Clinical signs
*Reduction or absence of lameness
*Resolution of signs of inflammation
*Tendon still palpably enlarged and soft
*Signs of re-injury if exercised too early
Pathology
*Angiogenesis
*Fibroplasia
*++ fibroblasts
*collagen III
*small collagen fibrils formed
Remodeling/maturation phase – (Months)
Clinical signs
*Tendon size decreases
*Tendon less pliable
*Reduced fetlock extension
*Contractures
Pathology
*Collagen transformation from III to I
*Cross-linking
*Thicker collagen fibrils
Tendon injury - first aid
Prevent injury becoming worse
Reduce pain
Reduce inflammation
Provide stability
Reduce tendon loading
NSAIDs
Steroid
External support
Cold therapy
Confinement
Intralesion therapy
At start of repair phase - 2-3 weeks after injury - after inflammatory phase
Only when a hole or space is present
Therapy is injected into lesion under US guidance
Improve speed and quality of healing - supraphysiological healing
Not a substitute for long term rest and controlled exercise
Aims of soft tissue injury rehab
Hasten return to function
Improve function of structure involved
Reduce pain and inflammation
Reduce re-injury rates
Improve quality of life
Improve range of motion or flexibility
Improve proprioception and balance
Adopt whole animal approach
What will help improve core/dynamic stability in rehabilitation
What rehab to use
Water treadmill - adds resistance to cranial phase, increases stride height, increased ROM of axial skeleton, buoyancy
Swimming - not for sport horses as encourages extended neck and spine - reduced bone stimulation so limited use sometimes
Ridden or in hand exercise
Hillwork - trot up walk down
Pole exercises - raised
Range of surfaces
Cross training
What are 4 phases of wound healing
Haemostasis/coagulation - first 5-10 minutes
Inflammatory phase - debridement pahse - 1-3 days after wounding (excess granulation tissue phase)
Proliferative phase - wound bed fills with fibroblasts - weeks after - fibroplasia and angiogenesis
Proliferative phase - epithelialisation - 24-48h after wounding, inhibited by infection, dessication of wound surface, exuberant granulation tissue, repeat dressing changes
- Can only work if granulation tissue underneath - no divots or large lumps
Proliferative phase - contraction - 2 weeks after wounding - accelerate closure
Maturation - remodelling - from 3 weeks to 2 years - strength of new tissue
Wound lavage
Clean potable tap water
povidone iodine (clean as organic matter inactivates)
Protocol for wound management
History first
Physical exam
Sedation
Pain relief
Hosing
Clip
Cleaning
Rinse
Tetanus vaccine - when
Wound evaluation
Clean or sterile prep
Digital palpation
Probe digitally or sterile probe - position of limb at time of injury - skin penetration may not be atop of deeper pathology
Radiography
US
Pressure test - can you distend synovial capsule after aspirating joint fluid - inject saline
Wound treatment
Desensitisation - mepivicaine
Debride - remove devitalised tissues, foreign material
- Scalpel blade
Osmotic dressing
Lavage
Repair - suture (appositional or tension relieving
Resect edges, suture fully, partially, or drain
Monofilament prevents bacteria tracking
Physiology of increased digital pulses
Injury to foot
Inflammation
Increased blood flow
Swelling
Hoof capsule cannot expand
Increased pressure
Blood pressure within digital artery increased
Bounding pulse
History questions for bounding digital pulses
How to feel
What is the horse used for?
How is it managed?
Any recent changes in management?
Any previous lameness / foot problems?
When did the problem start?
Has it improved or worsened?
What exercise had the horse been doing recently?
When were the feet last trimmed / shod?
Have the owners given any treatments?
On abaxial margin of the lateral and medial sesamoid bones
Run finger from side to side to feel the neuro vascular bundle
Place finger & thumb on either side
Gentle pressure
Be patient
Assess strength
Normal pulse is not always easy to feel - faint, harder with thick skin
Raised is easier - bounding compared to other legs
1 limb or more? assists with diagnosis
LamesStatic exam increased digital pulses
Dynamic exam
Recumbent?
Stance?
Generalised distal limb swelling?
Localised heat / pain / swelling?
Effusions in digital flexor tendon sheath or fetlock / coffin joints? (pastern joint effusion is hard to palpate)
Hoof temperature?
Wounds?
Hoof cracks?
Abnormal hoof rings?
Defects in the sole?
Shoe type and integrity?
Unable to move
Lame at walk?
Lame at trot?
Worse on turns?
Grade of lameness?
Worse on hard?
Which leg or legs?
How is/are lame foot/feet placed on ground?
Worse on lunge?
Response to flexion?
Remove shoe
Repeat hoof tester examination
Pare foot with hoof knives
- Discolouration
- Discharge
- Deviation of white line
Lameness grading
0 - sound
1 - mild inconsistent lameness
2 - mild consistent lameness
3 - moderate consistent lameness
4 - severe consistant lameness
5 - unable to bear weight
Ddx for increased digital pulses
Laminitis
Subsolar abscess
Fracture
Bruising
Corns
Keratomas
Septic pedal osteitis
Thrush in frog clefts
diagnosis by
History
Clinical exam -static and dynamic
Radiography
Rarely MRI CT
Define laminitis
Inflammation of laminae of the foot
Bone between dermal and epidermal lamellae are strongly bonded, released to allow hood growth through action of MMP - metalloproteinase - catabolic enzyme
Excessive MMP
Causes of laminitis - endocrine
Obesity, EMS
- Increased fat reduces cellular response to insulin - insulin resistnace/dysregulation
Cells remove less glucose from blood - hyperglycaemia
Body produces more insulin - negative feedback - hyperinsulinaemia
Excess insulin - stimulates MMP production
EMS
- Excess body condition
- Abnormal fat distribution
PPID - pars pituitary intermedia dysfunction
- excesss ACTH also causes hyperinsulinaemia
PPID
- Hirsuitism
- Decreased muscle mass
- Pot belly appearance
- Supraorbital fat pads
Non endocrine causes of laminitis
Toxic
- Compromised bowel - colitis, enteritis, strangulation
- Severe infection - RFM/sepsis
Bacterial endotoxin enters blood stream - endotoxaemia
MMP production increased
Support limb laminitis
- Severe lameness in one limb - excessive weight bearing in contralateral - prolonged pressure reduces blood flow so hypoxia so inflammation and MMP production
Corticosteroid induced - exogenous corticosteroid - rare
Stress
- Endogenous glucocorticoids increase
Induce hyperinsulinaemia and subsequent increase MMP - greater risk if susceptible already
Signalment for laminitis
Age – No consistent predisposition, but foal & weanlings rarely affected
Breed - Occurs in all breeds of horse, but native breeds / ponies predisposed
- Donkeys can be severely affected
Sex – No predisposition
Peaks in spring and autumn
Most cases are endocrine
History taking for laminitis
When did signs begin?
Progression – getting better or worse?
Any recent management changes?
Previous episodes of laminitis?
Any concurrent disease / injury?
Received any medications recently?
Current diet?
When last trimmed / shod?
Horse’s use?
Exercise history?
Clinical exam laminitis
Recumbent?
Stance?
- leaning backwards
- weight shifting
Resp. rate / panting?
Heart rate?
Temperature?
Sweating?
Pained expression?
Often affects both front limbs
Maybe all 4, or just 1
Increased digital pulses
Hooves warm to touch
Visible growth rings indicate previous episodes
Able to lift legs?
Often show pain to hoof testers at point of frog
Shod/unshod/type of shoe
Depression at coronary band and concavity of sole suggests severe disease - sinking
Dynamic
Degree of lameness varies
May be mild - walks almost normally - to severe - unable to walk
Usually worse when turning on hard ground
Foot lands heel first to spare the toe region from weight bearing
Sometimes show a high stepping gait with hindlimb laminitis
Laminitis grading
0 - sound
1 - weight shifting at rest, sound in straight line, stilted gait when turning or trotting
2 - stilted gait when walking in straight line, clearly lame when turning, legs can be lifted without difficulty
3 - reluctant to walk, legs can only be lifted with great difficulty
4 - will only move when forces, long periods recumbent
What radiographs to do for laminitis
Lateromedial - will see if any p3 rotation - should be parallel with hoof wall, >10 degree is severe - and assess sole depth, and remodelling at tip of p3
Dorsopalmar/plantar
Metabolic tests for laminitis
EMS - baseline insulin (serum)
- Feed only hay/grass 12h prior
Increased baseline insulin is positive - EMS
normal baseline insulin is negative - does not rule out disease
Oral sugar challenge tests
Feed only hay/grass for 12 hours
Dextrose powder and blood sample for insulin 60-90 mins later
PPID
Baseline ACTH - EDTA
Usually diagnostic, reference range changes throughout year, most accurate in autumn
TRH stim test
Rarely required
Collect baseline ACTH
Inject TRH
Collect ACTH 10 mins later
All results inaccurate if animal is in pain - wait few days until comfortable
Repeat samples to assess response to tretament and adjust management and drug dosages
Initial management for laminitis
Pain relief - NSAIDs - PBZ, paracetamol, opiates
Vasodilator - improve blood supply to distal limbs, ACP - and an anxiolytic
Support feet - deep bed, remoev shoes, frog supports
Diet - weight loss 1.5-2% body weight dry weight hay, soaked for 1h to reduce sugar
- Tiny amount of alfafa - low sugar feed - to put medication in
Vitamin/mineral balancer
Warn owner this is not quick fix
Euthanasia also not wrong
Longer term management of laminitis
Regular re examination
Adjust medication and management accordingly
Endocrine testing once pain reduced
EMS - metformin, levothyroxine, ertugliflozin
PPID - pergolide, cabergoline
Farriery - trim heels and toes, heart bar shoes
Careful introduction of exercise
Repeat radiographs if not improving or as required from farrier
Euthanasia
Can do DDFT tenotomy - mid cannot cut DDFT - removes palmar traction on P3 - salvage
Prognosis of laminitis
Lameness severity
Degree of rotation
Sinking
Patient weight
Ability to control endocrine
Improvement takes many months - as new hoof grows down - 1 year
Repeat episodes are common
Risks for hoof abscess
Poor hoof quality
Unhygienic environment - dirty bedding, wet turnout
History of laminitis - seedy toe, white line disease
Clinical signs of hoof abscess
Acute onset lameness
Often severe
Bounding digital pulse
Localise the lame limb
Examine foot for anything obvious - penetrating injury and foreign body
Hoof testers - around hoof wall, percuss different regions of sole, not always reactive
How to find hoof abscess
How to treat
Remove shoe
Remove entire sole surface
Explore white line with loop knife
Look for abnormalities - black patches
Explore
Once found
Pare using hoof knives and nippers
Likely to be reactive at this stage
Consider sedation or palmar digital nerve block to desensitise
Pare until pus
Leave suitable drainage area - prevent refilling
Wet poultice the foot
Repeat daily whilst abscess drains
After 2 days of clean poultices - replace with dry poultice for 2 days to harden foot
NSAIDs
Tetanus (antitoxin and/or vaccination)
Box rest - prevent tracking to coronary band which will prolong treatment time
If you dont get put - may need a day to brew - place poultice and revisit next day
Consider radiographs
- Locate and rule out other ddx
Most do not need antibiotics - can prevent draining and encapsulate abscess
Only use when soft tissue infiltration or in a readily draining abscess you are struggling to get ontop of
Causes and types of p3 fractures
Clinical signs
Acute onset trauma, developmental/osteochondral fragments, repetitive wear and tear/chronic disease
Types - small fragments, large complete fractures, stable or unstable, articular and non articular
Navicular and p3 within hoof - minimal displacement
Careful palpation of hoof and pastern for heat, pain and swelling - synovial effusions
Use hoof testers
Clinical signs depend on fracture site and severity
Small extra articular fragments – low grade lameness with minimal localising signs
Significant / complete fractures – acute onset, severe lameness with localising signs (bounding digital pulses, heat in hoof, positive response to hoof testers)
Articular fragments – Distal interphalangeal joint effusion (pedal bone and navicular bone)
Tendon involvement – digital flexor tendon sheath effusion (navicular bone)
Diagnosing p3 and navicular fracture
Radiography
MRI
CT
Gamma scintigraphy
Nerve and joint blocks for mild/chronic - avoid in severe fracture
Radiography - fracture may not be visible until 7-10 days later until some bone resorption has occured
Some only heal with fibrous union - line on radiographs but stable, chronic fracture may need additional tests to determine significance
Radiographs - navicular bone
Lateromedial
Dorsoproximal palmarodistal 60 o oblique
Palmaroproximal palmarodistal oblique
Radiographs - p3
Lateromedial
Dorsopalmar/ dorsoplantar
Dorsoproximal palmarodistal 60 o oblique - either erect balet toe or angle machine - pack hoof to avoid air artefact
Dorsolateral proximal palmaromedial distal oblique
Palmaroproximal palmarodistal oblique
Is it really a fracture??
A fragment at the site of the extensor process can have a number of possible causes:
Recent fracture
Previous fracture, now healed and stabilised
Separate centre of ossification
Dystrophic mineralisation in the extensor tendon
Treatment plan for navicular or p3 fracture
Fixation - internal screw
Conservative - box rest
External coaptation - foot cast
Fragment removal - bursoscopy
What are sole bruises
Blunt trauma to solar surface of hoof during locomotion
Haemorrhage into tissues of foot
Tissues become inflamed, vascularity increased - increase in tissue fluid
Increased fluid content of inflamed tissues
Hoof is a sealed non compliant structure and thus leads to focal increases in pressure
Clinical signs of sole bruising
Acute, severe unilateral lameness - ddx - subsolar abscess, pedal bone fracture
Mild bilateral (or quadrilateral) pain - ddx - laminitis, bilateral forelimb lameness
Increased digital pulses to affected hooves
Increased hoof temperature
Sensitivity to hoof testers
When is solar bruising called a corn?
At the seat of corn - i.e. points of heel either side of frog
Hoof testers will localise focus of pain
Can be dry or suppurative as tissue fluid leaks through the epidermal tissues
Management of corn/sole bruising
If lameness is acute, unilateral, severe - manage as subsolar abscess and assess response
- If horse has bruising, lamenss will improve rapidly without any pus drainage
If lameness is mild or multilimb
- Box rest, NSAIDs (PBZ), lameness should rapidly improve
If significant haemorrhage then can progress to subsolar abscess - blood is excellent culture medium
Risk factors for sole bruising
Surface:
* Uneven or highly concussive surfaces
Shoeing/farriery:
* Barefoot horses will be more prone
* Long shoeing interval (particularly corns)
Activity type:
* Horses used for hacking will be more likely
Activity level:
* Repetitive concussive forces
Conformation:
* Horses with flat foot and low heel conformation
Maintain shoeing intervals - 6 weeks is the “norm” - but consider individual variation
In at-risk horses or at-risk environments consider ways to prevent concussion and contusion:
* Shoes fitted to horses that are barefoot
* Pads fitted between the shoe and the hoof
* Packing material injected between the pad and the sole
Horses with poor hoof conformation should be actively corrected:
* Sparing the heel when trimming
* Avoid working on firm or uneven ground
Keratoma - pathogenesis
Hyperplastic keratin mass within the hoof
Originates from epidermal horn producing cells of coronary band
May be benign neoplasm
Grow distally towards toe with the hoof
Acts as a space occupying lesion within hoof capsule
- Pressure necrosis in adjacent distal phalanx
- Hoof deformation
- Loss of white line integrity - entry of bacteria - hoof abscess
Most common in toe region
May occur following insult to germinal cells at coronary band - hoof abscess, trauma, hoof crack
Keratoma history and exam
May be mild intermittent long term lameness
Usually recurrent severe lameness
Recurrent hoof abscesses at same location
Raised digital pulse - single foot
Possible hoof wall distortion
Deviation of white line with cork like growth visible
Localised pain with hoof testers
Drainage from abscess
Lameness abolished by perineural anaesthesia of foot - palmar digital
Dorsoproximal palmar/plantar distal oblique 60 o - upright pedal
Smoothly demarcated radiolucent lesion in distal border of distal phalanx
Can be tubular or spherical
Treatment by excision through hoof wall
Takes several months for hoof defect to grow out - good prognosis
But recurrance in <20% cases
Septic pedal osteitis
Follows a solar penetration of distal phalanx
Usually nail
Bacteria enters bone and causes osteomyolitis
Sequestrum formation follows
Raised digital pulse
Discharge and pain with hoof testers at site of penetration
Initial radiographs may be normal - ideally radiograph with nail still in place
Manage with poultice, abx, NSAIDs, tetanus antitoxin
Lameness does not resolve - septic pedal osteitis diagnosed on repeat radiographs
Can treat with surgical excision - osteolytic bone removed - hospital plate screwed on so dressing changed every day
Excellent prognosis
Coffin joint OA
Progressive degenerative joint disease of middle/older horses
DIP - low ringbone OA - common, all types of horse, front more than hind
PIP - pastern OA - high ringbone - uncommon, heavier breed, cobs and hunters, hind more than front
Predisposing factors
- Workload - repetitive, faster gait, landing after jumps, hard surface, hoof imbalance, usually LTLH (long toe low heel) with broken back HPA (hoof pastern axis), early life nutrition, previous injury
Concussive forces
Low grade lameness, often bilateral, often insidious but can be sudden
Disease progresses subclinically prior to clinical signs - when threshold of disease is reached
Effusion in coffin joint - 1cm proximal to coronary band on midline
Careful attention to hoof balance and shoeing
Broken back hoof pastern axis
Long toe low heel
Usually sound at walk, mild lame at straight trot
- more obvious on lung with lame on inside of circle, worse on hard ground, moderately positive to distal flexion
PD nerve block - 10-15 mins then reassess
or DIP - coffin joint block- wait only 5 mins to prevent diffusion out of joint
Radiography - may see osteophytes on extensor process of P3 - should be smooth and round
Periosteal new bone where joint capsule joins to pastern where insertion onto p2
May see osteochondral fragmentation at extensor process of p3 - mineralised opacity and periosteal new bone on p2
Treatment
Oral NSAIDs - PBZ, suxibuzone
Intraarticular corticosteroids - triamcinalone, methylprednisolone
6 month duration - could cause laminitis, joint sepsis
Can try hyaluronic acid or polyacrylamide gel (arthromid)
Corrective farriery - LTLH
- shorten toe, rasp back use rolled toe shoe
Support heels - bar shoe, sometimes heel elevation
Add cushioning - rubber pad or sole packing under shoe
Surgery - arthroscopy to remove fragment, debride necrotic tissue - dorsal only
Palmar digital neurectomy
What is the navicular bone
Distal sesamoid bone
- Attached with suspensory collateral ligament
- Impar ligament
- DDFT
What is navicular degeneration
Focal loss of the medullary architecture with medullary sclerosis
Fibrocartilaginous change of the flexor surface of the bone
Traumatic fibrillation of the deep digital flexor tendon which may lead to adhesion formation between the tendon and bone
Enthesiophyte formation on the proximal and distal borders of bone
Diagnosing navicular degeneration
Treatment
Positive response to PDNB
- Typically complete resolution
- lameness switches to other leg
Not definitive to navicular degeneration
Anaesthesia of navicular bursa more specific
- Not done often
- harder
- Requires radiographic guidance and contrast
Lateromedial
DPr - PaDi oblique - 85 o upright navicular
Pa45pr - PaDi oblique skyline
Analgesics - NSAIDs - PBZ
Corrective farriery - wedges, rolled toe, bar shoes
Corticosteroids - triamcinolone, methylprednisolone
Bisphosphonates
Vasodilators
Palmar digital neurectomy - pain relief - but complications - neuroma, catastrophic DDFT breakdown, pedal oesteitis
Management only - no cure
Soft tissue injuries within foot
Some have acute injury and acute history
Some have degenerative pathology and insidious history
Can be unilateral or bilateral
Palpation often unremarkable - Some acute have increased digital pulses apart from severe colateral ligament injuries
Sometimes sensitivity to hoof testers in heel region
Dynamic often unpredictable - usually worse on hard
Usually worse on inside rein
Not usually positive to flexion
Soft tissue injuries within foot
Some have acute injury and acute history
Some have degenerative pathology and insidious history
Can be unilateral or bilateral
Palpation often unremarkable - Some acute have increased digital pulses apart from severe colateral ligament injuries
Sometimes sensitivity to hoof testers in heel region
Dynamic often unpredictable - usually worse on hard
Usually worse on inside rein
Not usually positive to flexion
DDFT pathologies
Core lesions - various severities, different locations along length of tendon, can propagate proximally/distally with time
Sagittal splits - often seen at level of navicular bone, often propagate proximally/distally with time - especially after neurectomy
- Involve tendon surface so can lead to adhesion formation and bursitis
- lameness often severe but very variable
Dorsal border
- Dorsal border fibrillation
- Often causes bursitis and adhesion formation
More of a degenerative pathology rather than acute injury
Navicular bursa treatments
Intrabursal medication - biologics in acute phase
Corticosteroids to manage long term
Navicular bursoscopy - indicated for all lesions seen to communicate with bursa - sagittal splits and dorsal fibrillation particularly
Can break down adhesions surgically
Debride fibrillated tissues - drivers for synovitis
