Horses 3 Flashcards
Locating source of lameness what are the 3 main presentations and what to do
1. Pain and swelling • Tendon injury and septic arthritis • NO NERVE BLOCK -> ultrasound to confirm -> WILL BE LAME ON BOTH SOFT AND HARD SURFACE 2. Swelling not associated with pain • Effusion in joint, tendon sheath swelling 3. No pain no swelling • Most common • Pain but nothing externally
What are the 5 main diagnostic techniques and what good for
- Radiography - cheap, easily available
○ Osteoarthritis -> osteophytes present, arthritic change -> BUT IS IT CAUSING THE ISSUE? - Ultrasound - soft tissue but can only image small areas at the time - miss the pathology
○ To ultrasound the whole limb can take days -> NOT A GOOD SCREENING MODALITY - CT - soft tissue but same as ultrasound -> only small areas
- MRI
- Scintigraphy - highly sensitive and can do the whole limb
○ Show lots of hot spots but how do we know which is important
Golden rules for lameness diagnostic
- Allow plenty of time - can take hours and days
- Follow a routine
- Avoid cutting corners
- Use nerve blocks
What are the 6 main steps in the diagnostic approach
1) history
2) clinical examination
3) diagnostic analgesia
4) imaging
5) further diagnostic analgesia
6) response to therapy
History with lameness examination
○ Signalment § Race horses different to hobby horses § Ponies -> laminitis ○ Duration ○ Onset § Associated with work § Sudden/gradual ○ Shoeing § Often if recent will be the issue ○ Changes with work § Often gets worse with work ○ Response to treatment
What are the main aspects of the clinical examination in a lamness examination
Observe and palpate
1) examine at rest
2) examine moving (gait)
3) flexion test
clinical examination lameness what are the general steps
i. Observe □ Symmetry - need to get the horse to stand square ® Muscle mass ® Conformation ® Feet □ Swelling ® Synovial structures □ Feet ® Shoeing and Balance ii. Palpate □ Joint capsules □ Tendons and suspensory ligament □ Muscles □ Bony prominences iii. Flex and extend - NOT FLEXION TEST □ Testing for -Range of motion, Pain iv. Hoof testers □ Apply across hoof wall and sole, frog □ Repeatability, unreliable - soft feet false +ve, hard feet false -ve
What is involved with the lameness examination at rest and moving (gait)
○ Examine at rest § Quiet confined area - important § Examine whole horse - all the legs ○ Examine moving (gait) § Straight line - walk, trot § Lung - walk, trot, canter □ Soft and hard surfaces □ Allows more time to examine lameness □ Lower limb problems often worse § Ridden - some lameness only observed when ridden § Tips □ Keep it simple □ Take your time □ Practice
What are the 3 steps in giat examination for lameness and describe
- Determine the lame legs or legs - ALWAYS STEP 1
® Which leg is the horse unweighting
◊ Forelimbs -> head, forequarter drops of the non-lame limb
} Subtle lameness may not have head nod looks at forequarter
◊ Hindlimbs -> lifts hindquarter on lame limb
} Look at the midline at base of tail will go up higher when on lame limb
◊ Lower limb issues generally don’t like turning and worse on hard lunge - Characterise the lameness
® Foot flight
® Length of stride - Lameness grade
0 – no lameness
1 – subtle lameness - no real head bob
2 – obvious consistent lameness - can tell straight away
3 – pronounced unweighting
4 – severe lameness, difficult to trot
5 – non weightbearing
What is involved with an objective assessment of lameness
□ Inertial sensors -> lameness locator - sensor on head and rump
□ Measure asymmetry, allows objective comparison over time and between nerve blocks
Again not always the best with subtle lameness
What is involved with flexion tests, which joint and how to perform
§ Following joints
□ Fetlocks
□ Carpi
□ Hindlimbs
§ Hold flexed for 1 minute then trot off
§ Difficult to interpret
Many sound horses have positive flexion tests
Nerve block what does it do, types and what time needed to give
§ Only objective means of determining site of pain § Types □ Regional -> preferred □ Intra-articular ® Pain may be extra-articular ® More invasive - needle in synovial structure risk of infection or reaction ® More proximal limbs have to do here § Allow appropriate time □ Lower limb - 10 and 30mins □ Upper limb - 20 and 40mins □ Intraarticular 5-10mins □ Why you don't want to do too many in the field -> have to stay there
How to test for adequate anaglesia with nerve block and which nerve blocks for pleasure and racehorse
□ Deep pain
® Hoof testers
® Suspensory palpation
® Skin sensation - may not be the best indicator
Pleasure horse
1. palmar digital 2. abaxial 3. low 4 point 4. subcarpal 5. median/ulnar
Racehorse
1. pastern ring block 2. low 4 point 3. midcarpal 4. subcarpal 5. median/ulna
Carpus what also called, bones in proximal and distal row and the synovial structures
(knee)
Bones
Knee
- Proximal row -> (medial to lateral) -> radial, intermediate, ulnar and accessory
- Distal row -> first to forth carpal bones
○ The first is small and inconstant
Synovial structures
- Carpal sheath - surrounds both the superficial and deep digital flexor tendon as they pass the carpus
- Extensor tendon sheaths
What are the 3 joints in the carpus and the pouches with how high motion
- Antebrachiocarpal joint (radiocarpal) -> high motion joint so will be able to feel
○ Palmar pouch - lateral aspect immediate palmar to the radius and proximal to accessory carpal bone - Mid carpal joint -> high motion joint so will be able to feel
- Carpometacarpal joint -> low motion joint so won’t be able to feel (communicates with mid-carpal joint)
Fetlock synovial structures and joint with pouches
Synovial structures
- Digital sheath - contains the deep digital and superficial digital flexor tendons as they pass the fetlock joint
○ Swelling will be palmar to the suspensory ligament and dorsal to the flexor tendons
Joints
- Metacarpo-phalangeal joint - has dorsal and palmar pouches
○ Palmar pouch -> between the third metacarpal bone and suspensory branch - most commonly see swelling here first
§ Common injuries -> suspensory branch tears, sesamoid fractures, palmar osteochondral disease
○ Dorsal pouch -> either side of the sagittal ridge of the third metacarpal bone -> swelling when more severe
Pastern what joint and its pouch
- Proximal interphalangeal joint - a small dorsal pouch with large palmar pouch between branches of SDFT and P1
What is the main synovial structures in the hoof and pouches and the joint with its pouches
- Navicular bursa - lies between the DDFT and the navicular bone
○ Proximal pouch - proximally on the dorsal aspect of the DDFT
○ Lateral and medial pouches - can be penetrated by deep wounds to the heel
Joints
1. Coffin joint (distal interphalangeal joint) - lies mostly within joint capsule
○ Dorsal pouch - extends above the coronary band axially 2cm
○ Palmar pouch - immediately dorsal to palmar pouch of navicular bursa
Palmar digital nerve block what nerve blocking, what blocks and how to perform
blocking the palmar digital nerve - 2mls
○ Blocks -> whole sole, all the foot and the contents EXCEPT for the dorsal coronary band
a. Left thumb is placed on the ergot and is pulled proximally to tense the ligaments of the ergot which passes distally to the collateral cartilages - palpate these
b. Injection site is the intersection of the collateral cartilage and the palmar aspect of the pastern
Pastern ring block what nerve blocked, what blocks and how to perform
palmar digital nerve and its dorsal branch
○ Blocks -> whole foot and distal and proximal interphalangeal joint
a. Blocked mid pastern where the palmar digital nerve comes out from under the ligament of the ergot
b. 2 ml is injected at this site and needle is partially withdrawn and redirected dorsally injecting slowly as needle is pushed to expand the subcutaneous space
c. Another 2ml is deposited dorsal to the first injection site to block the dorsal branch
Abaxial sesamoid nerve block what nerve blocks, what blocks and how to perform
palmar nerve - 2-3mls
○ Blocks -> whole foot, distal and proximal interphalangeal joint, proximal sesamoid bones
a. Palmar vein, artery and nerve are palpated on the abaxial surface of the sesamoid bone and the needle is placed parallel and immediately palmar to them
Low four point nerve block what nerve block, what blocks and how to perform
palmar and palmar metacarpal nerves are blocked
○ Blocks -> mid metacarpus all the way down to the hoof
a. Block palmar nerve are blocked mid metacarpus in the groove between the suspensory ligament and the flexor tendon
b. Palmar metacarpal nerve are then blocked where they emerge from under the buttons of the splint bones -> proximally to hit the button of the splint bone
Subcarpal nerve block what nerve block, what blocks and how to perform
lateral palmar metacarpal nerve
○ Blocks -> metacarpal bone
a. The level of injection just below the level of the carpometacarpal joint where the flexor tendons are pushed axially and needle passes axial to the splint bone to hit palmar aspect of the metacarpus at its junction to splint bone
b. 3ml injects at both lateral and medial sites
How to perform nerve block in the distal interphalangeal joint
- dorsal pouch of the joint (above the coronary band of the midline)
a. Horse weight bearing on the limb with needle placed axially 10mm above coronary band, perpendicular to the skin, passed through common digital flexor tendon and onto dorsal aspect of P2
b. If unable to inject withdraw slightly until fluid goes in easily
c. Inject 5mls of local anaesthetic
How to perform nerve block in the proximal interphalangeal joint and fetlock joint
Proximal interphalangeal joint
a. Palpate the V formed by the lateral branch of the SDFT and the palmar aspect of P1, the depression in the distal part of this V is the injection site
b. Pass needle axially and slightly distally so you hit palmar aspect of P1 -> should be nearly full length of needle
Fetlock joint
a. Place a needle between the lateral proximal sesamoid bone and the third metacarpal bone with the limb flexed
How to perform nerve block in digital sheath and midcarpal and antebrachiocarpal joint
Digital sheath
a. Method involves passing a needle along the abaxial surface of a proximal sesamoid bone
Midcarpal and Antebrachiocarpal joints
a. Flex the limb and place the needle either lateral or medial indentation either side of the extensor carpi radialis tendon
b. Pass needle until you hit the cartilage
Stifle what are the 3 joints, how interact and palpate
- Femoropatellar joint - swelling can be palpable between and overlying the patellar ligaments
- Medial femorotibial joint - palpated medial to the medial patellar ligament and cranial to medial collateral ligament
- Lateral femorotibial joint - deep so generally not possible to palpate swelling
What is the stay apparatus of the hindlimb and the 3 things it consists of
The stay apparatus is defined as the combination of structures, and especially the elastic tendons and ligaments, which allow horses to rest while standing up -> passively support the trunk against gravity
- Horse limb can only undergo extension and flexion -> resisted by the stay apparatus
Consists of :
1. medial patellar ligament
2. reciprocal apparatus - (ties the movement of the hock and the stifle together so reciprocal movement occurs ○ (SDFT (superficial digital extensor tendon) +peroneus tertius (from the region of the extensor fossa of femur down to metatarsus))
3. suspensory apparatus (interoessweous ligament)
Tarsus (hock joint) what bones are present
- Proximal row -> talus (has trochlea that articulate with cochlea of tibia) and calcaneus (sustentaculum tali -> DDFT)
- Middle row -> central tarsal bone
- Distal row -> tarsal bones 1-4 of which the first and second are fused, third rests on large metatarsal bone and forth is lateral and projects proximally into the level of the middle row
What are the 4 joints in the tarsus joint and where sweling
- Tarsocrural joint - largest joint space and only one that will notice swelling from
○ Swelling noticed on the dorsal aspect -> medial and lateral to extensor tendons and palmar aspect -> between calcaneus and the tibia laterally and medially - Proximal intertarsal joint - communicate with tarsocrural joint -> Don’t need to block separately
- Distal intertarsal joint - very small
- Tarsometatarsal joint -
Syonvial structure and ligaments and tendons within the tarsus
Synovial structures
- Tarsal sheath - through which the DDFT runs
○ Swelling is seen cranial, lateral and medial to the gastrocnemius and SFT tendons
- Calcaneal bursa - SDFT runs within
Ligaments and tendons
- Superficial and deep digital flexor tendons
- Plantar ligament - calcaneus to head of 2nd metatarsal bone
- Collateral ligaments - either side of tarsal joint
What are the different nerve blocks with the tarsus compared to carpus
- Similar to forelimb
1. Palmar digital block - same
2. Pastern ring block - same
3. Abaxial sesamoid block - same
4. Low 6-point block - slightly different
5. Subtarsal block - similar
What tendons run the palmar aspect of the distal hindlimb and how does their shape change as move distally
Green -> superficial digital flexor tendon
- As move distally it becomes more bow shaped as become thinner
Blue -> deep digital flexor tendon
- As move distally it becomes more rounded and larger
Yellow -> Inferior check ligament (Accessory ligament of the deep digital flexor tendon)
- As move distally merges into the deep digital flexor tendon
Red -> interosseous ligament (suspensory ligament)
As move distally the ligament splits into medial and lateral as insert onto sesamoids
For lameness exam what is involved with clinical examination of the hoof
- Shape and symmetry ○ Collapsed heel (hoof almost parallel to surface), upright feet - Shoeing - Digital pulse - Coronary band Test with: - Hoof testers - Hoof knife ○ Need to remove stuff from the bottom of the Swelling - Hoof capsule rigid - Often pushed up limb
For hoof lamness what is important with the gait examination
- Surfaces most foot pain worse on hard surface
- Usually also worse on the turn -> lunging
What are the 3 nerve block that are important for hoof lameness
1) palmar digital nerve block
2) distal interphalangeal joint block
3) navicular bursa block
Radiography of hoof lameness, what is important for foot preparation and the 5 main views and why
○ Foot preparation - IMPORTANT
§ Remove shoes
§ Remove debris
§ Dress foot
§ Pack sulci within the frog - playdo to prevent shadows from the grooves
○ Views
1) Lateromedial - place metal onto hoof to determine slope
2) sanding dorsopalmar - assessment of balance
3) upright pedal bone - navicular and pedal bone exposure
4) obliques - fractures
5) skyline of navicular bone
Ultrasound and schintigraphy for hoof lameness what can examine
○ Limited by hoof capsule
○ Dorsal
§ DIP joint, collateral ligaments of DIP joint
○ Palmar
§ DDF tendon, navicular bursa
Scintigraphy
○ Phases
§ Flow phase - from circulation into soft tissue
§ Pool (soft tissue) - coming out of the tissues
§ Bone phase - just within the bone
○ Determine significance of radiographic changes
○ Detect bone pathology not observed on radiographs
MRI and CT and Athroscopy for hoof lameness what good to examine
MRI and CT
○ Best method for investigation of soft tissues within the foot
○ Only definitive method for diagnosis of DDF tendon lesions
○ Good for bone sequestra especially of pedal bones
Arthroscopy
○ Synovial structures
§ Distal interphalangeal joint
Navicular bursa
What are the 7 main conditions of the foot/hoof
- Subsolar abscess
- Subsolar bruising
- Pedal bone osteitis
- Laminitis
- Navicular disease
- Quittor
- Pedal bone fracture
Subsolar abscess what is it, when common, history and examination
- Infection in subsolar tissue
- More common during wet conditions
History - Sudden onset usually not associated with work
- Severe lameness
- Distal limb swelling
Examination - Severe lameness
- Increased digital pulse
- Pain on hoof testers
Subsolar abscess diagnosis and differential diagnosis
- Positive palmar digital, abaxial sesamoid nerve block - not the first option but if unsure can do
○ There may be swelling up the leg but caused by the focus of infection in the hoof
○ If swelling up the leg but nerve blocked to the hoof -> take off shoe and examine foot - No changes on radiographs
○ Except if draining may see a gas line out of the hoof - Purulent material localised
Differential diagnosis - Fracture
- Acute subsolar bruise - hard to differentiate but just blood not puss (not infected)
- Synovial sepsis
- Laminitis
Subsolar abscess treatment and what if don’t resolve
- Drain abscess - dig in the foot and find the puss
- NSAIDs
- NO ANTIBIOTICS -> want the abscess to come to a head and break down - contraindicated
- If unable to drain
○ Poultice and re-examine in a few days
§ Poultice helps soften the hoof and easier to dig, also abscess may grow and come out on its own at this point - Make sure tetanus is up to date if deep within the hoof
Failure to improve -> should be comfortable in a week
○ CANNOT IGNORE -> very painful and can lead to further issues
○ P3 osteitis
○ Keratoma
○ Synovial structure infected
Subsolar bruising what caused by and general history
- Trauma to solar soft tissues
- May be single event or repeated concussion
History - Acute
○ Sudden onset associated with work
○ No localising signs - Chronic
○ Insidious onset/recurring lameness
○ No localising signs
Subsolar bruising examination and diagnosis
Examination - Conformation ○ Thin flat soles ○ Collapsed heels - Increased digital pulse - Pain on application of hoof testers - Bruising only observed in white feet Diagnosis - Positive response to palmar digital nerve block - No changes on radiographs - Scintigraphy ○ Increased uptake of radiopharmaceutical at pedal bone solar margin
Pedal osteitis what is it and radigraph importance
- Subsolar bruising involving the distal phalanx
- Can miss with an overexposed X-ray
Laminitis results from and results in
- Inflammation of the laminae
- Exact cause unknown
○ insulin - Results from -> Breakdown of bond between hoof wall and laminae
○ Basement membrane - Results in ->
○ Pedal bone sinking
○ Pedal bone rotation
○ Compromised blood supply in the dorsal area of the hoof
What is laminitis associated with in horses and ponies
In horses associated with: - Systemic disease ○ Endometritis ○ Colitis ○ Grain overload ○ Equine cushings disease (PPID) ○ Equine metabolic syndrome - Excessive weight bearing - from injury with the other foot - Corticosteroid administration In ponies associated with: - Systemic disease ○ Lush pasture ○ Equine metabolic syndrome ○ Equine cushings disease (PPID)
What are the clinical signs associated with laminitis and radiography changes
- Increased digital pulse
- Tachycardia
- Pain on hoof testers
- Lameness
○ Location
§ Quadralateral - usually
§ Bilateral forelimb
§ Bilateral hindlimb
○ Reluctant to move
○ Leaning back
○ Short stepping - Indentation of coronary band
○ Can place fingers within the indentation - Chronic hoof changes
○ Dropped sole
○ Non-parallel rings
Radiography - Pedal bone
○ Sinking
○ Rotation
○ Gas lines - resulting from separation on dorsal wall
Pedal bone modelling, lysis
What is involved with management of acute cases of laminitis
○ Treat cause ○ Pain relief - NSAIDS ○ Minimise P3 movement § Restrict exercise - box confinement, deep bedding sand -> want them to lie down § Sole support - Cast § DDF tenotomy ○ Cold therapy § Prevents mediators accessing laminae § Only effective early - use prophylactically § Involved lots of labour - 24 hour monitoring ○ Sole support § Dental impression material § High density foam § Wedge to reduce tension on DDFT ○ DDF tenotomy - incise § The thing that is causing the pedal bone to rotate § Salvage procedure § May not improve long term survival
Management of laminitis in chronic cases
○ Assume the pedal bone is now stable in its new position ○ Maintain alignment of P3 ○ Prevent weight bearing on sole § Trim the sole from the frog backwards - also improves blood low § Constant management issue ○ Improve blood flow to coronary band ○ Remove necrotic tissue § Pedal bone, laminae □ Pedal bone generally soft so if hard - dead ○ Shoeing § Only when pedal bone stable § Elevate painful areas of sole § Types of shoes □ Reverse shoe, Heart bar shoes ○ Diet § Maintenance § Good quality feed § Do not starve
Prognosis for laminits what does and doesn’t depend on
- Depends on: ○ Extent of tissue necrosis ○ Stabilisation of P3 - Not dependent on: ○ Degree of rotation
Navicular disease what is it and how easy to diagnose and causes
- Degenerative condition of the flexor surface of the navicular bone
- Difficult diagnosis
○ Be cautious when reading the literature
§ Case definition often poor
Causes - Repeated loading
- Single traumatic event
- DDF tendon strain
- Sepsis
Navicular disease pathogensis, history and clinical findings
Pathogenesis - Horse unweights heel by DDFT contraction - Results in greater pressures on navicular bone -> further degeneration History - Variable - Classic ○ Gradual onset ○ Bilateral forelimb lameness - Clinical findings ○ Variable ○ Unilateral or bilateral Foot conformation variable -> low or high foot conformation
Navicular disease gait examination and diagnostic anaglesia positive to
- Gait examination ○ Often worse on lunge ○ Often worse on hard surface ○ Flexion test positive - Diagnostic analgesia positive to: ○ Palmar digital ○ Intra-articular DIP joint block ○ Navicular bursa block
Navicular disease imaging findings
○ Radiography § Changes only when disease is advanced § Flexor surface skyline view - cystic structures ○ Ultrasound § May observe bursa effusion ○ Scintigraphy § Increased uptake of radiopharmaceutical in navicular bone § Non specific ○ MRI - most useful § DDF tendon lesions § More sensitive for bone lesions -> look at changes in navicular bone itself ○ Bursoscopy § Assess fibrocarilage § Surface injury to DDF tendon
Navicular disease treatment
- Remove pain
○ NSAIDS, intra-thecal corticosteroids, neurectomy - Improve foot balance -> conformational changes, shoeing
○ Lateromedial balance
§ Move centre of pressure palmarly (backwards) -> take pressure off navicular bursa - Antiarthritic drugs
- Bisphosphonates?
Infammatory acute laminitis pathogensis and what is the general first presentation
grain overload
- How occurs -> ferment starch in caecum -> lactic acid produced will result in breakdown of the caecal wall allowing other toxins produced to get into the mucosa and access to blood stream -> changes in blood flow
○ Possible toxin includes matrix metalloproteinases -> produced in the hoof and respondible for breakdwn of basement membrane resulting in causing sinking and rotation
First presentation - profuse watery diarrhoea
What is teh clinical progression of inflammatory acute laminitis
- Dehydrated, PCV 50
- Responded to 20L normal saline IV
- Heart rate mildly elevated, peaked at 60
- Diarrhoea transient, reducing in severity
- Few hours later, horse reluctant to walk out of his stable, especially onto hard concrete surface
- Stiff gait at the walk; turns with great difficulty
- A forefoot can be lifted off the ground with difficulty
- Lameness progressively worse
- Uncomfortable to stand
- Hoof heat
- ‘bounding’ digital pulses
What occurs to the foot during acute laminitis
- Breakdown of hoof wall tissues -> laminae coming apart
○ Histopathology -> movement and pulling away of the secondary laminae from the basement membrane
○ Also inflammation, apoptosis and enzymatic breakdown of the basement membrane
§ Separation of basement membrane from epidermal epithelial cells - Rotation of pedal bone away from the hoof wall
- Unstable leg
Outcome of acute lamnitis
- Sinker - palpable depression at coronary band
- Recumbent
POOR PROGNOSIS - - euthanise - need to prevent this from occurring
Management of acute laminitis what phase can occur and what need to do
at the developmental phase
- Minimise acute phase to prevent mechanical collapse
ONCE MECHANICAL COLLAPSE -> so severe that cannot do much
Management
- Already significant structural damage to laminar bonds – even if just grade 1 or 2
- Very fragile
- Damage limitation
1) First aim: STABILISE
○ Frog support -> relieving loading on the toe
§ Shoes that provide extra frog support
§ Place on sand -> goes up in the gaps and support around sand
2) Icing feet - 2-3 days
○ Effects on blood flow
○ Prevents reperfusion injury and Inhibition of enzymes
3) Anti inflammatories/analgesics
○ e.g. phenylbutazone
○ Novel analgesics (gabapentin)
4) Vasodilators - NOT GIVEN NOW
Endocrinopathic laminitis pathogensis
eating grass - insulin
- Generally in spring time -> lush pasture
How does grass cause laminitis ?
- Fructan carbohydrates -> Hindgut fermentation BUT also foregut and NOT ENOUGH metabolism at this point to change the pH of the gut enough to result in wall damage and sepsis -> DIFFERENT TO ABOVE
- Fructans plus simple sugars plus amino acids: = Insulin response - the issue here
Why do some horse/ponies get laminitis while others don’t, 5 reasons
- Ponies; some horse breeds
○ Pony breeds:
§ Shetlands, Welsh, New Forest, Dartmoor, Exmoor, Connemara, etc..
○ Horse breeds:
§ Andalusians, Paso Finos, Tennessee Walkers, Morgans, Spanish Mustang, some Quarterhorses
- Metabolically efficient: ‘good doers’; ‘easy keepers’
§ Ancient relatives -> western Europe in the sparse harsh environments
§ Thoroughbreds and standardbreds -> eastern Europe -> different metabolism so less effective - Insulin dysregulation
- Insulin itself can cause laminitis - Obesity
- Abnormal fat deposition - crusty neck
- Laminitis predisposition
What is the effect of insulin on lamellae
- Frequent mitotic figures are a feature of insulin affected lamellae
- Insulin has a proliferative effect
- Results in stretching of lamellae and eventual breakdown - weakening -> exact mechanism unknown
- Possible -> Insulin acting like IGF -> resulting in increased growth of epidermal lamellar basal epithelial cells
Chronic laminitis ongoing management
1) Correct orientation of hoof capsule in relation to distal phalanx (P3)
- Allow well bonded lamellae to grow down from coronary band region
- Loss of use -> months - years maybe permanently - PREVENTION OF THIS
2) Restricted access to grass- Dirt yard; grazing muzzle
3) Antibiotics?
- Founderguard
4) Low GI diet
- No grain
5) Weight loss - control insulin and obesity in the equine metabolic syndrome
- Soak hay; 1.25 – 1.5% bwt (DM) /day
§ Careful not doing it too rapidly as can lead to hyperlipidaemia
- Exercise -> may be beneficial but diet the best
What problems may arise with chronic laminitis if it isn’t treated properly
- Damaged lamellae don’t re-attach
- Ongoing instability
- Attempt at healing with excess keratin laid down
- forms a wedge
- Hoof wall continues to grow apart from the vascular dermis
- Compromised blood supply
Pastern lameness where possible swelling and response to flexion test
Swelling ○ Distal interphalangeal joint § Dorsal coronary band ○ Proximal interphalangeal joint § Synovial distension rarely recognised § Firm periarticular swelling common ○ Distal palmar soft tissue structures § Injury to flexor tendons results in swelling of digital sheath § Distal sesamoidean ligaments rarely recognised Flexion tests ○ Generally positive for flexion test
Pastern lameness lameness when worse and diagnostic anaglesia
Lameness ○ Often worse on hard surface and on lunge Diagnostic analgesia ○ Regional nerve blocks § Palmar digital nerve block § Pastern ring block § Abaxial nerve block ○ Intra-articular nerve blocks § Distal interphalangeal joint Proximal interphalangeal joint
Pastern lameness diagnostic imaging which use, why and views
- Radiography
○ Often negative particularly down lower limb
○ Views
§ Lateromedial
§ Dorsopalmar
§ Flexed obliques - Ultrasound
○ Assessment of palmar soft tissue structures
§ Always indicated with digital sheath swelling
§ More difficult than metacarpal area
○ Collateral ligaments - Scintigraphy - not common
○ Stress fractures
○ Osteoarthritis of distal and proximal interphalangeal joints
ringbone what is it and the 3 locations present, which more common and associated with
- Osteoarthritis with associated periosteal bone production on phalanges
- Fibrous and then bony thickening
1) Low-DIP joint
§ Not common
§ Often associated with intra-articular fractures or collateral ligament injury
§ Difficult to differentiate from other foot conditions due to poor specificity of IA (intra-articular) block
2) High-PIP joint
§ More common
§ Chronic low grade lameness
§ Young horses –subchondral cystic lesions, fractures
§ Mature horses –chronic degenerative condition
3) Non-articular - bony proliferation on pastern that isn’t associated with a joint
Not common
Ringbone in proximal interphalangeal joint diagnosis and treatment
§ Diagnosis □ Local analgesia □ Radiographs ® Unreliable unless condition advanced ® Identification of fractures, cysts □ Scintigraphy § Treatment □ Intra-articular medication □ Arthrodesis
Pastern fractures most common types in the proximal phalanx and middle what most common in
Proximal ○ Sagittal § Racing injury § Short fracture –chronic lameness § Long fracture –acute lameness ○ Comminuted § All types of horses § Can be repaired if a single strut of bone identified Osteoarthritis if can’t reconstruct joint surfaces Middle phalanx ○ Sport horse injury ○ Palmar process fractures ○ Comminuted most common ○ Treatment § Arthrodesis - going to end up with osteoarthritis anyway
Fetlock most important diagnostic technique and general examination for lameness
- Diagnosis difficult without local analgesia Examination 1. Swelling ○ May be none ○ Differentiate joint and digital sheath ○ Suspensory branch desmitis 2. Palpation ○ Suspensory ligament desmitis § Localised swelling and pain 3. Pain on flexion ○ Positive flexion test -> need a really good response to be worried about this injury
Fetlock lameness diagnostic analgesia what use
○ Regional § Abaxial □ May block sesamoids § Low 4 point - everything down - certain ○ Intraarticular - less common § Via collateral ligament of sesamoid
Fetlock lameness diagnostic imaging radiograph what views ad interpretation
§ Views 1) Lateromedial 2) Dorsopalmar-elevate 10 ® Lift sesamoids away from the joint - easier to see 3) Obliques ® Elevate 10°forelimbs ® Elevate 35°hindlimbs ◊ Separate base of sesamoids to P1 4) Flexed lateromedial 5) Highlight plantar aspect of condyle ® Elevated oblique ® Dorsopalmar with leg forward § Interpretation □ Challenging -> Significant pathology with no radiographic changes
fetlock lameness ulrasound what examine and scintigraphy
○ Ultrasound § Suspensory ligament branches - useful for this § Synovium □ Dorsal synovial pad § Digital sheath □ Annular ligament □ Flexor tendons ○ Scintigraphy § Useful for Subchondral bone injury § Increased uptake in lateral condyle of hind fetlock normal in race horses
Subchondral bone injury when commonly occur, where commonly occur and pathogenesis
- Under diagnosed condition of racehorses
○ After horse been resting going back to high intensity training
○ OR new race horse training -> need to ease them into training when young - Lateral condyle in hindlimbs
- Medial and lateral condyles in forelimbs
- Pathogenesis
○ Occurs in area of condyle that articulates with sesamoid
○ Subchondral bone modelling in response to training
Subchondral bone injury what makes diagnosis difficult and the diagnosis techniques
No localising signs - rarely swelling - CHALLENGING
○ Local analgesia
§ Plantar metatarsal nerve block - button of the splint bone block
□ Low 4 point
○ Radiographs
§ Flexed extended limb view
§ Dorsolateral elevated oblique - separates sesamoid away from condyle
§ Majority no changes
○ Scintigraphy
§ Diagnostic in combination with local analgesia -> if not seeing much on radiograph
○ MRI - not necessary
Subchondral bone injury treatment
○ 3 months rest minimum - more severe 6 months
§ Longer the better
○ Most race again but performance often compromised
○ Poor prognosis if recurs or RG changes
Metacarpus how to differentiate the tendons, palpation weight and non-weight bearing and structures feeling for
§ SDFT - sharp edges § DDFT - rounded edges § SL - > Body and Branch ○ Weight bearing § Dorsal aspect of MC3 § Swelling of palmar soft tissue structures § Effusion in tendon sheaths ○ Non weight bearing § Flexor tendons not painful § Interosseous body - normally painful § Interosseous branches (around the fetlock) - not painful
Metacarpus injuries what structures result in what level of lameness
○ Tendon injuries § Often not lame - if lame substantial injury § Lameness indicates significant injury ○ Suspensory injuries § Mild lameness □ Branch lesions □ Forelimb body lesions § More severe lameness □ Proximal suspensory □ Hindlimb body lesions
Metacarpus lameness diagnostic analgesia when needed and which perform
○ Rarely needed if swelling present - palpation is good for identifying pain
○ No swelling
§ Subcarpal/tarsal block following low 4 point
§ Ulnar or tibial block
§ Intra-articular nerve blocks
□ Need to be aware that intra-articular midcarpal block may also block proximal suspensory ligament
Metacarpus lameness what are the 3 diagnostic imaging, what views, how asses and which best
1) Radiography
§ Views
□ Lateromedial
□ Dorsopalmar
□ Obliques - important for splint bones
2) Ultrasound - BEST FOR TENDON INJURIES
§ Assessment of palmar soft tissue structures
§ Assess each structure from proximal to distal
§ Echogenicity and fibre alignment assessed
□ Normal echogenicity
□ Hypoechoic
□ Anechoic
§ Measure Cross-sectional area -> generally enlarged if issue
□ Compare with contralateral limb
□ Normal SDFT hourglass shape
3) Scintigraphy - would go for ultrasound first
§ Indications
□ Lameness localised to site but no radiographic changes
□ Assessing the significance of radiographic changes
Superficial digital flexor tendonitis how common, which limb and clinical signs
- Common injury of racing horses, eventers
- High recurrence rate
- Predominantly forelimb
- Many treatments but little evidence of efficacy
Clinical signs - Swelling and pain on palpation
- Lameness mild or none
- Locations
○ Most mid metacarpus - no swelling of either sheath at this point
○ Distal injuries - digital sheath swelling
○ Proximal injuries - carpal sheath swelling
Superficial digial flexor tendon pathogensis
- Limited collagen turnover in adult tendon
○ Fatigue failure of collagen fibres occurs with repetitive loading
§ Higher strain leads to lower number of cycles to failure - Once injured -> Tendon repair
○ Type I collagen replaced with type II - NO TYPE 1
○ Well aligned fibres replaced with poorly aligned fibres
○ Increased tendon cross sectional area - typical scar - lifelong thickened tendon
○ Recurrence generally occurs at junction of normal and repaired tendon
§ Due to increased stiffness at injury leaving a difference in stiffness at junction
-> stress concertation at this points
Superficial digital flexor tendonitis ultrasound changes with acute and chronic
- Acute
○ Hypoechoic core lesion
○ Hypoechoic peripheral lesion -> if injury on the periphery
○ Mottled hypo-echogenicity
○ Increased cross-sectional area - measure is important - Chronic
○ Core lesions persist with gradual increase in echogenicity
○ Focal areas of increased echogenicity
○ Poor fibre alignment
Superficial digital flexor tendonitis treatment options and which are best
- Initial rest and anti-inflammatories
- Controlled exercise programme
- Other treatment options - not much evidence on these
a. Superior check ligament desmotomy -> check ligament associated with superficial digital flexor tendon
§ Thought to reduce risk of injury, but increase risk of superficial tendon injury
b. Stem cells -> some evidence
c. Platelet rich plasma -> little evidence
d. Shockwave therapy -> improve initial but no evidence to improve long term injury
Suspensory ligament desmitis what are the 4 main locations
1) proximal suspensory
2) body of suspensory
3) branch of suspensory
4) distal sesamoidean
Proximal suspensory desmitis what horses present within, localising signs, which limb poorer prognosis and diagnosis techniques
○ All types of horses
○ No localising signs - very different to other tendon injuries
○ Forelimb and hindlimb
§ Hindlimb poorer prognosis
○ Diagnosis
§ Subcarpal/subtarsal block
§ Scintigraphy - only if bone is involved will get positive -> if only tendon no response
§ Radiographs - chronic changes
□ To determine whether painful or old -> nerve block
§ Ultrasound
MRI - some cases only visible here
Proximal suspensory desmitis treatment and prognosis
○ Treatment
i. 3 months rest - only if going to get better
ii. Shockwave therapy - some benefit
iii. Fasciotomy +/- neurectomy - most common
□ Cutting fascia over back of proximal suspensory
iv. Stem cells - no evidence
○ Prognosis
§ Forelimbs – good
Hindlimbs – poor - surgery straight away for this one
Body and branch suspensory desmitis what horse most common in, localising signs, ultrasound and treatment
○ Predominantly TB and SB race horses § TBs-forelimbs § SBs-forelimb and hindlimb ○ Pain and swelling ○ Lameness variable ○ Ultrasound § Core lesions § Diffuse lesions ○ May have concurrent splint bone fracture ○ Treatment § Initial rest followed by controlled exercise § Prognosis poor in TBs, fair in SBs □ Some SBs can continue racing with low grade branch lesion
Splint bone fractures common cause and treatment
- Common traumatic injury
○ Oblique RG of metacarpus/metatarsus
§ Swelling following trauma
§ Open injuries - osteomyelitis
Treatment - Amputation - depending on the bone involved
○ MT4 - whole bone - lateral splint bone in hindlimb
○ MC2 - distal half - medial splint bone in forelimb -> anymore may become unstable
○ Others - distal 2/3 - Removal of greater amounts requires stabilisation of proximal fragment
Internal or external fixation may be needed -> plate and screws
Dorsal metacarpal disease what also called, what results in, is it commonly seen at veterinary clinics
Shin soreness
- Pain over dorsal aspect of MC3 due to rapid periosteal bone production
○ Adaptation to training
- Rarely presented to veterinarians - trainers generally aware, diagnose and treat
○ Most young horses spelled for 6 weeks
- Occasionally recurrent -> veterinarian then called
○ May progress to stress fracture - need to rule out in these cases -> detailed radiographs needed
