Lameness Flashcards
DDX for animals presenting with abnormal gaits
* Musculoskeletal pain or dysfunction
* Neurological conditions
* Intra-abdominal pain
* Skin conditions
What are ways musculoskeletal pain may present?
* poor performance, lameness, reluctance to move, recumbency
Components of a lameness exam
* History, examination of the environment, physical exam, examination of the gait, nerve blocks, imaging, the response to treatment
Most common location of lameness in an adult horse?
Foot and affected sites decrease in frequency as we move up the limb…shoulder lameness is very rare.
What is the most common location of lameness in race horses?
* Fetlock and carpal injuries due to high loads generated in these joints in horses travelling at speed (feet problems are also common)
What is the most common cause of lameness in foals? Yearlings?
Septic arthritis or septic osteitis
** septic focus should be assumed until proven otherwise in any lame foal due to the need for aggressive treatment
** In yearlings developmental condtions are the most common cause of musculoskeletal problems (osteochondrosis & subchondral bone cysts)
Exam question tip
* Which diagnostic techniques you will use
* Mention the nerve blocks even if you aren’t going to use them and tell him why you aren’t
Challenges with equine lameness
* often few localising signs
* Accurate diagnosis time consuming (come in the morning, often will come back or refer)
* Diagnostic aids often equivocal (none are stand alone, often have to do more than one, prep client)
Locating source of lameness? Diagnostic techniques?
* Pain and swelling…
* Swelling not associated with pain
* No pain and no swelling
How do we localize the source of pain?
Nerve blocks
How does the stay apparatus affect a lameness exam?
Makes it difficult to localize pain in a horse limb
Diagnostic approach to lameness?
Golden rules of a lameness exam?
History in a lameness exam
* Signalment, duration, onset (associated with work, sudden/ gradual), shoeing, changes with work, response to treatment
Has the owner already tried phenylbutazone? If so, how did it respond?
Clinical exam in a lame horse
- Examine at rest- quiet place (stable), examine the whole horse: symmetry (muscle mass, conformation, feet), swelling (tendons, synovial structures), feet (shoeing, balance, hoof wall, sole, frog quality, must clean out shoe), palpation (joint capsules, tendons and suspensory ligament, muscles, bony prominence e.g. tubera sacrale, flex and extend, hoof testers
- Examine moving- gait eval– straight line, lunge (trot and canter soft ground, hard ground), ridden… which leg is horse unweighting?
- Flexion Tests- may h ave positive flexion tests, difficult to interpret, not specific- fetlock flexion test stresses all lower joints as well as navicular apparatus
- Nerve Blocks- only objective means of localising lameness, time consuming
- Diagnostic imaging
Lameness grading system when trotting!! What do you say when walking?
Mild, moderate or severe when walking
Usual sequence for a pleasure horse for nerve blocks?
* Palmar digital
* Abaxial
* Low 4 point
* Sub carpal
* Median/ulnar
Usual sequence for a racehorse with nerve blocks
* Pastern ring block
* Low 4 point
* Midcarpal joint
* Subcarpal
* Median/ulnar
Show me where you palpate fetlock swelling, midcarpal swelling… etc.
With hoof testers, why unreliable?
* All horses with soft feet will be positive
* All horses with hard feet will be negative
Gait evaluation process
- Determine the lame leg or legs (have to do this first)- which leg is the horse unweighting? Look at the head. Drop the head, neck and forequarter on the non lame limb.
- THEN characterise the lameness– foot flight, length of stride
Worse on the turn and a hard surface?
Generally mean sFoot or pastern problem
What should you look for in terms of gait with hindlimb lameness?
Lift is faster than the drop in the hind quarters… lifts hindquarter on lame limb
** will also look lamb in the ipsilateral forelimb because they use their head as a fulcrum to lift the hind quarters to keep the weight off
What will allow you to evaluate a horse for a longer time when evaluating gait?
on lunge
* Lower limb injuries often worse
What is the problem with flexion tests?
* not specific
* hard to interpret
* many sound horses have positive flexion tests
Pros and cons of nerve blocks? Preferred?
Cons: time consuming, understand limitations
** Regional vs. intra articular– complications uncommon but still severe– painful, more invasive, also don’t know what we are blocking
Appropriate time limits for nerve blocks?
Bigger nerves take longer to block– tibial and peroneal e.g.
What do you need to do with nerve blocks?
Test whether they have worked…. e.g. hoof testers, most horses hate you squeezing suspensory apparatus, skin sensation not a great taste– we aren’t checking the skin
Why different routines for pleasure v. racehorse?
* In practice most common cause of lameness in race horses is carpal lameness… so more efficient
What might you see in a hindlimb bilateral problem?
Bunny hop
What is 1? What occurs here?
Sagittal ridge
* flap and fragment formation tend to occurs at the margin of weight bearing and non weight bearing areas
* the sagittal ridge of MC/MT3
What also occurs here?
flap and fragment formation tend to occurs at the margin of weight bearing and non weight bearing areas
flap and fragment formation tend to occurs at the margin of weight bearing and non weight bearing areas
What occurs here?
flap and fragment formation tend to occurs at the margin of weight bearing and non weight bearing areas
What occurs in regards to the arrow on the cranial side?
Fragmentation– distal intermediate ridge of the tibia in the tarsocrural joint
What is the bottom lines joint? What normally happens here?
fetlock joint where fragmentation of the proximal plantar P1 fragments
What tends to occur here?
Subchondral cysts tend to occur in weight bearing areas such as the medial condyle of the femur in the stifle
What happens on the medial proximal x in the elbow joint?
Subchondral cysts (weight bearing areas)
What happens with the glenoid cavity of the shoulder?
Subchondral cysts (weight bearing areas)
H? And what happens here?
Proximal interphalangeal joint
Subchondral cysts (weight bearing areas)
What is the pastern in a horse?
Consequences of limb trauma in horses
Middle 1/3rd of the MC has no tendon sheath
* Digital tendon sheath on the bottom
Is it okay to lose one extensor tendon in a horse?
Okay to lose one, but more than one–>
Lose extensor function and start knuckling
Remove one extensor tendon for stringhalt
What flexor tendons can be involved in limb injuries in horses?
A really deep one can involve all 3
lose the DDFT- Toe up the in air
lose the suspensory ligament- fetlock sinking
Treatment of tendon injuries
Suture- clean simple transection only
Special suture patterns– locking loop, tendon pulley suture
** in practice rare to get a nice clean simple transection of the tendon
Support:
- extensor tendons– bandage, simple splint, toe extension shoe
- flexor tendons– support bandage, rescue splint, cast, heel extension shoe, raised heel shoe
Prognosis of extensor tendon injuries
* depends on extent of wound
* Open tendon sheaths heal well
* Stringhalt (causing exaggerated bending of the hock) occasional complication in hind limbs
Flexor tendon injury prognosis
** Flexor tendons:
tendon lacerations involving the tendon sheath: poorer prognosis, heal poorly, adhesions between tendon and surrounding sheath which can affect performance (reduced mobility of the leg)
Consequences for synovial structure injury? What is key with this?
* proper diagnosis as early management improves prognosis
Palmar aspect of the fetlock– digital tendon sheath likely involved
coffin joint (pastern?)
Carpal joint- have a feel to see if you can palpate the articular cartilage– if you can feel a tendon, may be in the tendon sheath depending on anatomy– or inject sterile fluid on the other side and if it comes out then you know you are in the joint
affecting navicular bursa
Where is the contrast material?
Digital sheath– synovial structure
Diagnosis of synovial injuries in horses
Treatment of synovial injury in a horse
* Aggressive early treatment will improve prognosis (more aggressive than if the joint was not involved)
* Open well draining wounds better than small puncture wounds– often the little ones you have to worry more about then the big ugly open wound
* Debridement, lavage, broad spectrum antibiotics (penicillin + gentimycin), monitor carefully
** Casting will assist healing
What is a possible sequelae if synovial structures are involved in an injury? What are some causes?
Septic synovitis
(haematogenous in foals)
Clinical signs of septic synovitis
Severe lameness and swelling
Tarsocrural joint
Septic synovitis
Echogenic fluid (normal synovial fluid is anechoic- black)
Definitive diagnosis septic synovitis
* Culture- positive only in 50% of cases (because lots of means of synovial fluid to stop bacterial growth)
* Fluid directly into blood culture
** NO bacteria does not mean it is not infected!!!
Treatment for septic synovitis
IV antibiotics of the leg with a tourniquette
* Intra-articular to get very high levels and easier
(systemic antibiotics: penicillin + gentamycin)
Causes of luxation
Diagnosis of luxations
Treatment of luxations
Fetlock
Prognosis guarded due to infection and often develop OA
What don’t you use to diagnose a fracture in a horse limb?
* nerve blocks
* Diagnosis based on clinical examination and radiographs
Diagnosis of fractures in proximal limb
** scintigraphy won’t be positive for a week because not yet increased osteoblastic activity
Emergency treatment in the field for a fracture
* Analgesics, sedation (low dose), stabilise the leg
Cannon bone fracture
Stablisation of fractures
Helps prevent anxiety as well
Stablisation of distal metacarpus and below
Stabilisation from midmetacarpus to distal radius
Stablising fractures of mid to proximal metatarsus
Stabilisation of fractures of mid to proximal radius
Stabilisation of mid to proximal tibia (common in a young horse)
Stabilisation of more proximal fractures?
Cannot be stabilised
Transportation of a horse with a fracture
Prognosis of fractures in a horse
What does circumferential wire injury often cause?
Avascular necrosis– wire has cut off the blood supply therefore delayed sloughing of tissue distal to the injury
* early diagnosis is challenging because they all have cold limbs, all have some vasoconstriction
** usually just treat and warn the owners
* Flow phase scintigraphy can help but generally wait and see
Where horses have no alternative other than to graze oxalate dominant plants in pasture, what do you need to do? What are symptoms of too much oxalate?
Provide supplements of calcium and phosphorous as well as vitamins A & D to counteract the reduced uptake of available calcium from the feed
* shifting intermittent lameness, failure of young horses to grow to expected height… advanced: fractures of pelvic bones, ribs and splint bones, spinal column collapse and hind limb in-coordination
** Big head– swollen forehead, nasal and jaw bones, loose teeth, inability to chew food, distortion of the nose and noisy breathing due to restricted nasal passages
What are good sources of Ca if horses are consuming grain as well?
* Lucerne hay or molasses
Horses on diets high in cereal grains (including bread), tropical grasses containing oxalates (e.g. kikuyu, panicum)– what can happen?
High serum phosphate antagonises serum Ca2+–> low Ca2+ stimulates PTH–> Ca2+ resorbed from bone–>nutritional secondary hyperparathyroidism–> osteodystrophia fibrosa e.g. big head in a pony or shifting lameness
How can we assess secondary nutritional hyperparathyroidism?
* Urinary P excretion… compare urein: serum % of phosphorous and creatinine (baseline metabolite that the kidney doesn’t reabsorb)
How much calcium do you need to add to a diet to fix Ca:P ratio?
Grazing animal diet
* Enough energy, protein, Ca, sunlight, Cu
* Ca: P balance especially with cereal supplements
How can nutrition affect lameness?
Three presentations of osteochondrosis
- Flap and fragment formation
- Fragmentation alone
- Subchondral bone cysts
Where do flap and fragments occur of osteochondrosis? Predilection sites?
Where does fragmentation occur?
Where do subchondral cysts occur? Predilection sites?
Pathogenesis of osteochondrosis
Pathogenesis of OC with diet
Retained cartilage
Flap and fragment formation in OC
Lumped under OC because young growing horses at particular predilection sites
3 most common sites in the tarsus of OC in order of frequency
Three most common sites in the stifle of OC
Most common sites in the fetlock of OC
Most common sites of OC in the shoulder
Most common sites of subchondral bone cysts
Presentation of OC
* Swelling (except not in shoulder joint because covered in muscle)
Presentation of subchondral bone cysts
* swelling less obvious: medial FT joint swelling
Shortened cranial phase of stride
Proximal limb lameness
Lameness in OC?
Young horse presenting shortened cranial stride phase, no foot abscess, no obvious trauma…
suspect shoulder OCD
Diagnosis of OCD
Conservative Treatment of OCD
* Restrict exercise
* Restrict diet
* Monitor radiographically
Surgical treatment of OCD
* Removal of osteochondral fragments
* Debridement of subchondral cystic lesions
Stifle osteochondrosis swelling in a yearling, very common presentation (occasionally an older horse)
** can ID lateral because the medial has the big prominence where the stay apparatus hooks
Treatment stifle osteochondrosis
has to be the tarsal crural joint because of the amount of swelling
tarsal sheath never swells cranially
fragmentation of the distal lateral trochlear ridge
Tarsal Osteochondrosis treatment
Fetlock OC
Ununited plantar eminence P1- fetlock osteochondrosis
Presentation of shoulder osteochondrosis
end up lame because swelling isn’t obvious enough early on
Treatment for subchondral bone cysts
If corticosteroids do not work (once or twice)–> surgical debridement (intra-articular, extra-articular…. arthrodesis)
What is arthodesis?
Arthrodesis, also known as artificial ankylosis or syndesis, is the artificial induction of joint ossification between two bones by surgery. This is done to relieve intractable pain in a joint which cannot be managed by pain medication, splints, or other normally indicated treatments.
Prognosis of subchondral bone cysts
Problem with lower limb trauma
“proud flesh”- exuberant granulation tissue
Laceration to lower limb tx
* Suture- rarely successful without casting
* open wound
* Most substances placed on wounds delay healing– as little as possible
* Initially: reduce bacteria numbers, stimulate granulation tissue–> debride and lavage
* When wound has granulated– inhibit granulation tissue with pressure from a cast (bandage only provides pressure for a very short while) and topical corticosteroids (rub in 2 x daily), remove excessive granulation tissue (excise= cut it off, topical caustic substances- copper sulphate, which affects epithelialisation however)
what encourages excessive granulation tissue?
Excessive granulation tissue DDX
Sarcoid
What is required for epithelialisation?
* Level granulation tissue bed required
* easily traumatised
What do you need for skin grafting?
Punch grafting easiest
- donor site = neck
- biopsy punch
- immobilise limb
* Complications
- subcutaneous emphysema
- elbow joint sepsis (avoid with penicillin and gentamycin instead of just penicillin, if elbow is involved)
** uncommon as nice open wounds that drain well
What structures can heel wounds affect?
DIP= distal interphalangeal joint
* Difficult to determine extent of wound without surgical exploration
* field: sedate the horse, abaxial nerve blocks, if finger goes in more than a few centimeters– then recommend sending the horse off
Heel wound treatment
* Debridement: under GA, extensive debridement of collateral cartilage
* debride and ligate digital vessels
* sharp sectioning of nerve (blunt sectioning could result with a neuroma)
* Synovial structures involved– then inject sterile fluid at remote site to see if it comes out of the wound to see if it is involved– if it does then you need to flush the synovial structure to remove foreign material + bacteria
Injured coronary band
* Careful apposition
* large mattress sutures through skin and subcutaneous tissue
Heel wounds aftercare
* restriction of exercise e.g. confined to a yard
Complications in heel wounds
Quittor- infection of the collateral cartilages
Puncture wounds of the foot can affect which structures
Problem because not as open, important to determine which structures involved– serious injuries: navicular bursa, DIP joint, digital sheath
Diagnosis of puncture wound foot injury in a horse
* Determine which structures are involved
* Careful trimming of sole/frog
* Radiograph- plain, sterile probe and take a radiograph, contrast material
* You can also try and collect synovial fluid to see if a synovial structure is involved– if we can’t collect fluid– can put saline in and see if it runs out the hole
Treatment of puncture wounds in a foot
Pedal bone– debride, curette pedal bone (healthy pedal bone is hard to remove, whereas unhealthy is soft)
- bandage initially
- hospital plate (keeps it dry and clean)
** once it has filled in with hard horn you can stop bandaging it
Prognosis of puncture wounds that involve the pedal bone
* Good prognosis but healing is long
Treatment if navicular bursa is involved
* street nail procedure– problem defect in DDFT resulting in serious complications
* Arthroscopic debridement is the modern treatment– instrument through wound
* Broad spectrum antibiotics– locally intrathecal, intravenous perfusion
* Elevate heel
* hospital plate
Prognosis with involvement of navicular bursa
Expensive with guarded prognosis
Interosseous ligament aka suspensory ligament
name the bones that sit within the hoof capsule (below the coronary band)
Clinical exam of the hoof
* Shape and symmetry
* Shoeing
* Pulse over the sesamoid bones- struggling to feel is what we want
* Coronary band– injuries or swelling
* hoof testers- looking for a painful response, keep going and come back to it– to ensure they aren’t just playing up that there was actually focal pain
* hoof knife- clean it up to see defects, bruising
* Swelling around the pastern, sometimes even the fetlock can be associated with the foot as the foot can’t swell
* most foot problems are worse on a hard surface
After clinical exam of the hoof, what is the next step likely?
Nerve blocks
What nerve are you aiming to block
Don’t want to block the pastern joint, problem is the local diffuses
* sole, heel, hoof capsule, etc.
Pink?
Joint also blocks the palmar digital nerve, but you don’t block the heel as you’re not getting the branch
Pink?
Foot preparation for imaging in the foot
* Radiography, ultrasonography, scintigraphy, MRI, CT, arthroscopy
(pack sulci with playdo)
Radiographic views of the hoof
* Standing lateromedial
- foot on block
- beam centered on solar surface of pedal bone
- parallel to bulbs of the heels (since horse may stand toe in for example)
* Standing dorsopalmar
- assessment of lateromedial balance
* Upright pedal bone
- pedal bone exposure
- navicular bone exposure
* Obliques- important for fractures
* Skyline navicular bone
- assess flexor surface
- corticomedullarly junction
Problems with ultrasound with the hoof? What is it good for?
What is scintigraphy good for with hooves?
* determine significance of radiographic changes
* detect bone pathology not observed on RGs
Best uses of CT in hoof problems
* Better definition of bone changes
* Contrast allows visualisation of blood flow in the foot
MRI uses in the hoof
3 names for this bone
* Coffin bone, P3, pedal bone
Arthroscopy in the hoof good for?
History? Exam? Diagnosis? DDX? Treatment?
*History: sudden onset usually not associated with work, severe lameness, distal limb swelling
* Exam: increased digital pulse, pain on hoof testers
* Diagnosis: positive palmar digical, abaxial sesamoid nerve block; no changes on radiographs (pus similar density to hoof wall, can see air but not pus), purulent material localised
** DDX: Fracture, acute subsolar bruise, synovial sepsis, laminitis
* Treatment: drain abscess, NSAIDs (pain relief), if unable to drain: poultice (softens the foot easier to work with next time, common thought that it helps drain the abscess by soaking up moisture but unlikely), reexamine… failure to improve? P3 osteitis, keratoma, synovial structure
** if they are not getting better and keep recurring: abscesses generally don’t form next to the pedal bone– should not keep reforming– might be in the bone due to laminitis– sometimes have to remove part of the bone to actually resolve the problem
Chronic bruising growing out in the picture
* HIstory: acute: sudden onset with work, no localising signs (may not see it at all if it has black feet); chronic- insidious onset/ recurring lameness, no localising signs
* Exam: often poor conformation– thin flat soles, collapsed heels…. increased digital pulse due to chronic or acute inflammation in the foot, +/- pain on application of hoof testers
** Increase the sole depth to protect the bottom of the foot
* Diagnosis: positive response to palmar digital nerve block, no changes on radiograph, scintigraphy– increased uptake of radiopharmaceutical at pedal bone solar margin
If it becomes really chronic and causes changes
Big things to remember about foot lameness in horses
* Breakdown of bond between hoof wall and laminae- basement membrane
* Pedal bone sinking
* Pedal bone rotation
* Compromised blood supply from pressure of the pedal bone
Causes of laminitis
* in ponies associated with
- systemic disease
** lush pasture
** equine metabolic syndrome
** PPID
Clinical signs of laminitis
* Increased digital pulse
* Tachycardia
* pain on hoof testers
* Lameness: quadralateral, bilateral forelimb, bilateral hindlimb (less common)… reluctant to move, leaning back, short stepping
* Indentation of coronary band (if pedal bone sinks or rotates)
* Chronic hoof changes (dropped sole, non-parallel rings)
* sinking– bigger gap between hoof wall and pedal bone
* gas lines- lamina is weak and breaks down
* pedal bone modelling, lysis
Management of laminitis
* Acute
- treat cause
- prevent mediators accessing laminae (cold therapy, only effective early)
- pain relief (NSAIDs– phenylbutazone)
- minimize P3 movement (restrict exercise- box confinement, deep bedding, sand, sole support, cast, DDF tenotomy)
Chronic laminitis management
* generally collapsed sole around the tip of the pedal bone– the most painful area when they bear weight on it
* Only trim if pedal bone is stable (if unstable and you try this, the horse will become more uncomfortable, so you can try trimming just a little): trim the sole from the point of the frog back and remove excess toe– don’t want to remove any of the sole in front of the frog because you want to protect the tip of the pedal bone with as much sole as possible
* improve blood flow to coronary band
* Remove necrotic tissue: pedal bone (debride, large amount can be removed successfully), laminae
* Shoeing– only when pedal bone stable, elevate painful areas of sole
** Diet: maintenance, good quality feed, do not starve
Prognosis in laminitis
* how quickly the pedal bone stabilizes – even with a lot of rotation, pedal bone can still stabilize
Causes of navicular disease
Pathogenesis of navicular disease
Diagnosis?
* navicular bursa block- most specific block you can do
* Radiograph changes only seen when disease is advanced– flexor surface skyline view
* Ultrasound- may observe bursa effusion (not that useful)
* Scintigraphy- increased uptake of radiopharmaceutical in navicular bone, non specific
* MRI- DDF tendon lesions, more sensitive for bone lesions
* Bursoscopy– not usually for diagnosis but if you want to consider a procedure– assess fibrocartilage, surface injury to DDF tendon
Swelling above the fetlock could mean?
An injury may be on the pastern because it could be affecting the digital sheath which runs the whole way
How do you diagnose a pastern or fetlock problem?
* worse on the lunge and hard surfaces
Palmar digital nerve– try to do it low enough that you avoid blocking the proximal interphalangeal joint (will block DIP joint and it does block PIP joing a lot)
* Intra-articular nerve blocks another possibility– DIP and PIP- not as specific
* Radiography– lateromedial, dorsopalmar, flexed oblique
* Ultrasound– useful for palmar soft tissue structures– always indicated with digital sheath swelling, more difficult in metacarpal area…. collateral ligaments of both PIP and DIP
* Scintigraphy useful for stress fractures– esp P1 or OA
12 yo eventer
Right Forelimb lamness worse when lunged to the right (pastern or foot)
* Blocks to palmar digital (can’t rule out pastern joint)
* radiographs- nothing
** later– navicular bursa block with a 30% improvement (not helpful….partial block of a tendon that spans a large part of the leg OR multiple problems)
* Scintigrpahy– uptake medial pedal bone and navicular bone
* MRI would have been great for this
* Ultrasound both legs
collateral ligament injury of DIP joint
** collateral ligament attaches to P2 and P3
BUT two problems
DIP joint Ringbone
PIP joint Ringbone
PIP joint diagnosis:
- local analgesia
- radiographs– unreliable unless condition is advanced, ID of fractures, cysts is helpful; scintigraphy
* TX: intra-articular medication, arthrodesis
Subchondral bone injury
Pathogenesis of subchondral bone injury
* area of condyle that articulates with sesamoid
* subchondral bone modelling in response to training
subchondral bone injury under electron microscopy
* 1st one is normal horse
* 2nd is race horse
* 3 subchondral bone
* 4 resting for weeks turning over subchondral bone
start off with subchondral bone cartilage–> collapse of underlying subchondral bone–> cartilage erosion–> secondary degenerative changes
Diagnosis of subchondral bone injury
* Local analgesia– plantar metatarsal nerve block
** SCINTIGRAPHY BETTER THAN XRAY– diagnostic in combination with nerve block
(MRI is good for diagnosis shows lysis in white– darker area is sclerosis)
Synovial structures in the tarsus?
Bony prominences of the tarsus?
Tendons and ligaments in the tarsus?
Clinical examination of tarsus
*Swelling
- tarsocrural joint
- tarsal sheath
- calcaneal bursa
- extra-synovial
* Pain on flexion
- only severe inflammatory disease or injury
* Flexion test: not specific, fetlock and stifle problems often positive
Bone Spavin Treatment
Radiographs NAD
U/S- tarsocrural joint effusion… tarsal sheath– synovial swelling
Calcaneal bursa NAD
Next step- collect fluid and send to the lab
* Tarsocrural arthrocentesis- cell count 1.5 x 10^9/L… 60% Neutrophils….. not convinced this is sepsis but wouldn’t rule it out
Next time:
* Surgical exploration- we find that tarsal sheath open– the wound went straight in
* RG again 7 days later and find lysis on the bone
* tarsal sheath is overtly infected– lots of swelling all over the place not just over the tarsal sheath
… kick broken the skin, damaged the bone, after 7 days enough lysis that we have a bony lesion under the sheath– big problem…. debrided this…
* Multiple synovial structures
* Radiographs unreliable for distal joints
Joint compartments in the stifle
Soft tissue structures in the stifle
Boney prominences of the stifle
Clinical examination of the stifle
* Examine for swelling:
- femoropatellar joint
- medial femortibial joint
* Palpate patellar ligaments
* Flexion test- may have pain on flexion
Stifle osteochondrosis
Stifle osteochondrosis
Diagnosis of stifle osteochondrosis
Treatment of stifle osteochondrosis
Hindlimb lameness sudden onset
* Examine carefully for swelling
If no effusion:
* Intra articular nerve block to localise
Pain on flexion is useful but not specific for stifle.
* Significant soft tissue injuries may have no changes on radiographs
Pelvic injury challenges? What do you assess (clinical exam)?
* however if it has been going on for a long time you will get muscle atrophy… examine pelvic symmetry
* Rectal exam e.g. haematomas with acute fractures
* Diagnostic analgesia: Sacroiliac joint, sacroiliac ligaments
* Radiography– need GA
* U/S- assessment of ligaments and muscles, bony surface of pelvis
* Scintigraphy- pelvic fractures, hip joints
** Bottom line: difficult to assess clinically… easily examined rectally and ultrasound… some acetabular fractures you need to go to x-ray
* what does not fit foot abscess?
* What is something else you might worry about in a race horse?
* Do we nerve block it?
* Assess at the trot not overly lame
* Hoof testers- no reaction
* Trainer requested fetlock radiographs NAD
* PD mild improvement, abaxial– 70% improvement (therefore definitely in the foot)… you might have expected that PD would block it but we did have some improvement.
* Does not necessarily fit foot abscess because it hasn’t improved over 4 weeks
* You might also worry about stress fracture of the condylar, split P1 (vertical fracture common in race horses)
* Nerve block could be dangerous if it is a stress fracture but it is 4 weeks later so probably not
* Pedal bone fracture
Why perfuse watery diarrhoea? (MOA) What could happen?
Acidosis- SI is not able to digest all of the starch–> getting through to the caecum–> bacterial overgrowth producing lactic acid–> osmotic effect producing watery diarrhoea
* acidity could wear away the mucosa and allow toxins into the blood stream
** bacteria can change a thousand fold in a few hours
** bacteria fermenting the starch in the hindgut and growing– it is not those toxins that will cause the horse to be sick, it will be the endotoxic from the gram negative bacteria that will wear away the endothelial lining and allow the endotoxin into the blood stream
* few hours later, horse reluctant to walk out of his stable, especially onto hard concrete surface
* Stiff gait at walk; turns with great difficulty
* A forefoot can be lifted off the ground with difficulty
** affecting all 4 feet
* lameness progressively worse, uncomfortable to stand, hoof heat, “bounding” digital pulses
WHAT CAN YOU DO??
* you can give them hay to keep things moving along
* if it just happened, you could try virginiamycin but unlikely to help because it would come behind the start
Classic laminitic stance
What is happening in acute laminitis?
** laminae are supporting the whole weight of the horse
–> severe laminitis pulling apart of the dermis from the epidermis and rotation of the pedal bone
Pathogenesis of acute laminitis?
Basement membrane is the glue that holds the epidermis to the dermis
** all about the epithelial cells and their attachment to the basement membrane and what causes them to pull apart
*caused by inflammation (gram negative endotoxins– sepsis/ septicaemia type situation) and enzyme activation– epithelial cells secrete enzymes normally but if they secrete excess it chews away the membrane
* rotated pedal bone, distance between top of the hoof wall and pedal bone– hole hoof has sunk– happens frequently sinking and rotation
* so sore he can’t stand up
Acute laminitis
Prevention of acute laminitis
*First Aim: STABILISE: Support the frog– relieving loading on the toe (glue on shoes or styrofoam pads and duct tape, deep sand optimal surface)
* Icing the feet
- effects on blood flow
- prevents reperfusion injury
- inhibition of enzymes
* Anti-inflammatories/ analgesics
- e.g. phenylbutazone
- Novel analgesics (gabapentin)
* Vasodilators - ACE promazine (out of favor these days)
* matrix metalloproteinase (MMP) inhibitors - none currently available
Sequence of events in acute laminitis
* 15% of all ponies in Australia have had laminitis at some point in their lives– ponies aren’t adapted to a high sugar diet
* good doer - aka easy keeper
* Obel grade 3 laminitis (grade 4 can’t walk, grade 5 recumbent)
HOW IS THIS DIFFERENT TO ACUTE LAMINITIS?
** these cases tend not to over rotate
* can be managed
How does grass cause laminitis? Who is predisposed?
Equine Metabolic Syndrome
* High amounts of sugar
* fructan carbs are the storage type of carbs
* Stimulate insulin response– it is actually insulin that causes laminitis in this situation
* Ponies; some horse breeds
* insulin dysregulation
* obesity
* Abnormal fat deposition- nuchal ligament
* Laminitis predisposition
Breed susceptible to laminitis
* bred to survive in harsh conditions… metabolically extremely efficient (storing fat well, etc.)
Fed horses a meal containing glucose
* ponies and andalusians were getting a massive swing in insulin
What causes chronic laminitis?
Insulin
** high concentrations will trigger laminitis but mechanisms are unknown– causes the epithelial cells to proliferate and letting go of the membrane
Case management of chronic laminitis
* Weight loss: can soak hay to leach out water soluble carbohydrates… OR poor quality hay (but with mineral supplement then) & EXERCISE
* analgesics and NSAID’s
* Will be okay in a few days… but it will be a recurring problem if the animal is on grass… a lot of work.
** grazing muzzle- can still get to grass but less
* OR restricted access to grazing (dirt yard)
* Low GI diet– no grain
What happens down the track with chronic laminitis?
* Correct orientation of hoof capsule in relation to distal phalanx (P3)
* Allow well bonded lamellae to grow down from coronary band region
What are the two forms of laminitis?
Horse carpal valgus
What fold increase do horses blood flow increase to the muscles during moderate exercise? How do horses cool? How is increased blood flow achieved?
Horses are inefficient coolers– rely on evap from sweat
Heat from contracting muscle conducted to the skin by the blood– fluid evaps on the skin and removes heat from the body
** lose a lot of electrolytes in their sweat
Thermoregulation of a horse
Blood volume and hydration during exercise
What is rhabdomyolysis? Non-exertional rhabdomyolysis? Exertional rhabdomyolysis?
Causes of non-exertional rhabdomyolysis
* nutritional- vitamin E and/or Se deficiencies
* Toxicities- ionophores, coffeeweed (Cassia occidentalis), white snakeroot
* Traumatic
What is atypical myopathy?
What is exertional rhabdomyolysis? Types?
How many cases of Sporadic Exertional Rhabdomyolysis will horses have? What are the inciting/ predisposing factors?
What is Chronic exertional rhabdomyolysis? Predisposing/ inciting factors?
When does chronic exertional rhabdo occur?
What are the types of chronic exertional rhabdo?
What is recurrent exertional rhabdo?
* Recurrent episodes of muscle stiffness, sweating and reluctance to move
* occurs most commonly in young THB, STB and arabian racing fillies as they begin race training
* Intrinsic muscle abnormality–> defect in muscle contraction
* Speculated that calcium handling by muscle cell SR is abnormal
What is Polysaccharide Storage Myopathy (PSSM)? Who does it occur in?
* Glycogen accumulation is a result of increased production–> rather than impaired glycogen breakdown
* Glycogen in affected animals is slightly different from that found in normal animals–> less branched
* Mutation is GYS1 gene of QH–> encodes glycogen synthase
* Functional analysis has revealed that GS activity is increased in horses with mutation
- mutation causes gain of function of the GYS1 gene
- enhanced activity and/or poor regulation of the mutant enzyme
- cause of rhabdo in PSSM is unclear– likely related to some defect in energy metabolism
General diagnosis of ER
Typical clinical signs of Sporadic Exertional Rhabdo
Changes in CK and AST compared to each other over time after single insult in Rhabdo
** CK of 5,000 is normal– but 10,000s or 100,000s or more not normal!
Typical clinical findings of Polysaccharide Storage Myopathy
Typical clinical signs and history in Recurrent Exertional Rhabdomyolysis
Prognosis of ER
After diagnosing ER, what do you need to consider straight away?
Treatment of severe, acute rhabdo
Management of Chronic Rhabdomyolysis
Where is the inferior check ligament in relation to SDFT and DDFT?
In the metacarpal region, what causes swelling?
Palpation weight bearing clinical exam of the metacarpal area
Palpation of the metacarpus non-weight bearing, where would you expect to see pain even in a normal horse?
Lameness localised to the metacarpus is likely?
What can you do in the metacarpus for diagnosis? (rarely done)
What will an intra-articular mid carpal block also block?
What radiographic views would you use for diagnosis of metacarpal injury?
What would you use U/S for in a metacarpal injury?
Assessment of palmar soft tissue structures
Assess each structure from proximal to distal
Echogenicity and fibre alignment assessed
- normal echogenicity
- hypoechoic
- anechoic
* cross sectional area
- compare with contralateral limb
- normal SDFT hourglass shape
Indications for scintigraphy in the metacarpal region?
Pathogenesis of digital flexor tendonitis
* tendon repair
- type I collagen replaced with type II
- well aligned fibres replaced with poorly aligned fibres
- increased tendon cross sectional area
- recurrence generally occurs at junction of normal and repaired tendon
Clinical signs of supf digital flexor tendonitis
- swelling and pain on palpation
- lameness mild or none
Acute findings on U/S in supf digital flexor tendonitis
DDFT is always a bit brighter
U/S findings in chronic tendon injuries
** also get a mottled appearance– but increased cross sectional area
Look at it longitudinally– poor fibre alignment
Treatement of digital flexor tendonitis
* Initial rest and anti-inflammatories
* controlled exercise program
** problem with superior check ligament desmotomy– increases risk of suspensory ligament injury so it has gone out of favor
* Body and branch lesions
- predominantly TB and SB race horses
- TBs forelimbs
- SBs forelimb and hindlimb
- pain and swelling
- lameness variable
U/S findings of suspensory ligament desmitis
always check splint bone
Suspensory ligament desmitis Treatment
* 6- 12 months for most horses to come right
Proximal suspensory desmitis
Diagnosis of proximal suspensory desmitis
Treatment of proximal suspensory desmitis?
Prognosis?
Prognosis of forelimb is good, hindlimb is poor
* shockwave therapy is hit or miss
* fasciotomy and neurectomy– surrounded by splint bones
Treatment of splint bone fractures
Likely diagnosis in shin soreness
Rarely presented to vets
most young horses get it and are spelled for 6 weeks
occasionally recurrent
occasionally stress fractures– may progress to stress fractures (common in the states where they race on dirt a lot)
Palmar digital -ve
Abaxial -ve
Low 4 pt mild improvement
Subcarpal 50% improvement
Median/ulnar mild LF lameness
** RG carpus and proximal metacarpus- NAD
** U/S proximal suspensory ligament- bony protrusion in suspensory origin and associated hypoechoic lesion
Proximal suspensory desmitis
- no swelling
- local analgesia
** improvements in multiple nerve blocks = either multiple problems or a problem that is spanning the whole region
Reasons for carpus injury
Synovial structures associated with the carpal joint
bones associated with midcarpal joint
bones associated with antebrachiocarpal joint
Pathophysiology of carpus injuries
* Joint in extension throughout stance phase
* Modelling of subchondral bone in response to exercise– sclerosis of third carpal bone; chip fracture; slab fracture
* Failure of subchondral bone to adapt to increased stress
- subchondral bone necrosis
- chip fracture
- slab fracture
Clinical exam of carpus
* OR lateral swelling– carpal sheath, antebrachiocarpal joint
* Flexion test- limited use; pain on flexion useful
* Lameness- often bilateral; mild lameness– chip fracture OA; marked lameness– significant pathology
Diagnostic analgesia of the carpsu
Radiography views to take of the carpus? Two most common places for carpal injury?
flexed lateral view shown much better than a standing lateral– separates radial carpal bone from intermediate carpal bone
distal radial carpal bone
proximal intermediate
Skyline of 3rd carpal bone
U/S findings in carpal injuries
Scintigraphy diagnostic imaging in carpus injuries
Uses of arthroscopy in carpus injuries
* need to remove chip fractures– therefore arthroscopy is common
* Nerve blocks- pastern ring block- no response
* Low 4 point- no response
* midcarpal joint block– changes to right front lame– carpal problems are often bilateral problems
** subtle mottling of 3rd carpal bone– if unsure CT but overkill
** Could arthroscope if money wasn’t a problem– but just time off
What do you do first?
* 3/5 is alarming– severity
* Possible slab fracture or something else nasty
* 1– radiograph because you don’t want to block the horse if he has a decent fracture
** in a racehorse a skyline is mandatory
** will need to get our arthroscope in there and tidy up
Clinical exam of the shoudler
** could see– hardly bring leg past the vertical
Diagnostic analgesia of the shoulder
Radiography- views of the shoudler?
Scintigraphy views with a shoulder injury
U/S– structures you can assess?
Conditions of the shoulder
Conditions of the elbow
Dropped elbow appearance
Clinical exam of the elbow? Diagnostic analgesia?
* Intra-articular
Radiography views of an elbow injury
Scintigraphy used for what in elbow injuries
Treatment of ulnar fractures
Knee angular limb deformities usually? Fetlock usually?
Pastern flexural deformity
Pastern? flexural deformity
Types of congenital flexural deformity? Angular deformity?
Pathogenesis of acquired flexural deformity? Angular?
How does an acquired angular limb deformity occur?
Pathogenesis of acquired flexoral limb deformity?
Clinical assessment
OR acquired
* age, radiographs
Management of acquired flexural deformity
Angular deformity from growth plate
- confinement, maintain foot balance, lateral/medial extension, surgery (growth acceleration– periosteal strip OR growth retardation– bridge growth plate)
- foot extension- to side want limb to deviate to
Osteochrondosis
- angular deformity from growth plate
- foot extension to side want limb to deviate
* knee
- 8-20 degrees- periosteal strip
- > 20 degrees- physeal bridge
- prognosis guarded if angle greater than 25 degrees
What is this? Management? Joint affected?
* Angular deformity from growth plate
- fetlock
5-8 degrees- periosteal strip
>8 degrees- physeal bridge
prognosis guarded if angle greater than 12 degrees
Management of tendon laxity
Management of congenital flexural deformities
Management of acquired flexural deformities
* Tetracycline
- 3 grams IV
- large dose
- warn owners potential for side effects
Surgical management of flexural deformities
Crank on the leg and feel which tendon is tightest during surgery
* most commonly inferior check ligament desmotomy
** Check ligament desmotomy– must combine with aggressive reshaping of foot
Management of carpal flexural deformities
Management of pastern flexural deformity
* splinting
* Inferior check ligament desmotomy
Most common cause of lameness in foals
Presentation of septic arthritis
DDX- owners may think mare stood on foal but rare– tend to assume is septic joint
How do you make a definitive diagnosis of septic arthritis?
Treatment of septic arthritis? Prognosis?
Prognosis- guarded if bone involved
Take aways for angular limb deformity
Take aways for flexural limb deformity
Take aways for septic arthritis/ osteomyelitis
When you palpate back pain, what could this mean?
Axial skeleton? How many cervical? Thoracic? Lumbar?
C- 7, T- 18, L-6
Sacroiliac joint cartilage?
Ligaments of the sacroiliac joint?
Biomechanics of the axial skeleton
Biomechanics of the sacroiliac joint
Horse back pathology, is it important?
poor relationship between pathology and pain
Diagnostic analgesia to assess back pain?
Only objective means of assessing back pain
* Local injection– dorsal spinous processes, sacroiliac region
* Dorsal SI ligament- local infusion
OR
* SI joint– regional analgesia; Peri-articular
Radiography of dorsal spinous processes? Cd lumbar spine? SI region?
* different exposures required– facet joints (seen in RG here)
** Can’t assess caudal lumbar spine or sacroiliac region
Scintigraphy of the spine
DDX of sacroiliac pain
The only way to know for sure is blocking out– block structures separately dorsal SI ligaments, SI articulation
Back pain take aways
When do you use ultrasound for horses?
Monitoring healing in tendon/ muscle injuries using U/S
Rhabdomyolysis
Limitations of Scintigraphy
Uses of CT
Limitations of equine CT
Equine Condylar Fracture
Foal osteomyelitis
Equine MRI
MRI Equine Foot
