Equine Fetlock and Metacarpus/tarsus

Question 1

what is the fetlock made up of? (bones)

Answer 1

1. distal MC/MT III
2. proximal first phalanx
3. proximal sesamoids

Question 2

describe the synovial cavity/joint capsule of the fetlock

Answer 2

a single synovial space extending approx 5-7cm proximal to joint surface just below joint surface on the palmar surface

dorsally, extends from just above sagittal ridge to just below the joint surface;

dorsally, a bilobed synovial pad is located along the dorsal proximal articular border

Question 3

describe the soft tissues of the fetlock

Answer 3

1. med and lat collateral ligaments
2. med and lat sesamoidean ligaments
3. SDFT and DDFT
4. suspensory branches: number 1 supporting structure of fetlock joint
5. distal sesamoidean ligaments: continuation of suspensory = hella important
6. intersesamoidean ligament

Question 4

describe blood supply of fetlock and innervation

Answer 4

1. medial and lateral palmar/plantar
2. med and lat palm/plant MC/MT

same but for nerves

Question 5

what are the 3 categories associated with traumatic/degenerative causes of disease to the fetlock

Answer 5

1. acute or repetitive overload injuries
   -capsulitis/synovitis
   -chronic proliferative synovitis
   -subchondral bone disease
   -sesamoiditis
   -OA
   -all build on each other, start with top and if dont treat will keep moving through list
2. articular fragmentation: traumatic and developmental
   -dorsal
   -palmar/plantar fragmentation
   -proximal sesamoidean fragmentation
   -sagittal ridge fragmentation (OCD/developmental)
3. articular fractures
   -condylar fractures
   -proximal phalanx fractures
   -proximal sesamoid fractures: unfit/unconditioned horse = soft tissues weak and bone is strong, but as train and get stronger, ST strong and bone weak

Question 6

describe capsulitis/synovitis; include diagnosis and treatment

Answer 6

1. common, esp in younger horses
2. heat, effusion, positive to flexion
3. subtle lameness that may subside once warmed up
4. onset with increased workload
5. untreated = chronic thickening, effusion, reduced ROM, and poor performance

diagnosis: based on clinical exam; palpate effusion in fetlock, rads not super helpful would just see soft tissue thickening in front and back of joint but helpful to xray anyway just to check for other injuries
-ultrasound: can see how thick joint capsule is

treatment: REST is most important! but if can’t rest or take off work, meds
1. rest and training adjustment
2. non-steroidal medication
3. topical anti-inflammatories: diclofenac sodium (surpass)
4. intra-articular therapy:
-hyaluronan
-HA + steroids
-biologics
5. oral or injectable therapy:
-glucosamines, chondroitin sulfates
-polysulfated GAGs

Question 7

describe chronic proliferative synovitis; including clinical signs

Answer 7

1. villonodular disease
2. repetitive trauma to dorsal aspect of fetlock joint through hyperextension leads to inflammation and thickening of the normal synovial pad and eventually chronic fibrosis of pad

clinical signs:
1. heat, effusion, positive to distal limb flexion
2. focal thickening of dorsal aspect to joint distal to capsular attachments

Question 8

describe diagnosis and treatment of chronic proliferative synovitis

Answer 8

diagnosis:
1. clinical exam
2 low palmar nerve block or IA anesthesia
3. radiographs:
-soft tissue thickening over dorsal joint
-bone resorption on dorsal aspect of distal MCIII proximal sagittal ridge
4. contrast arthrogram: filling defect
5. US: marked thickening of pad overlying dorsal aspect of MCIII

treatment:
1. rest and reduced training
2. NAIDs: often not as effective
3. aggressive IA therapy: HA, HA + steroids, biologics, repeat therapy
4. failed medical mgmt = arthroscopic excision of pad
5. commonly concurrent articular disease like OA

Question 9

describe subchondral bone injury; include 2 common sites of injury

Answer 9

1. palmar osteochondral disease (PODS)
2. common in any horse that works hard for a living; more in front limbs than hindlimbs
3. seen on front medial condyle or hind lateral condyle
4. variable degrees of lameness based on stage of disease; may not see typical signs of fetlock disease
5. very important to recognize and dx early before irreversible cartilage damage

common sites of injury:
1. distal palmar MCIII: possible focal overload injury at point of impact from base of prox sesamoids during maximal weight bearing
2. proximal phalanx under central articular surfaces

Question 10

describe diagnosis of subchondral bone injury (7)

Answer 10

1. clinical exam
2. low palmar nerve block
3. medial and lateral palmar metacarpal nerve block alone can help differentiate from other causes
4. variable response to IA anesthesia; intact cartilage may prevent complete response
5. radiographs: signs don’t always mean disease!
   -linear to crescent shaped lucency in palmar third of the condyles
   -nontraditional views often beneficial: flexed horizontal beam dorsal palmar projection highlights palmar articulation; DLPMO and DMPLO highlight palmar articulation
6. nuclear scintigraphy: high sensitive, low specific; detects early bone activity
7. MRI: high sensitive and high specific! gold standard!
   -defines location and type of bone lesions

Question 11

describe treatment and prognosis of subchondral bone injury

Answer 11

treatment:
1. REST 60-90 days (not stall rest, just not working)
2. NSAIDs
3. IA therapy in advanced cases
4. podiatry: correct an imbalance if present

prognosis: depends on the degree of structural damage and the presence of cartilage damage

Question 12

describe articular fragmentation-dorsal proximal P1 fragments; include diagnosis and treatment

Answer 12

1. common; more in frontlimb than hindlimb; medial (95%) >lateral
2. see acute swelling and heat and subtle short duration lameness, positive fetlock flexion, and poor performance (right when fracture chips off)
3. +/- incidental finding in yearlings and non-racehorses in prepurchase exams

diagnosis:
1. clinical exam
2. low palmar nerve block
3. IA anesthesia: once nerve block wears off, if lameness resolves with this is more common that fragment = source of/contributing to lameness and may benefit from removal!!
4. radiographs: need a good straight rad or might miss small fragment!
-best seen on straight lateral and DLPMO
-fragments can be: sharply marginated or rounded, varying sizes, single or multiple, varying amounts of displacement

treatment: as conservative as you can, not ALL fragments need to come out, likely not the source of lameness if the horse is lame; if going to spend money to remove, want to make sure good chances of having a sound horse at the end of that treatment
1. if small fragments, low level work, or economics involved, can try to manage with IA therapy BUT
2. working a horse with unstable chip fracture can lead to more rapid irreversible degenerative changes in the fetlock like extensive score lines, thin cartilage, or more advanced OA
3. surgical treatment: arthroscopy, 6-8 weeks rehab; give excellent prognosis if no other degenerative changes in the joint

Question 13

describe articular fragmentation- proximal palmar/plantar P1 fragments- Type I; include diagnosis and treatment

Answer 13

1. osteochondrosis vs trauma
   -common in young, untrained animals, due to avulsion of immature bone fragments attached to short sesamoidean ligament, still classified as fragments! not OCD lesions
2. much more common in hindlimb than frontlimb, medial > lateral
3. variable lameness, often found in sound horses; if horse lame will see effusive joints

diagnosis:
1. clinical exam
2. low palmar nerve block
3. IA anesthesia
4. radiographs:
-best seen on oblique DLPMO, DMPLO, and flexed lateral
-fragments can be: sharply marginated or rounded, varying size and shape, single or multiple, with varying amounts of displacement

treatment: conservative
1. if low level work, try to manage with NSAIDs, oral joint supplements, injectables, IA therapy (corticosteroids, corticosteroids + HA, biologics (IRAP, pro-stride)
2. arthroscopy is controversial!
-if upper level jumper or racehorse more likely to recommend to prevent possible future lameness BUT
-may lead to irreversible degenerative changes in the fetlock (score lines, cartilage thinning)
-fragments are much more challenging to take out

Question 14

describe articular fragmentation- proximal palmar/plantar P1 fragments- Type II

Answer 14

1. extra-articular, large, abaxial and extend 2-3cm
2. less common than Type I
3. uncommon to see lameness so removal not receommended

Question 15

describe the bony structures of MC/MT

Answer 15

1. MC/MT III
2. MC/T II and IV

there is substantial articulation and weight transference through the carpus and MC II and IV, and through the tarsus and MT II, but minimal articulation between the tarsus and MC IV

Question 16

describe soft tissues of MC/MT

Answer 16

syndesmosis: fibrous joint between two parallel bones (MC 3 and 4, MC 3 and 2), united by fibrous connective tissue
-narrow gap joined by ligamentous tissue or a wdie gap joined by a broad sheet of connective tissue called the interosseous membrane
-attaches splint bones to cannon bone
-ossifies to a variable extent during skeletal maturity

-in front leg, quite a bit of stress on splint bone, twisting and turning/daily activity can cause inflammation within syndesmosis, can lead to syndesmopathy

Question 17

describe syndesmopathy

Answer 17

1. inflammation within syndesmosis
2. osseous union between the splint bones and MCIII can occur
3. desmitis of interosseous ligament with enthesophyte formation or endosteal new bone can cause pain and lameness

Question 18

describe exostosis- splints (6)

Answer 18

1. exostosis formation on splint bones from blunt trauma or strain trauma
2. palpable pain can be elicited (Cold or Hot)
3. palpable swelling usually present
4. most common on proximal half of the limb
5. may or may not cause lameness, usually worse on hard ground
6. axial proliferation may cause impingement on the suspensory ligament

Question 19

describe diagnosis and treatment of metacarpal/metatarsal disease

Answer 19

1. clinical exam: focal reaction to palpation
2. perineural anesthesia: M/L palmar MC/MT nerves
3. local infiltration
4. radiographs: difficult to fully appreciate axial proliferation
5. ultrasound is useful! US suspensory and can follow to see bony proliferation at axial margin of splint bone and suspensory ligament

treatment:
1. ID early and rest: 2-3 weeks to 2-3 months; rest until cold
2. NSAIDs
3. topical therapy: protective compression wraps, diclofenac/surpass, cryotherapy in acute phase
4. local infiltration with corticosteroids: dexamethasone
5. surgical intervention:
-if nonresponsive to medical therapy, impingement on suspensory ligament; can do amputation/segmental ostectomy of bony proliferation and part of splint bone (but in front leg esp is super important to leave enough splint for weight bearing)