• low cellularity
• collagen
• proteoglycan
• noncollagenous proteins
• water
• subsynovium-fibrous, areolar, or adipose
• synovium- incomplete layer 1 to 4 synoviocytes thick with no basement membrane

type A-phagocytic activity

type B-synthetic activity

• proprioceptive and nociceptive
• nerve fibers terminate in joint capsule, ligaments, menisci
• cartilage not innervated

• ultrafiltrate of plasma plus hyaluronan 
• (responsible for viscosity)
• low cellularity
• 90% mononuclear cells
• low total protein concentration

• water (70-80%)
• chrondrocytes (1-2%)
• extracellular matrix (20-30%)
• collagen II
• proteoglycan
• glycoproteins
• protease inhibitors, lysozyme, fibronectin, chondronectin, mineral and lipid

1. synthesize, organize, degrade, regulate composition of ECM
2. receive oxygen and nutrients via diffusion from synovial fluid

1. mechanical environment
2. cytokines
3. growth factors

1. chondroitin sulfate
2. keratan sulfate
3. dermatan sulfate
4. hyaluronan

proteoglycans

why are proteoglycans so resistant to compression?

what about tensile forces?

• hi density negative charges keep molecules separated and trap water. osmotic properties provide for resistance
• collagen helps to resist tensile forces

• I (superficial/tangential): chondrocytes small and flat, cells and collagen parallel to articular surface
• II (middle/transitional): chondrocytes larger and rounded, collagen fibers oblique to perpendicular surface, many branching fibers
• III (deep/radiate): chondrocytes larger and rounded, perpendicular and in columns, collagen perpendicular to surface
• tidemark: demarcation between calcified and noncalcified cartilage
• IV: calcified cartilage

• important in degradation of articular cartilage ECM

• MMP-collagen
• aggrecanases-aggrecans
• cytokines-can stim MMP
• prostaglandins-proteoglycan depletion
• oxygen derived free radicals-proteoglycan, collagen, hyaluronan

• accelerated degradation of articular cartilage collagen and proteoglycan
• inability of chondrocytes to adequately replace damaged collagen and lost proteoglycans
• weakened articular cartilage is less resistance to loading and shear stresses
• gross cartilage lesions develop with continued use unless inciting cause corrected
• wear particles from damaged cartilage can initiate further mediator production by synovium
• spontaneous repair of gross cartilage lesions is incomplete or may not occur.

1. intrinsic: increased metabolic activity of chondrocytes increases leading to cell division and synthesis of proteoglycans and collagen
2. extrinisic: mesenchymal elements from subchondral bone respond with the production of connective tissue that undergoes metaplasia to yield fibrocartilage (NOT collagen II)
3. matrix flow: cartilage produced at periphery of lesion and wave-like lips of cartilage migrate toward center of defect; very limited movement

• partial: minimal to no inflammatory response, some intrinsic
• full thickness: exposed subchondral bone results in inflammation, granulation tissue, fibroblasts recruited to produce collagen. fibrous tissue undergoes chondrification to produce fibrocartilage. new cartilage mechanically inferior to hyaline cartilage

a progressive and permanent deterioration of articular cartilage resulting in loss of function

due to aging or post-traumatic

• joint pain and lameness
• decreased range of motion
• joint effusion
• varying degrees of local inflammation

• decreased joint space
• osteophyte/enthesophyte formation
• subchrondral bone sclerosis

• irregularly distributed partial or full thickness cartilage loss, loss of shiny surface
• may see wear lines
• osteophyte/enthesiophyte
• increased density of subchondral bone
• synovial inflammation and soft tissue swelling

• depends on many factors (use, age, size, disposition, $)
• even a few days rest can help
• reduction of acute inflammation will reduce production of cytokines and enzymes which may cause cartilage destruction
• surgery
• PT
• nutritional 
• NSAIDS
• corticosteroids
• slow-acting disease modifiers
• nutraceuticals

• remove fragment,
• debride,
• internal fixation/joint reconstruction,
• lavage and removal of inflammatory mediators,
• soft tissue debulking and debridement,
• arthrodesis

• hydrotherapy
• ice
• swimming
• acupuncture
• soft laser therapy
• glavanic/faradic electrical stim
• therapeutic US
• counterirritants
• radiation
• extracorporeal shock wave therapy
• massage
• superficial heat

• NSAIDS (reduce matrix catabolism, synthesis)
• phenylbutazone, 
• flunixin meglumine
• corticosteroids (reduce GAG synthesis, NOT if articular fracture present)
• methylprednisolone acetate (Depo-medrol),
• tramcinolone acetonide (Vetalog)
• slow-acting disease modifiers (anti-inflam, lubrication, chondroprotective)
• hyaluronic acid
• polysulfated GAGs (Adequan)
• nutraceuticals

1. primary-direct penetration
2. secondary-extension of infection from adjacent tissues
3. tertiary- hematogenous; septicemia or metastasis from another infected area

• S type (synovial)-infection confined to joint space without osteomyelitis
• E type (epiphyseal)-osteomyelitis of epiphysis
• P type (physeal)- osteomyelitis adjacent to growth plate

• non-weight bearing
• heat and swelling
• fluid distention and edema
• foals may present with septicemia first
• depressed, off-feed
• sweating/febrile

• early- cannot confirm, but may see soft tissue swelling and increased joint space
• later- see narrowing of joint space, lysis of subchondral bone, and periosteal proliferation

• yellow, greyish, blood-tinged
• cloudy to frank pus
• pH <6.9
• clots readily and may contain fibrin
• 20-200k leukocytes/mm3 with 90% neutrophils
• elevated protein
• should culture for aerobic and anaerobic

• cattle: Arcanobacterium pyogenes, strep, salmonella, E. coli, mycoplasma
• foals: enterobacteria: E. coli, salmonella, enterobacter, klebsiella, proteus, providencia. strep, rhodococcus equi, actinobacillus equuli
• adult horses: staph aureus, enteric gram negatives

• time is critical!
• culture, but treat empirically, conservatively
• parenteral antibiotics (broad): penicillin and gentamicin
• lavage
• arthoscopy to remove clots, etc
• if frank pus: isotonic fluid lavage with arthrotomy 
• regional antibiotic perfusion
• DMSO joint lavage (free radical scavenger)
• supportive bandage and cold therapy
• NSAIDS
• IV sodium hyaluronate

• multifactorial
• polygenetic trait
• environmental factors
• disparity in growth and development of soft tissues relative to bone so that the joint is lax. 
• leads to abnormalities of acetabulum and femur

what is the pathogenesis of hip dysplasia?

1. soft tissue abnormalities lead to skeletal developmental abnormalities
2. joint is lax
3. abnormalities of acetabulum and femur
4. thickening of joint capsule and increased trabecular bone thickness
5. erosion of articular cartilage due to abnormal articulation
6. exposes subchondral bone and associated inflammatory/nociceptive properties
7. capsular stretching and subchondral trabecular micro fractures

1. restricting growth of at-risk animals 
2. breeding dogs with normal hips only

1. <12 months of age with marked hip pain and palpable laxity. no radiographic signs of DJD. sx to increase congruency of hip joint to avert later degenerative changes
2. >2 years with signs attributed to DJD. laxity usually not palpable. sx to relieve pain and restore function

• younger: lameness, reluctance to exercise, difficulty climbing stairs, difficulty rising after rest, bunny hopping, audible clicking or popping in hip area, laxity, muscle atrophy, painful palpation
• older: similar signs including lameness, exercise intolerance, crepitus, decreased range of motion (notes say pelvic muscle atrophy, lecture does not)

• lameness, muscle underdevelopment or atrophy
• pain upon manipulation of hips, esp. extension and abduction
• young animals: Ortolani signs
• radiographs: subluxation in young, arthritic changes in older
• OFA score or Penn hip score

how is an Ortolani sign elicited?

what does it mean?

• Force hip into dorsal subluxation by compressing femur along long axis with limb slightly abducted. stifle flexed 90degrees. Limb is then abducted while maintaining compression. If femoral head falls back into acetabulum with a click, this is a + Ortolani sign. 
• only indicates lip laxity.
• usually only seen in younger patients

• NSAIDS and exercise restriction in young animals
• non-surgical treatment ineffective in older patients
• nutraceuticals and chondroprotectives may help

1. pubic symphysiodesis
2. triple pelvic osteotomy
3. femoral head and neck ostectomy
4. etc: pectineal myectomy and intertrochanteric osteotomy

1. FHO (femoral head and neck ostectomy)
2. THR (total hip replacement)

• pubic symphysis is insulted (electrosurgery or staples) early in development (3-4 months of age) to cease endochondral ossification for pelvic growth. 
• focal disturbance results in relatively less growth of ventral pelvis, resulting in bilateral acetabular rotation and increased femoral head coverage
• benefit: minimally invasive
• drawback: needs early diagnosis 

• osteotomy of ilium, pubis, ischium with reattachment of ilium using angled plate to rotate acetabulum over femoral head 
• benefit: slows/prevents osteoarthritis, animals usually do well with this if selected properly
• drawback: animals selected need to have NO radiographic evidence of DJD and <10 months of age (so diagnose by PennHip (>16 weeks of age))

aggressive, permanent with less predictable outcome.

can always be done later to alleviate clinical signs

• replaces femoral head and neck with prosthetic (cobalt chrome) cemented into femoral canal
• replaces acetabulum with prosthetic cup (polyethylene) cemented into pelvis
• benefit: 96% of dogs have excellent outcome
• drawback: most complications are severe and require implant removal

• older animals
• tend to get proximal femoral physeal fractures
• most are craniodorsal
• round ligament torn/avulsed
• actabular rim and femoral head avulstion fractures commonly associated

1. non-weight bearing on affected limb 
2. limb usually adducted and help in external rotation
3. if hips extended or neutral, affected limb is shorter due to dorsal luxation, best assessed in dorsal recumbency 
4. if hips flexed, affected limb appears longer
5. greater trochanter in line with ischiatic tuberostiy and iliac crest rahter than forming triangle.
6. "thumb test" -thumb in space between greater trochanter and ischiated tuberosity will be displaced when hip is externally rotated in normal dogs. failure to displace thumb indicates luxation or fracture

• closed-asap (before 3-4 days post-luxation), after radiographs to rule out fractures. under anesthesia, externally rotate femur to disengage femur from ilial shaft. pull leg distally and caudally until head pops over acetabulum. internally rotate and abduct limg to reduce luxation. apply pressure medially to greather trochanter, rotate hip to displace hematomy and work joint capsule out of acetabulum. apply Ehmer sling 10-14 days 
• open-capsulorrhaphy, synthetic capsule repair, toggle pin (mimics round ligament)

• mimics round ligament
• made of Kirschner wire and suture threaded through. 
• placed medial to acetabular wall through hole at level of round ligament origin. suture placed thru a hold drilled from femoral head to subtrochanteric area and secured. 

• congenital malalignment of extensor mechanism (quads, patellar tendon, patella, patellar ligament, tibial tuberosity) 
• luxation exacerbates deformity in immature animals resulting in shallow trochlear groove depth, tibial and femoral angular and rotational malformation

• I: can be luxated manually. immediately returns to original position. no clinical signs.
• II: patella in normal position most of the time, but can be manually luxated, and stays until extension. may have clinical signs. 
• III: patella luxated most of the time, can be manually replaced but reluxates
• IV: patella luxated and cannot be reduced except by sx. significant limb deformity. prognosis even with sx is guarded

• grade II: lifting limb before resuming normal gait. no lameness.
• grade III, IV: lameness, gross conformational abnormalities, inability to extend stifle. 
• can have different grades between stifles
• rarely medial and lateral between stifles. 

• deepending of femoral trochlea (wedge recession, modified recession, sulcoplasty)
• tibial tuberosity transposition
• corrective femoral and itbial osteotomies

• retinacular/capsular imbrication
• capsulectomy followed by capsular closure
• fabellar-patellar suture
• fabellar-tibial antirotational suture
• transposition of the rectus femoris origin

degenerative usually, but can occur due to trauma,

traumatic: usually in dogs <4yrs of age (unilateral, avulsion of tibial attachment), gross instability

• craniocaudal stability
• limits hyperextension of stifle
• limits internal rotation of tibia

acute onset lameness or more gradual lameness

severe lameness that improves with time

diagnosis confirmed by: cranial drawer test

radiographs to assess degree of osteoarthritis in both stifles. 

• animal in lateral recumbency with affected limb up.
• one thumb on lateral fabella an dipsilaterla index finger on patella
• other thumb on fibular head and ipsilateral index finger on tibial tuberosity. 
• while holding femur still, attempt to force tibia cranially in various degrees of flexion/extension
• immature dogs may have a few mm with distinct stop, adults should have no drawer motion. 

• intracapsular
• extracapsular
• osteotomy

prognosis 85-90% success rate overall, maybe extracapsular favored

• autogenous tissue to replace CCL. 
• secured to femur and tibia
• over the top and under and over techniques
• often done with extracapsular technique on top

autogenous tissue or synthetic material placed outside capsule to stabilize stifle. 

fibular head transposition- moving insertion of lateral collateral ligament cranially and securing it to tibia so lateral collateral ligament is now oriented caudal to cranial direction

fabellar-tibial suture-suture from fabella to tibial tuberosity, mimicking CCL

• defect in endochondral ossification, so a thickened area of articular cartilage develops
• deeper areas have abnormal metabolism and may separate from subchondral bone. 
• if separation develops into a free flap, synovitis develops. 
• large breed male dogs 6-12 months of age
• usually stifle and hock
• lateral aspect of femoral condyle
• medial trochlear ridge 
• sx: remove chondral flap and curett underlying subchondral bone
• prognosis: good for stifle, guarded for hock

• lateral aspect of femoral condyle
• medial trochlear ridge 

subjective scale 1-7

animals must be 2 years old

objective measurement of laxity

greater predictive value than OFA

valid in animals >16 weeks of age

1. round ligament
2. joint capsule
3. dorsal acetabular rim

1. acetabular labrium
2. pelvic muscles

64% excellent limb function

18-25% reluxation

14% lameness and OA

Steinmann pin, usually with a threaded tip, underneath the attachment of the hamstring muscles at the ischium, through and overtop of the external rotators and sciatic nerve, over the neck of the femur, and into the wing of the ilium.

Complications: sciatic nerve injury, migration, tract drainage, injury to femoral head, septic arthritis. success rate 73%.

The pin often migrates along the epaxial musculature of the back and has been known to penetrate the brain and the heart.

indications: recurrent or chronic luxations

complications: rectal perforation, pin migration, breakage

80% success rate. 

pin penetrates greater trochanter and femoral head

• primary: cranial and caudal cruciates
• secondary: menisci, collateral ligaments, joint capsule

• early: mild lameness, effusion, 
• mild OA
• no instability
• often bilateral
• more common in mature dogs
• chronic: intermittent lameness
• periarticular fibrosis, more on medial aspect
• instability
• moderate OA
• often bilateral

cranial menisco-tibial ligament

caudal menisco-tibial ligament

joint capsule

medial collateral ligament

cranial menisco-tibial ligament

menisco-femoral ligament

osteochondritis of humeral head

panosteitis of humerus

ununited anconeal process

fragmented coronoid process

osteochondritis of humeral condyle

panosteitis of radius/ulna

retained cartilage core

loss of fibroblasts-->chondroid metaplasia

unsuccessful remodeling in responses to cyclic loading

50-90% incidence

• usually > 6 months
• mild to profound intermittent weight bearing forelimb lameness
• atrophy of regional muscles
• flexion and extension elicits marked pair response

• subchondral bone defect in the caudal aspect of the humeral head on lateral radiographs. arthrography needed to diagnose OCD
• intact thickened cartilage over subchondral bone defect is favorable prognostic sign. 

subtantial lameness

chronic lameness

what is panosteitis? who is affected?

acquired inflammatory condition affecting diaphyseal and metaphyseal regions of the long bones of (male) large/giant breed dogs

• often cyclic/recurrent
• shifting leg lameness
• lethargy, anorexia, fever
• pain response elicited when digital pressure applied to affected region of long bones

increased radiolucency of medullary cavity in region of nutrient foramen(degeneration of medullary adipocytes) occurs early; almost never seen

hazy, granular increased radiopacity within medullary cavity due to endosteal or periosteal bony proliferation. seen 10-14 days post onset of lameness

ununited anconeal process

osteochondrosis

fragmented coronoid process

1. lameness, stiff stilted gait 4-5 mos age
2. pain upon extension
3. joint effusion

what is seen on radiographs of the elbow with osteochondrosis?

which view?

subchondral bone defect affecting trochlea of humeral condyle which is most easily visualized on

slightly oblique, craniocaudal view

degenerative changes may be present

 excision of cartilage flap

soft padded for a couple of days, exercise restricted 3 weeks

prognosis guarded depending on size of lesion

• german shepherds and basset hounds
• male=2xfemale
• 30% bilateral

• intermittent lameness as early as 4 months
• exacerbated by exercise or prolonged rest
• sit with carpus in valgus position (knock-knees)
• elbow abducted,
• circumduct the antebrachium during swing phase of stride
• hyperextension and flexion may elicit pain 
• pain upon anconeal process pressure when elbow is flexed
• crepitus
• synovial effusion
• joint capsule thickening

diagnosis should be made AFTER 20 (24 in german shepherds) weeks of age due to distinct center of ossification separate from the ulna which later fuses with ulna

flexed lateral radiograph

often will have proximal subluxation of radial head

excision, stabilization (lag screws, proximal diaphyseal ulnar osteotomy

union following ulnar diaphyseal osteotomy 

prognosis is good, but may develop extensive DJD later

large breed dogs

retrievers, rotties, german shepherds. 

• rarely <5 months
• subtle weight bearing lameness
• exacerbated by exercise, prolonged rest
• insidious onset of gait abnormality
• no pain response usually
• limb held in exaggerated externally rotated position when sitting or standing
• circumduct antebrachium during swing phase of stride
• carpus in flexed, externally rotated positition when elbow extended
• joint effusion 

• rarely identified bc of superimposition of medial coronoid process
• mediolateral view with elbow maximally extended and supinated may help, but not really. 
• degenerative changesin elbow in absense of UAP or osteochondrosis
• increased density of ulna hear coronoid 
• osteophyte development on anconeal process
• CT helpful
• definitive diagnosis made at exploratory arthrotomy or arthroscopy

humeral head

humeral condyle

femoral condyles

patella

trochlear ridges of talus 

1. weight bearing lameness
2. prominent muscle atrophy
3. pain in flexion/extension of shoulder
4. subchondral defect/sclerosis of caudal humeral head

1. craniolateral
2. caudolateral
3. caudal

diffuse microcracks in subchondral bone

consistent with fatigue microdamage

uncommon, characteristic lameness in hunting dogs

sudden onset lameness from vigorous exercise

pain in one shoulder, reluctant to bear weight

subsides 1-2 weeks

then several weeks later, persistent lameness wtih external rotation of humerus resulting from fibrosis of infraspinatus

most likely a primary myopathy

• standing hyperextension of limb
• adduction of elbow
• abduction of paw
• restricted shoulder movement
• marked scapular muscle atrophy
• lateral circumduction of distal forelimb with carpal flip while ambulating

tenotomy of insertion

approach: cranial to deltoid muscle with caudal retraction

• inflammatory condition affecting bicipital tendon and tendon sheath within intertubercular groove of humerus
• assumed result of chronic strain or trauma
• synovial hyperplasia,
• chondromalalcia of intertubercular groove,
• osteophytosis,
• calcificaiton of bicipital tendon
• pain elicited upon pressue to tendon and tendon sheath

• limiting exercise and oral admin of anti-inflammatories
• intra-articular injeciton of steroids (depomedrol) can be tried if lameness persists
• surgical transposition of bicipital tendon to greater tubercle of humerus in refractory cases

small/toy breeds: medial (congenital)

large dogs: lateral can be seen (usually due to trauma)

• extending forelimb and lifting humeral head into glenoid cavity
• use velpeau sling with paw placed near opposite shoulder 17-21 days.
• avoid internal rotation of humeral head
• often limited success

craniomedial approach

medial transposition of biceps tendon to creat lateral force on humeral head. 

spica splint 17-21 days

• nonweight-bearing lameness
• affected limb in flexion, adducted, internally rotated
• crepitus on extension, flexion
• prominent greater tubercle
• difficulty in finding acromion process
• chronicity-->ankylosis, some weight bearing

• can do closed within a few days of occurence. better success rate
• extending limb and applying lateral pressure to proximal humerus, spica splint 17-21 days
• open if persistent, reluxates
• lateral transposition of bicipital tendon, spica splint

radius and ulna displace laterally, causing pronation of antebrachium with limited range of motion of elbow

displaces laterally bc medial portion of condyle (trochlea) extends further distally than the lateral portion (capitulum) and resists medial displacement

•  antebrachium and carpus abducted and elbow flexed
• paw does not touch the ground while standing/sitting
• manipulation is painful
• laterally displaced radius and ulna are very prominent
• NEED TWO ORTHOGONAL VIEWS

congenital- guarded

traumatic-good if dx/tx within first few days

• closed reduction-elbow flexed and antebrachium pressed cuadalyl with pressure applied to radial head
• antebradium internally rotated to position anconeal process in supratrochlear foramen as the limb is gradually extended. 
• radiographs taken to confirm
• spica splint 7-14 days
• exercise restriction 3-4 weeks

• remaining growth potential
• degree of retardation or physeal growth
• percentage of growth involving physis that contributes to bone's overall length
• single or paired with another bone

antebrachium 

distal ulna

conical conformation

asynchronous, with proximal and distal plates contributing different amounts to overall length

proximal/distal radius: 40/60%

proximal/distal ulna: 15/85%

valgus bc radius is bowing from continued growth,

carpus will continue to grow and take oncaual displacement

1. ostectomy
2. resect or suture periosteium over ends of osteotomy to prevent rapid healing
3. interpose free autogenous fat graft in ostectomy site
4. warn owner that quick healing may warrant another surgery. 

• splinting can be attempted by rarely successful (placed in flexion), coapted 4-8 weeks
• primary open ligament repair, rarely attempted
• arthrodesis (partial or pancarpal) with plates on dorsal surface (compression side easier to access), protected via coaptation for 1-3 months

trauma

developmental disturbances

inflammatory disease

radiography

CAT

scintography

US

thermography

video analysis

blood chem

xerography

no longer available in North America

CAT scan is amenable in examining what? 

head

antebrachium

neck

tarsus

stifle

• areas of increased blood flow
• areas of increased bone turnover

labelled compound accumulates in bone

large gamma camera detects photons emitted by isotope (Technetium99m attached to methylene diphosphonate)

converts to voltage signal

• advantages: 
• small radiation dose
• elimination in urine
• image 2-4 hours post injection
• half-life 6 hours
• disadvantages:
• radiation safety hazard

1.  injection angiogram-image of vessels for short time
2. blood pool (soft tissue)-regional blood flow 
3. bone scan- also damaged muscle tissue (2-4 hrs)

1. scanning patients with lameness that cannot be blocked out or imaged another way
2. imaging entire skeletal system of horse with multiple limb involvement
3. source of pain localized by nerve blocks but rads show nothing
4. judging clinical relevance of rads
5. monitoring fracture healing

1. imaging tendons
2. surface fractures not readily seen on rads
3. other soft tissue (heart, abdomen, thorax, musculoskeletal) 

more readily

darker

• edema
• decreased capillary circulation
• capillary thrombosis
• vasoconstriction secondary to nerve root or peripheral nerve damage

• stationary position of horse allows examiner to view from all sides for longer periods of time. can evaluate asymmetry, different speeds, different gaits, etc. 
• however, the gait is NOT the same as on the ground (no preservation of momentum (also, expensive)

• creatine kinase (CK)
• skeletal and cardiac muscle, brain
• <6 hours after injury
• half life 1-2 days
• aspartate aminotranferase (AST)
• skeletal, cardiac muscle, liver, RBC, etc.
• rise slower than CK (12-24 hours-7 days)
• lactate dehydrogenase (LDH)
• skeletal and cardiac muscle
• more difficult test

• phalangeal fractures-middle phalange
• sesamoid fracture-Fetlock
• stress fractures -"bucked skins"
• intra-articular fractures- condylar fractures and carpal fractures
• long bone fractures
• arthritis-fetlock and tarsus
• tendonitis-"bowed tendon"

1. corticosteroid (systemic of intra-articular)
2. hyaluron (intra-articular)
3. GAGs
4. NSAIDS

• inhibit destructive enzymes (collagenase), inflammatory mediators (IL-1), neutrophil function
• depress chondrocytes
• increase risk of infection
• negative effects on hyaluron and proteoglycan production

• reduces inflammation/inhibits neutrophil function
• suppresses endogenous steroid production
• weakens connective tissue

• lubricates synovial membrane and articular surfaces
• reduces inflammation
• stimulates production of normal synovial fluid

anti-inflammatory agent

free radical scavenger

• consituent of joint fluid and cartilage matrix
• anti-inflammatory properties
• can cause flare post injection intra-articularly
• chondroprotective
• stimulates chondrocytes
• Adequan also used for sinusitis

• inhibit prostaglandin synthesis (COX I, II) (interfere with arachidonic acid cascade)
• blocks tissue response to injury
• reduces pain

COX I- constitutive

COX II-inflammatory mediator

cast and transfixation pins,

requires lots of intensive nursing and horse can suffer fractures of metacarpus through proximal pin hole. 

arthroscopy

lag screws

plating

casting

cast/transfixation pin

1. reduce fragments
2. overdrill fragments
3. tap hole in parent bone
4. tighten screw to compress fragments

• 4.5 or 5.5 screws and broad plates used (sometimes multiple)
• prognosis guarded
• some fractures not repairable

• due to mechanical trauma or stress
• chip fractures of pastern (rare)
• severely comminuted fractures (common)
• avulsion of either caudal emmences from pull of collateral ligaments of pastern joint (intermediate freq)
• severe lameness
• acute onset
• swelling
• crepitation
• diagnosed radiographically

• prognosis: depends on severity
• tx: depends on severity of lameness
• small intraarticular fractures: leave
• avulsion fractures/communuted: sx with fusion, or cast with pins
• caudal eminence: precise repair otherwise DJD
• prognosis better for hindlimb in general

• sesamoid fractures
• intra-articular fractures of phalanx
• condylar fractures
• arthrosis

• apical- TB and standardbreds. excessive strain from repeated pull of suspensory apparatus and compression of metacarpal/metatarsals. 
• apical is most common 
• large apical  (>1/3 body) -poor prognosis
• midbody-poor prognosis
• basilar-poor prognosis
• dx: radiographs
• signs: lameness, swelling, heat
• sx removal if possible
• prognosis depends on fracture

transverse fractures of both sesamoids in one limb

severe lameness

interferes with circulation of distal limb

• renal
• stomach ulcers
• large colon

mechanical injury leads to: 

• cartilage damage,
• capsular damage,
• synovitis,
• peri-articular bone formation

• joint distention
• lameness
• pain
• reduced range of motion

resting

immobilixation

PT

controlled exercise

counter-irritation (um, no)

corticosteroids, hyaluronan, GAGs

1. bucked shins
2. dorsal cortical fractures
3. condylar fractures
4. midshaft fractures
5. sequestra
6. splint bone

you see a horse with swelling over and proximal to the lateral condyle with fetlock joint effusion and lameness.

what do you suspect? what force causes this? how do you confirm your suspicion?

• condylar fracture
• cause: excessive dorsiflexon and axial rotation of the metacarpals. 
• radiograph-fracture from articular surface lateral to middle sagittal ridge of distal MCIII runing thru distal MCIII and thru lateral cortex, or entire thing fissured

what is the treatment for condylar fractures?

prognosis?

lag screws

fair to good for returning to athletic performance, depending on time, DJD, cartilage erosion, palmar chip fractures, step formation in joint after repair

bucked shins-not radiographically evident

dorsal cortical fractures-evident

how are bucked shins prevented?

in whom do they occur?

reduced and controlled training

young TB's

rest

sx: osteostixis, intra-cortical screwing 

drill 5-7,  2.7-3.5mm holes across fracture

holes fill with bone

how does a cannon bone diaphyseal fracture present?

how are they repaired?

acutely, severely lame

lay screwing with casting

trauma and inflammation to splint bones. can present as lame, but usually painful upon deep palpation

tx: rest with or without steroid injection, cold application, anti-inflammatories

exostosis removal if necessary, but can return as superostosis

• sx: remove infected fragment
• curette the cloaca
• remove exostosis surrounding
• bandaging and Abx

fractures, especially chip fractures

what carpal fractures do racing horses get?

TB and quarterhorses?

standardbreds?

steeplechase?

racing horses -chip and slab (3rd carpal)

TB and quarterhorses- chip fractures of intermediate and radial

standardbreds- chip fracures of radial

steeplechase- accessory carpal fractures

how do intraarticular carpal fractures present?

how are chip fractures treated?

mild to moderate lameness

arthroscopic removal

• true, BUT, may not correlate with clinical condition
• peri-articular spurring, narrowing of joing space, lytic changes in central tarsal, 3rd tarsal, and 3rd metatarsus. 
• may have loss of joint space and anylosis fo distal two joints

Churchill's Hock test

squeeze dorsal on medial splint bone. positive response is for horse to elevate the legs upward and outward

yearlings and 2yrs old-IA cortocosteroids...meh

older horses-IA hyaluronan, GAG, corticosteroids

1. improper shoeing
2. improper bandaging
3. inadquate conditioning

fiber damage

hemorrhage

inflammation

• anti-inflammatories (parenteral corticosteroids, phenylbutazone)
• controlled exercise (no free paddock exercise)
• cold packing
• Robert-Jones
• ULTRASOUND to check alignment 
• REST FOR 2-12 monts

• visual
• passive
• examination in motion
• supportive examination

soreness in the strap muscles of the neck indicates: 

• upper limb, bicipital bursa soreness
• distention in carpus
• heat
• withdrawal
• enlargements
• effusion 
• edema
• consistency
• twitching
• pain upon palpation (splints and tendons)

all, but definitely including:

coronary band

collateral cartilages

DDFT

sheath

balls of fingers, not fingernails

push across muscles

note contraction and withdrawal

patellar fixation

drawer sign

collateral ligament

rotation

apply pressure to patella and have horse move forward a step. 

0-no perceptible lameness

1-lameness difficult to observe under any circumstance

2-lameness consistent under some circumstances

3-lameness consistent at trot under all circumstances

4-lameness obvious at walk

5-lame limb non-weight bearing

depends

slow-good for evaluating subtleties in gait

trot-most useful for identifying lameness

fast-can help to identify pain

head down on sound in forelimb lameness

lame hip is lower, with more motion up and down in hindlimbs

1. anatomic nerve variation amonst individuals
2. difficult to determine if entire area anesthetized
3. high proximal limb pain hard to block
4. difficult to assess with subtle lameness
5. fractious horses-safety issue
6. dusty, contaminated areas
7. avoid if hairline fractures possible/suspected
8. motor paralysis

relax. apply a pressure bandage, 

remember that local anesthetics are irritating and this is expected. 

where is a palmar digital nerve block injected?

abaxial?

palmar digital- mid pastern, palmar

abaxial-sesamoid level, palmar

 1-2 ml

bruises around angle of bar

abscesses possible result, but not often

caused by trauma, esp with improper shoeing

red stains seen with chronicity

rest, caustics, packing, proper shoeing

I- fracture of non-articular wing

II-articular wing

III-saggital fracture that divides into equal parts (can use lag screws)

IV- all forms of extensor process fractures

V-everything else

caudal heel pain. degenerative

can involve navicular bone, DDFT, navicular bursa, impar ligament, prox suspensory ligament

bilateral forelimb lameness in one leg more severely than the other. 

short, choppy stride

turned clockwise, lameness noticeable on right

land on toe rather than flat on hoof

more affected foot is smaller

• small feet
• upright conformation
• 7-14 years of age
• quarterhorses, TB, SB
• familial
• GELDINGS

• changes to flexor surface
• osteoporosis of navicular bone
• calcification of NS ligament (navicular suspensory ligament)
• calcification or fragments of bone within DIL (distal interphalangeal ligament)

history

lameness exam

palmar digital nerve block

radiographs (changes in shape of distal foramina to mushrooms)

scintigraphy (look at flexor tendon),

MRI

• intermittent lameness
• both front feet (rarely hind)
• may point one or both
• contracted heels
• may buildup bedding under heel
• shortened, choppy stride
• suspensory ligament 

• corrective shoeing (full bar, rolled toe, raise heels, slipped heels)
• palmar digital neurectomy (guillotine), proximal navicular suspensory desmotomy, tendon/ligament splitting
• continued exercise!!!!
• NSAIDS
• isoxsuprine hydrochloride
• corticosteroids
• adequan
• cosequin
• acupuncture
•  
• NOT WARFARIN

1. allowing several days between palmar digital nerve blocks and neurectomy
2. incising tissues cleanly and avoiding trauma
3. pressure wraps
4. phenylbutazone
5. 6 weeks before returning horse to use

• black spot on sole
• nerve blocks
• gas on radiographs
• foreign bodies (DO NOT REMOVE THESE UNTIL YOU RADIOGRAPH TO ASSESS EXTENT OF INJURY)

subsolar-drain, pare, magnesium sulfate, bacteriostatic dressing

submural- caused by puncture in white line, predisposed by seedy toe. dx by seeing one nail placed higher in wall. pull all nails and inspect.  treatment same as above. 

puncture wound thru frog likely cause 

severely painful

• drainage via street nail operation
• central 1/3 frog removed
• window is cute in aponeurosis and thru tendon and bursa drained. 
• pack and bandage
• flush dialy with bacteriostatics
• prognosis guarded to unfavorable

• bounding digital pulse
• warm feet
• camped in front stance
• abnormal "walking on eggshells" gait

chronic phase when only toe is involved (leads to infection and euthanasia). sinking if quarters and heel involved

radiographs needed (look for air)

look if coronary band sinks below most proximal hoof wall. 

heat rings on hoof

flat sole instead of concave

• as an emergency! relieve underlying cause!
•  DMSO
• phenoxybenzamine, acepromazine  (vasodilators)
• nitroglycerin and heparin (meh)
• cold therapy
• wrapping
• stand in sand
• packing
• trimming and shoeing 
• hoof wall resection (allows gas in and drainage)
•  elevate heel, lower heel/trim toe, protect sole
• deep flexor tenotomy (last ditch effort)
• shoes: hart, egg*, reverse