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Orthopaedic conditions of foals (Osteochondrosis (Predilection sites…
Orthopaedic conditions of foals
Osteochondrosis
Aetiology
Abnormal endochondral ossification resulting in thickened cartilage that is vulnerable to trauma.
Risk factors
Multifactorial disease: rapid growth/genetics, nutrition/mineral imbalances, abnormal loading (shearing/trauma).
Predilection sites
Femoropatellar joint: LTR > MTR > Patella
Femorotibial joint: medial femoral condyle cysts
Tarsocrural joint: DIRT (use DMPLO to view) > LTR of talus > medial malleolus
Fetlock (metacarpo-/metatarso-phalangeal): Mc(t) III saggital ridge or palmar/plantar aspects of condyles
Clinical presentation
Joint distension (+/- lameness) typically occurs first (usually 6 mths of age onwards)
Diagnosis
Radiography
Subchondral bone defect (+/- "kissing" lesion or joint mouse), flattening of articular surface, joint effusion. Take DMPLO to view DIRT.
Definitions
Osteochondrosis: abnormal cartilage/bone formation
Osteochondritis: disruption of articular surface with inflammation
OCD: loose osteochondral fragments
Subchondral cyst-like lesions: invagination of cartilage surrounded by rim of endochondral ossification. May also occur subsequent to articular disruption or synovial penetration
Therapy
Surgical
Generally not done if < 1yr. Involves arthroscopic debridement of lesion. Medial femoral condyle cysts generally have lag screws placed across them (causes them to fill in).
Conservative
Generally done if < 6 mths. Diet adjustment (early weaning, low CHO/high fibre diet), confinement, joint injections (HA), analgesia (meloxicam, firocoxib).
Angular limb deformities: deviation in the frontal and/or saggital plane (judged from in front/behind)
Definitions
Varus (medial deviation/"bow legged")
Valgus (lateral deviation/"knocked knee")
Both are caused by abnormal bone growth (one side of the physes grows too rapidly)
"True" ALDs cannot be straightened on palpation
Risk factors
Perinatal
Periarticular soft tissue flaccidity, soft tissue trauma, placentitis, premature/twins
Incomplete ossification predisposing to pressure-induced deformity, as well as joint laxity leading to abnormal loading
Developmental
Unbalanced nutrition, excessive exercise/loading, external trauma
Abnormal physeal growth or early physeal closure
Clinical presentations
Carpal valgus
Medial > lateral physeal growth (limb bends in)
Longer window of opportunity for treatment (up to 10-12 mths)
Fetlock varus
Lateral > medial physeal growth (limb bends out)
Shorter window of opportunity for treatment (within 2-5 mths of age)
"Windswept" foals have combined varus & valgus affecting pairs of fore-/hindlimbs
Diagnosis
Palpation
Indicates if joint laxity is involved or if there is physitis (heat, pain, swelling)
Visual assessment
At birth many normal foals have both forelimbs externally rotated (corrects as the chest broadens)
Radiography
Assess for incomplete ossification and degree of angulation
Therapy
Stall rest
Avoids further damage to bones and soft tissue (indicated for both joint laxity and true ALDs). Generally 2-6 wks.
Splints and casts
Indicated if joint laxity or incomplete ossification (NOT for abnormal physeal growth). Change casts every 7-10 days.
Corrective trimming and shoe extensions
Used alone or in combination with other treatments.
Carpal valgus: foot trimmed laterally and medial extension applied.
Fetlock varus: foot trimmed medially and extension applied laterally.
Surgery
Indicated for severe deviations or poor response to conservative therapy.
Growth acceleration (concave side of limb): periosteal stripping. Performed < 4 mths for carpus, and < 4 wks for fetlock.
Growth retardation (convex side of limb): transphyseal bridging. Performed < 6-10 mths for carpus, and < 2-5 mths for fetlock
Corrective osteotomy/ostectomy: ceases bone growth.
Cut-off points for therapy
Carpus
Conservative management: < 10 degree deviation
Surgical management: > 10 degree deviation, generally done at 2-3 mths but can wait longer
Fetlock
Conservative management: < 5 degree deviation
Surgical management: > 5 degree deviation, generally done at 1-2 mths
Flexural deformities: deviation in the sagittal plane (judged from the side)
Aetiology
Typically contractures (congenital or acquired)
Congenital usually carpus/tarsus and fetlock joints, but are relatively uncommon
Acquired much more common. Typically occur at 6 & 18 mths (growth spurt points) due to disproportionate bone/tendon growth.
Clinical presentation of acquired deformities
6 mths
"Clubfoot": steep dorsal hoof wall. Due to DDFT contracture.
Conservative treatment if < 90 degrees.
18 mths
Fetlock flexion: SDFT contracture but DDFT may be involved.
Stage 1 (dorsiflexion with occasional knuckling) and stage 2 (permanent knuckling) deformities.
Therapy
Clubfoot
Conservative if < 90 degrees: meloxicam & high-dose oxytet, inferior check desmotomy, dorsal shoe extension. Good prognosis.
Fetlock flexion
Stage 1 deformities: meloxicam, physio, heel wedged shoes, splints to extend fetlock.
Stage 2 deformities: meloxicam, superior/inferior check desmotomy.
Septic arthritis
Aetiology
Usually haematogenous spread of bacteria, but may be due to focal infection (e.g. umbilical remnants). Usually Enterobacteriaceae, Strep and Staph.
Pathophysiology
Rich and slow blood flow through developing physes/epiphyses provides optimal conditions for bacterial seeding. Results in bone/cartilage necrosis.
Clinical presentation
Acute, rapidly progressing moderate/severe lameness, joint swelling/periarticular soft tissue swelling.
DDx
Fracture, foot abscess, trauma. Treat as septic arthritis until proven otherwise.
Diagnosis
Aseptic synoviocentesis
Serosanguinous
Watery
TP 30-60 g/L (turbid)
Neuts > 90%
NCC 20-150 x 10^9/L
Radiography
False negatives early on. If no evidence of boney involvement, re-image 7-10 days later.
Therapy
Antiobiotics
Pen/Gent (oxytet is an alternative, esp if osteomyelitis). Treat for 1 wk post-clinical signs.
Joint lavage
3-5 L of sterile Hartmann's per joint. Can be done with sedation/GA, but best done using an arthroscope.
NSAIDs
Low-dose flunixin.
Box rest with limb bandaging
Aggressive treatment of concurrent/primary disease (e.g. endotoxaemia, septicaemia)
Risk factors
High risk foals predisposed
Incomplete cuboidal ossification
Due to perinatal (IUGR, premature/dysmature, twins) and/or developmental (abnormal loading, trauma).
Treatment involves confinement, splints and/or casts.
Physeal dysplasia
Inflammation of growth plates (physitis)
Multifactorial (genetics, nutrition, exercise, obesity, toxicoses)
Commonly affects distal radius, tibia, Mc(t) III, or proximal P1.
Treatment as per conservative osteochondrosis management