Orthopaedic conditions of foals (Osteochondrosis (Predilection sites…
Orthopaedic conditions of foals
Abnormal endochondral ossification resulting in thickened cartilage that is vulnerable to trauma.
Multifactorial disease: rapid growth/genetics, nutrition/mineral imbalances, abnormal loading (shearing/trauma).
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
Joint distension (+/- lameness) typically occurs first (usually 6 mths of age onwards)
Subchondral bone defect (+/- "kissing" lesion or joint mouse), flattening of articular surface, joint effusion. Take DMPLO to view DIRT.
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
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).
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)
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
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
Unbalanced nutrition, excessive exercise/loading, external trauma
Abnormal physeal growth or early physeal closure
Medial > lateral physeal growth (limb bends in)
Longer window of opportunity for treatment (up to 10-12 mths)
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
Indicates if joint laxity is involved or if there is physitis (heat, pain, swelling)
At birth many normal foals have both forelimbs externally rotated (corrects as the chest broadens)
Assess for incomplete ossification and degree of angulation
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.
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
Conservative management: < 10 degree deviation
Surgical management: > 10 degree deviation, generally done at 2-3 mths but can wait longer
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)
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
"Clubfoot": steep dorsal hoof wall. Due to DDFT contracture.
Conservative treatment if < 90 degrees.
Fetlock flexion: SDFT contracture but DDFT may be involved.
Stage 1 (dorsiflexion with occasional knuckling) and stage 2 (permanent knuckling) deformities.
Conservative if < 90 degrees: meloxicam & high-dose oxytet, inferior check desmotomy, dorsal shoe extension. Good prognosis.
Stage 1 deformities: meloxicam, physio, heel wedged shoes, splints to extend fetlock.
Stage 2 deformities: meloxicam, superior/inferior check desmotomy.
Usually haematogenous spread of bacteria, but may be due to focal infection (e.g. umbilical remnants). Usually Enterobacteriaceae, Strep and Staph.
Rich and slow blood flow through developing physes/epiphyses provides optimal conditions for bacterial seeding. Results in bone/cartilage necrosis.
Acute, rapidly progressing moderate/severe lameness, joint swelling/periarticular soft tissue swelling.
Fracture, foot abscess, trauma. Treat as septic arthritis until proven otherwise.
TP 30-60 g/L (turbid)
Neuts > 90%
NCC 20-150 x 10^9/L
False negatives early on. If no evidence of boney involvement, re-image 7-10 days later.
Pen/Gent (oxytet is an alternative, esp if osteomyelitis). Treat for 1 wk post-clinical signs.
3-5 L of sterile Hartmann's per joint. Can be done with sedation/GA, but best done using an arthroscope.
Box rest with limb bandaging
Aggressive treatment of concurrent/primary disease (e.g. endotoxaemia, septicaemia)
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.
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