- Definition
- Pathophysiology
- Systems Affected
- Genetics
- Incidence/Prevalence
- Signalment
- Signs
- Causes
- Risk Factors
BASICS
Acute or chronic injury of tendon and/or musculotendinous junction; most commonly refers to SDFT and DDFT injury.
- Normal SDFT of galloping Thoroughbreds elongates by up to 16% of its original length. SDFT failure occurs with elongations (strains) of ≥20%. This small safety margin is probably a major factor in the high incidence of SDFT injury in Thoroughbred racehorses
- Excessive tendon loading results in disruption of collagen fibrils and extracellular matrix. Intratendinous hemorrhage and hematoma occurs. Fibrin and inflammatory cells are released in proportion to injury size
- Scar formation begins type III collagen production, which provides early stability but little tensile strength. Type III collagen predominates in the first 6–8 weeks of healing
- Remodeling begins after 6–8 weeks. Type I collagen slowly replaces type III collagen. The tendon is resized and reshaped. Collagen fibers become aligned in the direction of stress and tendon tensile strength improves. Remodeling continues for many months
- Abnormal type III collagen quantities, small collagen fibrils, and lack of linear fiber arrangement can persist for up to 14 months. This slow rate of healing contributes to the high rate of reinjury
Musculoskeletal—tendons, musculotendinous junctions, areas of tendon insertion, tendon sheaths.
- SDFT injury—Thoroughbred racehorses: 8–43%; event horse: CCI competitors higher than 1 day eventers; show jumpers: unusual except international competitors or >15 years of age
- SDFT injury front >hindlimb. Bilateral injury common
- DDFT—most common in hindlimb of dressage and show jumpers
- SDFT—Thoroughbred racehorses, upper level eventers, Grand Prix jumpers. Infrequent in Standardbreds, racing Arabians and Quarter Horses, polo ponies, fox hunters, cutting horses, barrel racers
- DDFT—most common in jumpers or dressage >10 years of age
- Acute unilateral lameness that responds to rest
- Swelling, focal sensitivity, and/or heat along palmar/plantar metacarpus/metatarsus
- Tendon enlargement with chronic injury
Physical Examination Findings—SDF Tendonitis
- Bowed (convex) tendon profile when standing
- ±Digital sheath effusion
- “Curb” if injury to tarsus
- Variable lameness depending on severity, location, and chronicity; ± lame in mild and/or chronic injury; acute transient lameness in moderate or moderately severe injury
- Carpal canal injury—carpal sheath distention, lameness, worse with carpal flexion, ± stands with carpus slightly flexed
- Pastern branch lesions often lame
- Complete rupture—severe lameness, dropped fetlock
Physical Examination—DDF Tendonitis
- Mild to moderate lameness
- ±Positive distal limb flexion
- Distal injury (within the foot)—unilateral lameness with no physical abnormalities
- Digital tendon sheath effusion
- Tarsal sheath distention with penetrating or blunt trauma to hock
- ±Carpal sheath effusion with injury to radial head of deep digital flexure muscle near musculotendinous junction
- Excessive biomechanical load
- Direct blunt or penetrating trauma
- Sepsis owing to penetrating wound of tendon sheath
- Encircling bandages (“bandage bow”)
DIAGNOSIS
TREATMENT
MEDICATIONS
FOLLOW-UP
MISCELLANEOUS