Tendon and ligament injuries are among the most common causes of lameness and early retirement in performance horses, accounting for approximately 43-54% of all musculoskeletal injuries in equine athletes.
Overview and Clinical Importance
Tendon and ligament injuries are among the most common causes of lameness and early retirement in performance horses, accounting for approximately 43-54% of all musculoskeletal injuries in equine athletes. Complete rupture represents the most severe form of these injuries and carries significant implications for athletic soundness and prognosis.
The majority of tendon injuries (75-93%) involve the superficial digital flexor tendon (SDFT), with the mid-metacarpal region of the forelimb affected in 97-99% of cases. The prevalence of SDF tendinopathy is particularly high in racing Thoroughbreds (11-30%), making this topic highly relevant for the NAVLE examination.
| Aspect |
Details |
| Etiology |
Acute overload injury during high-speed exercise, accumulated microdamage, age-related stiffening (older horses at higher risk for proximal rupture) |
| Common Location |
Mid-metacarpal region (97-99% of cases); proximal rupture at carpus more common in older horses |
| Clinical Signs |
Acute onset lameness (moderate to severe)
'Bowed tendon' appearance - swelling on palmar metacarpus
Heat and pain on palpation
Fetlock hyperextension (dropped fetlock) with complete rupture
Proximal rupture: swelling over back of knee, reluctance to extend carpus |
| Diagnosis |
Clinical examination (palpation, observation)
Ultrasonography: hypoechoic lesions, fiber disruption, increased cross-sectional area; perform at 7 days post-injury for optimal prognostic value
MRI for intra-thecal lesions or when ultrasound is inconclusive |
| Treatment |
Acute phase: Cold therapy, bandaging, NSAIDs, stall rest
Regenerative: PRP, mesenchymal stem cells (best evidence for SDFT injuries)
Rehabilitation: Controlled exercise program over 9-12 months
Surgical: Superior check ligament desmotomy (reduces reinjury in racehorses) |
| Prognosis |
Guarded for return to high-level performance; 56% reinjury rate with rest alone. Stem cell therapy may reduce reinjury to approximately 18% |
Functional Anatomy
Understanding the anatomy and biomechanical function of equine tendons and ligaments is essential for recognizing injury patterns and determining prognosis.
Flexor Tendons
Superficial Digital Flexor Tendon (SDFT)
The SDFT is the most commonly injured tendon in horses. It arises from the superficial digital flexor muscle at the level of the carpus and runs down the palmar aspect of the limb. The accessory ligament (superior check ligament) connects the SDFT to the radius, preventing overstretching of the muscle-tendon unit. The SDFT splits into two branches that insert on the proximal and middle phalanges (P1 and P2).
Key Function: Energy storage and release during locomotion (acts as a biological spring), flexion of the fetlock and pastern joints.
Deep Digital Flexor Tendon (DDFT)
The DDFT arises from three muscle bellies that fuse proximal to the carpus. It passes through the carpal canal and continues distally, reinforced by the inferior check ligament (accessory ligament of the DDFT) in the mid-metacarpal region. The DDFT passes over the navicular bone within the navicular bursa before inserting on the flexor surface of the distal phalanx (P3).
Key Function: Flexion of the coffin, pastern, and fetlock joints; only flexor tendon inserting on P3.
High-YieldComplete DDFT rupture results in a pathognomonic 'toe-up' stance because the DDFT is the only structure inserting on P3. This presentation should immediately suggest DDFT rupture on the NAVLE.
Suspensory Apparatus
Suspensory Ligament (Interosseous Muscle)
The suspensory ligament originates from the proximal palmar metacarpus and distal carpal bones. It courses distally between the splint bones, bifurcates into medial and lateral branches, and inserts on the proximal sesamoid bones. Extensor branches continue dorsally to join the common digital extensor tendon.
Key Function: Primary support of the fetlock joint; prevents hyperextension. The suspensory apparatus continues distally as the distal sesamoidean ligaments.
Reciprocal Apparatus of the Hindlimb
The reciprocal apparatus mechanically couples stifle and hock flexion/extension, meaning both joints must flex or extend together. This apparatus consists of:
- Peroneus tertius (cranial component): Entirely tendinous structure from extensor fossa of femur to dorsoproximal metatarsus and calcaneus
- Gastrocnemius and SDFT (caudal component): Form the common calcaneal tendon inserting on the tuber calcanei
NAVLE TipPeroneus tertius rupture = hock can extend while stifle is flexed (pathognomonic). Gastrocnemius rupture = hock flexes while stifle extends (dropped hock). Know these pathognomonic presentations - they are frequently tested!
| Aspect |
Details |
| Etiology |
Laceration, chronic navicular disease with adhesions, severe trauma |
| Pathognomonic Sign |
'Toe-up' stance - dorsiflexion of the coffin joint because DDFT is the only flexor inserting on P3 |
| Clinical Signs |
Severe lameness
Toe elevated off ground at rest
If within digital sheath: effusion present |
| Treatment |
Supportive care with heel wedge shoeing
Casting for stabilization if complete rupture
Tenoscopy if within digital flexor tendon sheath |
| Prognosis |
Poor for athletic soundness; may be salvaged for pasture soundness or breeding |
Specific Tendon and Ligament Ruptures
Superficial Digital Flexor Tendon (SDFT) Rupture
Deep Digital Flexor Tendon (DDFT) Rupture
Suspensory Ligament Rupture/Severe Desmitis
Exam Focus: Degenerative Suspensory Ligament Desmitis (DSLD) is a systemic connective tissue disorder (not just suspensory ligaments) with proteoglycan accumulation. Affects Peruvian Pasos, Arabians, Quarter Horses. Presents with progressive bilateral hindlimb fetlock drop ('coon-footed'). No cure; prognosis is poor.
Peroneus Tertius (Fibularis Tertius) Rupture
Gastrocnemius Muscle/Tendon Rupture
Collateral Ligament Injuries
Collateral ligaments restrict joint motion to the sagittal plane. Rupture causes joint instability and is often associated with concurrent soft tissue or meniscal injuries.
| Region |
Clinical Features and Prognosis |
| Proximal (PSD) |
Forelimb: Subtle lameness, worse on soft ground; 90% return to work with conservative treatment
Hindlimb: More challenging; may require fasciotomy of deep plantar fascia; 14% return to work with conservative treatment, 85% with surgical fasciotomy |
| Body |
Most common in racehorses (especially Standardbreds); enlargement, heat, pain; ultrasonography confirms diagnosis; shock wave therapy, PRP, stem cells used as adjunctive treatment |
| Branch |
Common in Standardbreds and jumping horses; often associated with sesamoiditis or avulsion fractures; radiography to evaluate sesamoid involvement essential |
| Complete Rupture |
Catastrophic; significant fetlock drop (hyperextension); most common cause of breakdown injuries in Thoroughbred racehorses; surgical fetlock arthrodesis for salvage |
Diagnostic Imaging
Ultrasonography
Ultrasonography is the primary diagnostic modality for tendon and ligament injuries. Optimal timing for initial prognostic scan is 7 days post-injury.
High-YieldThe palmar metacarpal region is divided into seven zones (1A, 1B, 2A, 2B, 3A, 3B, 3C) from proximal to distal, each 4 cm in length. Always document the zone of injury for accurate monitoring during rehabilitation.
| Aspect |
Details |
| Etiology |
Hyperextension of hock (limb trapped, horse struggles); falling, slipping; caught in bars; laceration; full-limb cast application |
| Pathognomonic Sign |
Hock can be extended while stifle is flexed (normally impossible due to reciprocal apparatus) |
| Clinical Signs |
Able to bear weight on affected limb
At walk: gastrocnemius and SDFT appear flaccid
Characteristic 'dimple' on caudodistal aspect of gaskin
At trot: obvious lameness with delayed protraction due to hock overextension |
| Diagnosis |
Clinical signs are pathognomonic; ultrasonography confirms location (usually mid-tibial region) |
| Treatment |
Strict stall rest for 4-6 weeks, then controlled rehabilitation for 3-4 months; surgical intervention not recommended |
| Prognosis |
Generally good (78% return to previous level of exercise); avulsion at origin carries worse prognosis |
Treatment Options
Conservative Management
Rest is the most universally accepted component of any tendon/ligament treatment protocol. A controlled exercise rehabilitation program typically spans 9-12 months.
Acute Phase (0-14 days)
- Cold therapy (ice water immersion or ice packs) 2-3 times daily
- Supportive bandaging to reduce swelling
- NSAIDs (phenylbutazone, flunixin meglumine, firocoxib) for inflammation and analgesia
- Strict stall rest
Rehabilitation Phase
- Controlled hand walking beginning at 3-4 months (for mild-moderate injuries)
- Gradual increase in exercise intensity based on ultrasound monitoring
- Serial ultrasound examinations every 60-90 days
Regenerative Therapies
NAVLE TipOrthobiologics (PRP, stem cells) are administered INTRALESIONALLY under ultrasound guidance. They work by delivering growth factors or modulating inflammation. Evidence is strongest for stem cells in SDFT injuries. Remember: these therapies supplement, not replace, the 9-12 month rehabilitation period.
Surgical Options
| Aspect |
Details |
| Etiology |
Adults: Rare; severe trauma
Foals: Associated with dystocia, assisted delivery, uncoordinated attempts to stand |
| Pathognomonic Sign |
'Dropped hock' - hock flexes during weight bearing while stifle extends (opposite of peroneus tertius) |
| Clinical Signs |
Complete rupture: unable to bear weight (adults)
Swelling in crus region with hematoma
Tuber calcanei displaces distally during weight bearing
Internal rotation of limb (outward movement of calcaneus) may be present |
| Treatment |
Foals: Splinting/casting, sling support; favorable prognosis (82% race in Thoroughbreds)
Adults: Modified Thomas splint-cast combination; guarded prognosis |
| Prognosis |
Foals: Favorable for partial and complete ruptures
Adults: Poor for complete ruptures; favorable for partial ruptures with conservative management |
Prognosis Summary
| Joint |
Clinical Features |
Treatment/Prognosis |
| Fetlock |
Acute lameness, effusion; joint instability with complete rupture; medial and lateral CL present |
Immobilization, stall rest produces favorable results despite severe initial injury |
| Stifle |
Severe lameness, joint effusion; medial CL more common than lateral; often concurrent meniscal injury |
Mild sprains: 6-8 weeks rest then rehab; mild sprains = fair prognosis; severe = poor; often leads to DJD |
| Coffin (DIP) |
Subtle lameness; requires MRI for diagnosis; may have concurrent DDFT lesions |
Poor prognosis with conservative management; orthobiologics sometimes attempted (requires MRI guidance) |
| Finding |
Interpretation |
| Hypoechoic lesion |
Acute injury with hemorrhage, edema, fiber disruption; core lesions appear as dark areas within tendon substance |
| Anechoic lesion |
Complete fiber disruption with fluid accumulation; represents core lesion or complete rupture |
| Increased CSA |
Cross-sectional area increase indicates swelling/inflammation; can predict impending severe injury |
| Fiber pattern disruption |
Loss of normal parallel fiber pattern in longitudinal view; indicates partial or complete tearing |
| Peritendinous edema |
Subcutaneous fluid around tendon; early indicator of subclinical injury |
| Therapy |
Mechanism/Source |
Indications/Notes |
| PRP |
Platelet-rich plasma from patient's blood; concentrated growth factors (TGF-beta, PDGF) |
SDFT, DDFT, suspensory injuries; can be combined with shock wave; improves tissue organization |
| MSCs (Stem Cells) |
Bone marrow (sternal or tuber coxae) or adipose-derived; 3-4 week culture expansion for bone marrow; adipose can be same-day |
Best evidence for SDFT injuries; reduces reinjury rate; preferred for severe injuries with poor prognosis |
| IRAP/ACS |
Interleukin-1 receptor antagonist protein; anti-inflammatory |
Primarily for joint disease; limited use for pure tendon/ligament injuries |
| ESWT |
Extracorporeal shock wave therapy; sound waves stimulate healing, provide analgesia |
Chronic/recurrent PSD (41-53% return to work); often combined with PRP |
| Procedure |
Indication |
| Superior check ligament desmotomy |
SDFT tendinitis in racehorses; reduces tension on SDFT, decreases reinjury rate |
| Inferior check ligament desmotomy |
Flexural deformity (club foot); releases tension on DDFT |
| Plantar fasciotomy |
Hindlimb proximal suspensory desmitis; relieves pressure on proximal SL; 85% return to work |
| Fetlock arthrodesis |
Catastrophic suspensory apparatus failure; salvage for breeding |
| Tenoscopy |
Digital flexor tendon sheath injuries; debridement of DDFT tears, manica flexoria tears, adhesion removal |
| Structure |
Return to Athletic Function |
Key Factors |
| SDFT |
Guarded (44-55% with rest alone; improved with stem cells) |
Lesion size, chronicity, intended use |
| DDFT (complete) |
Poor |
May salvage for pasture/breeding |
| Proximal SL (forelimb) |
Good (90%) |
Uncomplicated, acute cases |
| Proximal SL (hindlimb) |
Guarded-Fair (14% conservative; 85% with surgery) |
Often requires fasciotomy |
| Peroneus tertius |
Good (78%) |
Avulsion at origin = worse |
| Gastrocnemius (foals) |
Favorable (82% race) |
Concurrent illness worsens |
| Gastrocnemius (adults) |
Poor (complete); Fair (partial) |
Severity of rupture |