Tendons passively transfer force from muscle to bone to effect locomotion whereas ligaments restrict distraction of two bony surfaces. The digital flexor tendons and the suspensory ligament (SL) on the palmar aspect of the limb in the horse have additional supportive functions because of the large weight bearing loads on the hyperextended metacarpophalangeal joint (MCPJ). Furthermore the superficial digital flexor tendon (SDFT) acts to store energy and promote efficient locomotion.

Determining which structures are involved?

Use your eyes! Look at the palmar aspect of the metacarpus; it should be perfectly vertical with no evidence of bowing; look at the level of the metacarpophalangeal joint, it will be dropped if there is significant injury to the SDFT. Palpate all the palmar tendons and ligaments with the limb loaded and unloaded checking for heat, pain and adhesions. If the horse has sustained a wire wound the extent of tendon involvement can be determined by assessment of the position of the foot and fetlock: if the SDFT alone is fully transected then the metacarpophalangeal joint will be dropped when the limb is loaded, if the deep digital flexor tendon (DDFT) and SDFT are transected then the horse will knuckle the toe upwards (think where the DDFT inserts), when the SDFT, DDFT and SL are transected the horse has a plantarograde stance and the metacarpophalangeal joint bears weight. 

Emergency management of any of these conditions involves, application of supportive bandaging, administration of non-steroidal anti-inflammatory drugs ± cold hydrotherapy.

Superficial digital flexor tendinopathy

The horses’ limb has evolved for speed so there is limited muscle mass on the distal limb that has resulted in long tendons and a hyperextended MCPJ. The SDFT sustains large loads during normal galloping and operates very close to its’ functional limit hence incidence of injury to this structure in racehorses and 3 day event horses is high (10-30% as reviewed by Patterson-Kane and Firth 2009). Tendons are predominantly composed of type I collagen secreted in perfect parallel alignment to provide the property of tensile strength. Tendon as a tissue has a relatively low cellularity and once damaged the resident cells fail to regenerate normal tendon tissue such that it heals with a fibrous scar that has inferior biomechanical properties. Consequently re-injury rates are high (56% in National Hunt horses Dyson 2004)

High speeds, hard ground, fatigue, weight of horse and shoe have al been implicated as risk factors for tendinopathy (Williams et al 2001). Clinical superficial digital flexor tendinopathy varies from individual collagen fibril slippage to single fibril or fibre rupture through to complete rupture of the whole tendon as the number of affected fibres increases. There are three main theories to describe the aetiopathogenesis of tendon injury:

1. Repetitive subthreshold mechanical overstimulation resulting in microdamage and activation of degradative enzymes and extracellular matrix destruction.
2. Understimulation; Loss of local homeostatic strain results in activation of degradative enzymes
3. Aberrant differentiation of resident progenitor cells to causing lipid, cartilage or bone formation within the tendon and weakening mechanical properties.

Horses typically present acutely, severely lame with a soft, painful ‘bowed’ tendon in the mid canon region. When the limb is loaded the MCPJ can appear ‘dropped’ if the SDFT injury is severe. Lameness often resolves quickly in non-severe injuries. Diagnosis is based on ultrasonography carried out 10-14 days after initial injury to confirm the extent of the fibre damage. Tendons should be evaluated in both transverse and longitudinal ultrasonograms. It is important to be familiar with the normal appearance of the palmar metacarpus (Figure 1). A central ‘core’ lesion is usually apparent (anechoic (black) area within hyperechoic (white) tendon) (Figure 2); the length of damaged tendon, total cross sectional area and % cross sectional area fibre damage should be documented on the first ultrasound to allow monitoring of healing.

There are 3 phases of tendon repair and treatment should be targeted accordingly: the acute inflammatory phase; the subacute fibroplastic phase and the chronic remodelling phase. Acute management in the inflammatory phase involves strict box rest, cold hosing for 15-20 minutes twice daily, supportive bandaging, non-steroidal anti-inflammatory medication (phenylbutazone) with controlled walking exercise introduced as soon as the horse is sound at the walk.

The aim of treatment in the remodelling phase is to promote parallel longitudinal fibre alignment. “Of the many treatments that have been advocated there is little evidence that any of them have enduring beneficial effects” (Dowling and Dart 2000). Treatment options include:

4.     Thermocautery (pin or bar firing).

Deep digital flexor tendon (DDFT) is less common than injury to the SDFT injury but can occur at several locations;

1. within the hoof capsule
2. within the digital flexor tendon sheath (DFTS)
3. within the tarsal sheath
4. within the carpal sheath (associated with osteochondromas)
5. associated with desmitis of the acceossory ligament of the deep digital flexor tendon (see below)

Diagnosis and treatment of deep digital flexor tendinopathy

Injury to the DDFT within the hoof capsule is most common in horse that jump and pleasure horses. Clinically cases present with sudden onset severe unilateral lameness that resolves and recurs when exercise is reintroduced, lameness can usually be abolished by palmar digital analgesia just proximal to the collateral cartilages. Lameness will respond to intra-articular analgesia of the distal interphalangeal joint or intrathecal analgesia of the navicular bursa in some cases. Radiography of the foot is frequently unremarkable but occasionally demonstrated remodelling of the facies flexoria of the third phalanx with insertional lesions. Ultrasonography is usually only useful if the DDFT lesions extends proximally to the level of the pastern. Definitive diagnosis is made using magnetic resonance imaging with the horse standing and sedated. Three types of lesions are described within the hoof capsule (dorsal fibrillation, core lesions and sagittal splits). Treatment is focussed on box rest, controlled exercise and corrective farriery (raising the heels reduces the tension on the DDFT BUT increases the tension on the SDFT and SL). Prolapse of tendon fibres into the navicular bursa can be treated surgically, with debridement of torn fibres under arthroscopic guidance.

Injury to the DDFT within the DFTS is most common in horses that jump. Marginal tears of the DDFT present clinically with effusion of the DFTS and sudden onset lameness. The lameness usually is improved following intrathecal analgesia of the DFTS. These lesions are often missed during ultrasonography of the DFTS and definitive diagnosis is made tenoscopically. Treatment can be conservative involving box rest, controlled exercise and intrathecal corticosteroids and hyaluronan or surgical debridement of frayed tendon fibres (Smith et al 2006).

The interosseous ligament in the horse has evolved to become a ligamentous support structure (the suspensory ligament [SL]) that bifurcates in the mid canon into 2 branches that insert on the proximal sesamoid bones (PSB). The suspensory apparatus then continues as sets of paired distal sesamoidean ligaments to provide support for th palmar apstern. The suspensory apparatus can fail at several locations:

1. Complete breakdown when both proximal sesamoid bones fracture in the race horse. This is almost exclusively a condition of racehorses occurring predominantly in the forelimbs and more commonly in the USA than the UK. Horses pull up non-weight bearing lame with a dropped fetlock, radiography can demonstrate bilateral PSB fracture. This is a career ending injury but does not qualify for humane destruction as treatment options are available, i.e. fetlock arthrodesis.
2. Proximal suspensory desmitis (PSD) in the forelimbs is different to PSD seen in the hind limbs. Forelimb PSD usually present as bilateral lameness with the lamer leg on the outside of the circle. Lameness is alleviated by analgesia of the lateral palmar nerve, ultrasonography can demonstrate heterogenous fibre pattern and increased depth of the ligament. Forelimb PSD usually responds well to 3 months rest and controlled exercise. Hind limb PSD can present acutely or have an insidious onset, more common in dressage horses with an upright hock conformation. Diagnosis can be difficult but is based on analgesia of the lateral plantar nerve, radiography and ultraosonography. Treatment options include rest and controlled exercise, extracorporeal shock wave treatment (ESWT) or surgery (neurectomy of thedeep branch of the lateral plantar nerve and fasciotomy).
3. Mid-body suspensory desmitis
4. Suspensory branch desmitis
5. Desmitis of the distal sesamoidean ligaments.

Desmopathy of accessory ligament of the deep digital flexor tendon (ALDDFT)

Present clinically as acute onset moderate to severe lameness with swelling of the ALDDFT (also know as inferior check ligament). Possibly a higher incidence in ponies and horses that jump. Diagnosis is based on clinical findings and ultrasound, the typical ultrasonographic diagnosis demonstrates enlargement of the ALDDFT rather than core lesion formation as seen in the SDFT. Treatment is again based on box rest and controlled walking exercise for 3 months with ultrasonographic re-evaluation prior to introduction of trot work    

DIPJ collateral ligament desmopathy

Recurrent forelimb lameness usually with no localising clinical signs. Severe cases demonstrate palpable enlargement of the collateral ligament of the distal interphalangeal joint. Lameness improves following PDNB but often requires ASNB to fully abolish lameness. Some cases are apparent on ultrasonographic or scintigraphic evaluation but definitive diagnosis requires MRI. Treatment is aimed at correcting hoof imbalance and maintaining box rest and controlled exercise for 6-12 months. Prognosis for return to athletic function is poor.