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Suspensory Ligament Desmitis

Ashlee E. Watts

■ Definition and Etiology The suspensory ligament (SL), also known as the interosseous muscle, is a strong, flat, tendinous band that contains a variable amount of muscle fibers.1 The SL originates from the palmar carpal ligament and the proximal palmar aspect of the third metacarpus (MCIII) and in the hindlimb from the proximal plantar third metatarsus (MTIII).

Coursing distally, it descends between the second and fourth metacarpal/metatarsal bones and divides into the medial and lateral branches before inserting on the abaxial aspect of the proximal sesamoid bones. The suspensory apparatus continues distally as the straight, oblique, cruciate, and short distal sesa- moidean ligaments, which originate from the base of the proximal sesamoid bones and insert in the palmar pastern. The SLs main function is to prevent hyperextension of the fetlock joint.1 Its branches also help stabilize the rotational forces on the joint. Injury to the SL occurs when it is overloaded with stress (overstretched) and its structural integrity is com­promised. As with tendons, the repair process is characterized by inflammation (desmitis) and resultant fibroplasia. Healing occurs over many months, and repaired tissue is subject to re-injury due to the accumulation of scar tissue. SL desmitis is a common injury in all breeds of performance horses. Both forelimb and hindlimb injuries occur, and bilateral desmitis is not uncommon. Desmitis of the SL can be divided into three regions of interest: the proximal (origin) portion, the body, and the branches. Proximal SL desmitis is likely due to hyperextension of the carpus/tarsus in conjunction with severe overextension of the fetlock joint.1 Straight hock conformation and hyperextension of the fetlock joint may be predisposing factors or may exacerbate the injury in the hindlimbs.
Exercise in deep soft footing may also increase risk of injury.2 Avulsion fracture, bone sclerosis, and/or enthesophyte formation in the proximal palmar/plantar MCIII/MTIII can also occur. Proximal SL desmitis occurs most frequently in sport horses, racehorses, and Western performance horses.1 Injury to the body of the SL is less common and occurs predominantly in racehorses, specifically Standardbreds.1,2 Desmitis of the SL branches is most common in Standardbreds and jumping horses.1 In the SL branches, injury is frequently associated with fetlock lame­ness, which suggests that the twisting motion of the fetlock predisposes horses to injury.

Catastrophic traumatic disruption of the suspensory apparatus occurs almost exclusively in the forelimbs of Thoroughbred racehorses and is the most common cause of breakdown injuries.3 Fatigue and high speed are components of this career-ending injury. Degenerative suspensory ligament desmitis (DSLD) is a disorder characterized by progressive degeneration and enlarge­ment of the SL, resulting in excessive fetlock hyperextension (dropping). Affected horses are generally dropped in both hind fetlocks and variably painful. The condition occurs sporadically in many breeds, usually older horses and broodmares.1 Peruvian Paso4 horses may be at risk and often are affected in all four limbs. The pathogenesis is unknown.

■ Clinical Signs Horses with proximal SL desmitis fre­quently have no localizing clinical signs. Heat, swelling, and edema are transient or absent, and lameness is variable. Horses with bilateral injury, especially in the hindlimbs, may have subtle gait abnormalities that are only apparent during ridden work. Lack of impulsion, resistant behavior, and loss of hindlimb activity are frequent complaints. In horses with desmitis of the body and branches of the SL, heat, pain, ligamentous enlargement, and lameness are common. Associated fetlock effusion and concurrent distal splint bone fractures may also be noted.

Acute severe traumatic disruption of the suspensory apparatus results in obvious swelling, grade 4 to 5 lameness, and a hyperextended fetlock. Affected horses require first-aid treatment by application of a splint for weight-bearing stability. DSLD is characterized by bilateral chronic lameness, painful and enlarged SLs, dropped fetlocks, prolonged periods of recumbency, and reluctance to move.1,4

■ Diagnosis Perineural analgesic techniques help localize the site of lameness pain to the SL. For proximal SL desmitis, analgesia of the deep branches of the lateral palmar nerve1,5 or lateral plantar nerve just distal to the tarsus1,6 will alleviate lameness in the forelimb or hindlimb, respectively. Desmitis of the SL body and branches is localized using low palmar/ plantar analgesia.

Ultrasonography is the imaging modality of choice for all but the proximal SL of the hindlimb, where high field MRI is the modality of choice.7 Lesion severity is assessed by obtain­ing cross-sectional and longitudinal views of the ligament and cross-sectional area measurements. Ultrasonographic changes include cross-sectional area enlargement, focal or diffuse areas of hypogenicity, core lesions, loss of normal fiber pattern, and periligamentous thickening. Mild injuries to the SL may be difficult to identify because of the wide variation in its normal ultrasonographic appearance. This is especially true in the proximal SL, since its origin is more heterogeneous than other tendons and ligaments because of variable amounts of fat and muscle tissue. Comparison between the affected and nonaffected limbs in the same horse are recommended because of individual variations and the large variation between breeds.1

Radiographic examination should be performed to identify concurrent bony lesions. Subchondral sclerosis, avulsion fracture, and enthesophyte formation have been identified in the proximal palmar/plantar MCIII/MTII regions of horses with proximal SL desmitis.1,8,9 Axial exostosis along the second and fourth metacarpal/metatarsal bones10 or fractures can contribute to SL body desmitis.

Sesamoiditis and sesamoid fractures may be noted in horses with desmitis of the SL branches. In acute traumatic disruption of the suspensory apparatus, comminuted fractures of both sesamoid bones are common.

Nuclear scintigraphic findings are normal in the majority of horses with SL desmitis.11 Increased radiopharmaceutical uptake associated with the proximal palmar/plantar MCIII/ MTIII can be identified in horses with avulsion fractures and other stress-related bone injuries seen in complex SL desmitis.8,9 MRI is not necessary but should be considered if no ultraso­nographic abnormality is identified, or for the proximal SL in the hindlimb. MRI has identified fibrous adhesions between the SL and the small splint bones.10

■ Treatment Treatment of acute SL desmitis is aimed at reducing inflammation with systemic NSAIDs, local cold hydrotherapy, limb bandages, and controlled exercise. Initial clinical signs dissipate quickly even when there is significant SL fiber disruption, so it is strongly recommended to assess the ligament using ultrasonography. In uncomplicated desmitis, a controlled graded exercise program is recommended. The duration of rehabilitation will depend on the extent and severity of the desmitis. Fractures of the small metacarpal/metatarsal bones or sesamoid bones should be removed prior to rehabilita­tion. Horses are confined to a stall and hand walked daily. Ligamentous healing should be monitored every 60 days using ultrasonography. Ideally there should be a progressive reduction in cross-sectional area, improved echogenicity, and fiber align­ment. Gradual increase in exercise can be prescribed depending on healing. The reparative process is slow, and return to competition or racing may not be possible for 12 to 18 months.

Damaged SLs have been injected with a wide assortment of therapeutics, and recommendations are similar to those outlined for tendinitis earlier in this chapter. Extracorporeal shockwave therapy1,12 may be beneficial.

The effects of intralesional platelet­rich plasma13 and autologous stem cells14 are currently under investigation, and clinical results are promising.

Successful treatment of proximal hindlimb SL desmitis is particularly challenging, and most horses treated conservatively remain lame. Neurectomy of the deep branch of the lateral plantar nerve,1,15,16 desmotomy,17 and fasciotomy14-17 may be beneficial in these horses. Fasciotomy surgery allows decompres­sion of the compartment-like syndrome that occurs when the damaged proximal SL becomes edematous and swells within the surrounding retinaculum. The deep branch of the lateral plantar nerve within the damaged SL becomes inflamed and damaged, so a neurectomy of this nerve is performed at the same time as the fasciotomy surgery.18

For horses with acute traumatic suspensory desmitis, it is crucial to place the affected limb in a protective splint that aligns the metacarpus with the phalanges in a straight column to prevent fetlock bending. Surgical management involves fetlock arthrodesis using a dorsal plate and wires or cables to reestablish the palmar tension band. Treatment for horses with DSLD is palliative, and rest versus turnout or barefoot versus shod does not appear to alter the long-term outcome. When there is deterioration or uncontrolled clinical signs despite treatment, options include surgical fetlock arthrodesis or euthanasia.

■ Prognosis Prognosis of SL desmitis depends on the location and severity of the injury. Uncomplicated cases with minimal disruption of the ligament can recover, and 90% of horses with acute proximal SL desmitis in the forelimb will return to full athletic function.2 Complicated, chronic, or recurrent desmitis has been associated with a worse prognosis. Chronic hindlimb proximal SL desmitis has a particularly poor prognosis, and only 14% of horses treated conservatively return to full work.2 Adjunctive medical and surgical treatments can improve prognosis in these problematic horses. Most horses with traumatic disruption of the SL can be salvaged for breeding after surgical repair. Prognosis for horses with DSLD is extremely poor, although these horses can also be salvaged with surgical arthrodesis of the fetlock joints.

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Source: Smith Bradford P., Van Metre David C., Pusterla Nicola (eds.). Large Animal Internal Medicine. Part 2. 6th edition. — Elsevier,2020. — 2279 p.. 2020

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