Proximal suspensory desmopathy in horses

Proximal suspensory desmopathy in horses

An overview of the causes, diagnostic approach and treatment options for this common condition in performance horses.
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Mar 01, 2014


Performance horses are particularly at risk for this condition, due to the stress placed on the proximal suspensory ligament during exercise. (GETTY IMAGES/KOJI AOKI)
Proximal suspensory desmopathy (PSD) of the hind limb is a commonly seen problem in many types of performance horses, especially those equine athletes that are required to heavily load their hind legs while performing in their respective disciplines. Dressage horses, cutting horses and jumpers are particularly at risk for this condition. In these horses, damage often occurs proximally in the tendon, and the diagnosis and treatment at this location can be frustrating for both practitioners and horse owners.

Many different treatment approaches have been tried—from complete rest to shock wave therapy to the use of regenerative medicine via intra-lesional injection (extracellular matrix powder, autogenous bone marrow, autogenous stem cells, platelet rich plasma and others). Recently another treatment approach, based on what is known about the anatomy and physiology of the hind limb proximal suspensory ligament (PSL), has been increasingly utilized. This procedure combines fasciotomy of the PSL and neurectomy of the deep branch of the lateral plantar nerve.

Though this procedure was first reported in 2006 and expanded upon in 2008, it has become more popular recently and is offering major relief to many affected horses. There are still some important issues with hind limb PSD diagnosis, patient selection and staging, and postsurgical rehabilitation, but it seems that fasciotomy-neurectomy can be a positive step and should be considered in the management of hind limb PSL damage.

Probable causes and pathology


(GETTY IMAGES/LYNN KOENIG)
Injury to the PSL occurs when the ligament is stretched beyond its normal physiological limit. Many factors contribute to this stress-induced injury, including straight, upright hind limb conformation, poor surfaces or uneven footing in the ring, fatigue and other underlying pathology.

It is currently thought that many cases of PSL injury are the result of accumulated, submaximal damaging events (athletic work trauma), rather than a single catastrophic incident. It is further believed that work trauma is superimposed on progressive degeneration of the ligament itself.

Sue Dyson, MA, PhD, a specialist in equine orthopedics at the Centre for Equine Studies at the Animal Health Trust in Newmarket, U.K., believes there should be a name change for this condition that better reflects both the actual ligamentous damage incurred and its probable cause.

"Proximal suspensory desmopathy, as opposed to desmitis, might be a more appropriate term in some horses in view of the degenerative histological characteristics of injured ligaments and the absence of signs of inflammation in the majority," she says.

According to Dyson, pain and the resulting lameness in these cases may originate from the suspensory ligament itself and from compression of associated nerves (i.e., plantar neuritis) and less from inflammation. It is the special anatomical architecture of the hind limb proximal suspensory ligament that is both the cause of problems in this area and the reason for success of the fasciotomy-neurectomy procedure.

The hind limb suspensory ligament is confined by the plantar aspect of the third metatarsal bone (MTIII), the second and fourth metatarsal bones (MTII and MTIV), and the deep fascia running between the plantar aspects of MTII and MTIV. Repetitive injury to this ligament results in increased tendon size due to initial intraligamental hemorrhage and edema, which is followed by removal of injured tissue and proliferation and migration of fibroblasts. When this normal repair process is not fully accomplished due to repeat stress trauma, there is resultant production of inelastic, cartilage-like tissue within the ligament. This chronically thickened, swollen ligament in its restricted "compartment" exerts significant pressure on the lateral plantar nerve, which is adjacent to this area, causing the pain and lameness that is often seen in these horses upon exercise.

Ferenc Tóth, DVM, PhD, a former researcher at the University of Tennessee's College of Veterinary Medicine, and his coworkers have summarized the clinical relevance of their observations on lameness caused by PSD, stating, "Horses lame because of PSD of the pelvic limb may remain lame after desmitis has been resolved because of compression of the deep branch of the lateral plantar nerve."

Tóth's final suggestion is that "excising a portion of this nerve may resolve lameness," foreshadowing future developments in treatment.1