Degenerative Suspensory Ligament Desmitis (DSLD) is a
syndrome being recognized with greater frequency. The
condition has been recognized in the Peruvian Paso, Peruvian
Paso crosses, Arabians, American Saddlebreds, American Quarter
Horses, Thoroughbreds and some European breeds such as the
Irish Thoroughbred and Swedish Warmbloods. Drs. Pryor, Pool
and Wheat first described DSLD at the University of California
at Davis in 1981 as Passive Suspensory Ligament Failure in an
unpublished paper. Recognition of DSLD with its grave
prognosis is essential among equine practitioners.
Horses present with a history of an obscure lameness
problem that has developed over time. Cases may be mildly
affected and have only a painful response to palpation of the
suspensory ligaments, especially the suspensory branches. DSLD
is unique in its bilateral distribution, which can affect both
front legs, both hind legs or all four legs. No other
suspensory injury matches this pattern of distribution. As the
condition progresses there may be filling in the fetlock
joints (windpuffs). An exaggerated dropping of the fetlocks
while in motion may be noted. The pasterns eventually become
horizontal and secondary degenerative joint disease (ringbone)
may occur. There is a gradual straightening of the stifle and
hock angle if the hind legs are affected. Some horses become
resistant to having their feet picked up and shoeing becomes
an ordeal. Some horses will dig holes to rest the affected
legs in a position with the toes down and the heel elevated.
When standing on a hard surface, the horse may rock back and
forth, relieving one leg while loading the other painful leg.
Laminitis might also be misdiagnoses. Acute rupture of the
suspensory apparatus is possible.
1. Palpation of the suspensory ligaments will indicate a
bilateral distribution of suspensory ligament branches with a
pain response, thickening and hardening of the mid-body or
2. Ultrasound imaging will confirm the diagnosis. There
will be a poor fiber pattern noted at the origin of the
suspensory or at the bifurcation and branches. The
circumference of the medial/lateral suspensory branches will
be enlarged (greater than 1.2 cm)
3. Radiographs will reveal a lowering of the sesamoid bones
relationship0 to the fetlock joint with possible
mineralization noted in the soft tissue areas of the
suspensory branches. Degenerative joint disease may be present
in the pastern joint. Subluxation of the pastern joint is
obvious as the horse becomes coon footed.
4. Thermography will show significant warming over the
areas of the suspensory branches.
5. Nuclear scintigraphy clearly demonstrates a unique
distribution in both the soft tissue phase and bone phase. The
suspensory branches are quite reactive on soft tissue and the
proximal sesamoid bones as well as the pastern joint 'light
up' on the bone phase.
Gross pathology will reveal the extent of damage that has
been sustained by the suspensory ligament. The ligament is
enlarged and has a hard fibrous feel. There may be adhesions
of the suspensory ligament to the cannon bone, the splint
bones and the deep flexor tendon. The bifurcation between the
suspensory branches may be totally filled with fibrocartillage.
Histopathology on more than 30 cases (Pool 1992) showed a
consistent pathological process. Speculation is that, at some
point in the life of a predisposed horse, a previously normal
suspensory ligament begins to undergo failure when resisting
normal forces of tension (strain). With normal tissue, a
strain is repaired with fibroblasts (cells that produce type
III collagen). Fibroblasts 'bridge' the damage and, in time,
repair the damaged tissue. The new collagen fibers then orient
themselves in line with the stress on the tissue as the
healing progresses. Horses affected with DSLD have an abnormal
healing response. Regardless of the causes of the injury or
strain, the damaged tissue heals with cartilage instead of
collagen. Fibroblasts defect and become chondrocytes and the
ligament is unable to restore itself to normal tissue
strength. The ligaments continue to 'break down' even with
just the strain of normal weight bearing. Some Peruvian Pasos
have spontaneously exhibited DSLD as yearlings (1).
1. Stall confinement and rest for 9 - 12 months. Slow
up-hill walking may help the superficial flexor muscle and
tendon unit to handle the increased load due to the lack of
suspensory ligament support.
2. Egg bar support with wedging to comfort. Patten shoes
can be used behind (4). This gives immediate relief. Horses
are gradually lowered as level of comfort improves. Recent
research shows that raising the angle loads the dorsal
branches of the suspensory ligament itself (5). Clinically the
horses show great relief from pain with the angle elevated.
Although this shoeing philosophy is controversial, the horse
clinically improves in comfort and the ultrasound confirms
"healing" of the affected area of the suspensory ligaments,
although once again, it heals with cartilage.
3. Analgesics as needed.
4. Supportive leg wraps, similar to Sports Medicine Boots,
will improve the level of comfort for the horse, but can be
only left on for a maximum of 12 hours a day.
5. MSM does seem to help the horse's level of comfort and
some horses can handle light riding and go lame if taken off
6. Acupuncture may give some relief.
DSLD has a grave prognosis for the equine athlete. The
question of heredity must be answered as there are several
sire/son, dam/daughter and full sister combinations of
affected individuals. A pasture comfortable animal seems to be
the best result at this time. The Peruvian Paso cases tend to
continue the 'break down' process despite heroic efforts by
the veterinarian, the farrier and the owner. Euthanasia for
humane pain relief is, unfortunately, the outcome.
The DSLD syndrome should be included in the list of
differential diagnoses of a horse that presents with symptoms
of dropped fetlocks, horizontal pasterns, straight hocks and
stifles and bilateral or quadrilateral limb lameness. DSLD
should also be considered when the horse exhibits difficulty
standing when the opposite leg is held up along with signs of
discomfort and when enlargement and/ or hardening of bilateral
or quadrilateral suspensory ligaments and associated branches
is noted on palpation. Accurate and early diagnosis by
ultrasound, therapeutic shoeing, stall confinement, analgesics
(when indicated for pain) have appeared to aid in the healing
of affected horses to the point of pasture soundness. One must
remember that when healing, cartilage is substituted for
normal collagen tissue; therefore weak non-painful suspensory
ligaments are the best to be expected through the healing
process. The question of heredity needs to be addressed, as
these horses are only returning to breeding soundness rather
than to previous athletic ability. Although DSDL is a
relatively uncommon disease entity, it unfortunately carries a
poor prognosis for the affected equine athlete.
Pool R, Wheat J, et al (1981) Clinical and pathological
characterization of suspensory apparatus failure in Peruvian
Paso horses. Unpublished paper.
Pool R, (1991) Pathology of tendons and ligaments, 13th
Bain-Fallon Memorial Lecture Proceedings, Melbourne. Australia
Young J, (1993) Degenerative Suspensory Ligament Desmitis,
Hoofcare and Lameness, pp 6-19.
Stashak, T.S. (1987) Traumatic rupture of the suspensory
apparatus. In: Adams "Lameness in Horses", Lea & Febiger,
Philadelphia, p 585.
Thompson, Cheung, Silverman (1993) The effect of toe angle on
tendon, ligament and hoof wall strains in vitro. Journal of
Equine Veterinary Science 13, p. 651.
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