Lameness of the hind limbs caused by proximal suspensory desmitis (Proceedings)

Inflammation of the proximal aspect of the interosseus medius muscle, or suspensory ligament (i.e., proximal suspensory desmitis, PSD) of the hind limb, is a common cause of acute or chronic lameness of horses and is most commonly diagnosed in competition horses 4 to 10 years old.1,2 Horses that are excessively straight in the hocks or that have hyperextension of the fetlock may be predisposed to developing PSD of the hind limbs.3 Discerning whether hyperextension is a cause or a result of PSD may be difficult.

Diagnosis of PSD of the hind limbs is based on the results of physical examination, regional analgesia, and ultrasonographic and radiographic examination of the proximal plantar aspect of metatarsi.1-6 Nuclear scintigraphy is unreliable in establishing a diagnosis of PSD.3 Lameness of a hind limb caused by PSD is temporarily exacerbated by flexion of that limb in about 85% of affected horses.6 Pain causing lameness is determined to be localized to the proximal aspect of the suspensory ligament of one or both hind limbs by observing that lameness improves substantially after anesthetizing either the tibial nerve 8 to 10 cm proximal to the tuber calcis, the dorsal branch of the lateral plantar nerve (DBLPN) 2 or 3 cm distal to the tarsometatarsal joint, or the lateral and medial plantar metatarsal nerves 4 to 5 cm distal to the tarsometatarsal joint.1,3 These nerve blocks are administered after observing a negative response to desensitization of the fetlock and structures distal to it after anesthetizing the medial and lateral plantar nerves and the medial and lateral dorsal and plantar metatarsal nerves at the level of the distal end of the second and fourth metatarsal bones.

Ultrasonographic evidence of PSD includes abnormal fiber pattern, enlarged cross-sectional area (defined as a cross-sectional area greater than 1.5 cm2),7 and poor definition of the margins of the suspensory ligament. One study evaluating the value of ultrasonographic examination in the diagnosis of PSD of the hind limb found that ultrasonography correlated poorly with MRI and histology in establishing the cross-sectional area of the proximal aspect of the suspensory ligament.8

Radiographic abnormalities of the proximal aspect of the metatarsi associated with PSD of the hind limbs include new periosteal bone on the proximoplantar aspect of the 3rd metatarsal bone, most apparent on a lateromedial projection, and trabecular sclerosis, which is seen best on the dorsoplantar projection.2 Dyson1 found radiographic abnormalities of the proximoplantar aspect of the 3rd metatarsal bone in 55% of hind limbs affected with PSD, whereas Crowe et al.4 found radiographic abnormalities of the proximoplantar aspect of the 3rd metatarsal bone in only 24% of hind limbs affected with PSD.

Treatments of horses lame because of PSD of the hind limbs include prolonged confinement followed by a regimen of controlled, gradually increasing exercise.1,9 Although approximately 90% of horses with PSD of one or both fore limbs return to soundness with this treatment,10 horses with PSD of one or both hind limbs usually remain lame.1,9 In one study, confinement followed by a regime of controlled, gradually increasing exercise enabled only 14% of horses with PSD of one or both hind limbs to return to their previous level of activity, without recurrent lameness, for more than a year.1

Treating horses with PSD of the hind limbs with a combination of confinement and shock wave therapy improves the prognosis for return to soundness.4 Rapid improvement in lameness after treatment may be due to analgesic provided by the therapy,4 and sustained improvement may be the result of an increased rate of deposition of collagen fibrils and greater expression of transforming growth factor β-1.11 In one study, treatment with shock wave therapy, in addition to restricted exercise for 12 weeks allowed 41% of horses suffering from PSD of one or both hind limbs to return to their previous level of activity, without recurrent lameness, for more than 6 months.4

Hewes et al., reported that 85 % of horses lame because of PSD of the hind limbs characterized by a core lesion, were able to return to full work after being treated by a combination of desmotomy and fasciotomy, in addition to restriction of exercise for 30 days.9 These investigators speculated that horses improved because fasciotomy decompressed the enlarged suspensory ligament, and desmoplasty facilitated angiogenesis in the damaged portion of the ligament.9

Other treatments of horses affected with PSD include infiltration of a glucocorticoid around the insertion of the affected suspensory ligament of acutely affected horses, injection of bone marrow or bioscaffold material into the ligament, and systemic or local administration of glycosaminoglycans.5,9,12

The suspensory ligaments of the hind limb receive sensory and motor innervation from the DBLPN and from its branches, the medial and lateral plantar metatarsal nerves. The tibial nerve supplies the lateral plantar nerve from which the DBLPN originates.1 The proximal aspect of the suspensory ligament, the distal most segment of deep branch of the lateral plantar nerve coursing plantar to the suspensory ligament, and the plantar metatarsal nerves running axial to the second and fourth metatarsal bones, are rigidly restrained by the plantar aspect of the 3rd metatarsal bone, the axial borders of the 2nd and 4th metatarsal bones, and the deep fascia covering the suspensory ligament.3

Lameness of the hind limbs caused by PSD may be due, in part, to damage to DBLPN and the plantar metatarsal nerves that occurs when these nerves are compressed within their confines by the swollen suspensory ligament. Compression of these nerves may be the cause of the poor response of horses lame from PSD of the hind limbs to treatment by rest alone. Pathological changes are usually present in the DBLPN of horses with lameness of the hind limbs caused by PSD and include myxomatous expansion with formation of Renaut bodies in the subperinerium and nerve fascicles, and axonal degeneration, all changes associated with entrapment neuropathy.

Excision of a segment of the deep branch of the lateral plantar nerve to desensitize the suspensory ligament, either alone or combined with transection of the fascia plantar to the suspensory ligament to decompress the ligament, has been used to treat horses for lameness of one or both hind limbs caused by PSD.13 To transect the DBLPN, horses are positioned in dorsal recumbency with hind limbs flexed, and the region of each hind limb between the gaskin and the fetlock is prepared for aseptic surgery. Neurectomy is usually performed on both hind limbs of horses affected with PSD, even if only one of the limbs is lame because unilaterally affected horses sometimes become lame on the limb that did not receive surgery when strenuous exercise is resumed (Ger Kelly, personal communication, 2007). To locate the DBLPN, an 8- to 10-cm skin incision, centered at the tarsometatarsal joint, is made at the lateral border of the tendon of the superficial digital flexor muscle. The incision is extended through the flexor retinaculum, and the lateral plantar nerve is identified coursing next to the lateral margin of the superficial digital flexor tendon. A 3- to 4-cm section of the lateral plantar nerve is separated from fascia and retracted laterally using a Penrose drain. The DBLPN is isolated between the tendon of the deep digital flexor muscle and the suspensory ligament using a curved mosquito hemostat to bluntly separate fascia, and a 2-cm section of the nerve is excised. To perform fasciotomy, the deep digital flexor tendon is retracted medially, and the U-shaped proximal border of the fascia plantar to the suspensory ligament is identified. The fascia is split longitudinally about 4 cm using Metzenbaum scissors.

The incisions in the flexor retinaculum and the subcutaneous tissue are closed separately using 2-0 PDS. The skin incision is closed with skin staples or 0-polypropylene sutures placed in a vertical mattress pattern. The wounds are covered with a sterile, non-adherent, synthetic pad, which is secured with sterile cast padding and elastic, adhesive tape. An absorbent cotton pad is applied to the hock and secured with elastic gauze and elastic, non-adhesive tape. At subsequent bandage changes, application of the inner layer of elastic, adhesive tape is omitted.

Horses receive phenylbutazone (2.2 mg/kg) orally twice daily for 4 to 7 days, and the limbs are re-bandaged every 3 to 4 days until skin staples or sutures are removed at 14 to 16 days after surgery. Horses are confined to a stall for 3 weeks and are walked daily during this time. At 3 weeks, the horses are placed into a small paddock for several more weeks before being returned gradually to full exercise.

In one study, decompressive fasciotomy combined with excision of a segment of the DBLPN enabled 18 of 20 (90%) horses to resume their previous level of exercise, without suffering from the recurrence of lameness.13 In an unpublished study, 16 of 19 horses (84 %) determined to be lame in one or both hind limbs because of PSD that were treated by excision of a segment of the DBLPN alone returned to soundness (Toth, Schumacher, et al, 2007).

Transection of the DBLPN likely causes neurogenic atrophy of at least a portion of the suspensory ligament (Schumacher, personal observation), and although the clinical significance of neurogenic atrophy of the ligament is not known, it could increase the risk of catastrophic failure of the ligament. The effects of excising a segment of the DBLPN on the integrity of the suspensory ligament need to be investigated to determine the long-term risk of complications associated with the treatment.

References

1. Dyson S: Proximal suspensory desmitis in the hindlimb: 42 cases. Br Vet J 150:279-291, 1994

2. Dyson S: Proximal suspensory desmitis: clinical, ultrasonographic and radiographic features. Equine Vet J 23:25-31, 1991

3. Dyson SJ, Genovese RL: The suspensory apparatus, in Ross MW, Dyson S (ed): Diagnosis and Management of Lameness in the Horse. Philadelphia, PA, W. B. Saunders Company, 2002, pp 654-672

4. Crowe OM, Dyson SJ, Wright IM, et al: Treatment of chronic or recurrent proximal suspensory desmitis using radial pressure wave therapy in the horse. Equine Vet J 36:313-316, 2004

5. Dyson S: Proximal suspensory desmitis in the forelimb and the hindlimb. Proc 46th Annual Convention of the American Association of Equine Practitioners, San Antonio TX, pp 137-142, 2002

6. McIlwraith CW: Diseases of joints, tendons, ligaments, and related structures, in Stashak TS (ed): Adams' Lameness in Horses (ed 5), Philadelphia, PA, Lippincott Williams & Wilkins, 2002, pp 459-644

7. Reef VB: Musculoskeletal ultrasonography, in Reef VB (ed): Equine Diagnostic Ultrasound, Philadelphia, PA, W. B. Saunders Company, 1998, p 61

8. Bischofberger AS, Konar M, Ohlerth S, et al: Magnetic resonance imaging, ultrasonography and histology of the suspensory ligament origin: a comparative study of normal anatomy of warmblood horses. Equine Vet J 38:508-516, 2006

9. Hewes CA, White NA: Outcome of desmoplasty and fasciotomy for desmitis involving the origin of the suspensory ligament in horses: 27 cases (1995-2004). J Am Vet Med Assoc 229:407-412, 2006

10. Dyson S: The suspensory apparatus, in Rantanen N, Mckinnon, A. (ed): Equine Diagnostic Ultrasonography (ed 1), Baltimore, Williams & Wilkins, 1998, p 454

11. Caminoto EH, Alves AL, Amorim RL, et al: Ultrastructural and immunocytochemical evaluation of the effects of extracorporeal shock wave treatment in the hind limbs of horses with experimentally induced suspensory ligament desmitis. Am J Vet Res 66:892-896, 2005

12. Herthel DJ: Enhanced suspensory ligament healing in 100 horses by stem cells and other bone marrow components. Proc 47th Annual Convention of the American Association of Equine Practitioners, San Diego, CA, pp 319-321, 2001

13. Bathe A: Neurectomy and fasciotomy for the surgical treatment of hindlimb proximal suspensory desmitis. Proc 40th British Equine Veterinary Association Congress, Newmarket, UK, p 118, 2001