The treatments of navicular syndrome vary widely, which probably reflects the treatment of multiple causes. By determining the most likely cause of the syndrome, the most specific problem can be treated. The treatment of navicular syndrome is as controversial as any aspect of this disease. However, it has been shown that correct shoeing should be basis of all treatment. Any medicinal or surgical therapy should be as an adjunct to shoeing.

The most successful approach to shoeing is that based on individual case needs rather than a standard formula. The following principles should be followed: (1) Correct any pre-existing problems of the hoof, such as underrun heels, contracted heels, sheared heels, mismatched hoof angles, broken hoof/pastern axis. (2) Use all weight bearing structures of the foot. (3) Allow for hoof expansion. (4) Decrease the work of moving the foot. Shoeing is most effective when corrections are made within the first 10 months of lameness, up to 96% success. This is in contrast to when shoeing changes are not made until after 1 year of lameness, where only 56% of the cases have been successfully treated.

These principles can be accomplished using many different methods and techniques. Shoeing is of utmost importance in dealing with hoof pain causing the signs associated with navicular syndrome or remodeling of the bone (osseous form). It is necessary to insure proper hoof balance and support in order to eliminate the pain and stop or decrease the stresses, which are causing the problem.

Horses that respond to coffin joint anesthesia should be treated for inflammation of that joint. This may include systemic non- steroidal anti-inflammatory therapy but intra-articular therapy or specific joint therapy should also be considered. The use of hyaluronic acid and corticosteroids as anti-inflammatories within the joint is well documented. I prefer to use a combination of high molecular weight hyaluronic acid (10mg) and triamcinolone (8mg) injected intra-articularly followed by a second shot of hyaluronic acid in 2 weeks. In addition, the use of intra-articular or intramuscular polysulfated glycosaminoglycans (Adequan) has been useful in the control of joint disease. Most frequently I use PSGAGs if I suspect cartilage damage (500mg IM, weekly for 4 weeks). Cartilage damage, at least on the flexor surface, can most easily be assessed by contrast navicular bursagraphy.

Occasionally horses affected with coffin joint synovitis also have a chronic broken forward hoof axis. Many of these cases appear to be mild flexural deformities. Because of the mal-articulation of the short pastern and coffin bones, the joint remains inflamed despite therapy. In these cases, inferior check desmotomy to allow correction of the broken forward axis has been a very useful in treatment of these types of cases.

Vascular forms of the disease can be treated with vasoactive drugs. Isoxsuprine Hcl is the most common drug used to increase the circulation to the podotrochlea. It is dosed at 0.6-1.2mg/kg b.i.d. until sound, then decreased to s.i.d. for 2 weeks then further decreased to every other day.

Other drugs have been studied. Metrenperone is a serotonin antagonist and thereby increases circulation. It has been used at a dose of 0.1mg/kg b.i.d. However, the drug has not been shown to be as efficacious as isoxsuprine. A new drug that is showing promise is pentoxifylline, which increases RBC deformability and thus aids circulation. The drug is dosed at 4.5-7mg/kg t.i.d. Clinical trials in Canada have shown much promise.

Some surgeries have been suggested to be useful in the treatment of vascular forms of the disease. Palmar digital neurectomy causes vasodilation and the effect lasts as long as the neurectomy. Fasciotomy of the palmar digital nerve has also been suggested but the effect does not last and may cause more damage to the nerve.

In cases where desmitis of the navicular suspensory ligament is suspected there are basic 2 treatment alternatives. Treatment is designed to reduce strain on the ligament. This can be achieved by either raising the heels of the horse's foot or by cutting the collateral sesamiodean ligaments (CSL). Collateral sesamoidean desmotomy is a surgery that has become popular in Europe and has been effective on selected cases of navicular syndrome. The surgical approach is made just proximal to the collateral cartilages, just cranial to the digital vein. A 2cm incision is made, the vein is retracted palmarly, and the CSL can be located as it courses proximally and dorsally over the short pastern bone. A hemostat is used to dissect around the ligament and then transection is performed. Closure is standard. The horses are allowed to rest for 2 weeks for skin incision healing, then they are returned to work.

Similarly, when the deep flexor tendon is involved, raising the heels of the hoof will decrease strain on the tendon. But in addition, desmotomy of the inferior check ligament has also recently been shown to be effective in treatment of these cases.

Podotrochlear bursa lavage has been suggested for the treatment of true cases of navicular bursitis. Ingress and Egress needles are placed in the bursa and isotonic fluid is flushed through the bursa to remove any inflammatory debris.

When all other treatments have failed or have not had the desired affect, palmar digital neurectomy remains a viable treatment alternative. Numerous techniques are available but all follow some basic rules. First, the neurectomy will not improve the lameness any more than a palmar digital nerve block. Therefore, it is highly recommended that the nerves be anesthetized with the owner/rider present so that they can decide whether the horse has sufficiently improved. Second, neuromas are a common problem but can be avoided by atraumatic surgical technique. Atraumatic surgery can really only be learned by practice. Neuroma formation can be decreased by allowing the surgical wounds to heal as well as possible before returning to work. This usually requires 4 to 6 weeks rest after the surgery. Third, the horse will lose skin sensation in the back half of its foot but probably loses all or most of its sole sensation. However, the horse will always know where the foot is. The foot should then be protected by using a pad.

REFERENCES

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10. Colles CM. Concepts of blood flow in the etiology and treatment of navicular disease. in Proceedings, 29th Annu Conv Am Assoc Equine Practnr 1983; 265-275.

11. Lose MP. Contracted flexor tendons as related to the etiology of navicular disease. Eq Vet Sci 1991; 11:308-311.

12. Turner TA. Navicular disease management: shoeing principles, in Proceedings. 32nd Annu Conv Am Assoc Equine Practnr 1986; 625-633.