Navicular Syndrome

Robert Webster

Karen Romagosa

Dr. Daniel J. Burba

Navicular syndrome is one of the most common causes of lameness in horses. This condition occurs especially in performance horses, particularly middle age to older animals. This syndrome consists of several clinical signs, including but not limited to pain in the palmar region of the hoof (heel area) and gait abnormalities associated with degenerative changes in the navicular bone (distal sesamoid bone). The degenerative process affects both the bone and the navicular bursa surrounding the bone, as well as the deep digital flexor tendon that runs behind the bursa. This process more often occurs in the forefeet but rarely can affect the hind feet in some cases. The typical horse suffering from navicular syndrome presents with a history of intermittent lameness that subsides with rest. This is usually a bilateral disease (affecting both the right and left sides) with one foot often worse than the other. These horses may point the more painful foot when standing, and may alternate which foot is pointed. Since the heel of the foot is the more painful region, owners may notice excessive wear on the toe of the shoe or foot. The horse often has a short-strided, stilted gait and many times it leads people to believe the lameness is arising from the shoulder. Sometimes the complaint is that the horse will not take a barrel or seems off when making a turn.

The clinical signs of navicular syndrome may be a result of several different processes. There are three main theories with regard to the cause of navicular syndrome. The first theory suggests that increased or abnormal force on the navicular bone has increased the amount of bone remodeling. This force could be created between the navicular bone and the deep digital flexor tendon. Increased bone remodeling can lead to both pain and lameness. A second theory contends that changes in the blood supply to the navicular bone could contribute to navicular syndrome. Damaged vessels may become blocked by clots (thromboses), which cause pain and death of the surrounding tissues. Once tissue death occurs, the bone structure breaks down and is reabsorbed, resulting in the clinical signs of navicular syndrome. Hypertension of the veins in the hoof causes the vessels to stretch, resulting in another type of vascular pain and subsequent lameness. A final hypothesis suggests that breakdown of the cartilage and joint structure in the navicular bone and surrounding navicular bursa may contribute to the signs that make up the navicular syndrome. This process is known as degenerative joint disease, a painful arthritic condition. Although the exact mechanism by which navicular syndrome occurs is unknown, these hypotheses suggest feasible pathways toward the disease state that may be analyzed and treated.

Diagnosis of this condition is controversial since the syndrome itself is not clear cut. However, a diagnosis may be reached by the veterinarian on the basis of clinical signs, localization of pain to the heel region of the foot, radiographic signs (if present), ruling out other causes of lameness, and a history of intermittent lameness which subsides with rest or worsens with exercise/work, or a history of inconsistent performance. In order to support the diagnosis, other clinical tests may also be performed. The first is a hoof tester response. A positive response to the hoof testers should be uniform over the navicular area. However, a negative response does not rule out navicular syndrome. Wedge tests are another diagnostic aid used for this condition. The “toe wedge test” increases strain on the deep digital flexor tendon, exacerbating any lameness associated with the navicular bone by increasing pressure on the bone. The “frog wedge test” exacerbates lameness associated with the navicular bone by applying pressure to the bone via a block placed directly under the frog. Regional anesthesia is another method of diagnosis used by veterinarians for navicular syndrome. A palmar digital nerve block should be performed first on the foot that is exhibiting the most lameness. The veterinarian should evaluate the horse for lameness before the other foot is blocked. The animal may shift the lameness to the opposite foot following the first block, and a marked improvement in gait should occur after both feet are blocked. Many horses may also have coffin joint synovitis, which can be ruled out by performing local anesthesia of the coffin joint. A final method that can be employed as a diagnostic tool is bone scintigraphy. The increased uptake of radioisotope in the region of the navicular bone will be observed on a bone scan. This imaging method shows the area of the navicular bone that is undergoing bone remodeling.

There have been numerous treatments directed toward the clinical resolution and/or slowing of the degeneration of the navicular bone. The treatment is aimed at providing palliative pain relief as well as ceasing the progression of navicular disease. Management of the disease in younger animals with mild radiographic changes should be conservative in nature. Initial treatment should begin with corrective trimming and shoeing, rest, and nonsteroidal anti-inflammatory medications (NSAIDs). Other treatment options may be considered for adjunct therapy, but the aforementioned protocol is essential.

Foot abnormalities should be addressed with proper trimming and corrective shoeing. The goal of shoeing is to reestablish a normal foot/pastern axis and to provide proper mediolateral balance for the animal. This process involves shortening of the toe and elevating the heels to increase the hoof angle by two to four degrees. The toe of the shoe is rolled or rounded in a vertical plane to enhance break over. This method is thought to decrease deep digital flexor tendon tension and relieve loads exerted by the collateral and distal sesamoidean ligaments on the navicular bone. In addition, applying full pads and packing the sole with silicone rubber may reduce concussion. A bar shoe is used to provide added support to the heels.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are frequently used for their analgesia, antiinflammatory, and platelet aggregation inhibitory effects. Phenylbutazone is the antiinflammatory drug of choice for navicular syndrome. The primary goal of treatment with antiinflammatory drugs is to use the minimum dose possible to maintain maximum comfort and to reduce inflammation, while avoiding adverse toxicity such as gastrointestinal ulceration. The recommended dosage is 2.2 mg/kg twice a day. The lowest dose and shortest duration of treatment is recommended. Sometimes, horses can be effectively managed by giving the NSAIDs the day before and day of competition or riding. Intrarticular (injected into the joint space) corticosteroids, alone or in combination with hyaluronic acid, may provide temporary relief to inflamed structures relating to navicular disease. The corticosteroids of choice are triamcinolone and methylprednisolone acetate. This treatment should be used with caution because of the potential for abuse, and their ability to mask signs of lameness. Your veterinarian may choose to inject these into the coffin joint or navicular bursa. Polysulfated glycosaminoglycans (Adequan), isoxsuprine hydrochloride (peripheral vasodilator), and pentoxifylline (hemorreologic agent) are additional treatment options that may be used. They should not be viewed as sole treatment modalities, but research suggests there are potential benefits for their use as adjunct therapy. Response to these treatment options should be considered when determining their continuation and/or duration of use.

Surgical options should be considered for animals exhibiting signs of chronic navicular disease, such as marked radiographic changes and lack of response to medical therapy. Two surgical procedures of choice are navicular suspensory desmotomy and palmar digital neurectomy. The goal of the navicular suspensory desmotomy is to reduce forces on the navicular bone and its ligaments. Increased tension on these ligaments is responsible for a broken-back foot/pastern axis. The palmar digital neurectomy should be considered for cases unresponsive to medical therapy, and those animals that are not candidates for the navicular suspensory desmotomy (i.e. increased age, severe lameness, angular limb deformity, and radiographic evidence of flexor cortex defects). This procedure provides palliative pain relief by eliminating sensation from the palmar aspect of the foot. However, there are several potential drawbacks to the neurectomy, such as the possibility of regrowth of the nerve, painful neuroma development, or foot infection postoperatively. The postoperative care of the affected horse is an important contributing factor to the success of any surgery. Following surgery for navicular syndrome, the surgical wounds should be allowed to heal for four to six weeks. This requires resting the horse for that period of time as well as providing pain medication. In addition, the foot should be protected by using a pad.

Navicular disease is a syndrome with a complex pathogenesis. The disease does not involve an infectious component, therefore prevention is challenging. Preventative measures involve early recognition of conformation problems, such as small or narrow feet, excessive concussion (i.e. cutting, racing, and roping horses), and improper shoeing or trimming techniques that result in a backward broken hoof/pastern axis. If these conditions can be recognized and corrected early, the disease process may be slowed. Although the prognosis for the syndrome is guarded, a carefully designed therapeutic protocol can prolong the usefulness of the animal. Over a period of months to years, most affected horses will reach a point of unresponsiveness to treatment, however, some horses can have reversal of the process if caught early in the disease process and treated correctly.