Navicular syndrome

What it is

Navicular syndrome (podotrochlosis, palmar foot pain) groups the lesions of the podotrochlear apparatus: the navicular bone (distal sesamoid), its ligaments (the collateral sesamoidean ligaments and the distal sesamoidean impar ligament), the navicular bursa and the part of the deep digital flexor tendon that glides over the bone. The term "navicular disease" is reserved for degeneration of the bone itself: remodelling of the distal border, erosion of the fibrocartilage of the flexor surface, sclerosis of the medullary cavity and adhesions to the tendon.

Its origin is mainly attributed to repeated mechanical overload: the deep digital flexor tendon compresses the navicular bone against the second phalanx at the end of the stance phase. Conformations that increase this pressure, such as a long toe with low heels and a broken-back hoof-pastern axis, are considered risk factors. Magnetic resonance imaging has shown that many horses with "navicular syndrome" actually have lesions of the tendon or ligaments, alone or together with those of the bone.

Who it affects

Adult horses, mainly between 4 and 15 years of age, of sport and working breeds: Quarter Horses, Thoroughbreds and warmbloods. It is rare in ponies and uncommon in the pelvic limbs. Showjumpers, with tight turns and abrupt landings, are considered at higher risk.

Anatomy involved

• Phalanges of the thoracic limb: the navicular bone (distal sesamoid) lies on the palmar aspect of the distal interphalangeal joint, between the second and third phalanges, and acts as a pulley for the deep digital flexor tendon. Its distal border is attached to the third phalanx by the impar ligament and its ends to the first phalanx by the collateral sesamoidean ligaments. The distal interphalangeal joint communicates with the bone and its inflammation is part of the differential diagnosis.
• Deep digital flexor muscle: its tendon passes over the flexor surface of the navicular bone, separated from it by the navicular bursa, and inserts on the flexor surface of the third phalanx. Tendon lesions (core lesions, sagittal splits and dorsal border abrasions) are very common at the level of the bone.
• Hooves (ungulae): the podotrochlear apparatus lies inside the hoof capsule, above the frog and between the heels. Hoof shape (low or contracted heels, long toe) influences the load on the bone.

Clinical signs

Insidious and often intermittent lameness of the thoracic limbs, almost always bilateral although one limb is worse; the horse may therefore just look "stiff" or "short" in its stride. Lameness worsens on a circle on hard ground, with the affected limb on the inside. The horse tends to land toe first to unload the heels and may rest each forelimb forward in turn. Hoof testers over the middle third of the frog may be painful, although this is an unreliable sign. Over time the feet become narrower with contracted heels.

Diagnosis

• Lameness examination with trotting in a straight line and on a circle on hard and soft ground, and a distal limb flexion test.
• Diagnostic analgesia: a palmar digital nerve block usually abolishes the lameness; analgesia of the navicular bursa and the distal interphalangeal joint helps to localise it, but is not specific because the anaesthetic diffuses to neighbouring structures.
• Radiographs (lateromedial, dorsoproximal-palmarodistal oblique and the palmaroproximal-palmarodistal oblique "skyline" view): enlarged synovial invaginations along the distal border, fragments, cysts, medullary sclerosis and defects of the flexor cortex. Some sound horses have radiographic changes and some lame horses have normal radiographs.
• Magnetic resonance imaging: the reference method; it shows lesions of the bone, tendon, ligaments and bursa. Computed tomography and bursoscopy are alternatives in some centres.

Treatment and prevention

• Corrective trimming and shoeing: shortening the toe, easing breakover, supporting the heels and correcting the hoof-pastern axis; egg-bar shoes or wedges are sometimes used.
• Non-steroidal anti-inflammatory drugs during painful phases, and rest and controlled exercise if the tendon or ligaments are injured.
• Corticosteroid injection (with or without hyaluronic acid) into the navicular bursa or the distal interphalangeal joint; its effect depends on the type of lesion.
• Bisphosphonates (tiludronate, clodronate), which inhibit bone resorption; the evidence comes from a few small trials.
• Palmar digital neurectomy as a last resort in cases that do not respond: it removes sensation from the heel, but can cause painful neuromas and is not suitable if there are severe lesions of the deep digital flexor tendon, because of the risk of rupture. Competition rules may restrict neurectomised horses.
• The horse is a food-producing animal in many countries and drug use is subject to national regulations and withdrawal periods. In the EU, the equine identification document (passport) states whether the horse is excluded from slaughter for human consumption, and this decides which medicines may be given.

Key studies

• Dyson and Murray (2007), magnetic resonance imaging study of 264 horses with foot pain. Deep digital flexor tendon lesions were present in 82.6% of limbs, mainly at the level of the collateral sesamoidean ligament (59.4%) and the navicular bone (59.0%). Lesions of the impar ligament (38.2%) were more common than those of the collateral sesamoidean ligament (10.5%), and both were associated with navicular bone abnormalities. It shows that bone, tendon and ligaments are injured together. It is a referral-centre series without healthy controls.
• Parkes et al. (2015), retrospective study of 702 horses with foot pain diagnosed by magnetic resonance imaging, in five diagnostic groups (62 with primary navicular bone lesions). Clinical examination, response to diagnostic analgesia and the radiographic grade of the navicular bone did not distinguish lesions of the podotrochlear apparatus from other causes of foot pain. Horses with deep digital flexor tendon injury showed pain on turning more often. It is a single referral centre.
• Denoix et al. (2003), randomised, double-blind, placebo-controlled clinical trial of intravenous tiludronate for 10 days in 73 horses with navicular disease (50 in the final efficacy analysis). The 1 mg/kg dose improved lameness and allowed a return to normal activity at 2–6 months, with greater efficacy in recent cases; the 0.5 mg/kg dose was not effective. Diagnosis was radiographic, without MRI, and almost a third of the horses were not included in the analysis.
• Mitchell et al. (2019), randomised, blinded trial in 12 competition horses with navicular syndrome: clodronate (n = 6) or placebo (n = 6). Clodronate slightly reduced forelimb lameness at one week and coaches reported improved performance more often at 8 weeks, with no change in bone turnover markers. It is a very small trial and two control horses received joint injections.
• Marsh et al. (2012), retrospective series of 101 horses with navicular syndrome examined with high-field magnetic resonance imaging and treated with corticosteroid and hyaluronan injection of the navicular bursa. 75% returned to their previous use for a mean of 9.7 months and 35% were sound at follow-up. Horses lame for less than 6 months and those with primary tendon lesions or bursitis responded best; adhesions and multiple lesions worsened the outcome. It has no control group.