Navicular disease can no longer be considered a single disease, with a single pathogenesis. This chapter discusses the functional anatomy of the podotrochlear apparatus (PTA) together with the various forms of injury that affect it. Clinical features, uses and limitations of diagnostic analgesia, radiologic findings consistent with navicular disease, and the use of ultrasonography, nuclear scintigraphy, computed tomography, and magnetic resonance imaging for definitive diagnosis of various forms of navicular disease and injury of the PTA are described. Possible management strategies are outlined.
Podotrochlear Apparatus and Related Structures—Functional Anatomy
The distal sesamoid or navicular bone is an integral part of the distal interphalangeal (DIP) joint and provides a fulcrum for the deep digital flexor tendon (DDFT). The palmar compact bone is covered by fibrocartilage; the dorsal compact bone is covered by articular cartilage. The spongiosa is principally comprised of trabeculae and adipose tissue. The distal border has articular and nonarticular components, separated by a fossa with synovial invaginations from the DIP joint projecting into the spongiosa. The navicular bone is part of the PTA, together with the collateral sesamoidean ligaments and the distal sesamoidean impar ligament. The bone has a close relationship with the navicular bursa and the DDFT.
The navicular bone, which articulates with both the middle and distal phalanges, provides a constant angle of insertion for and maintains the mechanical advantage of the DDFT, which exerts major compressive forces on the distal one third of the bone. Tension in the DDFT and the distal digital annular ligament promotes stability of the DIP joint.
What is Navicular Disease?
No form of navicular disease has ever been reproduced experimentally, and the pathophysiology underlying all forms of navicular disease remains open to speculation. Navicular disease is not a single condition, but rather is a complex group of injuries and disease processes. Classical navicular disease results in erosion of the fibrocartilage and palmar compact bone, frequently with either lesions of the DDFT in the same sagittal plane or adhesions of the DDFT. More recently, other causes of navicular pain have been recognized, including acute trauma, primary lesions of the spongiosa characterized by increased signal intensity in fat-suppressed magnetic resonance (MR) images and decreased signal intensity in T1-weighted gradient echo sequences, and modeling of the navicular bone in association with lesions of the collateral sesamoidean ligaments and distal sesamoidean impar ligament. There may be thickening of the palmar compact bone. Distal border fragments are often seen together with other lesions of the navicular bone and are frequently associated with distal sesamoidean impar ligament pathology. Occasionally, proximal avulsions of the collateral sesamoidean ligaments are seen. Periarticular osteophyte formation on the dorsoproximal aspect of the navicular bone is a manifestation of osteoarthritis of the DIP joint. A congenital bipartite navicular bone may be a primary source of pain or can cause secondary DDFT injury. It is now recognized that primary lesions of the DDFT are an unrelated condition. All forms of navicular disease are more common in the forelimbs than in hind limbs.
A genetic component may be a component of some forms of navicular disease, with Quarter Horses being at particularly high risk. Theoretically, a small angle of the distal border of the distal phalanx results in increased stress exerted by the DDFT on the navicular bone, but there is no direct relationship between the angle of the distal phalanx and the shape of the hoof capsule. No relationship between hoof capsule shape and navicular disease has been demonstrated. This issue is confounded by the tendency for a lame limb to develop a more upright, boxy hoof capsule. In a recent study, risk factors for PTA injury were the following: age, with horses 10 years and older being at higher risk than horses younger than 6 years; breed, with Thoroughbred crossbreds having increased risk, compared with Warmbloods; and weight-to-height ratio, with horses with a ratio of greater than 3.45 having a higher risk than those with a ratio of less than 3.19. Show jumpers also had a higher risk for PTA injury, compared with dressage horses.
Lameness may be unilateral or bilateral and sudden or insidious in onset. There may be an increase in digital pulse amplitudes, but this is a nonspecific finding. Some horses show pain on compression of the heel or pressure on the frog applied with hoof testers, but many do not. The horse may stand pointing the lame limb or stand camped-out with both forelimbs, but these signs can also be seen in horses with primary lesions of the DDFT. The degree of lameness at the walk and trot is highly variable and is related to whether the lameness is unilateral or bilateral and to the severity of the disease process. A horse with bilateral lameness may have a short striding gait, whereas a horse with unilateral pathology may have severe forelimb (or hind limb) lameness. Affected horses often have increased discomfort in turning. Lameness is often accentuated during lungeing, especially on firm surfaces and usually, but not always, with the lame limb on the inside of a circle. In some affected horses, lameness may improve somewhat with work. In the presence of adhesions of the DDFT to the palmar aspect of the navicular bone, the caudal phase of the stride may be shortened, which may be particularly apparent at the walk.
Distal limb flexion tests produce a variable response. Lameness may be accentuated in the load-bearing limb because of prolonged extension of the DIP joint. Elevation of the toe, using the board or wedge test, may accentuate lameness, but this test is highly unspecific and may also accentuate lameness associated with a primary DDFT injury or collateral ligament injury of the DIP joint.
Uses and Limitations of Diagnostic Analgesia
Palmar digital nerve blocks often result in improvement in lameness, but may not abolish lameness, particularly in the presence of adhesions of the DDFT to the navicular bone. Lameness is usually eliminated by palmar (at the base of proximal sesamoid bones) nerve blocks. However, occasionally more proximal limb nerve blocks are required for complete resolution of lameness, if lameness is severe or if there are adhesions between the DDFT and the navicular bone. Intraarticular analgesia of the DIP joint may result in rapid resolution of PTA pain, but a negative response does not preclude navicular bone pathology. Intrathecal analgesia of the navicular bursa usually improves lameness unless there are extensive adhesions between the DDFT and navicular bone.
Lateromedial, dorsoproximal-palmarodistal oblique, and palmaroproximal-palmarodistal oblique radiographic images of the foot are required as a minimum. The navicular bone should be assessed for the presence of proximal border enthesiophytes; length of the palmar compact bone; thickness of the palmar compact bone; regularity of the dorsal aspect of the palmar compact bone; opacity of the spongiosa; trabecular architecture; the number, size, position, and shape of distal border radiolucent zones; the presence of distal or proximal border fragments; the size, position, and shape of radiolucent lesions in the spongiosa; radiolucent lesions in the palmar compact bone; and new bone on the palmar compact bone at the sagittal ridge (Table 199-1; Figures 199-1 to 199-6).
Radiologic Interpretation of the Navicular Bone
|0||Excellent||Good demarcation between the palmar compact bone and the spongiosa; fine trabecular architecture within the spongiosa. Palmar compact bone of uniform thickness or thickest proximally and uniform opacity. No lucent zones along the distal border of the bone, or several (<7) narrow conical lucent zones along the horizontal distal border. No distal extension of the palmar aspect of the navicular bone. Right and left navicular bones symmetrical in shape.|
|1||Good||As above, but lucent zones on the distal border of the navicular bone more variable in shape. Small enthesiophyte on the proximolateral aspect of the navicular bone. Mild distal extension of the palmar aspect of the navicular bone.|
|2||Fair||Slightly poor definition between the palmar compact bone and the spongiosa secondary to increased opacity of the spongiosa. Crescent-shaped lucent zone in the sagittal ridge. Several (<8) lucent zones of variable shape along the distal horizontal border of the navicular bone. Moderate enthesiophyte formation on the proximal border of the navicular bone. Navicular bones asymmetrical in shape. Proximal or distal extension of the palmar aspect of the navicular bone. Distal border fragment without associated radiolucency.|
|3||Poor||Poor definition of the palmar compact bone and the spongiosa secondary to increased opacity of the spongiosa. Thickening of the palmar ± dorsal compact bone. Poorly defined radiolucent area or areas in the palmar compact bone. Many (>7) variably sized and shaped radiolucent zones along the distal horizontal or sloping borders of the navicular bone. Lucent zones along the proximal border of the bone. Large enthesiophyte formation on the proximal border of the bone. Discrete site of mineralization within a collateral sesamoidean ligament. Radiopaque fragment on the distal border of the navicular bone with associated radiolucent zone in the adjacent bone. Periarticular osteophyte on the dorsoproximal aspect of the bone.|
|4||Bad||As above, plus cystlike lesion within the spongiosa of the navicular bone. Radiolucent region in the palmar compact bone of the navicular bone. New bone on the palmar compact bone of the navicular bone.|