Page 432 - Adams and Stashak's Lameness in Horses, 7th Edition

398 Chapter 3

and scintigraphy for lesions responsible for lameness, at the insertion on the distal phalanx, at the level of
resulting in a more accurate, early diagnosis and prog­ the flexor surface of the navicular bone, at the level of
VetBooks.ir priate specific treatment protocol. Many of the causes of mal recess of the navicular bursa, or at any combina­
the collateral sesamoidean and T‐ligaments in the proxi­
nosis and allowing for the selection of the most appro­
tion of these three levels at the same time. Lesions are
foot lameness we know today thanks to the use of MRI,
can only be identified conclusively with MRI. usually restricted to one lobe but may change their
One study, using cadaver limbs of horses with distal morphology while transitioning from one level to
limb lameness, found that anatomical structures another. There is a good correlation between the MRI
appeared similar in both high‐field and low‐field sys­ appearance of tendon lesions and their pathological
tems but that the margins of some structures were less classification into core lesions (Figure 3.220), parasag­
clearly defined with low‐field MRI likely due to partial ittal plane splits and tears (Figure 3.221), insertional
volume effect. It was concluded that the level of lesions (Figure 3.222), and dorsal surface erosions and
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detection of moderate to severe lesions in the foot was fibrillations (Figure 3.223). 18,32,121,156,158 Generalized T1
similar between high‐ and low‐field systems. However, signal increase in one tendon lobe may constitute an
small tendon, articular cartilage, ligament, and bone artifact rather than diffuse tendinopathy. Insertional
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lesions were better detected using a high‐field enthesopathy can result in cortical irregularity, caused
system. 122 by focal bone resorption or enthesophyte formation at
There have been several reports on the incidence the insertion of the tendon to the flexor surface of the
of injuries diagnosed with both low‐ and high‐field distal phalanx, and in diffuse osseous signal change in
MRI systems in horses with foot lameness. Some of the palmar aspect of the distal phalanx, caused by osse­
these 24,46,48,75,103,113,157,168,179 are summarized in Table 3.3. ous fluid or sclerosis. Dorsal lesions may be accompa­
Overall, injury of the DDFT was the most prevalent nied by adhesions between the dorsal surface of the
lesion, while navicular bone lesions were the next most tendon and the palmar surface of the collateral sesa­
common diagnosis followed by injuries of the collateral moidean and impar ligaments within the navicular
ligaments of the DIP joint. Abnormalities in the DIP bursa. Torn collagen fibers arising from the tendon’s
joint and navicular bursa were diagnosed frequently in damaged dorsal surface may recoil proximally in the
low‐field studies but less commonly in high‐field stud­ navicular bursa, resulting in the dorsal protrusion of a
ies. Injuries to all other structures occurred with mark­ tendon granuloma into the proximal recess of the navic­
edly lower frequency, generally in less than 10% of ular bursa. Adhesions are suspected when one or
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horses. The absence of significant abnormalities was more bands of hypointense (T2) or hyperintense (T1)
mentioned in up to 14% of horses in four studies in material are present between the dorsal surface of the
which an MRI diagnosis was not made. Although MRI DDFT and the collateral sesamoidean ligaments, oblit­
is the most sensitive and specific diagnostic modality for erating the normal synovial fluid signal in this space.
the diagnosis of injuries of a3l tissues in the horse’s Sometimes lack of separation extends across the entire
foot, not all causes of foot lameness can be readily surface of both structures in the proximal recess of the
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identified (Table 3.3). navicular bursa. Other signs of navicular bursitis
accompanying lesions of the dorsal surface of the
intrabursal portion of the tendon include fluid disten­
sion of the proximolateral and proximomedial pouches
MRI Abnormalities in the Foot of the bursa (proximolateral pouch is always larger)
and thickening and proliferation of the bursal synovium
Tendinopathy of the DDFT
in the proximal recess of the navicular bursa. Thickening
The normal DDFT can be clearly recognized as a of the collateral sesamoidean and distal impar liga­
well‐delineated, bilobed, double elliptical structure of ments may also be seen. Resorptive lesions of the flexor
homogeneous low signal (black) with a hyperintense cortex of the navicular bone are frequently accompa­
midline septum. From the navicular bone distally, the nied by fibrous adhesions between the eroded bone sur­
midline septum is no longer visible, and the tendon face and the dorsal surface of the tendon. Unfortunately,
becomes progressively flatter to finish in a crescent‐ adhesion detection is difficult in the absence of normal
shaped distal insertion on the distal phalanx. A general­ synovial fluid volume between the opposing structures
ized signal increase in the portion of the tendon in the navicular bursa, as may occur in chronic bursitis
comprised between the distal border of the navicular with synovial proliferation. Distension of the navicular
bone and its insertion to the distal phalanx can be caused bursa or DIP joint with 4–6 mL of 0.9% saline is useful
by the magic angle effect (Figure 3.212). The appearance as it should cause separation of the tendon from the col­
of the normal DDFT has a strong left to right limb as lateral sesamoidean ligaments and the navicular bone if
well as medial to lateral lobe symmetry in both signal no adhesions are present. 100,102,159 Lack of separation
intensity and cross‐sectional area measurements. The after injection is indicative of fibrous adhesions between
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tendon contains a dorsal layer of high T1 and PD signal adjacent structures.
both at the level of the navicular bone and proximal to It may be possible to use T1‐to‐T2 signal differences
the navicular bone. 17,159 to estimate the age or stage of healing of a tendon
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Tendon lesions are characterized by focal or linear, lesion. Early tendinopathy has been characterized by
marginal or central, intratendinous signal increase on increased signal in T2, STIR, and T1 images. In the
both T1 and T2 images, variably accompanied by some chronic stages of tendon healing by fibrosis, signal inten­
enlargement of the affected lobe in the acute stage of sity in core lesions generally decreases in T2 images but
injury. Lesions may occur distal to the navicular bone remains high in T1 and PD images. 160
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