|A 10y Percheron gelding presented to the Ohio State University for humane euthanasia. The gelding had a history of difficulty rising, low ringbone affecting the forelimbs, and pelvic limb lameness. There was a flexural deformity of the right hind fetlock and the horse was unable to extend the pastern to appropriately bear weight. Post-mortem MRI of the bilateral proximal metatarsi were performed for unrelated research purposes. Ultrasound examination of the right proximal metatarsus was performed in a non-weight bearing position.|
Left Hind: The accessory ligament of the deep digital flexor tendon (ALDDFT) is moderately to severely diffusely enlarged, PDw hyperintense, and poorly defined from the periligamentous tissues, which are also thickened. There are several focal, strongly PDw hyperintense tears along the proximal dorsomedial margin near its origin on the plantar tarsus. The medial aspect of the mid body of the SDFT is mildly enlarged and rounded with mildly increased PDw signal intensity, worse at the level of insertion of the ALDDFT. The DDFT is normal. There is mild general enlargement and rounding the proximal suspensory ligament with flattening of the lateral lobe. The fat/muscle bundles are well-defined. There are small osteophytes with subchondral sclerosis along the dorsal margins of the central and 4th tarsal bones with increased fluid in the distodorsal recess of the tarsocrural joint.
Right Hind: Similar to but worse than the left, the accessory ligament of the deep digital flexor tendon (ALDDFT) is severely, diffusely enlarged, PDw hyperintense, and poorly defined from the periligamentous tissues, which are also thickened. The plantar metatarsal fascia is moderately thickened and heterointense. There is a strongly PDw hyperintense, linear tear along the plantaromedial margin of the ALDDFT 1.5cm distal to the MTPJ. There are irregularly distributed small pockets of PDw hyperintense fluid in the distal tarsal sheath surrounding the lateral head of the DDFT and the synovium is thickened and isointense to the ALDDFT. There is also asymmetrically distributed hyperintense fluid surrounding the medial head of the DDFT. The plantar proximal suspensory ligament is contacted by the enlarged ALDDFT, but is otherwise normal. The SDFT and DDFT are normal. There is increased fluid in the distodorsal recess of the tarsocrural joint.
The ALDDFT is diffusely, severely enlarged, approximately 1.5x the size of the DDFT. There areheteroechoic to hypoechoic regions throughoutwith severe, diffuse alteration of the fiberpattern. The dorsal margin of the ligament is poorly defined from the overlying DDFT and thereis heteroechoic tissue between the plantar margin of the ALDFFT and the suspensory ligament.
- Severe, chronic, bilateral hind limb desmopathy of the accessory ligament of the DDFT with likely adhesions to the regional soft tissue structures and tarsal sheath, worse on the right.
- Mild left hind proximal suspensory ligament desmopathy and superficial digital tendinopathy; consider secondary to increased weightbearing on the left pelvic limb. Minor changes in size and shape of the flexor tendons may also be attributable to post-mortem evaluation and lack of tension on these structures.
- Mild bilateral tarsocrural effusion and mild right distal intertarsal degenerative joint disease.
The ALDDFT is underdeveloped in the equine hindlimb and lameness secondary to desmitis of this structure is uncommon. Reciprocal action of the tarsus reduces tension on this ligament during the late stance phase and it is presumed to have only a minor supporting role in the hindlimb. Chronic desmopathy of the ALDDFT has been associated with unilateral or bilateral lameness with acute or insidious onset of a postural change. This is usually characterized by the inability to extend the affected fetlock in general purpose pony or cob-type horses greater than 10 years of age (Smith et al. 2005). This is in contrast to desmitis of the ALDDFT in the forelimb, which is usually associated with acute onset of lameness in mature performance horses following strenuous activity. It has been suggested that the tendency of the horse to rest the hindlimbs may predispose the horse to develop flexural contracture following acute injury; however, the difference in onset and progression of disease in horses with ALDDFT injury with and without contracture remains unclear. Once postural deformity is present, these changes are irreversible and prognosis is poor. Desmotomy of the ALDDFT is offered as a treatment option, but slow relapse and/or deterioration with persistent lameness has been reported.
Although advanced imaging such as MRI is unnecessary to diagnosis this condition, the ultrasound, MRI, and gross anatomic findings in this case complement the current ultrasonographic literature and confirm a diffuse, severe, and uncommon manifestation of desmopathy of the ALDDFT. Ultrasound findings in horses with flexural contracture and ALDDFT desmopathy are reported to show moderate to severe enlargement of the ALDDFT (affecting 1/3 to the entire ligament) with heterogeneous to hypoechoic echogenicity and periligamentous thickening, which were seen in the right hindlimb of this patient. Injury to neighboring soft tissue structures is uncommon, although adhesions may be identified. Adhesions are difficult to identify without dynamic evaluation, but the soft tissue thickening surrounding the ligament on both modalities is highly suggestive of adhesion formation in this patient. Due to multiple limb lameness, this patient was humanely euthanized and treatment was not pursued. However, it is unlikely that medical or surgical intervention would have been successful in this case.
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