Get access

Lameness associated with tarsocrural joint pathology in 17 mature horses (1997–2010)




Pain originating from the tarsus is a common cause of lameness; however, there are limited descriptions of tarsocrural joint (TCrJ) pathology in mature horses. The objectives were to describe the clinical features and diagnostic imaging findings of skeletally mature horses with TCrJ pathology, and to determine the clinical outcome. Case records and images of 17 horses examined at the Animal Health Trust, between 1997 and 2010, with pathology associated with the TCrJ were evaluated and follow-up information obtained. TCrJ pathology was associated with a range of conditions and resulted in mild to severe lameness. Perineural analgesia of the tibial and fibular nerves improved lameness in all limbs, whereas intra-articular analgesia of the TCrJ improved lameness >50% in 12/17 limbs (70.6%), <50% in 3/17 limbs (17.6%) and in 2 limbs produced no change. Radiological abnormalities of the TCrJ were identified in 8/19 (42.1%) limbs. Nuclear scintigraphy detected abnormalities of the TCrJ in 4/11 (36.4%) limbs. Ultrasonographic abnormalities of the TCrJ were identified in 4/10 (40%) limbs; all horses had chronic synovitis. In addition, one horse also had a large amount of fluid, of heterogeneous echogenicity, consistent with haemarthrosis, confirmed by arthrocentesis. Abnormalities on magnetic resonance images were identified in one limb. Abnormalities of the TCrJ were identified arthroscopically in 4/5 (80%) lame limbs; however, one horse that responded positively to intra-articular analgesia had no detectable abnormality. Two horses returned to full athletic function following rest: one with TCrJ haemarthrosis, and one with an incomplete parasagittal fracture of the talus. Intra-articular medication resulted in improvement in lameness and return to work in one horse with osteoarthritis (OA) of the TCrJ, but had no effect in any other horse. We conclude that the prognosis for return to work is poor for horses with both OA of the TCrJ, and osteochondritis dissecans and secondary OA.