HOW TO MANAGE HOOF LAMENESS II
Fig. 7. Caudal view of the dissected foot revealing the digital cushion and collateral (ungual) cartilages.
Fig. 5. Probe inserted into the collateral ligament of the distal interphalangeal joint.
desensitizing the DIP joint; therefore, a negative response to navicular bursa analgesia and a positive response to DIP joint analgesia is a strong indication that the DIP joint is the source of pain. Radio- graphs in acute cases rarely show much. In chronic cases, osteophytes, narrowed joint spaces, subchon- dral sclerosis, and enlarged synovial invaginations on distal border of navicular bone are all signs of joint disease. MRI is very helpful in evaluating the extent of the cartilage damage and peri-articular structures. MRI is also helpful in determining ac- tive inflammation and physiology of the adjacent bone.
Treatment of coffin joint disease involves manag-
ing the inflammation and its destructive action on the cartilage. Systemic and intra-articular anti- inflammatories, hyaluronic acid, and polysulfated glycosaminoglycan (PGAG)s are used.6 Acute con- ditions require rest and rehabilitation whereas chronic conditions require a more long-term man- agement program. Severe cases may require a decrease in performance level or retirement. Sys- temic or articular treatments with steroids, hyal- uronic acid (HA), and PGAGs have been shown to be of clinical benefit in decreasing inflammation and maintaining joint health. Special attention to trimming and shoeing is most likely to have the
biggest impact, especially in cases with poor confor- mation or foot-balance issues. Trimming to establish even loading medial to lat-
eral is the goal. Radiographs should be used in cases with a history of DIP disease, to help establish a balanced trim. Trimming perpendicular to the long axis of the pastern is recommended when ra- diographs are not available. When shoeing, pre- serving the natural function of the foot is the goal. Taking into consideration the shock absorbing mechanism and loading characteristics of a healthy barefoot. There are several mechanisms in place to accom- modate shock absorption: 1) hoof wall, 2) lamellar interface, 3) soft tissue (joint, joint capsule, sole co- rium, digital cushion, tendon/ligament, bone), and 4) movement of blood into and out of the foot. When the foot is loaded, the elastic hoof capsule deforms, soft tissue is compressed and stretched, and the elastic/pliable lamellar interface allows the bone col- umn to displace slightly within the hoof capsule. A well-formed hoof capsule with proper mass, shape, and moisture content are the foundation for a well- functioning foot. As the foot is loaded, the compression and tension
Fig. 6. Distal interphalangeal joint with the second phalanx removed showing the articular cartilage of the distal phalanx and navicular bone. A healthy joint is on the left and a degenerative joint is on the right with cartilage erosion.
406 2020 Vol. 66 AAEP PROCEEDINGS
within the foot squeezes the blood out of the foot and helps drive it up the limb through low-resistance vascular pathways in the collateral cartilages. The structure most responsible for transmitting ex- ternal shock into movement of blood are the bars, digital cushion, and collateral cartilages. It has been hypothesized, by Dr. Rooney,7 as the heels impact the ground, the bars receive vibrations and force, which then transmits it to the collateral car- tilages, which lie just deep to the bars (Fig. 7). The collateral cartilages are rich in vasculature and contain a pool of blood, which receives these vibra- tions and converts it to the movement of fluid/blood up the limb. Basically, the collateral cartilage and its vasculature provide a low-resistance pathway for the rapid movement of blood out of the foot during ground impact, acting as a hydraulic shock absorber. Feet, which are efficient at shock absorption, have thick, robust collateral cartilages (with abundant
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