Page 547 - Adams and Stashak's Lameness in Horses, 7th Edition

Lameness of the Distal Limb 513

(Figure 4.85). Poor conformation may predispose to pull- monly in the hindlimb and can be the cause of chronic
ing/tearing of the soft tissues surrounding the joint or to hindlimb lameness if unrecognized at the initial injury.
VetBooks.ir ern performance horses that are required to start and stop margin of the PIP joint or involving the collateral liga-
Direct blows to the pastern region and lacerations at the
incongruences within the joint surfaces. In addition, west-
ments may contribute to OA of the PIP joint. Infectious
suddenly or twist and turn abruptly appear to be prone to
PIP joint damage. arthritis is often associated with an existing laceration
Trauma to the periarticular soft tissues and the PIP or puncture wound that involves the PIP joint but may
joint may be repetitive or occur as a single, high‐energy also develop after a wound has completely healed.
event that does not cause a fracture or joint luxation.
Because the PIP joint is considered a low‐motion/high‐ Clinical Signs
load joint, the articular cartilage and subchondral bone
are placed under a greater workload, making these Focal or diffuse enlargement of the pastern region
structures more susceptible to injury from nonphysio- may be evident visually as well as on palpation
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logic loading. Overloading the PIP may cause direct (Figure 4.89). Palpable heat and pain with firm digital
articular cartilage damage and/or subchondral bone pressure may be appreciated. The affected pastern region
bruising that may contribute to the development of sub- may feel larger, particularly the dorsolateral and dorso-
chondral cystic lesions (SCLs) (Figure 4.86) or OA. medial surfaces, than the contralateral joint. In most
Trauma may also cause injury of the periosteal attach-
ments of the extensor tendons, ligaments, and joint cap-
sule, resulting in periostitis and new bone formation. In
addition, these injuries may cause joint instability or
subluxation leading to secondary cartilage damage and
OA. The OA may also result from an imbalance between
repetitive microtrauma sustained during athletic perfor-
mance and the adaptive repair mechanism of the skele-
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tal tissue. Whether primary synovitis/capsulitis is a
distinct entity involving the PIP joint is uncertain, but
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it is less commonly recognized than with other joints in
the horse. Lame horses that block to intra‐articular (IA)
anesthesia of the PIP joint that do not have radiographic
abnormalities may have PIP joint synovitis/capsulitis,
subchondral bone bruising, or other unrecognized bone
or cartilage damage that can only be recognized with
advanced imaging such as CT or MRI (Figure 4.87).
When bone bruising does not involve the subchondral
bone, it can be expected to heal without long‐term con-
sequences with rest alone (Figure 4.88).
OA of the PIP joint may develop secondarily to a
number of abnormalities within the joint. These include
OC, unrecognized palmar/plantar eminence fractures of
P2, traumatic blows or lacerations, septic arthritis, and
selective weight‐bearing in young horses. 16,23,71 OA of
the PIP joint secondary to OC is usually seen most fre-
quently in the hindlimbs of horses less than 3 years of Figure 4.86. Dorsoplantar radiograph of a trauma‐induced SCL
age, and more than one joint can often be affected. of the distal aspect of P1 (arrow) that was not apparent radiographically
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Single eminence fractures of P2 also occur most com- until 3 months after the original injury.

Figure 4.87. Proton density‐weighted (left and center) and STIR in the subchondral bone (arrow right). The lameness did not
(right) MR images from a horse with moderate to severe lameness improve with stall rest. The lameness persisted and the joint
of 1 month’s duration that blocked to the pastern joint. There were developed radiographically apparent signs of OA after 3 months of
no radiographic abnormalities. There is an articular cartilage defect stall rest and it was treated with a pastern arthrodesis.
(arrow left and center) and fluid signal intensity/bone marrow lesion