3/12/2010 - Anatomy and OCD

Vet tip of the Day: Significance of OCD based on anatomic location
Key Words: Osteochondrosis, lameness, joint, anatomy

This cute foal picture is here to remind you that OCD is a developmental orthopedice disease.  In other words, it develops as a foal grows, although it may not manifest itself clinically until later in life when joints are subjected to the rigors of training and controlled exercise.  When we consider the prognosis of various OCD lesions, then, there is one common sense rule to keep in mind: foals that develop significant lameness early in life due to OCD are likely to have more severe lesions than animals that do not show any clinical signs until they are older and in training. 

Regardless of the anatomic location, the larger and deeper the OCD lesion is in a given animal, the less likely it is that surgical treatment will be successful.  In general, the degree of lameness and age at onset correlate with the severity of the lesion.  Consider our mare Classy, a five year old just completing 60 days of fairly rigorous training and only demonstrating a grade 1 lameness and mild joint swelling.  Even before examining her radiographs, one can be hopeful that her prognosis for full function would be favorable.  And this is in fact the case.  Classy has an excellent prognosis for a full athletic career following surgical debridement of her stifle lesions.  On the other hand, a 6 month old weanling with grade 3 lameness and severe swelling of the stifle joint undoubtedly has a more conservative prognosis for an athletic career, even with appropriate treatment.

OCD can occur in any joint in the body. The most commonly affected joints are the stifle, hock and fetlock, and less commonly the shoulder and cervical spine (neck).  Within each of these joints there are several locations where lesions can occur.  In addition, lesions may occur as mineralized cartilage fragments that have separated from the underlying bone (see Classy's x-ray's for a beautiful example) or they may appear as cyst-like lesions, where the cartilage lining the bone is still intact, but is no longer attached in one region, with fluid and tissue debris filling the area between the detached cartilage and underlying bone. Remember our jump painting analogy?  The detached lesions are like paint chips, leaving the wood of the jump exposed, the cyst-like lesions are like bubbles in the paint, detached from the wood, but with the paint surface still intact. 

The prognosis for full athletic function for OCD of the lateral trochlear ridge in the stifle and most locations in the hock is excellent in the majority of cases, particularly when lameness is not severe, and does not become apparent until the horse enters training.  OCD of the fetlock is often treated successfully, but caries a more conservative prognosis in general than lesions of the hock or stifle.  OCD of the shoulder and cervical spine in general carry a guarded prognosis. There are certain anatomic locations where OCD lesions may be detected radiographically in a sound horse during a pre-purchase examination, for example, and be considered clinically insignificant, depending on their severity, and the horse's level of performance.

While surgical debridement (scraping the lesion just as you would scrape the paint on your jumps before correctly applying fresh paint) remains the gold standard for treatment of OCD, there are many emerging treatments under investigation which may alter our approach to this complex disease.  Intra-articular stem cell therapy is one of the most promising of these.  And still, many foals and weanlings with early diagnosis of less severe forms of OCD respond well to simple rest and careful rehabilatation with intra-articular chondoprotective therapy, allowing mother nature to do her own magic in healing lesions.

I've barely scratched the surface of the subject of OCD in these past few posts, but hopefully you will take away the message that in most horses this diagnosis does not mean the end of an athletic career.

I'm off to dinner after a long, cold day of work in windy, 45 degree rain spitting Reno today.

Enjoy.

Tuesday, February 7: The Fetlock and Metacarpus

Vet tip of the Day:

First a quick review: we've looked at the anatomy of the bones in the pastern and foot and the attachment of the deep flexor tendon onto the back of the second pastern bone and coffin bone. We've discussed how irregularities in the navicular bone can contribute to heel pain by irritating the flexor tendon and navicular bursa as the tendon slides up and down against the back of the navicular bone. And we've reviewed ring bone, an arthritic condition that occurs at the P1-P2 and P2-P3 joints.

Today we will move on to the bones and major soft tissue structures between the knee (carpus) and the pastern. The cannon bone, with a much smaller splint bone on either side, spans this distance. The bottom of the cannon bone rests on the top of P1, the long pastern bone, and forms the fetlock joint. The cannon bone and the splint bones are all metacarpal bones, which correspond to the bones in your hand between your wrist and your knuckles. At the level of the fetlock joint, just behind the cannon bone, lie the sesamoid bones. The suspensory ligament, which arises from the back of the knee, lies along the back of the cannon bone and splits just above the sesamoids, with one branch attaching to the top of each sesamoid bone. The deep and superficial flexor tendons originate behind the knee and attach at the level of the pastern. The deep flexor tendon attaches to the back of P1 and P2 (the long and short pastern bones), and the superficial tendon to P2 and P3 (the short pastern and coffin bones).

The distal, or lower cannon bone, suspensory branches and fetlock joint are like an amazing suspension bridge which is critical in supporting the weight of the horse during exercise. They are very common sites of injury in athletic horses. You may have seen pictures of the x-rays of Barbaro, whose catastrophic injury involved not only a fracture of the end of the cannon bone, but also his sesamoid bones, suspensory ligament and pastern. In our less extreme athletes, small strains in the suspensory branches, chip fractures in the fetlock, and inflammation of the sesamoid bones are all relatively common causes of lameness.

Pick up your horse's right front leg and hold the foot in your left hand. Place your right thumb on the inside, and your index finger on the outside, of the cannon bone mid-way between the knee and the fetlock. Squeeze firmly and let your fingers slide over the structures moving toward the back of the leg. The suspensory ligament is difficult to feel because it is very firm and lies closely attached to the back of the cannon bone. However, it is easy to feel the deep and superficial digital extensor tendons which lie just under the skin. Learn to distinguish between them, and then move your hand up and down the leg, feeling the length of each tendon from knee to fetlock. Just above the fetlock, on the inside and outside, it is possible to clearly palpate the branches of the suspensory ligament where they attach to the top of the sesamoid bones. Your hands are very sensitive indicators of changes in the soft tissue structures of the leg that can alert you to the presence of injuries.