Showing posts with label OCD. Show all posts
Showing posts with label OCD. Show all posts

Friday, March 12, 2010

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.

Wednesday, March 10, 2010

3/9/2010 - Osteochondrosis - What is it?

Vet Tip of the Day: Osteochondrosis - Understanding the disease Process
Key Words: Bone, Cartilage, Mineralization, endochondral ossication

Yesterday I discussed the lameness workup on Classy, a 5 years old thoroughbred mare with OCD of the stifle.  So what is OCD anyway?
Today Iwill describe the disease process, and some of the factors we believe predispose juvenile horses to this problem.  Tomorrow I will go over some of the more common location for OCD lesions.

OCD stands for Osteochondrosis dissecans.  Just to give you a hint at how complex this disease is, there is still debate over whether this even is an accurate name for the problem.  To understand this disease at all, you must first understand how bones grow.  A joint is a moving part, consisting of bones that slide along each other, separated and lubricated by joint fluid.  The surface of the bone is covered by a layer of cartilage, which is softer and more compliant than bone, and therefore stands up better than more rigid bone to the forces exerted on joints during athletic activity. 

Think about it - how do your foal's bones get longer and thicker as the foal grows?  What happens is a process called endochondral ossification.  The bones grow from the surface cartilage toward the underlying bone.  The cartilage cells, called chondrocytes, divide and increase in number.  As they mature, they become mineralized and eventually transform into bone.  This is a rapidly ongoing process in the growing foal.  If the transition from young chondrocyte to mineralized chondrocyte to bone doesn't occur correctly, there is a defect in bone maturation.  Thus, osteochondrosis is a defect in endochondral ossification. 

Try this image to help you imagine what happens.  You are painting the jumps in your arena.  You are getting tired, so instead of putting on several thin coats of paint, and allowing each to dry in between, you start globbing on thick layers of paint, not letting each layer dry.  When you lay the paint on correctly, each layer adheres to the one beneath and you end up with a shiny surface of smooth paint that doesn't crack or peel.  If you glob the paint incorrectly, you end up with bubbles underneath the surface and cracks and flakes on the surface soon after the paint dries.  Exactly the same thing happens in foals with OCD.  The cartilage to bone development is abnormal, and the resulting defects include cysts (just like the bubbles under your paint surface) and cartilage flaps that detach from the underlying bone just like your flaky paint, because the attachment to the underlying layers is not healthy. 

Cysts lying just below a thin layer of unhealthy cartilage, flaky, cracked cartilage, and actual flaps of calcified cartilage that separate from the underlying bone are all manifestations of OCD.  In all three cases, the smooth, gliding surface that is critical to pain free, athletic joint function, is lost.  The result is swelling and pain during athletic activity.  Many factors predispose horses to develop OCD.  The particular combination of events in a given foal that result in OCD are complex and inter-related.  Some of the major forces at play are: genetics, rapid growth and large body size, excess feeding of carbohydrate, abnormal stress and trauma, and mineral imbalance, specifically copper deficiency.

This is a very basic overview of the disease process called OCD.  Tomorrow we will look at some of the most common sites in the body where OCD occurs, and the clinical significance of some of these sites.

Tuesday, March 9, 2010

3/9/2010 OCD

Vet Tip of the Day: Osteochondrosis Dissecans - More Lameness!
Key Words: OCD, stifle, developmental orthopedic disease

I'm going to continue discussing lameness today.  I'm also going to confuse you by presenting another case in which I did not follow the cardinal rules of lameness diagnosis: 1) physical examination 2) gait evaluation 3) diagnostic nerve blocks 4) diagnostic imaging.  In the horse I will discuss today, I skipped step 3, and will explain why.

In today's discussion I am simply going to present this case, and tomorrow will discuss the disease process in more detail.  Look at the x-ray here - this is the horse's stifle, the joint which corresponds to our knee.  The patella is the triangular shaped bone at top right of the picture.  It rests against the bottom of the femur (your thigh bone) and slides up and down on two ridges called the trochlear ridges.  These ridges end in the condyles, which on the x-ray are the two rounded knobs at the end of the femur.  Below the femur is the tibia (your shin bone). 

Look on the trochlear ridge just below the tip of the patella and you will see a small piece of bone separated from the trochlear ridge by a black shadow.  This is a classic lateral trochlear ridge OCD lesion.  Now here is the case presentation.

Classy is a 5 year old thoroughbred mare.  She never raced, but did train for the track as a 2 year old.  She was pulled from training due to "splint bone issues" and was turned out to pasture for a few years.  Recently she was sent out for 60 days basic flat work training which she completed successfully without complaint of lameness from the trainer.  Upon return to her owner's barn, both the owner and trainer at the barn noted that Classy would buck when asked to canter and just "didn't seem right behind".

On physical examination Classy had no remarkable abnormalities execept for moderate fluid filling in her femoropatellar joints on both hind legs.  The filling was soft and non-painful.  On gait evaluation Classy was grade 1 lame (see previous post on lameness grading) on her right hind.  She had a mild positive response to right hind hock/stifle flexion.  She was sound and negative to flexion of the left hind.  When observed on a longe line on a soft surface, Classy did not show overt lameness, but her hind limb gait was characterized by a shortened step and a rapid downward placement of her feet at the trot.  When asked to canter, she had obvious difficulty executing a canter departure.  When travelling to the right, she would only canter disunited, with the forelimbs following a right lead foot cadence and the hindlimbs following a left lead foot cadence.  Tracking to the left she would occasionally canter in a united left lead canter, but also frequently cantered disunited.  Her hind limb gait at all times during the canter was characterized by poor independent motion of her two hind legs - they tended to move together, suggesting a "bunny hop" quality.

The combination of physical examination findings and gait evaluation were suggestive of a stifle problem.  Radiographs were performed immediately for three reasons.  First, intra-articular anesthesia (joint block) of the femoro-patellar joint to identify subtle lameness such as Classy exhibited is not routinely reliable - horses will not always "block out" even though the stifle is the source of the lameness. In general, lameness should be at least a grade 2 before intra-articular anesthesia is relied upon as a diagnostic tool.  Secondly, from a strictly practical point of view, we were under time constraints, the intra-articular anesthesia would incur cost without a high likliehood of definitive results, and Classy was a somewhat fractious 5 year old likely to be uncooperative during placement of needles in her stifle without significant sedation.  Thirdly, OCD was the most likely presumptive diagnosis for Classy, and radiographic confirmation of this diagnosis in combination with Classy's signs is considered definitive without intra-articular anesthesia.

Classy was sedated and 3 views of each stifle were taken.  The radiographs confirmed OCD in both stifles, the right significantly worse than the left.  The x-rays were reviewed by a board certified surgeon and surgery is scheduled for next week!  Cost $2500 - prognosis for soundness and full athletic function excellent - layup time 6 weeks.

In Classy's case, the owner's astute attention to a relatively mild gait abnormality resulted in a timely diagnosis of a problem that left untreated would likely result in degenerative changes in the joint with resultant chronic lameness.  Over the next few days we will look at OCD in more depth, and then return to Classy's case and discuss why her particular manifestation of this developmental orthopedic disease carries with it an excellent prognosis following surgical repair.

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