Failed a PPE: Calcification from clyde itch?

[heartbroke]

So I'm heartbroken. My lovely clydeX mare just failed a Pre-Purchase Exam for a lovely lady who would have been a perfect match. I could have believed a small bone chip or one of those 'its there but its nothing' xrays, but the results took my breath away. The vet said that if he hasn't seen the horse himself he'd think she was dead lame. She's never been lame a day in her life! Vet even flexed her and she was perfectly sound but her xrays are terrible.

So there is one of three things going on. Xrays show calcification on the front of the foreleg pastern, slightly on one leg but significant on the other leg. This mare had a severe case of clyde itch at one time in her life and still has scar tissue on her legs from the damage. So option 1: scar tissue on the skin of her pastern is creating a false positive on the xray for calcification. Option 2: the scaring and skin trauma from the clyde itch (chorioptic mange) actually caused calcification on the pastern bone. Option 3 the horse has calcification on the pastern bone - ringbone - that is unrelated to her having had clyde itch. I just can't wrap my head around this, vet says my horse should be lame and she had an easy (broodmare) start to life, then hacked and hunted for last two years in perfect health and soundness. He can't believe that he flexed her and even then she went sound, he says she should be lame based on the xray alone even without flexion.

Has anyone ever heard anything like this before? The purchaser really wants this horse to pass and is requesting that the Vet who did the PPE seek a second opinion on the xrays, but I'm still in shock. Can clyde itch cause any of this? Is it possible to have scaring on the skin that effects xray results? Can skin damage alone cause enough scaring to cause actual calcification on the bone?

I'm so in shock. I thought I'd be celebrating my horse finding the perfect home tonight.

 

[Box_Of_Frogs]

That's terrible! Something similar...my 20 yr old cob x mare suddenly showed some occasional very mild lameness. Treated as an abscess for a few weeks. No improvement so had x-rays. Expected to find minor ringbone. What we actually found, on the long pastern of the foot in question, was extensive calcification, so bad that the vets said it looked as if someone had repeatedly hit her pastern with a hammer. Said she should be almost unable to walk. They said they had no idea what it was. They said to ride her if she was sound but no bute because they weren't sure if there was soft tissue injury there. No real options for "cure" so I decided to let Bridie herself dictate her exercise levels. And now, 3 months or so after the original diagnosis, she's permanently sound, is enjoying long hacks, some fast work, keeping up with big horses (she's only 14.1hh) and shoving her way to the front most of the time! Weird! She's always been a door kicker and some questions were asked about that but I honestly can't see kicking a door, or mange, affecting the pastern bone to that degree. It's an obvious option for me to have Bridie re-x-rayed but I'm not going to as it would only be out of curiosity and woudn't change how she's managed either way. I'll be interested in what others have to say about your horse. Thinking of you xxx

 

[Yertis]

See below, particularly the last bit about fibrosis, there are several papers on this if you do a google search. I have managed mine for the last 8 years now and the condition has not progressed - not cured either - but as long as the buildup is controlled should be o.k.

CHRONIC PROGRESSIVE LYMPHEDEMA (CPL) IN DRAFT HORSES

A condition characterized by progressive swelling, hyperkeratosis and fibrosis of distal limbs has been characterized in Shires, Clydesdales and Belgian Draft horses and unfortunately affects numerous horses within these breeds. The disease has also been recognized in Gipsy Vanners; however, only a few horses have been evaluated at this point of time. This chronic progressive disease starts at an early age, progresses throughout the life of the horse and often ends in disfigurement and disability of the legs, which inevitably leads to the horse's premature death. The pathologic changes and clinical signs closely resemble a condition known in humans as chronic lymphedema or elephantiasis nostras verrucosa. The condition has therefore been referred to as chronic progressive lymphedema (CPL). The lower leg swelling is caused by abnormal functioning of the lymphatic system in the skin, which results in chronic lymphedema (swelling), fibrosis, decreased perfusion, a compromised immune system and subsequent secondary infections of the skin.

The clinical signs of this disease are highly variable. It is often first addressed as a marked and “therapy-resistant” pastern dermatitis (scratches). The earliest lesions, however, are characterized by skin thickening, slight crusting and possible skin folds in the pastern area. While readily palpable, these early lesions are often not appreciated visually as the heavy feathering in these breeds covers these areas. Upon clipping of the lower legs, it becomes obvious that the lesions are far more extensive than expected. Secondary infections develop very easily in these horse's legs and usually consist of chorioptic mange and/or bacterial infections. Pigmented and non-pigmented skin of the lower legs are affected. Appropriate treatment of the infections (pastern dermatitis) is not successful as underlying poor perfusion, lymphedema and hyperkeratosis in association with the heavy feathering present perfect conditions for repetitive infections with both chorioptic mange as well as bacterial infections. Recurrent infections and inflammation will enhance the lymphedema and hence, the condition becomes more chronic. As a result, the lower leg enlargement becomes permanent and the swelling firm on palpation. More thick skin folds and large, poorly defined, firm nodules develop. The nodules may become quite large and often are described as "golf ball" or even "baseball" in size. Both skin folds and nodules first develop in the back of the pastern area. With progression, they may extend and encircle the entire lower leg. The nodules become a mechanical problem because they interfere with free movement and frequently are injured during exercise. This disease often progresses to include massive secondary infections that produce copious amounts of foul-smelling exudates, generalized illness, debilitation and even death.

 

[Heather 1]

Hi so sorry to hear about this. Bearing in mind that I’m not a vet! my understanding is that, at least in people some calcification isn’t unusual, and it’s significance depends on things like whether there’s an underlying condition causing it, where it is, and if it’s causing problems e.g. kidney stone, but often it’s not a problem. Calcification can be a response to inflammation – persistent door kicking does sound a possible cause!

Recent research suggests that arthritis is a dynamic process, many who have significant changes on x rays have no symptoms of this, and two thirds of arthritis ‘cases’ clear up significantly or completely, the body is continually changing.

We probably all know of a horse who developed ringbone, was turned away, and once it had settled down came back into full time, productive work. Many horses with active lives wouldn’t get through a vetting, but it all depends on what other factors are involved e.g. what they’re now going to be used for. And of course, a horse may get through a vetting with flying colours, only to do a tendon the first week after it’s sold, that’s horses! Buying a horse does involve a significant financial outlay so caution is always advised, but when all factors are taken into account, the situation may be brighter than it seems now.

It’s highly unlikely that irritated or fibrosed soft tissue would be mistaken for calcification or bone on an x ray, and the tissue folds seen in chronic progressive lymphoedema also look quite different.

CPL is a disease of the lymphatic system and affects soft tissues, the UC Davis article quoted is now quite dated, the basic description of the condition is still relevant but it’s describing CPL in horses which for various reasons were severely affected, many horses with CPL do not develop it as badly as they had, and I think that this article has unintentionally scared some owners of horses vulnerable to the condition. We were hoping to update it as there’s a lot more information available now but so far it hasn’t been done.

I do hope you manage to resolve this so that everyone is happy.