Showing posts with label Gordon. Show all posts
Showing posts with label Gordon. Show all posts

Thursday, September 29, 2011

Laminitis In Action: Coffin Bone Rotation Time Lapse Video (International Laminitis Conference Preview)

Laminitis, caught in the act: The foot of a horse suffering from Potomac Horse Fever is recorded as it goes through two processes subsequent to the damage in the foot caused by the disease: the coffin bone appears to be rotating away from the hoof wall at the toe and down at its tip; it is also "sinking" within the foot. These two processes are called rotation and sinking, or sinker syndrome. Many laminitis terms have parallel names in other parts of the world or even within the same country. (Andrew Van Eps video)

(You might have to watch this a few times, and if you have a slow connection, you might need to click on the stop button. Once the video is buffered, it should play smoothly. Watching it in full-screen mode helps.)

What you are seeing is a time-lapse of the radiographic view of a horse going through the process commonly called "rotation". What rotation actually is and which part of the foot is the chicken and which is the egg is perpetually debated. This particular foot is also "sinking" within the hoof capsule.

Andrew Van Eps
The video was created by Andrew Van Eps, BVSc, PhD, MACVSc, DACVIM of the University of Queensland. Dr. Van Eps earned a PhD while he was researching laminitis at the Australian Equine Laminitis Research Unit under Dr Chris Pollitt. Among the insights Dr. Van Eps' PhD research has contributed to the treatment of laminitis is the efficacy of cryotherapy in the prevention of laminitis. He created the video of the Potomac Horse Fever case during a residency at the University of Pennsylvania School of Veterinary Medicine.

At the Sixth International Equine Conference on Laminitis and Diseases of the Foot in West Palm Beach, Florida next month, Dr. Van Eps returns once again to speak. Among his subjects will be suggestions for ways to apply cryotherapy, clinical techniques to prevent support-limb laminitis and his intriguing-sounding lecture, "Lamellar Bioenergetics Studied Using Tissue Microdialysis".


You might be interested in reading "Equine laminitis: cryotherapy reduces the severity of the acute lesion" and "Equine laminitis model: cryotherapy reduces the severity of lesions evaluated seven days after induction with oligofructose" by van Eps and Dr. Pollitt, originally published in 2004 and 2009, respectively, in the Equine Veterinary Journal.

He's probably forgotten all about this video. But to anyone dealing with laminitis, the question of whether or not rotation is inevitable in a given horse remains a paramount concern. How many horses technically experience laminitis and have damaged laminae, but have minor rotation or none at all, and why is there such variation between horses? How many horses have bouts of laminitis that their owners never even notice? Is it still laminitis if no one notices but the farrier, the next time the horse is due to be trimmed or shod?

And what is rotation? Is the deep digital flexor tendon, which attaches on the underside of the coffin bone, actually pulling up and back on the bone as the laminae at the toe loosen their hold on the bone, as we've been taught, and as this video would so nicely illustrate? Or is it the weight of the horse on the compromised structures, compounded by unusual posture, that encourages a combination of those forces to work in concert?

A paper from New Zealand published in this month's (September 2011) Equine Veterinary Journal proposes that the soft tissue structures in the back of a contracted, bar-humped foot make it possible for the palmar processes of the coffin bone to act like a fulcrum around which the coffin bone rotates, and that the tendon has no involvement. (See "The effect of hoof angle variations on dorsal lamellar load in the equine hoof" by Ramsey, Hunter and Nash.)

Lead author Gordon Ramsey was kind enough to send his paper and this section begs to be highlighted; using a Finite Element analysis model, Ramsey calculated forces on the proximal hoof wall at the toe when the heels are raised, as recommended in some laminitis therapy regimen. Extrapolating from that finding, he challenged the mainstream concept of coffin bone rotation in laminitis.

Please note that the author is from the University of Auckland in New Zealand and so uses "lamellae" instead of "laminae" in his text; instead of referring to raising the heels of the foot, he refers to mechanically altering the palmar angle of the coffin bone. It's food for thought whether measurements of heels and coffin bone palmar angles are interchangeable.

C0004P0141
A typical laminitis foot, with increased heel growth, which would elevate the palmar angle of the coffin bone as per Ramsey's FE model. According to his calculations, as that palmar angle is intentionally increased in some laminitis treatment protocols, the stress on the proximal (closer to the coronet) laminae inside the hoof wall at the toe would be increased. (University of Nottingham vet school photo)


Ramsey writes:

"The first stage of structural failure in a laminitic hoof involves a stretching of the laminar junction (Pollitt 2007), with rotational displacement occurring subsequently. This seems consistent with a mode of failure that begins at the most loaded proximal part of the lamellae, as predicted by this model, with rotation only occurring after the lamellae have been weakened. 

"It has been proposed that rotational displacement of the distal phalanx, as a sequel to weakening or failure of the laminar junction, is a result of the forces imposed by the deep digital flexor tendon (DDFT) and leverage of the dorsal wall on the ground during breakover (Hood 1999). Experimental results have shown that in laminitic ponies the DDFT force is zero for the first 40% of stance and only approaches a normal value near the end of stance, but that the peak vertical ground reaction force (GRF) is only reduced by 13 percent compared to normal ponies (McGuigan et al 2005). 

"Since the peak lamellar load, predicted by this model to occur at the proximal (not the distal) region of the laminar junction, is more strongly influenced by the GRF than the DDFT force and does not occur during breakover, then this mechanism seems unlikely. 

"An alternative proposed mechanism is that the digital cushion and the region of the attachment of the DDFT are a fulcrum about which the distal phalanx rotates (Coffman et al 1970). As both the DDFT and the digital cushion are soft tissues, it seems unlikely that these could provide sufficient support. 

"However, if the hoof has contracted heels or ingrown bars (Strasser 1997), then these could provide support for the palmar processes to act as the fulcrum for rotation. This could explain why in some hooves the distal phalanx rotates but in other cases, where this fulcrum perhaps does not exist, it only displaces vertically."

Join in the discussion at the Laminitis Conference, October 29-31. The early registration discount ends soon!


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