I just saw a public FB post with the images below. I only show the images, not the whole post, as it is irrelevant who posted it.
The point is to be cautious when interpreting Digital Cushion (DC) based on cross-sections alone. It can be very misleading.
the 2 images at the bottom right are credited to Lindsey Field from The Study of the Equine Hoof
The top image with the two cuts next to each other is not even the same cut. The one on the right is almost through the midline, the left one is just about along the collateral groove (CG). Therefore, they are not comparable as they show a different anatomical location. A cut along the CG will always show less DC than a cut through the midline, even on the same hoof. That’s just how the anatomy is.
Now looking at the two images that say poor and great DC. The one that says great DC seems to have a compromised laminar connection and the short pastern is pulled up, aka stretching the DC. The image showing poor DC has the short pastern (P2) pushing down on the DC, but seems to show a better laminar connection. Both those hooves show as distinct downward bulge of the frog corium, leading to a thin frog in that area. This suggests there are significant other pathological aspects in those hooves, which are not visible in these views. Compare that to the frog at the top right image.
So, please, analyse the material properly and form a complete picture of what is going on in a certain hoof, before making conclusions on certain aspects alone.
We have just added this new section to the website. You can get to it via this link.
Simply go there, create an account if you haven’t got one, then click “Take the course”, and you are in.
It contains videos and articles on hoofcare related topics. The first few posts are establishing the basics in hoof anatomy, which is the foundation for anyone who would like to understand hooves, or even work on them.
It is supported via a chat group. You will find the links to that in the course description.
Feel free to make suggestions on what topics you would like to see covered, as well as how you like the format.
Just as Canterbury is drying out due to a series of North-West winds, a couple of clients sent me these photos of their newly built hoof-bath solutions.
What’s the point of this, you might say?
For hooves to stay functioning and healthy, certain parameters must be met.
the hoof-capsule must be maintained in a shape/proportions so it can expand on weight bearing
the ground needs to be sufficiently firm to facilitate such expansion (especially in winter)
the hooves need to be sufficiently hydrated to allow such expansion (especially in dry conditions)
the horse needs to move. Just standing around in a yard or around a hay feeder leads to insufficient steps and therefore hoof expansion.
Not having enough hoof hydration over summer affects the horse in the following way:
the hoof becomes stiff and less flexible to expand properly
less hoof function allows more build up of bars and sole
more build up of bar affects the way the horse loads the hoof – typically toe-heavy
this affects the regrowth pattern and stance – heels tend to grow too fast, increasing PA
chronic overload of toe lamellae and under-stimulation of lamellae towards the back. toe coronet overloaded
the trimmer cannot correct the situation properly has hooves are too hard to cut
If your horse is allowed to go through summer with this pattern, be prepared that it becomes sore once the hooves regain their ability to expand again. Typically that occurs when the rain sets in, in autumn – aka re-hydration. The return of hoof expansion and better blood flow to the compromised internal tissues, will lead to a patho-physiological response – inflammation. We will observe this as a tender-footed horse, probably with and elevated and strong digital pulse.
And of course, the grass starts growing again at the same time, and now it’s the grass’ fault.
When it comes to talking about causes and treatment of Laminitis, there are many opinions “out” there, and sometimes it appears they contradict each other. How can this be? Does that mean only some views are correct, and consequently the others must be incorrect?
Based on my experience over the last two decades, I have concluded that the confusion and different opinions we read are the result of mixing up different event mechanisms that lead to a situation we call laminitis. In other words, we are not talking about the same “thing”.
The common denominator is the word Laminitis and on the first glance they look similar on x-rays. While acute, the horse presents the same way, aka fronts camped out, hinds standing under, high pulse, stiff gait, etc. The management of the acute phase (< 72h) would typically be the same, too.
However, how the horse got to this stage is different. As far as I am concerned, there are two fundamentally different types of scenarios, 1) chemical overload of some sort, and 2) mechanical overload.
In the true sense of the first scenario, the hoof is healthy prior to the event. That means it is without wall separation and the consequences of the trigger event allows the hoof-capsule to potentially separate.
In the second scenario, the separation develops first as a result of mechanical deformation and overload, while the inflammation part is triggered later – often years apart.
As chemical overload I regard scenarios like insulin overload, carbohydrate overload, toxicity response from retained placenta, etc. They all create a toxicity effect that tends to affect the whole horse. In the hoof it inflames the laminae, and the laminar dermis and epidermis appear to separate. Interestingly enough, this tends to happen without physical damage of the lamellar structure, aka no ripping and breaking. Theoretically, this should happen within a healthy and tightly connected hoof-capsule (HC), free of distortion, because we would like to assume that the hoof was healthy prior to such event. In the first occurrence of such event within a healthy HC, there simply is no space for P3 to to go anywhere, due to the close proximity of inner hoofwall and P3. Unfortunately, we rarely find those healthy hooves to begin with.
The insulin and carbohydrate overload scenarios are have been studied and created in a pseudo-in-vivo environment, where a horse is forced to receive large amounts of these substances within a very short period of time, that in real life with normal boarding conditions would be extremely hard, if not impossible, to achieve in a 24h period.
Due to the “letting go” of the laminar connection, if one was to dissect hooves from this scenario, one could expect that the HC pulls away from the laminar corium relatively easily.
Sloughed-off, fairly healthy, Hoofcapsule showing smooth and harmonic lamellae arrangement.
The mechanical overload is by far more common in real life. Typically this starts in the back half of the hoof where discomfort is allowed to develop in the hoof. This can start as early as a few months after birth. The horse shifts weight away from that area and transfers it towards the front half of the hoof – 24/7. This paves the way for chronic overstressing and eventually stretching of the laminar connection, and sometimes even the laminar corium. Those horses commonly present symptoms like fast growing heels, steep pastern alignment, short stride, toe-first landing, possibly stumbles easily, tight muscles around the shoulders. Eventually we see flare in the toes and radiographically we would see P3 and the inner hoofwall are no longer parallel. That means the laminar connection is getting widened. All the while the horse does not show any signs of acute laminitis, but it would most likely be diagnosed with “signs of chronic laminitis”.
The space between P3 and the hoof-capsule is filled out with more laminar horn, often referred to as “laminar wedge”. More laminar horn over a wider space does not make the hoof stronger, but rather the opposite occurs. Usually the harmonic laminar arrangement is disturbed, making the lamellae look rugged and “ripped”. Nevertheless, when dissecting such a hoof, it is typically very hard to separate the laminar horn from its corium – often the corium rips off the bone instead.
Hoof with Laminar Wedge. However, also note the severe deformation in the back half of the hoof.
Typically, a trigger event of some sort (trauma, dietary disturbance, change of ground conditions, change of hoof hydration) occurs, and promotes and acute laminitis. Many horses only get x-rayed at this point, which then shows separation on a hoof with acute laminitis. A very common reason, why it is believed that the laminitis caused the separation.
The problem now is that we are trying to explain, and treat, this second scenario with the reasoning from the first scenario. However, it is to note that a hoof with mechanical distortion and toe overload will have a much lower trigger threshold to chemical overload. The long-term solution then is to lift that trigger threshold and focus on reducing the HC distortion.
A hoof of a 4-months old filly, already demonstrating significant HC distortion with symptoms of toe-overload and bottom-up separation in the dorsal hoofwall (left). On the right, the same hoof much improved.
Horse lame – Vet diagnosis: no signs of laminitis, but since the horse is lame and slightly overweight, it has to be laminitis.
This just happened to a client, and you can imagine how freaked-out the owner was. Unfortunately, it is not a single occurrence to get a laminitis diagnosis, when there is no laminitis.
The horse transitions well to barefoot trimming, is moving freer, muscle tension is going away, stance, loading, and movement patterns are improving. Suddenly, the horse presents with some temporary, often sudden, lameness. Emotions run high, the stressed client calls in a vet for lameness diagnostics. The vet assesses the hoof of concern as it presents, typically without further investigating how the hoof may have changed over the last few months, or how the whole horse has changed over the same period, aka hoof history.
X-rays get taken. No signs of laminitis. Sole thickness good. Bone alignment good. No response to hoof testers. Pulse, not reported on. Conclusion: it must be some low-grade laminitis since the horse is lame and slightly overweight. Restrict High Carb feeds and administer Bute.
Did the hooves show Hoof Mechanism (HM) on loading? Not checked.
A horse with laminitis is typically highly sensitive to hoof rasping. Well, this one wasn’t. No strong or elevated pulse. Happy to lift the hooves for trimming. But overall the hooves were too long and had full bars, due to being ridden less for the previous month, ground being softer, and left and extra week between trims. HM reduced to non-existent. Trim the hooves, get HM established, check for good loading pattern. Within a week the horse is fine again.
Learning to see how your horse loads its hooves and whether or not they have HM is so important. Many problems can be eliminated/prevented by just managing this.
The photo below shows how the inner hoofwall run parallel to the dorsal aspect of P3 (pink line). The blue contour shows the (still) deep Collateral Groove, which can easily lock up when the bar gets too long. The focus needs to be to further relax that region.
Other examples include where horses are lame and have a strong pulse. Diagnosis: Laminitis. Despite the horse standing on the hoof’s toe and unloading the heels. A few days later, a heel abscess opened up.
Don’t be afraid to get another opinion, when your horse gets a laminitis diagnosis.
