Transcript:

[0:01]

Hi everyone, welcome back to Mad Barn Academy, and if you’re new here, welcome. I hope that you’ll take some time to explore the other videos on our channel after you’ve watched this one. If you like this video and the other videos that we post, please like and subscribe. The ongoing support means a lot to us. I’m Dr. Fran Row, one of the veterinary nutritionists here at Mad Barn, and today I’m covering part two of the two-part series on laminitis.

[0:32]

If you haven’t watched part one, go ahead and do that now. In the first video, we went through an overview of laminitis, starting with the normal anatomy of the hoof, what happens when there’s inflammation, and finishing out with the mechanisms that lead to laminitis. Today we’ll be finishing up our discussion on endocrinopathic laminitis specifically, so let’s get started.

[1:01]

These are our objectives for today: we’ll be reviewing metabolic disease, the clinical signs of laminitis, and then strategies to prevent endocrinopathic laminitis. As a quick review, endocrinopathy is the most common mechanism of laminitis — it’s thought that 90% or more of horses that develop laminitis have an underlying metabolic disorder that results in insulin dysregulation and hyperinsulinemia. Additionally, it’s the mechanism of laminitis that we can address with dietary management, which we’ll cover later on.

[1:38]

Chronic insulin dysregulation leads to insidious, low-grade changes in the foot over time, and it’s important to realize that this damage is cumulative. This means these horses are more likely to develop acute laminitis because they have exaggerated reactions to changes in blood insulin levels compared to normal horses.

[2:06]

To better understand metabolic disease in horses, we have to understand insulin. So, let’s back up and review the basics of insulin dynamics in the body. Insulin is one of the hormones involved in blood sugar homeostasis. The body can only function properly if blood sugar levels are maintained within a fairly narrow range. The “sugar” in blood sugar refers to glucose, which is the end product of carbohydrate metabolism and the main energy substrate for cells in the body.

[2:41]

When carbohydrates are ingested, they are broken down in the stomach, and glucose is absorbed from the small intestine into the bloodstream. This stimulates the release of insulin from the pancreas. Insulin’s job is to tell cells to uptake glucose from the bloodstream. When insulin resistance occurs, normal insulin concentrations fail to stimulate tissues to uptake glucose. The body responds by releasing more insulin to prevent blood glucose from becoming too high, resulting in elevated blood insulin — or hyperinsulinemia.

[3:26]

For horses with metabolic disease, they are unable to metabolize carbohydrates normally, leading to insulin dysregulation and insulin resistance. Genetics is thought to be the most important predisposing factor for the development of EMS. It’s most commonly seen in “easy keepers” such as ponies, Mustangs, Morgans, Tennessee Walking Horses, donkeys, and Spanish breeds, to name a few. These horses are more metabolically efficient, meaning they can efficiently turn low-quality feedstuffs into energy and fat. While this was beneficial for their ancestors grazing poor-quality grasslands, it becomes a disadvantage in modern times.

[4:29]

Modern management practices have horses eating better-quality feed while also being less active. Not surprisingly, EMS often coincides with obesity or regional adiposity since these horses convert food into fat stores efficiently but may not exercise enough to burn excess calories. While obesity itself doesn’t cause EMS, it can exacerbate the condition, which is why weight loss is often discussed for horses with EMS.

[5:14]

For horses with PPID, overproduction of hormones by the pituitary gland results in generalized hormonal disruption throughout the body. In some of these cases, that disruption includes hyperinsulinemia, though the exact pathophysiology is still poorly understood. About one-third of horses with PPID exhibit hyperinsulinemia, making them at risk for laminitis. PPID, or Cushing’s disease, occurs due to age-related degeneration of the pars intermedia, a specific region of the pituitary gland. It most commonly occurs in horses over 15 years of age, with likelihood increasing with age.

[6:10]

Hyperinsulinemia is the underlying cause of laminitis in these horses. While they may not be acutely laminitic all the time, they are more likely to develop clinical disease. Some horses do not appear laminitic or show PPID signs outwardly, so we often have to rely on bloodwork to diagnose hyperinsulinemia. However, in most cases, there are clues we can look for that make us suspicious a horse is hyperinsulinemic and at risk for laminitis. Catching these changes early and intervening can reduce that risk.

[7:05]

Clinical signs of acute laminitis include increased digital pulses to the foot, increased heat over the hoof wall, and some degree of hoof pain. Horses may display weight-shifting behavior, rock back off their front feet, shift weight between feet, be reluctant to walk or pick up their feet, lay down more, or show sensitivity to hoof testers over the sole. As discomfort increases, other pain signs may appear: increased heart rate, increased respiratory rate, sweating, and muscle fasciculations or trembling.

[8:07]

For today, I want to focus more on chronic, insidious, or subclinical changes that clue you into pathology in the foot. I’ve also included a list of clinical signs of PPID you can review — that will be its own topic another day. Remember, horses with untreated PPID are at risk for laminitis, so it’s important to rule out PPID in suspected metabolic horses.

[8:42]

Some clues to look for include changes to the shape of the sole. Normally, the sole is concave, but with instability and coffin bone displacement due to laminitis, the sole can become flat or even convex (“dropped”). There may also be sole bruising where increased pressure from coffin bone displacement occurs — easy to mistake for a stone bruise, so it’s important to look for other clues.

[9:30]

Another sign is a widened white line due to laminar stretching. As the hoof grows out, so do the abnormal lamina, and we can see that wide white line at the sole. Growth rings on the hoof wall can also be a clue: normally concentric, they should be parallel all the way around the foot. Divergent growth rings indicate abnormal hoof growth from chronic laminitic change. The toe grows more slowly compared to the heel, which grows at a more normal rate, so rings become narrow at the toe and wider at the heel. Over time, this can lead to excess heel growth, tall heels, or even slipper foot in horses without regular farrier care.

[10:47]

Lastly, some of the changes that we look for we can only see on radiographs because we’re looking at changes in the coffin bone. With chronic laminitic change, we might see remodeling at the tip of the coffin bone. The bone remodels in this area because it’s attempting to protect itself when there’s increased pressure or concussion, particularly if that coffin bone has rotated down. In more mild cases, we’ll appreciate a little bit of lipping at that edge. In more severe cases, the bone can become quite lytic, and that normal bony architecture is destroyed.

[11:33]

Here’s a simple graphic illustrating the difference between a healthy foot and a laminitic foot. To review: when there’s inflammation in the lamina, we’ll see separation between the hoof wall and the coffin bone. If severe enough, the coffin bone can rotate down or sink into the hoof capsule. Over time, chronic changes can appear as abnormal hoof growth with more growth occurring at the heels, widening of the white line on the sole, flattening of the sole, and recurrent sole bruising. These changes, in combination with obesity or regional adiposity, or signs of PPID (Cushing’s disease), make us very suspicious of endocrinopathic laminitis caused by hyperinsulinemia.

[12:34]

Now, let’s talk about what we can do to intervene and reduce the risk of laminitis in these horses. Our prevention strategies involve both dietary and some management changes. For diet, our goals are to reduce hydrolyzable carbohydrates (HC) in the diet, maintain an ideal body weight or promote weight loss if applicable, provide sufficient protein, and meet vitamin and mineral requirements to balance the diet. For other management, we often look to increase exercise whenever possible. Additionally, your veterinarian may elect to use medications that accelerate weight loss (like levothyroxine), improve insulin sensitivity (such as metformin), and/or treat PPID with pergolide if applicable.

[13:47]

To reduce hydrolyzable carbohydrates, we focus on a forage-based diet. HC are the carbohydrates in the diet that contribute to a glycemic response, meaning they raise blood insulin levels. Because we want to minimize insulin dysregulation, our first objective is to feed a diet low in HC. You can calculate HC by adding ethanol-soluble carbohydrates (simple sugars) plus starch from the percent dry matter column on a forage analysis. We ignore water-soluble carbohydrates because that value includes non-digestible carbs that do not contribute to the glycemic response.

[14:43]

If the hay is too high in HC and sourcing another hay is not possible, we can soak the hay for 15–30 minutes in lukewarm water before feeding. Soaking leaches out excess sugars and can lower HC content. Pasture grasses, particularly during spring and fall, are quite high in HC, which is why we see cases of “grass founder” during these times. It’s recommended to limit pasture intake using a grazing muzzle or by managing horses on a dry lot. Lastly, remove concentrates or feeds high in HC. Even some ration balancers can be too high, so assess all feeds. If a carrier is needed for supplements or mental stimulation, suitable alternatives include grass forage cubes, pellets, or beet pulp.

[16:07]

Here’s an example of a forage analysis to show how to calculate HC content: add ESC and starch from the percent dry matter column. For metabolic horses, aim for HC less than 10%.

[16:35]

Next, aim to maintain horses at an ideal body weight. This may mean instituting a weight loss program for overweight horses. Horses at ideal weight can generally have free-choice hay, consuming about 2% of body weight in dry matter daily. For overweight horses, restrict to 1.5% of body weight in forage daily — the minimum requirement to maintain gut health and satiety. Monitor carefully, as these horses are prone to weight gain, and adjust rations as needed. For example, an 1,100 lb horse at ideal weight × 2% = 22 lbs forage/day; overweight × 1.5% = 16.5 lbs forage/day.

[18:03]

Provide sufficient protein, but not excess. Horses at maintenance or light work typically meet protein needs from hay; extra protein is generally unnecessary. Avoid high-protein diets for metabolic horses, as research shows excess protein can exacerbate insulin resistance over time. This means avoiding high-protein ration balancers or feeds like alfalfa.

[18:40]

Lastly, horses on a forage-based diet won’t meet vitamin and mineral requirements, so balance with a fully fortified, low-carbohydrate, low-protein product. At Mad Barn, we recommend AminoTrace+ because it meets these needs for metabolic horses.

[19:08]

For other management, regular exercise is important whenever possible. Increasing exercise promotes weight loss and improves insulin sensitivity. When ridden work isn’t possible, lunging, round penning, or ponying can be options. The amount of exercise depends on the horse’s soundness — acutely laminitic horses should be on stall rest.

[19:56]

That wraps up part two of Laminitis in Horses. Here are our references for today, and I’ve linked a couple of our articles on laminitis and metabolic disease in the description below. Don’t forget to check those out when you have time. I appreciate you taking the time to listen today, and if you liked this video, please like and subscribe to our channel. Until next time, thanks.