Cover Story | Orthopedics

Recognizing the laminitic horse

By Marie Rosenthal MS

The healing of laminitis that is not diagnosed early or managed correctly may no longer contribute to the mechanical function of the tissue, so early detection is crucial. However, recognition can be tricky because there are a variety of clinical presentations, and the condition can be subclinical, according to Andrew van Eps, BVSc, PhD, DACVIM-LA, who spoke at the 2026 ACVIM Forum in Seattle.

“Early recognition is probably number one in my 5-point plan to make life better for these horses,” said Dr. van Eps, who is a professor of large animal internal medicine and the Dean W. Richardson Endowed Chair of Equine Musculoskeletal Research at the New Bolton Center, the large animal hospital of the University of Pennsylvania School of Veterinary Medicine, in Kennett Square.

The second most important action is to aggressively treat the underlying cause of the laminitis.

The lamellae normally suspend the distal phalanx within the hoof capsule. Laminitis is the failure of the attachment between the hoof wall and the coffin bone. That attachment in a normal horse is 1 m2, and is intricate and strong, he explained.

No matter the underlying cause, laminitis once was thought to be an ischemic problem. “Back in 2007, we were only just realizing that laminitis was mechanistically different depending on the situation that it developed under,” he said, “and these mechanisms that led to laminitis are quite disparate and different.”

Today, veterinarians recognize 3 causes of laminitis:

1. Hyperinsulinemia (endocrine)
2. Sepsis
3. Supporting limb

Hyperinsulinemia
Hyperinsulinemia is the most common underlying cause of laminitis, causing up to 90% of cases, according to the Merck Veterinary Manual. Insulin appears to act through the receptors of insulin-like growth factors (IGF) to promote growth-factor signaling pathways that are similar to what one would see with epithelial-mesenchymal transition in cancer, according to Dr. van Eps. The cells detach and mobilize to get ready to move and/or divide. Since the horse’s hoof is under mechanical stress, the tissue stretches and elongates, resulting in a mechanical failure. “What’s becoming really clear with better means of identifying and treating hyperinsulinemia is that the nature of the lesion depends on the underlying cause, and that affects the prognosis,” Dr. van Eps said.

Despite this reaction, the basement membrane tends to stay intact, which improves the prognosis and healing. “With tight insulin control, dramatic improvements are possible even in chronic cases, because the lesion doesn’t involve fragmentation of the basement membrane,” he explained.

Sepsis
Like other forms of end-organ failure in sepsis cases, septic laminitis is complicated, and clinicians will see local and systemic inflammation and activation of epithelial basal cells. They respond quickly by ramping up inflammatory processes to foreign and local inflammatory signals.

Unlike in hyperinsulinemic cases, the basement membrane separates in septic laminitis. “We get the basement membrane pulling off those epidermal cells, and the basement membrane can fragment as well, and this is an important point,” Dr. van Eps said.

Once there is dermo-epidermal separation in acute laminitis, those epidermal basal cells divide, proliferate and fill that basement membrane template. “It’s a bit of a misconception that this tissue is not capable of healing; it’s well capable of healing—massive stem-cell potential,” he said. “The problem is that it has to heal back in an organized way, and that’s the difficult thing if the basement membrane gets fragmented, and that’s what we see with sepsis-type laminitis.

“So, that basement membrane gets fragmented, invaded by white blood cells, and it heals but not in a way that contributes to the mechanical function of the tissue anymore,” he said.

Another way that this tissue responds to injury is by forming a dysplastic hyperkeratotic horn on the hoof wall side, which is seen as a consequence of laminitis regardless of cause.

Supporting limb laminitis
In supporting limb laminitis, the cells closest to the keratinized axis of the lamellae die because they are farthest from the blood supply. There is a lot of apoptosis, necrosis and epidermal-dermal separation, according to Dr. van Eps.

Horses rely on walking and limb-load cycling to perfuse their entire foot with blood. If they stand still, even just under normal load, areas of the foot are not perfused, which appears to be the root cause of supporting limb laminitis.

But individual variations in these perfusion deficits, even just standing still under normal load, probably play a role in susceptibility to supporting limb laminitis, he said.

This is mostly seen in horses with fractures or other painful limb conditions that interfere with normal ambulation, but could potentially be related to a disease process such as pleuropneumonia, in which pleural pain tends to limit ambulation. However, laminitis often occurs well after the peak inflammatory period. “It often [occurs] weeks down the track when everything seems to be going okay,” he said.

Chronic laminitis
There are consequences of the lamellar failure that result in chronic laminitis. Displacement or rotation of the distal phalanx can occur, which forms a lamellar wedge. That then crushes the sole under P3, and there is lysis and remodeling of the distal phalanx.

“But in most of the cases that have a really big lamellar wedge, particularly in those hyperinsulinemic cases, it is mostly cap horn. And if you stop making cap horn, and the hoof grows down over it, it can go away. And that’s responsible, I think, for most of the improvements that we see in those chronic hyperinsulinemic cases with good insulin control.

“When the bone’s no longer supported by the lamellae, we get crushing of the sole underneath it because the bone is now pushing down on a solar surface,” he said. In some cases, the sole can start bulging.

“Pre-existing chronic laminitis without obvious clinical signs is really common,” Dr. van Eps said. In one study, 75% of horses with pituitary pars intermedia dysfunction (PPID) had radiographic evidence of chronic laminitis, and the owner or the veterinarian recognized fewer than 50% of those cases (J Vet Intern Med 2025;39[3]:e70109).

It’s particularly a problem in Warmblood sport horses—at least in his area, he added. “We see in barns sometimes up to 50% of active Warmblood sport horses with 2° or more of rotation. And I’d say 80% of those have no previous recognition that they have laminitis. So, subclinical laminitis is very common, and it can be performance-limiting, and it can be progressive.”

Therefore, it’s important to spot it early if possible. He said several signs could occur. Besides mild lameness, atypical presentations such as bucking or refusing to work can occur with subtle/subclinical laminitis in athletic horses.

“One of the earliest, most subtle signs is incessant weight shifting, and we see that probably most commonly in cases that develop in the hospital environment with septic-type laminitis,” he said. Often they rock back because they want to reduce tension on the deep flexor tendons of the forelimbs.

Pulses are generally higher. Hoof testing can be really variable. If they’re chronic enough, you can see divergent rings on the hoof. They can look a lot more painful on hard ground than on soft ground, so horses also should be walked on a hard surface.

However, clinical signs can be unreliable in early or subtle laminitis, so diagnostic imaging to look for the lesion is crucial. “It’s not always a clinical diagnosis,” Dr. van Eps said.

An important consideration is that the bone does not always rotate, especially in acute and subtle chronic laminitis. Acute laminitis is visible radiographically, and measuring the lamellar lucent zone (LLZ) is a sensitive way to diagnose acute and subtle chronic laminitis that is not associated with rotation. You can measure the lucent zone and, therefore, measure acute laminitis on a digital radiograph.

The inner hoof wall and the parietal surface of the distal phalanx should be parallel, and should be less than 7.5 mm in light breed horses without laminitis. “If it’s wider than that, you’ve either got stretch, which is more likely with hyperinsulinemic-type laminitis, or you’ve got separation, more common with septic or support limb, but does happen also with severe acute hyperinsulinemia,” Dr. van Eps explained.

Dr. van Eps and his colleagues published a study looking at the utility of measuring the lucent zone. They measured the LLZ in 32 healthy light breed horses that acted as controls, and their median score was 6.9 mm. “We had 18 acute laminitic cases that were in the first 3 days of their laminitis,” he said. The median score was close to 9 mm (Equine Vet J 2025 Jul;57[4]:931-942).

To measure the LLZ, measure the thickness of the dark gap (LLZ) running parallel with the length of the coffin bone. In a normal horse, it should be about 7.5 mm.

“At a cut-off of >7.5 mm for middle LLZ, sensitivity was 87% [95% CI, 73%–94%] and specificity 91% [95% CI, 81%-96%] for diagnosis of acute laminitis. Using the ratio of middle LLZ to distal phalanx cortical length, sensitivity was 95% [95% CI, 81%–99%] and specificity was 95% [95% CI, 87%–99%] (cut-off >0.11),” the authors wrote.

The development of positron emission tomography (PET) scanning for the standing horse is a major advance in diagnosing laminitis, according to Dr. van Eps, but it is expensive and mostly used by researchers. However, it may someday be a clinically useful tool in the toolbox.

“[Right now], I think the value in it is what we’re learning that we can then apply to the field and to clinics,” Dr. van Eps said. MeV