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Kaydence Sports Medicine & Rehab, 12635 County Road 130, Carthage, MO (2026)

06/24/2026

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06/22/2026

Understanding Equine Muscle Atrophy

Muscle is the tissue that turns a skeleton into a mobile body. Attached to bones via tendons, muscles contract and relax to maneuver that skeleton. Then there’s the smooth muscle that allows all sorts of functions that keep our horses alive and active, from digestion to tissue oxygenation. Muscular activity keeps legs moving, head turning, heart beating, and the lungs breathing. A common skeletal muscle issue is atrophy—the shrinkage or loss of muscle cells called myocytes. Stemming from a wide range of causes and linked to potentially serious diseases, muscle atrophy warrants a deeper look.

A Real Impact on Your Horse’s Health and Performance
With the crucial role musculature plays in every aspect of life, it’s easy to imagine the consequences of faulty, diseased muscles. “If muscle mass is insufficient, which can occur with muscle atrophy, a horse’s welfare can be significantly impaired,” says Alisa Herbst, PhD, of Rutgers, The State University of New Jersey, in New Brunswick, who recently developed and evaluated a muscle atrophy scoring system for horses. “For example, that horse might not be able to get up after lying down, or he might be unable to avoid an attacking horse,” she says. “Aside from compromised quality of life, horses with low muscle mass are limited in their ability to perform athletically. Lack of proper muscling increases the risk of injury, especially if high-intensity work or performance is requested.

“The full extent of the impairment on performance depends on the extent of strength lost from muscle loss compared to the amount of strength required for a given type and intensity of work or performance,” she adds.

The Culprits
We can divide the root causes of muscle atrophy into five main categories:

Sarcopenia is the Greek-originating scientific name for “age-related flesh loss.” It refers to a loss of muscle mass, quality, and strength, all of which are common in senior horses. In addition to giving geriatrics a sunken or skinny appearance, with the vertebrae and hip bones protruding, this generalized muscle loss can cause weakness. Some theories suggest sarcopenia is linked to inflamm-aging, a progressive bodywide inflammation affecting older horses and humans (Liang et al., 2022). In people it is also well-established that malnutrition correlates with sarcopenia (Ligthart et al., 2020).

Underuse of muscles leads to atrophy. Senior and retired horses are especially at risk of muscle atrophy because of naturally occurring sarcopenia, their tendency to develop pituitary pars intermedia dysfunction (more on that later), and the sedentary aspect of their lifestyle. Prolonged inactivity causes both atrophy and functional deconditioning of skeletal muscle, meaning muscle function is lost when unemployed. Muscle misuse can cause atrophy, as well.

“If a saddle is incorrectly fitted to a horse, that saddle will create painful pressure points on muscles,” explains Stephanie Valberg, DVM, PhD, Dipl. ACVIM, ACVSMR, emeritus Mary Anne McPhail Dressage Chair in Equine Sports Medicine and professor and director of the Neuromuscular Diagnostic Laboratory at Michigan State University’s McPhail Equine Performance Center, in East Lansing. “The pain and soreness will prompt the horse to avoid using affected muscles, manifesting as trouble lifting the back and engaging the hindquarters. The horse won’t develop proper musculature because using the muscles hurts.”

Neurologic diseases, including problems with the nerves innervating the muscle (neurogenic cause), can also lead to atrophy in horses. This could be focal (limited to a specific area) loss of muscle mass from traumatic nerve damage or originate from central neurologic systemic diseases such as equine protozoal myeloencephalitis (EPM) and equine motor neuron disease (EMND).

Myopathy is an umbrella term that encompasses all muscular diseases. Common myopathies in horses are classified as three types:
1. Those that cause muscle degeneration with exercise, such as exertional rhabdomyolysis, or tying-up.
2. Those that cause damage not associated with exercise (nonexertional rhabdomyolysis).
3. Those that cause muscle atrophy. “Common muscle diseases that cause atrophyinclude vitamin E responsive myopathy (VEM), as well as myosin heavy chain myopathy (MYHM) and polysaccharide storage myopathy (PSSM), both inherited diseases of Quarter-Horse-related breeds,” says Valberg.

Systemic disease that causes generalized weight and muscle loss—but is not primarily muscular or neurologic in nature—can also lead to this issue. Most commonly, this refers to pituitary pars intermedia dysfunction (PPID, formerly known as equine Cushing’s disease). “We’ve established that muscle atrophy is an important clinical sign of PPID and seems to affect roughly 50% of cases,” says Herbst. “The visible loss of muscle mass in PPID-affected horses is considered to result from the loss of certain muscle fibers.”

Study results further suggest muscle atrophy in PPID cases is linked to proteolysis—the breakdown of muscle proteins by enzymes. Pergolide, the treatment for PPID, has not been shown to improve muscle atrophy (Banse et al., 2021). Aside from PPID, other systemic causes of muscle atrophy include cancer, chronic infections, degenerative disorders such as degenerative suspensory ligament disease (DSLD), and malabsorptive disorders, the most common one being leaky gut syndrome.

Finding the Cause
With so many possible origins of muscle atrophy—some as benign as insufficient exercise and others as grave as cancer—getting to the root cause can quickly turn into a detective mission. Rather than a standalone disease, loss of muscle mass is considered a symptom of many conditions.

“Atrophy can have a range of clinical presentations and underlying causes,” says Valberg. “This complexity can make diagnosing and treating its underlying cause challenging.”

To guide veterinarians through the diagnostic process, Valberg has published a diagnostic tree for equine muscle atrophy.

As with nearly all health concerns affecting our horses, the recommended first step in diagnosing muscle atrophy is your veterinarian gathering a detailed history and performing a thorough physical exam. In this preliminary stage, the main goal is to simply determine if the origin of the muscle atrophy is muscular, neurogenic, or systemic. Veterinarians have a range of diagnostic tools available to help).

Evaluating Atrophy the ScientificWay Using MASS
Until recently, quantifying muscle loss required expensive, hard-to-obtain equipment, such as the three-dimensional photonic scans Valberg and her team use in research settings. That changed in 2022 when Herbst and her team published the Muscle Atrophy Scoring System (MASS). This provides an objective, repeatable, and standardized option for practitioners—and horse owners, with some training—to identify, monitor, and compare muscle atrophy in a particular horse by evaluating muscle in places such as the neck, back, and hind end.

Like the Henneke body condition scoring system, MASS scores are based on descriptions of how body regions feel and look, Herbst explains. Using a four-point scale, the MASS scores indicate muscle mass instead of fat. While developing the system Herbst and her team also found that higher MASS atrophy scores correlated with increasing age and with PPID status. These findings support further evaluation of the potential benefits of MASS to identify and monitor muscle atrophy in horses, she says.

Building Back: Recovering From Muscle Atrophy
The best treatment plan depends on the underlying cause of your horse’s muscle atrophy. In ridden horses a saddle fit check is a good first-line solution in cases of topline muscle atrophy. “Beyond that initial measure, in some cases treatment will take the form of an oral treatment with medications such as vitamin E—crucial for muscle health and function—or it may involve a corticosteroid for immune-mediated diseases,” says Valberg. “To help muscle recover its full form, additional therapies such as physical rehabilitation therapy, therapeutic ultrasound, and electrical muscle stimulation may be indicated. Your veterinarian will guide treatment based on the underlying cause of atrophy.”

Often, following the treatment plan for a given condition also helps resolve the associated muscle atrophy. “Take a horse with osteoarthritis, for example,” says Herbst. “That horse moves less because of pain and, therefore, develops disuse-related muscle atrophy. Once the pain is resolved, or at least managed, the horse will be willing to put weight on the affected leg again and might be able to tolerate normal exercise. Similarly, if a horse does not eat sufficiently due to a bad infection (e.g., pneumonia) and, therefore, loses muscle, treating the infection will help with food intake and halt, or even reverse, muscle atrophy.”

Prevention for Healthy Horses
Maintaining healthy muscles in your horse starts with the basics: proper nutrition and exercise. Because vitamin E deficiency is a direct cause of muscle malfunction and atrophy, ensuring appropriate blood levels of the vitamin is crucial. Vitamin E is found naturally in fresh grass. For horses with limited or no access to pasture, ask your veterinarian about blood testing and supplementation. Secondly, barring any physical limitations, your horse will benefit from a regular physical conditioning program to build and maintain healthy musculature. This includes not only your typical ring work but also hill work, longeing with equipment appropriate for your horse’s individual fitness level, and muscle-building programs such as dry and water treadmills

For owners of healthy horses looking to build strength and stability in the topline musculature, veterinarians often recommend physiotherapeutic stretches. “Dynamic mobilization exercises—aka carrot stretches—were found to increase the size of stabilizing muscle in the horse’s back,” reports Herbst, citing a 2015 study by De Oliveria et al.

“From a diet standpoint, amino acid supplements may support muscle growth and might also help prevent or slow down muscle atrophy, especially when used in conjunction with an exercise prescription,” she says. This being said, supplementation isn’t as straightforward as “more is always better,” says Valberg.

“If the diet is already well-balanced for muscle health, diet changes are unlikely to affect atrophied muscles,” she says. “However, if the diet lacks vitamin E and amino acids (the building blocks of protein), then balancing diet accordingly can positively affect muscle health and tone.”

Take-Home Message
You can strive to keep your horses’ muscles at a healthy mass and tone with two of the most commonsense management practices: a balanced diet and a regular exercise regimen. If you’re managing your equine partner through an atrophic episode, there’s hope. “Luckily, muscle possesses a remarkable ability to regenerate, and many horses do return to a normal muscle mass and full function, depending on its cause,” says Valberg. To maximize your horse’s chances of overcoming muscle loss, communicate with your veterinarian at the earliest sign of muscle pain, loss, or dysfunction, and encourage him or her to use the new Muscle Atrophy Scoring System to track progress.

The Horse

06/19/2026

Don’t Gamble With Green Grass

How to manage horses and their pastures to prevent laminitis
Grazing is a natural exercise for equids, but it isn’t without risk. For some horses, overingesting certain grasses can lead to laminitis, a painful, life-altering hoof disease that can be fatal in severe cases. It occurs when the laminae—the tissues that suspend the coffin bone within the hoof capsule—become damaged and inflamed.

So what is it about grass that creates such an issue for these animals? It boils down to the density of the nonstructural carbohydrates (NSCs), which are the sugars (glucose, fructose, sucrose), starches, and fructans that grasses create during photosynthesis. When a horse digests NSCs, his body breaks them down into glucose and fructose, which the small intestine absorbs. This can result in an increase in blood glucose concentration that can trigger an insulin surge.

“In the horses that are predisposed to metabolic disorders, when they ingest a high amount of NSCs, they secrete too much insulin,” explains Kathryn Watts, Colorado-based researcher and founder of Safergrass.org. “Abnormally high insulin can be a feature of pituitary pars intermedia dysfunction (PPID, formerly equine Cushing’s disease), or they can have high insulin as a standalone condition.”

Shannon Pratt-Phillips, PhD, a professor of equine nutrition and physiology at North Carolina State University, in Raleigh, studies obesity, metabolic issues, and glucose disturbances in horses. “Horses that tend to eat regular diets that are rich in starch and sugar can develop insulin dysregulation (ID), and for horses that are already at risk, consuming something that’s extra high in starch and sugar can send them over the edge where they might have a laminitic crisis,” she says.

Grasses and other plants photosynthesize to create sugar on sunny days. The plants generate more and more sugar throughout the day, so each plant’s sugar content is at its peak by the time the sun sets. If the temperatures are above 40 degrees F overnight, plants use those sugars to grow. So, by the time the sun rises in the morning, each plant’s overall sugar content is low again.

“In the spring and fall the ambient temperatures at night are too cool for the plant to use its sugar stores for growth, resulting in a higher concentration of sugars the next day, and the concentrations just get bigger and bigger every day,” Pratt-Phillips says.

“That can happen at any time of year depending on where you live,” adds Watts. “It is possible to founder (cause the coffin bone to rotate or sink in) a healthy horse in just a couple of hours if they’re predisposed and allowed to overeat grass that’s high in NSCs. Even if the concentration of NSCs in the grass is not maxed out, that same horse might still run into problems if they are allowed to overeat.”

When Is Grass a Risk?
A common misconception is that the only time of year grazing poses a risk to horses is in the spring. But, again, the issue depends more on where you live than what time of year it is. “In marine climates, like the Pacific Northwest, the U.K., and the coastal regions of Australia, there is no seasonality for laminitis,” says Watts. “There isn’t a lot of snow, and the grass stays green all winter long.”

Is Your Horse at Risk?
To determine how to manage horses on pasture, you must first identify the ones most at risk for laminitis. “Most veterinarians are suggesting to proactive owners that all horses over the age of 15 get tested annually for ACTH (adrenocorticotropic hormone, excessive levels of which can lead to PPID) and insulin concentration,” says Watts. “Most of the epidemiological studies are saying that it’s the undetected metabolic disease that is implicated in most of the new cases of laminitis. So, risk management is all about testing horses to find out which ones are at high risk and then managing that risk.”

Thanks to modern veterinary medicine and better nutrition, horses are living longer than they used to and have more time to develop diseases such as PPID. Horses over age 15, therefore, are at higher risk of developing pasture-related laminitis than younger animals.

“Not all PPID horses have high insulin,” says Watts. “Those that do not may be able to graze with less risk, but PPID is a progressive disease, and insulin dysregulation may develop later. ID as a standalone condition is not age-dependent, although symptoms generally do not display until after the horse or pony is done growing.”

Tips for Low-Risk Horses
If your horse is getting plenty of exercise, has been tested for ACTH and insulin levels, and is already in a setting where he has access to pasture 24/7, managing his health boils down to monitoring his body condition so you can make sure he isn’t consuming too much grass. Having constant pasture access means he’ll be naturally adapting to changes in grass throughout the year—the surges in growth in spring and summer and the dormancy of fall and winter. Even with that ongoing adaptation, however, be mindful of intake.

“Do they ever come up for air?” says Pratt-Phillips. “Or is their head buried in grass the whole time? Most horses will walk around and take breaks, but if you have a horse that never picks his head up, that might be a horse that’s more prone to overeating.” That healthy horse can soon become an unhealthy horse by consuming too many nutrients.

“If you have a horse that was on a drylot over the winter, and suddenly the horse has access to a perfectly manicured pasture, then that’s a very different type of situation,” she adds. “You have to introduce them to pasture very slowly, perhaps starting with 30 minutes each day for a week and slowly increasing from there.”

Tips for High-Risk Horses
Horses with signs of high circulating insulin levels (e.g., ridges on hooves, abnormal fat deposits) are particularly at risk of developing pasture-associated laminitis, says Watts. Horses with body scores above 6 (on the 1-to-9 scale, with 9 being obese) or that have PPID or a history of laminitis also need to be watched carefully. For these horses the best time for pasture turnout is before dawn (again, after nights when it hasn’t dropped below 40 F).

“When you rise at dawn, graze your pony on your lawn,” recites Watts. “Sugars rise in the afternoon; for foundered ponies this spells doom.”

Watts says using a grazing muzzle can be a good solution for some horses. “The goal is to minimize intake, but we want them out there (on pasture) for as long as possible, because we want them moving and eating,” she says.

Consider any pony to be at risk for laminitis. Pasture is like an all-you-can-eat buffet, and for ponies, which evolved in harsh environments and often have higher insulin levels and metabolic rates, this can be disastrous.

“Ponies can really pack in the pasture,” says Pratt-Phillips. “They can eat twice as much as a horse can per unit of body weight. So even grass with a relatively low sugar concentration can potentially be problematic.” Grazing muzzles and timed grazing can be helpful when managing your pony on pasture.

The horse with a history of laminitis should probably never have full access to grass, says Pratt-Phillips. “If you don’t have a facility that allows you to keep your horse off grass, you should have that horse wear a grazing muzzle all the time so that they can only eat sparse amounts of grass,” she explains. “You can be more relaxed with these horses if you know your pasture is composed of low-sugar or warm-season grasses (e.g., Bermuda grass, crabgrass, bahiagrass), but I probably wouldn’t risk it.”

Watts recommends every owner pay close attention to their pastured horses: “Every horse with ID seems to have a preferred ‘fat depot,’ ” she says. “Feel those fat pads on a regular basis. If you have a horse that has a tendency to have a cresty neck, after a couple of hours of grazing, you can sometimes feel their neck harden.”

Any dramatic changes to those fat pads can indicate a reaction to sugar. “A journal is very useful for detecting small changes that occur over time,” she adds. “Measure their neck and write it down, take pictures of their fat depots once a month, have your farrier take pictures of their feet, and compare the changes over time.”

It’s also very important to watch at-risk horses move—every day. Watts suggests owners teach their horses to trot on command, either at liberty or in-hand, so they can monitor changes in their movement, which can be red flags. “For any horse that is high risk for laminitis and is out on grass, I want to see them trot,” she says. “It takes an expert to see changes in the walk, but at trot most people can see it.”

Pasture Management
Managing your horses’ pasture is another key way to reduce their risk of developing laminitis or to allow at-risk horses access to grass. Consider these steps:
2. Keep your pasture fertilized. “There are a lot of data in plant physiology journals that show that grass that’s deficient in nitrogen tends to be higher in sugar,” says Watts. “If there isn’t enough nitrogen to create protein, the plant can’t grow, and it tends to accumulate sugar.”
4. Manage your weeds—they can also be high in sugar. Clover, dandelions, plantain, chicory, thistles, and other broad-leaf weeds can be problematic.
6. Don’t let grass go to seed. “The growth points where the seeds develop is where the sugar accumulates,” says Watts. “As the grass starts to head out, the portion of the plant that’s highest in sugars is now elevated and easier to graze.”
8. Plant warm-season grasses if you have mild winters. Bermuda grass, teff, and bahiagrass don’t tend to accumulate as much sugar as cool-season grasses such as Kentucky bluegrass, timothy, orchardgrass, brome, and fescue.
10. Strip graze, or divide your pasture into smaller areas or “strips” that reduce horses’ risk of overeating. As you move horses from one strip to the next, you can maximize the pasture usage without impacting its nutritional value.

Take-Home Message
If you’ve determined your horse is at low risk for developing laminitis, and you can manage pasture quality and quantity, then by all means give him access to it. “Grazing is one of the best things a horse can do,” says Pratt-Phillips. “Grass fulfills almost all the protein requirements, calories, and vitamins that a horse needs.”

With high-risk horses, remember that grazing risks don’t disappear at the end of spring, and every horse must be managed as an individual. “If the insulin stays high,” Watts says, “there are some horses that just can’t ever have grass again.”

The Horse

06/17/2026

We have some last minute appointment slots available tomorrow at Longhorn Arena. All appointment types available.

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Please text 417-448-0131 to schedule.

06/17/2026

Gastric Health
Ulcers Happen. Strike Back.

The complex nature of the horse’s digestive tract can predispose them to many problems, such as:

* Colic commonly caused by gas, impactions with feed or sand, and abnormal motility
* Equine gastric ulcer syndrome (EGUS), more commonly referred to as gastric ulcers
* Infectious diseases caused by bacteria, viruses, parasites, and other organisms
* Non-infectious diseases caused by overeating, poor-quality food, toxins, obstruction, inflammation and neoplasia

What is Equine Gastric Ulcer Syndrome (EGUS)?

EGUS encompasses a variety of lesions within the stomach that occur when acid has damaged the stomach lining. The horse has what is known as a complex stomach, meaning it has two different linings. The squamous mucosa (1) is the area above the margo plicatus. The glandular mucosa (2) includes the area below the margo plicatus extending through the antrum to the pylorus.

Lesions of the squamous mucosa are recognized as equine squamous gastric disease (ESGD), while lesions of the glandular mucosa are referred to as equine glandular gastric disease (EGGD). Although lesions can occur in either location, they behave differently in terms of risk factors and response to treatment.1 Veterinarians must perform a gastroscopy exam to accurately and definitively diagnose EGUS.

The economic impact of this disease is difficult to calculate because the impact on athletic performance varies from individual to individual. However, there are well-defined costs attributable to diagnosis, medication and the labor required for treatment.

What causes EGUS?
Any horse at any age can develop EGUS. The two leading risk factors are how and what we feed them (e.g. episodic feeding, withdrawal of feed before exercise and high concentrate/low forage diets), and stress (e.g. injury, transport, stall confinement).

Feeding: Lack of forage in a horse’s diet is a contributing factor of EGUS. Continual intake of forage helps horses naturally produce saliva, a buffer to stomach acid. Today’s horses are often subjected to a concentrate-rich diet and longer periods between feedings. More concentrate (especially high starch concentrates) along with less access to grazing leads to the following:

* Reduced amount of chewing
* Reduced saliva production
* Less physical buffering of acid by forage in the stomach
* More acid production
* Higher likelihood of gastric ulcer syndrome

Stress: Some horses are more prone to stress than others, but for many, even the smallest changes in routine can cause stress. Physical and behavioral changes, such as injury, transportation, change in herd dynamics and stall confinement, can cause stress in horses. It’s important to identify and anticipate moments of stress so they can be managed properly.

What are the clinical signs of EGUS?
Unfortunately, EGUS is not top-of-mind for many horse owners until their horse is already showing signs. Help your clients get ahead of EGUS by educating them on the clinical signs, which include:

* Poor performance
* Changes in behavior
* Recurrent, low-grade colic (especially after eating)
* Inappetence, weight-loss and/or poor body condition

Boehringer Ingelheim

06/12/2026

Diagnosing Equine Hock Joint Problems

With multiple rows of uniquely shaped bones, several distinct joint spaces, and a plethora of soft-tissue attachments, the horse’s hock (tarsus) plays a crucial role in equine locomotion. However, its complex anatomy can prove a diagnostic challenge for veterinarians.

“Unlike the forelimbs, lameness related to the distal extremity is less common in hind limbs, yet the hocks are a common source of pain/discomfort causing lameness,” says Pablo Espinosa-Mur, DVM, DVCs, Dipl. ACVSMR, assistant professor of diagnostic imaging at Ontario Veterinary College, in Canada.

Horse Hock Anatomy
The hock joint is made up of three rows of bones and three distinct joints. The bulbous ends of the horse’s tibias, called the malleoli, come to rest on top of each talus, a uniquely shaped bone in the hock forming the tarsocrural joint. Each talus has two obliquely oriented (slanted or at an angle) ridges extending from the dorsal (towards the back) aspect of the bone that interlock with the malleoli and the distal (lower) intermediate ridge of the tibia.

The flat bottom of the talus articulates with the rectangular central tarsal bone, forming the talocalcaneal-centroquartal (or proximal intertarsal) joint. The bottom of the central tarsal bone overlies the small cuboidal bones, numbered one through four, forming the centrodistal joint. Finally, the small cuboidal bones articulate with the metatarsal bones (primarily the third metatarsal bone, which is the cannon bone) forming the tarsometatarsal joint.

Several soft-tissue structures such as muscles, ligaments, and tendons pass alongside the hock. This includes the digital flexor tendons coursing along the plantar aspect (toward the rear) of the joint, the extensor tendons running along the dorsal aspect, and the medial and lateral (located closer to and further away from the median plane of the horse, respectively) collateral ligaments extending from the lateral aspects of the tibia to the third metatarsal bones.

“However, there is sometimes communication between other joints as well, which means intra-articular (IA) anesthesia may not be specific,” adds Sue Dyson, MA, VetMB, PhD, an independent consultant based in the U.K. Joint communication refers to the interconnection between different joint compartments, which allows synovial fluid to flow between them.

“There are many attachments as well as deep and superficial parts both medially and laterally that have different orientations and attachments. These structures can get injured individually or together, complicating the workup,” Dyson explains.

Common Horse Hock Pathology
Dyson says common pathologies (disease or damage) causing lameness in the horse’s hock include:
1. Osteoarthritis (OA) in the distal hock joints, particularly the centrodistal (distal intertarsal) and/ or tarsometatarsal joints;
3. Osteochondrosis dissecans (loose cartilage or bone fragments in the joint) in the distal cranial (toward the horse’s head) aspect of the intermediate ridge of the tibia (DIRT lesions) or the trochleas of the talus, often combined with secondary osteoarthritis of the tarsocrural joint; and
4. Traumatic injury of the deep and superficial collateral ligaments.
“In some cases, osteoarthritis of the distal tarsal joints and desmitis (damage of a ligament and surrounding structures) of the proximal suspensory ligament (originates at the top of the cannon bone and supports the fetlock) can be seen in the same horse,” says Espinosa-Mur. “These conditions can be clinical while others can be subclinical (not visible to the eye) at the time of presentation.”

Diagnostic Analgesia in the Hock
Because the hock’s structures lie in such proximity to one another, performing nerve blocks to localize lameness to one location can be challenging for veterinarians, says Espinosa-Mur. Some of these structures share innervation or are close enough that diagnostic analgesic can diffuse and cause false results, he adds. For example, the anesthetic agent can diffuse from the tarsometatarsal joint into surrounding structures. This means the veterinarian unintentionally desensitizes the surrounding area, including the suspensory ligament.

“This is particularly true if too much local anesthetic solution is used as it will leak out from the tarsometatarsal joint and influence the suspensory ligament,” says Dyson. “Ideally, practitioners will cross-block, meaning they will block the suspensory ligament on one occasion and the tarsometatarsal joint on a separate visit.”

It is important for veterinarians to recognize that IA anesthesia will not remove bone pain, says Dyson. “So with OA that involves subchondral bone (beneath the cartilage) damage, an intra-articular block may be negative.”

Imaging the Horse’s Hock
Veterinarians can use X rays as a first-line method to evaluate the structures in the hock. When they cannot reach a clear answer using this imaging modality, advanced imaging is the next step.

To help home in on the specific source of hock lameness, Espinosa-Mur and colleagues recently published a studyusing 18F-sodium fluoride (18F-NaF, a radioisotope) PET for imaging the tarsus and proximal metatarsus (the upper aspect of the cannon bone near the hock). They took 18F-NaF PET images of 25 horses with lameness localized to these regions and compared them to computed tomography (CT) scans of those same 25 horses.

Espinosa-Mur says he and colleagues believe imaging modalities capable of distinguishing active injuries from chronic or incidental (found unexpectedly, typically without clinical signs or need for treatment) lesions would benefit equine practitioners, especially when evaluating the hock. In this case 18F-NaF PET provides an image that helps veterinarians detect active lesions by highlighting areas where the bone takes up the radioisotope—similar to a bone scan but in 3D.

In some cases the PET scan results correlated with those from the subjective and objective lameness evaluations. “Advanced imaging with PET could definitively help determine the (lesions) that display higher osseous (bony) turnover, which in some cases can be the ones that are causing lameness,” says Dyson.

Take-Home Message
The equine hock is a complex collection of joints, which makes diagnosing hock pain challenging. “With a good clinical examination, systematic use of nerve blocks, and good radiography and ultrasonography, many diagnoses of hock-related injury can be achieved,” says Dyson. Since the advent and wider availability of advanced imaging, including CT and PET, veterinarians can more easily diagnose hock problems and determine their clinical relevance, allowing targeted treatment options.

The Horse

Kaydence Sports Medicine & Rehab

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