EHM is a devastating neurological disease in horses that is caused by equine herpes virus 1 (EHV-1). It has gained more notoriety over the last 10 years, affecting horses at boarding facilities, large stables, racetracks and horse shows, resulting in widespread quarantines. One of the largest EHM outbreaks in U.S. history was in 2011; it started at a horse show in Utah and ended up exposing 242 horse premises in 19 states.

The first sign of the disease is often fever, which can go unnoticed. About seven to 10 days later, the most common symptoms include hind limb weakness and/or incoordination, incontinence (dribbling urine) and stumbling. These signs can worsen into more severe neurological symptoms such as sitting like a dog, severe ataxia, paresis (“drunk walking” and weakness), and difficulty getting up. The worse the clinical signs, the worse the prognosis. Those that can’t get up are often humanely euthanized.

By the Numbers

Equine herpesvirus is a widespread, common virus in horses. It has nine different forms, but the most common are types 1 and 4 (also known as rhinopneumonitis)—and each type can have subtypes. Type 4 typically localizes in the upper airway (nose and throat), causing a snotty nose and mild to moderate fever. In other words, type 4 is usually just a horse cold, and thankfully it’s the more common form.

Type 1 is much more invasive and causes not only respiratory disease but also abortions and myeloencephalopathy (disease of the nervous system). Respiratory disease and abortions are the most common effect of this virus.

Vaccines for EHV and EHM

Both viruses can be vaccinated against; this is the “rhino” part of the flu/rhino vaccine. EHM, the neurological disease caused by subtypes of EHV-1, is very uncommon. It’s most often associated with a subtype of the herpes virus referred to as the “neuro form.” This is a very important factor when managing outbreaks where horses are tested to determine quarantine status.

The vaccines currently available are not labeled to protect against the neurological form of herpes (EHM), but researchers are currently studying if there is some protection provided.

By vaccinating the general horse population, the overall amount of herpes virus shed is decreased, and thus decreases the chances of the neuro form from occurring.

What we do know is that by vaccinating the general horse population, the overall amount of herpes virus shed is decreased, and thus decreases the chances of the neuro form from occurring.

Horse owners and facility managers can also help protect horses by becoming aware of the disease and learning good biosecurity. Follow vet-recommended vaccination programs to manage shedding of the virus among the general horse population.

The Challenge of EHV-1

EHV-1 is a difficult virus in many ways. It is highly contagious, gaining access to the body through the nose from nasal secretions of infected horses. At the nose level, it replicates and causes disease there. But type 1 goes deeper into the tissue, getting into white blood cells that transport it throughout the body.

Invasion

Here is where it creates the most harm. These infected white blood cells attach to the lining of blood vessels, most notably in the uterus of pregnant mares or the blood vessels of the spinal cord and brain stem.

It invades those cells, lining the blood vessels, causing damage and essentially destruction of the blood vessel. Once this happens, the blood supply to the tissue is compromised and the tissue dies. In the case of abortions, the placenta dies. In EHM, the spinal cord tissue dies, causing the varying advancing neurological symptoms, depending on location and severity of damage.

Immune to Immunity

In addition to causing such a damaging disease, herpes virus in general has also adapted itself to evade the immune system. It moves from cell to cell without entering the blood (where the antibodies are). This is one reason why the vaccine, which stimulates the body to produce antibodies, has difficulty protecting against this disease.

The virus can also stop the infected white blood cell it has invaded from producing markers on the surface of that cell that alert the other white blood cells to the infection and signal destruction of the infected cell.

Hidden Threat

Finally, it literally “hides out” in lymph tissue and the nervous system, becoming dormant and undetectable by the body. It’s in this latent state that most horses are infected. Many are infected as foals by their dam, and the virus remains dormant until some physical stressors activate the virus.

Diagnosis

It is not completely known what exactly reactivates the virus and causes EHM. The disease itself appears to be occurring more frequently, and is considered an emerging disease.

As such, much of what we do know has been from studying the outbreaks that have occurred. From these studies it appears that older horses and mares are more at risk. Introduction of new horses to a herd and showing are common factors in outbreaks. It’s theorized that these events cause stressors in the horses, creating the right conditions for activation of the virus.

Events that cause stress in horses create the right conditions for activation of the virus.

This disease is reportable, meaning when it occurs it must be reported to the United States Department of Agriculture (USDA) state regulatory veterinarian. All horses on the affected premises must be quarantined, and horses that have been in contact with the affected horses are monitored for disease. Alerts about these outbreaks are issued nationwide; you can stay up to date via the Equine Disease Communication Center (www.equinediseasecc.org) and sign up for email notifications.

How to Diagnose EHM

Currently the best available diagnostic tests are nasal swabs and blood testing to look for a rise in antibody titers over a seven-day interval. Antibody levels are compared, and a four-fold increase indicates active infection. Later-stage tests include virus isolation, cerebral spinal fluid analysis and tissue sampling.

This disease can look like West Nile virus, Eastern and Western encephalitis, wobbler’s, severe arthritis of the neck, EPM or rabies, so when clinical symptoms first show it can be very challenging to make a proper diagnosis.

Treatment of EHM

There is no direct treatment for EHM. Efforts are directed at providing supportive care with fluids and IV total nutrition, as well as minimizing the damage with anti-inflammatory drugs like Banamine, steroids and DMSO.

Antiviral Drugs:

There are two antiviral drugs that have been used with some success: acyclovir and valacyclovir, with the latter currently the more promising, although neither is proven. There is a small amount of data in the literature that suggests zinc supplements might help prevent and cure the disease.

Management:

Biosecurity is key in minimizing the spread of this disease. Infected horses should be removed from the herd and isolated on the same property. All items that were in contact with the infected horse must be disinfected, since the virus can survive in the environment for a long time. Some of the techniques for managing infected horses include foot baths and separate clothes for handlers, separate stall cleaning tools, and ideally, separate handlers when possible.

Prevention of EHM

Horses that have been exposed to infected horses need to be closely monitored. This includes taking their temperature twice daily, serial nasal swabs and blood antibody titers. No vaccine has been shown to prevent EHM, but herd vaccination has been shown to decrease the virus shed and could potentially help prevent the disease.

The recommended vaccination frequency is once every six months, or three months for horses at higher risk. Horses must remain quarantined for 28 days after the last horse has shown signs of the disease and nasal swabs show no more infection. Horses that have recovered from the disease typically don’t have relapses and aren’t contagious. However, they may have lasting neurological changes.

What’s Next?

EHM’s status as an emerging disease has focused a lot of research on it and as a result, a lot more is known now than 15 years ago. Unfortunately, there are still so many unanswered questions that horse owners and veterinarians continue to struggle to conquer this disease.

EHM will most likely never be eradicated, but much work is being done to find better treatments and a vaccine. Until then, the horse community must work hard to combat this disease by implementing good vaccine protocols, quarantining horses new to a herd, and monitoring temperature for at least two weeks before introducing to the group.

Other steps include good nutrition, not overworking horses (especially while at shows), and trying to minimize physical stress as much as possible.

This article about Equine Herpes Myeloencephalopathy originally appeared in the August 2018 issue of Horse Illustrated magazine. Click here to subscribe!

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As veterinarians, there are always those horses we’ll never forget. For me, when it comes to horse dentistry, there are four.

The first is Shiloh. During my second year out of vet school, the old, beloved mare couldn’t eat for two weeks after my boss floated her teeth with hand floats.

About five years later, there was Mariah, who for some strange reason kept breaking her teeth. It seemed every few months I’d be called out and find yet another of her molars broken. We were at a loss as to how she was doing it.

Next was Roulette, who was so mouth-shy that no one could get near her with a dewormer. When I floated her teeth, a process part of horse dentistry, I found the smelliest, rotten broken tooth in her upper molars. I can only imagine the constant tooth pain she was in.

Finally there was Opie, whom I had taken care of for 15 years and a favorite patient. He too got a fractured tooth, and they called in a vet specializing in horse dentistry to fix it when I couldn’t. That put me on the path to improve my horse dentistry skills. I knew I had to do better for Opie and my other clients.

Modern Improvements

Equine vets have stepped up the horse dentistry game big time. Now we have a board certification association that creates actual equine dentists, which is a great deal different than a dental school that certifies non-vets.

We take X-rays of the teeth and we look at tooth root health. We treat gum disease. We have the ability to fill cavities. We no longer expose the sensitive pulp chamber of the teeth. It’s much more than having Joe from down the road come out and float your horse’s teeth.

The Horse’s Mouth

Equine teeth, adapted by nature to constantly chew grass all day, are being constantly worn down. To accommodate this, the horse’s teeth constantly erupt (grow) from the gums. They essentially have very long teeth hidden inside their jaws that emerge as the surface wears down from grinding food.

The horse’s upper jaw is slightly wider than the lower jaw, so the back molars are not completely aligned from side to side. The upper outside and lower inside of the cheek teeth do not touch, and as the teeth are worn down, sharp ridges and points develop on the inside lower teeth and outside upper teeth, or the teeth become slanted from side to side.

The points can become so sharp that they cut the cheeks and tongue, causing ulcers, and after a while, poor grinding causes the horse to drop food. These points, ridges and slants are what need realigning, or what is known throughout the horse world as “floating.” In the horse dentist world, the new term is “occlusal alignment,” which is essentially restoring the grinding surfaces of the teeth­—the occlusal surfaces—back to their original alignment for the most effective and efficient chewing.

How the Tooth Works

So why was Shiloh so mouth-sore after being floated that she couldn’t eat, and why did Mariah get so many broken back teeth? It turns out there are some areas of the horse’s teeth that we shouldn’t touch. The structures that allow us to grind down the sharp points and ridges are also the structures that can become diseased or get damaged during attempts to realign the teeth.

Horses’ teeth have a strong enamel covering along with hard reinforcement, called dentin, within a large cavity. This cavity is called the infundibulum. Like us, they have pulp chambers that hold the sensitive nerves.

As the tooth erupts, dentin and enamel are laid down to protect the pulp chambers and harden the center of the tooth within the infundibulum. When we correct the alignment by floating the teeth, we grind down only the edges of the teeth, not the middle of the teeth that touch and grind (called the occlusal surface).

The grinding (occlusal) surfaces interlock with each other in a zigzag pattern with what is known as the transverse ridges. Sometimes teeth are ground down on this occlusal surface in an attempt to flatten those ridges. Only excessive ridges should be taken down.

The danger in grinding down the occlusal surface is exposing the pulp cavity. If this happens, the underlying nerve is exposed and the tooth becomes extremely painful and has the potential to die over the next several months. Studies have shown that there can be as little as 1 to 3 mm of enamel covering the pulp chambers, which makes exposing them and damaging the teeth easy to do.

Wave Mouth

In the case of Shiloh, because of her advanced age, her teeth had worn into what is known as a “wave mouth.” Horses have front teeth, called incisors, used for ripping grass. These are the teeth you see when you lift up the horse’s lips. There are six upper and six lower incisors.

If you are able to open the horse’s mouth and look in the back, you will see the teeth that do all the hard work—grinding hay and grass. There are six upper and six lower large molars on the left and right sides of the mouth, often referred to as the cheek teeth.

The small wolf tooth, if present, is just in front of the first cheek tooth, typically only on the top jaw, and the canines are just behind the front teeth. In the case of wave mouth, the lower cheek teeth form a hump and over-wear the upper cheek teeth, causing a wave.

Where we get in trouble is when we try to correct these misalignments. Sometimes when grinding down the waves and humps to flatten the teeth, we expose the pulp cavity, or the heat generated from the grinding causes heat damage to the pulp chamber.

The front teeth can also get a wave, known as smiley face, or slant from side to side, known as a slant. Where we get in trouble is when we try to correct these misalignments. Sometimes when grinding down the waves and humps to flatten the teeth, we expose the pulp cavity, or the heat generated from the grinding causes heat damage to the pulp chamber.

If attempting to make the teeth look aligned, it is possible to take so much down that the back cheek teeth no longer touch each other and can’t do their normal grinding anymore. This also puts more pressure on the front teeth, making them sore and possibly causing the beginning of a serious disease called equine odontoclastic tooth reabsorbtion and hypercementosis (EOTRH).

Tooth Death

Shiloh was most likely overfloated, something that often happened 20 years ago. If the pulp cavity becomes exposed, sometimes the tooth fixes itself with a patch of dentin to seal off the exposed chamber, but if it doesn’t, the nerve dies slowly, a very painful process.

Since the cheek teeth have multiple pulp chambers that often communicate with each other, this causes the tooth to die. Once it dies, it has the potential to fall out. The process can take months or years.

Dental Caries

In Mariah, Roulette and Opie’s case, their problem wasn’t over-floating or misalignment of the teeth, but rather the tooth itself developed what are known as caries. These weaken the teeth and cause them to fracture.

As mentioned earlier, one of the adaptations of horses’ teeth is the infundibulum. This cavity in the center of the tooth is quite large and runs deep within the tooth. It gets filled in with dentin to help strengthen the tooth.

Only the front teeth and the upper cheek teeth have these specialized cavities. Unfortunately, sometimes these don’t fill in properly with dentin, and a small hole develops in the center of the tooth. This hole can get packed with food and other bacteria and grow in size.

Caries can get very large and involve the pulp chambers. They can get so big and so impacted with food that the tooth splits open, causing a fracture. If left in the mouth, the fractured tooth becomes very painful and can cause gum disease or sinus infections, since the upper cheek teeth are within the sinus cavity.

Diseases

Other areas of concern in the horse’s mouth are the gums and the front teeth. Horses can and do get gum disease. The most common form is a space between the cheek teeth, called a diastema, which allows food to get impacted between the teeth.

This impacted food is a source of infection, and if left unchecked, causes gum disease by creating deep, infected pockets. These pockets can cause loosening of the teeth, leading to possible tooth loss and pain.

EOTRH is a dental disease that is being more commonly recognized. This is a disease of the incisors (front teeth), where the bone surrounding the teeth becomes inflamed.

The initial response by the jawbone to this inflammation is loosening of the teeth because the bone surrounding them becomes reabsorbed. Once the body realizes the teeth are loose, it overcompensates by laying down extra calcium to try and strengthen the area and save the tooth. Instead, there is a lot of pain, destruction of the tooth, excessive enlargement of the tooth roots, and fractures in the teeth.

Begin with an Exam

We’ve come a long way from the days of Shiloh. Now the accepted practice is the oral exam, not just floating the teeth. We sedate each horse and open the mouth fully with a speculum to look at each tooth with a bright light and a mirror or endoscope (special camera that can get to the back of the mouth).

We examine the infundibulum and pulp chambers for caries, fractures or damage to the chambers. We look at the gums with a mirror or endoscope for signs of gum disease. We use special picks and probes to determine how big and deep the caries or gum pockets are. We take X-rays, computer topography (CT) scans and bone scans of the teeth to determine if the tooth roots are healthy.

We clean out caries and fix diastemas by opening the gaps between teeth, which prevents food from becoming trapped. We extract diseased cheek teeth and incisors in a much more humane and pain-free way.

And we’ve gone back to school. Now there are many specialized courses for vets to learn these new techniques. For those who want to take it to the next level, a true veterinary dental association board-certifies veterinarians that want to become dental specialists.

These specialized horse dentists and others are developing new techniques to try and save teeth. They are working on ways to fill in caries before they fracture, giving the tooth a filling and doing root canals.

Horse dentistry is no longer your average Joe’s float job. It’s real dentistry, and vets are getting on board.

Janice Posnikoff, DVM, was the owner and principal vet at Orange County Equine Vet Services in Orange County, Calif., for over 20 years. After spending time in Maryland and Virginia, she now brings her love of dressage and expertise in sport horse medicine to her hometown city of Winnipeg, Canada at Elders Equine Vet Services as an associate vet. She lives and practices there with her five bunnies, close to family and friends.

This article about horse dentistry originally appeared in the March 2018 issue of Horse Illustrated magazine. Click here to subscribe!

Further reading:

Everything You Ever Wanted to Know About Equine Dentistry 

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Poor conformation such as long, sloping pasterns can predispose a horse to tendon and ligament damage.

There are several factors that contribute to overload and breakdown of tendons and ligaments. The first is conformation. Long sloping pasterns and/or long toes/low heels create more tension and load on tendons and ligaments.

Next is conditioning. Regular exercise creates strong bones, tendons and ligaments. However, exercise should be increased gradually over time to higher levels. Horses that are not properly conditioned and then ridden hard are very prone to tendon/ligament tearing. With conditioning also comes proper warm-up. Cold tissues are less pliable and therefore are more susceptible to injury.

Footing can also be problematic. Deep or slippery footing can cause the fetlock to drop too much, increase breakover, or create tremendous torque from twisting, all of which can lead to injury.

And finally, these injuries can sometimes happen simply from the horse exerting so much power during work that tissue tears. However, I feel this is a rare occurrence in properly conditioned horses.

I believe many of these injuries can be prevented by being aware of the above factors and taking necessary precautions. Address hoof balance issues, such as long toe/low heel, with your vet and farrier. Condition your horse carefully, and don’t overwork him. Watch the footing: Deep sand, a slick base, and rocky or uneven ground are the enemies of tendons and ligaments.

Another consideration is protective legwear for horses. In general, I do recommend using boots that fit properly; a bad fit can do more harm than good. Look for boots that “sling” under the fetlock to support tendons and ligaments. Beware of some types of neoprene boots, which cause unwanted increased heat in the leg. Also, some horses are allergic to neoprene and will blister under these boots.

Back to Tendon and Ligament Injuries.

The post Tendon and Ligament Injuries: Causes and Prevention appeared first on Horse Illustrated Magazine.

Cycle of Inflammation

A joint is comprised of two bones that need to move independently of each other. A cartilage layer on the ends of each of those bones acts as a shock absorber, and joint fluid facilitates movement and also absorbs shock. A joint capsule holds the joint fluid in and keeps the bones together. It’s a very simple design with many complicated features. And the greater a joint’s motion is, the more susceptible it is to problems.

Joint inflammation is the body’s way of trying to fix a problem. The problem usually starts off as some sort of tissue damage or infection. Inflammatory cells, which are white blood cells, move into the area and start a whole cascade of reactions. These inflammatory cells do a great job killing bacteria and absorbing damaged tissue, but they also release chemicals into the surrounding tissue that actually destroy it. This is where arthritis can develop—and this is why inflammation is so destructive and why we do as much as possible to stop it.

Over time, the self-feeding cycle of inflammation results in joint surface (cartilage) deterioration, painful joint capsule thickening and the break down of joint fluid. The body, in an attempt to heal the damage, lays down scar tissue and bone that decrease flexibility and overall joint function.

All of the above are also very painful. As cartilage is destroyed and the underlying bone becomes unprotected,  it hurts. Some of the chemicals released by inflammatory cells actually stimulate pain. This is the body’s defense mechanism, designed to stop the horse from using damaged tissue so it can heal. Unfortunately, in the case of arthritis, all this accomplishes is further break down of the joint due to decreased circulation from inactivity.

Arthritis Management

There are several areas of prevention and management that focus on stopping the inflammation and supporting the structures of the joint, including proper trimming/shoeing, exercise, good footing, balanced nutrition, injections and responsible breeding. New therapies are being investigated that are aimed at stopping cartilage destruction, but arthritis prevention is the best treatment of all.

Exercise

A great natural anti-inflammatory is circulation. Increased circulation improves the body’s ability to remove toxins produced by inflammation cells, and therefore decreases joint damage. Increased circulation also removes fluid from the inflamed tissue and increases joint mobility.

Increased circulation occurs with exercise. The simple act of walking increases blood flow. Often, arthritic horses will start out “stiff” during work, but warm up after a period of walking.

Regular exercise routines are key for arthritis prevention and management. Turnout paddocks and pastures are great for constant walking to keep joints limber. Daily riding also helps prevent and treat arthritis.

The amount and type of exercise should be tailored to the horse’s ability and conformation, and the footing should be considered. Hard, rocky footing will add more concussion to the legs, so good footing is preferred. This means riding in well-maintained arenas; when trail riding, walk the hard, rocky stretches and save trot/canter exercise for nice parts of the trail.

Fitting the horse’s career to his conformation is also very important. Horses with poor conformation, such as toed in, toed out, sickle or cow hocked, upright pasterns and straight hind legs are more prone to arthritis due to abnormal concussion on the joints. These horses can often perform while young but are at greater risk of developing arthritis. Therefore, the type of work they do should be carefully chosen. A wise trainer or rider will keep these horses at lower levels of competition, even though the horse may be more talented, in an effort to preserve the joints.

A great example of career choice based on conformation is the western pleasure horse, which is typically bred to be straighter in the hind legs. This type of conformation allows the western pleasure horse to perform the soft jog and lope required for the sport. However, a horse built for western pleasure would have much difficulty doing extended and lateral work required for dressage. These horses can do other types of work but tend to have poorer performance and are at more risk of developing problems sooner in life.

Trimming/Shoeing

Trimming and shoeing are very important in both the prevention and management of arthritis. Improper trimming can cause abnormal concussion on the joint. The most common error is uneven trimming, with one side of the hoof higher than the other. This imbalance causes one side of the hoof to land first and creates increased concussion on one side of the joint. Over time this can develop into a type of arthritis most commonly known as ringbone.

Long toes/low heels are also bad for the joints, causing added stress on the joints from the increased breakover. Overall, horse owners should strive for balanced trimming from side to side, and keeping the toe short. For horses with hock arthritis, I like to see the hind toes squared off so the leg can roll over the toe easier, decreasing the stress on the front of the leg and the hock.

Supplements

Joint supplements offer management and prevention at once. There are many products available aimed at stopping joint cartilage breakdown by supplying the body with the building blocks for cartilage production. These building blocks—chondroitin sulfate and glucosamine—are the main molecules supplied in these joint supplements.

There are also many herbs available; the two most common anti-inflammatories are yucca and devil’s claw. The effectiveness of these herbs is questionable, but many horse owners report good results for their horses when used for low-level arthritis.

Joint Injections

The tried-and-true management strategy for arthritis is joint injections. The main goal of this therapy is to reduce the inflammation within the joint and help restore it to a more healthy state, therefore reducing pain and returning the horse back to his regular exercise routine.

Most joints are injected with a corticosteroid along with hyaluronic acid. Corticosteroids are very strong anti-inflammatory drugs that break the cycle of inflammation. Hyaluronic acid is synthetic joint fluid that replaces the weak, thin, joint fluid that is no longer doing its job. There are many types of corticosteroids used for joint injections, but the most common are betamethasone, Depo-Medrol and triamcinolone. Triamcinolone has been shown to be chondroprotective when used in small doses; this means it actually helps produce stronger cartilage and thicker joint fluid.

Intramuscular and Intravenous Injections

Hyaluronic acid is also available in an intravenous preparation under the brand name Legend. When given intravenously, it migrates to the joint and stimulates the joint to produce more joint fluid and also acts as an anti-inflammatory drug. (HA is also available in oral supplements, but research on efficacy is still pending.)

Polysulfated glycosaminoglycan (Adequan) is available in an intramuscular preparation that helps strengthen the cartilage and also stimulates the joint to produce more joint fluid.

Non-steroidal anti-inflammatory drugs (NSAIDs), such as bute and Banamine, are also used to help alleviate pain and decrease inflammation within the joint. This class of drugs has some side effects, such as ulcers, kidney or liver damage, if not used cautiously. In an effort to avoid side effects, a topical cream called Surpass has been developed. It acts as an anti-inflammatory at the site where it is applied.

Personal Notebook

In my practice I deal mostly with hock arthritis and ringbone, with a few knees thrown in for good measure. I work with the owner to develop a tailored program based on degree of lameness, degree of arthritis determined by radiographs (X-rays), career of the horse and the resources available.

Horses with mild hock arthritis are usually not lame but rather have performance problems, such as not striding out, swapping canter leads, difficulty picking up correct canter leads and refusing jumps. For these horses, oral joint supplements, intravenous Legend and intramuscular Adequan are the first line of treatment if the horse is in low-level work, such as trail riding.

I also try to make sure the horse is not spending too much time in a stall, and I encourage daily turnout and under-saddle exercise. In many urban areas pasture is not available and horses are stabled in stalls. Spending time standing in stalls leads to problems. Horses that walk around all day in turnout keep their joints healthier due to increased circulation.

Athletic horses that suffer arthritis usually need joint injections to return them to the level of work they were at or to resolve lameness. Depending on the amount of work the horse is doing and the severity of arthritis, the joint injections usually only have to be done once a year. Concurrent use of Legend, Adequan and oral joint supplements (chondroitin sulfate and glucosamine) help prolong the duration of the joint injections. Squaring the toes of the hind hooves and setting the shoes a little back from the toe eases breakover—allows the toe to roll over faster—and therefore reduces the stress on the joints.

Many performance horses are given oral joint supplements, intravenous Legend and intramuscular Adequan as preventative care in an effort to stop or minimize joint damage created by the demands of high-impact sports. This regimen also helps keep the performance horse as comfortable as possible. By keeping arthritis pain in check and keeping the horse moving as much as possible, we also help prevent secondary injuries, such as joint sprains, tendon injuries and sore backs.

Show horses in full competition often receive Legend and Adequan shots monthly, while others get the shots quarterly. Once again, all of these programs are tailored to the individual and depend on response to treatment.

New Horizons

There are some wonderful scientific minds out there trying to find solutions to what causes arthritis and how to fix it. The current focus is on extracorporeal shockwave therapy; drug therapies; chemicals released by inflammatory cells; and the cellular structure of the tissue that make up the joint.

ESWT
Extracorporeal shock wave therapy (ESWT) is a treatment that has proven to work very well for equine arthritis. It has been around for a decade, but over the last few years has been clinically proven to resolve lameness due to arthritis. At this time it is unknown how exactly ESWT works, but it’s a very active field of research. The research has so far proven that arthritic horses do respond positively to the treatment, and many prominent clinicians are recommending it. There had been some concern that ESWT causes microdamage to the bone tissue, leading to fractures. Thankfully, current data doesn’t support this theory.

Drugs
Tildren, a new drug that’s being used in Europe to manage arthritis and navicular disease, stops the breakdown of bone. No word yet on when this treatment might be available in this country.

Chemical Mediators
Research examining the bad chemicals that trigger tissue damage, as well as the good chemicals that stimulate tissue development, is hot right now and may revolutionize management and prevention of arthritis. Gene therapy is a related topic, with researchers hoping to find a way to introduce genes that stimulate joint cells to produce joint-friendly proteins, create synthesis of cartilage and block formation of destructive enzymes.

Tissue Transplants
For years researchers have been trying to transplant cartilage to restore damaged joints. So far they have been unsuccessful, but they are still trying. Cell transplants into the joint or cartilage to stimulate tissue production are also being studied. This is extremely encouraging and would be less invasive than actual tissue transplants.

All of these areas of treatment are showing great promise and some successes. In the last 10 years we have advanced dramatically in the recognition and management of arthritis. In the next 10 years we can expect to see more great advancement in the prevention and treatment of this debilitating disease.

Further Reading
HorseChannel’s Joint Care Guide

This article originally appeared in the October 2005 issue of Horse Illustrated. Click here to subscribe.

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Cancer is the uncontrolled growth of cells that develop into masses, commonly known as tumors. They may invade healthy tissue sometimes as a more diffuse blanket of cells throughout the tissue similar to roots of a tree spreading throughout the ground. The tumors themselves release chemicals into the body that cause several different side effects such as weight loss, depression, anorexia, fever, anemia just to name a few. Once a cell type or tissue becomes cancerous it can spread through the blood or lymph system to all regions of the body and become tumors anywhere. 

In the case of lymphosarcoma, the lymph tissue becomes cancerous, often starting with one lymph node and spreading to others. The lymphatic system is the body’s defense network and lymph nodes are small nodules throughout the body that filter lymph, destroy infections, and produce white blood cells. People often refer to these nodes as “glands.” Along with the lymph nodes, there is also lymph tissue that is diffusely spread throughout organs such as the intestines and the skin. Any one of these “glands” or lymph tissue can become cancers, hence the symptoms of the disease can vary greatly depending on the location of the cancerous tissue. There are four general types of lymphosarcomas which are categorized on location. The four main types are generalized (multi-centric), intestinal, mediastinal and cutaneous. 

The generalized form is the most common and includes multiple peripheral and internal lymph nodes. Basically, it is tumors through the lymph nodes of the body. Common sites are the nodes (glands) around the throatlatch, in between the jaw, at the base of the neck, superficial inguinal, mesenteric, and the pectoral region. The most common clinical sign of this type of lymphosarcoma is large masses on the chest, at the base of the neck, under the jaw, and at the throatlatch. Ventral edema is very common as well as weight loss. Sometimes the diffuse lymph tissue within the skin can also be affected which manifests itself as a severe ulcerative dermatitis, where the skin literally erupts with crusting sores that don’t heal. This form also has the lowest survival rates, often only weeks to a few months.

Intestinal lymphoma involves the diffuse tissue within the intestinal wall. Involvement in this area causes malabsorption problems of the intestines. This leads to severe weight loss, diarrhea and sometimes colic. Mediastinal refers to the lymph nodes within the chest in between the lungs. Tumors in this region can cause coughing, increased heart rates, fluid on the chest and even fluid within the chest.

The best and least deadly form of this disease is the cutaneous form which, is lymph nodes that turn into tumors under the skin and don’t migrate throughout the body. Horses with these types of tumors typically do very well and live fairly long with minor clinical symptoms.

Unfortunately, if large tumors are not visible, diagnosis can be difficult. There is also overlap of the different types, which leads to further diagnostic challenges. A biopsy of the tumor can confirm the diagnosis, but can sometimes introduce tumor cells into the blood stream which could cause the cancer to spread further. An ultrasound of the tumor is typically very characteristic and diagnostic. Often a diagnosis is made from clinical signs such as weight loss, masses, depression, edema of belly and legs, fever, diarrhea, skin crusting and scaling, coughing, high heart rate, blood changes such as anemia and a variety of other symptoms caused by the tumors that affect the tissue they are close to.

Treatment is also difficult; many horses don’t survive longer than a few weeks or months. Chemotherapy has been proposed, but often financial constraints and side effects severely limit their use. Some herbal remedies have been helpful for those horses with a less aggressive disease. Corticosteriods have been shown to be helpful but high levels are often needed and secondary laminitis has been documented. Interestingly, some tumors have progesterone receptors and sometimes pregnancy can reduce or eliminate some cutaneous tumors, but the use of progesterone for treatment is not widely accepted.

Dr. Posnikoff has been a longtime contributor to Horse Illustrated. She currently heads her own practice, Orange County Equine Veterinary Services, in Orange County, Calif.

Other articles by Dr. Posnikoff:

The Truth About Ringbone >>
Tendon and Ligament Injuries >>
Colic Surgery Guide >>
Advances Against Cushing’s Disease >>

The post Lymphosarcoma Horse Cancer appeared first on Horse Illustrated Magazine.

After his long winter off, you’ve put your horse through a springtime conditioning regimen, and he’s ready for competitions, weekend camping trips or plenty of pleasure riding on the local trails. You’ve been slowly putting him through his paces, and all is well except an unusual swelling on one of his forelegs that popped up after a romp in the pasture with his buddies. Your one-two punch of icing, bute and standing wraps is helping, but he’s off. So you call out the vet—and get the bad news. Your horse has a tendon injury, and you won’t be doing much riding this summer.

Every breed and riding discipline has its own set of tendon and ligament injuries, but across the board there are four major structures in the forelimbs that are most commonly injured. Here’s a look at those injuries and the prognosis for each, which in many cases is quite good thanks to veterinary advancements. 

Anatomy and Physiology of Tendons and Ligaments

Tendons and ligaments are made from the same basic tissue and have the same basic structure. The tissue is a very strong fibrous material that groups together in bundles, forming long cords. 

Tendons join muscle to bone and as a result, when the muscle contracts, the bone moves. Most tendons are designated as either flexor or extensor. Flexor tendons allow a joint to bend inward, toward the body (joint closes), and extensor tendons allow a joint to extend (joint opens).

Ligaments join bone to bone. They are stabilizing structures that essentially hold bones together and stop them from overextending, overflexing or overrotating.

There are four main tendons and ligaments at the back of the horse’s leg that do the majority of the work: suspensory ligament, inferior check ligament, deep digital flexor tendon and the superficial digital flexor tendon. In a horse’s forelegs, these four structures are the most commonly injured tendons and ligaments. When injury does occur in these structures, the infamous “bowing out” along the back of the leg is visible—in layman’s terms, the horse has a bow.

When Injuries Happen

Medically speaking, a bow can be different “types” of injuries involving tendons and ligaments: Strains that cause tendons and ligaments to stretch are described as type I lesions. They result in swelling of the tendon or ligament. Depending on the location and amount of swelling, the horse’s leg is usually only slightly enlarged, warm and painful, and lameness may or may not be present.

Fiber tearing is more serious and often results in increased swelling, more heat and often, but not always, lameness.  Mild tearing is classified as a type II lesion. Severe tearing, classified as a type III lesion, causes increased signs of heat, swelling and pain; often, these horses are lame. The worst injury is massive tearing, classified as a type IV lesion; the damage causes severe lameness, with very obvious heat, pain and swelling.

In general, strains are better than tears, small tears are better than large ones, and damage that occurs away from bone is better than damage right at the bone. 

The location of these injuries is classified into different zones along the back of the leg, but the general layman terms classify the injury into high, middle or low “bows,” corresponding with high, middle or low along the back of the cannon bone.

Most of these injuries occur in the forelimbs since they bear 60 percent of the horse’s weight and are therefore most prone to being overloaded. Of all the tendon and ligament injuries that can occur, the inferior check ligament is the least severe. The role of this ligament is to help stabilize the leg during weight bearing. Inferior check ligament injuries often cause a large swelling, but little pain or lameness. 

The superficial digital flexor tendon is responsible for stability and flexion of the lower leg. When this tendon is injured, there is generally some lameness, but even severe damage may not be career ending.

The deep digital flexor tendon is a workhorse of a tendon: It not only stabilizes the leg during maximum load (full weight bearing), but also flexes all of the lower leg joints during hoof flight. If it’s significantly damaged, there is lameness, heat, pain and swelling, and it could be career ending.

Suspensory ligament in-juries are the most serious and can be the hardest to treat. Like the deep digital flexor tendon, an injury here causes lameness and swelling. The job of this ligament is to stabilize the leg during maximum load; it stops the fetlock from dropping to the ground.

With all of these structures, one thing is certain: The more severe the injury, the more lameness there is. 

Depending on the tendon or ligament affected, and the type of injury that has occurred, a horse can have varying degrees of lameness, from mild to severe.

Signs of Trouble
Being familiar with what is normal in your horse’s legs, along with his normal way of going, will help you know when something isn’t right. The more severe or recent the injury, the more heat, pain and swelling that occur. Sometimes there is an enlargement in the area without lameness or obvious pain. When these enlargements occur though, it is still cause for concern. A veterinarian can palpate (feel) the leg and tell which tendon or ligament is involved, but a confirmed diagnosis comes from ultrasounding the affected area.

Ultrasound is the most basic and useful tool to evaluate these soft tissue injuries. From these images we can see which structure is damaged, the extent of damage, the location, and we can measure the damage. MRI is also used to diagnose soft tissue injury, as well as scintigraphy (scan).

The Healing Process

In the old days many horses were simply “turned out” for six months to heal a tendon/ligament injury and then rechecked. Certainly our minds have changed in this area over the last five years. If your horse is unlucky enough to get one of these injuries, today there are many options to help him recover.

The current thinking is to decrease inflammation and rest the horse to prevent any further damage. Icing and cold hosing are very effective for reducing inflammation within the first 48 to 72 hours after injury. The leg is wrapped for support and may be poulticed in an effort to decrease the inflammation further. I often use a gelcast, which is a special bandage that has magnesium salts in it that act like a poultice. It is combined with four other layers of wrapping and looks like a soft cast. It supports the fetlock and minimizes the pull on the back of tendons and ligaments, essentially resting the damaged area.

Anti-inflammatory drugs can be useful to keep pain and swelling down. If the injury is mild enough that it can be managed without these medications, sometimes the pain keeps the horse off the leg, which allows for rest and healing.

Depending on the severity of damage, the horse is usually stall rested for a length of time, then hand walked, and then put back to modified work until the area is healed. This process can be very subjective and variable depending on the horse, owner, environment and veterinarian. The current theory and practice is to start the horse back to modified work earlier in an effort to strengthen the tissues and help them realign as close as possible back to their original fiber pattern. However, under-saddle work is typically limited to a walk only within the first few months of injury.

Treatment Advances
Aside from rest, we now have many new treatments that are clinically proven to help tendons and ligaments heal stronger and get horses back to their performance lives. For some horses this means returning back to the level of previous workload, while others may need to step down to less demanding careers.

Extracorporeal shock wave therapy (ESWT) has become a very valid therapy for these types of injuries with a good deal of success. At this time it is unknown exactly how ESWT works, but it is thought that it increases blood flow, stimulates healing and possibly numbs pain.

Another treatment proven to be successful is bone marrow transplant. Bone marrow from the horse’s sternum is extracted and then transplanted into the area of damage. Here again, the full mechanism of how this works is unknown, but it is believed that within the bone marrow are chemical and cell mediators that stimulate healing, including stem cells.

This leads us into another area of exciting treatment options: stem cell therapy. It is now possible to extract stem cells from a horse’s own fat, and then use those cells for healing. Stem cells are those that haven’t differentiated into any specific type ofcell yet: They still have the potential to become skin, bone, tendon, ligament, et cetera. It’s an exciting concept because it means these cells can be placed in damaged tissue, allowing the tissue to then  regenerate. 

Another therapy is IRAP (interleukin-1 receptor antagonist protein). IRAP is a chemical mediator in the blood that stops the bad chemical mediators in the blood produced by inflammation from being able to do damage, and allows the good chemical mediators to work more effectively. Blood from the horse is taken and incubated on special glass beads which grow the IRAP. The IRAP is then harvested and injected into the injury site. Unfortunately, this therapy is not widely available yet, but that may change.

With the exception of stem cell therapy from fat, I have personally used all of these therapies on tendon and ligament injuries and have seen great success to the point of horses returning to their former level of competition or life. They are all exciting wonderful treatments that have opened the door for many horses and owners.

Our ability to diagnose, treat and prevent tendon/ligament injuries has improved tremendously over the last few years. Although these injuries are still extremely serious, they’re not as overwhelming as they once were. With good care and treatment, many tendon and ligament injuries can now be overcome.

Learn about updated diagnostic tools: Miracles of MRI.

Tendon and ligament injury Causes and Prevention.

Janice Posnikoff, DVM, heads up Orange County Equine Veterinary Services in Southern California.

This article originally appeared in the June 2006 issue of Horse Illustrated. Click here to subscribe.

The post Equine Tendon and Ligament Injuries appeared first on Horse Illustrated Magazine.

What is Equine Cushing’s Disease?

Over the years, the disease has had a few name changes, with equine Cushing’s disease the most commonly accepted. But labels such as “equine ‘Cushing’s-like’ disease,” “equine Cushing’s syndrome,” “equine pituitary pars intermedia adenoma,” and the most currently accepted name in the veterinary community, “equine pars intermedia dysfunction,” have all been used to describe the condition.

Equine Cushing’s disease is a primary problem of the pituitary gland, located inside the brain. This gland is like a dispatch center, where hormones and other chemical mediators called “proopiomelanocortin peptides” (POMC) are produced and then released into the body to control body functions. Horses with Cushing’s disease have a breakdown of the control of the pituitary gland—it literally doesn’t shut down and continues to produce POMC.

The overactive pituitary gland of a Cushing’s horse can grow in size and even develop benign pre-tumor and tumor cells that press against the brain. In the advanced stages of the disease, this compression can be severe and cause neurological problems if the gland becomes big enough. Cushing’s disease has often been described as a benign tumor of the brain, but there is still debate whether it’s a tumor or hypertrophy, which is tissue enlargement as a result of increased work (similar to the way that muscles enlarge from exercise). Indeed, the pituitary gland can develop cells that grow to become a tumor, but it’s unknown which comes first, hypertrophy or the tumor.

An overactive pituitary gland also affects the horse’s adrenal glands (located near the kidneys). Stimulated by increased POMC production, the adrenal glands overproduce cortisol, which contributes to a host of health problems. Increased cortisol levels have been the traditional marker for detecting and diagnosing equine Cushing’s disease.

New research is leading to a lot of answered questions and development of new questions for this disease. It’s now known that specific nerve cells in the brain secrete dopamine. In normal horses these cells inhibit an overactive pituitary gland and are present in large numbers. Horses with Cushing’s disease have dopamine-producing cells with decreased antioxidation capacity that are more susceptible to dying. But the question remains as to why. What is known is that fewer dopamine-producing cells means pituitary gland activity goes unchecked.

Clinical Signs

The classic Cushing’s case is an old, skinny, hairy horse that grows a long, wavy hair coat year-round. Many people unwittingly believe that their horses are just getting older. In reality these horses are often sick. Along with being very hairy, Cushing’s horses are generally lethargic, sweat easily, tend to run high temperatures, drink and urinate excessively, and have fertility problems. Horses with this disease are also at increased risk of developing laminitis. The high cortisol levels in the body lower the immune system, making the horse more susceptible to infections, such as delayed healing, reoccurring hoof or tooth abscesses, sinus infections and chronic fungal, bacterial or parasite infections. Pneumonia is even possible.

As Cushing’s disease progresses, more and more body changes occur, and symptoms become more obvious. This can take years to happen and it’s really a snowball effect. Cushing’s horses metabolize protein at a higher rate that causes muscle breakdown and wasting, which can be very noticeable along the topline and haunches as the disease progresses. Weakened abdominal muscles become stretched from the weight of the intestines,creating a “pot belly” appearance. Intermittent front limb stiffness can also be seen.

In the advanced stages of the disease, severe neurological problems can occur if the pituitary gland becomes big enough and causes compression in the brain. Symptoms of compression include ataxia (uncoordinated movement of the limbs), fever, hyperventilation and possibly recumbency leading to death. If treatment is not provided—and sometimes even if it is—the pituitary gland gets larger, the immune system weaker and the body condition worsens to the point of real debilitation for the horse. These horses look and act very old. Their hair coats are extremely long, sometimes several inches long, and very wavy. They breathe heavily and sweat in their stalls and seem extremely lethargic. They might start to sway when walking, and in the most extreme cases get to the point where they can’t get up.

Disease Diagnosis

There are several ways to diagnose equine Cushing’s disease. The classic method is to measure body cortisol levels in response to an outside stimulus, most notably dexamethasone (a corticosteroid). Dexamethasone, when administered to a healthy horse, tells the pituitary gland to shut down. Horses with Cushing’s disease don’t respond to dexamethasone stimulus—their pituitary glands continue to produce POMC, and their adrenal glands continue to produce high levels of cortisol. This dexamethasone testing procedure is known as the “dexamethasone suppression test.” The higher the dose of dexamethasone used, the more the pituitary gland should be suppressed.

There are actually two types of “dex” suppression tests: high-dose dex suppression and low-dose dex suppression. It may seem obvious that the high dose is more accurate and should be the test of choice, but it’s not without its complications: The biggest risk is increased chance of developing laminitis. For this reason researchers and clinicians alike are trying to find alternative ways to test for equine Cushing’s disease. And they have found a few.

One alternative is the low-dose dex suppression test. This test has become the standard and is theoretically safer, due to the lower dose of dexamethasone, especially for the horse that has already had an episode of laminitis. Some researchers suggest avoiding the test during autumn months, as hormone levels in horses can vary seasonally. During fall, researchers are pointing to a higher possibility of false-positive results.

Taking it to the next level, a new test is being developed that combines thyrotropin-releasing hormone and dexamethasone, referred to by some veterinarians and researchers as the “DST/TRH” test. This test allows for increased accuracy in testing in the early stages of the disease.

Other testing methods have also been developed, mostly in an effort to avoid administering dexamethasone to horses that have laminitis or are at greater risk of developing it. One such method is to evaluate the levels of ACTH (adrenocorticotropic hormone) in the body, which has been shown to be higher in Cushing’s horses. Unfortunately, this test can have false negatives, meaning even though the ACTH levels are low, the horse can still have Cushing’s—the disease is just not advanced enough for the test to pick up on it.

There are researchers who suggest that high insulin levels in the horse are an indicator of this disease, and some research is being devoted to testing cortisol levels in saliva.

Another test monitors and measures the day and night levels of cortisol. In normal animals it’s been shown that morning levels of cortisol are high, and in the evening levels drop off. The difference between morning and night should be more than 30 percent; if not, it’s theorized that the cortisol remains at a constant level as a result of the pituitary gland not shutting down.

One final method used quite often in the field is response to treatment. Instead of testing what appears to be an obvious case of Cushing’s, a veterinarian treats the horse with medication and watches for clinical signs to resolve. This has its drawbacks, especially if we are mistaking the disease for something else that should have a completely different treatment.

Treating the Cushing’s Horse

A few drugs have emerged for treating equine Cushing’s disease that are better than others. Today, the most commonly used drug for treating the disease is pergolide. This drug, also used to treat Parkinson’s disease in humans, stimulates dopamine release, which in turn tells the pituitary gland to shut down. There are good anecdotal results and very limited side effects with this drug, as well as a lot of research available that has shown its effectiveness. In some of my patients, owners report that their horses act 10 years younger after starting treatment.

Cyproheptadine was the original drug of choice for treating equine Cushing’s disease, but many studies are now showing that its effectiveness is not nearly as good as pergolide. Some reports indicate that cyproheptadine used with pergolide can be more effective, however.

A human drug called trilostane offers promise for treating equine Cushing’s disease. This drug works at the level of the adrenal gland to slow down cortisol production. Current research has shown that this drug has reversed some of the symptoms of equine Cushing’s disease.

More research is on the way to reproduce these findings and prove the drug’s safety in horses. Trilostane is available in the United Kingdom, and also to veterinarians here through special arrangement with drug compounding companies. At this time trilostane is very expensive, but hopefully, as has been the case with pergolide, when demand grows and efficacy and safety are established, this drug will become more available and affordable.

Diet is gaining significance in the management of Cushing’s disease. Antioxidants, such as vitamins E and C, could play a role in helping to support Cushing’s horses. Chasteberry (Vitex agnus castus) is emerging as an organic source of dopamine stimulation; while it hasn’t completely stood up to the rigors of scientific testing, many researchers are still looking into it as a source of treatment for equine Cushing’s disease.

Feeding a Cushing’s horse can be very challenging, and unfortunately there are no set rules. However, it is safe to say that horses with Cushing’s disease do well on the same type of low-sugar, low-starch diet that horses prone to laminitis do. This type of feeding plan usually rules out alfalfa and grain, and leaves us with grass hay and grass hay pellets. If the disease symptoms aren’t too severe, then extruded feeds utilizing soy and beet pulp can help keep weight on. Generally I try to keep Cushing’s horses on mostly timothy and orchard hays, along with pelleted feeds, like those mentioned above, to keep weight on, and I minimize sugar as much as possible. Since Cushing’s horses are difficult to keep weight on, dedication has to be put into balancing diet with exercise.

Insulin Resistance

One real misconception about Cushing’s disease is that affected horses are hypothyroid and fat. They’re not. We don’t know enough about the thyroid gland and its hormones, but currently it’s believed that the thyroid does not play a direct role in equine Cushing’s disease. In the past, many older horses that were “easy keepers” were diagnosed with Cushing’s disease and put on thyroid medication. Thyroid supplementation hasn’t been proven to help horses with Cushing’s disease. In fact, many horses that are true hypothyroid are not fat at all and can often be thin.

It is the horse with insulin resistance that is fat. Insulin resistance is fast becoming a buzzword as the culprit behind easy keepers. The pituitary gland has nothing to do with this disease. Instead, as its name suggests, cells become resistant to insulin. When this happens, sugar (carbohydrates) circulating in the bloodstream is no longer drawn into the cells by insulin. This leaves excess sugar in the blood that gets converted to fat. In horses this often causes a cresty neck and large fat pads in abnormal places. Mustangs are genetically engineered for this condition so that they can put on fat stores in times of plenty to rely on when food is sparse. This leads us to believe that genetics play a large role in insulin resistance.

The trouble with modern horsekeeping is that we often provide plenty of food all the time for our beloved equines, so they just keep making fat stores—some better than others. Insulin resistance can create dire health problems, especially in the hoof, where laminitis can occur.

In the End

Cushing’s is an easily recognized and treatable disease, but unfortunately it can’t be cured yet. It is a slow-progressing disease that often goes unrecognized in the early stages. Sadly, Cushing’s disease usually gets diagnosed once the clinical signs are more advanced. When caught early, treatment is very successful in reducing clinical signs and allowing affected horses to live almost normal lives. For those horses in advanced stages of the disease, treatment still offers improved quality of life and longevity.

This disease hits close to home for me since my own horse Prophecy was diagnosed with it at the age of 9 using the morning and night cortisol levels testing method. I have had him on pergolide since that time, which was about four years ago. His symptoms at the time of diagnosis were for the most part very mild and very subtle. He had many episodes of “ain’t doing right,” laziness in the arena and a mild case of laminitis. His owner at that time, having had a dog with Cushing’s disease, asked me to test him. I’m happy to report that he is symptom free today. However, to be on the safe side, I’m starting Prophecy on higher dose vitamin E supplements and will test him using low-dose dexamethasone suppression combined with TRH stimulation. If he tests positive with that method, I will seriously consider trilostane for him.

In my practice area, horses with Cushing’s disease do very well and can lead an active lifestyle. Those undergoing treatment do much better for a longer period with fewer problems; I rarely have to deal with laminitis in these horses. I have one 18-year-old Grand Prix dressage horse with Cushing’s disease that is still competing and doing well. She has been on pergolide for three years, but we are starting to see a few more symptoms, so we are increasing her dosage and are considering trilostane for her.

Overall, horse owners shouldn’t fear this disease, but we must all have a healthy respect for it.

Further Reading

Optimal Diet for Cushing’s Disease

What is safe to feed a horse with Cushing’s?

This article originally appeared in the November 2005 issue of Horse Illustrated. Click here to subscribe.

The post Advances Against Cushing’s Disease appeared first on Horse Illustrated Magazine.

What is Ringbone?

Ringbone is a horseman’s term for osteoarthritis, or bony arthritis, of the pastern and/or coffin joints—ringbone in the pastern joint is called high ringbone, and in the coffin joint low ringbone. Arthritis is any condition that causes inflammation of the joint. Osteoarthritis forms when the inflammation within the joint creates enough damage that the body lays down bone in an effort to heal the damaged tissue. Typically the bony development occurs at the joint surface or the attachment sites of the joint capsule to the bone. Another term to describe this type of damage to a joint is degenerative joint disease (DJD).

The preferred veterinary terminology for high ringbone is osteoarthritis or DJD of the proximal interphalangeal joint (pastern joint); or in the case of low ringbone: osteoarthritis or DJD of the distal interphalangeal joint (coffin joint). For convenience, I will refer to the condition as ringbone.

Some also classify the type of ringbone as articulating, meaning involving the joint surfaces, or nonarticulating, meaning not involving the joint surface but rather the joint capsule where it attaches to the bone. Ringbone can start out as nonarticulating and advance into articulating. Non-articulating is less painful since it doesn’t involve the joint surface where weight bearing occurs and is therefore considered less serious.

The pastern and coffin joints are located in the lower limb of all four legs. The coffin joint is a large high-motion joint within the hoof; the next joint up is the pastern joint. The pastern joint is a small joint that doesn’t move very much but carries a lot of weight. It is located between the top of the hoof and the fetlock. Most people don’t even realize that a joint exists here.

How Does Ringbone Occur?

The most common cause of ringbone is abnormal stress on the joint, causing joint surface damage and subsequent bony development. The abnormal stress can be in the form of poor conformation, imbalanced shoeing or working on poor ground surfaces. Base-narrow or base-wide conformation, combined with a toed-in or toed-out stance, creates increased weight-bearing forces on the inside or outside of the joint by causing the horse to land first on the outside or inside of the leg. These increased forces can cause microdamage to the cartilage on the joint surface and microtearing of the joint capsule or of the collateral ligaments (stabilizing ligament on either side of the joint). The body reacts to this microdamage initially as inflammation. Inflammatory cells release toxins that create more tissue damage and thin the joint fluid. More tissue damage creates more inflammatory cells, and a cycle begins of increasing damage. As the damage increases the body attempts to heal initially with scar tissue, which then progresses into bony development.

The length of time it takes for this to occur varies and is dependent on many factors. The more trauma, and the more severe the conformational abnormalities, the quicker the disease progresses. Hoof balance, proper trimming and shoeing, footing and exercise are very big factors in this disease. Unbalanced hooves, as well as long toe/low heel, can cause severe stress on the joints. Shoeing a horse with shortened toes to increase breakover decreases the stress on the joints and helps reduce the inflammation, and can help slow the development of disease. Hard footing increases trauma on the joints, while deep footing increases the flexion of the joints leading to possible overflexion and damage to the joint capsule.

Other causes of ringbone include blunt trauma or lacerations to the joint, and osteochondritis dissecans (OCD). OCD is a malformation of the cartilage layer during a horse’s formative years—the disease leads to large flaps of cartilage within the joint. When a cartilage flap or “chip” is present in the joint, it creates a cycle of inflammation. In the case of trauma, a single trauma event, such as direct hit to the joint or a laceration, can cause the initial joint damage and start the cycle of inflammation.

How Do We Diagnose Ringbone?

Radiographs (X-rays) of the leg are the best way to diagnose the disease. The joint surfaces are usually very smooth, but when ringbone is present extra bone is seen on X-ray.

But it’s not always so easy. In the early stages of the disease, the bony changes may not be so evident. Often only a small “spur” is seen on the front of the joint, or some calcification away from the joint surface is visible where the joint capsule or collateral ligaments attach to the bone. Pain, and therefore lameness, is caused by inflammation within the joint. Sometimes a horse is more lame at this stage of the disease.

In these situations your vet must determine if the cause of lameness is from the joint or some other disease process; therefore it’s always important to perform a thorough lameness exam. This exam should include watching the horse move on hard and soft ground, jogging straight and in circles. Flexion tests and diagnostic nerve blocks are also important. Horses with ringbone flex positive in thelower limb, meaning lameness results when the lower limb is held in flexion for one minute and then jogged off.

Nerve blocks are invaluable in determining the location of the pain. Once the pain has been localized to the lower leg by response to an abaxial nerve block (block around the fetlock), the pain can be further localized by blocking out each joint. If low ringbone is the cause of pain, then the lameness resolves when the coffin joint is blocked out; in cases of high ringbone, lameness resolves when the pastern joint is blocked out. Diagnostic nerve blocks are very important in the cases where the X-rays are not so obvious.

The severity of the disease varies. Lameness doesn’t always correlate with radiographic changes. Some horses with mild bony changes on radiographs are very lame and vice versa. There are many sound horses with obvious ringbone in their pasterns. When a horse has significant high ringbone it can be seen on the front and sides of the pastern as hard lumps or a “ring” of extra bone around the front and sides of the pastern. If the ringbone can be seen easily it is already very advanced. Ringbone in the coffin joint is much more significant and always causes severe lameness since this is the higher motion joint.

As the disease advances it can spread into the joint, causing severe cartilage deterioration and joint collapse, ending in full fusion of the joint. During the process, the horse is severely lame. Sometimes the lameness can become so severe that the quality of life for the horse is very poor and humane euthanasia is chosen.

How Do We Treat Ringbone?

Dealing with ringbone is not a single treatment but rather a whole management scheme that is lifelong for the horse. Everything is aimed at decreasing the inflammation in the joint and saving the cartilage surface.

We start by trying to balance the hoof and increase the breakover for the horse. This means making sure the hoof is level from side to side and the toe is short so that the leg can roll over the front of the hoof quicker, decreasing the stress on the joints.

Next we address the inflammation in the affected joint. Often this means injecting the joint with anti-inflammatory drugs such as corticosteroids, along with synthetic joint fluid called hyaluronic acid that helps replenishthe existing thin, weak joint fluid. This helps stop the disease progression and hopefully slows down the damage to the joint surface.

Along with joint injections comes complementary therapy in the form of supplements, exercise management and physical therapy. Oral joint supplements given daily, such as chondroitin sulfate, glucosamine, MSM and more recently oral hyaluronic acid, may help the body to develop more cartilage and joint fluid.

Intravenous hyaluronic acid, called Legend I.V., and Adequan I.M. (polysulfated glycosaminoglycan) are also used quite successfully to preserve the joint. Legend works to produce more joint fluid and act as an anti-inflammatory. Adequan works at the joint surface helping the cartilage. Both are very effective and are often used together.

Herbal supplements may be given in feed to help support the joint. Yucca and devil’s claw are common herbal anti-inflammatories. A host of other products are available that combine all of these ingredients as well some others not mentioned in this article. Most appear to help, but none seem to be outstanding in resolving pain for ringbone. Care must be given when feeding herbal products to avoid allergic reactions or colic. Product concentrations are often inconsistent, and many of these herbs haven’t been studied fully in horses.

Horses with ringbone do best with consistent low-level exercise. Horses that stand excessively all day long tend to get more inflammation in the joints and therefore more lame. Constant walking around all day on pasture helps stimulate circulation and decrease inflammation within the joint, therefore decreasing lameness. The amount of exercise varies depending on the degree of ringbone and the tolerance of the horse. Some horses with this condition are able to maintain careers in the lower levels and often do better if kept in a consistent work program. Soft footing is better than hard, but too soft causes overflexion of the joint and increased inflammation.

Physical therapy is also available for these horses. Warm therapy helps loosen joints; liniments and wraps help support the joint. Massage therapy, acupuncture, chiropractic and other alternative therapies have varying degrees of efficacy, but all aim to loosen tissue and decrease inflammation, as well as help other muscles and joints that are compensating for the ringbone.

One promising new therapy called extracorporeal shockwave therapy (ESWT) is proving to be very effective for horses with ringbone. The true nature of how shockwave therapy works is still unknown, but it is the focus of much research right now by many major institutions.

What is known is that many horses show dramatic improvement with ESWT, so it’s become a therapy that is now being tried for a variety of problems. For ringbone it has proven to be effective for horses that are not too severe. I personally have seen many horses respond to the therapy, including my own horses.

Response to shockwave therapy appears to depend on severity of the ringbone and the aftercare. More severe cases require more than one treatment, typically one treatment weekly for three weeks. Many horses with less severe changes respond after only one treatment. It also appears that if the horse returns to regular exercise, the lameness resolves, but if the horse stands idle for any length of time, the lameness can return. Horses with severe ringbone don’t appear to respond to this therapy. As with all therapies, ESWT should be discussed with your veterinarian.

The Big Picture

The time between when a small spur forms and the joint fuses is our time to help the horse with ringbone. I use a combination of all the therapies mentioned above, and in most cases I can keep a horse active and happy for many years before the ringbone gets too severe. Thankfully, I haven’t had too many ringbone cases that I have had to put down, but I currently have a couple that I know I will have to sooner or later. These severe cases are lame but comfortable, and I usually inject their joints approximately once a year. Each time though, it becomes harder to inject the joint, and I know there will come a time where I won’t be able to due to the severe joint collapse and bony development.

For my ringbone patients that are doing well, I attribute it to good management on the owner’s part—essentially catching the problem early and giving good joint support. However, I have seen some of these horses become very lame, even with good joint management. Unfortunately I can’t predict which horses will do well and which won’t. Ringbone can affect any horse.

Janice Posnikoff, DVM, heads up Orange County Equine Veterinary Services in Southern California

This article originally appeared in the June 2005 issue of Horse Illustrated. Click here to subscribe.

The post The Truth About Ringbone appeared first on Horse Illustrated Magazine.

While colic episodes are cause for concern, most cases can be managed with non-surgical veterinary treatment: a shot for pain, a dose of mineral oil, a rectal exam, and the horse usually gets better. But then there are the other cases. Those horses that don’t get better with one or two or three shots for pain relief, that keep on lying down, pawing, trying to roll, kicking at their belly, looking at their sides, et cetera. This is the dreaded 10 percent that require surgery.

Classic Colic

The large intestine of the horse is designed to digest forage. It’s composed of a very large cecum, which can be compared to our appendix, and a large and small colon. Gas or spasmodic colics occur when the cecum and large colon become distended with gas. The gas distention overstretches the intestinal wall, making the intestine very painful and unable to contract in a nice wave-like motion that moves gas along and out. Instead the intestine spasms, allowing gas to stay and creating a cycle of more and more distention. In these cases horses will often paw violently, pace, lie down and kick at their bellies. Walking will sometimes help get the intestines moving again and push the gas out; if not, then Banamine and Xylazine for pain relief, along with rectal massage and nasogastric tubing (a tube passed up the nose and down into the stomach, which allows the veterinarian to administer mineral oil with a stomach pump) usually fixes these colics.

Impaction colic is similar to gas colic: The intestine becomes distended and stops moving properly. But instead of gas, food material fills the intestine and gets stuck (impacted). These types of colics can be very painful but often the horse is not as violent. A rectal exam by a veterinarian, which may include pulling out manure, helps provide some relief. Also, a nasogastric tubing with mineral oil helps soften and lubricate the manure so it can pass.

Spotting Surgical Colic

Surgical colics are much different. In most cases there is an immediate difference in the horse’s eye that most surgeons recognize immediately. These horses don’t respond to pain medications, and the nasogastric tubing and rectal exam provide little, if any, relief. The pain is constant and can be severe or subdued, but not completely relieved with painkillers. In very obvious cases, the horses are throwing themselves down with pain, rolling and won’t get up, even with drugs on board. The onset of clinical signs is usually rapid, and the pain typically increases quickly. Getting into the trailer and to the nearest equine hospital, before the intestines become too damaged and the horse becomes too overcome with pain, is critical.

The causes of surgical colics vary, but the common denominator is a blockage of the intestines that can’t resolve without opening up the horse’s abdomen and fixing the problem.

A Colic Surgery Candidate

Surgical colics have very high heart rates, often above 60 beats per minute and can be over a 100 bpm. The respiration rate is usually elevated, and fever (101.5 degrees F and above) is sometimes present. These horses usually show signs of pain, such as pawing or trying to lie down. They typically have no gut sounds, and their gums are an abnormal color. The gums can range from cyanotic to bright red. Cyanosis is a grayish-blue color that indicates decreased oxygen supply. Bright red gums indicate toxins in the blood that are causing the blood to clot and slug in the small capillaries. A variant of red gums is a toxin line—a red line in the gums over the teeth—that is usually the first sign of toxin absorption

Surgical Colics

Colon torsion or “twisted gut” is one of the most common, and most dramatic, types of surgical colics. The large colon is separated into sections folded into left and right, upper and lower quadrants. The left quadrants are not attached to the body wall; these parts of the large colon are free moving in the abdomen and can twist 180 to 360 degrees causing a complete blockage. Not only is gas and food material trapped inside the twisted gut, but blood supply is cut off, causing damage or death to the intestine. As the gut dies, toxins are released into the body, causing severe illness or even death. For some horses, pain medication helps keep them quiet for approximately an hour. But some horses are so painful that the drugs seem to help very little.

Strangulating lipomas and epiploic foramen entrapment are situations where blood supply to the small intestine is completely cut off and the intestine dies. When a lipoma (fatty tumor) develops, it is connected to the intestines by a thin strand of tissue. This strand of tissue acts like a string and the lipoma acts like a weight, wrapping around a section of small intestine then tightening and cutting off the intestine completely.

Epiploic foramen entrapments occur when a section of small intestine falls into the epiploic foramen—a triangular window created by the body wall, the liver and the vena cava (large abdominal vein carrying blood back to the heart). The trapped small intestine gets irritated from the partial obstruction and swells, getting heavier and pulling more intestine through the window, eventually causing complete strangulation of the small intestine.

Both of these types of colic are very painful; the intestines die from lack of blood supplyand toxins are released into the body. Horses with these types of colic are very sick. Often it’s difficult to get them to stay up, and they are minimally responsive to pain medications.

Enteroliths, commonly called intestinal stones, can cause colic and need to be removed surgically. These stones develop inside the large intestine and can get so big that they either irritate the colon or get stuck within the colon, potentially cutting off circulation to the intestine. Without proper circulation, the area of intestine around the stone dies and then ruptures, releasing intestinal contents into the abdomen and a massive amount of toxins into the body, which causes death.

The above are by far the most dramatic cases, but there are also mild to moderate displacements of the large colon, adhesions, scar tissue constrictions, parasite migration, blood clots and more, that can create a surgical colic.

Surgical Status

Time is of the essence in a situation where intestines are dying, so the sooner the horse gets to surgery, the better his chances of survival. A vet’s rule of thumb is that if a horse has to be medicated more than three times within a one- to two-hour period, he should be sent to a surgical facility for evaluation.

Some horses are so painful on presentation at the hospital that there is no question surgery is needed, but others may have varying degrees of symptoms so more diagnostic tests are performed.

The two most widely used tests done at the hospital, invaluable for determining the surgical status of a colic, are the abdominal tap and the abdominal ultrasound. The abdominal tap involves obtaining a sample of peritoneal fluid (the fluid that surrounds the abdominal organs) to check for elevated protein and white cells. Normally peritoneal fluid is a clear amber color, but in very sick horses it can become cloudy, red-tinged, or in the case of a ruptured intestine, the fluid appears green with food particles within.

Abdominal ultrasound allows the surgeon to evaluate the small and large intestines. The ultrasound can also help determine the motility of the gut by actually looking at the intestines move.

If an intestinal stone is suspected, then abdominal radiographs (X-rays of the belly) are done. Since the possibility of rupture is always present, if an intestinal stone is seen on abdominal radiographs, surgery is always warranted, even if the horse is pain free.

The call to go to surgery is usually determined quickly once all of the above factors are put together. For the horses that are not as obvious, often there is a period of monitoring at the hospital to see if the clinical signs resolve or worsen. If a horse doesn’t appear painful but has abnormal ultrasound or abdominal tap findings, surgery is usually recommended in order to help save the intestine from further damage. There are some horses that may not be good surgical candidates and are better served by humane euthanasia, such as those that have suffered for days and have consequently experienced significant damage. Horses severely compromised by diseases such as laminitis, liver disease, kidney disease or Cushing’s disease, might not be surgical candidates either. But even Cushing’s horses can do well if they are somewhat stable before surgery.

On the Table

At many of the hospitals there are observation rooms where you can watch your horse’s surgery. The surgery itself involves fully anesthetizing the horse, getting him onto a surgery table, then opening up the abdomen. Once the horse is completely anesthetized and laid down, a tracheal tube is passed through the mouth and into the lungs to get the horse on gas anesthesia and oxygen. The horse is then moved onto the table by shackling the lower legs and lifting him with a winch. The horse is on his back and is secured to the table by the shackles. His belly is shaved and scrubbed to meet surgical standards. The surgeons prepare themselves by scrubbing their hands and dressing in full surgical gowns and gloves. Colic surgery in the horse is treated with the same standards as human surgery.

These horses can be very sick, and the anesthesia can be very dangerous for them. Some horses stop breathing or have other complications. Special equipment is used to constantly monitor blood pressure, heart rates, respiration rates and blood gas levels, so appropriate measures can be taken to treat problems as they arise. If the blood pressure drops too low, long-term damage to the kidneys and brain, or even death, can occur.

The surgery itself consists initially of making an incision into the abdomen down the midline of the horse’s belly. The surgeon then reaches in to find the problem: Twisted large left quadrants of the colon are untwisted; a displaced large colon is put back into the right spot; in the case of problems with the small intestine, the dead or damaged gut is cut out and the good intestine reconnected back together; intestinal stones are removed or severe impactions extracted. During surgery the large left quadrants of the colon are usually pulled out of the abdomen and emptied by making a small incision at the pelvic flexure (a section of the large intestine ), and the contents dumped into a bucket.

During the operation, the surgeon can estimate how the horse will do afterward depending on the problem and the state of the intestines. Sometimes the damage is so extensive that the surgeon may recommend euthanasia while the horse is still on the table or will warn the owners that the post-surgery prognosis is not good. Other times the surgeon will see minimal damage, and the prognosis is favorable.

If colic is caught early, surgery can be performed in time to save the intestines and minimize complications. But complications can occur and may start as early as recovery. After surgery the horse is allowed to wake up, but is encouraged to stay down until he is more coherent and stable to support standing. Very rarely a horse will get up too soon and hurt himself falling, sometimes even breaking bones. Other times the surgery fails to resolve the pain, and the horse begins to colic again. Sometimes this pain can be resolved with medical management, sometimes not and another surgery is needed.

Recovery

The first 72 hours after surgery are the most critical. This is when the intestines are trying to reorganize themselves from being manipulated, cut open, et cetera. As a result the intestines sometimes stop moving, which is very painful for the horse. Also, if the circulation to the intestines was cut off for too long, the lining of the intestines sometimes reacts by becoming inflamed, or dies, resulting in severe diarrhea. If the horse had intestine cut out, the site of reattachment may fail, causing either another blockage or rupture at the site. After surgery the horse’s immune system is compromised from stress, and infection is a concern. Laminitis, although rare, may also occur.

After the first 72 hours, other long-term complications can set in. Scar tissue formation, adhesions and intestinal constriction may decrease the motility of the intestines and cause more colics. Persistent diarrhea from salmonella infections, microflora imbalance or inflammation of the lining of the colon, is a possibility. Horses may become hard keepers and require additional supplements to maintain. Hernias or infections along the incision line on the belly are also possible.

With the improved surgical techniques and experienced surgeons we have today, a great majority of horses get to go home after colic surgery and make a full recovery. Typically horses need 90 days to recover after colic surgery. The first 30 days are stall rest and hand walking, which allow the intestines and the incision line to strengthen up. The following 30 days are light turnouts in small paddocks or sun pens. The final 30 days are light exercise under saddle, mostly walking or easy trotting.

Difficult Decisions

Once a horse has had colic surgery, the chances of colicking again vary and depend mostly on the type of colic surgery and the extent of damage that occurred. Colon torsion and small intestinal resections (sections cut out and reconnected) have the highest rate of colic recurrence requiring surgery. Some horses appear more prone to colon torsion and displacements; for these horses the colon is actually tacked down to the abdominal wall. In the case of small intestinal resections, the area of reattachment can be an area of food blockage due to poor flow through the connection site. Typically these horses tend to colic again one to two years after surgery. Horses that have intestinal stones removed can form new stones; this regrowth takesyears, usually four to seven.

When in the moment, trying to decide to do surgery can be very difficult but should be decided as soon as possible. Survival is based on the speed of getting the horse to the surgery table and who’s doing the surgery. Waiting to see if the horse gets better increases the risk of the surgery failing. Often financial constraints limit our ability to give this option to our horses. For this reason, I strongly recommend all horses getting surgical/medical insurance. This allows freedom of judgement based on medical facts only.

For more information on colic:

When should you call the vet for a colicky horse? Read more >>
Colic prevention tips. Read more >>

This article originally appeared in the March 2005 issue of Horse Illustrated. Click here to subscribe.

The post Colic Surgery Guide appeared first on Horse Illustrated Magazine.