Frequently Asked Questions

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Distal tarsitis often referred to as “bone spavin”, is the most common cause of clinical lameness associated with the tarsus (or “hock”) in horses. Distal tarsitis is osteoarthritis and periostitis (inflammation) of the distal intertarsal, tarsometatarsal, and occasionally the proximal intertarsal joints. Distal tarsitis is a clinical diagnosis.

In other words, demonstration of pain in distal tarsal joints is diagnostic. Pain is demonstrated upon clinical examination, lameness characteristics, response to Churchill’s Hock testing, hock flexion, and response to intra-articular anesthesia. Radiographs are frequently used to assess the presence and severity of distal tarsitis. It is important to note, however, that joint inflammation (arthritis) is invisible on a radiograph (which provides only structural information). Since the tarsus is a slow-motion area, radiographic changes and the presence of distal tarsitis do not always correlate.

The low-motion nature of the distal tarsal joints also allows veterinarians to be very aggressive regarding treatment, which usually involves intra-articular (joint) injections. Typically, a combination of steroids and hyaluronan is used. Although the excessive use of steroids can be harmful to joints, the lack of movement within the distal tarsal joints presents a little risk in regard to future function and performance. In fact, horses that are refractory to distal tarsal injections may be candidates for chemical fusion, which eliminates the joints altogether and produces soundness.

This is a very common question in our neck of the woods. Clients commonly find urine spots that appear red in color and become concerned that it may be blood. In 99 percent of the cases, the red color is not due to blood, but rather, it is due to the oxidation of some of the compounds in urine. We see it more in the winter because it stains the snow.

A horse with blood in its urine may show abnormal urinary behavior (including colic, and inconsistent stream or stopping and starting) or abnormal drinking behavior (increased or decreased drinking). Blood clots may also be seen, and a red color would also occur in the shavings. If your horse is acting normal, then we recommend that you collect a urine sample and bring it to our clinic for analysis. This way we can determine if the red color is due to blood in the urine or its by-products.

Literally, cryptorchidism means “hidden testicle”. Abnormal location of the testicle occurs when one or both of the testicles fail to descend completely from the fetal position behind each kidney through their respective inguinal canals into the scrotum. An abdominal cryptorchid has testicle(s) within the abdominal cavity. A horse with testicle(s) in the inguinal canal is called an inguinal cryptorchid or “high flanker”. Since cryptorchidism is heritable, cryptorchid horses are considered genetically unsound. For this reason, registration of cryptorchid horses is disallowed by many breed associations.

Cryptorchid castration requires general anesthesia and is, therefore, more involved than routine castration. The procedure, however, is relatively simple. By using the inguinal extension of the gubernaculum, the testicle can be retrieved without having to dilate the inguinal canal and increase the potential for herniation of the bowel into the scrotum. Aftercare consists of one week of stall rest prior to resuming exercise.

Before answering your question, let’s first review what the term “colic” means. The term “colic” refers to abdominal pain. Of course, abdominal pain can be a result of many things including kidney disease, peritonitis, and estrus (in mares). In horses, we typically use the term colic to describe the pain associated with intestinal obstruction and/or distension. Obstruction can occur subsequent to impaction, displacement, torsion (twisting), entrapment, strangulation, and/or incarceration (trapping) of intestine(s). Regardless of the cause of obstruction, the inability of the ingesta to move at a normal rate results in excessive gas production and fluid accumulation. This in turn causes intestinal distension and pain (colic).

In some cases of severe obstruction, vascular occlusion can occur. Consequently, a portion of the intestine does not receive an adequate supply of blood (and therefore not enough oxygen and nutrients). Endotoxins are absorbed through compromised bowel walls into the bloodstream. Since this condition (called endotoxemia) is life-threatening, surgery is indicated to prevent/treat decreased blood flow and compromise of the affected bowel.

Endotoxemia usually manifests as increased heart rate, compromised mucous membrane color, and/or moderate to severe persistent pain. The presence of any of these symptoms justifies sending your horse to a surgical hospital, particularly if your horse has been refractory to conservative treatment.

Won’t the tendon tighten up even more and make the problem worse if we do this?

The angle of the LF pastern and foot, the contracted heels, and the evidence of wall delamination (i.e. the dished dorsal wall) all suggest that he has too much tension in his DDF tendon (i.e. it is too “tight”). It seems that alleviating the tension on the tendon by raising his heels with the wedged pad would only allow it to contract further (become even tighter), whereas stretching it by imposing greater tension (i.e. dropping the heels) would normalize its length and tension.

Although this makes perfect sense, it is extremely difficult to achieve in older horses. We find that some horses develop contractural deformity(ies) in one or both thoracic deep flexor muscles/ tendons when they reach their mid to late teens. Although we are not sure as to the cause, it does appear to be a progressive problem.

Generally, dropping the heel and increasing the tension on the DDF tendon in older horses does not effectively stretch/ lengthen the tendon. Rather, it accentuates the problems occurring as a result of excessive DDF tension: laminitis, navicular inflammation, dorsal wall delamination, contracted heels, DDF tendinitis, etc. We would expect that lowering your horse’s heels would do the same.

We do recommend massage therapy of the flexor tendons in an attempt to discourage further contraction. Although we’re still not certain as to it’s effectiveness, it can only help.

A foot that is taller and more contracted than its contralateral counterpart is commonly referred to as “clubbed”. By definition, a clubbed foot has more than the appropriate amount of heel length; the extra heel results in a broken-forward distal limb axis. A foot becomes clubbed as a result of excessive tension on the deep digital flexor (DDF) tendon tension. The DDF tendon arises from the DDF muscle behind the radius and courses all the way down the back of the limb to insert on the underside of the third phalanx (P3). Excessive tension on the DDF tendon can cause several things, including excessive pressure on the navicular bone, mechanical rotation of the third phalanx, pedal osteitis, and delamination of the hoof wall (“white line” disease). Treatment options for excessive DDF tension include corrective shoeing, massage therapy, acupuncture, and/or surgery.

The West Nile Virus is an arthropod-borne virus similar to the viruses that cause Western and Eastern Equine Encephalitis (EEE). Encephalitis cases are seen in the warm months of the year when the primary vector, the mosquito, is present. The West Nile Virus was first identified in the US in New England in 1999. It has gradually spread over the east coast. Pathogenesis: birds are the usual host for West Nile, it is spread from bird to bird via the intermediate host, the mosquito. Humans, horses, and perhaps other mammals are dead-end hosts, infected via the bite of an infected mosquito, and cannot transmit the virus to others. Not every individual who contracts the virus will become seriously ill. Most will have subclinical infections or develop mild symptoms such as fever, malaise, body aches, etc. similar to other viral infections. Development of neurologic signs such as severe depression, circling, seizures, etc. occurs in a small percentage of cases; some of these cases will ultimately be fatal.

A vaccine for horses currently exists and is recommended by most veterinarians on a biannual basis. Mosquito control is the most important preventive measure for all species, however. Spraying, removing free-standing water, stall confinement during mosquito feeding times, etc. are highly encouraged.

Cribbing is a common vice in which horses grasp a solid object with their upper incisors, contract ventral neck muscles and arch their necks, retract their larynx and pull backward. Horses that swallow air during this maneuver are called “wind suckers”. Cribbing is considered unsoundness, causing excessive wear on the incisors and enlargement of ventral neck muscles. Horses with aerophagia may exhibit weight loss, unthriftiness, poor performance, digestive disturbances, and flatulence.

Cribbing can be corrected in many cases through surgical intervention, especially when nonsurgical management is unsuccessful. Surgery involves partial removal of two muscles and resection of a nerve that supplies a third muscle. Consequently, “wind sucking” becomes impossible for the horse.

Lameness is by far the most common cause of inadequate performance in the horse. The majority of horses currently in training have experienced lameness at one time or another. An accurate diagnosis of lameness requires a comprehensive understanding of equine anatomy and a methodical approach to examination. Causes of lameness can be divided into two categories: primary causes and secondary causes. Primary causes represent abnormalities that did not occur as a result of another problem. Foot abscesses, acute fractures, soft tissue injury (e.g. from trauma) and some forms of arthritis are common primary causes of lameness. Secondary causes of lameness are present as a consequence of one or more other problems. Laminitis, stress fractures, and soft tissue inflammation (e.g. myositis or desmitis) are common examples of secondary causes of lameness. They occur as a result of the horse’s compensating for a primary cause of pain. Although treating secondary causes of lameness often improves the horse’s performance, they will recur and lameness will persist as long as the primary cause(s) of lameness goes untreated. It therefore behooves both the horse and client to accurately diagnose the primary problem(s) as soon as possible. Once the primary lameness is eliminated, all secondary problems should disappear.

A complete understanding of the horse’s anatomy, conformation, gait, and intended use(s) are essential in determining an accurate diagnosis. A proper lameness examination should include 1) conformation evaluation, 2) passive lameness evaluation, and 3) active lameness evaluation. Performing a lameness examination is much like putting a jigsaw puzzle together. There is always 1 piece that makes everything else fit!

Extracorporeal High-Energy Shockwave Therapy (ESWT) is a new treatment methodology that is currently gaining popularity in the world of performance horse medicine. ESWT was first developed for humans as a treatment for the disintegration of kidney stones. Subsequently, it was recognized that ESWT might have applications in orthopedics as well. High-intensity waves apply mechanical pressure and tension on tissues. These forces stimulate osteogenesis (new bone formation) and removal of excessive osseous tissue (calcification). The effects of shock waves occur in regions where tissue density changes, such as bone/ tendon or bone/ ligament interfaces. Therefore, it has shown promise in treating such conditions as stress fractures, navicular disease, distal tarsitis, suspensory desmitis, ligament and tendon fibrosis and/or ossification, etc. Preliminary research shows better quality healing and improved recovery rates.

Degenerative joint disease (DJD) is a common cause of decreased performance in equine athletes. Lack of performance often precedes overt lameness and/or radiographic changes. The degenerative cycle is initiated as a result of joint instability. Instability may occur pursuant to trauma/injury, damage to the supporting soft tissue structures of the joint (ligaments), and overuse. Inflammation of the joint’s synovial membrane (a condition called synovitis) occurs secondary to joint instability. The presence of inflammatory cells within the synovial membrane results in 1) increase in hydrostatic pressure within the joint and 2) release of catabolic enzymes (lysozymes) and other chemical mediators into the joint. The increased hydrostatic pressure results in the influx of fluid into the joint, distension of the joint capsule, and pain (the joint’s nerve endings are within the joint capsule). The enzymes released into the joint degrade hyaluronan (the molecule that gives synovial fluid its thick and slippery characteristics) as well as the articular (cartilage) surface. Erosion of the cartilage surface results in loss of articular congruency, which in turn causes increased joint instability. And the cycle begins.

The slapping of the back foot is often referred to as “goose-stepping”. This characteristic gait abnormality is specific for fibrotic or ossifying myopathy of one or more of the hamstring muscles on the back of the pelvic limb, which includes the semi tendinosis, semi-membranosis, and biceps femoris groups. The semi-tendinosis muscles are most commonly affected. Pelvic limb myopathies are most frequently observed in Quarter Horses, due to the type of work they perform.

Normally, the hamstring muscles move independently of each other and are able to stretch very easily when the limb is extended cranially (out in front). However, a trauma in the form of muscle strain/tearing (resulting from hyperextension of the pelvic limb) or reaction to intramuscular injection results in the development of scar (fibrotic) tissue within the muscle(s). The scar tissue organizes, matures, and contracts, creating a “rope-like” band where there was once normal pliable muscle tissue. The lack of elasticity of the scar tissue causes the pelvic limb to be pulled caudally (backward) before the full length of the stride is reached. The foot “slaps” the ground as a consequence.

Fortunately, this problem is very easy to treat and carries a good prognosis. Treatment involves a minor surgical procedure that is performed with the horse standing/sedated and the area locally anesthetized. Scar tissue is transacted through a 1-to-2-inch incision along the back of the leg. Most horses can return to normal work after 3-4 weeks.

Windpuffs is a term that denotes synovial effusion (i.e. extra fluid) within the fetlock joint and/or digital flexor sheath. It can occur in the front legs, the back legs, or both. Extra fluid results in a soft fluctuant swelling behind and just above the fetlock joint. It is more common in older horses but can occur at any age.

Although the digital flexor sheath and fetlock joint are in close proximity with one another, effusion in one structure can be identified by its specific location. Swelling behind the suspensory ligament branches is consistent with digital flexor sheath effusion. Swelling in front of the suspensory branches suggests fetlock joint effusion.

In the vast majority of cases, the swelling is a result of extra fluid within the palmar (front leg) or plantar (back leg) digital sheath rather than the fetlock joint. The plantar digital sheath acts as a sleeve that houses the superficial and deep digital flexor tendons as they course around the back of the fetlock joint. Normally, a very small amount of synovial fluid is present within the sheath to provide lubrication to the tendons as they slide around the back of the joint.

Excessive fluid within the sheath develops in response to increased hydrostatic pressure which in turn occurs due to the presence of inflammatory cells (inflammation) within the sheath. The synovium can become inflamed for a variety of reasons such as flexor tendonitis, trauma to the synovial membrane, infection, etc. In most cases, however, the source of the inflammation is undetermined.

Although plantar digital effusion can cause clinical lameness, this is rare except in severe cases (e.g. infection or tendon damage). Therefore, the problem is considered primarily cosmetic in nature. Consequently, most horses are left untreated.

Treatment options include intrasynovial injection (steroids/ hyalronan) or surgical debridement. Injection usually dramatically reduces the size of the swelling, although recurrence is very common and usually expected. Surgical manipulation can result in the formation of scar tissue within the sheath, which in turn can cause adhesion formation and lameness. Therefore, this strategy is reserved for only the most severe of cases.

Navicular Inflammation

Navicular inflammation, often referred to as “Navicular Disease” or “Podotrochleosis”, is one of the most common causes of intermittent, often-shifting, thoracic limb lameness in horses between 4 and 15 years of age. Although the pelvic limbs may be affected, for all intents and purposes it is a disease of the thoracic limbs.

Where is the “Navicular Bone”?

The navicular bone resides palmar to the coffin joint in the back 1/3 of the foot. It serves as a fulcrum for the deep digital flexor (DDF) tendon as this structure passes around the back of the foot to attach on the third phalanx (P3 or “coffin bone”). The navicular bone consists of a hard cortical exterior and a soft cancellous interior (medulla or marrow). The soft marrow interior allows the navicular bone to compress when under pressure. The navicular bursa is a synovial “sac” between the navicular bone and DDF tendon and serves to lubricate the tendon as it slides over the back of the navicular bone.

How Does Navicular Inflammation Arise?

Simply, inflammation in the palmar foot or navicular area develops as a result of excessive tension of the deep digital flexor (DDF) tendon. Since the DDF tendon uses the navicular bone as a fulcrum, increased DDF tension results in increased pressure across the navicular bone. In the normal situation, the navicular bone responds by compressing. However, if the pressure is persistent and/or severe, the navicular bone will begin to remodel in an attempt to adapt to the biomechanical stimulus. During remodeling, osteoblasts (hard bone cells) are laid down along the palmar surface of the marrow cavity. This results in a higher hard bone:soft bone ratio which increases the bone’s stiffness and decreases its compressibility. If the pressure is of low intensity and/or of limited duration, navicular bone remodeling may successfully absorb, diffuse, and redistribute the load. In this situation, horses will remain asymptomatic. However, if the pressure is of high intensity and/or persistent, inflammation (and pain) may ensue.

Why Does Navicular Inflammation Occur? Other contributors to navicular inflammation include navicular bursitis (inflammation of the navicular bursa) and venous congestion/hypertension within the navicular bone. Both may also occur as a result of excessive DDF tension.

Horses can have excessive DDF tension for a number of reasons. The horse’s breed, size, type of work, frequency of work, the intensity of work, conformation, etc. can all play a role in the development of navicular inflammation. Since it is our goal to keep your horse performing at its intended level, we will only discuss factors that are treatable. Many are related to confirmation. The most common are:

• Broken-back Distal Limb Axes. This conformation results in an increased distance between the DDF tendon’s origin in the DDF muscle along the back of the radius and its insertion on the palmar aspect of the third phalanx. Since this tendon stretches very little, increasing its traveling distance increases its tension. Increased DDF tension results in increased pressure across its fulcrum (the navicular bone).

• Low Heels/Long Toes. This conformation delays the breakover of the limb. The more delayed the breakover, the greater the DDF tension prior to advancing the limb. The more DDF tension, the more pressure on the navicular bone.

• Underslung Heels. Due to the anatomy of the fetlock joint, a horse’s center of gravity is actually behind (palmar to) where the footrests on the ground surface. Weightbearing force is therefore greatest on the palmar aspect of the foot closest to the limb’s center of gravity. The greater the distance between the foot and the center of gravity, the greater the weight bearing force on the back of the foot. Underslung heels are farther from the center of gravity of the limb, and are therefore subject to greater weight bearing or concussive forces. Frequently, the navicular bone lies just above the point where the heel meets the ground and the force is the greatest. Underslung heels, therefore, result in increased concussive pressure on the navicular bone.

• Sheared Heels. This refers to unbalanced heels; i.e. where the heels are at different levels relative to the ground surface. Since the navicular bone lies across the back of the foot, it experiences differences in forces from one side of the foot to the other. This abnormality, therefore, may not only increase overall navicular pressure but result in differences in pressure from one side to the other.

What are the clinical signs?

Affected horses often have a history of intermittent thoracic limb lameness that improves with rest. Although both forefeet are usually involved, the lameness is only observed in the more affected limb. It is not until perineural anesthesia is used to anesthetize the more severe foot that contralateral lameness is manifested. Subsequent perineural anesthesia of the contralateral limb often produces a sound horse. Following are some common clinical and lameness characteristics of horses with navicular inflammation:

• High and/or contracted heels on the affect foot (often thrush is present).

• Grade 2-3/5 thoracic limb lameness.

• Consistent pointing with the affected limb.

• May stand in the stall with the toes stuck down in the bedding.

• Chronic bruising of the sole and/or toe.

• Worse when trotting with the affected limb on the inside of a circle.

• Horse tends to land on the toe during movement.

• Sensitivity to pressure (hoof testers) over the frog of the affected limb.

• 100% soundness is achieved with palmar digital (PD) perineural anesthesia of the limb.

How is Navicular Inflammation Diagnosed?

Navicular Inflammation is a clinical diagnosis. In other words, demonstration of pain in the palmar aspect of the foot is diagnostic of navicular inflammation. Pain is demonstrated upon clinical examination, hoof testing of the frog, and response to PD perineural anesthesia. Radiographs are frequently used to assess navicular inflammation. It is important to note, however, that inflammation is invisible on a radiograph. Since this is a relatively low-motion area, radiographic changes and the presence of navicular inflammation don’t correlate very well. Therefore, we must rely on our clinical findings to determine the presence of navicular inflammation and pain.

How is Navicular Inflammation Treated?

• CORRECTIVE SHOEING

  • Maintain straight distal limb axes (to decrease DDF tendon tension)

  • Trim, broaden, and rocker the toes (to quicken breakover and decrease DDF tendon tension during movement)

  • Apply full (egg) bar shoes (to stabilize the heels relative to one another and prevent shearing)

  • Extend the shoe palmarly (to move the point of weightbearing closer to the limb’s center of gravity)

• MEDICATION DESIGNED TO ENHANCE PERIPHERAL BLOODFLOW

  • Aspirin: Prevents platelet aggregation and therefore “thins” the blood

  • Isoxuprine: A vasodilator (increases the diameter of the vessels)

  • Phenylbutazone: A vasodilator

• SYSTEMIC ANTI-INFLAMMATORY MEDICATION

  • Phenylbutazone: Functions as both a vasodilator and anti-inflammatory

  • Previcox: A long-term anti-inflammatory

• SYSTEMIC ARTHROTHERAPY

  • Adequan, Legend, Cosequin, Flex-Free, etc. can help normalize the synovial environment within the navicular bursa and reduce inflammation/pain.

• LOCAL ARTHROTHERAPY

  • In cases of chronic moderate to severe navicular inflammation, we often elect to perform intrasynovial injection. This may involve direct navicular bursa injection and/or indirect delivery of medication to the bursa via the distal ingterphalangeal (or coffin) joint.

• TILDREN

  • This product has proven to be very effective at alleviating inflammation and clinical signs associated with navicular inflammation in our hands.

• EXTRACORPOREAL SHOCK WAVE THERAPY (ESWT)

  • Shock wave therapy has shown to be an effective treatment modality for navicular inflammation, especially if concurrent deep digital flexor tendon (DDFT) pathology exists.

• PERMANENT ANESTHESIA OR PD NEURECTOMY

  • This is the ultimate “pull the wool over your eyes” technique. Eliminating the horse’s ability to feel pain certainly improves soundness; however, it also greatly increases the risk of the horse sustaining injury to the numbed portion of the foot. Therefore, this approach should only be considered as a last resort.

In summary, navicular inflammation appears to be a disorder triggered by an excessive bone remodeling response. Bone remodeling occurs as a result of excessive pressure across the navicular bone by the DDF tendon. Excessive DDF tendon tension may occur due to faulty conformation that is acquired or inherited. Navicular inflammation can be successfully managed via early recognition and correction of the predisposing factors as well as a proper therapeutic plan.

Distal Tarsitis

Distal tarsitis often referred to as “bone spavin”, is the most common cause of clinical lameness associated with the tarsus (or “hock”) in horses. Distal tarsitis is osteoarthritis and periostitis of the distal intertarsal, tarsometatarsal, and occasionally the proximal intertarsal joints.

What are the distal tarsal joints?

The tarsus, or “hock”, is very similar in structure to the human heel. The tarsus consists of 4 joints: the tibiotarsal joint, the proximal intertarsal joint, the distal intertarsal joint, and the tarsometatarsal joint. During movement, the tibiotarsal joint performs approximately 98% of the motion of the tarsus. The proximal intertarsal joint, just below the tibiotarsal joint, performs approximately 2% of the motion. The lowest 2 joints, the distal intertarsal and tarsometatarsal joints, move very little. In fact, if the horse did not have these joints (i.e. if there was solid bone across the distal tarsus) we would not be able to detect any unsoundness or alteration in gait.

How does distal tarsitis arise? Although the distal tarsal joints are not essential to normal locomotion of the horse, they are prone to instability. Chronic joint instability results in the development of joint inflammation (i.e. arthritis). Repeated compression and rotation of the tarsal bones and excessive tension on the attachment of the major dorsal ligaments have been implicated as causes of distal tarsitis. Factors which can affect the development of distal tarsitis include the horse’s age, weight, breed, job description, frequency of work, intensity of work, and conformation.

Following are conformational abnormalities that may increase the horse’s chances of developing distal tarsitis:

• Straight pelvic limbs

• Sickle hocks

• Cow hocks

What are the clinical signs?  Horses with distal tarsitis usually exhibit a gradual onset of pelvic limb lameness. Lameness is most apparent during the trot and may be characterized by a hypermetric “stabby” pelvic limb flight pattern. Horses will commonly pull the pelvic limbs underneath their body and “stab” them to the outside as the foot strikes the ground surface. Although lameness is frequently bilateral, horses will favor the more affected limb during exercise. A “hip hike” (pelvic excursion) is typically apparent, particularly when the horse is trotting with the affected limb to the inside of a circle. Lameness may worsen following a period of rest. Affected horses usually exhibit stiffness when first starting to exercise but can often “work out of it”. In chronic cases, firm enlargement on the inside of the hock may become visible; the swelling represents excessive proliferation of bone associated with the distal tarsal joints. Horses with moderate to severe tarsitis will usually exhibit a positive Churchill’s Hock Test, a procedure that is performed during the passive lameness evaluation. A positive response to this test is manifested by pelvic limb abduction. Pelvic limb flexion (“spavin testing”) during active lameness evaluation is an accurate and widely used detector of distal tarsitis. A positive response results in increased lameness and hypermetria following 60-90 seconds of pelvic limb flexion prior to trotting.

It is very common for horses to exhibit secondary symptoms as a consequence of favoring one or both pelvic limbs over an extended period of time. Common compensatory problems include:

• Thoracolumbar ebaxial (back) soreness due to an asymmetric pelvic limb gait

• Proximolateral thoracic limb suspensory desmitis as a result of chronic overloading of the thoracic limbs

• Greater Trochanteric Bursitis (“whorlbone”)

• Increased wear on the outside of the pelvic foot or shoe– in an attempt to relieve hock pain

Since these abnormalities are often secondary to distal tarsitis, successful treatment of the tarsitis alone frequently results in resolution of these problems. In our opinion, horses that exhibit one or more of the above-mentioned clinical signs should be evaluated for the presence of distal tarsitis as a potential primary cause.

How is distal tarsitis diagnosed? Distal tarsitis is a clinical diagnosis. In other words, demonstration of pain in distal tarsal joints is diagnostic. Pain is demonstrated upon clinical examination, lameness characteristics, response to Churchill’s Hock Test and hock flexion, and response to intra-articular anesthesia. Radiographs are frequently used to assess the presence and severity of distal tarsitis. It is important to note, however, that joint inflammation (arthritis) is invisible on a radiograph (which provides only structural information). Since the tarsus is a low-motion area, radiographic changes and the presence of distal tarsitis do not always correlate. Nuclear scintigraphy (bone scanning) may be a more accurate assessor of the presence of distal tarsal inflammation since it provides functional information (i.e. measures blood flow). In our experience, this diagnostic modality has proved to be very useful in the identification of distal tarsitis.

How is distal tarsitis treated? Two basic forms of treatment exist for distal tarsitis. The first involves the reduction and possibly the elimination of inflammation within the distal tarsal joints. This is achieved by the use of systemic and/or intra-articular anti-inflammatory therapy. Reduction of inflammation (arthritis) results in improved comfort. Intra-articular therapy usually involves the use of steroids, which are extremely effective at reducing local inflammation and pain. This approach also involves an attempt to maintain normal synovial integrity within the distal tarsal joints. Systemic medications such as Adequan®, Legend®, Cosequin®, etc. are designed to improve synovial function and general joint comfort in the horse. Clinicians at The Atlanta Equine Clinic also use intra-articular hyaluronan therapy (in combination with steroids) to enhance the effect of the treatment locally.

The other form of distal tarsal therapy involves fusion of the distal intertarsal and tarsometatarsal joints. This can be accomplished surgically or by the use of a chemical agent which is infused into the distal tarsal joints. Since these joints have almost no motion, their fusion results in minimal alteration in the horse’s gait. By eliminating the joints, however, instability and therefore inflammation and pain are also eliminated. This approach is generally reserved for those horses that have proved to be refractory to anti-inflammatory treatment and have advanced osseous changes associated with the distal tarsal joints. If you would like to learn more about distal tarsal fusion, please ask one of our staff. We will be glad to discuss this topic in more detail.