What services does South Shore Equine Clinic provide to the horse community?
I see a lot of horses getting their hocks injected. Some horses get theirs injected every few months. Is this healthy?
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 an 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 low-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 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.
I have been finding red urine spots in the snow, should I be worried?
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, an inconsistent stream or stopping and starting) or abnormal drinking behavior (increased or decreased drinking). Blood clots may also be seen, and the 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 it’s by products.
My horse is a “cryptorchid”. What does this mean?
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 bowel into the scrotum. Aftercare consists of one week of stall rest prior to resuming exercise.
How do I know when I need to send a horse with colic to your hospital versus treating it at the farm?
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 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 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 intestine does not receive an adequate supply of blood (and therefore not enough oxygen and nutrients). Endotoxins are absorbed through compromised bowel wall into the bloodstream. Since this condition (called endotoxemia) is life-threatening, surgery is indicated to prevent/treat decreased blood flow and compromise of 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.
I have a horse with a clubbed foot. My vet would like me to further increase the angle of the foot to reduce tension on the deep digital flexor (DDF) tendon, which he says is too tight. 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 it’s length and tension.
Although this makes perfect sense, it is extremely difficult to achieve in older horses. We find that some horses develop contactural 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.
What is all this about West Nile Virus? Should I be worried?
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. The 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.
My horse is a chronic cribber. I have tried everything, but nothing seems to work. Any ideas?
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 an 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.
My horse has been lame for over 2 years. No one can seem to find out what the problem is. Any suggestions?
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. 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!
I have heard a lot about “shockwave therapy” lately. What is this and what does it do?
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.
My horse has been diagnosed with “degenerative joint disease”. What does this mean?
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.
Since we are limited in our ability to enhance joint stability in the horse, we rely on medications designed to reduce inflammation and enhance/normalize synovial (joint) environments in the face of instability. These medications are referred to as “arthrotherapy”, and include both systemic (e.g. Adequan®, Legend®, Bute) and local (HA, steroids) forms.
Why does my horse “slap” one of his back feet on the ground at a walk?
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 include the semitendinosis, semimembranosis, and biceps femoris groups. The semitendinosis muscles is 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, 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 transected through a 1-to-2-inch incision along the back of the leg. Most horses can return to normal work after 3-4 weeks.
My horse has swelling around all four fetlock joints. When I asked my trainer about it, she told me that they were “windpuffs”. What are “windpuffs”?
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.