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Treatment Options for Kissing Spine
Lori Smolkovich, DVM
Overriding dorsal spinous processes, better known as "kissing spine" is a condition that many horse owners fear, because, until recent years, treatment options were very limited. In this article, the anatomy of the horse’s back, clinical signs, and treatment options will be discussed.
Individual bones called vertebrae fit together to form the spine. The vertebrae are named for their location. Starting at the head and moving toward the tail, the equine spine consists of seven cervical or neck vertebrae (#1 in image), 18 thoracic vertebrae (#2 in image), 6 lumbar vertebrae (#3 in image), 5 sacral vertebrae (#4 in image), and approximately 20 caudal or tail vertebrae (#5 in image). When discussing kissing spine, the area of interest is the thoracic and lumbar vertebrae (#2 and #3).
As you can see in the picture, there are bony "protuberances" that project dorsally (or up) along the spine. These "protuberances" are part of the vertebrae called dorsal spinous processes (DSPs). There are ligaments that are in between each DSP called the interspinous ligament, and a ligament and several muscles that run over the top of the DSPs. These muscles and ligaments make up the top line of the horse and help support the vertebrae to give it strength. Kissing spine occurs most frequently when the dorsal spinous processes come in contact with each other because the back muscles are weak and do not provide the support the spine needs. When the DSPs "kiss", or touch, the repetitive rubbing causes inflammation and bony changes. As a result of inflammation, the horse develops back pain. The bony changes in the DSPs can be easily diagnosed with radiographs.
Radiograph #1 illustrating normal DSPs
Radiograph #2 illustrating kissing spine. Notice the lack of space between the DSPs and the increased bone density where the rubbing and pressure has occurred.
There are two broad categories of treatment for kissing spine; medical management and surgical intervention. Medical management commonly consists of shockwave therapy, bisphosphonates, corticosteroid injections, and physical therapy. Shockwave therapy is utilized to modulate pain and discomfort. Bisphosphonates and corticosteroid injections treat and quiet inflammation. Physical therapy is required to strengthen the back muscles and build the top line so that the DSPs have more support and are less likely to contact each other. If medical treatment is not able to manage the horse's clinical signs, surgical intervention is often the next step.
There are several ways to surgically approach kissing spine. Two of the more common procedures will be discussed in this article. One surgical option is a subtotal ostectomy of the impinging dorsal spinous processes (SODSP). This means that a portion of the DSP is removed to create a wider gap between the DSPs thus preventing them from touching or "kissing". This procedure has been performed under general anesthesia and on horses standing with heavy sedation. The decision to perform the surgery standing or under general anesthesia is often dependent on which DSPs are affected, surgeon's preference, and risk factors specific to the individual horse. The other surgical option is an interspinous ligament desmotomy (ISLD). Unlike the SODSP, which is a surgery that removes a portion of bone, the ISLD approaches “kissing spine” by altering the soft tissue structures around the affected DSPs. As previously discussed, in between each DSP, there is a ligament called the interspinous ligament. In an ISLD, those ligaments are incised or cut, allowing the DSPs to not be held so tightly together. As a result the DSPs can spread apart and therefore do not “kiss”. The ISLD is surgery that is performed standing under heavy sedation so general anesthesia is not required.
Regardless of the surgical procedure that is utilized, physical therapy plays an integral role in the success of the horse following surgery. Once the DSPs are no longer kissing, the back must be strengthened to ensure the DSPs are supported as much as possible so that the condition does not reoccur. Physical therapy often begins after surgery with carrot stretches, later on, the horse is worked on a lunge line in a chambon, Pessoa, or other rig to encourage the horse to use his body and back properly while not adding the weight of a rider. Once the horse is ready, under saddle work that encourages engagement of the back and hind end is necessary to continue to build strength and to maintain the back muscles.
Kissing spine is a painful condition for horses and a frustrating one for riders. Fortunately there are many ways to help your horse achieve relief. If you think your horse may be affected by kissing spine, have your veterinarian evaluate him and discuss which options may be best for you and your horse.
Jacklin, B.D., et al. (2014). A new technique for subtotal (cranial wedge) ostectomy in the treatment of impinging/overriding spinous processes: Description of technique and outcome of 25 cases. Equine Veterinary Journal, 46, 339-344.
Brink, P. (2014). Subtotal Ostectomy of Impinging Dorsal Spinous Processes in 23 Standing Horses. Veterinary Surgery, 43, 95-98.
Coomer, Richard P.C., et al. (2012). A Controlled Study Evaluating a Novel Surgical Treatment for Kissing Spines in Standing Sedated Horses. Veterinary Surgery, 41, 890-897.
Catarina Ruksznis, DVM
Despite its relatively small size, the equine eye is a complex organ which can go very seriously wrong, very quickly when injured. If your horse comes in from the pasture with his eye swollen shut, take no chances- have your vet take a look as soon as possible. These clinical signs could be due to anything from a bump, to a foreign body, to a disease process within the eye. One of the more common problems we see are corneal ulcers. In order to understand this problem, let's first think about the anatomy of the eye.
In its most simple conception, the eye is a round structure divided into two compartments: the anterior ("forward") chamber and the posterior ("behind") chamber. The two compartments are separated from one another by a divider made up of the iris and lens. The anterior chamber lies between the cornea and the iris/lens, while the posterior chamber lies behind the iris/lens and the back of the eye. The cornea is the clear "window" at the front of the eye through which light enters and we can see. It is made up of different layers of cells like layers of a sandwich. The bread is formed by epithelial layers and the contents by the stromal layers, which form the majority of the corneal thickness. In total, the thickness of the equine cornea is only about 1 mm. The cornea is by necessity a very specialized tissue (it's clear!) and contains various mechanisms through which water is excluded from the stroma and transparency is maintained. The remainder of the outside of the eye is covered with a fibrous layer of white tissue (the "whites of the eye"), which is called the sclera.
Corneal ulcers are injuries, abrasions or erosions, to the cornea. While superficial corneal ulcers only involve the outermost epithelial layer (the 'top slice' of bread), deeper ulcers may include loss of the stromal layers and even expose the inner endothelial layer. Any depth of ulcer is painful, and horses may display squinting, tearing or rubbing at the offending eye. You may also see redness, swelling of the eyelids or thick, abnormal discharge from the eye.
When examining an eye, your vet will begin with a careful ocular exam. This will include looking for causes of the ulcer, such as a foreign body stuck in the eye, decreased tear production or the inability to blink. Corneal ulcers can then be definitively diagnosed by staining the eye with a colored dye called fluorescein. Fluorescein stain is not taken up by the normal corneal epithelium, but does stick to the inner stromal layers of the cornea (the filling of the sandwich) in places where the epithelium has been scraped away. While the stain appears yellow/green to the naked eye, it fluoresces green when viewed under a blue light. Ulcers appear as areas of intense green on the cornea. It is important to note that deep corneal ulcers, ones which have gone through all of the stromal layers, will only show a thin ring of stain uptake on the edges of the ulcer. This is because the endothelial layer which forms the bottom of the ulcer does not adhere to the stain but the sides of the ulcer, where the stroma is exposed, do. Other stains may also be used to evaluate the eye, such as rose bengal and lissamine green, to look for viral or fungal infection.
Management of corneal ulcers involves both systemic (oral or intravenous) treatment and treatments applied directly to the eye. Pain from the corneal ulcer is managed with systemic banamine, a non-steroidal anti-inflammatory medication similar to ibuprofen, along with topical atropine. Atropine is an anticholinergic agent which stops the spasmotic contraction of muscles within the eye secondary to pain, allowing the pupil to dilate.
Corneas, like your skin, are constantly exposed to the environment. Once there is a breech in the epithelial barrier, there is an opportunity for infection to occur. Bacterial or fungal infection may cause significant corneal damage and even corneal melting (keratomalacia) as the body tries to respond. Topical antibiotic therapy is therefore an essential part of treatment for corneal ulcers. There are a wide variety of antibiotic choices available, the most common of which is triple antibiotic ointment, composed of three antibiotics (Neomycin, Polymixin B, Bacitracin). This product has a broad spectrum of activity against many of the probable bacterial contaminants and is a good choice for an uncomplicated ulcer. It is essential to remember that this product is composed of only antibiotics and is often referred to as NeoPolyBac. There is a very similar product known as NeoPolyDex, which contains a steroid in addition to antibiotics. Steroids should never be applied to a corneal ulcer, as they inhibit healing. In cases of more complicated or non-healing ulcers, corneal scrapings can be taken to sample the cells and bacteria/fungi within the cornea and to guide antibiotic choice. In addition to an antibiotic, an antifungal is often added to the treatment regime in more complicated cases.
In the case of an uncomplicated corneal ulcer, healing should be complete within 7 to 10 days. If the ulcer does not heal or worsens, more intensive treatments or diagnostics are warranted.
Irby, Nita L. "Ophthamology." Equine Emergencies Treatment and Procedures. Fourth ed. St. Louis: Elsevier Saunders, 2014. 400-07. Print.
Gilger, Brian C., ed. Equine Ophthalmology. Second ed. Maryland Heights: Elsevier Saunders, 2011. Print.
Equine Protozoal Myeloencephalitis: An overview
Equine Protozoal Myeloencephalitis (EPM) is a commonly diagnosed neurologic disease of the horse that has captured the attention of equine veterinarians and horse-owners alike since it was first documented 30 years ago. It is a progressive and degenerative disease of the equine central nervous system, and is caused most commonly by the protozoan species, Sarcocystis neurona. (There have been few documented cases identifying Neospora hughesi as the causative agent, though the two species are clinically indistinguishable from one another.) Recent studies show that approximately 22-65% of horses in the United States are seropositive with antibodies from S. neurona, but only a small portion of these horses will go on to develop clinical disease.
The definitive host of Sarcocystis neurona is the opossum. This is the host in which sexual reproduction of the parasite occurs. Infected opossums shed sporocysts in their feces which are in turn transmitted to the intermediate host when ingested. Intermediate hosts include cats, armadillos, skunks, raccoons, and sea otters, and once infected, they develop sarcocysts in their skeletal muscle. Once this muscle is ingested by the opossum, the life cycle is completed. In the pathogenesis of EPM, horses are considered aberrant, or dead-end hosts, which halt the life cycle of the organism. Horses become infected through ingestion of contaminated feed or water and once infection is established, disease progression ensues.
While the pathogenesis of EPM infection is still widely a mystery, it is postulated that the ingested sporocysts are able to penetrate the intestinal wall and enter the cells that line the horse's arteries. The organism develops within the arterial walls until they rupture into the bloodstream where they can spread to other parts of the body. At this point it is possible for the horse to clear the infection on his own, leaving him seropositive, but without any clinical signs or evidence of disease. It is unknown how S. neurona enters the CNS in horses, though once the protozoa gain access they can establish infection in any area of the brain or spinal cord. Horses infected with S. neurona are unable to transmit the disease to other horses.
EPM can manifest itself through a variety of clinical signs, though the most classic are the three As: Ataxia, Asymmetry, and Atrophy. A common appearance of a horse with EPM is one with severe asymmetrical gluteal muscle atrophy. Since the organism can infect any area of the central nervous system, ataxia, or incoordination, is frequently observed in horses with EPM. Moreover, a variety of neurologic deficits can be seen, ranging from cranial nerve abnormalities in the form of a head tilt or facial paralysis to a dull or depressed mentation. Various gait abnormalities may also be seen and can occasionally be mistaken for lameness. The timeline for disease progression is variable, but if left untreated, in its most severe form, EPM can lead to seizures, coma, and even death.
Obtaining a diagnosis for EPM can be challenging, and it's important to know that a truly definitive diagnosis may not be attainable during a horse's lifetime. That being said, tests for EPM in live horses include the Western blot, indirect fluorescent antibody test (IFAT), and surface antigen-1 ELISA test (SAG-1 ELISA). Simple seropositivity for S. neurona antigen is not sufficient for a diagnosis, as that only relays if there are circulating antibodies within the vasculature. All exposed horses should be seropositive, but it takes the protozoan entering the central nervous system from the systemic circulation for the horse to actually have EPM.
To make a diagnosis of EPM, cerebral spinal fluid (CSF) and blood samples should ideally be submitted together for paired testing and analysis. The Western blot test looks for IgG antibodies against S. neurona within the CSF, though false positives are possible, especially if there is blood contamination of the sample. With a specificity of only 44-60%, it is likely that the immunoblot tests are best to rule out the presence of EPM, rather than provide a diagnosis for the disease. The IFAT test has shown comparable sensitivity, better specificity, and it is less affected by blood contamination. However, this test might give positive results for the protozoa S. fayeri, which might or might not cause disease in the horse. The newest test, the SAG-1 ELISA, looks for the presence of a particular surface protein of S. neurona, but not all strains express this particular protein. Therefore, false negative results are common.
The gold standard for diagnosing EPM in the horse is based on finding characteristic lesions on post-mortem exam within the CNS. However, due to the small number of organisms needed to cause the disease, the diagnosis can be missed even with a full neurologic necropsy. In general for the live animal, a clinical diagnosis is best established in horses with clinical signs of neurological disease consistent with EPM combined with positive CSF testing. Another option for diagnosis of EPM is looking for improvement in clinical signs in response to treatment. Since test results can take days to weeks to come back, horses are often started on treatment for the disease once they begin showing signs of neurologic disease while other possible causes continue to be ruled out.
Treatment for EPM is generally successful with studies indicating clinical improvement in 60-70% of cases. However, a portion of horses that are treated will have some residual neurologic signs that do not completely resolve with treatment. Relapse of disease once treatment is stopped is possible, though uncommon. There are four drugs that have been approved by the FDA for treatment of EPM: pyrimethamine, sulfadiazine, ponazuril and diclazuril. The most common oral medication used for the treatment of EPM is ponazuril (Marquis). It is administered once daily for 28 days or more depending on disease severity. While studies show ponazuril can effectively rid horses of S. neurona, it does not improve the CNS damage that occurs before treatment begins. Regardless of which medication is instituted, early detection and prompt treatment are essential for a positive outcome and a full recovery.
If you have any questions regarding this article or the health of your horse, please contact your veterinarian or the doctors at New EnglandEquineMedical & SurgicalCenter.
Tessa Lumley, DVM
New England Equine Medical & Surgical Center, 15 Members Way, Dover, NH03820
Volunteer Management Survey Kicks Off
It probably comes as no surprise that volunteers are the life blood of the horse industry. Recruiting and retaining volunteers can be challenging, and it can be one of the key obstacles to growth. It can also be difficult to figure out where to start to improve volunteer management.
Blue Ribbon Consulting, LDO, LLC is conducting a volunteer management survey to develop a white paper that will provide a snapshot on where the horse industry stands. The survey results can help nonprofits to determine next steps to strengthen their volunteer management practices. Those that operate an equine oriented nonprofit, or on the board of directors are invited to take a few moments to participate in this survey. Answers are confidential and will only be used in aggregate to produce a white paper that will be posted to the Blue Ribbon Consulting website. If you don't run an equine nonprofit but know someone that does, please send the link along to them.
Find the survey here: https://www.surveymonkey.com/r/FFV9S3Y . Please complete the survey by December 15, 2014. The white paper will be available in early 2015.
Since 1995, Blue Ribbon Consulting has provided evaluation, planning, research, marketing and problem-solving services to clients around the world to take their horse businesses successfully through their business transitions. Lisa Derby Oden, Blue Ribbon Consulting’s founder and principal, has also been a nonprofit founder, board member, and executive officer for state and national organizations. She has worked with nonprofits in strategic planning, program development, corporate development, fundraising, grant writing and grant administration. Lisa has delivered business development, marketing, and leadership seminars throughout the United States. In addition to her horse business books, she has also been a columnist and freelance writer for many equine trade publications. Lisa has received state and national awards for her work in the horse industry.
Contact: Lisa Derby Oden
Blue Ribbon Consulting, LDO, LLC
Synovial infections in adult horses
Elizabeth Taylor, DVM, MS
Septic arthritis and tenosynovitis are orthopedic conditions in horses that develop following penetrating trauma or less commonly following an injection. They can carry serious complications for the horse if left untreated. Potential complications of synovial infections include arthritis, irreversible cartilage damage, adhesions, and severe lameness sometimes requiring humane euthanasia. It is important that these conditions be recognized promptly in order to instill immediate and accurate diagnosis and treatment aimed at eliminating the infection, reducing pain and inflammation and ultimately returning the horse to function.
In adult horses, joint or tendon sheath infection usually results from contamination via wounds. Because the lower leg of horses is poorly covered with soft tissue, joints and tendon sheaths are located very superficially and are prone to contamination following many lacerations, including heel bulb lacerations, and lacerations to the front or back of the pastern or fetlock.
It is important to contact your veterinarian if your horse has a laceration of the lower leg in a location near a synovial structure. Typically, horses with a synovial infection are quite lame (grade 4/5), however if the affected joint or tendon sheath is open and draining, lameness can be less severe. Frequently there is marked effusion (swelling), heat and sensitivity to the touch.
Analysis of synovial fluid is key in diagnosing and treating an infection. A sample should be obtained for both cytology and culture. Culture of the fluid is the “gold standard” for the diagnosis of an infection, however this only occurs in approximately 50% of cases. Therefore, analysis of the fluid’s cell count and protein, as well as examination under a microscope can help with an immediate diagnosis.
Diagnostic imaging can also aid in the diagnosis of a synovial infection. Ultrasonography can be helpful in the acute phase, when effusion is most prominent and accurate aspiration of fluid can be obtained. Radiography is less helpful in the acute phase, as soft tissue swelling is the only evidence of infection, but it can be useful to identify osteomyelitis (infection of the bone) should the infection spread.
The mainstay of treatment is to remove bacteria, devitalized tissue and other debris and reduce pain and inflammation. The goal of treatment is to return the articular cartilage to a normal environment, thus preventing cartilage loss. Cartilage health is imperative in maintaining an athletically sound horse.
Physical removal of bacteria and inflammatory mediators is best accomplished early and with a high volume of fluid. This can be done via needle lavage, arthroscopy or open drainage. Arthroscopy is advantageous because it also allows evaluation of the articular cartilage and removal of debris.
Antimicrobial therapy is directed by culture results, however because results may take days and positive results are not always obtained, therapy should be broad spectrum. In addition to systemic administration of antimicrobials, local administration of antimicrobials results in high concentrations directly at the site, while avoiding untoward systemic effects.
Lastly, synovial infections are very painful and can lead to support limb laminitis if proper analgesia is not maintained. Non-steroidal anti-inflammatory drugs (NSAIDs), such as phenylbutazone or flunixin are used to decrease the pain and inflammation associated with synovial infections. Their use must be judicious as serious side effects (gastric ulcer formation, colitis and renal toxicity) can arise with long-term use.
It is important to monitor synovial infections very closely as they can become life threatening if the horse has continued pain and lameness. Early recognition, accurate diagnosis and aggressive therapy of synovial infections greatly increase the prognosis for a horse to return to full athletic function.
Seat Bones from the Horse's Side of the Saddle
By Nancy Wesolek-Sterrett
Dressage Department Head, Meredith Manor International Equestrian Centre
When a horse has trouble moving straight or difficulty bending in one direction or another, or the rider cannot circle without pulling on the inside rein, the first thing I think of is not, “What’s wrong with this horse?” I consider that the crookedness may be feedback and immediately check the rider’s position. Is she sitting up straight?
Sitting straight means that the rider is centered over the horse’s center of gravity with equal weight on both seat bones. As well as, the rider’s shoulders directly over the seat bones. This is important because unless a rider can sit this way, she will not be able to subtly modify those seat bone pressures correctly to communicate direction, bend, speed and other information to her horse. When the rider’s seat bones contradict other aids, the horse gets confused, crooked, or offers other feedback that telegraphs the message, “What did you say?”
At the halt, the horse’s spine should be straight from poll to tail. The rider’s nose, chin, breastbone, belly button and spine all align with the horse’s spine. From the side, the rider’s ear, shoulder, hip and heel should align. As the horse begins to move, the rider keeps equal weight on both seat bones to indicate a straight direction of travel. Or she weights and unweights her seat bones in nuanced ways that influence the direction of travel in bends, circles, canter leads, lateral movements, etc. To get a square halt, she needs to put her weight equally on both seat bones again.
If the rider pays attention, the horse broadcasts clear feedback about as to how he feels the weight distribution in her seat bones and what it suggest that he do with his body. Take the example of a crooked rider whose default position puts more weight on her left seat bone than on her right. When going to the left, the horse probably bends and circles correctly. However, when the rider asks the horse to circle right, the horse may drift out to the left, fall in through the right shoulder, or have difficulty picking up the right lead. Ridden continually this way, the horse may develop more muscle on the left side to carry the rider’s crooked weight and become asymmetrical in the pelvis or hips.
Small things can make a huge difference for the horse. I recall one horse whose rider trained him correctly to turn on with the rider’s weight slightly heavier on the inside seat bone. He was sold to a rider who used a ‘spiraling seat’ to turn her horse. While this is very useful seat imagery, the rider misunderstood the full concept and overturned her shoulders, pushing her weight onto her outside seat bone. The horse was confused and the new rider was frustrated. (Sit on a swivel chair and try it.)
If rider sits heavily on the left seat bone, horse may dive to right or may drift to left to get more underneath the rider. The horse may have difficulty getting the right canter lead, refuse to yield from the right leg because the left seat bone is blocking the request. A jumper may run out to the left in front of a jump or drift to the left on landing. Unequal weight may put a lazy horse behind the leg and slow him down. Given confusing signals, a hot horse might get hotter and run from the pressure.
Understanding how to sit with equal weight on both seat bones, understanding how to weight and unweight each seat bone independently of the other, and keeping shoulders aligned with the hips can make many riding problems go away. A very slight shifting of weight onto one seat bone or the other can help the horse give the right answer as he follows the rider’s weight. For example, when the rider starts from the halt sitting straight with equal weight in both seat bones, she can give the horse clear communication when they start circles and eventually lateral work. Later on in the training scale, the rider’s ability to shift slightly from one seat bone to the other while staying straight and centered over the horse’s spine is essential to correct flying changes.
Many riders blame the horse when he goes crooked rather than considering that he may be giving them feedback about their own crookedness. A horse may act out because of a sore back and the rider may blame the saddle instead of realizing that continual riding with her seat bones unequally weighted could be the cause.
The question “Is it me or is it my horse?” can be hard to answer when you ride the same horse all the time. The rider with just one horse will benefit from the help of an instructor or experienced observer who can give them feedback about whether the rider’s crookedness is making the horse crooked or vice versa. Gradually, both horse and rider can develop a feel for ‘straight’ and help each other stay centered. Our students have the opportunity to test their seat skills by riding horses of all sizes, personalities and training levels. They learn a lot from their mounts as they adjust to these differences.
Riders with their own horse might take lessons on other mounts from time to time to help them figure out, “Is it me or is it my horse?”
Certainly a horse with unevenly developed musculature, saddle soreness, teeth issues, or dozens of other major or minor issues may compensate in ways that put the rider crooked in the saddle. Regardless of the cause, however, if the rider matches the horse’s crookedness, it will never go away. The rider that becomes responsible for being ‘straight’ herself, helps her horse feel what ‘straight’ should be so that he can figure out how to get there.
Riders ambitious to get to the next level in their sport sometimes hope that buying a horse that is at or above that level is the way to move up. Once they are in the saddle, however, they find themselves stuck right where they were. Worse yet, the higher level horse they thought would be their ticket to ribbons winds up ‘dumbing down’ its performance to the rider’s lower level. Often, the problem is very basic. The rider has never really learned how to sit truly straight with equal weight on both seat bones.
The seat bones are literally the seat of all communication with the horse. Correctly or incorrectly they are always sending information to the horse. Riders who pay attention to their seat bone messages and the feedback their horse gives about them will become able to truly influence their horse stride by stride. Remember, nothing replaces a correct, independent, influencing seat.