Dr. Ashley M. Stokes

Assistant Research Professor

Equine Health Studies Program

Equine Health Studies Program

School of Veterinary Medicine

Louisiana State University

Baton Rouge, LA  70803

Telephone: 225-578-9500

Telefax: 225-578-9605

E-mail: equine@vetmed.LSU.edu

Website: www.equine.vetmed.LSU.edu

Laminitis (founder) is a severely debilitating, excruciatingly painful, and potentially career-ending and life-threatening disease of the soft tissues (sensitive and insensitive laminae) of the equine foot.  These laminar tissues secure the coffin bone to the hoof wall, and when disrupted due to some of the causes listed below, the tissues may separate allowing rotation and/or sinking of the coffin bone. Gastrointestinal tract disease is the most common primary disease associated with the development of laminitis; however, many of the other causes listed below are associated with management practices. Laminitis is important to all horse owners, trainers and enthusiasts because it can occur in adult horses and ponies of any breed or use (athletes or companions/pets). Knowing some of the causes and risk factors leading to the development of this devastating disease are of tremendous benefit. Early identification of these factors can aid in the prevention of laminitis or may decrease the severity of disease if appropriate steps are taken (such as calling your veterinarian before signs of laminitis are evident).

1. Grain overload or abrupt changes in diet (i.e. when a horse breaks into the feed room) Do not wait until symptoms develop to call your veterinarian, call immediately so corrective measures can be implemented before tissue damage occurs.
2. “Grass founder” is associated with sudden access to excessive amounts of lush forage, such as in the spring, and often leads to successive episodes of founder each year.
3. Conditions that cause high fever, release of bacterial toxins within the horse’s system, or serious metabolic disturbances (i.e. severe colic or pleuropneumonia) are risk factors for the development of laminitis.
4. Retained placenta and metritis predisposes a mare to laminitis. Post-foaling, monitor your mare for retained placenta, and have the mare examined by your veterinarian if she does not pass the placenta within 1-3 hours.
5. “Road founder” is due to excessive concussion to the feet. Use caution in exercising your horse vigorously on a hard surface for prolonged periods, especially if not appropriately shod.
6. “Contralateral overload limb laminitis” is associated with excessive weight bearing on one leg due to injury of the opposite leg. Therefore, if your horse develops a severe lameness you should have it examined immediately by your veterinarian in order to initiate appropriate treatment.
7. Examine your bedding (wood shavings) to ensure that it doesn’t contain black walnut shavings (most companies selling bedding for horses guarantee black walnut-free products).
8. Prolonged use or high doses of corticosteroids has been associated with, but not proven to lead to, the development of laminitis. Use caution in using these drugs.
9. Heavy breeds, such as draft horses are at risk.
10. Monitor your horse’s diet since overweight horses or those on a high nutritional plane are at a higher risk for laminitis. Putting your horse on a weight-reduction diet and exercise regimen may help reduce the likelihood of an episode of laminitis.

Rustin M. Moore, DVM, PhD, Diplomate ACVS

Professor, Equine Surgery

Director, Equine Health Studies Program

Equine Health Studies Program

School of Veterinary Medicine

Louisiana State University

Baton Rouge, LA  70803

Telephone: 225-578-9500

Telefax: 225-578-9605

E-mail: equine@vetmed.LSU.edu

Website: www.equine.vetmed.LSU.edu

1. Establish a regular routine including feeding and exercise schedules, and adhere to it! Horses seem to be creatures of habit and any change in feed, water, exercise or environment should be done gradually to prevent an “upset” to their gastrointestinal tract.

2. Feed a high quality diet comprised primarily of roughage. Horses should eat 1-2% of their bodyweight in roughage (pasture or good quality hay) each day, which equates to 10-20 pounds of hay in an adult 1,000 pound horse. Hay is best fed free-choice. Horses’ digestive tracts are better designed for continuous grazing or eating rather than feeding at intervals such as twice daily.

3. Minimize concentrates (grain) in the diet. An adult horse that is not in strenuous exercise or lactating does not actually need concentrates in their diet if they have adequate amounts of good quality roughage and they should not be fed more than ¼ to ½ of a pound of grain per each 100 pounds of body weight (thus, a 1,000 pound horse should not be fed more than 5 pounds of grain per day). At least one-half (and preferably ¾ of the horse’s energy needs should be supplied through hay or forage. The grain should be divided into at least two feedings if possible.

4. A regular parasite control program should be established with the help of your veterinarian. Several of the intestinal parasites (ascarids, large and small strongyles, and tapeworms) afflicting horses have been associated with different types of colic.

5. Provide exercise and/or turnout on a daily basis. Change the intensity and duration of an exercise regimen gradually.  Horses used to exercise (free roaming in pasture or regular riding) seem predisposed to certain types of colic (especially impaction of the cecum and large colon) when their exercise is abruptly halted for extended periods.

6. Provide fresh, clean water at all times. The only exception is when the horse is excessively hot, and then it should be given small sips of water until it has recovered. A typical 1,000 pound adult horse should drink about 6-8 gallons of water per day; requirements increase if the horse is in strenuous exercise, sweating excessively or lactating.

7. Avoid putting feed on the ground, especially in areas where there is sand in the soil, or in a paddock or stall. Although it is of questionable efficacy, horses in areas where sand is present can be fed psyllium hydrophilic muciloid (Metamucil) on a regular basis to facilitate evacuation of the sand.

8. Check hay, bedding, pasture, and environment for potentially toxic substances, such as blister beetles, noxious weeds, and other undigestible materials such as fibrous foreign bodies (nylon rope, string from baled hay, plastic, etc.), or metal objects which could serve as a nidus for enterolith (stone) formation within the large intestine.

9. Reduce stress! Horses undergoing a change in environment or exercise are at greater risk of intestinal dysfunction. Special attention should be given to horses when transporting them or changing their surroundings, such as at shows or other activities.

10. Be aware that some medications, especially nonsteroidal anti-inflammatory drugs such as phenylbutazone (Butazolidin) and flunixin meglumine (Banamine) can have adverse effects on the gastrointestinal tract (ulcers). Use these drugs cautiously and only under the supervision of your veterinarian.

Martin A. Vidal, BVSc, MS, MRCVS

Resident, Equine Surgery

 Rustin M. Moore DVM, PhD, DACVS

Professor, Equine Surgery

Director, Equine Health Studies Program

Equine Health Studies Program

Department of Veterinary Clinical Sciences School of Veterinary Medicine

Louisiana State University

Baton Rouge, LA 70803

(225)-578-9500

www.equine.vetmed.LSU.edu

INTRODUCTION

Tendon and ligament injuries are painful and debilitating diseases affecting horses in all aspects of the competitive equestrian industry, and are one of the most important orthopedic injuries related to the loss of horses from their intended use. The superficial digital flexor tendon (SDFT) is usually the most commonly affected tendon and the incidence of injuries has been reported as high as 43% in racing Thoroughbreds. Depending on the breed and the activity of the horse, however, other tendons (deep digital flexor tendon, DDFT) and ligaments (suspensory ligament, SL, and its branches, inferior check ligament, ICL), below the knee or the hock and the various sesamoidean ligaments (SesL) below the fetlock may also be affected.

Tendon and ligament injuries are usually strain-induced and tend to occur within the middle (core) portion of the tendon/ligament. The exceptions are traumatic injuries occurring as a result of an external insult often associated with skin trauma and age-related tendon or ligament degeneration usually evident in older horses with a characteristic dropped fetlock appearance. Common predisposing factors to exercise-induced tendon/ligament injuries are fatigue, abnormalities of conformation and foot balance as well as poor surface conditions. A major dilemma regarding tendon and ligament injuries is that they unfortunately heal slowly and often inadequately, and the tissue remodeling that occurs during the chronic reparative phase tends to result in scar tissue formation. The characteristic appearance of such scarred tendons is commonly referred to as a ‘bowed tendon’ (Figure 1).

The prognosis for return to racing in Thoroughbreds with SDFT injuries is guarded (20 to 60%) since the repair tissue cannot withstand the same rigor of exercise as normal tendon and therefore reinjury has been reported for up to 80% of these horses. Perhaps the two most important factors determining the prognosis for return to competitive athletic function and recurrence of reinjury are the severity of the initial injury and the nature of the exercise program during the rehabilitation period. Equine veterinarians have long struggled with these frustrating injuries and the multitude of treatment modalities commonly employed by clinicians suggests that few if any of these standard treatments have been very effective in reliably facilitating healing, promoting return to athletic soundness and preventing re-injury.

ANATOMY

The microstructure of tendons is arranged such that the primary collagen fibers (predominantly Type I), the principal structural component of tendons and ligaments, are arranged in bundles surrounded by a thin layer of richly vascular (blood supply) and elastic connective tissue, which provides nutrient supply to the tendons and allows them to glide freely beneath the skin. The SDFT and DDFT are extensions of their respective muscle bellies, which are located above the knee and hock, and they course along the back of the cannon bone and insert onto the phalangeal bones in the pastern and the foot. These tendons, their accessory ligaments such as the ICL and SCL and the adjacent SL and SesLs in the lower limb serve as a shock absorption apparatus allowing the horse to accelerate and decelerate its tremendous body mass.

The microstructure of tendons and ligaments is uniquely adapted to handle the type and degree of load (force) experienced by an exercising horse. Collagen (type I) is a molecule with an elastic property partly related to its crimped, parallel and longitudinal fiber arrangement within the tendon, lending the tendon its ability to absorb shock during the horse’s stride. Biomechanically, tendons/ligaments like other materials, when exposed to mechanical forces will experience a stress-strain relationship due to the muscular forces, which stretch and thereby deform the tendon during movement. Provided the relationship between the stress within the tendon due to the muscular forces pulling on the tendon and the resultant strain measured as deformation are mathematically linear, the tendon remains within an elastic phase during which the integrity of the tendinous ultrastructure remains intact upon relaxation of the muscles. If the deformation is continued beyond the yield point, which separates the elastic phase from the plastic phase, it results in damage or failure of the collagen fibrils, causing an inflammatory response leading to the condition know as tendinitis or desmitis. The SDFT strain measured in galloping horses is very close to that of SDFT failure, which signifies the small margin between normal peak deformation and failure. This indicates how close the SDFT is to mechanical failure during routine galloping, and how factors such as foot balance, shoeing and track surface would influence the stress/strain relationship and contribute to development of tendinitis.

TENDON HEALING AND THE EFFECT OF AGE AND EXERCISE

The unique function of tendons to carry loads and maintain their tensile forces while avoiding oxygen depletion and subsequent cell death is due to their low metabolic rate and their ability to efficiently generate energy. However, the low metabolic rate is also responsible for the relatively slower healing capacity of tendons and ligaments compared with other tissues. Tendon healing occurs in three phases: (1) the acute inflammatory phase, (2) the subacute reparative phase, and (3) the chronic remodeling phase. The inflammatory phase lasts 1 to 2 weeks and is characterized by inflammation, hemorrhage, and the release of inflammatory mediators which may further damage the surrounding uninjured tissues. The reparative phase begins a few days after the injury and peaks at approximately 3 weeks. During this period, new blood vessels are formed and cells such as stem cells involved in tissue repair are recruited and accumulate at the site of injury. The initial repair collagen (type 3) is deposited in a random orientation and establishes a cross-linking network to lend strength to the repair tissue. Finally, during the remodeling phase the collagen cross-linking undergoes re-organization and maturation and the repair collagen (type 3) is transformed into more linear, stronger and elastic collagen (type 1). Collagen fibers are gradually aligned along the longitudinal axis and collagen fiber bundles increase in diameter, imparting greater mechanical strength to the healing tendon.

Much of the mechanical strength of a tendon or ligament depends on the maturity of collagen cross-linking, collagen fiber diameter and the crimp morphology of the collagen. All of these characteristics of collagen can be affected by a number of factors, including age, training and injury, and will influence the manner in which tendons ultimately heal. Collagen fiber diameter and crimp morphology of SDFTs and DDFTs collected from Thoroughbreds have been shown to change dramatically within the first two years of life. It is believed that the complicated and synergistic effect of exercise and age on crimp morphology and changes in collagen fiber diameter, both intimately related to the mechanical properties of tendons, are involved in the maturation process of tendon and ligaments in young growing horses. Galloping exercise causes cumulative micro-trauma, resulting in partial to complete rupture of collagen fibrils. This damage has been shown to occur preferentially within the core region of the tendon, because of the relatively greater degeneration and remodeling of collagen fibril diameters and the crimp morphology in the center of the tendon in exercised horses. This phenomenon is believed to explain why most excessive strain injuries typically result in core lesions.

DIAGNOSIS

The initial diagnosis of tendon injuries based on clinical signs of soft tissue swelling, heat, pain on palpation and lameness depends greatly on the degree of tendon injury. Mild injuries, however, are often quite difficult to detect as they are associated with subtle clinical signs, and often go unnoticed until continued exercise strain exacerbates the lesion severity and thus the clinical signs. Although important, lameness examination and palpation alone are often inadequate to assess subtle tendon/ligament injury as well as their healing progress. Ultrasonography is currently the most common, practical and effective diagnostic tool to evaluate and monitor tendon and ligament injuries. Figure 2 shows cross-sectional (2A) and longitudinal (2B) ultrasonographic images of an obvious severe SL lesion in the right front cannon bone area of a Thoroughbred race horse. However, it is often more difficult to assess the presence and quantity of torn tendon fibers during the acute inflammatory stage of the injury due to a combination of hemorrhage and inflammatory fluid accumulation within the lesion, which may obscure the lesion severity. Therefore, frequent ultrasonographic re-evaluations of the injury are crucial to monitor the healing progress after the inflammatory process has subsided, which may take up to several weeks depending on the nature of the initial injury and treatment.

TREATMENT OF TENDINITIS

Acute Inflammatory Phase Therapy

The principal goal after a tendon injury is first to reduce the inflammatory response, which may have deleterious effects on the surrounding healthy collagen fibers and connective tissue due to the inflammatory mediators released from injured cells. Secondly, it is important to promote restoration of tendon structure and function and thereby minimize scar tissue formation, which has known inferior mechanical and elastic properties. Promoting adequate collagen fiber alignment and remodeling, crucial to the functional restoration of the tendon, requires a controlled program of rest and exercise, which is time-consuming, costly, labor-intensive and frustrating for both the horse owner and the veterinarian.

The initial inflammation is most commonly and most effectively treated with nonsteroidal anti-inflammatory drugs (NSAIDS) such as phenylbutazone (Butazolidin^®), flunixin meglumine (Banamine^®) and/or ketoprofen (Ketofen^®). A new and recently FDA-approved product called Surpass™ (1% diclofenac sodium) is believed to have reduced systemic side effects because of the relatively low dose used its local action at or near the site of its topical application. The effectiveness of this preparation for acute inflammation associated with tendinitis/desmitis is unknown. Local and systemic corticosteroids are also frequently used to reduce inflammation, edema and adhesion formation. However, it has been shown that corticosteroids can be detrimental to tendon healing, and especially corticosteroids injected into the tendon have been shown to cause collagen fiber destruction, cell death and tendon calcification, resulting in prolonged reduction of tensile strength. Topical anti-inflammatory products such as dimethyl sulfoxide (DMSO) are frequently used for their ability to penetrate cell membranes and scavenge free radicals released from injured cells, which may also damage surrounding non-injured tissues. However, topical DMSO has been shown to affect healing properties and may therefore not be suitable for long-term use. Tendons are routinely bandaged during the acute injury stage to minimize swelling and edema due to fluid emanating from the inflamed and injured tissues. Cold water (hydrotherapy) and ice (cryotherapy) are also commonly used to reduce swelling and inflammation by causing local vascular constriction (thereby reducing the concentration of inflammatory mediators) as well as decreasing the cellular metabolic demand and nerve conduction velocity, which reduces pain perception.  

Reparative and Chronic Remodeling Phase Therapies

A number of other therapies have been commonly used to medically treat tendon/ligament injuries medically during the reparative phase of healing. Initial ultrasonographic studies demonstrated that intralesional injections of beta-aminoproprionitrile fumarate (BAPTEN^®) appeared to encourage more linear collagen fiber arrangement during the early period of the repair phase. However, the perception of an improved prognosis for return to racing was refuted by a study which later showed that one of the side effects of BAPTEN^® was significant suppression of collagen production, and therefore it was concluded that BAPTEN^® actually suppressed tendon healing at a cellular level. BAPTEN^® is no longer manufactured.

Sodium hyluronan has been shown to affect proliferation, migration, and differentiation of precursor cells into tendon cells (tenocytes) and to stimulate vascular (blood vessel) ingrowth. However, despite some evidence of improved repair tissue formation and ultrasonographic appearance, scientific data regarding the response of injured tendons to sodium hyaluronate as well as to polysulfated glycosaminoglycans (PSGAGs) formulations has been conflicting, indicating the need for more research into these therapeutic options.

Anecdotal reports have suggested the use of heparin for treatment of tendinitis but studies have never demonstrated any beneficial effects of heparin. Additionally, some have suggested deleterious effects of intralesional heparin administration.

Alternative Therapies

Counter irritation methods, such as pin firing and blistering, have been commonly used as treatments for tendinitis. However, it is known whether these methods cause severe inflammation and fibrosis, which could be counterproductive to tendon healing, cause further damage and invariably prolong tendon healing. It has been suggested that additional scar tissue would provide greater strength due to an increased tendon cross-sectional area; however, this would occur only to the detriment of its elastic properties. Therefore, the prognosis for return to racing, compared with other forms of therapy, is doubtful.

Therapeutic (low-power) lasers have been used in several species including humans and horses for various soft tissue and skeletal disorders. However, there are no reports that prove its efficacy in horses and one human clinical study involving soldiers with Achilles tendinitis demonstrated no significant effect of this treatment. Similarly, there is a lack of evidence for any effect of electrical currents used in electromagnetic therapy or therapeutic ultrasound, which is commonly applied in humans to improve healing of soft tissue injuries and scar tissue reduction. Extracorporeal shock wave therapy (ESWT) (Figure 3) has shown promise in the treatment of equine tendon and ligament injuries, especially those involving the origin and insertion of the suspensory ligament at the bone-ligament junction. The perception and scientific evidence for this treatment modality has so far been promising as some investigators have reported a 21 to 30% increase in the number of horses with suspensory desmitis that were able to return to their previous level of work after application of ESWT, compared with other therapeutic modalities. However, controlled long-term studies are still needed to assess the efficacy of ESWT on structures such as the flexor tendons.

Surgical Treatment

The technique of superior check ligament desmotomy (SCD) involves the transsection of a short accessory ligament (also called the superior check ligament, SCL) between the SDFT and the bone (radius) in the area just above the knee. This is believed to enhance the elasticity of the musculo-tendinous unit of the SDFT and its muscle belly in the upper limb. Variable success rates (40% to 82%) of horses returning to racing, and recurrence rates (13% and 33%) have been reported. Although still commonly used, the effectiveness of this technique has been debated more recently because it has been suggested that horses undergoing a SCD were more likely to suffer from recurrent or new injuries, especially involving the suspensory ligament. It has been suggested that this could possibly be attributable to overextension of the fetlock after the superior check ligament has been transected.

The theory behind surgically splitting tendons is to reduce core lesion size by evacuating the contents (blood, edema, inflammatory cells), releasing inflammatory mediators from the injury site and to encourage ingrowth of new blood vessels. Ultrasonographic and histological studies have reported favorable results. However, its merit is believed to be limited to the acute tendinitis stages and could in fact be detrimental in more chronic tendon injuries.

Injuries and thickening of the SDFT within the fetlock region may result in increased friction along the annular ligament, which is a broad structure encircling the back of the fetlock, which helps to contain the flexor tendons (SDFT and DDFT) in that area.  The resultant inflammatory-mediated swelling of the annular ligament can contribute to or exacerbate the lameness. Transsection of this ligament is often indicated in horses with “low bows” in order to restore the gliding function of the tendon over the back of the fetlock.

TISSUE ENGINEERING AND THE FUTURE

During the mid 1990s, veterinarians began to inject core lesions of flexor tendons and suspensory ligaments with aspirates of the horse’s own (autologous) sternal bone marrow (Figure 4). The presumption is that stem cells and growth factors in the marrow will promote or facilitate tendon healing. Although no controlled studies have yet been published to provide scientific evidence for the effectiveness of this therapy, an initial report described an 86% success rate for return to intended function after this technique. Such data and anecdotal success stories have stimulated a plethora of research and the emergence of stem cell therapy companies such as Vet-Stem™ and VetCell BioScience Limited both in the private and academic sectors. The concept of tissue engineering using bone marrow- or fat-derived stem cells is based on research which has shown that these cells augment tendon repair as evident by the significant improvement of structural, geometrical, and most importantly, biomechanical tendon properties.

Tissue engineering is the development of biological substitutes to restore, maintain or improve tissue or organ function.  In broad terms, this approach involves isolating cells from the body, placing them on or within structural matrices, providing growth factors and implanting the new system inside the body.  Stem cells are precursor cells which are found in bone marrow, fat, and skin as well as around blood vessels. These cells have widely been recognized for their potential to promote healing and replace injured or diseased tissues due to their ability to differentiate into many different tissues such as bone, cartilage, tendon, muscle, fat and nerve. Hence, a number of companies and academic institutions have begun to use stem cells harvested either from bone marrow (VetCell BioScience Limited, UK) or fat (VetStem, Inc., USA) for therapy of equine tendinitis/desmitis. Stem cells, however, may also require suitable scaffolding for implantation. A commercially available biodegradable animal (pig urinary bladder submucosa) product (ACell™) has been used for injection into tendon/ligament injuries with the intention to provide a suitable matrix for the body’s own stem cells to migrate and establish themselves within the injured tissue. This technique, which involves reconstituting the powdered material and injecting into the site of tendon/ligament injury, has so far shown some reasonable anecdotal success, but this also requires further controlled research to validate its application in equine tendinitis.

More recently, new molecular approaches to the therapy of injured tissues have emerged. Results of early reports have been promising demonstrating growth factors such as insulin-like growth factor-I (IGF-I) can be placed either directly (growth factor therapy) or indirectly into an injured tissue by injecting cells with the genetic information coding for these growth factors (gene transfer). The transfer of genes into the healing tendon environment can thereby be manipulated for extended periods of time. More research, however, is still required before these techniques will gain FDA (Food and Drug Administration) approval for the use in human and veterinary medicine.

In most circumstances, a combination of the above therapeutic options is used by the clinician to treat tendinitis. However, the ability of tendons to heal adequately depends to a large extent on a controlled exercise program, designed to stimulate the remodeling of the tendon ultrastructure without re-injuring the tendon. Thus, a gradual, controlled increase in exercise duration and intensity over the course of 6 to 9 months or more is required. During this period, diligent hoof care and balance avoiding toe overgrowth are important to minimize unnecessary leverage and increased strain on the affected tendon(s)/ligament(s).

CONCLUSION

Despite considerable information regarding the anatomy and physiological maturation and aging process of equine tendons, the pathophysiology of tendinitis/desmitis in athletic horses remains elusive and the most effective and appropriate treatment of these conditions still require further research. Many of the current treatment techniques employed by the equine veterinarian are still based on personal preference and may vary widely in their success rate. The multitude of treatment options indicate that no single treatment has yet stood the test of time and research, which suggests that they are not particularly efficacious. The use of recombinant growth hormones and stem cells in equine tendinitis are still in their infancy, but appear to show considerable potential for successful treatment, judging by early anecdotal success and the success of tissue engineering in basic and applied research in other species and tissues. For more information on some of these newer techniques, including extracorporeal shockwave therapy, bone marrow transfer and stem cell therapy, or to discuss whether these might be appropriate for your horses with tendinitis/desmitis, please contact the authors by telephone (225)-578-9500 or e-mail (equine@vetmed.LSU.edu). You can also visit the LSU Equine Health Studies Program website (www.equine.vetmed.LSU.edu) for more information.

By Dr. Rustin Moore

The LSU School of Veterinary Medicine hosted the grand opening of the Equine Intensive Care Unit, the newest addition to the School’s Equine Health Studies Program on October 22. This new 10-stall facility will enable the School to provide comprehensive, advanced veterinary care for the ever increasing number of horses requiring emergency and critical care services.

Dr. Michael G. Groves, dean of the School of Veterinary Medicine, made the opening remarks and introduced Dr. Rustin Moore, director of the School’s Equine Health Studies Program. “Today’s event signals another significant accomplishment in the growth and development of the equine programs here at the LSU School of Veterinary Medicine,” said Dr. Groves. Dr. Moore explained the function of the new facility and commented on the fact that this facility was built with private funds. He then thanked each of the major donors and presented them with certificates of appreciation. LSU System President Dr. William Jenkins was also present. He thanked the donors and complimented the School on its continuing progress.

Each of the donors present was asked to take part in the ribbon-cutting. Ms. Saundra Lane Garrett, representing Gerry Lane Enterprises, and Ms. Nadine Carter Russell, representing Mrs. Paula Manship, cut the ribbon, officially opening the new intensive care unit. The other major donors present were Ms. Sydney Hines of Pass Christian, Miss., on behalf of Mrs. Jeanne H. McDaniel; Yvette Barbazon, representing Clear Creek Stud; and Ms. Francois Stirling, representing the Downman Family Foundation. Donors not present were Mrs. Ruth Hubert of the Hubert Charitable Foundation and Ms. Sydney Biedenharn of the Biedenharn Foundation. Naming opportunities still exist for Equine ICU stalls with gifts of $50,000 or more, as well as a naming of the entire unit. “These funds will help us to continue to deliver state-of-the-art advanced veterinary medical care for horses in Louisiana and the surrounding area and will enable us to construct additional facilities that will enhance our program,” said Dr. Moore.

The emergency and critical care field has been rapidly evolving and becoming a more common practice in veterinary medicine. According to the Veterinary Emergency and Critical Care Society (VECCS), an Emergency & Critical Care Center is a facility specifically designated to be operated, staffed and equipped 24 hours a day to provide a broad range of veterinary emergency and critical care services.

The LSU Equine Clinic is open for emergency admittance, evaluation and treatment of critically ill and injured horses 24 hours a day, 365 days a year. On-duty veterinarians are available for consultation or for referral of horses. The Equine ICU is staffed by veterinary technicians or nurses that provide around-the-clock monitoring, administer treatments to hospitalized horses, and assist with the diagnostic work-up of horses admitted on an emergency basis. A team of boardcertified veterinary specialists provide comprehensive, advanced veterinary medical, surgical and reproductive (obstetrical) care. Veterinary specialists in anesthesiology, clinical pathology, ophthalmology and radiology are on call to provide consultations, ancillary services or assist with horses admitted on an emergency basis.

Construction of the new Equine Intensive Care Unit (EICU) expands our ICU from a two-stall to a 10-stall centralized, climate-controlled, state-ofthe- art facility that contains 6 (12′x12′) stalls for housing adult horses and 4 (12′x16′) stalls specially designed for housing mares with sick foals. Additionally, one of the stalls is designed to accommodate horses with orthopedic/neurologic injuries/illnesses; the walls and floor of this stall are heavily padded and it is equipped with an overhead mechanical hoist to assist horses that are unable to stand alone via sling support. The EICU also has an on-site clinical pathology laboratory for monitoring blood biochemical, blood gas and metabolic parameters. The facility is immediately adjacent to the equine surgery suites, diagnostic procedures rooms and the imaging (radiology, ultrasound and CAT scan) facilities. Additionally, television monitors in the EICU enables remote monitoring of horses in isolation and enteric precaution stalls by the on-duty ICU personnel.

Approximately 20-25% of horses admitted to the LSU Veterinary Teaching Hospital and Clinics require some level of emergency and critical care services. Critically ill horses are generally referred to this 24-hour facility by veterinarians in Louisiana and surrounding states. The level of care required is dependent upon the underlying disease and the extent of the accompanying abnormalities. Some of the emergency and critical care services include: around-the-clock monitoring; assisting with thermoregulation (body temperature control) by altering the environmental temperature in cases of environmentally induced hyperthermia, particularly in foals with Rhodococcus equi pneumonia or horses that are anhidrotic (unable to sweat); administering intravenous fluids for horses that are dehydrated or in shock or those that have electrolyte, acid-base or metabolic disturbances; administering medications as well as enteral and parenteral nutrition; administering intranasal oxygen to foals or adult horses with respiratory disease, drainage or evacuation of fluid that accumulates in the pleural (chest) cavity due to pleuropneumonia; and emergency surgical intervention and intensive postoperative medical care in horses with acute gastrointestinal tract disease (colic). With the diagnostic and therapeutic advances made in the last several years in equine medicine and surgery, many critically ill horses with life-threatening diseases can be successfully treated, and even returned to athletic performance.

Approximately 60-65% of horses that are admitted to LSU Veterinary Teaching Hospital requiring emergency and critical care services have acute gastrointestinal tract disease (colic) and approximately one-half of these colics necessitate exploratory surgery. The second most common presentation involves neonatal foals with lifethreatening illnesses and these cases comprise approximately 10% of our emergency and critical care caseload. This is followed by traumatic injuries (lacerations, fractures, open joint injuries), respiratory distress, acute neurologic disease, obstetrical or other emergencies of the reproductive tract, and ophthalmologic emergencies such as melting corneal ulcers or ocular/periocular trauma.

“The new facility will enable us to more effectively and efficiently deliver comprehensive advanced veterinary care to the ever-increasing number of critically ill and injured horses admitted to the LSU Equine Clinic”, said Dr. Rustin Moore, EHSP director. These critically ill and injured horses are referred to us from private equine veterinarians from the state and around the region. For more information on the LSU Equine Clinic, please visit our website: http://www.equine.vetmed.lsu.edu or contact us via telephone (225)-578- 9500.

PDF version of the article is available here.

Polysaccharide Storage Myopathy (PSSM)is a condition in horses where there is abnormal glycogen storage occurring in muscles resulting in the accumulation of excessive amounts of glycogen and an unusable polysaccharide.

The accumulation of these compounds can result in symptoms that might range from reluctance to “move out”, in its mildest form, to an acute episode of “tying up” or rhabdomyolysis. Another term for this condition is “Equine Polysaccharide Storage Myopathy” or “EPSM”. The term “PSSM” was initially used by Dr. Stephanie Valberg (University of Minnesota) when she first described the condition in Quarter horses while Dr. Beth Valentine (Oregon State University) used the term “EPSM” when she described a similar condition in draft horses. While symptoms may vary depending on the breed, there is so much similarity that the two terms probably represent two ends of a spectrum of a single metabolic muscle disorder. A recent article from Spain documented PSSM in 9 show jumpers and dressage horses showing back pain. Those horses included “warmbloods”, Anglo-Arabs and Andalusian breeds. In addition to these breeds, PSSM/EPSM has been recognized in Morgans, Arabians, Thoroughbreds, Standardbreds, American Sadddlebreds, Tennessee Walking Horses, Appaloosas, Paints and many crossbreed horses.

(For simplicity, the condition will be referred to as PSSM in the rest of this article).

The purpose of this article is to describe our current knowledge of the metabolic abnormality involved, the resulting symptoms exhibited by horses with the condition, how to diagnose the condition and the diet and husbandry used to successfully manage the condition. In addition, the author would like to share some anecdotal insight gained by personally dealing with the condition in my own Morgan.

Metabolic Abnormalities

Glucose is normally stored as an energy source in the form of polysaccharide (“polysaccharide” means “many molecules of glucose”) called glycogen in the liver and muscles. Horses with PSSM actually have an excessive accumulation of glycogen molecules in muscle cell cytoplasm. Over time, this glycogen combines with certain proteins present in the cytoplasm to form abnormal glycogenprotein complexes. How these abnormal polysaccharides damage the muscle cell is not exactly clear but may involve interfering with intracellular pathways for generating energy and thus result in cell necrosis or death. There are several “glycogen storage diseases” recognized in humans and other species but they are usually characterized by accumulation of excessive glycogen due to deficiencies in the enzymes that break down glycogen for energy utilization. In horses with PSSM, the enzymes to break down glycogen are present and work appropriately. Instead, the problem seems to be that these horses are too efficient in storing glucose as glycogen in muscle cells. Muscle cells are one of the cell types in the body that utilize the hormone insulin to help glucose enter the cell. Insulin serves to aid cell membrane proteins called “Glucose Transporters” (GLUTs) in transporting glucose into the muscle cells. Studies have shown that horses with PSSM actually have increased insulin sensitivity so that they are more efficient in moving glucose into the cells. (This would be the opposite of type 2 diabetes where cells have decreased insulin sensitivity which is also called insulin resistance)

Symptoms Associated with Excessive Polysaccharide Storage

With the excessive accumulation of these polysaccharides, the muscle cell can be damaged and die. When this occurs, depending on the number of muscles involved, duration of the process and other stress factors, multiple symptoms can be shown by the affected horse. While symptoms can occur in 6 month or younger foals, most often signs are not apparent until the horse goes into training at 2-4 years of age. Depending on the severity of involvement, symptoms can include any of the following: generally stiff, difficulty rising, reluctant to “move out”, tires easily, saddle issues (sore back), bucking, resistance to holding up the hindfeet for shoeing, subtle lamenesses, abnormal gaits, cranky attitude, muscle tremors or sensitivity, kicks at flies that aren’t there (muscle cramps), swishes tail excessively (muscle pain), looks at belly or flanks as if colicky (muscle pain), having a preference for rubbing or rolling a lot, or the opposite, with resistance to brushing/grooming, especially over the back and rump. Affected horses may show a stiff, tense gait with difficulty getting that nice relaxed rhythmic swing that is so desirable in the dressage horse or any other athletic, sport horse. Symptoms of “shivers” where there is an abnormal hindleg action and muscle quivering have been described in draft breeds. If left unmanaged, over time the muscles can atrophy and the horse can show severe muscle wasting. The horse may eventually be unable to rise from a lying down position.

In its most severe manifestation, an affected horse can “tie up” (also known as exertional rhabdomyolysis or Monday morning disease or azoturia). While the horse is exercising, they will stop moving, often quite abruptly, or sometimes just slow down. They may come to a complete standstill, refusing to move. Their muscles tremble all over their body and they break out in profuse sweating due to extreme pain as the muscles, especially their rump muscles, go into severe cramps. As these affected muscles are severely damaged, they will release a cellular pigment called myoglobin which is normally involved with oxygen utilization within the muscle cell. Released myoglobin is then transported in the bloodstream and is filtered by the kidneys, appearing in the urine as a dark brown color. Unfortunately, myoglobin can be toxic to the kidneys and result in renal failure if not treated aggressively. It can take weeks to recover from an episode of rhabdomyolysis.

Symptoms can be exacerbated by nervousness and can occur after being rested from exercise for a couple of days or longer. A history of recent respiratory infection may serve as a precipitating event. Not gradually warming up in cold weather may also precipitate symptoms.

Diagnosis of PSSM

A presumptive diagnosis can be made based on a typical history of symptoms described as above, as well as the presence of typical physical findings such as sore back or rump muscles, resistance to pick up hind limbs or in extreme cases muscle wasting. To support the diagnosis, it is helpful to document elevations of muscle enzyme concentrations in the blood. The two most commonly evaluated muscle enzymes are creatine kinase (CK) (also known as creatine phosphokinase, CPK) and aspartate aminotransaminase (AST) (also known as serum glutamate transaminase, SGOT). CK has a shorter half life and therefore will become elevated sooner and return to normal range sooner after an acute episode of muscle damage and is therefore the preferred muscle enzyme to evaluate when diagnosing and monitoring muscle recovery. Horses with PSSM may have normal or elevated CK concentrations prior to exercise. After exercise the concentrations of CK will rise to higher levels than normal horses. One recommended protocol for diagnosis is to measure CK concentrations 4 hours after after mild walk/trot exercise for 15 minutes. A CK concentration greater than 800U/L would suggest significant muscle damage. While elevated CK concentrations are not diagnostic for PSSM, since any condition that damages muscles can elevate CK, elevations would be supportive of the diagnosis and warrant pursuing a definitive diagnosis by muscle biopsy. It is recommended that the veterinarian performing the biopsy contact the laboratory prior to doing the biopsy to learn the best way to collect, handle and transport the tissue to the lab. Because the histopath diagnosis is very dependent on tissue handling (temperature (freezing/thawing), duration of time from biopsy to processing), staining and processing, it is recommended that only labs knowledgeable in diagnosing PSSM be used (2 contacts are listed at the end of the article). The muscle tissue is stained with PAS (periodic acid-Schiff) stain to show glycogen within the muscle cells. In addition, the tissue is then treated with amylase to differentiate glycogen from the abnormal polysaccharide complexes (glycogen is digested by the amylase whereas the abnormal polysaccharide complexes are resistant to digestion by amylase). The amount of PAS positive muscle cells that are and are not digested by amylase help in making the diagnosis. While greater than normal amounts of PAS positive muscle cells are usually present, increased amounts of amylase resistant PAS positive tissue may or may not be present, depending on the duration of the condition in the horse (probably increases with increasing duration). In addition, there may be other intracellular changes that suggest muscle damage that can be visualized in the evaluation.

Management of PSSM

The successful management of PSSM is based on a combination of changes in dietary and exercise programs, tailored to each individual horse. Since these horses have an increased sensitivity to insulin and therefore are more efficient at taking in glucose circulating in the bloodstream into muscle cells, dietary modification is oriented at minimizing the amount of glucose and therefore carbohydrates in the diet (The so-called “Horsekins Diet”).

An attempt to eliminate all grains should be made. Since carbohydrates are a major source of calories, this energy source needs to be replaced. A very good source of calories is fat in the diet since fat has twice as many calories as carbohydrate or protein on a per gram basis. Sources of fat that can be used in horses include rice bran and corn oil. In addition to being a good source of calories, fat has been shown to be “muscle sparing” in horses used for athletic competition. That is, when fat is incorporated in the diet in greater quantities, studies have suggested that muscle cells are somewhat protected from some of the negative oxidative processes that occur with high levels of exercise and the muscles seem to recover better after an athletic event even in normal horses. In diets high in fat, there may be an increase in the need for fat soluble vitamins such as Vitamin E. Since both Vitamin E and selenium are important for muscle health, it is important to make sure adequate levels are available. However, excessive levels of selenium (and other nutrients) can be toxic; therefore, care should be taken in formulating an individual diet.

Also attention to electrolyte needs that are vital to proper muscle and other cell functions should be addressed, especially in hot, humid climates.

When electing to use fat sources other nutritional factors need to be considered. While rice bran is an excellent source of fat (10-20% fat, Dry Matter Basis, depending on the source), it is also high in phosphorus so that a source of calcium must be fed to maintain an ideal Ca:P ratio. Good sources of calcium include alfalfa and beet pulp. Caution should be used in just feeding alfalfa as your only source of hay since it can be a source of higher available carbohydrate than grass hays. The importance of adequate fiber cannot be over emphasized in any horse’s diet and hay at volumes of at least 1.5-2% of body weight should be fed or have plenty of high quality grass available. Sugar content of grass is also a consideration in certain grasses at certain times of the year. Another good source of fiber and “safe calories” is beet pulp. Since it is also high in calcium it can be used to balance the high phosphorus in rice bran if fed in a 3:1 ratio of beet pulp to rice bran on a weight basis. When shopping for sources of beet pulp, be sure to purchase beet pulp that has not had molasses added! When feeding corn oil, the limiting factor can often be palatability. As much as 16 ounces per day can be fed. Recent suggestions that corn oil (3 oz /day) can be protective against gastric ulcers would be an additional plus to using corn oil.

If trying to figure out your own balanced diet seems a little overwhelming, the good news is that there are several feed companies that have diets available that could be used for PSSM. Manufacturers include Kentucky Equine Research (ker.com) (Equi-Jewel, balanced rice bran and other protein mineral supplements), Hallway Feeds (hallwayfeeds.com) (Releve, a complete, balanced diet specifically developed for PSSM), Moorman’s Natural Glo Rice Bran, Buckeye Ultimate Finish and others. In addition, Purina has recently marketed their Ultium which has rice bran and beet pulp; however, there is some grain/molasses content to that diet. Be sure to work with a good nutritionist to make sure that your diet is well balanced in calories, protein, electrolytes, minerals and vitamins.

The other good news is that a high fat, low carbohydrate diet high in fiber is also optimum for preventing other equine diseases including colic, laminitis, gastric ulcers and recurrent rhabdomyolysis in race horses which is due to another mechanism than PSSM. It is helpful in managing these disorders as well as in the management of equine pars intermedia dysfunction (Equine Cushings) as well as in the management of Peripheral Cushings or so called Metabolic Disorder, if calories are appropriately regulated.

Studies have suggested that optimum response to management must not only utilize a dietary change but must incorporate daily, regular exercise so that muscle gycogen is used daily and not allowed to accumulate. Horses should get as many hours as possible of turn out to exercise, even if you have to use a grazing muzzle to limit caloric intake in quality pastures for fat horses.

Workouts should be done daily on a consistent basis with “days off” limited to one or two a week. When prolonged lay offs cannot be avoided due to schedules, illness or injury, starting back to work should be gradual.

Prognosis for a horse diagnosed with PSSM

While PSSM could be fatal if a horse has a severe episode of tying up or if he/she becomes debilitated by muscle wasting, most horses can do very well if diagnosed early and managed successfully. In fact, according to Dr. Valentine, there is the suggestion that horses with PSSM, when managed correctly, are superior in temperament, conformation and performance. And in fact, while breeding for these characteristics, we may have been unknowingly breeding for this type of “over-efficient” muscle metabolism.

An anecdotal case of PSSM

My personal experience with PSSM began on a chilly November evening 2 years ago. I had been to a 2 day show the weekend before and given my horse 2 days rest before starting back to work. I was riding my then 5YO Morgan gelding at canter when he came to an abrupt stop and started shivering and sweating all over. We were some 100 yards from the barn and it took me 15 minutes to walk him back to his stall. With each step I began to realize that my horse had just “tied-up”. As I instituted IV fluids, Banamine and acepromazine therapy to stabilize him, I mentally went through my differentials for rhabdomyolysis. In retrospect, I realized that he had shown a lot of those subtle symptoms like the sore back (I had to have a custom made saddle built for him), resistance to the farrier lifting his hind feet, ticklish when being brushed, loving to roll after any exercise, swishing his tail a lot when being ridden, and kicking at non existent flies. He would often get mad when you asked him to do certain tasks while riding. While we had only shown in 2 recognized shows at training level, the judges’ comments consistently included “seems tense”, “resistant”, and “needs to relax”. So I decided to confirm my suspicions (his CK was >35,000!) by sending a muscle biopsy to Dr. Valberg at Minnesota. While my gelding had to have 2 weeks of complete rest to recover from the severe muscle damage, I didn’t wait for biopsy results before I started instituting dietary changes. I did my homework on commercial diets available and finally came up with a diet that has seemed to work for us. I formulated the diet, consulted a feed company that ran it through a nutrition software program to make sure it was well balanced and gradually introduced it to my horse. The diet basically consists of Ca:P balanced rice bran, beet pulp (non-molassesed), a protein/mineral supplement, corn oil, a Vitamin E/Selenium supplement (grass and hay in my area is selenium deficient), an electrolyte supplement, 1 to 2 flakes of alfalfa hay, 1- 3 flakes of grass hay and 8-12 hours of grazing (quantities depend on time of year and thus grass quality). My exercise program did not have to change since he was already getting 8-12 hours of grazing and when stalled he has free access to a 50×50 paddock. He is exercised 5-6 days a week being either ridden, driven or longed. When I go out of town for several days, if I can’t get friends to exercise him, I start exercise back very gradually. When I go to horse shows, I take a portable electric paddock so that he can have some turn out time even at shows. When the weather is cold, he gets ridden or at least warmed up with a rump rug on his back. He loves getting massages from our local equine massage therapist as often as I can afford it. Slow warm-ups are very important to our daily training. After, about 4 months, I could start to see a difference in how he moved. It took at least a year before I could say that he had a lovely relaxed swishy trot. Realizing that I am a relatively new dressage rider working with a trainer, we have made slow steady progress. We are consistently scoring in the mid 60s at training level, and are strongly schooling 1st level with aspirations to show first level at our next recognized show. In addition, we have recently started to drive and hope to do some dressage driving as well as pleasure driving. We have competed in a 17 mile “fun” endurance race, a 6 mile Hunter’s Pace and trail ride weekly. We do have to be careful about long rides and chilly, damp weather. Since I have always felt that good things always come from bad, I feel fortunate to have made the diagnosis in my horse because I now have a better knowledge of good nutrition as well as a better feel for exercise physiology and muscle movement after all the research I have done to understand and manage his condition. His attitude is that of a typical, happy Morgan that loves to work. I think I have a happier, better athlete and we hope to ride and compete for many years to come!

Conclusions

In conclusion, it is important that we educate ourselves about this possibly under-diagnosed condition. What else can we do besides educating ourselves and our colleagues, looking for it in our own horses and adjusting dietary/exercise management? We can contribute to the advancement of knowledge about the condition by helping researchers. We can help them by offering blood and tissue from our own horses for biochemical and genetic studies so we can have a better understanding of the incidence within our breeds. We can support research by donating dollars to those investigators that are producing quality research data to better inform us. Recognition is the first step towards the elimination of the negative aspects of this unique metabolic condition.

PDF version of this article can be found here.