Assessing the approaches to diagnosing and treating proximal suspensory desmitis

Article by Connor Parsons DipWCF

Diagnosing proximal suspensory desmitis in the hind limb can be difficult. However, the modern diagnostic modalities available to the industry today makes it possible to isolate injuries, allowing both veterinarians and farriers to work together to achieve the best diagnosis and prognosis possible for the equine in question.

In this article, Connor Parsons reviews the anatomy and function of the suspensory ligament, causes and signs of proximal suspensory desmitis and whether there is an ideal procedure for diagnosing, treating and formulating a prognosis for the horse as part of his DipHE Farriery studies. 

ANATOMY

The equine limb is complex yet effective. The suspensory ligament is made up of dense white fibrous connective tissue which suspends the fetlock and prevents hyperextension.

Originating at the proximal, plantar aspect of the third metatarsal/carpal attaching to two palmar depressions distal to the carpometacarpal and tarsometatarsal joints descending the channel formed by the 2nd, 3rd and 4th metatarsal/carpal, bifurcating two thirds of the way down the 3rd metatarsal/carpal, making a firm attachment to the palmar aspect of the proximal sesamoids, pulling the sesamoids proximally, then travelling dorsally and distally at an oblique angle to merge with the common digital extensor tendon. This forms a sling to support the fetlock joint. The ligament and its branches are strong but only slightly elastic (Devereux, 2006).

The suspensory ligament also forms a part of the hindlimb stay apparatus which is a system of ligaments, tendons and muscles that work together to allow the horse to stand and doze with minimal muscular effort. Also known as the fright and flight mechanism (Colles & Ware, 2020).

DAMAGE TO THE SUSPENSORY LIGAMENT

Suspensory ligament damage can affect horses of all breeds and ages. However, it is most common in competition horses. Proximal suspensory desmitis (PSD) is inflammation or damage of the main body at the origin of the ligament at the proximal end of the third metacarpal/metatarsal.

The suspensory ligament can be inflamed or there can be changes to the fibre pattern of the ligament. These cases will present with lack of performance, being worse on soft surfaces. In more severe cases a core lesion (hole) can be seen on an ultrasound scan, where a number of fibres have ruptured. This type of injury will have a more sudden onset of lameness (Dyson, 1994). Injury can be solely within the ligament, involve tearing of the fibres of the ligament or be connected to avulsion fractures at the origin, involving the proximal 3rd metacarpal/tarsal (Baxter, 2020). Complete rupture is possible, however, very rare. The prognosis for a complete rupture is not favourable (Dyson, 1994).

Although the suspensory ligament has a slight elasticity to its make-up, if it is stretched it tends to heal with a loss of elasticity making it susceptible to recurrent damage (Colles & Ware, 2020).

SIGNS OF PROXIMAL SUSPENSORY DESMITIS

Proximal suspensory desmitis is a difficult condition to diagnose as the hind limb is complex and many of the functioning structures work in unison. A horse suffering with inflammation or damage to the main body of its hind suspensory can present one of three ways. It may have a unilateral lameness, a bilateral lameness or just a general decrease in performance (Dyson,1994).

CAUSES OF PROXIMAL SUSPENSORY DESMITIS OF THE HINDLIMB

Although there has been extensive research into proximal suspensory desmitis, there is no primary cause in all cases. 

Proximal suspensory desmitis is a common injury in both front and hind limbs of the equine athlete. Usually bilateral in the hind limb (Dyson, 2016). All types and breeds of horses are susceptible to this type of injury. Poor conformation is a contributing factor to proximal suspensory desmitis.

Conformational defects such as straight hocks, sloping pasterns and long-toe, low-heel conformations would be at higher risk to injury. These conformational defects will all apply unnecessary pressure to the suspensory ligament. Horses that have suffered with this condition will be predisposed to a repetitive strain injury of this ligament (Devereux, 2006). Overextension of the tarsus as a result of overextension of the fetlock has been linked to proximal lesions. The higher the severity of trauma, the higher the severity of ligamentous lesion. Working horses on deep, soft surfaces will increase the risk of this injury (Baxter, 2020).

The hindlimbs are more frequently affected with this condition than the forelimbs with a much lower success rate of the horse returning back to performance prior to rest (69% hind vs 80% forelimb) (Colles & Ware, 2020).

DISCUSSION

In a study of six horses, this is an extremely small cohort of horses to be able to state an average age a horse is likely to present with this condition. This study also shows that all of the horses studied were of varying fitness levels, therefore stating that this does not affect the likelihood of injuring the hind suspensory ligament. There was only one horse in this study that was unfit and overweight. The rest were all competition fit with good muscle mass, showing that fitness doesn’t necessarily decrease the risk of this injury happening. The case history of the six horses studied did not include which discipline or level the horse was working at. This would be an interesting factor to consider when looking at which horses would be more susceptible to proximal suspensory desmitis.

Each individual case was being looked after by different veterinarians, giving a clear picture of different approaches on how to diagnose and treat this condition. Although for the purpose of a study the varying opinions will make the comparison more difficult. All horses presented with a reduction in performance prior to veterinary contact. Only one horse was reported with a bilateral lameness behind. Flexion testing appeared to aggravate the lameness making it more prominent to see. Local analgesia has been shown to be effective in isolating the area to be investigated. Also, showing lameness on the other hind once the worse limb has been blocked out.

Using digital diagnostic modalities such as ultrasonography to diagnose this condition allows the veterinarian to study the changes in the fibre pattern of the suspensory ligament. This will allow the veterinarian to see the severity of damage caused and allow them to provide the best treatment plan possible. In this study only one horse had a lesion while the other five horses had thickening and slight changes to the fibre pattern. Horse 2 had lesions on both hind limbs however the veterinarian didn’t medicate, box rest was recommended. His prognosis was guarded.

Although radiographs of the feet don’t directly help with the diagnosis of proximal suspensory desmitis, they do allow the farrier to trim accordingly to restore the hoof back to correct hoof pastern axis and mediolateral foot balance. This will reduce lever arm forces thus reducing any unnecessary pressures on the plantar aspect of the limb.

Horses were radiographed for foot balance to aid with remedial trimming and shoeing. This will increase the equines prognosis allowing the farrier to have a clear picture of what is being dealt with. All of the horses that were radiographed presented with a negative sole plane and weak heels.

The question is whether this foot conformation is because the horses are wanting to apply more pressure to the caudal aspect of the hoof in the landing phase, reducing the movement of the metacarpophalangeal articulation. This is an attempt to reduce the loading forces applied to the suspensory ligament. However, it will also cause the heels to become weak. Or, if this conformational defect has caused the suspensory ligament to become inflamed or damaged, thus causing proximal suspensory desmitis.

Proximal suspensory desmitis can be secondary to other conditions such as hock conditions or sacroiliac problems which cause the horse to adopt a different gate. Therefore causing unnecessary loading on the suspensory ligament. It is important that the primary cause is diagnosed and treated when treating proximal suspensory desmitis. This is where scintigraphy can be a useful tool to get a clear picture of the cause involved in individual cases. Scintigraphy is an expensive diagnostic modality which carries significant health and safety risks, this must be taken into consideration when dealing with cases.

All horses studied were worse on a soft surface where it is harder for the horse to guard itself from soft tissue injuries. Horses that are worse on soft surfaces generally are suffering from soft tissue pain. However, nerve blocks will help the veterinarian pinpoint the structures involved when diagnosing lameness.

Although it is possible to have a unilateral lameness with proximal suspensory desmitis in the hind limb it is most common for the lameness to be bilateral. All of the horses in this study had a bilateral lameness, generally worse on one limb than the other. Although presenting prior to veterinary contact as lack of power or struggling to strike off on the correct canter lead.

When a veterinarian is deciding on a treatment plan, the horse is looked at carefully including its previous history as some treatments come with higher risks, although can be extremely effective for reducing inflammation. Shockwave treatment comes with minimal risks involved and is effective; however, many racing authorities require a mandatory 5 day Stand-Down period from racing following the administration of extra-corporeal shockwave therapy. Findings from this study show that the horses with the best prognosis of getting back to competitive work have undergone surgery. Understandably this is the last resort treatment as it is invasive and expensive for the client. 

Only one horse from this study did not have any medical intervention and this horse had the least favourable prognosis. This would suggest that box rest alone is not generally enough if the horse is expected to get back to full athletic fitness. The most common veterinary treatment is steroidal injections into the area of interest and shockwave therapy with rest. However, the use of corticosteroids in horses in training often adopt a clear 14-day exclusion on the use of intra-articular (joint) injections before racing in line with different racing authority regulations.

Water based therapy can also be considered as part of the recovery process when bringing the horse back into work. It’s known to reduce limb oedema, stimulate nerves, and improve circulation, which speeds the healing process and provides pain relief. It also aids in joint stability, providing all-around support to the limbs. 

Cold water therapy is typically prescribed when the goal is to reduce heat and inflammation. Applying cold water or ice reduces the amount of accumulating fluid to an injured area and can somewhat numb the area, causing a topical analgesic effect. 

Underwater treadmills are often used for horses with tendon and ligament injuries to provide a gradual transition back into exercise and regain the range of motion. Swimming is also used to condition the horse without putting a load on the skeletal system. It is often used in the early stages of tendon and suspensory injuries due to no pressure being placed on the lower limb. Trainers who use swimming as part of their routine often find that, in addition to the cardiovascular workout, it also helps the horse relax and settle its mind.

This is not always successful and horses are then admitted for surgery. While the surgery for this condition is successful, there must be consideration taken into the fact that it is not legal to compete at certain levels once this surgery has taken place.

The study shows that the farriery treatment involved when dealing with this condition is varied, depending on which veterinarian the horse is being looked after by. However, the author has had positive results from many different shoeing styles. The main importance of trimming and shoeing for this condition has been shown to restore the best possible hoof pastern axis through trimming, supporting the entire limb and fitting a shoe with an early breakover. This will reduce the lever arm on the metacarpophalangeal articulation, thus minimising unnecessary pressure on the suspensory ligament.

CONCLUSION

Having such a small cohort of horses in a study makes it difficult to finish with a conclusive result. This small study however, has given a positive result in the diagnosis stages of dealing with this condition. At this stage nerve blocks are invaluable along with ultrasonography. In less obvious cases MRI is useful to gain a diagnosis and occasionally scintigraphy will be used to locate the problem. Radiography is a useful tool when dealing with PSD and checking the origin area for avulsion fractures.

This study has also shown that there is a link between a negative solar angle and proximal suspensory desmitis. However, this would need to be studied further and on a greater scale to determine why there is a link between this conformational defect and this condition.

It is paramount that correct foot balance is achieved by the farrier. To achieve this foot balance radiographs are required. This study has shown that there is no definitive way to shoe for this condition, however it has shown a positive result from an early breakover shoe, allowing the horse relieve pressures on the caudal aspect of its hoof. Horses that had the best prognosis underwent surgery, allowing them to get back to competitive fitness.

REFERENCES

Baxter, G. M., 2020. Adams and Stashak's Lameness in Horses. 7th Edition ed. Hoboken, NJ: John Wiley & Sons.

Colles, C. & Ware, R., 2020. The Principles of Farriery. 2nd edition ed. Marlborough: J.A.Allen. 

Devereux, S., 2006. The Veterinary Care Of The Horse. 2nd Edition ed. London: J.A.Allen. Dyson, S., 1994. Proximal suspensory desmitis in the hindlimb: 42 cases. British Veterinary Journal, 150(3), pp. 279-291.

Dyson, S., 2016. American Association of Equine Practitioners. [Online] Available at: https://aaep.org/horsehealth/lowdown-high-suspensory-disease-proximal-Suspensory-desmitis [Accessed 19 11 2022].

Smith, M., 2022. Newmarket Equine Hospital. [Online] Available at: https://www.newmarketequinehospital.com/media/pm1beabc/hah349-Vet_susp_desmitis-final.pdf [Accessed 9 April 2023].

There's more to it than meets the eye!

Article by Adam Jackson MRCVS

The horse’s eyesight has evolved to scan its environment rather than picking up sharp details, in order to survive from predators.  As a prey animal, the horse’s eyes are eight times larger than a human’s eye; however, this makes them more vulnerable to injury and disease that may be catastrophic.  Horses develop many of the same eye problems as humans such as glaucoma, corneal ulcers, cataracts and other issues.   

The working of the eye 

Vision is provided by light entering the eye, which is made into an image by the brain through various complex biomechanical and physical processes.  

As light enters the eye, it is targeted to the retina by the cornea and the lens bending the light.  This light reaches the sensory tissue at the back of the eye.  In fact, the retina or nervous tunic is made of cells that are extensions of the brain coming off the optic nerve.  The retina consists of 2 types of photoreceptors called rods and cones.  The rod cells are more light-sensitive, thus providing night vision, whereas the cones are less light sensitive but provide visual acuity and the ability to see colour.  The optic disc in the retina does not contain photoreceptors and is the location the optic nerve leaves the eye to transmit the visual information to the visual cortex of the brain.   

Visual field of the horse 

Because the horse’s eyes are positioned on the side of the head, the range of vision is roughly 350 degrees, thus, allowing the horse to spot potential predators.  Due to the positioning of the eyes, the horse has two blind spots that include in front of the face and behind its head extending over its back and behind the tail.   

The horse has both binocular and monocular vision. Monocular vision means vision in one eye only and binocular vision means seeing with two eyes.  65 degrees of the 350 degree vision consists of binocular vision while the remaining 285 degrees is monocular vision.  As a result, the horse has a smaller field of depth perception compared to a human.  The horse must raise or lower its head in order to increase its range of binocular vision.  By introducing a bit and making the horse hold its head perpendicular to the ground, the binocular vision becomes less focused on distant objects and more focused on what is immediately in front of the horse.  Show jumpers and jump jockeys allow the horse to raise its head a few strides before a jump so that the horse can properly assess the jumps to allow appropriate take-off. 

Sensitivity to light 

Horses’ eyes have evolved to allow them to have good vision in dim light and due to this evolution they have better vision on slightly cloudy days compared to sunny, bright days.  There are two particular structures that allow them to have superior night vision, which include a high proportion of rods to cones (20:1) and the presence of the tapetum lucid.   

The horse’s large pupils allow a large amount of light to enter and the size of the retina allows a high number of cells to be involved in the capturing of light. In addition to the rods and cones, the horse's tapetum lucidum is a reflective structure in the back of the eye that bounces light back to the photoreceptors for a second time, thus further increasing the ability to capture more light.  Ultimately, this structure allows greater night vision.   

Interestingly, horses have also evolved structures to protect their eyes from photic damage during bright sunny days.  The pupil has the ability to significantly constrict in order to reduce the amount of light entering the eye.  In addition, there is a structure referred to as the corpora nigra, which is a bulbous structure extending from the iris into the space of the pupil that acts as a shade.    

Colour Vision 

Horses have dichromatic vision; therefore, they are not colour blind but they have a smaller spectrum than humans typically do.  Horse’s dichromatic vision means they see in the green-blue spectrum and the ocular variations based upon them.  They cannot distinguish red and are often thought to have a red-green colour blindness.  The horse’s colour vision must be taken into account when designing obstacles for horses to jump.   

Eyelids 

There are three layers to the eyelids that include a thin layer of skin covered in hair, a layer of muscles that allow the opening and closing of the eyelid and the palpebral conjunctiva, which lies against the eyeball.  The horse also has a third eyelid, also known as the nictitating membrane which has the function of protecting the cornea.   

Non-pigmented third eyelids are more susceptible both to solar-induced inflammation and to squamous cell carcinoma. Therefore, careful scrutiny of this structure is important.  Prominence of the third eyelid may be a result of inflammation caused by solar-induced inflammation or conjunctivitis (inflammation of the conjunctiva).  Inflammation and neoplasia should be differentiated on the basis of clinical appearance.  For example, squamous cell carcinoma has a plaque-like appearance and erosion. Conjunctivitis is the inflammation with thickening and reddening of the transparent membrane that lines the eyelid and eyeball.  Any suspected tumour should be excised and undergo histopathology to determine if it is indeed neoplasia or a type of inflammation.  Other neoplasia that may occur in the eyelids are melanomas or periocular sarcoids.   

Entropion is the inversion of the eyelid margin and lashes.  Often seen in foals as a consequence of either anatomical imperfection or of dehydration and debility, it is the inward rotation of the eyelid that leads to the rubbing of hair in the cornea leading to keratitis.  Later onset entropic is usually a consequence of a traumatic injury and can result if primary repair of an eyelid laceration has not been performed.   

Trauma to the eyelids may result in bruising or a laceration.  If bruising has occurred, a warm compress may be helpful if the horse will tolerate it.  If a laceration has occurred it should always be repaired. 

Lacrimal system  

The horse has a pair of nasolacrimal ducts that carry lacrimal secretions, commonly known as tears, from the eye to the nasal cavity.   

Keratoconjunctivitis sicca is a deficiency in the acqueous portion of the tear film and is relatively rare.  If it occurs, it is a result of damage to the facial nerves or direct damage to the lacrimal gland or duct. With the lack of tears the cornea appears dull and lacklustre and may lead to corneal ulceration.  It is often associated with a mucopurulent eye discharge as well as pain and inflammation.  This condition can be managed with regular cleaning and the application of a tear replacement solution.  

Acquired stenosis/occlusion of the lacrimal drainage system may be a consequence of infectious, trauma, neoplastic or inflammatory disease within the drainage system or external to it. It is often presented with epiphora (tear overflow) or a mucopurulent discharge if infection is involved.  Following treatment of the underlying cause, the goal is to re-establish the drainage system with flushing of the duct with saline solution, or a combination of steroid, antibiotic (if required) and saline solution.  

Conjunctiva/Sclera 

The sclera is the white of the eye which is the relatively tough outer layer of the eye and is covered by a thin mucous membrane, referred to as the conjunctiva, and runs from the edge of the cornea and covers the inside of the eyelid.  

Conjunctivitis is the inflammation and swelling of the conjunctiva and includes a primary conjunctivitis or a secondary conjunctivitis.  Primary conjunctivitis is inflammation caused directly by irritants, chemicals, toxins and bacteria.  However, conjunctivitis may be secondary to another ocular disease such as disorders of the lacrimal system, eyelid problems, and keratitis.  In addition, conjunctivitis may be a non-specific symptom of other systemic diseases such as a respiratory viral infection.  Conjunctivitis presents with a reddened inflamed conjunctiva with mould, purulent, serous or a combination of these discharges.  The horse will have discomfort of the eye with this ailment.   

Conjunctival foreign bodies are often acute and unilateral and caused by organic material resulting in excessive tearing, inflammation of the conjunctiva and ocular discomfort.   

Conjunctival neoplasia is most often a squamous cell carcinoma (SCC) as this tumour usually affects areas of epithelial transition such as the mucocutaneous junction of the eyelids.  The extent and appearance of the lesion is variable but SCC should always be considered especially in those horses lacking pigment in those areas. The symptoms range from mild ocular discomfort with discharge to plaque-like and cauliflower-like masses without ulceration.   

Cornea 

The cornea is the transparent front part of the eye that covers the iris, pupil and anterior chamber.  It is a domed-shaped structure that acts as the eye’s windshield protecting the eye from insult such as an infection.  Along with the tear film, it provides a proper anterior refractive surface for the eye, in fact, it contributes two-thirds of the refractive power of the eye.  Congenital problems of clinical significance are rare in horses but acquired corneal problems as a result of trauma are common in horses. 

Traumatic keratitis due to lacerations or penetrating injuries are common and in most cases involve full thickness penetration, acqueous loss and iris prolapse.  This condition presents with sudden and severe pain accompanied with excess tearing and blepharospasm (involuntary tight closure of the eyelids).  The extent of the damage to the cornea can be determined by the use of fluorescein dye.  If the wound is not repaired quickly then the iris may become incarcerated and the restoration of the normal eye anatomy is difficult.  

Abrasions to the surface of the cornea is a common condition seen by equine practitioners.  Some simple scratches heal quickly while others may become more complex, involving fungal or bacterial infections resulting in a protracted recovery. 

Corneal ulcers are a defect in the surface of the epithelium of the cornea that involves the underlying stroma.  They are often described as sores on the cornea.  It is important that they are diagnosed and treated promptly as there is potential that the horse’s vision may be affected. The clinical symptoms are often ocular discomfort with excessive tearing, squinting or blepharospasms. Discolouration and swelling of the cornea and the eventual development of blood vessels around the ulcer and an irregularity of the cornea. The depth of the ulcer must be established and it may range from superficial to deep.   

Liquefactive stromal necrosis (melting ulcers) are not an uncommon condition in the horse and may present acutely or as a progression from a corneal ulcer.  It should be deemed as an emergency because corneal perforation may result.  This disease may be accompanied by uveitis.   

Corneal foreign bodies are usually organic material and present with blepharospasm, excess tearing and pain.  Various illuminations, magnifications as ophthalmic stains may be used to identify it and aid in removal.  

Bacterial keratitis is often seen after a corneal injury especially if an ulcer is present. The horse will demonstrate acute eye pain with serous discharge that quickly becomes mucopurulent or purulent.  The clinical appearance is not usually diagnostic and cultures and scrapings should be taken from the edge of the ulcer. This procedure ensures the correct selection of treatment and pain relief.  

Mycotic keratitis is uncommon in the UK but with the changing climate it may become more prominent.  This type of keratitis is a result of fungal growth so tends to occur in climates supportive of this type of growth. Diagnosis is based on the history, clinical appearance and the demonstration of fungal hyphae and positive fungal culture. This disease may be a consequence of inappropriate drug therapy (such as corticosteroids) or from previous corneal trauma. Following the identification of the fungus, topical treatments can be used but may take weeks to months.  

Uveal Tract  

The uveal tract consists of three parts that include; The choroid which is the tissue layer filled with blood vessels; The ciliary body that is the ring of tissue containing muscles that change the shape of the lens as well as producing the clear fluid that fills the space between the cornea and the iris; The iris which is the coloured part of the eye.   

Persistent pupillary membranes are vascular arcades and developing tissue of the eye that fail to atrophy as the eye matures.  These are very common in horses and usually have no consequence and no treatment is needed.  

Cysts may arise in various parts of the uveal tract and are not uncommon in the horse.  Irrespective of their origin, they may vary between pigmented to unpigmented and are smooth, round and do not invade neighbouring tissue. No treatment is required except on rare occasions when they interfere with the horse’s vision.  

Neoplasia of the uvea is not common but may arise and are often melanomas that are locally invasive but without cellular malignancy. 

Trauma of the iris may result from direct trauma, or a secondary consequence of corneal perforation or a whiplash injury.  Any uveitis that is caused by trauma can be treated medically.  If there is an iris prolapse, then the iris is placed back into the anterior chamber provided they are not contaminated. Any foreign bodies must be removed and any hyphaema (bleeding in the anterior chamber between the cornea and iris) is usually left to be resorbed naturally. 

Uveitis is inflammation of the uveal tract and can cause eye pain and alterations in vision. There are many causes of uveitis that include trauma, lens-associated uveitis, general viral infections (such as equine viral arteritis) and bacterial disease (such as Rhodococcus equi in foals).  However, many situations of uveitis are an immune-mediated uveitis often referred to as equine recurrent uveitis (also known as moon blindness). Uveitis may present as an acute or a chronic condition. 

This disease can be treated medically often with the use of a sub-palpebral or nasolacrimal lavage system.  In addition, the patient should be placed in a quiet fly-free and dust-free environment.  

Lens 

The lens is a clear curved disk that sits behind the iris and in front of the vitreous of the eye, which bends light as it enters the eye to develop an image.  The horse’s lens is large and minor opacities associated with embryonic remnants are common.  

Cataracts are the most common lens abnormality to be encountered causing an opacity of the lens.  Cataracts may be acquired from trauma or post-inflammation situations.  However, cataracts may be congenital commonly seen in Arab and thoroughbred foals.   These opacities can be classified in various ways: 

Age of onset – juvenile, senile or congenital 

Cause - post inflammation (uveitis) or trauma   

Location – cortical, capsular, nuclear, polar, equatorial 

Stage of development – immature, mature, hypermature

Most cataracts cause no obvious visual deficits unless they are dense and obstruct the visual axis.  in which cataract surgery may be considered.  

Acqueous drainage 

The acqueous humor is a transparent water-like fluid similar to blood plasma but containing low protein levels. It is secreted from the ciliary body (a supporting structure of the lens) and fills both the anterior and posterior chamber of the eye.  

Glaucoma is a pathological elevation of the intraocular pressure resulting in the optic nerve becoming damaged . Primary glaucoma in horses is exceptionally rare while secondary glaucoma is uncommon but may occur after anterior segmental inflammation. Often there is little to no pain but an enlarged globe and raised intraocular pressure with the lack of pupillary light reflex may be seen.  Treatment may be attempted if the vision is present with various medications to reduce the intraocular pressure.  If the horse is blind it may be left without treatment. 

Conclusion

Good eye care is vital as the horse relies on its site to receive a great deal of information on its surrounding environment.  Even with the horse holding its head forward it has remarkable peripheral vision but the horse’s vision is a little blurrier and less colourful compared to humans.  In addition, both the strengths and weaknesses of the visual abilities of the horse must be seriously considered when looking at various techniques for training. 

Gut issue biomarkers and their use in signalling dysbiosis

Article by Jackie Zions

Gastrointestinal issues (GI) are the number one cause of morbidity in horses other than old age.   An unhealthy digestive system can cause poor performance, pain, discomfort, diarrhoea, and a whole host of issues that can sideline your horse.  It’s no wonder researchers are paying close attention to the ‘second brain’ and its billions of inhabitants.  Ontario Veterinary College (OVC) researcher, Dr. Luis Arroyo has been studying the equine gastrointestinal systems for many years with several research projects receiving funding from Equine Guelph.  Arroyo discusses what we know about equine gut health, causes of GI disorders and the extensive continuing research to understand what unstable and stable gut populations look like.

Starting with some basic anatomy Arroyo says, “The gastrointestinal tract of a horse is extremely large, and there are many things that can cause disturbances to the normal functioning or health of the gut.”  A healthy gut microbiome is essential for the horse’s entire body to function optimally.

Signs of GI issues

Common signs of disorders could include abdominal pain, bloating, changes in faecal consistency (including diarrhoea or constipation), excessive drooling, decrease in water consumption, lack of or poor appetite, weight loss and low body condition score.  

“Some cases are more obvious to owners,” says Arroyo, “like poor performance, or acute or chronic diarrhoea.” 

Changes of behaviour such as becoming cranky or moody can be tell-tale signs there is unrest in the GI system.  Biting at the flanks can signal abdominal pain as well as reactivity to being saddled.  When the horse stops wanting to perform and athletic abilities suddenly decline, if there is no obvious lameness, GI issues are high among the considerations.

“Horses are herbivores, designed to consume a diet of forage, and to break down complex sugars within that forage.” says Arroyo.  “The gut microbiota does this job and is very important for healthy digestion.”  Recent research is connecting the changes in diversity of microbial communities to conditions like colic, colitis, and gastric ulcers.

Causes of GI Issues

Colic is the number one clinical condition occurring in horses.  It is well-known that sudden dietary changes can be a major contributor as well as diets that are high in grain.  This can create changes in the volatile fatty acids produced in the GI system, which in turn can lead to the development of gas colic.  Arroyo provides the example of switching from dry hay fed in the winter, to rich, lush, spring grass as a big cause of rapid fermentation that can cause colic.  

Any abrupt change, even if it’s a good quality feed to a different good quality feed, can be a source of colic.  Then there is the more obvious consumption of mouldy, poor quality hay.  So not only the quality but the transition/adaptation period needs to be considered when making feed changes and this goes for both changes to forage or concentrates.

A table of feed transition periods on the Equine Guelph website states an adaptation period of at least 10 – 14 days is recommended.  Transition periods under seven days can increase colic risk over 22 times!  (https://www.equineguelph.ca/pdf/tools/How%20to%20Transition%20Feedstuff.pdf)

“Decrease in water consumption can be an issue, especially in countries with seasons,” says Arroyo.  When water gets really cold, horses often drink less, and if it freezes, they don’t drink at all, which can lead to impaction colic.   Parasite burden can also cause colic. If your horse lives in a sandy environment, like California, ingesting sand can cause impaction colic.  

Non-steroidal anti-inflammatory drugs (NSAIDS) can cause colic or ulcers. NSAIDS can interfere with blood supply to the GI tract causing ulceration, for example in the mucosa of the stomach. Prolonged use can cause quite severe ulceration.

NSAIDS are not the only drugs that can contribute to GI issues.  “Antibiotics - as the name says - kill many kinds of bacteria,” says Arroyo. “They are designed for that!  Invariably they deplete some bacterial populations including in the intestine, and that is a problem because that may allow some other bacteria, potentially pathogenic or harmful, to overgrow, and that can cause dysbiosis.”  
In a recent study, by fellow OVC researcher, Dr. Gomez and co-workers, it was determined that damage to the intestinal microbiota could occur after only 5 days of administering antibiotics to horses.  Damage to the intestinal microbiota resembled dysbiosis that can potentially result in intestinal inflammation and colitis predisposing the horse to diarrhoea.  Judicious use of antibiotics and antimicrobials are advised.

There are infectious and non-infectious causes of colitis.  Infectious examples include salmonella and then there is Neorickettsia risticii, which if ingested from contaminated sources, can cause Salmonellosis or Potomac horse fever, respectively.

“Any stress factors such as transportation, fasting or intense exercise like racing, can be a factor for developing stomach ulcers,” says Arroyo.  

Current Diagnostics

Putting together a picture of the horse’s health status includes gathering clinical history from the horse owner and performing a physical examination for motility and hydration status. A biochemistry profile and complete set count can be gathered from blood testing.

Gastric ultrasound allows veterinarians to view the wall of the intestine, noting if it has thickened or distended, which could occur in cases when there is colic.  They can assess appearance and find out if the intestine is displaced or if there is a twist.  Gastroscopy is commonly used to find ulcers in the stomach and can reach as far as the first part of the duodenum. 

GI Research

“DNA sequencing has been a breakthrough in science in terms of understanding the communities of different microorganisms living in many different niches from the skin to the lungs to the upper airways to the intestine,”  says Arroyo.

It has allowed in-depth study of the population of microorganisms, providing a big picture of the different inhabitants in various areas of the GI tract, such as the lumen of the small intestine and the small and large colon.  “The microorganisms vary, and they have different functions in each compartment,” says Arroyo.  

DNA sequencing has allowed researchers to study microbial populations and gather information on what happens to bacterial communities when impacted by diseases like colitis.  “We can see who is down, and who is up,” explains Arroyo, “and determine what populations have been depleted.”  It has led to a better knowledge of which of the billions of factors are harmful to the system and which can compromise the health of the horse.

Robo-gut is one example of a fantastic system where bacterial communities are being replicated in the lab to mimic what would be found in a natural environment.  

Researchers at the University of Guelph have measured metabolic profiles of the bacterial population after the addition of supplements like probiotics and prebiotics.  They found they can dramatically change the metabolites that are being produced, according to what is being added to the system.

Exciting new research that could impact the future of diagnostics includes screening for biomarkers as indicators of intestinal health among equine microbiota.  Dr. Arroyo is currently working with research partner, Dr. Marcio Costa, from the University of Montreal, looking for biomarkers that indicate changes in the inhabitants of the equine gut that take place during the early onset of illness.

“A biomarker is a biological molecule that you can find in different places,” explains Arroyo.  “For example, you might find them in tissue, blood, urine, or different body fluids.  They can signal normal or abnormal processes or could reveal a marker of a disease.  For example, a biomarker can be used to see how well the body might respond to a treatment or to a disease condition.”

“The objective of a dysbiosis index is quantifying ‘X’ number of certain bacteria that are important to us,” says Arroyo.  In this case, the dysbiosis derives from sequencing of the bacterial population in faecal samples.  

Changes in the intestinal microbiota (dysbiosis) are present before and during the outset of diseases and after treatment with antibiotics.  Arroyo cites the example of decreased Lachnospiraceae commonly observed when there is intestinal inflammation.  

Bacterial biomarkers are currently being used in other species to accurately predict intestinal dysbiosis, for example in cats and dogs.  One canine study quantified the number of seven different taxa of importance of the total bacterial populations.  This information is entered into a mathematical algorithm that comes up with results explaining which bacteria have increased or decreased.  Based on those numbers, one can use a more specific taxa to identify dysbiosis.  In a feline study, it was discovered that six bacterial taxa could be accurately used to predict diarrhoea in 83% of cases.

It is hoped the same results could be accomplished for horses.  Developing PCR testing to screen for biomarkers could be a game changer that could potentially provide speedy, economical early diagnostics and early treatment.

So far, the most remarkable finding in the preliminary data reveals that in horses with colitis, the whole bacterial population is very depleted.

“At this stage we are in the process of increasing our numbers to find significant differences in which bacterial taxa are more important,” says Arroyo.  “Soon we hope to share which bacteria taxa are more promising for predicting dysbiosis in horses with gastrointestinal disease.”

The researchers are delving into a huge biobank of samples to identify potential markers of intestinal dysbiosis in horses, utilising PCR testing as a faster and more economical alternative to the complex DNA sequencing technologies that have been used to characterise changes in microbiota thus far.  The goal is to develop simple and reliable testing that veterinarians can take right to the barn that will result in early treatment and allow closer monitoring of horses at the first onset of GI disease.

Top Tips to Protect Digestive Health

1. Horses are hind gut fermenters who rely on adequate amounts of fibre in the diet to maintain healthy gut function.

2. Make dietary changes slowly as abrupt changes disrupt the microbiota.

3. Avoid large grain meals as huge portions of highly fermentable diets can be quite harmful to the microbiota and can also be a source of risk for developing gastric ulcers.  Opt to spread out concentrates into several smaller rations.

4. Prevent long periods of fasting which can also lead to ulcers.  Horses are continuous-grazers, and they need to have small amounts of feed working through their digestive system to keep it functioning optimally.

5. Have a parasite prevention programme.

6. Provide fresh water 24/7 to maintain good hydration and keep contents moving smoothly through the GI tract.

7. Keep up to date on dental appointments. 

8. Motion is lotion – turn out and exercise are extremely important to gut function.
   

In closing, Arroyo states, “These top tips will help keep the horse happy and the gastrointestinal tract functioning properly.”

The importance of good hoof balance to improve performance

The equine foot is a unique structure and a remarkable feat of natural engineering that follows the laws of biomechanics in order to efficiently and effectively disperse concussional forces that occur during the locomotion of the horse.  Hoof balance has been a term used by veterinarians and farriers to describe the ideal conformation, size and shape of the hoof relative to the limb.  

Before horses were domesticated, they evolved and adapted to survive without any human intervention. With respect to their hoof maintenance, excess hoof growth was worn away due to the varied terrain in their habitat.  No trimming and shoeing were required as the hoof was kept at a healthy length.

With the domestication of the horse and our continued breeding to achieve satisfactory performance and temperament, the need to manage the horse’s hoof became essential in order to ensure soundness and performance.  The horse’s foot has evolved to ensure the health and soundness of the horse; therefore, every structure of the foot has an essential role and purpose. A strong working knowledge of the biology and biomechanics of the horse’s foot is essential for the veterinarian and farrier to implement appropriate farriery.  It was soon concluded that a well-balanced foot, which entails symmetry in shape and size, is essential to achieve a sound and healthy horse.  

Anatomy and function of the foot

The equine foot is extremely complex and consists of many parts that work simultaneously allowing the horse to be sound and cope with the various terrains and disciplines.    Considering the size and weight of the horse relative to the size of the hoof, it is remarkable what nature has engineered.  Being a small structure, the hooves can support so much weight and endure a great deal of force.  At walk, the horse places ½ of its body weight through its limbs and 2 ½ its weight when galloping.  The structure of the equine foot provides protection, weight bearing, traction, and concussional absorption.  Well-balanced feet efficiently and effectively use all of the structures of the foot to disperse the forces of locomotion. In order to keep those feet healthy for a sound horse, understanding the anatomy is paramount.   

The foot consists of the distal end of the second phalanx (short pastern), the distal phalanx (pedal bone, coffin bone) and the navicular bone.  The distal interphalangeal joint (coffin joint) is found between the pedal and short pastern bone and includes the navicular bone with the deep digital flexor tendon supporting this joint.  This coffin joint is the centre of articulation over which the entire limb rotates.  The navicular bone and bursa sits behind the coffin bone and is stabilised by multiple small ligaments. The navicular bone allows the deep digital flexor tendon to run smoothly and change direction in order to insert into the coffin bone.   The navicular bursa is a fluid-filled sac that sits between the navicular bone and the deep digital flexor tendon.

The hoof complex can be divided into the epidermal weight-bearing structures that include the sole, frog, heel, bulbs, bars, and hoof wall and the anti-concussive structures that include the digital cushion, lamina, deep digital flexor tendons, and ungual (lateral) cartilage.  The hoof wall encloses the dermal structures with its thickest part at the toe that decreases in thickness as it approaches the heel.  The hoof wall is composed of viscoelastic material that allows it to deform and return its shape in order to absorb concussional forces of movement.  There is enough deformation to diminish the force from the impact and load of the foot while preventing any damage to the internal structures of the foot and limb.  As load is placed on the foot, there is deformation that consists of:

• Expansion of the heels

• Sinking of the heels

• Inward movement of the dorsal wall

• Biaxial compression of the dorsal wall

• Depression of the coronary band

• Flattening of the sole

The hoof wall, bars and their association with the sole form the heel base with the purposes of providing traction, bearing the horse’s weight while allowing the stability and flexibility for the expansion of the hoof capsule that dissipates concussional forces on foot fall.  The sole is a highly keratinised structure like the hoof wall but made up of nearly 33% water so it is softer than the hoof wall and should be concave to allow the flattening of the sole on load application. The frog and heel bulbs serve a variety of special functions ranging from traction, protection, coordination, proprioception, shock absorption and the circulation of blood.  

When the foot lands on the ground, the elastic, blood-filled frog helps disperse some of the force away from the bones and joints, thus, acting as a shock absorber.  The venous plexus above the frog is involved in pumping blood from the foot back to the heart when the foot is loaded.  In addition, there is shielding of the deep digital flexor tendon and the sensitive digital cushion (soft tissue beneath the sole that separates the frog and the heel bulb from the underlying tendons and bones).  Like the heel bulbs, the frog has many sensory nerve endings allowing the horse to be aware of where his body and feet are and allows the horse to alter landing according to the condition of the ground (proprioception and coordination).  

The soft tissue structures comprise and form the palmar/plantar aspect of the foot.  The digital cushion lies between the lateral cartilages and above the frog and bars of the horse’s hoof.  This structure is composed of collagen, fibrocartilage, adipose tissue and elastic fibre bundles.  The digital cushion plays a role in shock absorption when the foot is loaded as well as a blood pumping mechanism.  Interestingly, it has been found that the digital cushion composition varies across and within breeds.  It is thought the variation of the composition of the digital cushion is partially dictated by a genetic predisposition.  In addition, the composition of the digital cushion changes with age.  As the horse ages the composition alters from elastic, fat and isolated collagen bundles to a stronger fibrocartilage.  Finally, the digital cushion and connective tissue within the foot have the ability to adapt to various external stimuli such as ground contact or body weight.   The lateral cartilage is a flexible sheet of fibrocartilage that suspends the pedal bone as well as acting as a spring to store and release energy. The lamina is a highly critical structure for hoof health.  The lamina lies between the hoof wall and the coffin bone.  There are two types of lamina known as the sensitive (dermal) lamina and insensitive (epidermal) lamina.  The insensitive lamina coming in from the hoof wall connects to the sensitive lamina layer that is attached to the coffin bone and these two types of lamina interdigitate with each other to form a bond.

Hoof and Musculoskeletal System

The hoof and the musculoskeletal system are closely linked and this is particularly observed in the posture of the horse when resting or moving.  Hoof shape and size and whether they are balanced directly affects the posture of the horse.  Ultimately, this posture will also affect the loads placed on the skeletal system, which affects bone remodelling. With an imbalance, bone pathologies of the limbs, spine and pelvis may occur such as osteoarthritis.  In addition, foot imbalances result in postural changes that lead to stress to the soft tissue structures that may lead to muscle injuries and/or tendon/ligament injuries.  

Conformation and hoof balance 

The terms balance and conformation are used frequently and used to describe the shape and size of the limb as a whole as well as the individual components of the limb and the spatial relations between them.  Balance is the term often used to describe the foot and can be viewed as a subset of conformation.  

Conformation should be considered when describing the static relations within the limb and excludes the foot.  Balance should be considered when describing the dynamic and static relationship between the horse’s foot and the ground and limb as well as within the hoof itself.  

These distinctions between conformation and balance are important to assess lameness and performance of the horse.  Additionally, this allows the veterinarian and farrier to find optimal balance for any given conformation.

The term hoof balance does lack an intrinsic definition.  The use of certain principles in order to define hoof balance, which in turn can be extended to have consistent evaluation of hoof balance as well as guide the trimming and shoeing regimens for each individual horse.  In addition, these principles can be used to improve hoof capsule distortion, modify hoof conformation and alter landing patterns of the foot.  These principles are:

• Evaluate hoof-pastern axis

• Evaluate centre of articulation

• The need for the heels to extend to the base of the frog

Assessing the horse’s foot balance by observing both static (geometric) balance and dynamic balance is vital.   Static balance is the balance of the foot as it sits on a level, clean, hard surface.  Dynamic balance is assessing the foot balance as the foot is in motion.  However, horses normally do not resemble the textbook examples of perfect conformation, which creates challenges for the farriers and veterinary surgeons.  The veterinarian should instigate further evaluation of the foot balance and any other ailments, in order to provide information that can be used by the farrier and veterinarian in formulating a strategy to help with the horse’s foot balance. With the farrier and veterinarian working cooperatively, the assessment of the hoof balance and shoeing of the foot should deliver a harmonious relationship between the horse’s limb, the hoof and the shoe.  

Dynamic Balance

The horse should be assessed in motion as one can observe the foot landing and placement.  A balanced foot when in motion should land symmetrically and flat when moving on a flat surface.  When viewed from the side, the heels and toe should land concurrently (flat foot landing) or even a slight heel first landing.  It is undesirable to have the toe landing first and often suggests pain localised to the heel region of the foot.  When observing the horse from the front and behind, both heel bulbs should land at the same time.  Sometimes, horses will land first slightly on the outside or lateral heel bulb of the foot but rarely will a horse land normally on the medial (inside) of the foot.  If the horse has no conformational abnormalities or pathologies the static balance will achieve the dynamic balance.  

Static Balance 

Hoof –pastern axis (HPA)

The hoof pastern axis (HPA) is a helpful guideline in assessing foot balance. With the horse standing square on a hard, level surface, a line drawn through the pastern and hoof should be parallel to the dorsal hoof wall and should be straight (unbroken).  The heel and toe angle should be within 5 degrees of each other. An underrun heel has been defined as the angle of the heel being 5 degrees less than the toe angle. The heel wall length should be roughly 1/3 of the dorsal wall.  In addition, the cannon (metacarpus/metatarsus) bone is perpendicular to the ground and when observed from the lateral side, the HPA should be a straight line.  When assessing the foot from the side, the dorsal hoof wall should be aligned with the pastern.  The optimal angle of the dorsal hoof wall is often cited as being 50-54°.  The length of the dorsal hoof wall is variable but guidelines have been suggested according to the weight of the horse. 

It is not uncommon that the hind feet are more upright compared to the fore feet at approximately 5 degrees.  A broken hoof-pastern axis is the most common hoof imbalance.  There are two presentations of a broken HPA known as a broken-back HPA and a broken-forward HPA.  These changes in HPA are often associated with two common hoof capsule distortions that include low or underrun heels and the upright or clubfoot, respectively.    

A broken-back hoof-pastern axis occurs when the angle of the dorsal hoof wall is lower than the angle of the dorsal pastern.  This presentation is commonly caused by low or underrun heel foot conformation accompanied with a long toe.  This foot imbalance is common and often thought to be normal with one study finding it present in 52% of the horse population.  With a low hoof angle, there is an extension of the coffin and pastern joints resulting in a delayed breakover and the heels bearing more of the horse's weight, which ultimately leads to excess stress in the deep digital flexor tendon as well as the structures around the navicular region including the bone itself.  

This leads to caudal foot pain so the horse lands toe first causing subsolar bruising.  In addition, this foot imbalance can contribute to chronic heel pain (bruising), quarter and heel cracks, coffin joint inflammation and caudal foot pain (navicular syndrome).   The cause of underrun heels is multifactorial with a possibility of a genetic predisposition where they may have or may acquire the same foot conformation as the parents.  There are also environmental factors such as excessive dryness or moisture that may lead to the imbalance.

A broken-forward hoof-pastern axis occurs at a high hoof angle with the angle of the dorsal hoof wall being higher than the dorsal pastern angle.  One can distinguish between a broken-forward HPA and a clubfoot with the use of radiographs.  With this foot imbalance, the heels grow long, which causes the bypassing of the soft tissue structures in the palmar/plantar area of the foot and leads to greater concussional forces on the bone.  This foot imbalance promotes the landing of the toe first and leads to coffin joint flexion as well as increases heel pressure.  The resulting pathologies that may occur are solar bruising, increased strain of the suspensory ligaments near the navicular bone and coffin joint inflammation.

Center of articulation

When the limb is viewed laterally, the centre of articulation is determined with a vertical line drawn from the centre of the lateral condyle of the short pastern to the ground.  This line should bisect the middle of the foot at the widest part of the foot and demonstrates the centre of articulation of the coffin joint.  The widest part of the foot (colloquially known as “Ducketts Bridge”) is the one point on the sole that remains constant despite the shape and size of the foot.  The distance and force on either side of the line drawn through the widest part of the foot should be equal, which provides biomechanical efficiency.    

Heels extending to the base of the frog

With respect to hoof balance, another component of the foot to assess is that the heels of the hoof capsule extend to the base of the frog.  The hoof capsule consists of the pedal bone occupying two-thirds of the space and one-third of the space is soft tissue structures. This area is involved in dissipating the concussional and loading forces and in order to ensure biomechanical efficiency both the bone and soft-tissue structures need to be enclosed in the hoof capsule in the same plane. 

To achieve this goal the hoof wall at the heels must extend to the base of the frog.  If the heels are allowed to migrate toward the centre of the foot or left too long then the function of the soft tissue structures have been transferred to the bones, which is undesirable.  If there is a limited amount to trim in the heels or a small amount of soft tissue mass is present in the palmar foot then some form of farriery is needed to extend the base of the frog (such as an extension of the branch of a shoe).    

Medio-lateral or latero-medial balance 

The medio-lateral balance is assessed by viewing the foot from the front and behind as well as from above with the foot raised.   To determine if the foot has medio-lateral balance, the hoof should be bisected or a line is drawn down the middle of the pastern down to the point of the toe.  

You should be able to visualise the same amount of hoof on both the left and right of that midline.  In addition, one should observe the same angle to the side of the hoof wall.  It is important to pick up the foot and look at the bottom.  Draw a line from the middle quarter (widest part of foot) on one side to the other then draw a line from the middle of the toe to the middle sulcus of the frog.  

This provides four quadrants with all quadrants being relatively the same in size (Proportions between 40/60 to 60/40 have been described as acceptable for the barefoot and are dependent on the hoof slope).  The frog width should be 50-60% of its length with a wide and shallow central sulcus.  The frog should be thick enough to be a part of the bearing surface of the foot.  The bars should be straight and not fold to the mid frog.  The sole should be concave and the intersection point of both lines should be the area of optimal biomechanical efficiency.  

The less concavity means the bone is nearer to the ground, thus, bearing greater concussional force.  Finally, assess the lateral and medial heel length.  Look down at the heel to determine the balance in the length of both heel bulbs.  Each heel bulb should be the same size and height.  If there are any irregularities with the heel bulbs then sheared heels may result, which is a painful condition.  Medio-lateral foot imbalance results in the uneven loading of the foot that leads to an accumulation of damage to the structures of the foot ultimately causing inflammation, pain, injury and lameness.   Soles vary in thickness but a uniform sole depth of 15mm is believed to be the minimum necessary for protection.  

Dorso-palmar/plantar (front to back – DP) balance

Refers to the overall hoof angle and the alignment of the hoof angle with the pastern angle when the cannon bone is perpendicular to the ground surface.  When assessing the foot from the side, the dorsal hoof wall should be aligned with the pastern.  The optimal angle of the dorsal hoof wall is often cited as being 50-54°.  The length of the dorsal hoof wall is variable but guidelines have been suggested according to the weight of the horse. 

The heel and toe angle should be within 5 degrees of each other. An underrun heel has been defined as the angle of the heel being 5 degrees less than the toe angle. The heel wall length should be roughly 1/3 of the dorsal wall.  

A line dropped from the first third of the coronet should bisect the base.  A vertical line that bisects the 3rd metacarpal bone should intersect the ground at the palmar aspect of the heels.

Radiographs

A useful way to assess trimming and foot balance is by having foot x-rays performed.  Radiography is the only thorough and conclusive method that allows one to determine if the foot is not balanced and the bony column (HPA) is aligned. 

Shoes should be removed and the foot cleaned before radiographs are executed.  The horse is often placed on foot blocks to elevate the feet off the ground so that the foot can be centred in the cassette and x-ray beam.  

Latero-medial view – The side view of the foot allows one to assess the dorsal and palmar aspects of the pedal bone as well as the navicular bone.  The horse should be standing squarely on a flat, level surface.  This projection is useful in determining the point of breakover and the hoof pastern axis should be parallel with the hoof wall.  The lateral view will demonstrate the length of the toe and the alignment of the dorsal surface of the pedal bone with the hoof wall, which should be parallel.  This view also allows one to determine the depth of the sole and inadequate solar depth is usually accompanied with excessive toe length (broken-back HPA). One may observe a clubfoot, broken forward.  

One can distinguish between a clubfoot and a broken-forward HPA with radiographs.  The broken-forward HPA the hoof angle of the heel is greater than the angle of the dorsal hoof wall.  The clubfoot also demonstrates these steep/high hoof angles but additionally the alignment of the coffin, short and long pastern bones are broken forward.

Dorsopalmar/plantar views - this “front to back” view is also performed with the horse standing squarely on 2 positioning blocks.  This projection allows the evaluation of medial to lateral balance and conformation of the foot with observation and measurement of the medial and lateral wall length and angle.  Horses with satisfactory conformation present with a parallel joint surface of the pedal bone to the ground.  The coffin joint should be even across its width.  In addition, the lateral and medial coronet and the lateral and medial walls are of equal thickness and the distance from the lateral and medial solar margins to the ground are similar. 

With foot imbalance, this author has observed that fore feet may have a higher lateral hoof wall, whereas, the hind feet may have a higher medial hoof wall.  It is worth noting that the pelvis, stifle and hocks are adapted to move laterally allowing a slight rotating action as it moves.  This action may cause uneven wear or poor trimming and shoeing may cause this limb movement to be out of line.  

Trimming

Often, trimming and shoeing are based on empirical experience that includes theoretical assumptions and aesthetic decisions.   The goals of trimming and shoeing are to facilitate breakover, ensure solar protection and provide heel support.  Trimming is the most important aspect of farriery because it creates the base to which a shoe is fitted.  Hoof conformation takes into account the function and shape of the foot in relation to the ground and lower limb both at rest and exercise.  Each individual foot should have a conformation that provides protection and strength while maximising biomechanical efficiency often viewed as foot balance. 

An important question that initially needs to be addressed is whether the horse requires shoes or not.  The answer does depend on what type of work the horse performs, what is the amount of workload, the conformation of the horse (especially the limbs and foot) and are there any previous or current injuries.  It must be stressed that the most important aspect, whether the horse is shod or not, is that the trim ensures an appropriately balanced foot for the horse. If there is poor trimming then this may lead to uneven and increased workload on the limb leading to an increased strain of the hoof and soft tissues (i.e. ligaments, tendons) that increase the risk of injury and developing acute and chronic lameness. 

The foot can be evaluated, trimmed and/or shod in a consistent, reproducible manner that considers:

Hoof-pastern axis (HPA)

The centre of articulation

Heels extending to the base of the frog

Appropriate trimming and shoeing to ensure the base of the foot is under the lateral cartilage; therefore, maximising the use of the digital cushion, can help in creating a highly effective haemodynamic mechanism.  Shoeing must be done that allows full functionality of the foot so that load and concessional forces are dissipated effectively.  

To implement appropriate farriery, initially observe the horse standing square on a hard service to confirm that the HPA is parallel.  If The HPA is broken forward or backward then these balances should be part of the trimming plan.  To determine the location of the centre of rotation, palpate the dorsal and palmar aspect of the short pastern just above the coronary band and a line dropped vertically from the centre of that line should correlate with the widest part of the foot. 

Shoeing

When the shoe is placed on the horse, the horse is no longer standing on its feet but on the shoe; therefore, shoeing is an extension of the trim.  The shoe must complement  the trim and must have the same biomechanical landmarks to ensure good foot balance.  It is this author’s view that the shoe should be the lightest and simplest possible.  The shoe must be placed central to the widest part of the foot and the distance from the breakover point to the widest part of the foot should be equal to the distance between the widest part of the foot and the heel. 

It has been shown that the use of shoes that lift the sole, frog and bars can reduce the efficient workings of the caudal foot and may lead to the prevalence of weak feet.  A study by Roepstorff demonstrated there was a reduced expansion and contraction of the shod foot but improved functionality of solar and frog support.   With this information, appropriate shoeing should allow increased functionality of the digital cushion, frog and bars of the foot, which improves the morphology and health of the hoof and reduces the risk of exceeding the hoof elasticity.  

Disease associated with hoof imbalance

Foot imbalance can lead to multiple ailments and pathologies in the horse.  It must be noted that the pathologies that may result are not necessarily exclusive for the foot but may expand to other components to the horse’s musculoskeletal system.  In addition, not one but multiple pathologies may result.  Diseases that may result from hoof imbalance are:

Conclusion

Foot balance is essential for your horse to lead a healthy and sound life and career. With a strong understanding of the horse anatomy and how foot imbalance can lead to lameness as well as other musculoskeletal ailments, one can work to assess and alter foot balance in order to ensure optimal performance and wellbeing of the horse.  It is essential that there is a team approach involving all stakeholders as well as the veterinarian and farrier in order to achieve foot balance. With focus on foot balance, one can make a good horse into a great horse.

Stem Cell Therapy - the improved diagnostics available to treat lameness

Article by Jackie Zions (interviewing Dr. Koenig)

Prevention is the ideal when it comes to lameness, but practically everyone who has owned horses has dealt with a lay-up due to an unforeseen injury at some point. The following article will provide tools to sharpen your eye for detecting lameness, review prevention tips and discuss the importance of early intervention. It will also begin with a glimpse into current research endeavouring to heal tendon injuries faster, which has obvious horse welfare benefits and supports horse owners eager to return to their training programs. Dr. Judith Koenig of Ontario Veterinary College (OVC) spends half of her time as a surgeon and teacher with a strong interest in equine sports medicine and rehabilitation, and the other half as a researcher at the OVC.

Lameness is a huge focus for Koenig, whose main interest is in tissue healing. “I think over the past 20 or 30 years we have become very, very good at diagnosing the cause of lameness,” says Koenig. “In the past, we had only radiographs and ultrasound as a diagnostic tool, but by now most referral centres also have MRI available; and that allows us to diagnose joint disease or tendon disease even more. We are much better now [at] finding causes that previously may have been missed with ultrasound.” 
Improvements in diagnostics have resulted in increased ability to target treatment plans. With all the different biologics on the market today, Koenig sees a shift in the management of joint disease with more people getting away from steroids as a treatment.

The following list is excerpted from Equine Guelph’s short course on lameness offered on TheHorsePortal.ca. It outlines the different diagnostics available:

When asked for the latest news on research she has been involved in, Koenig proclaims, “I'm most excited about the fact that horses are responding well to stem cell treatment—better than I have seen any response to any other drug we have tried so far!”

Koenig has investigated the use of many different modalities to see if they accelerate tissue healing and has studied which cellular pathways are affected. Two recent collaborative studies have produced very exciting findings, revealing future promise for treating equine osteoarthritis with stem cell therapy.  

In a safety study, Koenig and her team at the Ontario Veterinary College have shown equine pooled cryopreserved umbilical cord blood, (eCB) MSC, to be safe and effective in treatment of osteoarthritis.  

“These cells are the ones harvested from umbilical cord blood at the time of foaling and then that blood is taken to the lab and the stem cells are isolated out of it,” explains Koenig. The stem cells are then put through a variety of tests to make sure they are free of infectious diseases. Once given a clean bill of health, they are expanded and frozen. 
The stem cells harvested from multiple donors of equine umbilical cord blood [eCB, (kindly provided by eQcell), MSC] were compared to saline injections in research horses. “This type of cells is much more practical if you have a cell bank,” says Koenig. “You can treat more horses with it, and it’s off the shelf.” There were no systemic reactions in the safety study. Research has also shown no different reactions from sourcing from one donor or multiple donors.  

In the second study, 10 million stem cells per vial were frozen for use in healing OA from fetlock chips in horses that were previously conditioned to be fit. After the fetlock chip was created, exercise commenced for six more weeks, and then osteoarthritis was evaluated by MRI for a baseline. Half the horses were treated with the pooled MSC stem cells, and the control group received saline before another month of exercise. Then MRI and lameness exams were repeated, and arthroscopy was repeated to score the cartilage and remove the chip.

Lameness was decreased and cartilage scores were improved in the group that received stem cell therapy at the time of the second look with arthroscopy.

Many diagnostics were utilised during this study. MRIs, X-rays, ultrasounds and weekly lameness evaluations all revealed signs of osteoarthritis in fetlock joints improved in the group treated with (eCB) MSCs. After six weeks of treatment, the arthroscopic score was significantly lower (better cartilage) in the MSC group compared to the control group. 

“Using the MRI, we can also see a difference that the horses treated with stem cells had less progression of osteoarthritis, which I think is awesome,” says Koenig. “They were less lame when exercised after the stem cell therapy than the horses that received saline.”

This research group also just completed a clinical trial in client-owned horses diagnosed with fetlock injuries with mild to moderate osteoarthritis changes. The horses were given either 10 million or 20 million stem cells and rechecked three weeks and six weeks after the treatment. Upon re-evaluation, the grade of lameness improved in all the horses by at least one. Only two horses presented a mild transient reaction, which dissipated after 48 hours without any need for antibiotics. The horse’s joints looked normal, with any filling in the joint reduced.
There was no difference in the 18 horses, with nine given 10 million stem cells and the other nine 20 million stem cells; so in the next clinical trial, 10 million stem cells will be used.

The research team is very happy with the results of this first-of-its-kind trial, proving that umbilical cord blood stem cells stopped the progression of osteoarthritis and that the cartilage looked better in the horses that received treatment. The future of stem cell therapy is quite promising!
Rehabilitation
Research has shown adhering to a veterinary-prescribed rehabilitation protocol results in a far better outcome than paddock turn out alone. It is beneficial for tendon healing to have a certain amount of controlled stimulation. “These horses have a much better outcome than the horses that are treated with just being turned out in a paddock for half a year,” emphasises Koenig. “They do much better if they follow an exercise program. Of course, it is important not to overdo it.”

For example, Koenig cautions against skipping hand-walking if it has been advised.  It can be so integral to stimulating healing, as proven in recent clinical trials. “The people that followed the rehab instructions together with the stem cell treatment in our last study—those horses all returned to racing,” said Koenig.  

“It is super important to follow the rehab instructions when it comes to how long to rest and not to start back too early.”

Another concern when rehabilitating an injured horse would be administering any home remedies that you haven't discussed with your veterinarian. Examples included blistering an area that is actively healing or applying  shockwave to mask pain and then commence exercise.

Prevention and Training Tips
While stating there are many methods and opinions when it comes to training horses, Koenig offered a few common subjects backed by research. The first being the importance of daily turnout for young developing horses.  

Turnout and exercise
Many studies have looked at the quality of cartilage in young horses with ample access to turn out versus those without. It has been determined that young horses that lack exercise and are kept in a stall have very poor quality cartilage.
Horses that are started early with light exercise (like trotting short distances and a bit of hill work) and that have access to daily paddock turnout, had much better quality of cartilage. Koenig cited research from Dr. Pieter Brama and similar research groups.

Another study shows that muscle and tendon development depend greatly on low grade exercise in young horses.  Evaluations at 18 months of age found that the group that had paddock turnout and a little bit of exercise such as running up and down hills had better quality cartilage, tendon and muscle.  

Koenig provides a human comparison, with the example of people that recover quicker from injury when they have been active as teenagers and undergone some beneficial conditioning. The inference can be made that horses developing cardiovascular fitness at a young age stand to benefit their whole lives from the early muscle development.

Koenig says it takes six weeks to regain muscle strength after injury, but anywhere from four to six months for bone to develop strength. It needs to be repeatedly loaded, but one should not do anything too crazy! Gradual introduction of exercise is the rule of thumb.

Rest and Recovery
“Ideally they have two rest days a week, but one rest day a week as a minimum,” says Koenig. “I cannot stress enough the importance of periods of rest after strenuous work, and if you notice any type of filling in the joints after workout, you should definitely rest the horse for a couple of days and apply ice to any structures that are filled or tendons or muscles that are hard.” 

Not purporting to be a trainer, Koenig does state that two speed workouts a week would be a maximum to allow for proper recovery. You will also want to make sure they have enough access to salt/electrolytes and water after training.

During a post-Covid interview, Koenig imparted important advice for bringing horses back into work methodically when they have experienced significant time off.
“You need to allow at least a six-week training period for the athletes to be slowly brought back and build up muscle mass and cardiovascular fitness,” says Koenig.  “Both stamina and muscle mass need to be retrained.”

Watch video: “Lameness research - What precautions do you take to start training after time off?” https://www.youtube.com/watch?v=zNHba_nXi2k

The importance was stressed to check the horse’s legs for heat and swelling before and after every ride and to always pick out the feet. A good period of walking is required in the warmup and cool down; and riders need to pay attention to soundness in the walk before commencing their work out.

Footing and Cross Training
With a European background, Koenig is no stranger to the varying track surfaces used in their training programs. Statistics suggest fewer injuries with horses that are running on turf. 

Working on hard track surfaces has been known to increase the chance of injury, but delving into footing is beyond the scope of this article.

“Cross training is very important,” says Koenig. “It is critical for the mental and proper musculoskeletal development of the athlete to have for every three training days a day off, or even better provide cross-training like trail riding on these days." 

Cross-training can mitigate overtraining, giving the body and mind a mental break from intense training. It can increase motivation and also musculoskeletal strength. Varied loading from training on different terrain at different gaits means bone and muscle will be loaded differently, therefore reducing repetitive strain that can cause lameness.

Hoof care
Whether it is a horse coming back from injury, or a young horse beginning training, a proficient farrier is indispensable to ensure proper balance when trimming the feet. In fact, balancing the hoof right from the start is paramount because if they have some conformational abnormalities, like abnormal angles, they tend to load one side of their joint or bone more than the other. This predisposes them to potentially losing bone elasticity on the side they load more because the bone will lay down more calcium on that side, trying to make it stronger; but it actually makes the bone plate under the cartilage brittle.  

Koenig could not overstate the importance of excellent hoof care when it comes to joint health and advises strongly to invest in a good blacksmith. Many conformational issues can be averted by having a skilled farrier right from the time they are foals. Of course, it would be remiss not to mention that prevention truly begins with nutrition. “It starts with how the broodmare is fed to prevent development of orthopaedic disease,” says Koenig. Consulting with an equine nutritionist certainly plays a role in healthy bone development and keeping horses sound.

Lower limb anatomy and how it can be conditioned for racing

Article by Adam Jackson MRCVS 

Better understanding the appropriate levels of exercise and training while the horse’s body grows and develops has been a topic of research for many years. Although it has been shown that young, growing horses are well-suited to adapt to conditioning, it is vital that continued research is performed in order to develop thoughtful and strategic training methods to promote healthy, fit and sound horses with long careers and lives.  

Horses’ limbs consist of dozens of muscles, bones, tendons, ligaments, and joints that allow the horse to move as well as support its body weight. The limbs function to provide thrust and movement while absorbing impact and bearing weight.  Most of the horse’s weight is supported by the fore limbs, while the propulsion of the horse is provided by the hind limbs. In addition, the horse has two apparatuses referred to as the stay apparatus and suspensory apparatus. The stay apparatus allows major joints in the limbs to lock so that the horse may rest and relax while standing. The suspensory apparatus is designed to absorb shock, carry the horse’s weight, and prevent the overextension of joints. Finally, the hooves are important structures that maintain support and traction as well as provide additional shock absorption.  

Since the cardiovascular system provides blood supply throughout the body, by responding to various stimuli, it can control the velocity and amount of blood carried through the vessels, thus, delivering oxygen, nutrients, hormones, and other important substances to cells and organs in the body.  It plays a very important role in meeting the body’s demands during exercise, stress, and activity.  

Exercise is used to increase the body’s ability to withstand repeated bouts of similar exercise with less impact.  With a strong and healthy cardiovascular system, there is an improved ability of the musculoskeletal system receiving oxygen, thus, allowing muscles to better their capacity to use oxygen and energy.  However, the adaptation period for each of these physiological systems do differ as the cardiovascular system adapts faster compared to the musculoskeletal system. This is often an overlooked consideration when developing training programmes for horses. 

It is important to understand the various functions, structures, and adaptive processes of the horse’s musculoskeletal system such as bone, articular cartilage, tendons, and ligaments in order to develop appropriate training regimens. 

Bone has many important roles that involve locomotion, the storage of minerals (especially calcium and phosphate), soft tissue and vital organ protection, and the support and containment of bone marrow. Bone is a specialised connective tissue, and together with cartilage forms the strong and rigid endoskeleton.  The bone is continuously altering through two processes called bone modelling and bone remodelling, involving four cells referred to as osteoclasts, osteoblasts, osteocytes and bone lining cells.  

Osteoblasts secrete bone matrix in the form of non-mineralised osteoid, which is then mineralised over a few weeks to form a bone matrix.  Osteoclasts are involved in resorption of bone as this process occurs faster than the formation of bone. When the bone surfaces are not in the development or resorption phase, the bone surface is completely lined by a layer of flattened and elongated cells termed bone-lining cells.  Osteocytes are derived from osteoblasts and are highly specialised to maintain the bone matrix.  They are designed to survive hypoxic conditions and maintain biomineralisation of the bone matrix.  Osteocytes also control osteoblastic and osteoclastic activities allowing bone remodelling.

The function of bone modelling is to alter and maintain shape during growth. As the horse grows and develops, bone modelling occurs with the acquisition and removal of bone.  While the young horse grows and develops, bone modelling allows the bone to endure strains from everyday work and exercise. The adult skeleton undergoes a minimal amount of bone modelling. Due to the presence of the high frequency of bone modelling in young horses, their skeletal strength is highly influenced by strains to their bones during exercise and daily use. With this knowledge, it has been concluded and confirmed that short-term dynamic exercise of an adolescent can lead to beneficial changes to its bone morphology.  

Bone remodelling is a different process, in which old and damaged bone is renewed, which enables the bone to respond and adapt to changing functional situations. Bone remodelling is usually a coordinated relationship between bone resorption and bone formation. This process occurs throughout the horse’s life with the renewal of primary, damaged or old bone. Osteoclasts absorb old and damaged bone, and the osteoblasts form new bone and lay down new bone matrix until the earlier absorbed bone is replaced. In those animals with musculoskeletal disease or damage, there is an imbalance of osteoblast and osteoclast activity. With the knowledge that osteoblast activity to make new bone takes months whilst osteoclast activity of removing old and damaged bone only takes a few days to two weeks, bone that is being repaired is at a high risk of further injury as bone removed has not been completely replaced.   Multiple studies have shown that exercise while growing can provide lifelong benefits; however, it must be done with care and knowledge.

In addition, many studies have shown that exercise of a dynamic nature in moderate distances, such as that achieved in the pasture or prescribed short-distance high-speed work is beneficial to musculoskeletal development and may prevent injuries when entering race training. It has also been observed that long slow work does not increase bone strength. Below is a summary of the young horse response of the various types of exercise.

Articular cartilage is a highly specialised connective tissue found in joints with the role of providing a smooth, lubricated surface of articulation and to help transmit loads with a low amount of friction. The articular cartilage is a hyaline cartilage (flexible and strong tissue providing a smooth, slippery surface) with a dense “ExtraCellular Matrix” (ECM) consisting of specialised cells called chondrocytes, collagen and proteoglycans. These components help to retain water in the ECM that is required for the joints mechanical properties. As age increases, hydration of the matrix does decrease, resulting in stiffness. Chondrocytes are residential cells in articular cartilage that play a role in the development, maintenance, and repair of the ECM. They do respond to a variety of stimuli, including mechanical loads, growth factors, hydrostatic pressures, piezoelectric forces (formation of electric charge with force). Because of the lack of blood vessels, lymphatics, and nerves as well as being a harsh biomechanical environment, there is a limited capacity to heal and repair. In addition, chondrocytes have limited potential for replication, thus, have limited healing capacity; and chondrocytes survival depends on an optimal chemical and mechanical environment.  

Maintaining joint health is vital, which requires the preservation of healthy cartilage tissue. Inactivity of joints is detrimental to articular cartilage; thus, regular movement of joints and dynamic loads is needed to provide a normal articular cartilage structure and function. Biochemical responses of the cartilage to exercise are not nearly as well known compared to bone. While the confinement of young horses stunts joint development, excessive straining of cartilage can also reduce joint development. It has been observed that pasture access was optimal for the development of joints and the confinement or excessive sprint exercise (12–32 sprints of 40 metres for 6 days a week for 5 months) causes detrimental effects on the joint and may be deemed as unnatural exercise.  It is also thought that exercise is needed well before two years of age to allow cartilage thickening as well as the avoidance of confinement. It can be concluded that further studies are required with respect to level of exercise and type of exercise in order to achieve healthy cartilage tissue as there is clearly a fine line between frequency and intensity of exercise.  

Tendons and ligaments are distinct but closely related tissues that have unique and important roles in musculoskeletal function and musculoskeletal disease. Tendons and ligaments are dense, fibrous connective tissues that connect muscle to bone or bone to bone, respectively.  These tissues transmit mechanical forces to stabilise the skeleton and allow body movement.  Tendons and ligaments consist mainly of collagen type I as well as small amounts of collagen III, IV, V, and VI. There are also various proteoglycans in tendons and ligaments that both organise and lubricate collagen fibre bundles. The elasticity of tendons and ligaments is due to the large amount of type I collagen. During locomotion, the tendon decreases energy cost to the horse by acting as a spring to store and release energy while stretching and recoiling in the stance and swing phases of each stride. Tendons and ligaments have blood vessels and nerves that allow the homeostasis and response to injury.  

Tenocytes are tightly regulated by a series of growth factors and transcription factors that allow the synthesis, maintenance, and the degradation of the tendon extracellular matrix. Tendons are elastic, but tearing may occur if there is excessive loading on the tendon and the repair of collagen is a slow process. In addition, tendons have crimp morphology where the tendons buckle in a state of relaxation and act as shock absorbers.  Unbuckling of the tendon occurs during loading.  This crimp morphology may be disturbed if an injury occurs and also is reduced in older horses.  

Due to the variation of activity of tenocytes in foals and young horses, it has been observed that both a lack of exercise and excess of exercise can impair tendon make-up and subsequent functionality. With the current data and research that has been gathered, it can be concluded that if horses take advantage of spontaneous exercise when in the paddocks (which they often do), the developing tendons may benefit and be at a lower risk of injury when racing training starts. 

Conclusion

It is clear that further research is needed in order to ascertain the optimal amount and type of exercise that is needed in order to provide a strong musculoskeletal system and functional performance. However, it has been shown that prescribed exercise during the growth of the horse can increase the longevity of the horse’s health and performance. It has been observed that confinement and the lack of loading can result in weaker tissues and the loss of function of none, tendons, ligaments and articular cartilage.  However, it must also be recognised that medical attempts to alleviate pain so that a horse can continue to train through an injury can greatly increase tissue damage which is detrimental to the horse’s health and career. It is far more beneficial to provide an adequate amount of time for the injury to heal, thus, putting the horse’s health and wellbeing as a top priority.  

Nutritional Perspective

Bone development in yearlings from the sales ring to racing

Article by Des Cronin B.Ag.Sc, MBA

Maintaining the equine skeleton is vital to ensure optimal development of the young growing horse, minimise risk of injury in the performance horse, and promote longevity and soundness.

The skeletal development and health of a young horse begins in utero and ensuring the broodmare receives the correct intake of key nutrients will be critical to the growth of the unborn foal. Producing high-quality milk places a significant drain on the mineral reserves of the mare. Maintaining mineral intakes during peak lactation is vital to ensure the foal receives the best nutrition to support the rapid skeletal development in the early weeks and months of growth. During this time, bone formation, body size, and muscle mass greatly increase. Risk of defective bone and related tissue formation increases with one of more of the following:

• Poor diet with the incorrect balance of energy and nutrients in the daily ration

• Inadequate amounts of calcium (Ca) and phosphorus (P)

• A reversed Ca:P ratio

• Low zinc (Zn) or copper (Cu) in the diet

• Low Vitamin D

Feeding a young horse for a maximum growth rate is undesirable because bone hardening lags greatly behind bone lengthening. At 12 months old, the young horse could reach about 90 to 95 per cent of its mature height but only about 75 per cent of its mature bone mineral content.

Ideally, young horses should gain weight at a rate that their developing bones can easily support. Growing bones and connective tissues don’t have the strength to support rapid weight gain from overfeeding, especially energy. Rapid weight gain can also make other skeletal anomalies worse. In these cases the risk of developmental orthopaedic disorders (DOD) and unsoundness increases.

DOD and unsoundness can also occur during uneven growth. For example, switching an underfed, slow-growing horse to a good diet that allows quick growth (compensatory growth), increases the risk of DOD. Foals between the ages of 3 and 9 months of age are at greatest risk of DOD.

Fresh forages, for example grazed grass, usually provide enough major minerals such as calcium (Ca) and phosphorus (P) for the growing horse. However, there can be significant variation in calcium and phosphorus levels in all forages but particularly preserved forages (hay and haylage). Forage analysis should always be undertaken to determine mineral composition. 

For young fast-growing horses, the diet must supply the quantities of calcium and phosphorus needed for normal bone formation. In terms of Ca:P ratio, the ratio must be positive in favour of calcium. Horses are much more tolerant of high-dietary calcium than other species. For practical purposes, a good guideline would be to keep the ratio Ca:P between 1.5 to 1 and 2.5 to 1.  Grains (e.g., oats) contain 10 per cent of the calcium level found in typical forages. Grains are poor sources of calcium, both in terms of the amount of calcium supplied and their effect on Ca:P ratio in the diet. Where grains are fed, supplementation will be necessary to balance the diet.  

While some forages may contain adequate calcium and phosphorus, they will typically supply less than 20 per cent of the daily requirements for trace elements. Supplementation of trace elements will generally be necessary to support normal bone development.

Where concentrates are fed (especially low levels), supplementation may still be necessary to balance the overall mineral and trace element intake. Nutritional advice should be sought to ensure the horse's diet is correctly balanced.

To meet the carefully balanced requirements of key minerals, it is advisable to supplement the daily rations of growing horses and young horses entering training with an appropriate nutritional product. 

Make sure that the supplement used contains the correct ratio of calcium and phosphorus, as well as other key nutrients such as vitamin D and chelated trace elements (copper, manganese, and zinc) to support normal bone development.

Supplementing branch chain amino acids in the diet ensures that growth is maintained. Lysine plays a key role when protein concentrations in the body are low. Vitamin A supports collagen formation, which is a key component of the supportive structures of joints (tendons and ligaments). Vitamin D3 is added to enhance calcium absorption.

Although growth rates slow after the age of two, they are still juvenile in their skeletal development with some growth plates, such as the shoulder and stifles, yet to completely close. Although they may look like fully grown adults, it is still important to meet nutritional requirements especially if starting training and work. With the addition of exercise and training, a young horse's nutritional needs change.  The added forces from groundwork on the long bones and increased requirements of other nutrients like electrolytes need to be considered. 

Finally, horses all grow and develop at different rates because of factors such as genetics. Some youngsters will need  more support for longer periods of time than others, so it is important to manage accordingly.

Air Quality and Air Pollution’s Impact on Your Horse’s Lungs

There’s nothing like hearing a horse cough to set people scurrying around the barn to identify the culprit. After all, that cough could mean choke, or a respiratory virus has found its way into the barn. It could also indicate equine asthma. Yes, even those “everyday coughs” that we sometimes dismiss as "summer cough" or "hay cough" are a wake-up call to the potential for severe equine asthma. 

Formerly known as heaves, broken wind, emphysema, chronic obstructive pulmonary disease (COPD), or recurrent airway obstruction (RAO), this respiratory condition is now called severe equine asthma (sEA). These names reflect how our scientific and medical understanding of this debilitating disease has changed over the years. We now consider heaves to be most comparable to severe asthma in people.

But what if your horse only coughs during or after exercise? This type of cough can mean that they have upper airway irritation (think throat and windpipe) or lower airway inflammation (think lungs) meaning inflammatory airway disease (IAD), which is now known as mild-to-moderate equine asthma (mEA). This airway disease is similar to childhood asthma, meaning  that it can go away on its own. However, it is still very important to call your veterinarian out to diagnose mEA. This disease causes reduced athletic performance, and there are different subtypes of mEA that benefit from specific medical therapies. In some cases, mEA progresses to sEA.

Equine Asthma and  Air Quality
What does equine asthma have to do with air quality? A lot, it turns out. Poor air quality, or air pollution, includes the barn dusts—the allergens and moulds in hay and the ground-up bacteria in manure, as well as arena dusts and ammonia from urine. Also, very importantly for both people and horses, air pollution can be from gas and diesel-powered equipment. This includes equipment being driven through the barn, the truck left idling by a stall window, or the smog from even a small city that drifts nearly invisibly over the surrounding farmland. Recently, forest-fire smoke has been another serious contributor to air pollution. 

Smog causes the lung inflammation associated with mEA. Therefore, it is also likely that air pollution from engines and forest fires will also trigger asthma attacks in horses with sEA. Smog and smoke contain many harmful particulates and gases, but very importantly they also contain fine particulate matter known as PM2.5. The 2.5 refers to the diameter of the particle being 2.5 microns. That’s roughly 30 times smaller than the diameter of a human hair. Because it is so small, this fine particulate is inhaled deeply into the lungs where it crosses over into the bloodstream. So, not only does PM2.5 cause lung disease, but it also causes inflammation elsewhere in the body including the heart. Worldwide, even short-term exposure is associated with an increased risk of premature death from heart disease, stroke, and lung cancer. This PM2.5 stuff is not trivial!

In horses, we know that PM2.5 causes mEA, so it’s logical that smog and forest-fire smoke exposure could exacerbate asthma in horses, but we don’t know about heart disease or risk of premature death.

Symptoms, Diagnostic Tests and Treatments

Equine asthma manifests with a spectrum of symptoms that vary in severity and the degree of debilitation they cause. Just like in people with asthma, the airways of horses with mEA and sEA are “hyperreactive.” This means that the asthmatic horse’s airways are extra sensitive to barn dusts that another horse’s lungs would just “ignore.” The asthmatic horse’s airways constrict, or become narrower, in response to these dusts. This narrowing makes it harder to get air in and out of the lungs. Think about drinking through a straw. You can drink faster with a wider straw than a skinnier one. It’s the same with air and the airways. In horses with mEA, the narrowing is mild. In horses with sEA, the constriction is extreme and is the reason why they develop the “heaves line”; they have to use their abdominal muscles to help squeeze their lungs to force the air back out of their narrow airways. They also develop flaring of their nostrils at rest to make their upper airway wider to get more air in. Horses with mEA do not develop a heaves line, but the airway narrowing and inflammation do cause reduced athletic ability.

The major signs of mEA are coughing during or just after exercise that has been going on for at least a month and decreased athletic performance. In some cases, there may also be white or watery nasal discharge particularly after exercise. Often, the signs of mEA are subtle and require a very astute owner, trainer, groom, or rider to recognise them.

Another very obvious feature of horses with sEA is their persistent hacking cough, which worsens in dusty conditions. “Hello dusty hay, arena, and track!” The cough develops because of airway hyperreactivity and because of inflammation and excess mucus in the airways. Mucus is the normal response of the lung to the presence of inhaled tiny particles or other irritants. Mucus traps these noxious substances so they can be coughed out, which protects the lung. But if an asthma-prone horse is constantly exposed to a dusty environment, it leads to chronic inflammation and mucus accumulation, and the development or worsening of asthma along with that characteristic cough.

Accurately Diagnosing Equine Asthma

Veterinarians use a combination of the information you tell them, their observation of the horse and the barn, and a careful physical and respiratory examination that often involves “rebreathing.” This is a technique where a bag is briefly placed over the horse’s nose, causing them to breathe more frequently and more deeply to make their lungs sound louder. This helps your veterinarian hear subtle changes in air movement through the lungs and amplifies the wheezes and crackles that characterise a horse experiencing a severe asthma attack. Wheezes indicate air “whistling” through constricted airways, and crackles mean airway fluid buildup. The fluid accumulation is caused by airway inflammation and contributes to the challenge of getting air into the lung. 

Other tests your veterinarian might use are endoscopy, bronchoalveolar lavage, and in the specialist setting, pulmonary function testing. They will also perform a complete blood count and biochemical profile assay to help rule out the presence of an infectious disease. 

Endoscopy allows your veterinarian to see the mucus in the trachea and large airways of the lung. It also lets them see whether there are physical changes to the shape of the airways, which can be seen in horses with sEA. 

Bronchoalveolar lavage, or “lung wash” is how your veterinarian assesses whether there is an accumulation of mucus and inflammatory cells in the smallest airways that are too deep in the lung to be seen using the endoscope. Examining lung wash fluid is a very important way to differentiate between the different types of mEA, between sEA in remission and an active asthma attack, and conditions like pneumonia or a viral lung infection. 

Finally, if your veterinarian is from a specialty practice or a veterinary teaching hospital, they might also perform pulmonary function testing. This allows your veterinarian to determine if your horse’s lungs have hyperreactive airways (the hallmark of asthma), lung stiffening, and a reduced ability to breathe properly. 

Results from these tests are crucial to understanding the severity and prognosis of the condition. As noted earlier, mEA can go away on its own; but medical intervention may speed healing and the return to athletic performance. With sEA, remission from an asthmatic flare is the best we can achieve.  As the disease gets worse over time, eventually the affected horse may need to be euthanised.

Management, Treatment and Most Importantly—Prevention
Successful treatment of mEA and sEA flares, as well as long-term management, requires a multi-pronged approach and strict adherence to your veterinarian’s recommendations.

Rest is important because forcing your horse to exercise when they are in an asthma attack further damages the lung and impedes healing.  To help avoid lung damage when smog or forest-fire smoke is high, a very useful tool is your local, online, air quality index (just search on the name of your closest city or town and “AQI”).  Available worldwide, the AQI gives advice on how much activity is appropriate for people with lung and heart conditions, which are easily applied to your horse. For example, if your horse has sEA and if the AQI guidelines say that asthmatic people should limit their activity, then do the same for your horse. If the AQI says that the air quality is bad enough that even healthy people should avoid physical activity, then do the same for you AND your horse. During times of poor air quality, it is recommended to monitor the AQI forecast and plan to bring horses into the barn when the AQI is high and to turn them out once the AQI has improved.

Prevent dusty air. Think of running your finger along your tack box – whatever comes away on your finger is what your horse is breathing in. Reducing dust is critical to preventing the development of mEA and sEA, and for managing the horse in an asthmatic flare. 

Logical daily practices to help reduce dust exposure:

• Turn out all horses before stall cleaning

• Wet down the aisle prior to sweeping

• Never sweep debris into your horse’s stall

• Use low-dust bedding like wood shavings or dust-extracted straw products, which should also be dampened down with water

• Reduce arena, paddock, and track dust with watering and maintenance

• Consider low-dust materials when selecting a footing substrate

• Steam (per the machine’s instructions) or soaking hay (15–30 minutes and then draining, but never store steamed or soaked hay!) 

• Feed hay from the ground

• Feed other low-dust feeds

• Avoid hay feeding systems that allow the horse to put their nose into the middle of dry hay—this creates a “nosebag” of dust

Other critical factors include ensuring that the temperature, humidity and ventilation of your barn are seasonally optimised. Horses prefer a temperature between 10–24 ºC (50–75 ºF), ideal barn humidity is between 60–70%. Optimal air exchange in summer is 142 L/s (300 cubic feet/minute). For those regions that experience winter, air exchange of 12–19 L/s (25–40 cubic feet/minute) is ideal. In winter, needing to strip down to a single layer to do chores implies that your barn is not adequately ventilated for your horse’s optimal health. Comfortable for people is often too hot and too musty for your horse! 

Medical interventions for controlling asthma are numerous. If your veterinarian chooses to perform a lung wash, they will tailor the drug therapy of your asthmatic horse to the results of the wash fluid examination. Most veterinarians will prescribe bronchodilators to alleviate airway constriction. They will also recommend aerosolised, nebulised or systemic drugs (usually a corticosteroid, an immunomodulatory drug like interferon-α, or a mast cell stabilisers like cromolyn sodium) to manage the underlying inflammation. They may also suggest nebulising with sterile saline to help loosen airway mucus and may suggest feed additives like omega 3 fatty acids, which may have beneficial effects on airway inflammation. 

New Research and Future Directions

Ongoing research is paramount to expanding our knowledge of what causes equine asthma and exploring innovative medical solutions. Scientists are actively investigating the effects of smog and barn dusts on the lungs of horses. They are also working to identify new targeted therapies, immunotherapies and other treatment modalities to improve outcomes for affected horses.

Conclusion

Both mild and severe equine asthma are caused and triggered by the same air pollutants, highlighting the need for careful barn management. The alarming rise in air pollution levels poses an additional threat to equine respiratory health. Recognising everyday coughs as potential warning signs and implementing proper diagnostic tests, day-to-day management practices and medical therapies are crucial in combating equine asthma. By prioritising the protection of our horse’s respiratory health and staying informed about the latest research, we can ensure the well-being of our equine companions for years to come.

Gastric ulcers in racehorses – what trainers should know

Article by Dr Michael Hewetson

Why are gastric ulcers so important in racehorses?

Gastric ulcers are very prevalent in racehorses, with between 52% and 93% of horses in active training affected. This is significant, because gastric ulcers can impact both the horse's performance and its overall health and welfare, which in turn can have financial and competitive implications for their owners, trainers, and the racing industry as a whole. 

Gastric ulcers can affect a horse's performance by causing abdominal discomfort and reduced appetite. This can lead to changes in stride length and decreased energy levels that may impact their racing performance. Horses with gastric ulcers may also exhibit changes in behaviour, such as nervousness, aggression, or reluctance to train or race, which again, can affect their overall performance and temperament. If left untreated, gastric ulcers can lead to more serious health concerns such as colic, potentially requiring costly medical intervention and downtime for the horse. But most importantly, gastric ulcers are a welfare issue for the Thoroughbred racing industry, and with growing public scrutiny on the industry, ensuring the well-being of racehorses is a priority, and addressing gastric ulcers promptly should be considered part of responsible horse management. This requires a close working relationship with your vet, who will be able to give you expert advice about diagnosis, treatment, and management of this frustrating disease. 

Understanding gastric ulcers

FIGURE 1

Equine gastric ulcer syndrome (EGUS) is a general term used to describe erosions and ulcers of the horse’s stomach and is similar to the term peptic ulcer disease in people. Unlike people however, the horse is unique in that the stomach lining (mucosa) is divided into an upper squamous and a lower glandular portion (figure 1); and it is important to realise that there are differences between these two regions with respect to how these lesions develop, their prevalence, associated risk factors and response to treatment. Therefore, when referring to EGUS, your vet may use the terms Equine Squamous Gastric Disease (ESGD) and Equine Glandular Gastric Disease (EGGD) to clearly distinguish the anatomical region of the stomach affected. 

FIGURE 2

There does not appear to be a clear relationship between the presence of squamous disease and glandular disease, and the fact that both conditions may occur concurrently in the same horse does not indicate that they are associated. In the case of squamous disease, the cause of the ulcers is well understood, with a variety of managemental risk factors (e.g. increase in exercise intensity, low roughage/high starch diet, stall confinement) contributing to an increase in the exposure of the squamous mucosa to acid. The squamous mucosa is not normally exposed to acid. As such it is inherently susceptible to acid injury, and with prolonged acid exposure, ulcers may develop (figure 2).

FIGURE 3

In contrast to squamous disease, the cause of glandular disease is poorly understood. The glandular mucosa is fundamentally different from the squamous mucosa in that it is exposed to a highly acidic environment under normal physiological conditions. As such, it is only when there is a breakdown of the normal defence mechanisms that protect the glandular mucosa from acidic gastric contents that glandular disease occurs. While ulcers are most commonly seen with squamous disease, horses with glandular disease rarely present with ulcers. Rather, the lesions are more consistent with an erosive inflammatory gastritis and can vary widely in their appearance (figure 3). There is a now evidence to suggest that stress, both psychological (e.g. multiple riders or caretakers; confinement; stress associated with transport and competition) and physiological (e.g. increases in the total amount and frequency of exercise without adequate rest periods) may increase the risk of glandular disease in horses. This may be due to a variety of mechanisms including a reduction in the mucus coating and blood supply to the glandular mucosa; both of which compromise the gastric barrier, resulting in acid injury.

The prevalence of gastric ulcers appears to vary with age, use, stage of training, as well as the region of the stomach affected. The prevalence of squamous disease is consistently highest in performance horses, with 52-93% of Thoroughbred racehorses found to be affected. The prevalence of glandular disease is less well reported, however up to 47% of Thoroughbred racehorses may be affected. 

Why are racehorses so susceptible to gastric ulcers?

It is most likely because of their unique management when compared to most other horse populations; and the intensity of exercise that is inherent of racing competition. For example, it has been shown that the risk of squamous disease increases with an increase in the intensity of exercise and the duration of time at work. Strenuous exercise causes an increase in intra abdominal pressure associated with contraction of the abdominal muscles1. This results in compression of the stomach, and exposure of the sensitive squamous mucosa to acidic gastric content (acid splash). Strenuous exercise has also been shown to cause an increase in a hormone called gastrin, which stimulates acid production in the stomach. 

Several factors associated with management have also been shown to increase the risk of squamous disease, many of which are imposed on racehorses at the commencement of training or during racing competition. These include a high starch/low roughage diet, intermittent fasting, stall confinement, transport, intermittent access to water and administration of hypertonic solutions of electrolytes. In fact, exposure to a combination of a high starch diet, stall confinement and strenuous exercise has been shown to induce ulcers in as little as 7 days; and intermittent fasting is so effective at inducing ulcers that it is used as a model for squamous disease in experimental studies. Thoroughbred racehorses are also exposed to many of the risk factors for glandular disease, most notably, multiple riders or caretakers; confinement; and stress associated with transport and competition.

How do you know if your horse has gastric ulcers and how might they affect performance?

A variety of clinical signs may suggest that a horse has gastric ulcers, however there is currently very little evidence to support a direct association between any of these signs and the presence or absence of ulcers seen on gastroscopy. This is likely because most of the clinical signs are non-specific and are often very subjective. This is complicated further by the fact that horses with gastric ulcers may not demonstrate clinical signs and if they do, the signs do not necessarily correlate with the severity of the lesions seen on gastroscopy. Clinical signs suggestive of gastric ulcers should therefore always be interpreted with caution, and most importantly, gastroscopy should always be performed to confirm the disease (figure 4).

In racehorses, gastric ulcers have been associated with poor appetite, poor body condition, changes in behaviour (including an aggressive or nervous attitude), post prandial colic, stereotypic behaviour and resentment of girthing. Any one of these clinical signs can potentially have an indirect effect on performance (for example, through reduced appetite or interruption in training), but the big question is if gastric ulcers themselves, in the absence of other clinical signs, have an effect on performance. Despite the fact that it is a well entrenched ’fact’ amongst trainers that gastric ulcers have a direct effect on poor performance or reluctance to train, there is surprisingly little evidence in the literature to back this up. This may be in part due to the difficulties in excluding the many confounding factors that might influence poor performance (e.g. lameness, respiratory disease etc.). 

The mechanism by which gastric ulcers may affect performance has not been identified but is likely to be related to epigastric pain. In people, epigastric pain is defined as pain localised to an area below the sternum and above the umbilicus and is common in athletes with gastro-oesophageal reflux disease (GERD). Acid reflux onto the sensitive squamous mucosa of the oesophagus during exercise causes a “burning sensation” that gets worse with increasing exercise intensity and has been shown to affect performance. Horses with squamous gastric disease have similar lesions to those causing GERD in human athletes, and the problem is likely to be exacerbated by the fact that the squamous mucosa extends from the oesophagus into the upper one-third of the stomach and is not protected by an oesophageal sphincter. Interestingly, a recent study in human athletes suggested that GERD may be associated with increased abdominal pressure during exercise, a mechanism that I have already alluded to in the equine athlete. How exactly epigastric pain impacts on athletic performance in the horse is a matter of ongoing speculation. One theory is that it may affect stride length. It has been shown that horses with gastric ulcers have a reduced stride length when galloping, likely due to abdominal discomfort. Stride length and lung ventilation are mechanically coupled in the galloping horse, and therefore, reduced stride length will result in decreased oxygen uptake, thus limiting aerobic capacity during peak exercise.

How are gastric ulcers treated and what can you do to prevent them?

Let’s turn our attention now to the treatment of gastric ulcers. Because there is currently little evidence to suggest an association between clinical signs and the presence or severity of gastric ulcers, treatment should always be based on gastroscopic evidence of ulcers. Some trainers may still choose to commence treatment based entirely on clinic signs without gastroscopy and assess for a clinical response. I would caution against this approach, as it can be costly if the horse does not have ulcers, and gastroscopy is still going to be necessary to conclusively rule out gastric ulcers if clinical improvement is not seen with treatment.

Treatment of gastric ulcers will vary depending upon the severity and the location of the ulcers and your vet will be able to give you advice on the best approach. In most cases treatment consists of management and dietary modification in conjunction with the use of proton pump inhibitors which suppress acid production. Oral omeprazole is the drug of choice and is currently the only licensed drug for the treatment and prevention of gastric ulcers in horses in the UK and Ireland.   

Administering oral omeprazole on an empty stomach can improve the bioavailability of the drug. This can be achieved practically by administering it first thing in the morning at least 1 hour prior to feeding. This ensures the stomach will be empty as horses eat very little during the night even if they have access to forage. 

The duration of treatment will depend on the location of the lesions, with squamous disease tending to heal faster than glandular disease. In most cases, your vet will prescribe oral omeprazole for 3-4 weeks and then the requirement for additional medication will be determined following a repeat gastroscopy. In the case of glandular disease, oral omeprazole is often combined with sucralfate, which adheres to the damaged mucosa, providing a physical barrier while also stimulating mucus secretion, both of which reduce potential exposure to acid. Omeprazole is a controlled drug, and therefore needs to be withdrawn prior to competition. The BHA published detection time for oral omeprazole is ≤ 48hrs, so withdrawal of the drug 3-5 days before competition would be prudent. There is, however, some concern that the requirement for withdrawal times might influence the efficacy of oral omeprazole treatment in racehorses. Many vets report reoccurrence of squamous disease following discontinuation of treatment with omeprazole, often within as little as 3 days, and this was demonstrated in a recent study comparing withholding periods for oral omeprazole treatments in racing Thoroughbreds6. The authors reported a squamous disease prevalence of 83% in horses after a “2 clear days'' recommended withholding period for oral omeprazole, which was an increase from 25% of horses with squamous disease before the recommended withholding period, and they theorised that ‘rebound acid secretion’ may be implicated. This phenomenon occurs following the discontinuation of proton pump inhibitor drugs such as oral omeprazole, and is linked to a loss of negative feedback from gastric acid during treatment that causes an increased secretion of the hormone gastrin that can persist for up to 2-4 days after the last dose of omeprazole has been administered. This results in a short period of increased gastric acid production when treatment is stopped. Whilst nothing can currently be done about the required withdrawal periods during racing, strict management practices should be implemented for the 2-4 days following cessation of omeprazole treatment to mitigate against development of squamous gastric disease. This could include ensuring provision of adequate roughage during this time, avoiding fasting or withholding water, and perhaps limiting exercise or transport if possible.

Additional management and dietary adaptations which may help prevent gastric ulcers and can be implemented longer term in a racing yard include free choice access to roughage (and if not, ensuring that roughage is provided at intervals of no more than 4-6 hours); turn out into a paddock with good quality grazing where possible; a low starch/high fat diet (or alternatively, smaller concentrate meals more frequently); reduction/avoidance of any potential stressors; and provision of regular rest days. Where possible, training schedules should be adjusted so that they occur later in the day when enough roughage has been consumed to ensure that there is a mat of roughage in the stomach to buffer acid in the upper squamous portion and to reduce acid splash during exercise. Alternatively, a handful of palatable chaff should be fed 20 minutes prior to exercise. 

Numerous supplements are marketed for prevention of gastric ulcers, however there is currently very limited evidence to support their use.

References

1. Lorenzo-Figueras M, Merritt AM. Effects of exercise on gastric volume and pH in the proximal portion of the stomach of horses. Am J Vet Res. 2002;63(11):1481–1487. 

2. Vatistas NJ, Sifferman RL, Holste J, et al. Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl. 1999;29:40–44. 

3. Murray MJ, Eichorn ES. Effects of intermittent feed deprivation, intermittent feed deprivation with ranitidine administration, and stall confinement with ad libitum access to hay on gastric ulceration in horses. Am J Vet Res. 1996;57(11):1599–1603.

4. Herregods TV, van Hoeij FB, Oors JM, Bredenoord AJ, Smout AJ. Effect of running on gastroesophageal reflux and reflux mechanisms. Am J Gastroenterol. 2016;111(7):940–946. doi:10.1038/ajg.2016.122

5. Nieto JE, Snyder JR, Vatistas NJ, Jones JH. Effect of gastric ulceration on physiologic responses to exercise in horses. Am J Vet Res. 2009;70(6):787–795. 

6. Shan R, Steel CM, Sykes B. The Impact of Two Recommended Withholding Periods for Omeprazole and the Use of a Nutraceutical Supplement on Recurrence of Equine Gastric Ulcer Syndrome in Thoroughbred Racehorses. Animals. 2023; 13(11):1823. 

7. Clark B, Steel C, Vokes J, Shan JR, Gedye K, Lovett A, Sykes BW. Evaluation of the effects of medium-term (57-day) omeprazole administration and of omeprazole discontinuation on serum gastrin and serum chromogranin A concentrations in the horse. J Vet Intern Med. 2023 Jul-Aug;37(4):1537-1543.

The Gerald Leigh Memorial Lectures 2023

The Gerald Leigh Memorial Lectures, is an annual  gathering devoted to the racing industry and the health and wellbeing of the horses involved.  

This year, equine veterinarians, researchers, students and industry professionals from around the world attended the event, held June 8, 2023, at the historic Tattersalls Sales in Newmarket, England.  

There were insightful and informative lectures that educated the attendants but also instigated a healthy, lively debate on the health and welfare of the training and competing of horses. The underlying theme that was present during the whole event was all members of the conference had a deep passion and commitment to continuously progress and improve on managing the welfare and wellbeing of the horses in the industry, both on and off of the track.  

Two very special guest speakers, Sir Mark Prescott and Luca Cumani, wonderfully illustrated these sentiments as they described their reflections on the improvement and enhancement of horse safety.  

Horse racing may be regarded as an elite sport, and all activities involving horses have an element of risk. All stakeholders in the racing industry must continuously work to ensure that the risks are minimised in order to reduce the number of injuries and fatalities that may occur in training and on the racecourse.  There are now well-publicised concerns regarding the acceptability of exposing horses to risk in racing.  These lectures and all of the attendees embraced the values of the public will so that there can be continued acceptance of horse sports.   

Reducing the incidence of fractures in racing 

Christopher Riggs of The Hong Kong Jockey Club clearly outlined the various strategies to reduce the risk of fractures in racehorses. There are two principal strategies that may used to reduce the incidence of severe fractures in horses while racing and training:

1. Identifying extrinsic factors that increase risk and take action to minimise them. 

An example would be investigating different racing surfaces in order to determine which may provide the safest racing surface. However, studies have provided limited evidence and support for subtle extrinsic factors.

2. Identifying individuals that are at increased risk and prevent them from racing or minimise that risk until the risk has subsided.  

There are many research routes that are being undertaken to identify those horses that may be at a higher risk of fractures. There are investigations involving heritability and molecular studies that may provide evidence of genetic predisposition to fracture. However, Dr. Riggs explained that further understanding of the relationship between genetic, epigenetic and environmental factors is required before genetic screening is likely to be of practical use.  

Pre-race screening of horses by diligent clinical examination is poor at reducing the incidence of fracture. Dr. Riggs described another strategy that may assist with a clinical examination that is the use of biomarkers in blood and urine.  

Unfortunately, the precision to be of practical value has so far remained relatively unrewarding.  Wearable technology that records biometric parameters, including stride characteristics, has shown some promise in identifying horses that are at increased risk of fracture; although Dr. Riggs explained that this work requires further development.  

Finally, Dr. Riggs described both the use and current limitations of  diagnostic imaging in identifying pre-fracture pathology in order to identify a horse at imminent risk of fracture.  He conceded that further knowledge of the significance of the range of abnormalities that can be detected by imaging is incomplete.

Dr. Riggs concluded his lecture by expressing that the implementation of  diagnostic imaging to screen  “high-risk” horses identified through genetic, epidemiology, biomarkers and/or biometrics may be the best hope to reduce the incidence of racing fractures. This field can be advanced with further studies, especially of a longitudinal nature.

Professor Tim Parkin of Bristol Veterinary School discussed the need for further investment in welfare research and education. One avenue of investment that should be seriously considered is the analysis of data related to (fatal) injuries in Thoroughbred racing over the last 25 years.  

It was expressed, with the abundance of data that has been collected, that some risk factors would be relatively simple to identify. An encouraging example in the collection and use of data to develop models in predicting and potentially preventing injury has been conducted by the Hong Kong Jockey Club funded by the Hong Kong Jockey Club Equine Welfare Research Foundation. This may provide an opportunity to pilot the use of risk profiling to contribute to decision-making about race entries.  In addition, the results of the pilot study combined with other sources of data may encourage race authorities to mandate the collection of veterinary and training data in order to help in risk mitigation.

Horse racing is an international sport, and there are different governing bodies that ensure racing integrity. However, the concept of social licence equestrian sports and Thoroughbred horse racing continues to gain significant public attention.  Therefore, racing governing bodies are increasingly aiming to provide societal assurances on equine welfare. 

Dr. Ramzan of Rossdales Veterinary Surgeons provided an eloquent and clear message during his lecture that race yard veterinarians and trainers are instrumental in ensuring good horse health and welfare and reducing serious injury of the horse both while training or racing, which will provide sufficient trust and legitimacy from the public and society.  This feasible goal can be reached with good awareness of members involved in the care and training of each individual horse and conveying this information and any concerns to their veterinarian.  The veterinarian can also contribute by honing their knowledge and skills and working closely with yard staff in order to make appropriate and better targeted veterinary intervention.   

In the last two decades, there has been an incredible evolution and exciting developments in diagnostic imaging in the veterinary profession. It is believed that these technologies can provide a significant contribution to helping in mitigating fracture risks to racehorses on the course and in training.  

Professor Mathieu Spriet of University of California, Davis, described how these improvements in diagnostic imaging has led to the detection of early lesions as well as allowing the monitoring of the lesions’ evolution.  

He continued by explaining the strengths and limitations of different imaging modalities such as computed tomography (CT), magnetic resonance imaging (MRI) and positron emission tomography (PET).  Being one of the leaders in the use of PET in equine veterinary medicine, he presented further insight on how this particular modality provides high-resolution 3-D bone scans while being very sensitive to the identification of bone turn-over prior to the development of structural changes and allowing one to distinguish between active and inactive processes when structural changes are present.  

He concluded his impressive lecture by providing evidence with amazing PET images that the role of imaging is not merely for diagnostic purposes to characterise clinical abnormalities, but can also be used as a screening tool in certain horse populations for fracture risk assessment or for the monitoring of lesions to provide clearance for racing. 

Fractures, due to bone overloading rather than direct trauma occur commonly in Thoroughbred racehorses and are the leading cause of euthanasia on the racecourse. Despite many changes to race conditions, the number of catastrophic fractures has remained relatively static, with approximately 60 horses a year having a fatal fracture during a race in the UK.  

Against this backdrop, there have been great developments in the diagnosis and treatment of fractures in the last 40 years. Prevention of racecourse and training fractures would be ideal so the development of efficacious techniques to screen horses at risk may reduce the incidence and preserve social licensing.  

One technique discussed by Dr. Ian Wright of Newmarket Equine Referrals was to help mitigate the impact of racecourse fractures, which would be acute immobilisation of racecourse fractures, thus, reducing associated pain and anxiety while optimising clinical outcome and reducing on course fatality rates. Because of our increased understanding of fracture pathogenesis and their associated biomechanics, effective fracture immobilisation has been made possible. The majority of fractures that occur in flat racing and between obstacles in jump racing, are a result of stress or fatigue failure of the bone and not associated with trauma.  

In addition, fractures seen on the racecourse are often found in the same specific sites (i.e., metacarpal/metatarsal condyles and the proximal sesamoid bones of the fetlock) and have repeatable configurations. With this understanding and knowledge, racecourse veterinarians can optimally immobilise a fracture in a logical and pre-planned manner.  

As Dr. Wright expressed, this allows the fracture patient to have reduced pain and anxiety and enable the horse to be moved from the course comfortably so that it can be further examined. Ultimately, this allows the veterinarian and all stakeholders to make effective and judicious decisions for the sake of the horse’s welfare and wellbeing. As Dr. Wright concluded, this benefits both horses and racing.

Dr. Debbie Guest of the Royal Veterinary College discussed a different approach in mitigating the risk of fractures during training and racing by developing novel tools to reduce catastrophic fractures Thoroughbreds. Because it has been found that some horses are more inherently predisposed to fractures than other horses, Dr. Guest and her team have developed a genome-wide polygenic risk score so that one can potentially calculate an individual horse’s risk of fracturing during training or racing compared to the population as a whole.  

This strategy may contribute in identifying genetically high-risk horses so that additional monitoring of the patients can be exercised during their careers and also leading to fracture risk, which are found to be the cause of approximately half of these incidents.  

The system of using DNA testing to identify biological processes that may or may not be present ultimately leading to fracture risk may be a powerful tool in lowering the risk of catastrophic fracture and requires further research and application.

Cardiac events & sudden cardiac death in training and racing

In racehorses, sudden death that is associated with exercise on the racetrack or during training is a serious risk to jockeys and adversely affects horse welfare and the public perception of the sport. It is believed 75% of race day fatalities result from euthanasia following a catastrophic injury. The other 25% of fatalities is due to sudden deaths and cardiac arrhythmias are found to be the cause of approximately half of these incidents. The lectures focused on this area of concern by providing three interesting lectures on cardiac issues in the racehorse industry.  

Dr. Laura Nath of the University of Adelaide, explained the difficulties in identifying horses that are at risk of sudden cardiac death. It is believed that part of the solution to this difficult issue is the further development and use of wearable devices including ECG and heart rate monitors.  

With the use of these technologies, the goal would be to recognise those horses that are not progressing appropriately through their training and screen these horses for further evaluation. This course of action has been seen in human athletes that develop irregular rhythms that are known to cause sudden cardiac death with the use of computational ECG analysis, even when the ECGs appear normal on initial visual inspection.  

Knowing that ECGs and particularly P-waves are used as a non-invasive electrocardiographic marker for atrial remodelling in humans, Dr. Nath recently completed a study on the analysis variations in the P-wave seen on ECGs in athletic horses and found that increases of P-waves in racehorses are associated with structural and electrical remodelling in the heart and may increase the risk of atrial fibrillation (cardiac event).

Dr. Celia Marr of Rossdales Veterinary Surgeons continued the discussion of cardiac disease in both the training and racing of horses. Unfortunately, cardiac disease knowledge does lag compared to musculoskeletal and respiratory diseases when considering the causes of poor performance in racehorses. Due to the fact that cardiac rhythm disturbances are fairly common, occurring in around 5–10% of training sessions in healthy horses in Newmarket and over 50% of horses investigated for poor performance, Dr. Marr expressed the need for further research and investigation in this area.  

In addition, this research needs to determine if there is indeed a link between heart rhythm disturbances and repeated episodes of poor performance and sudden cardiac arrest. ECGs and associated technologies are helpful, but there are limitations such as the fact that rhythm disturbances do not always occur every time the horse is exercised.  Therefore, it would be of great value that a robust criterion is established when evaluating ECGs in racehorses. The Horserace Betting Levy Board has provided funding for investigation by initially exploring the natural history of paroxysmal atrial fibrillation (self-correcting form) to understand risk factors and predict outcomes for affected horses.

Continuing the theme of the lectures on irregular heart rhythms and associated sudden cardiac death (SCD) in training and racing, Professor Kamalan Jeevaratnam described his exciting research in using artificial intelligence (AI) to identify horses at increased risk of developing irregular rhythms that may cause SCD.  

AI is an exciting and rapidly expanding field of computer science that is beginning to be implemented in veterinary medicine. With funding by the Horserace Betting Levy Board and the Grayson Jockey Club Research Foundation, Professor Jeevaratnam of the University of Surrey, has piloted three novel algorithms that help predict horses with rhythm abnormalities through the analysis of horses’ ECGs.  

It was acknowledged that further research is required to develop this technology by using data collected from multiple sources, but the initial results are promising in the development of an useful AI tool to identify horses at risk of SCD and prevent catastrophic events, thus, ensuring the welfare of the horse in racing.

Conclusion

The Gerald Leigh Memorial Lectures was a thoroughly successful and enjoyable event attended by a variety of different members of the horse racing industry. Not only did the lecturers provide interesting and valuable information but also excitement for the future of racing.  It was very clear that all the lecturers and attendees were passionate and committed to the racehorse welfare and wellbeing as well as retaining the social licence for an exciting sport. 

Thermoregulation in horses

Article by Adam Jackson - MRCVS

Exertional heat illness (EHI) is a complex disease where thoroughbred racehorses are at significant risk due to the fact that their workload is intensive in combination with the high rate of heat production associated with its metabolism.  In order to understand how this disease manifests and to develop preventative measures and treatments, it is important to understand thermoregulation in horses. 

What is thermoregulation?

With continuous alteration in the surrounding temperature, thermoregulation allows the horse to maintain its body temperature within certain limits.  Thermoregulation is part of the greater process of homeostasis, which is a number of self-regulating processes the horse uses to maintain body stability in the face of changing external conditions.  Homeostasis and thermoregulation are vital for the horse to maintain its internal environment to ensure its health while disruption of these processes leads to diseases. 

The horse’s normal temperature range is 37.5–38.5°C (99–101°F).  Hyperthermia is the condition in which the body temperature increases above normal due to heat increasing faster than the body can reduce it. Hypothermia is the opposite condition, where the body temperature decreases below normal levels as the body is losing heat faster than producing it.   These conditions are due to the malfunction of thermoregulatory and homeostatic control mechanisms.

Horses are colloquially referred to as warm-blooded mammals—also known as endotherms because they maintain and regulate their core body, and this is opposite ectotherms such as reptiles.  The exercising horse converts stored chemical energy into mechanical energy when contracting various muscles in its body. However, this process is relatively inefficient because it loses roughly 80% of energy released from energy stores as heat. The horse must have effective ways to dissipate this generated heat; otherwise, the raised body temperatures may be life threatening.

Transfer of body heat

There are multiple ways heat may be transferred, and this will flow from one area to another by:

1. Evaporation 

The main way body heat is lost during warm temperatures is through the process of evaporation of water from the horse’s body surface. It is a combination of perspiration, sweating and panting that allows evaporation to occur.

Sweating is an inefficient process because the evaporation rate may exceed the body heat produced by the horse, resulting in the horse becoming covered and dripping sweat. This phenomenon occurs faster with humid weather (high pressure).

Insensible perspiration is the loss of water through the skin, which does not occur as perceivable sweat. Insensible perspiration takes place at an almost constant rate and is the evaporative loss from skin; but unlike sweating, the fluid loss is pure water with no solutes (salts) lost. The horse uses insensible perspiration to cool its body.

It is not common for horses to pant in order to dissipate heat; however, there is evidence that the respiratory tract of the horse can aid in evaporative heat loss through panting.

2. Conduction

Conduction is the process where heat is transferred from a hot object to a colder object, and in the case of the horse, this heat transfer is between its body and the air.  However, the air has poor thermal conductivity, meaning that conduction plays a small role in thermoregulation of the horse.   Conduction may help if the horse is lying in a cool area or is bathed in cool water.  

The horse has the greatest temperature changes occurring at its extremities, such as its distal limbs and head.  The horse can alter its blood flow by constricting or dilating its blood vessels in order to prevent heat loss or overheating, respectively. 

Interestingly, the horse will lie down and draw its limbs close to its body in order to reduce its surface area and to control conduction. There also have been some adaptive changes in other equids like mules and burros, where shorter limbs, longer ears and leaner bodies increase its surface area to help in heat loss tolerance.

3. Convection 

Convection is the rising motion of warmer areas of a liquid or gas and the sinking motion of cooler areas of the liquid or gas.  Convection is continuously taking place between the surface of the body and the surrounding air. Free convection at the skin surface causes heat loss if the temperature is low with additional forced convective heat transfer with wind blowing across the body surface.

When faced with cold weather, a thick hair coat insulates and resists heat transfer because it traps air close to the skin; thus, preventing heat loss. Whereas, the horse has a fine hair coat in the summer to help in heat loss.

4. Radiation

Radiation is the movement of heat between objects without direct physical contact.  Solar radiation is received from the sun and can be significant in hot environments, especially if the horse is exposed for long periods of time.  A horse standing in bright sunlight can absorb a large amount of solar radiation that can exceed its metabolic heat production, which may cause heat stress. 

How the horse regulates its body temperature

The horse must regulate its heat production and heat loss using thermoregulatory mechanisms.  There are many peripheral thermoreceptors that detect changes in temperature, which leads to the production of proportional nerve impulses. These thermoregulators are located in the skin skeletal muscles, the abdomen, the spinal cord and the midbrain with the hypothalamus being instrumental in regulating the internal temperature of the horse.   A coordinating centre in the central nervous system receives these nerve incoming impulses and produces output signals to organs that will alter the body temperature by acting to reduce heat loss or eliminate accumulated heat.  

The racehorse and thermoregulation

The main source of body heat accumulation in the racehorse is associated with muscular contraction.  At the initiation of exercise, the racehorse’s metabolic heat production, arising from muscle contraction, increases abruptly.  The heat production does alter the level of intensity of the work as well as the type of exercise undertaken.  

During exercise, the core body temperature increases because heat is generated and the horse’s blood system distributes this heat throughout the body. Hodgson and colleagues have theorised and confirmed via treadmill studies that the racehorse has the highest rate of heat production compared to other sporting horses. In fact, the racehorse’s body temperature can rise 0.8°C per minute, reaching 42.0°C. But what core temperature can the horse tolerate and not succumb to heat illness and mortality?  The critical temperature for EHI (exertional heat illness) is not known, but studies have demonstrated that a racehorse can be found to have core temperatures between 42–43°C without any clinical symptoms. Currently, anecdotal evidence is only available, suggesting that a core temperature of 43.5°C will result in manifestation of EHI with the horse demonstrating central nervous system dysfunction such as ataxia (incoordination).  In addition, temperatures greater than 44°C result in collapse. 

Heat loss in horses

A horse loses heat to the environment by a combination of convection, evaporation and radiation, which is magnified during racing due to airflow across the body. However, if body heat gained through racing is not minimised by convection, then the racehorse’s body temperature is regulated entirely by evaporation of sweat. This evaporation takes place on the horse’s skin surface and respiratory tract.  

The horse has highly effective sweat glands found in both haired and hairless skin, which produces sweat rates that are highest in the animal kingdom.   Efficient evaporative cooling is present in the horse because its sweat has a protein called latherin, which acts as a wetting agent (surfactant); this allows the sweat to move from its skin to the hair.

Because of the horse’s highly blood-rich mucosa of its upper respiratory tract, the horse has a very efficient and effective heat exchange system.  Estimates suggest this pathway dissipates 30% of generated heat by the horse during exercise.  As the horse exercises, there is blood vessel dilation, which increases blood flow to the mucosa that allows more heat to be dissipated to the environment. When the respiratory tract maximises evaporative heat loss, the horse begins to pant. Panting is a respiratory rate greater than 120 breaths per minute with the presence of dilated nostrils; and the horse adopts a rocking motion. However, if humidity is high, the ability to evaporate heat via the respiratory route and skin surface is impaired. The respiratory evaporative heat loss allows the cooling of venous blood that drains from the face and scalp. This blood may be up to 3.0°C cooler than the core body temperature of 42.0°C. And as it enters the central circulatory system, it can significantly have a whole-body cooling effect. This system is likely an underestimated and significant means to cool the horse.

Pathophysiology of EHI  in the thoroughbred

Although it is inconsistent to determine what temperature may lead to exertional heat illness (EHI), it is known that strenuous exercise, especially during heat stress conditions leads to this disease.  In human medicine, this disease is recognised when nervous system dysfunction becomes apparent.  There are two suggested pathways that lead to EHI, which may work independently or in combination depending on the environmental factors that are present during racing/training.

1. Heat toxicity pathway

Heat is known to detrimentally affect cells by denaturing proteins leading to irreversible damage.  In general, heat causes damage to cells of the vascular system leading to widespread intravascular coagulation (blood clot formation), pathologically observed as micro thrombi (miniature blood clots) deposits in the kidneys, heart, lungs and liver.  Ultimately, this leads to damaged organs and their failure.

Heat tissue damage depends on the degree of heat as well as the exposure time to this heat. Mammalian tissue has a level of thermal damage at 240 minutes at 42°C, 60 minutes at 43°C, 30 minutes at 44°C or 15 minutes at 45°C.  This heat damage must be borne in mind following a race requiring suitable and appropriate cooling methods, otherwise inadequate cooling may lead to extended periods of thermal damage causing disease. 

The traditional viewpoint is that EHI is caused by strenuous exercise in extreme heat and/or humidity.  However, recent studies have revealed that environmental conditions may only cause 43% of EHI cases, thus, suggesting that other factors are involved.

2. Heat sepsis pathway

In some instances. a horse suffering from EHI may present with symptoms and clinical signs similar to sepsis like that seen in an acute bacterial infection. 

A bacterial infection leading to sepsis causes an extreme body response and a life threatening medical emergency.  Sepsis triggers a chain reaction throughout the body particularly affecting the lungs, urinary tract, skin and gastrointestinal tract.

Strenuous exercise in combination with adverse environmental conditions may lead to sepsis without the presence of a bacterial infection— also known as an endotoxemic pathway—causing poor oxygen supply to the mucosal gastrointestinal barrier. Ultimately, the integrity of the gastrointestinal tract is compromised, allowing endotoxins to enter the blood system and resulting in exercise-induced gastrointestinal syndrome (EIGS).

However, researchers have observed that EHI in racehorses is unpredictable as EHI may develop in horses following exercise despite “safe” environmental conditions.  Even with adequate cooling and resuscitative therapies, tissue damage that occurs demonstrates that thermoregulatory and inflammatory pathways may vary, and hyperthermia may be the trigger but may not necessarily be driving the condition.

Diagnosis of EHI

The diagnosis of EHI is based on the malfunctioning of the central nervous system.

Initially, hyperthermia reduces the blood flow to the cerebrum of the brain, leading to a decrease of oxygen to that area—also known as ischemia. As a result, the clinical signs are:

• Extreme restlessness

• Confusion

• Substantial headache

If this hyperthermia continues, then the blood-brain barrier (an immunological barrier between circulating blood that may contain microorganisms like bacteria and viruses to the central nervous system) begins to leak plasma proteins, resulting in cerebral oedema (build up of fluid causing affected organ to become swollen). If treatment is not initiated at this point, then neuronal injury will result especially in the cerebellum.

EHI follows and involves serious CNS dysfunction.  The clinical signs associated with EHI are:

• Delirium

• Horses unaware of their surroundings

The final stage of EHI occurs when the swollen oedematous brain compresses vital tissue causing cellular damage. The clinical signs of end-stage EHI are:

• Collapse

• Unconsciousness

• Coma

• Death

Definition of EHI

EHI most commonly occurs immediately after a race when the horse is panting, sweating profusely and may be dripping with sweat. The most reliable indication of EHI is clinical signs associated with the dysfunction of the central nervous system in the presence of hyperthermia. Researchers have provided descriptions of levels of CNS dysfunction, ranging from level 1 to level 4.

Level 1 – The earliest recognizable signs of CNS dysfunction

The horse becomes restless, agitated and irritable. There is often head nodding or head shaking. The horse is difficult to restrain and will not stand still.  Therapeutic intervention such as cooling can resolve these clinical signs, but if the horse is inadequately cooled then the disease can escalate. 

Level 2 – Obvious neurological dysfunction

Often misdiagnosed as colic symptoms, the horse becomes further agitated and irritable with the horse kicking out without any particular stimulus present. This stage is dangerous to all handlers involved as the horse’s behaviour is unpredictable. 

Level 3 – Bizarre neurological signs

At this stage, the horse has an altered mentation appearing vacant, glassy-eyed and “spaced-out”.  In addition, there is extreme disorientation with a head tilt and leaning to one side with varying levels of ataxia (wobbly).  It has been observed that horses may walk forward, stop, rear and throw themselves backwards.  It is a very dangerous stage, as horses are known to run at fences, obstacles and people. Horses may also present as having a hind limb lameness appearing as a fractured leg with hopping on the good limb.  These clinical signs may resolve with treatment intervention.

Level 4 – Severe CNS dysfunction

There is severe CNS dysfunction at this stage of EHI with extreme ataxia, disorientation and lack of unawareness of its surroundings. The horse will continuously stagger and repeatedly fall down and get up while possibly colliding with people or objects with a plunging action. Unsurprising, the horse is at risk of severe and significant injury.  Eventual collapse with the loss of consciousness and even death may arise.

Treatment of EHI

In order to achieve success in the treatment of EHI, it is imperative that there is early detection, rapid assessment and aggressive cooling. The shorter the period is between recognising the condition and treatment, the greater the chance of a successful outcome.  In particular settings such as racecourses or on particularly hot and humid days, events must be properly equipped with easily accessible veterinary care and cooling devices. It is highly effective if a trained worker inspects every horse in order to identify those horses at risk or exhibiting symptoms. 

If EHI is recognised, veterinary intervention will be paramount in the recovery to prevent further illness and suppress symptoms. It will be important to note any withdrawal periods of any non-steroidal anti-inflammatories (NSAIDs) and analgesics before returning to racing. There are a number of effective ways to cool the horse with easily accessible resources.

Whole body cooling systems

Cooling the horse with ice-cold water is an effective way to draw heat from the underlying tissues. In addition, cooling the skin redistributes cooled blood back to the central circulatory system thus reducing thermal strain with the cooling of core body temperature.

The system that works best for horses due to its size is spray cooling heat transfer. It is ideal to have two operators to spray either side of the horse. It is recommended to begin at the head and neck followed by the chest and forelimbs then the body, hind limbs and between the legs. Spray nozzles are recommended to provide an even coverage of the skin surface.   

Dousing is another technique in which horses are placed in stalls and showered continuously until the condition resolves. Pouring buckets over the entire body of the horse is not recommended as most of the water falls to the ground, thus, not efficient at cooling the horse. 

Because most horses suffer from EHI immediately after the race, the appropriate location for inspection, cooling systems and veterinary care should be in the dismounting yard and tie-up stalls.  There must be an adequate supply of ice to ensure ice-cold water treatment. 

When treating a horse with EHI, there must be continuous and uninterrupted cooling until the CNS dysfunction has disappeared. 
When the skin surface temperature decreases to 30°C, cutaneous skin vessels begin to disappear; CNS function returns to normal, and there is the normalisation of behaviour. Cooling can be stopped, and the horse can be walked once CNS abnormalities have resolved. It must remain closely monitored for a further 30 minutes in a well-ventilated and shaded region. It is important that they are not unattended.

Scraping sweat off of the horse must only be done if the conditions are humid with no airflow.  However, if it is hot and there is good airflow, scraping is unnecessary because the sweat will evaporate.

Cooling collars

During strenuous exercise, there is a combination of heat production in the brain, reduced cerebral blood flow, creating cerebral ischaemia as well as the brain being perfused with hot blood. It is believed that cooling the carotid artery that aids in blood perfusion of the brain might be a strategy to cool the brain. A large collar is placed on either side and around the full length of the horse’s neck and is cooled by crushed ice providing a heat sink around the carotid artery; and it is able to pump cooled blood into the brain. 

Another possible benefit of this device is the cooling of the jugular veins, which lie adjacent to the carotid arteries.  The cooled blood in the jugular veins enter the heart and is pumped to the rest of the body, hence, potentially cooling the whole body. In addition, it is thought that the cooling of the carotid artery causes it to dilate, allowing greater blood flow into the brain. 

Provision of shaded areas

Shaded areas with surfaces that reflect heat, dry fans providing air flow and strategically placed hoses to provide cool water is an important welfare initiative at racecourses in order to minimise risk of EHI and treat when necessary. 

Conclusion

The most effective treatment of EHI is the early detection of the disease as well as post-race infrastructure that allows monitoring of horses in cooling conditions, while providing easily accessible treatment modalities when they are needed.  

Evaluating the horse’s central nervous system dysfunction is essential to recognise both the disease as well as monitoring the progression of the disease. CNS dysfunction allows one to define the severity of the condition. 

Understanding the pathophysiology of EHI is essential. It is important to recognise that it is a complex condition where both the inflammatory and thermoregulatory pathways work in combination. With a better understanding of these pathways, more effective treatment for this disease may be found.

7 Simple Rules for Parasite Control in Racing Yards

Article by James Gibbons

When Benjamin Franklin wrote, in 1789, ‘in this world nothing can be said to be certain, except death and taxes’, he could, perhaps, have added another certainty to his list – worms in horses. Unlike most other infectious diseases of horses, such as strangles or influenza—which infect a small number of horses relative to the entire horse population at any one time—worms are present in almost all horses all of the time.  This fact leads to two obvious conclusions: first, it is not possible to eradicate parasites and the threat of parasitic disease from our horses; second, worm control is vital in any environment where horses are kept.  

The threat posed by intestinal worms to racehorse performance has long been recognised by horsemen the world over. For many years, regular treatment with anthelmintic drugs (‘dewormers’) was the mainstay of worm control in racing yards, as it was in most in areas of horse breeding and production. The emergence of resistance to these deworming drugs (referred to as ‘anthelmintic resistance’), in the last 10 years in particular, has meant that such regular treatments may no longer be effective and may in fact make the resistance situation in the yard or farm worse. With this in mind, it is important that we consider how best to control worms while preserving the efficacy of the few deworming drugs available to us. This can be achieved using control programs comprised of drug- and non-drug control measures. This article sets out seven points/rules to consider and implement when developing such a worm control programme for racing yards. 

1. Know your enemy

It is not possible to draw up a parasite control program without considering which worms it is you are trying to control. The three main types of worms we are concerned with are strongyles (large and small redworms), ascarids (roundworms) and tapeworms. The role of tapeworms in equine intestinal disease is debated, but they appear to be linked to certain forms of colic when present in high numbers. Notably, there is no evidence of age-related immunity to tapeworms. Ascarids are a cause of disease in foals primarily and yearlings and so are likely to be of less concern in most racing yards. However, unlike redworms, which are transmitted almost exclusively at grass, ascarids can be transmitted in the stable; and ascarid eggs survive for years in the environment so that a single infected animal can infect other young horses for years to come.  

Redworms are the most important parasite of horses and are found in horses of all ages where they can cause anaemia, weight loss, ill-thrift and diarrhoea. Large redworms can burrow into the walls of blood vessels that supply blood to the gut causing a very severe form of colic.  Small red worms can lie dormant in the gut wall for extended periods then emerge en masse to cause an acute shock-like syndrome with severe diarrhoea, which is often fatal.  

Faecal egg count (FEC) testing will identify if redworms or ascarid eggs are present in your horse’s droppings and this, in turn, tells you that the adult worm of that species is present in your horse’s gut. Tapeworm eggs can be detected by FEC testing, but it is not the most reliable method for their detection as the shedding of these eggs is not consistent. As redworms are the most relevant worm present in most yards, most of the information in this article relates specifically to the control of redworms rather than ascarids or tapeworms.

2. Know your horses’ risk

All trainers pride themselves on their knowledge of almost every aspect of their horses’ anatomy and physiology, but not all could tell you which of their horses are at greater or lesser risk of worms. As mentioned above, all horses are likely to carry some worms, but the adult worm burden and the number of worm eggs shed in faeces is far greater in younger horses than in mature stock.  Most horses between the ages of 5 and 15 years will have a lower worm burden, and a lower risk of parasitic disease, than horses below this age due to a degree of age-related immunity. Foals and yearlings can carry particularly high worm burdens and shed large numbers of eggs into the environment to infect other horses. 

It follows that any yard with yearlings—two- or three-year-olds—will need a comprehensive worm control programme; while yards with older stock may get away with less strenuous controls. Horses over the age of 15 may also have higher worm burdens. And while these are unlikely to be in training, they may be used as a riding horse or companion animal and act as a potential source of infection for the string.

3. Know your yard’s weak points

It is not unusual for our lab to get a call from a racehorse trainer wishing to express their disbelief that the faecal egg count test from their horses has tested positive for redworm eggs despite their horses having no access to grass. In these situations, careful questioning as to how the yard operates will usually reveal the use of turn-out paddocks for a short period at some point during the week. Invariably, these are shared, often quite small, paddocks which host many horses over time; and so they are more likely to be contaminated with worm eggs.  

While the intention is for the horse to get ‘a pick of grass’, it may be that it is more ‘a pick of worms’ they are getting in such paddocks! As part of a worm control plan, it is important to first identify high-traffic areas, which may be a pinch-point for worm transmission.  Once identified, the key to reducing the worm burden on such paddocks is ideally through the removal of droppings. This can be a labour-intensive exercise, but it only needs to be done twice weekly rather than daily. And there are now more automated methods for cleaning paddocks than the more traditional wheelbarrow and spade!  

4. Identify high shedders 

FEC testing not only tells you what type of worm is present in your horse’s droppings but also how many eggs there are per gramme of faeces.  Repeated FEC testing allows you to build up a picture of the shedding patterns of the horses within your stable. Horses in racing yards should have FEC testing carried out every three months. It is generally accepted that the shedding of worm eggs in horses follows the 80/20 rule; that is, 20% of the horses shed 80% of the eggs.  

If these high shedders in the group can be identified, then targeted treatment of them may be more beneficial (and cost-effective) than blanket treatment of the entire group.    Horses with a strongyle egg count in excess of 250 eggs per gramme (EPG) on repeated testing may be considered high shedders and require more frequent egg counts and treatment.  It is important to state that this figure of 250EPG is not absolute, and the threshold above which animals are considered high shedders or requiring treatment should be set in conjunction with your vet. Worm eggs are not distributed evenly within the droppings, so when collecting samples for FEC testing, make sure to take at least three faecal balls—each from a different area of the pile. 

FEC testing can only detect egg-laying adult worms, but the egg count is not a reliable indicator of the adult worm burden of the horse, i.e. a horse with a high FEC does not necessarily have a greater worm burden than a horse with a lower FEC; but the horse with the high FEC is more significant in terms of worm transmission to other horses. Immature worms that may be present in the horse are not detected by FEC testing. In recent years, new tests have been developed that can detect antibodies to tapeworms and small redworm in blood and/or saliva. These tests are a useful addition to any worm control programme. Regardless of the type of test used, dewormers are still necessary as part of any worm control programme, in foals and yearlings in particular, but also in high-risk environments, and in order to control the disease risks posed to horses of all ages by large strongyles.  

5. Know which drugs work

While it might seem like there is an endless range of deworming products for horses on the market, the number of active ingredients in these products is very limited with only four drugs (fenbendazole, ivermectin, moxidectin and pyrantel) available for the treatment of redworms and ascarids. With such limited availability, and no prospect of new worm treatments entering the market anytime soon, it is vital that we use the existing drugs judiciously so as to preserve their effectiveness into the future.  

The threat posed by anthelmintic resistance is very real. Already fenbendazole resistance in redworms is widespread, and ivermectin/moxidectin resistance in ascarids is becoming more common. This means that there are only one or two effective treatments remaining for these resistant worms. While thoughts of anthelmintic resistance may not keep any racehorse trainer awake at night, we do expect that the deworming treatments we use to be effective, not least because they cost quite a lot of money!  The only way to determine if our treatments are indeed effective is to carry out a faecal egg count reduction test (FECRT). 

This test follows on from the FEC test; any horse with a FEC of 500EPG or more should be treated with a dewormer and have a follow-up FEC carried out 10–14 days after that treatment. The percentage reduction in egg numbers is calculated and should be greater than 90–95% (depending on the drug). Reductions less than this are suggestive of a resistance problem. Because of the existing resistance situation, FECRTs should be carried out before using fenbendazole to treat redworms or ivermectin/moxidectin to treat ascarids. Equally, if you have any suspicion that a deworming product is not working effectively in your yard, then a FECRT for that drug should be carried out to investigate this.   

6. Don’t overtreat

Aside from the risk of anthelmintic resistance development and the significant costs incurred by frequent or blanket deworming of all horses in the yard, such treatments can have other effects on the horse, which may ultimately impact performance. Research has shown that anthelmintic administration is associated with a decrease in the diversity and abundance of certain bacteria in the horse’s gut, which may impact digestion and other metabolic processes. 

In humans, changes in the composition of the gut bacterial population have been shown to impact physiology, immunity and behaviour; and, while the structure of the gut may differ greatly between human and horses, there is no reason to believe the equine gut bacteria do not play a similarly important role in horse health. In recent years, the role of parasites in human health has been revaluated. And while they are still recognised as an important cause of disease, it is also accepted that they can play a beneficial role in the development of immunity and the prevention of some diseases. While we don’t have similar evidence of a benefit to horse health from parasites, it is not impossible that such benefits do really exist.  

A study of standardbred trotters in Denmark in 2011 found that horses with higher egg counts had better race finishing position than those with lower egg counts. So,  the presence of parasites does not always lead to poor performance! It was standard practice, in some racing yards, to deworm horses every eight weeks, but this seems excessive when one considers the biology of the worms involved. The small redworms take approximately eight weeks to develop to maturity in the horse, while the large redworms take approximately six months to do so. Treatment every eight weeks could only be justified if there were evidence of overwhelming worm exposure on an ongoing basis—something which is unlikely in a modern racing yard. Even if that were the case, other non-pharmaceutical controls would be necessary to get the situation under control.

7. Manage new arrivals

One of the challenges of worm control in a racing yard is the constant turnover of horses with some leaving the yard for rest or recovery from injury, others returning from such breaks and new horses joining the yard. When a horse leaves the yard, they leave the worm control programme as well. Evem if the yard’s deworming programme is followed while they are away, the risk factors in their new environment may be totally different and require an entirely different approach to treatment. More worrisome, the arrival of new horses or the return of others also risks the introduction of new or resistant parasites to the yard. In order to minimise this risk, all new arrivals should be isolated, tested and treated. Ideally, all new arrivals would be isolated for two weeks while a FECRT is carried out to ensure treatment has been effective.  

This may not be practical in all yards, but an isolation of period of at least three days after deworming should be observed to ensure all worms are shed before the horse joins the group. Treatment without isolation is not recommended as treated horses can shed viable eggs for a few days after deworming. There may be a temptation to let horses out to turnout paddocks for exercise or grass during the isolation period, but we have seen cases where this has led to the introduction of new parasites to the yard despite the horse being treated before it was turned out.   

There was a time when parasite control in racing yards was relatively simple and relied primarily on the regular use of deworming drugs. As with many aspects of horse racing, what was once considered acceptable is no longer so. Effective parasite control is not as simple anymore, and an overall plan designed to meet the needs of the individual yard is required. That is not to say that any trainer should be daunted by the prospect of drawing up such a plan. The seven points discussed here provide a basis to work from and your vet and laboratory are well placed to assist in building on this.  

Equine Neck CT: Advancing diagnostic precision in racehorses

Article by Rachel Tucker MRCVS

Introduction

When considering neck disorders in the racehorse, we most commonly think of severe conditions such as acute neck trauma and cervical vertebral myelopathy (Wobbler Syndrome). These represent the most severe end of the scale of orthopaedic and neurologic injury to the neck; and a diagnosis, or at least prognosis, is usually clear. However, neck conditions encompass a far wider range of clinical presentations. 

Horse positioned in ct scanner

At the milder end of the scale, signs may be subtle and easily missed, whilst still being responsible for discomfort and reduced performance. The recent ability to perform a computed tomography (CT) scan of a horse’s neck represents a major advancement in our ability to diagnose neck conditions. Timely and accurate diagnosis allows efficient and targeted treatment, the ability to plan schedules and improvement in welfare through the provision of appropriate treatment and earlier return to function. 

In neurologic cases, an accurate diagnosis facilitates risk management for both the horse, their handlers and riders, while improving safety for all.  As conditions and injuries of the neck are being better characterised using CT, new medical and surgical treatment options are being developed, giving the potential for improved outcomes and fewer losses from the racing industry. 

This article summarises how CT is being increasingly used by vets to diagnose conditions of the neck and how it is revealing previously unknown information and providing exciting new treatment opportunities. 

Presentation

Conditions of the neck can cause a range of signs in the horse, which are wide-ranging in their presentation and variable in their severity. The manner in which these conditions present depends on which anatomical structures are affected. Issues affecting the bones, joints and/or soft tissues of the neck can all cause neck pain, which can manifest in a number of ways. Cases of neck pain can be severe, resulting in a horse with a rigid, fixed neck carriage, an unwillingness to walk and struggling to eat, perhaps due to a traumatic event. Neck fractures are thankfully uncommon but can be catastrophic. 

More moderate signs might be displayed as a stiff neck, with reduced range of movement and resentment of ridden work. There may be pain on palpation of the neck and changes in the neck musculature. Increasingly, we are seeing horses with far more subtle signs, which are ultimately revealed to be due to neck pain and neck pathology. Typically, these horses might have an acceptable range of motion of their neck under most circumstances, but they suffer pain or restriction in certain scenarios, resulting in poor performance. This may be seen as tension through the neck, resisting rein contact, a reluctance to extend the neck over fences, or they may struggle on landing. 
Riders might report a feeling of restriction or asymmetry in the mobility of the neck. In addition, these horses may be prone to forelimb tripping or show subtle forelimb lameness. 

Any condition, which causes injury or disease to the spinal cord or nerves within the neck, also causes a specific range of neurologic signs. Compression of the spinal cord is most commonly caused by malformations or fractures of the cervical vertebrae, or enlargement of the adjacent articular process (facet) joints. This results in classic ‘Wobbler’ symptoms, which can range from subtle weakness and gait abnormalities, through to horses that are profoundly weak, ataxic and uncoordinated. This makes them prone to tripping, falling, or they may even become recumbent. 

Peripheral nerve deficits are uncommon but become most relevant if they affect the nerves supplying the forelimbs, which can result in tripping, forelimb lameness, or local sensory deficits. This lameness might be evident only in certain circumstances, such as when ridden in a rein contact. This lameness is difficult to pinpoint as there will be no abnormality to find in the lame limb, indeed a negative response to nerve and joint blocks (diagnostic analgesia) will usually be part of the diagnostic process.

Horses can present with varying combinations and severities of neck pain, neurologic signs and peripheral nerve deficits, creating a wide range of manifestations of neck related disease. 

Diagnosis

A diagnosis of neck pain is based on careful static and dynamic clinical examination and may be supported by seeing a positive response to treatment. Neurologic deficits are noted during a specific neurologic assessment, which includes a series of provocation tests such as asking a horse to walk over obstacles, back up, turn circles and walk up and down a hill. Confirming neck pathology as the cause of signs can be difficult. Until recently, radiography has been the mainstay imaging modality. Radiographs are useful for assessment of the cervical vertebrae and continue to play an important role in diagnosis; however the complex 3-dimensional shape of these bones, the large size of the neck and an inability to take orthogonal (right-angled) x-ray views means that this 2-dimensional imaging modality has significant limitations. High quality, well-positioned images are essential to maximise the diagnostic potential of radiographs. 

A turning point in our diagnostic ability and understanding of neck dysfunction has been the recent adaptation of human CT scanners to allow imaging of the horse’s neck. A number of equine hospitals across the United Kingdom and Northern Europe now offer this imaging modality. We have been providing this service at Liphook Equine Hospital since 2017, with over 150 neck scans performed to date.

The CT procedure

A computed tomography (CT) scan combines a series of x-ray images taken from different angles around the area of interest to create a 3-dimensional volume of imaging data. This data is presented as a grayscale image which can be viewed in any plane and orientation. It provides excellent bone detail, and post processing techniques can provide information on soft tissue structures too. Additional techniques can be employed such as positive contrast myelography to provide greater detail about soft tissue structures. Myelography delineates the spinal cord using contrast medium injected into the subarachnoid space and is indicated in any case showing neurologic signs suggestive of spinal cord compression. 

Neck CT is performed under a short general anaesthetic. Scans without myelography typically take less than 20 minutes to complete. The entire neck is imaged, from the poll to the first thoracic vertebra. The procedure is non-invasive and low risk, with anaesthetic-related complication presenting the main risk factor to the procedure. We have not encountered any significant complications in our plain CT scan caseload to date. Horses showing ataxia, weakness and incoordination (Wobbler’s), undergo CT myelography which adds around 20 minutes to the procedure. These horses are exposed to a greater level of risk due to their neurologic condition, the injection of a contrast agent and the increased chance of destabilising a more severe lesion during the procedure. 

Sagittal and transverse CT myelogram images of a young racing thoroughbred showing neurologic (Wobbler) signs. shows narrowing of the spinal canal at the base of the neck (arrow)

CT is revealing more detailed information about ways that spinal cord compression can occur in Wobbler cases, about compression of spinal nerves resulting in forelimb gait deficits and precise detail about fracture configurations. It gives us detailed images of articular process joint disease, intervertebral disc disease, developmental conditions and anatomic variations. It is also revealing information about rare diseases such as vertebral abscesses or spinal neoplasia. As our caseload and confidence in the imaging modality grows, we are learning more about the value of CT in examining more subtle neck conditions. We are also bringing the benefit of a more accurate diagnosis, allowing precise targeted treatment and a better ability to provide a prognosis about outcomes—likely progression or safety factors. CT myelography allows circumferential imaging of the spinal canal and yields significantly more information than traditional x-ray myelography. As a result, we hope to enable better case selection of horses that may benefit from Wobbler surgery, with the goal of resulting in improved success rates of the surgery.

Innovations in treatment

image shows a fracture of the articular process of the 3rd cervical vertebrae in the mid neck, which was not visible on x-ray. 

New treatment options are emerging as a result of our more accurate diagnoses of neck pathology. Of the first 55 horses which underwent neck CT at our hospital, we were surprised to discover that 13 (24%) had some form of osteochondral fragmentation within the articular process joints of their neck. Some of these horses were young Thoroughbreds, bred to race but showing Wobbler signs. These tended to have convincing CT evidence of type 1 CVM (Wobbler Syndrome) and osteochondrosis affecting their neck. Others had fragments which were larger and more discrete, with evidence of articular process joint enlargement/arthritis but no other bony lesions. These horses were typically older and of a range of breeds and uses. 

In those horses presenting with signs of neck pain but no neurologic deficits, surgical removal of these fragments was proposed. Following further consideration and cadaver training, we have begun to offer this surgery for horses that fit the appropriate criteria and have surgically accessible fragments.  We have performed arthroscopic or arthroscopic-assisted fragment removal from eight articular process joints in six horses to date. No intraoperative or postoperative complications have been encountered; and five of six horses showed complete resolution of neck pain. In the sixth horse, full recovery was not anticipated due to the presence of additional neck pathology, but partial improvement occurred for two years.  Fragment removal has relieved signs of neck pain and stiffness and caused improved performance in these horses. 

Two procedures that are emerging to treat spinal nerve root impingement are a targeted peripheral nerve root injection and a keyhole surgical procedure to widen the intervertebral foramen. Nerve root injection is performed in the standing sedated horse under ultrasound guidance. Surgery is performed under anaesthesia, using specialised minimally invasive equipment to widen the bony foramen using a burr. This surgery is in its infancy but offers an exciting treatment option.  

Additionally, CT gives us the ability to better plan for fracture repair, undoubtedly improving our case selection for Wobbler surgery; it more accurately guides intra-articular injection of the articular process joints. 

Summary

Computed tomography is transforming our ability to diagnose conditions of the horse’s neck. The procedure is low risk and now widely available in the UK and other parts of Europe. It is driving the innovation of novel treatment options with the goal of improving outcomes and reducing losses to conditions of the neck. Our CT findings are posing new questions about neck function, pain and neurologic disease and is an active area of ongoing research.

Anatomy of the cervical vertebrae

The neck vertebrae of the horse

The neck consists of seven cervical vertebrae which form a gentle S-shaped curve to link the skull at the poll to the thoracic vertebrae of the chest. Its primary functions are to protect the spinal cord, support the heavy weight of the head and to allow a large range of movement so that a horse can monitor his environment and run at speed, both being vital to this prey species. 

The first (atlas) and second (axis) cervical vertebrae are highly adapted to allow head mobility. The third to sixth vertebrae are very similar in shape, whereas the seventh is shortened as it starts to show similar features to the vertebrae of the thorax. The typical cervical vertebra consists of a cylindrical column of bone (vertebral body) articulating with adjacent vertebrae via an intervertebral disc. 

Running along the upper surface of this bony column is a bony canal created by the vertebral arch. This canal protects the spinal cord and associated structures that run through the centre. Above and to the side of the spinal canal sit the paired articular processes and below; and to the side sit the transverse processes. These are bony prominences to which muscles attach. The soft tissues of the neck are complex and intrinsically linked to the forelimbs and entire axial skeleton.  

The articular processes also form the articular process joints (facet joints) which create an additional two joints between each vertebra. Although highly adapted, these joints are similar to others in the body consisting of cartilage-lined surfaces, a joint capsule and joint fluid. The joint surfaces are oval in shape, approximately 3-4cm in diameter and sit at an oblique angle to the neck. They provide important additional support and mobility to the neck.

References:

Schulze N., Ehrle, A., Beckmann, I and Lischer, C. (2021) Arthroscopic removal of osteochondral fragments of the cervical articular process joints in three horses. Vet Surg. ;1-9. 

Swagemakers J-H, Van Daele P, Mageed M. Percutaneous full endoscopic foraminotomy for treatment of cervical spinal nerve compression in horses using a uniportal approach: Feasibility study. Equine Vet J. 2023. 

Tucker R, Parker RA, Meredith LE, Hughes TK, Foote AK. Surgical removal of intra-articular loose bodies from the cervical articular process joints in 5 horses. Veterinary Surgery. 2021;1-9.

Wood AD, Sinovich M, Prutton JSW, Parker RA. Ultrasonographic guidance for perineural injections of the cervical spinal nerves in horses. Veterinary Surgery. 2021; 50:816–822. 

Treating 'bucked shins' in the thoroughbred racehorse

Article by Adam Jackson MRCVS 

One of the most common causes of lost days to training and racing in racehorses is dorsal metacarpal disease (DMD), which is often referred to as “bucked shins” or “sore shins”.  

Often a frustration to trainers and owners, this problem rears its ugly head at the time of highest expectations, such as arising the last day of work before a horse’s first race; right after a horse’s first victory; or after a horse was purchased at a two-year old sale.

This disease presents with heat, pain with or without inflammation (swelling) on the dorsal (front) surface or the dorsomedial (front inside) surface of the third metacarpal bone (cannon) referred to as acute periostitis. With rest and reduced exercise, the condition can improve, but catastrophic fractures of the cannon may occur at the site of previous DMD episodes.  A good understanding of this disease and strategies of prevention are vital in order to improve the welfare of the horse and reduce the potential expenses to all shareholders.  

Introduction

The cannon bone is an important structure in the weight-bearing and absorbing shock. As the horse moves, the bone bends a little and then returns to its original shape like an elastic band, often referred to as elastic deformation.  In addition, it has been observed that horses that work slowly have tension on the front of the cannon bone; in other words, the bone is stressed by a stretching force rather than a compressing force. However, at higher speeds, these forces change from stretching to compressing forces.

Repeated bending forces (stress cycle) on the cannon bone causes dorsal metatarsal disease. When the horse is young, it has a thin bone cortex. As the horse grows and is repeatedly subjected to these forces, the bones remodel and the cortex thickens, making it stronger. However, if the bending forces exceed the bone’s ability to remodel, then this leads to stress fatigue and bone damage.

The occurrence of bucked shins is most common when horses are developing, typically two–three years old as training becomes more intensive. But it must be noted that if the horse is not bone fit, any aged racehorse is susceptible to these diseases when they begin training. Roughly at the age of five years old when a horse is fit, they are at a low risk of this disease. Within the first six months of training, DMD may present in one or both front limbs. If the condition does occur in both front limbs and the horse is being trained on a circular track, then it is likely the inside leg is where it will occur first.  In other words, if the training tends to be in a counterclockwise training circuit, then there are greater forces on the left limb than the right; thus the left is more likely to develop the disease before the right limb.

Risk Factors of DMD

Age: DMD occurs most commonly in 2–3 year olds, often within their first 6 months of training. It is rarely seen in horses with a mature skeleton (age 4 and over). However, this disease has been seen in 5 year olds especially if they have been stalled for a long amount of time after weaning and not racing until that age.

Gender: It is believed that the gender of the horse does not alter its risk to DMD.

Breed: Most common in thoroughbreds but may be seen in both standardbreds and quarter horses. 

Genetics: The risk of DMD is influenced by genetics as variation in limb bone geometry (inherited) behaves differently to force/strains on the bone. In addition, the longer the cannon bone, the greater the load is at flexion of the dorsal cortex of the bone, making it more susceptible to DMD.

Training and racing surfaces: The different types of training and racing surface alter the risk to DMD because there are variations in the force applied to limbs as well as the acceleration rates of hoof impact.  Furthermore, the impact of these forces is increased with greater speed.  Dirt tracks tend to be the hardest surface, whereas synthetic tracks reduce hoof and limb impact and loading force.  However, it is important to remember that the hardness of all of these surfaces can be altered by a number of other factors such as:

1. Different surface materials

2. Changes in weather, temperature and humidity

3. Surface maintenance (i.e., soaking, harrowing)

4. Changes in horse body weight

5. Age of surface – wear and tear of surface

6. Human opinion of track’s condition

Training: The length of time for bones to respond to different training practices is unknown. Although further research is required, it is suggested that fast work should be avoided in the early stages of training as it is thought that high-speed exercise introduced too quickly (within 1 month) was detrimental to bone health.

Direction of training: Track direction varies globally. Thoroughbreds tend to lead with the inside forelimb around turns then switch to the outer forelimb on the straight. It has been suggested that due to greater forces on the leading limb on the turn, that limb is more at risk of bucked shins. However, more research is required to make accurate conclusions.

Speed: Current research is contradictory. Some research indicates a reduction in the risk of DMD if the horse is trained at high speeds with every extra mile worked and canter work increases the risk. However, other research suggests that short periods of work (< 1 month) at high speed increases the risk of DMD.

Camber:  European tracks, with turf being the prevalent surface, tend to vary in their design, often including slopes, twists, turns, uphill sections, and cambers. In addition, races may be run straight, clockwise or counterclockwise. This is in contrast to the USA where the tracks are usually flat. Although it is known that this variation in track characteristics alters the horse’s gait, thus altering forces on the forelimbs, further research is needed to understand if these variations increase the risk of DMD.

How does DMD develop?

Buck shin is the formation of tiny stress fractures on the front or inside of the cannon bone of the horse’s front legs. DMD occurs when the stress on the legs with high-speed training exceeds the bone’s ability to adapt to those stresses. 

Bone is a dynamic tissue that is constantly adapting its structure. Once the bone is formed in immature animals, the bone grows and changes shape by a process called modelling. Bone remodelling is different from modelling in that its function is to renew the skeleton and involves both bone resorption and formation to occur at the same location in a sequential manner.   

With high-speed training, there is high-strain fatigue, which causes excessive compression of the bone. During this compression, there is insufficient amount of bone remodelling at the point of stress. At this site, this new bone is much weaker; thus, it is susceptible to inflammation and pain and may lead to fractures.

Treatment of dorsal metacarpal disease

Treatment of DMD is designed to alleviate pain and inflammation while allowing the remodelling process of the bone to catch up with the damage that has been caused from stress cycling.

The core of the treatment is rest and providing pain relief, followed by a slow and gradual increase in exercise levels. 

Fractures of the bone cortex can be treated with surgery using lag screw fixation and osteostixis. Osteostixis is the drilling of many holes around the site of fracture in order to promote bone healing. Lag screw fixation is the drilling of a screw across the fracture line to compress and stabilise the bone. However, fracture recurrence is common with both techniques and requires 5–6 months out of training.

There are additional treatments that may be used to complement core treatments. Extracorporeal shock wave therapy (ESWT) is commonly used for treatment and involves a highly concentrated, powerful acoustic (sound) energy source being applied to the site of injury. The rationale is that ESWT increases blood flow, increases growth of new blood vessels and increases the production of natural healing factors in the treated area. The research findings are limited on its effectiveness but anecdotally amongst the veterinary profession, it seems to work on bucked shins and stress fractures. 

In Europe, horses must not have had shock wave therapy on the day of racing, or on any of the five days before the race day in which the horse is declared to run. In North America, horses are not permitted to race or breeze for 30 days following treatment as per the Horseracing Integrity and Safety Authority’s (HISA) rulings. 

With all treatment options, there must be a careful and considered discussion with the veterinarian and all stakeholders on the desired outcome while bearing in mind the important factor of the horse’s welfare and wellbeing.

What about bisphosphonates?

Some clinicians are using a combination of shockwave and bisphosphonates (Tildren TM, OsPhos, TM) to treat DMD. Bisphosphonates were first seen in human medicine and used for osteoporosis. Bones are constantly remodelling in a process that removes old bone cells and deposits new ones. Bisphosphonates help prevent bones from losing calcium and other minerals by slowing or stopping that natural process that dissolves bone tissue, thus, helping bones remain strong and intact. Veterinary surgeons report mixed results with these therapies, and long-term use of bisphosphonates is expensive and has serious consequences. Bisphosphonates are toxic to the gastrointestinal and renal systems, thus, potentially causing colic and kidney disease. Their safety has not been evaluated for the use in horses younger than four years old nor in pregnant and lactating mares.

RULES ARE CHANGING - Bisphosphonates

Bisphosphonates are not to be administered to a racehorse under the age of three years and six months as determined by its recorded date of birth, on the day of the race or on any of the 30 days before the day of the race in which the horse is declared to run as per The International Federation of Horseracing Authorities rulings for Europe. 

In America, HISA’s Anti-Doping and Medication Control (ADMC) Program came into effect on March 27 and with it, new regulations regarding the presence and use of bisphosphonates.

The Horseracing Integrity & Welfare Unit (HIWU) states “The ADMC Program regulations categorise bisphosphonates as a Banned Substance, meaning that they are prohibited from being administered to, or present in, covered horses at any time. Covered horses that test positive for bisphosphonates under the ADMC Program are subject to lifetime ineligibility, and associated covered persons may incur an Anti-Doping Rule Violation.”

“HIWU will not pursue disciplinary action against Covered Horses or their associated covered person(s) for the presence of bisphosphonates if the covered person(s) can provide documentation (e.g. medical records or a positive test result) to HIWU of the administration or presence of bisphosphonates prior to the implementation date of the ADMC Program.” 

Training regimens

With DMD, it must be remembered that it is an appropriate response for new bone formation when the cannon endures cyclic stress and injury. This injury cannot be ignored but addressed to reduce the risk of serious consequences.  Exercise is the root of the problem; therefore, the solution is to alter the patterns of exercise.   

Dr David Nunamaker DVM of the University of Pennsylvania has developed a training programme, which is believed to reduce the risk of DMD. The rationale when developing this modified training programme is that horses are not born with the right bone structure for racing. The bones are to develop and adapt to racing. By providing training programmes that mimic racing, the bones can adapt to the forces that are applied during racing, thus reducing the risk of developing bucked shins.

When initiating this training regimen, it is assumed that young horses are broken to ride in autumn and able to gallop a mile by January so that training can start. 

Stage 1 (5 week duration) – Horses finish the gallops two times a week with the last 1/8th of the mile (last 200 metres of 1600 metres) completed in an open gallop in 15 seconds.

Stage 2 (5 week duration) – Twice a week open gallops for ¼ of a mile (400 metres of 1600 metres) in 30 seconds, including a 1 mile (1600 metres) gallop.

Stage 3 (7 week duration) – The addition of speed work once per week.  Breezing (moderate speed) for ¼ mile (400 metres) and daily gallops lengthened to 1 ¼ miles twice per week for 4 weeks. The following 3 weeks, the ¼ mile breeze is continued with a strong gallop out for another furlong (roughly 40 seconds total for a breeze).

Conclusion

The findings of exercise research are often varied and contradictory due to many research variables making comparisons and conclusions difficult. In addition, most of the research of musculoskeletal issues in racehorses uses racing data, but most injuries occur during training

Because more research is needed, there remain conflicting views of the effects of racing on horses before skeletal maturity and the most effective and safe way to introduce speed exercise. At present, the data suggests that distance and speed be implemented gradually and should include high-speed work at full racing speed.

The racing industry must continue to work cooperatively to address the welfare concerns associated with horses experiencing DMD.

The importance of the Sacroiliac joint

Article by Annie Lambert

Horses that present as sore in the hindquarters can be perplexing to diagnose. Sometimes the problem is found in the last place you look – the sacroiliac joint.

Even though the sacroiliac joint (SI) was on veterinary radars long ago, due to its location buried under layers of muscle in the equine pelvic region, the joint and surrounding ligaments were tough to diagnose and treat.

The sacroiliac joint is often a source of lower back discomfort in race and performance horses. Trainers may notice several clinical signs of a problem. These hints include sensitivity to grooming, objections to riders getting legged up, stiffness of motion, pain to manual palpation of the rump or back, resistance to being shod behind and poor performance.

Of course, those symptoms could describe other hind limb soundness issues, making the origin of the problem arduous to ascertain. A thorough physical examination with complete therapeutic options can relieve sacroiliac pain. The treatments are complicated, however, by the anatomy of the SI area. 

The equine pelvis is composed of three fused bones: ilium, ischium and pubis. The sacrum, the lower part of the equine back, is composed of five fused vertebrae. The sacroiliac joint is located where the sacrum passes under the top of the pelvis (tubera sacrale). The dorsal, ventral and interosseous sacroiliac ligaments help strengthen the SI joint. 

The SI and surrounding ligaments provide support during weight bearing, helping to transfer propulsive forces of the hind limbs to the vertebral column—creating motion much like the thrust needed to break from the starting gate.

Sound complicated? It certainly can be.

Diagnosing Dilemmas

It wasn’t until modern medical technology advanced that the SI could be explored seriously as a cause of hind lameness.

“The sacroiliac is one of the areas that’s very hard to diagnose or image,” explained Dr. Michael Manno, a senior partner of San Dieguito Equine Group in San Marcos, California. “[Diagnostics] of the area probably correlated with bone scans or nuclear scintigraphy. You can’t really use radiographs because the horse is so massive and there is so much muscle, you can’t get a good image.

“About the only time you can focus on the pelvis and get a decent radiograph is if the horse is anesthetized—you have a big [x-ray] machine and could lay the horse down. But, it’s hard because with anything close to a pelvic injury, the last thing you want to do is lay them down and have them have to get back up.”  

The nuclear scintigraphs give a good image of hip, pelvis and other anatomical structures buried deep in the equine body, according to Manno, a racetrack practitioner. “Those images can show areas of inflammation that could pretty much be linked right to the SI joint.”

The other modern technological workhorse in the veterinary toolbox is the digital ultrasound machine. Manno pointed out that veterinarians improved diagnostics as they improved their ultrasounding skills and used those skills to ultrasound areas of the body they never thought about before. Using different techniques, frequencies and various heads on the machine’s probe, the results can be fairly remarkable.

“The ultrasound showed you could really image deeper areas of the body, including an image of the sacroiliac joint,” Manno said. “It can also show some ligament issues.”

Where the SI is buried under the highest point of a horse’s rump, and under heavy gluteal muscles, there are two sets of ligaments that may sustain damage and cause pain. The dorsal sacroiliac ligaments do not affect the sacroiliac joint directly, but help secure the ilium to the sacral spine. The ventral sacroiliac ligaments lie deeper, in the sacroiliac joint area, which they help stabilize. These hold the pelvis tight against its spine. The joint itself, being well secured by these ligaments, has little independent movement and therefore contains only minimal joint fluid.

Diagnosing the SI can be complex because horses often travel their normal gait with no change from normal motion—no signs of soreness. Other horses, however, are sore on one leg or another to varying degrees, sometimes with a perceptible limp. 

“I don’t know that there is a specific motion,” Manno explained. “You just know that you have a hind end lameness, and I think a lot of performance horses have mildly affected SI joints. 

“The horses that are really severe become acutely lame behind, very distinct. You go through the basic diagnostics, and I think most of these horses will show you similar signs as other issues behind. We palpate along the muscles on either side of their spine and they are sore, or you palpate over their croup and you can get them to drop down—that kind of thing. Other times you do an upper limb flexion on them and they might travel weird on the opposite leg. So, it can be a little confusing.” 

In the years prior to the early 2000s, the anatomical location of the SI hindered a definite diagnosis; decisions on hind soreness were more of a shrug, “time and rest” treatment evaluation. As one old-time practitioner called it, a SWAG – “Scientific Wild Ass Guess.”

Even with modern tools, making a conclusive diagnosis can be opaque.

“The less affected horses, through exercise and with medications like Robaxin [muscle relaxer] or mild anti-inflammatories, seem to be able to continue to perform,” Manno said. “I don’t know how you can be perfectly sure of an inside joint unless you try to treat it and get results.”

“That’s why bone scans came into play and are really helpful,” Manno added. “You can image that [SI] area from different angles with the machine right over the path of the pelvis, looking down on it or an angle view into it, and then you see it from the side and the back very often. We can get an idea from the different views and angles of where the inflammation is and pinpoint the problem from that.” 

Once Manno has a generalized idea of where the problem is, he fine-tunes his hypothesis using more diagnostics with a digital ultrasound machine. 

“You can ultrasound from up above and see the joint that way,” he said. “As ultrasound has progressed, we’ve found that the rectal probes the breeding vets have used can also be tuned in to start looking for other things. If you turn them upwards, you can look at the bottom of the pelvis and the SI joint. You can see things through the rectum by just looking straight up. That is a whole new thing that we probably never thought about doing. I don’t profess to be very great at it; it’s not something I do a lot, but there are people that are just wonderful at it.” 

Treating a Theorem

But, if the diagnosis is incorrect, the prescribed treatment may be anything but helpful.

“In many cases, if a horse is really sore, you need to be very careful,” cautioned Manno. “What you don’t want to do is go from a strain or some sort of soft tissue injury into a pelvic fracture by trying to keep them going. In many cases you are back in the old rest and time type of treatment.”

Manno pointed out one treatment that has advanced over many years is injecting the SI joint directly. There are a couple of techniques used when injecting the SI. With a blind injection the practitioner directs a long, straight needle into the joint by relying solely on equine anatomy. The other technique employs an ultrasound machine to guide the placement of the needle into the joint.

“Normally we are just injecting cortisone in those cases,” Manno noted. “We are trying to get the inflammatory response to settle down. Hopefully that gives the horse some relief so that they’re a bit more relaxed in their musculature. You know how it is when you get a sore back; it’s hard to keep yourself from cramping, which makes everything worse.”

A slight tweak of that technique is to use a curved needle. When you are positioning the curved needle, it follows the curve of the horse’s anatomy and helps the practitioner direct the injection into the joint.

“It curves right into position for you; it gives you a little help,” Manno confirmed of the curved needle. “Some people are really good with that technique; others still like to go to the straight needle. [The curved needle] helps you approach the site without interference from the bones in that area.”

SI joint injuries affect most performance horses, including Standardbred trotters and pacers, Western performance athletes as well as hunters, jumpers and dressage horses.

The older show horses are often diagnosed with chronic SI pain, sometimes complicated by arthritis. These chronic cases—and admittedly some racehorses—are treated with different therapies. These conservative, nonsurgical treatments have been proven effective.

In addition to stall rest and anti-inflammatories, physical training programs can be useful in tightening the equine patient’s core and developing the topline muscles toward warding off SI pain. Manno, a polo player who also treats polo ponies, believes the hard-working ponies avoid having many SI injuries due to their fitness levels. 

“I think these polo horses are similar to a cross between a racehorse and a cutting horse,” Manno opined. “They are running distances and slide stopping and turning.”

Other treatments utilized include shockwave, chiropractic, acupuncture, therapeutic laser and pulsed electromagnetic therapy.

Superior Science

With the new diagnostic tools and advanced protocols in their use, veterinarians can pinpoint the SI joint and surrounding areas much closer. This gives them an improved indication that there definitely is an issue with the sacroiliac. 

When there is a question about what is causing hind end lameness, most practitioners begin with blocking from the ground up.

“In many cases with hind end lameness that we can’t figure out, we block the lower leg; if it doesn’t block out down low, we conclude the problem is up high,” Manno said. “Once you get up to the hock you’re out of options of what you can figure out. You start shooting some x-rays, but by the time you get to the stifle, you’re limited. Bone scans and ultrasounds have certainly helped us with diagnosing.”

Manno doesn’t see a lot of SI joint injuries in his practice, but he noted there were cases every now and again. He also opined that there were probably other cases that come up in racehorses on a short-term basis. He also noted that, although it may not be a real prominent injury, that’s not to say it has not gone undiagnosed.

“I think we realize, in many of the horses we treat, that the SI joint is something that may have been overlooked in the past,” Manno concluded. “We just didn’t have the ability to get any firm diagnosis in that area.”

International Codes of Practice on equine disease for 2023

Article by Victoria Colgate and Richard Newton

Horses are one of the most internationally travelled species, second only after humans, and this mobility, both between and within countries, means that the spread of equine infectious diseases is a very real and ever-present threat.

Indeed, infectious disease outbreaks are often related to new arrivals at, or movement of animals on and off premises, such as to competitions and race meetings. As well as having a negative impact on horse health and welfare, disease outbreaks can have further reaching consequences in terms of treatment costs, economic losses due to movement restrictions and an inability to compete, as well as disruption to the breeding schedule, which may have effects in racing in future years. Additionally, restrictions imposed in the face of the diagnosis of certain diseases can prevent the free export of horses between countries, impacting trade and equestrian sport. Infectious diseases are truly trans-boundary, and such a problem necessitates global cooperation and communication, echoing the mantra that ‘prevention is better than cure’. 

The origins and evolution of the Codes of Practice

figure 1

In 1977 in Newmarket, UK, there was widespread development of vulval discharge in thoroughbred mares post-covering that adversely affected their fertility and to an extent that caused temporary closure of stallion barns and stud farms. Initially unknown, the cause of this outbreak was later identified as the bacterium Tayorella equigenitalis, the causative agent of contagious equine metritis (CEM) and often referred to as the CEM organism, or CEMO. 

The impact on the 1977 breeding season was significant enough for the Horserace Betting Levy Board (HBLB) to consider a serious need to control CEM in future years and in reaction to this, the Codes of Practice (CoP) were created. First developed by HBLB committee discussion in the summer of 1977 and then formally published in 1978, the HBLB CoP outlined swabbing protocols in the weeks prior to covering in an attempt to prevent the venereal transmission of CEM. 

Despite the perceived draconian nature of these first codes, compliance was high and overall were highly successful—with CEM cases drastically falling following their introduction. In subsequent years, the CEM CoP was extended to include control measures on reproductive disease caused by the other venereal bacterial pathogens: Klebsiella pneumoniae (capsule types 1, 2 and 5) and Pseudomonas aeruginosa. Codes on the prevention and management of equine herpesvirus-1 (EHV-1) and equine viral arteritis (EVA) were also added following disease outbreaks of significant concern to the thoroughbred breeding industry in subsequent years. 

Today the CoP are referred to as the ‘HBLB International Codes of Practice’, with the 2020 CoP being the inaugural internationally branded edition and representing a comprehensive manual outlining a series of voluntary standards (codes) and advisories (guidelines), with accompanying appendices. They are intended to assist breeders, trainers and horse owners (in collaboration with their veterinary surgeons) to control and prevent a range of important infectious diseases in equids. The CoP have a broad application among thoroughbred breeders; and the UK, Ireland, France, Germany and Italy are all signatories. Additionally, in a translated form, they have formed the basis of written equine infectious disease advice in many other countries. The initial reduction and then sustained maintenance of low levels of infectious disease outbreaks experienced after the CoP’s introduction is testament to the document’s effectiveness and importance.  

The HBLB International Codes of Practice for the 2023 breeding season

The CoP are reviewed annually by a group of international veterinary breeding and infectious disease experts and stakeholder representatives. This review ensures that all advice is as current as possible regarding the latest scientific evidence and global disease situation. The CoP convey practical recommendations gained considering recent experiences with the occurrence and control of relevant outbreaks. 

The 2023 edition of ‘The CoP Manual’ (title cover, above Fig 1 and table of contents, below Fig 2) comprises:

figure 2

• Six Codes on the following diseases: CEM (covering CEMO, Klebsiella pneumoniae and Pseudomonas aeruginosa), EVA, EHV-1, equine coital exanthema (ECE, caused by EHV-3), equine infectious anaemia (EIA) and dourine 

• Five Guidelines on equine influenza (EI), piroplasmosis, strangles, West Nile Fever (WNF) and artificial insemination (AI) 

• Eleven Appendices with a range of  supporting information and guidance 

The CoP are published on the HBLB website (https://codes.hblb.org.uk/); a PDF download  (https://codes.hblb.org.uk/downloads/2023/Codes%20of%20Practice%202023.pdf) is also available. In Great Britain, the Thoroughbred Breeders Association (TBA) produces a spiral-bound printed hard copy for its members. 

The CoP outline each disease sequentially, using a standardised format of sections which include information on notification procedures, clinical signs, transmission, prevention, diagnosis, control, treatment, freedom from disease and export requirements. It is a document that continues to evolve over time in terms of both the diseases included and the expert advice imparted. 

Why ‘codes’ and ‘guidelines’?

Although the logic behind the distinction as to why specific diseases in the CoP are covered by a guideline rather than a code is not necessarily immediately initiative. It is worth remembering that a Code of Practice may be defined as ‘A documented set of recommended or preferred processes, actions or organisational structures to be applied in a given setting’, whereas a guideline is: ‘A general rule, principle or piece of advice’.  Therefore, the diseases applied as codes are those that directly relate to, and have an impact on, breeding and that necessitate particular actions either to prevent or control disease, should they occur. The guidelines, in contrast, are merely advisory measures to those involved in thoroughbred breeding businesses, but cover diseases and practices that are also highly applicable to other populations of horses. The remainder of the article outlines several of the important codes and guidelines.

Strangles

Strangles, caused by the bacterium Streptococcus equi, is a disease affecting the lymph nodes of the upper respiratory tract. Although endemic within the UK horse population, it only occasionally affects thoroughbred stud farms. Accordingly, it was first included in the CoP as an advisory guideline in 2004 and has since been periodically updated in line with developments in diagnostic testing and vaccination. Due to the ability of Streptococcus equi to develop persistent infection, remaining within material (pus/chondroids) in the guttural pouches long after resolution of clinical signs, one of the key elements in prevention and control is identification and treatment of these carrier animals. This involves performing guttural pouch endoscopy and lavage of strangles cases around 30 days after clinical recovery from infection, and also of any new arrivals at a premises during the quarantine period, before they are allowed to mix with the resident herd. 

Equine infectious anaemia (EIA)

figure 3

EIA, also known as swamp fever, is caused by the equine infectious anaemia virus (EIAV) and is transmitted between horses by the transfer of infected blood, either by insect vectors or contaminated veterinary equipment or through administration of infected blood products (e.g., plasma or whole blood transfusion). It is found in thoroughbred and non-thoroughbred populations worldwide, including parts of mainland Europe; but it is currently not present in Great Britain, where any suspicion of disease is notifiable by law to the Animal and Plant Health Agency (APHA) and would result in compulsory slaughter of the affected animal. Following an outbreak in Ireland in 2006, a CoP for EIA was developed by Defra in the UK in August that year and was included as an addendum for the 2007 breeding season (Figure 3) and subsequently as a full code from 2008 onwards. EIA has been included as a full CoP since 2008, and it recommends pre-breeding testing of all mares and stallions prior to commencement of the covering season as the best way to establish and maintain freedom from infection. 

Dourine 

A new code on dourine was added in 2012, following its re-identification in Sicily and the Italian mainland during 2011, which necessitated pre-import screening of horses arriving from this area. A notifiable venereal disease caused by the protozoan parasite Trypansoma equiperdum, once widespread, had largely undergone eradication and of late had only been reported in Asia, Africa, South America, Eastern Europe, Mexico and Russia. There is no cure for dourine, and euthanasia is usually the advised treatment option on the grounds of animal welfare and population health. As investigations into the 2011 Italian outbreak indicated subclinical seropositivity to dourine in many regions of Italy, it was evident that the disease was closer to our shores than anticipated. That led to its addition to the CoP in order to keep all owners/breeders informed and appropriately advised. 

Equine influenza (EI)

EI was added to the CoP in 2020 as an advisory guideline following the 2019 European epidemic, which saw a major outbreak in the UK (Figure 4), including cases of clinical disease in vaccinated thoroughbreds. This led to the cancellation of British horseracing for six days in February 2019 as a pre-emptive control measure, but still at significant economic cost to the industry. 

Figure 4

Although clinical EI is usually fairly mild and self-limiting, the resulting damage to the respiratory epithelium can impact performance for up to six months and leaves the horse vulnerable to secondary bacterial infections and potential pneumonia. Appropriate vaccination, biosecurity protocols and effective quarantining of new arrivals are outlined in the Code as the cornerstone to EI control. With such a highly contagious virus capable of spreading over large distances and with great speed, especially in the immunologically naïve, awareness and prevention are key.

West Nile fever (WNF)

WNF, caused by West Nile virus (WNV), is an infectious but non-contagious disease transmitted through the bite of an infected mosquito. Although the natural host-vector cycle is between birds and mosquitoes, horses and indeed humans can become infected but act as so-called incidental or ‘dead-end’ hosts; importantly, not presenting is a risk for onward transmission as there is insufficient WNV in their bloodstream. Many horses infected with WNV remain without signs, but approximately 10% will develop neurological disease, which can be fatal. Historically confined to Africa and the East, it entered North America in 1999 leading to widespread infection with many equine and human fatalities. Since then it has become endemic in the USA and continues to spread further into northern Europe as climate change alters vector habitats and life cycles. After the development of equine cases in Germany in 2018 and evidence of human and bird cases in the Netherlands in 2020, WNV was considered to pose an increasing threat to the UK horse population, especially animals that travelled overseas for competition and breeding purposes. WNF was therefore added as a guideline to the CoP in 2021. 

Piroplasmosis

The latest disease addition to the CoP was an advisory guideline on piroplasmosis in 2022, following concern that the disease was becoming increasingly important among the international equine population. Piroplasmosis is a tick-borne disease caused by the intracellular parasites Babesia caballi and Theileria equi. Although the UK is currently considered to be free from locally acquired endemic disease (referred to as ‘autochthonous’), cases have occasionally been confirmed in the UK and are endemic in other European countries. With no formal requirements for pre-import screening, infection could re-enter the UK through importation of infected horses. The code gives informative background information to raise awareness among thoroughbred breeders and owners/keepers of other horse populations.  

Improving accessibility and applicability of the CoP

Another way in which the CoP have more recently evolved is through the mechanisms of delivery to stakeholders. In July 2016, the accessibility and reach of the CoP took a further leap with the generation of the smartphone EquiBioSafe app (https://play.google.com/store/apps/details?id=com.veterinaryadvances.android.equibiosafe&hl=en_GB&gl=US&pli=1). With the HBLB Codes of Practice and National Trainers Federation Codes of Practice précised into key elements for the control and prevention of infectious diseases, the app allows interactive and stable-side access to advice, as well as assisting trainers to comply with sporting authority vaccine regulations and disease notification procedures. With the ability to send emergency notifications in the event of heightened disease threats in a particular area, the app provides real-time relevant information to assist with implementation of proactive biosecurity measures. This helps safeguard horse health and the socioeconomic livelihoods of all those involved in equestrian sport. Like the CoP, the EquiBiosafe app has mainly been targeted to a European audience, but downloads recorded from North America, Asia and Latin America demonstrate its international application. 

The HBLB International Codes of Practice act as broad, minimum requirement recommendations for the identification, treatment, prevention and control of a range of important equine infectious diseases—equally relevant across international borders and from pleasure to elite competition horses. They are also dynamic, evolving over time in line with the ever-changing disease situation, and therefore acting as a vital education and reference resource to all those involved in the equestrian industry. They form a user-friendly instruction manual of exactly ‘how (not) to’ allow infectious diseases to fulfil their devastating potential.  

EIPH - could there be links to sudden death and pulmonary haemorrhage?

Dr Peter W. Physick-Sheard, BVSc, FRCVS, explores preliminary research and hypotheses, being conducted by the University of Guelph, to see if there is a possibility that these conditions are linked and what this could mean for future management and training of thoroughbreds. 

"World's Your Oyster,” a three-year-old thoroughbred mare, presented at the veterinary hospital for clinical examination. She won her maiden start as a two-year-old and placed once in two subsequent starts. After training well as a three-year-old, she failed to finish her first start, easing at the top of the stretch, and was observed to fade abruptly during training. Some irregularity was suspected in heart rhythm after exercise. Thorough clinical examination, blood work, ultrasound of the heart and an ECG during rest and workout revealed nothing unusual. 

Returning to training, Oyster placed in six of her subsequent eight starts, winning the last two. She subsequently died suddenly during early training as a four-year-old. At post-mortem, diagnoses of pulmonary haemorrhage and exercise-induced pulmonary haemorrhage were established—a very frustrating and unfortunate outcome.

Across the racing world, a case like this probably occurs daily. Anything that can limit a horse's ability to express its genetic potential is a major source of anxiety when training. The possibility of injury and lameness is the greatest concern, but a close second is respiratory disease, with bleeding  from the lungs (most often referred to as exercise induced pulmonary [lung] haemorrhage or EIPH) being high on the list. 

EIPH is thought to occur in as many as 85 percent of racehorses, and may initially be very mild without obvious clinical consequences. In some cases it can be associated with haemorrhage of sufficient severity for blood to appear at the nostrils, even at first occurrence. In many racing jurisdictions this is a potentially career-ending problem. In these horses, an impact on performance is unquestionable. Bleeding from the lungs is the reason for the existence of ‘Lasix programs,’ involving pre-race administration of a medication considered to reduce haemorrhage. Such programs are controversial—the justifications for their existence ranging from addressing welfare concerns for the horse to dealing with the performance impacts. 

Much less frequently encountered is heavy exercise-associated bleeding from the nostrils (referred to as epistaxis), which can sometimes be accompanied by sudden death, during or shortly after exercise. Some horses bleed heavily internally and die without blood appearing at the nostrils. Haemorrhage may only become obvious when the horse is lying on its side, or not until post-mortem. Affected animals do not necessarily have any history of EIPH, either clinically or sub-clinically. There is an additional group of rare cases in which a horse simply dies suddenly, most often very soon after work and even after a winning performance, and in which little to nothing clearly explains the cause on post-mortem. This is despite the fact most racing jurisdictions study sudden death cases very closely.

EIPH is diagnosed most often by bronchoscopy—passing an endoscope into the lung after work and taking a look. In suspected but mild cases, there may not be sufficient haemorrhage to be visible, and a procedure called a bronchoalveolar lavage is performed. The airways are rinsed and fluid is collected and examined microscopically to identify signs of bleeding. Scoping to confirm diagnosis is usually a minimum requirement before a horse can be placed on a Lasix program. 

Are EIPH, severe pulmonary haemorrhage and sudden death related? Are they the same or different conditions? 

At the University of Guelph, we are working on the hypothesis that most often they are not different—that it’s degrees of the same condition, or closely related conditions perhaps with a common underlying cause. We see varying clinical signs as being essentially a reflection of severity and speed of onset of underlying problems. 

Causes in individual cases may reflect multiple factors, so coming at the issues from several different directions, as is the case with the range of ongoing studies, is a good way to go so long as study subjects and cases are comparable and thoroughly documented. However, starting from the hypothesis that these may all represent basically the same clinical condition, we are approaching the problem from a clinical perspective, which is that cardiac dysfunction is the common cause. 

Numerous cardiac disorders and cellular mechanisms have the potential to contribute to transient or complete pump (heart) failure. However, identifying them as potential disease candidates does not specifically identify the role they may have played, if any, in a case of heart failure and in lung haemorrhage; it only means that they are potential primary underlying triggers. It isn't possible for us to be right there when a haemorrhage event occurs, so almost invariably we are left looking at the outcome—the event of interest has passed. These concerns influence the approach we are taking.

Background

The superlative performance ability of a horse depends on many physical factors:

• Huge ventilatory (ability to move air) and gas exchange capacity

• Body structure including limb length and design - allows it to cover ground rapidly with a long stride

• Metabolic adaptations - supports a high rate of energy production by burning oxygen, tolerance of severe metabolic disruptions toward the end of race-intensity effort

• High cardiovascular capacity - allows the average horse to pump roughly a brimming bathtub of blood every minute

At race intensity effort, these mechanisms, and more, have to work in coordination to support performance. There is likely not much reserve left—two furlongs (400m) from the winning post—even in the best of horses. There are many wild cards, from how the horse is feeling on race day to how the race plays out; and in all horses there will be a ceiling to performance. That ceiling—the factor limiting performance—may differ from horse to horse and even from day to day. There’s no guarantee that in any particular competition circumstances will allow the horse to perform within its own limitations. One of these factors involves the left side of the heart, from which blood is driven around the body to the muscles.

A weak link - filling the left ventricle

The cardiovascular system of the horse exhibits features that help sustain a high cardiac output at peak effort. The feature of concern here is the high exercise pressure in the circulation from the right  ventricle, through the lungs to the left ventricle. At intense effort and high heart rates, there is very little time available to fill the left ventricle—sometimes as little as 1/10 of a second; and if the chamber cannot fill properly, it cannot empty properly and cardiac output will fall. The circumstances required to achieve adequate filling include the readiness of the chamber to relax to accept blood—its ‘stiffness.’ Chamber stiffness increases greatly at exercise, and this stiffened chamber must relax rapidly in order to fill. That relaxation seems not to be sufficient on its own in the horse at high heart rates. Increased filling pressure from the circulation draining the lungs is also required. But there is a weak point: the pulmonary capillaries.

These are tiny vessels conducting blood across the lungs from the pulmonary artery to the pulmonary veins. During this transit, all the gas exchange needed to support exercise takes place. The physiology of other species tells us that the trained lung circulation achieves maximum flow (equivalent to cardiac output) by reducing resistance in those small vessels. This process effectively increases lung blood flow reserve by, among other things, dilating small vessels. Effectively, resistance to the flow of blood through the lungs is minimised. We know this occurs in horses as it does in other species; yet in the horse, blood pressure in the lungs still increases dramatically at exercise. 

If this increase is not the result of resistance in the small vessels, it must reflect something else, and that appears to be resistance to flow into the left chamber. This means the entire lung circulation is exposed to the same pressures, including the thin-walled capillaries. Capillaries normally work at quite low pressure, but in the exercising horse, they must tolerate very high pressures. They have thin walls and little between them, and the air exchange sacs in the lung. This makes them vulnerable. It's not surprising they sometimes rupture, resulting in lung haemorrhage.

Recent studies identified changes in the structure of small veins through which the blood flows from the capillaries and on toward the left chamber. This was suspected to be a pathology and part of the long-term consequences of EIPH, or perhaps even part of the cause as the changes were first identified in EIPH cases. It could be, however, that remodelling is a normal response to the very high blood flow through the lungs—a way of increasing lung flow reserve, which is an important determinant of maximum rate of aerobic working. 

The more lung flow reserve, the more cardiac output and the more aerobic work an animal can perform. The same vein changes have been observed in non-racing horses and horses without any history or signs of bleeding. They may even be an indication that everything is proceeding as required and a predictable consequence of intense aerobic training. On the other hand, they may be an indication in some horses that the rate of exercise blood flow through their lungs is a little more than they can tolerate, necessitating some restructuring. We have lots to learn on this point.

If the capacity to accommodate blood flow through the lungs is critical, and limiting, then anything that further compromises this process is likely to be of major importance. It starts to sound very much as though the horse has a design problem, but we shouldn't rush to judgement. Horses were probably not designed for the very intense and sustained effort we ask of them in a race. Real-world situations that would have driven their evolution would have required a sprint performance (to avoid ambush predators such as lions) or a prolonged slower-paced performance to evade predators such as wolves, with only the unlucky victim being pushed to the limit and not the entire herd. 

Lung blood flow and pulmonary oedema

There is another important element to this story. High pressures in the capillaries in the lung will be associated with significant movement of fluid from the capillaries into lung tissue spaces. This movement in fact happens continuously at all levels of effort and throughout the body—it's a normal process. It's the reason the skin on your ankles ‘sticks’ to the underlying structures when you are standing for a long time. So long as you keep moving a little, the lymphatic system will draw away the fluid. 

In a diseased lung, tissue fluid accumulation is referred to as pulmonary oedema, and its presence or absence has often been used to help characterise lung pathologies. The lung lymphatic system can be overwhelmed when tissue fluid is produced very rapidly. When a horse experiences sudden heart failure, such as when the supporting structures of a critical valve fail, one result is massive overproduction of lung tissue fluid and appearance of copious amounts of bloody fluid from the nostrils. 

The increase in capillary pressure under these conditions is as great as at exercise, but the horse is at rest. So why is there no bloody fluid in the average, normal horse after a race? It’s because this system operates very efficiently at the high respiratory rates found during work: tissue fluid is pumped back into the circulation, and fluid does not accumulate. The fluid is pumped out as quickly as it is formed. An animal’s level of physical activity at the time problems develop can therefore make a profound difference to the clinical signs seen and to the pathology.

Usual events with unusual consequences 

If filling the left ventricle and the ability of the lungs to accommodate high flow at exercise are limiting factors, surely this affects all horses. So why do we see such a wide range of clinical pictures, from normal to subclinical haemorrhage to sudden death? 

Variation in contributing factors such as type of horse, type and intensity of work, sudden and unanticipated changes in work intensity, level of training in relation to work and the presence of disease states are all variables that could influence when and how clinical signs are seen, but there are other considerations.

Although we talk about heart rate as a fairly stable event, there is in fact quite a lot of variation from beat to beat. This is often referred to as heart rate variability. There has been a lot of work performed on the magnitude of this variability at rest and in response to various short-term disturbances and at light exercise in the horse, but not a lot at maximal exercise. Sustained heart rate can be very high in a strenuously working horse, with beats seeming to follow each other in a very consistent manner, but there is in fact still variation. 

Some of this variation is normal and reflects the influence of factors such as respiration. However, other variations in rate can reflect changes in heart rhythm. Still other variations may not seem to change rhythm at all but may instead reflect the way electrical signals are being conducted through the heart. 

These may be evident from the ECG but would not appear abnormal on a heart rate monitor or when listening. These variations, whether physiologic (normal) or a reflection of abnormal function, will have a presently, poorly understood influence on blood flow through the lungs and heart—and on cardiac filling. Influences may be minimal at low rates, but what happens at a heart rate over 200 and in an animal working at the limits of its capacity.

Normal electrical activation of the heart follows a pattern that results in an orderly sequence of heart muscle contraction, and that provides optimal emptying of the ventricles. Chamber relaxation complements this process. 

An abnormal beat or abnormal interval can compromise filling and/or emptying of the left ventricle, leaving more blood to be discharged in the next cycle and back up through the lungs, raising pulmonary venous pressure. A sequence of abnormal beats can lead to a progressive backup of blood, and there may not be the capacity to hold it—even for one quarter of a second, a whole cardiac cycle at 240 beats per minute. 

For a horse that has a history of bleeding and happens to be already functioning at a very marginal level, even minor disturbances in heart rhythm might therefore have an impact. Horses with airway disease or upper airway obstructions, such as roarers, might find themselves in a similar position. An animal that has not bled previously might bleed a little, one that has a history of bleeding may start again, or a chronic bleeder may worsen. 

Relatively minor disturbances in cardiac function, therefore, might contribute to or even cause EIPH. If a horse is in relatively tough company or runs a hard race, this may also contribute to the onset or worsening of problems. Simply put, it's never a level playing field if you are running on the edge.

Severe bleeding

It has been suspected for many years that cases of horses dying suddenly at exercise represent sudden-onset cardiac dysfunction—most likely a rhythm disturbance. If the rhythm is disturbed, the closely linked and carefully orchestrated sequence of events that leads to filling of the left ventricle is also disturbed. A disturbance in cardiac electrical conduction would have a similar effect, such as one causing the two sides of the heart to fall out of step, even though the rhythm of the heart may seem normal. 

The cases of horses that bleed profusely at exercise and even those that die suddenly without any post-mortem findings can be seen to follow naturally from this chain of events. If the changes in heart rhythm or conduction are sufficient, in some cases to cause massive pulmonary haemorrhage, they may be sufficient in other cases to cause collapse and death even before the horse has time to exhibit epistaxis or even clear evidence of bleeding into the lungs. 

EIPH and dying suddenly

If these events are (sometimes) related, why is it that some horses that die of pulmonary haemorrhage with epistaxis do not show evidence of chronic EIPH? This is one of those $40,000 questions. It could be that young horses have had limited opportunity to develop chronic EIPH; it may be that we are wrong and the conditions are entirely unrelated. But it seems more likely that in these cases, the rhythm or conduction disturbance was sufficiently severe and/or rapid in onset to cause a precipitous fall in blood pressure with the animal passing out and dying rapidly. 

In this interpretation of events, the missing link is the heart. There is no finite cutoff at which a case ceases to be EIPH and becomes pulmonary haemorrhage. Similarly, there is no distinct point at which any case ceases to be severe EIPH and becomes EAFPH (exercise-associated fatal pulmonary haemorrhage). In truth, there may simply be gradation obscured somewhat by variable definitions and examination protocols and interpretations.

The timing of death

It seems from the above that death should most likely take place during work, and it often does, but not always. It may occur at rest, after exercise. Death ought to occur more often in racing, but it doesn't. 

The intensity of effort is only one factor in this hypothesis of acute cardiac or pump failure. We also have to consider factors such as when rhythm disturbances are most likely to occur (during recovery is a favourite time) and death during training is more often a problem than during a race. 

A somewhat hidden ingredient in this equation is possibly the animal's level of emotional arousal, which is known to be a risk factor in humans for similar disturbances. There is evidence that emotions/psychological factors might be much more important in horses than previously considered. Going out for a workout might be more stimulating for a racehorse than a race because before a race, there is much more buildup and the horse has more time to adequately warm up psychologically. And then, of course, temperament also needs to be considered. These are yet further reasons that we have a great deal to learn.

Our strategy at the University of Guelph

These problems are something we cannot afford to tolerate, for numerous reasons—from perspectives of welfare and public perception to rider safety and economics. Our aim is to increase our understanding of cardiac contributions by identifying sensitive markers that will enable us to say with confidence whether cardiac dysfunction—basically transient or complete heart failure—has played a role in acute events. 

We are also looking for evidence of compromised cardiac function in all horses, from those that appear normal and perform well, through those that experience haemorrhage, to those that die suddenly without apparent cause. Our hope is that we can not only identify horses at risk, but also focus further work on the role of the heart as well as the significance of specific mechanisms. And we hope to better understand possible cardiac contributions to EIPH in the process. This will involve digging deeply into some aspects of cellular function in the heart muscle, the myocardium of the horse, as well as studying ECG features that may provide insight and direction. 

Fundraising is underway to generate seed money for matching fund proposals, and grant applications are in preparation for specific, targeted investigations. Our studies complement those being carried out in numerous, different centres around the world and hopefully will fill in further pieces of the puzzle. This is, indeed, a huge jigsaw, but we are proceeding on the basis that you can eat an elephant if you're prepared to process one bite at a time.

How can you help? Funding is an eternal issue. For all the money that is invested in horses there is a surprisingly limited contribution made to research and development—something that is a mainstay of virtually every other industry; and this is an industry. 

Look carefully at the opportunities for you to make a contribution to research in your area. Consider supporting studies by making your experience, expertise and horses available for data collection and minimally invasive procedures such as blood sampling. 

Connect with the researchers in your area and find out how you can help. Watch your horses closely and contemplate what they might be telling you—it's easy to start believing in ourselves and to stop asking questions. Keep meticulous records of events involving horses in your care— you never know when you may come across something highly significant. And work with researchers (which often includes track practitioners) to make your data available for study. 

Remember that veterinarians and university faculty are bound by rules of confidentiality, which means what you tell them should never be ascribed to you or your horses and will only be used without any attribution, anonymously. And when researchers reach out to you to tell you what they have found and to get your reactions, consider actually attending the sessions and participating in the discussion; we can all benefit—especially the ultimate beneficiary which should be the horse. We all have lots to learn from each other, and finding answers to our many challenges is going to have to be a joint venture.  

Finally, this article has been written for anybody involved in racing to understand, but covering material such as this for a broad audience is challenging. So, if there are still pieces that you find obscure, reach out for help in interpretation. The answers may be closer than you think!

Oyster

And what about Oyster? Her career was short. Perhaps, had we known precisely what was going on, we might have been able to treat her, or at least withdraw her from racing and avoid a death during work with all the associated dangers—especially to the rider and the associated welfare concerns. 

Had we had the tools, we might have been able to confirm that whatever the underlying cause, she had cardiac problems and was perhaps predisposed to an early death during work. With all the other studies going on, and knowing the issue was cardiac, we might have been able to target her assessment to identify specific issues known to predispose. 

In the future, greater insight and understanding might allow us to breed away from these issues and to better understand how we might accommodate individual variation among horses in our approaches to selection, preparation and competition. There might be a lot of Oysters out there!

For further information about the work being undertaken by the University of Guelph

Contact - Peter W. Physick-Sheard, BVSc, FRCVS.

Professor Emeritus, Ontario Veterinary College, University of Guelph - pphysick@uoguelph.ca

Research collaborators - Dr Glen Pyle, Professor, Department of Biomedical Sciences, University of Guelph - gpyle@uoguelph.ca

Dr Amanda Avison, PhD Candidate, Department of Biomedical Sciences, University of Guelph. ajowett@uoguelph.ca

References

Caswell, J.I. and Williams K.J. (2015), Respiratory System, In ed. Maxie, M. Grant, 3 vols., 6th edn., Jubb, Kennedy and Palmer’s Pathology of Domestic Animals, 2; London: Elsevier Health Sciences, 490-91.

Hinchcliff, KW, et al. (2015), Exercise induced pulmonary hemorrhage in horses: American College of Veterinary Internal Medicine consensus statement, J Vet Intern Med, 29 (3), 743-58.

Rocchigiani, G, et al. (2022), Pulmonary bleeding in racehorses: A gross, histologic, and ultrastructural comparison of exercise-induced pulmonary hemorrhage and exercise-associated fatal pulmonary hemorrhage, Vet Pathol, 16:3009858221117859. doi: 10.1177/03009858221117859. Online ahead of print.

Manohar, M. and T. E. Goetz (1999), Pulmonary vascular resistance of horses decreases with moderate exercise and remains unchanged as workload is increased to maximal exercise, Equine Vet. J., (Suppl.30), 117-21.

Vitalie, Faoro (2019), Pulmonary Vascular Reserve and Aerobic Exercise Capacity, in Interventional Pulmonology and Pulmonary Hypertension, Kevin, Forton (ed.), (Rijeka: IntechOpen), Ch. 5, 59-69.

Manohar, M. and T. E. Goetz (1999), Pulmonary vascular resistance of horses decreases with moderate exercise and remains unchanged as workload is increased to maximal exercise, Equine Vet. J., (Suppl.30), 117-21.

Small wounds leading to synovial infections

Article by Peter Milner

Most experienced trainers will know from bitter experience that a seemingly tiny wound can have a big impact if a horse is unlucky enough to sustain a penetrating injury right over a critical structure like a joint capsule or tendon sheath. Collectively, joints and tendon sheaths are called synovial structures, and synovial infection is a serious, potentially career-ending and sometimes life-threatening problem. 

A team of veterinary researchers from Liverpool University Veterinary School, published a study in Equine Veterinary Journal that examined factors influencing outcome and survival. This article was first published in European Trainer (issue 50 - summer 2015) but is being republished due to popular demand.

What is synovial infection?

Infection involving a synovial cavity, such as a joint or tendon sheath, is a common and potentially serious injury for the horse. The most prevalent cause is a wound, although a smaller proportion of cases result following an injection into a joint or tendon sheath, or after elective orthopaedic surgery to the area. Additionally, infection can occur via the bloodstream, particularly in foals that have not received enough colostrum.  Left untreated, the horse will remain in pain, and ongoing infection and inflammation can result in permanent damage. This can ultimately result in euthanasia on welfare grounds. 

What factors are important for horse survival?

When a synovial infection occurs there is a huge inflammatory response, leading to swelling and pain. The horse usually shows severe lameness but following a good clinical examination, the cause is often quickly identified.  Prompt veterinary recognition of involvement of a joint or tendon sheath and aggressive treatment (involving flushing the affected synovial cavity and the correct use of systemic and local antibiotics) will often result in a good outcome for the horse.  Flushing removes inflammatory debris including destructive enzymes and free radicals, and it eliminates contaminating bacteria in most cases. This is performed most effectively by arthroscopic guidance (“keyhole” surgery) under general anaesthesia. Using a “scope” to do this is considered superior to flushing through needles because arthroscopy allows the inside of the problem area to be inspected, foreign material (for example, dirt or splinters of wood) to be removed, and any concurrent damage (such as damage to the cartilage or a cut into a tendon) to be evaluated. In addition, targeted high volume lavage is best achieved via arthroscopy. 

Survival following arthroscopic treatment of synovial sepsis is good – approximately 80-90% of adult horses undergoing a flush are discharged from hospital.  In foals, however, the figure is much lower, at around 55%, and this likely due to complicating factors such as concurrent sepsis involving multiple organs.  Our study, recently published in Equine Veterinary Journal, investigated what factors might be involved in determining survival to hospital discharge in 214 horses undergoing arthroscopic treatment for synovial sepsis. We used statistical modelling to evaluate the interactions with different factors at three key time points during the management of the condition at Liverpool Veterinary School, one of the leading UK referral veterinary hospitals. Information collected on admission to the hospital included when the horse was last seen to be normal, the cause of the infection, the degree of lameness present, and the level of white blood cells and protein in synovial fluid collected from the infected joint or tendon sheath. These lab tests are an important method which veterinarians use to determine how severe the infection is. Additional data collected included whether the surgery was performed out-of-normal working hours, if foreign material was present, the amount of inflammation present in the area, and whether any additional cartilage or tendon damage was found at surgery. Post-operative information gathered included what the levels of white blood cells and protein were in the synovial fluid after surgery and whether the horse needed further surgical treatment.

All horses in this study were greater than six months old and the majority had sustained a wound that communicated with a joint or tendon sheath.  Eighty-six per cent of the 214 horses admitted to the hospital survived to hospital discharge.  Of the 31 horses that did not survive, 27 were euthanised due to persistent infection or lameness.

An angry, protein-soup

A high level of protein in the synovial fluid of the affected joint or tendon sheath on admission and levels that remained high after surgery were strongly associated with a poor outcome and loss of the horse.  Protein concentrations are normally fairly low in a normal joint or tendon sheath, but protein leaks into the synovial cavity from surrounding blood vessels when inflamed. Protein is also produced by cells in the synovial cavity when they are activated in response to a severe insult such as infection. Protein clots trap bacteria in the joint, making it harder to remove infection. The protein soup also includes lots of inflammatory mediators such as enzymes and signalling molecules, and these cause further inflammation, tissue damage, and sensitise pain receptors in the synovial cavity magnifying the inflammatory response and increasing the pain experienced by the horse. Unchecked, this angry, inflamed environment can result in cartilage degeneration, bone damage, and adhesion (scar) formation. This fits well with another observation from this study linking the presence of moderate or severe synovial inflammation at surgery as a negative factor for survival. 

Small wounds can lead to big trouble

Interestingly, horses presenting with an obvious wound (as opposed to a small penetrating injury or no visible wound) were more likely to survive to hospital discharge. This may be due to the injury being noticed earlier and hence prompting earlier veterinary intervention. Alternatively, open wounds may allow drainage of inflammatory synovial fluid and lessen the detrimental effects of increased pressure within the joint as well as reducing ongoing exposure to inflammatory mediators. This finding highlights the fact that trainers should act promptly when faced with a wound – it is easy to underestimate just how much damage may be going on under the surface.

Horses undergoing surgical treatment of a joint or tendon sheath infection out-of-hours (for example in the middle of the night) were three times less likely to survive to hospital. Often, horses with a synovial infection arrive stressed and painful and not in an ideal state for having an anaesthetic. Early identification of an infection and appropriate management is important but stabilisation of the horse and preparation for surgery appear to outweigh any perceived benefits of undertaking immediate surgery.  This is borne out by the finding that time from initial injury to treatment was not associated with outcome and is in agreement with previous findings from other researchers. It is important to reiterate that prompt recognition and treatment of a horse with an infection in a synovial cavity is essential but that surgical management within 12-24 hours of diagnosis, so that the horse is in the best condition for undergoing anaesthesia, does not affect outcome. 

Do horses return to work after a synovial infection?

The big question that owners and trainers want to know is whether the horse will regain full function of the joint or tendon sheath after having an infection. Figures for return to function following surgical (arthroscopic) treatment for a synovial infection vary between 54-81%.  Various factors appear to relate to outcome but when looking at a predominately thoroughbred racing population, the statistic for return to training appears to be at the higher end of this range. Factors associated with failure to return to athletic performance include the presence of thickened inflammatory tissue (known as pannus) at the time of surgery and that may relate to the development of fibrous adhesions and scar tissue within joint or tendon sheath longer-term. Some structures are particularly likely to compromise future function, and horses with an infection of the navicular bursa in the foot following a nail penetration generally do worse. 

Take home message

Horses sustaining an infection to a joint or tendon sheath have a good chance of the infection clearing up and surviving the injury, with the likelihood of racing as high as around 80%.  Our key message for trainers from this study is that it is essential that they recognise early when an infection involves one of these structures and have a veterinarian fully evaluate the injury. Aggressive treatment is important and involves flushing the synovial cavity using a “scope” under anaesthesia to remove as much inflammatory and infective debris as possible. 

Equine infectious disease surveillance in Northern Europe

By Fleur Whitlock

Equine infectious disease occurrences remain an ever-present threat, irrespective of the country where a horse resides. With climate change and increased international horse movements, monitoring and surveillance of infectious disease is more important than ever. But how is this conducted in our equine population?

In Northern Europe and the majority of countries worldwide, there are three infectious respiratory diseases commonly found to be circulating in horse populations (referred to as ‘endemic’). These include the viral diseases: equine influenza and equine herpes; and the bacterial disease: strangles. It is essential that horse keepers and their veterinary surgeons remain vigilant and knowledgeable around how these diseases present to ensure rapid implementation of control measures if they occur and more importantly what actions to take to prevent them in the first place. 

Why is surveillance vital?

Identifying and controlling infectious diseases when they occur is important to limit both the number of infected horses on a premises and the disruptive and costly effects that disease can have on commercial enterprises,  as well as avoiding the spread of infection to the wider horse population. To optimise control and prevention measures, diseases are monitored at a national and international level, through surveillance activities. 

How is surveillance conducted?

There are two main ways that equine surveillance is conducted:

1. Statutory reporting of notifiable diseases 

Diseases that are notifiable under veterinary or human health legislation in horses may include (but are not limited to and will have country-specific designation): African Horse Sickness (AHS), Contagious Equine Metritis (CEM), Dourine, Equine Viral Arteritis (EVA), Equine Infectious Anaemia (EIA), Glanders and West Nile fever. These diseases have been designated as notifiable, either due to their potential implications for human health, equine health or trade. Statutory reporting is required if a disease is suspected due to suspicious clinical signs or confirmed through diagnostic testing, such as those recommended by the HBLB International Codes of Practice before horses are bred each year. The specific approaches to their occurrences will be disease- and country-dependent but may include movement restrictions and testing of the in-contact population as a minimum. Information gathered from these outbreak investigations is evaluated and shared with the wider industry, through platforms such as the World Organisation for Animal Health - World Animal Health Information System (OIE-WAHIS) (https://wahis.oie.int). 

2. Voluntary disease investigation and reporting of positive laboratory test results for non-notifiable diseases

If a horse is examined and undergoes confirmatory diagnostic testing through a laboratory and either the veterinary surgeon or laboratory contributes to surveillance initiatives, the diagnosis may be reported (Figure 1). Alongside this, epidemiological data relating to horse-specific factors such as the horse’s age, breed, vaccination status and specific factors such as approximate geographical location, number of resident horses on the premises and history of recent horse movements may also be available. In addition to this, to increase our understanding about pathogens and how they are changing over time, further analysis of the pathogen isolated from the infected horse(s) may be conducted to determine factors such as the particular strain of the pathogen. Information such as this can then be utilised to inform factors such as vaccination requirements. However, given the necessary voluntary steps that are required for a confirmed disease diagnosis to reach the reporting stage through this surveillance method, reported cases may not reflect the true extent of disease in a particular region or country. Also, some bias in the type of outbreaks that get reported may exist as detection and reporting may favour more severe cases, particular groups that undergo required testing or be more likely to be sampled due to subsidised testing costs existing in a particular country. 

Figure 1: The pathway of surveillance.

Examples of surveillance initiatives 

Country-specific initiatives may be available to encourage diagnostic testing of suspect infectious cases through incentives such as subsidised laboratory fees. In the UK, equine vets can submit nasopharyngeal swab samples from horses with signs that could be indicative of equine influenza, for free PCR testing at a designated laboratory—with this scheme funded by the Horserace Betting Levy Board (HBLB) and overseen by Equine Infectious Disease Surveillance (EIDS), University of Cambridge, United Kingdom. In addition to this scheme, EIDS maintains a surveillance network of all commercial laboratories conducting equine influenza testing in the UK, encouraging the voluntary reporting of positive samples and the sharing of associated epidemiological and virological information. Both schemes enable monitoring of equine influenza in the UK, and this is essential given that equine influenza viruses naturally change and adapt, giving the potential for new strains to be more infectious or to emerge beyond the protection imparted by current vaccines. In addition to equine influenza, the UK closely monitors laboratory-confirmed occurrences of equine herpes virus-1 (EHV-1), given its ability to cause neurological signs and abortion in pregnant mares and death of newborn foals. Strangles is also under surveillance with epidemiological and bacteriological data collected and analysed to improve our understanding of this frustrating contagious disease and contribute to improving its control and prevention.

What disease reporting platforms are available?

Figure 3: Examples of the international and country-specific reporting platforms monitored by the International Collating Centre (ICC): an interim email report issued by ICC and a recent embedded disease alert.

Country-specific reporting platforms exist worldwide, and these predominantly notify stakeholders—usually through email alerts—about laboratory-confirmed disease occurrences in the reporting country. Examples in Europe include France’s Réseau D'épidémio-Surveillance En Pathologie Équine (RESPE, www.respe.net), the Netherlands Surveillance Equine Infectious Disease Netherlands (SEIN, www.seinalerts.nl), Belgium’s Equi Focus Point Belgium (EFPB, www.efpb.be) and Switzerland’s Equinella (www.equinella.ch). 

Figure 3: Examples of the international and country-specific reporting platforms monitored by the International Collating Centre (ICC): an interim email report issued by ICC and a recent embedded disease alert.

Complementary to this, the International Collating Centre (ICC) is overseen by EIDS and supported by the International Thoroughbred Breeders’ Federation (ITBF) and International Equestrian Federation (FEI) and has for over 30 years collated outbreak reports from available country-specific reporting contacts and platforms worldwide. In addition, EIDS receives reports directly from veterinary surgeons and diagnostic laboratories (Figure 2). Collated reports are sent to registered subscribers on an almost daily basis through an email that contains embedded links to specific ICC outbreak alerts. A quarterly summary report is also produced and emailed to subscribers four times a year and is available in the resources and archive section of the ICC website (https://equinesurveillance.org/iccview/). Reported outbreaks are predominately made up of at least one case that has had the diagnosis confirmed through laboratory testing. It is therefore expected that those outbreaks that reach the reporting stage by the ICC will not reflect true infectious disease frequency within the international equine population; and a country with no reported outbreaks of a disease does not necessarily mean that the disease is not present in that country. 

Figure 3: Examples of the international and country-specific reporting platforms monitored by the International Collating Centre (ICC): an interim email report issued by ICC and a recent embedded disease alert.

There is an interactive ICC website enabling analysis of all international infectious disease outbreaks reported through the ICC, which was launched in August 2019; and outbreak data for all of 2019 onwards is available through this platform. Through the ICC, infectious disease outbreak information is shared with stakeholders throughout the world, ensuring people remain up to date through this active communication network. 

In addition to the ICC, EIDS has an equine influenza-specific platform, EquiFluNet (www.equinesurveillance.org/equiflunet), which presents influenza outbreak reports for the UK and worldwide.

A summary of the recent findings of surveillance initiatives

Equine influenza 

Figure 2: European countries reporting equine influenza outbreaks in Europe through the ICC for 2019, 2020 and 2021.

During 2019, Europe experienced an epidemic of equine influenza with widespread welfare and economic effects, including the temporary ceasing of horseracing in the UK. During 2021, influenza occurrences in Europe reported by the ICC returned to a more expected level (Figure 3). However, the potential of viral strain changes alongside international horse movements makes monitoring and surveillance of this virus essential.

Equine herpesvirus-1 (EHV-1)

EHV-1 is endemic in Europe, and the ICC regularly reports on occurrences of EHV-1 disease. An example of an ICC report released during 2020 detailed an outbreak of EHV-1 neurological disease on a premises in Hampshire, United Kingdom, with multiple equine fatalities (Figure 4 – left panel). Another example of an ICC report included a widespread neurological EHV-1 outbreak that occurred in Spain at several international show jumping events during 2021 (Figure 4 – right panel).

Figure 4: The International Collating Centre(www.equinesurveillance.org/iccview) reports detailing outbreaks of equine herpesvirus-1 neurological disease in Hampshire, United Kingdom in January 2020 (left) and Valencia, Spain in February 2021 (right). 

West Nile fever (WNF)

Figure 5: European countries reporting equine WNV outbreaks in Europe reported through the ICC from 2019, 2020 and 2021.

WNF is caused by West Nile virus (WNV) by biting mosquitoes, with birds acting as sources of the virus. It is a zoonotic disease, meaning humans can become infected if bitten by an infected mosquito. The ICC has reported equine cases across Europe over recent years (Figure 5). Given that many countries in Europe remain ‘free’ from WNV, it is still possible  for horses to have neurological signs such as weakness and incoordination or even death following infection. Humans can also be affected if bitten by an infected mosquito, so monitoring and surveillance of equine WNF occurrences, alongside mosquito, bird and human surveillance are essential. By way of example, WNV was confirmed in birds and humans in the Netherlands for the first time in 2020, but as of March 2022, it has not yet been confirmed in horses.

Summary

Having an appreciation of how and why surveillance of equine infectious diseases are conducted helps to improve engagement with and encourage an increased contribution to surveillance initiatives. A well-informed view on equine infectious disease outbreaks worldwide ensures continued advancements in enhancing control and prevention measures. This in turn will help reduce the risk from disease outbreaks and ensure the industry can continue to operate to its full potential.

Sources for further information about equine infectious diseases and their control and prevention are available

More information about equine infectious diseases and prevention/control:

• Horserace Betting Levy Board’s International Codes of Practice 2021: https://codes.hblb.org.uk/

• Equine Infectious Disease Surveillance (EIDS) website, hosting the International Collating Centre (ICC) and Equiflunet: www.equinesurveillance.org

• Sign up to receive International Collating Centre reports by contacting EIDS: equinesurveillance@gmail.com

Racecourse Fracture Support System

By Ian Wright

Figure 1: The fracture support system is provided in two mobile impact-resistant carrying boxes that protect the equipment and allow it to be checked before racing. All boots and splints are permanently labelled with individual racecourse identification to ensure return of equipment that may have left the racecourse. 

The year 2022 heralds a major step forward in racehorse welfare and a world first for British racecourses. With a generous grant from the Racing Foundation and additional support from the RCA, ARVS and NTF, all British racecourses are to be provided with fracture support systems (Figure 1). These consist of two compression boots and two flexion splints—both for use in the forelimbs—and a set of aluminium modular adjustable splints. One size of each compression boot and flexion splint fits the majority of flat racehorses and the other larger jump racehorses. Together, these provide appropriate rigid external support for the vast majority of limb fractures that occur during racing. The general principles are that management of all fractures is optimised by applying rapid and appropriate support to provide stability, reduce pain and relieve anxiety. 

In the last 25 years, there have been major improvements in fracture treatment due to significant advances in surgical techniques (particularly with internal fixation), minimally invasive approaches (arthroscopy) and the use of computed tomography (CT). Arthroscopy and CT allow accurate mapping and alignment of fractures, which is important for all horses and critical for athletic soundness. All have contributed to improving survival rates; and it is now safe to say that with correct care, the vast majority of horses that sustain fractures in racing can be saved. Equally importantly, many can also return to full athletic function including racing. 

Fracture incidences and locations vary geographically and are influenced by race types, track surfaces and conditions. There is good evidence that the majority of non-fall–related fractures (i.e., those occurring in flat racing and between obstacles in jump racing) are caused by bone fatigue. This is precipitated by the absolute loads applied to a bone, their speed/frequency and the direction of force application. As seen with stress or fatigue, failure in other high-performance working materials such as aeroplanes or formula one cars—in which applied forces are relatively consistent—fractures in racehorse bones occur at common sites, in particular configurations and follow similar courses. Once the fracture location has been identified, means of counteracting forces that distract (separate) the bone parts can therefore be reliably predicted and countered. 

Worldwide, the single most common racing fracture is that of the metacarpal/metatarsal condyles (condylar fracture). In Europe, the second most common fracture is a sagittal/parasagittal fracture of the proximal phalanx (split pastern). Both are most frequent in the forelimbs. In the United States, particularly when racing on dirt, fractures of the proximal sesamoid bones (almost always in the forelimbs) are the most common reason for on-course euthanasia. They occur less frequently when racing on turf but are seen at increased frequency on all-weather surfaces in the UK. 

There is no specific data documenting outcomes of horses with sustained fractures on racecourses. However, there is solid data for the two commonest racing injuries. The figures below are a meta-analysis of published data worldwide.

CONDYLAR FRACTURES

• Repaired incomplete fractures; 80% returned to racing

• Complete non-displaced fractures; 66% of repaired fractures returned to racing

• Displaced fractures; 51% raced following repair

• Propagating fractures; 40% raced following repair

SPLIT PASTERN

• Short incomplete fractures; 65% returned to racing

• Long incomplete fractures; 61% returned to racing

• Complete fractures; 51% returned to racing

• Comminuted fractures in most circumstances end racing careers but with appropriate support and surgical repair, many horses can be saved. There is only one comprehensive series of 64 cases in the literature of which 45 (70%) of treated cases survived. 

Figure 2: Newmarket Compression Boot.

The science behind the development of fracture support systems comes from two directions. The first is data collected from racecourse injuries and the second, improved understanding of fracture courses and behaviour. Data collected from UK flat racecourses between 2000 and 2013 demonstrated that 66% of fractures occurred in the lower limb (from knee and hock down); and of that, over 50% of fractures involved the fetlock joints. Condylar fractures are most common, representing 27% of all reported fractures; and of these, approximately two-thirds occurred in the forelimbs. Split pasterns were the second most common, accounting for 19% of all fractures with three quarters of these occurring in the forelimbs. These fractures have predictable planes and courses which means that once recognised, they can effectively be immobilised in a standard manner that is optimal for each fracture type. For condylar fractures and split pasterns, this principally involves extension of the fetlock joint. By contrast, in order to preserve soft tissues and blood supply to the lower limb, fractures of the sesamoid bones (which represent 7% of recorded fractures in UK flat racing) require fetlock flexion. 

Figure 3: Compression boot fitted to a horse with a condylar fracture, allowing safe comfortable movement.

The compression boot (Figure 2) is readily applied “trackside” and can be used to stabilise most distal forelimb fractures sufficiently for horses to be moved off of the course. It is the temporary immobilisation of choice for forelimb condylar fractures and split pasterns (Figure 3). Radiographs can be taken with the boot in place (Figure 4), and this can be maintained for transport. The boot is a rigid construct of fibreglass made from a single mould. The divided front portion is contiguous with a foot plate on which the back of the boot is hinged. Removable foot inserts are provided to make minor adjustments for hoof size. The boot is lined with foam rubber and has a rubber sole plate, which protects the shell and provides a cushion grip for the foot. When the boot is opened, the injured limb is placed into the front of the boot while the back is closed and secured by sequential adjustment of ski boot clips. When the boot edges are opposed (it cannot be over-tightened), immobilisation is secure. It is made with a fixed fetlock angle of 150o which counteracts distracting forces and allows horses to weight-bear and load the limb to walk. 

Figure 4: X-ray of horse with a condylar fracture (arrows) taken with a compression boot fitted.

Figure 5: a & b) Fitted flexion splint. c & d)  X-rays of horse with bilateral sesamoid fractures taken before (c) and after (d) fitting a flexion splint, correcting hyperextension (dropping) of the fetlock and closing the fracture gap.

Flexion splints (Figure 5) are critical for the survival of horses with breakdown injuries such as sesamoid fractures. They are also suitable for other lower limb injuries, which are supported by fetlock and pastern flexion. The splints are made of aluminium with a secure footplate and conjoined foam-lined front splint, which is angled at 30o at the level of the coffin joint and extends to the top of the cannon. There is a shallow foam-covered concavity in which the upper cannon sits, allowing the horse to lean into the splint and load the leg while flexed. The splint is secured to the leg with nylon and Velcro straps. 

The aluminium splints (Figure 6) are lightweight, adjustable and modular to fit individual horse and regional needs. They are spring-locked and light but rigid, secure and are tolerated well. In the hindlimb, the reciprocal apparatus that combines stifle, hock and fetlock joint positions precludes use of a compression boot. However, modular splints provide rigid support for condylar fractures and split pasterns in hindlimbs and are secured over a bandage to create a parallel sided tube, on the inside and outside of the limb. The splints can also be adjusted and assembled to splint fractures that occur less commonly above the fetlock (Figure 7). 

Figure 6: Adjustable aluminium splints and application to a hindlimb to splint a condylar fracture.

Figure 7: Modular use of aluminium splint suitable for splinting (a & b) knee and (c) forearm fractures.

Appropriate immobilisation effectively stops fracture progression (i.e,. getting worse), which not only improves the horse's prospects for recovery but also provides effective relief from pain and anxiety. As flight animals, loss of limb control or function is a major contributor to stress. The relief provided by effective immobilisation is substantially greater than provided by any pain killer or sedative. It is also recognised that when fractures occur in the high adrenalin environment of racing, horses exhibit latent pain syndrome. Application of appropriate rigid support at this time (i.e., on the course) limits pain generation and allows humane movement for considered evaluation, X-ray, etc. away from the racetrack. 

Techniques for application of the boots and splints are taught to racecourse veterinary surgeons at annual seminars facilitated by the Association of Racecourse Veterinary Surgeons (ARVS). The RCA has provided forms to record use and to collect data centrally which, in the fullness of time, will determine impact and help guide future welfare strategies. The equipment is currently being rolled out and will be available at all British racecourses at the start of the 2022 flat race season. 

The initiative has been widely welcomed by the industry. “This new equipment will provide the best possible chance for an injury to be properly assessed while discomfort to the horse is significantly reduced [to] give the best chance of future rehabilitation.” Caroline Davies, RCA Racecourse Services Director.

“The fracture support kit is a major advance in the treatment of horses on the racetrack. It allows immediate effective support to be applied to an injured horse, resulting in pain control and stability, facilitating safe transport from the racecourse to a centre of excellence without risk of exacerbating the injury. This will optimise the chance of horses to return to athletic function. This innovation must be seen as a major step forward in horse welfare for the participants in racing and all other equine disciplines.” Simon Knapp, Horse Welfare Board

“As a clerk of the course, my number-one priority is the safety of the horses and riders who participate in racing, and we constantly seek ways to improve in that area. The equine fracture support kits are an excellent addition to the equipment available to racecourse veterinary teams and a vital step forward in horse welfare. It is so important for both the immediate comfort and long-term prognosis of a horse who suffers a fracture that the injury is immobilised, and the fracture support kits provide that stability quickly and effectively.” Andrew Cooper, Clerk of the Course, Sandown Park and Epsom Downs

“The introduction of these boots and splints to all racecourses in Great Britain represents a major advancement for the welfare of racehorses. This demonstrates the collective desire of all the sports participants to show to a wider society the ambition to continually improve racehorse welfare.” James Given, BHA Director of Equine Health and Welfare

“The importance of the fracture support kits cannot be overstated. In providing stability and support, it gives horses the best possible chance of recovery.” Emma Lavelle, NTF President

“I have no doubt that in time no racecourse in the world which purports to take equine welfare seriously will be without a set of fracture support kits.” Marcus Armytage, Daily Telegraph

Orthopaedic problems in young Thoroughbreds

Helping these future athletes achieve a protective conformation is vital with respect to their welfare, athletic career and sales potential: Orthopaedic conditions have the potential to blight a promising athletic career and prevent young horses reach their full potential. Early diagnosis and management are critical if horses are to be given the best chances of a successful and long career. And this, of course, depends on horsemen being able to pick up on problems as early as possible so they can be dealt with effectively. The Beaufort Cottage Educational Trust is a charity that aims to help disseminate knowledge in the Thoroughbred breeding and racing communities with the ultimate goal of improving horse welfare.

Each year, the charity organises the Gerald Leigh Memorial lectures which are fantastic resources for horsemen. The lecture series is supported by the Gerald Leigh Trust in honour of Mr. Leigh's passion for the Thoroughbred horse and its health and welfare. Most years, the lectures are presented in person in an event at the UK’s National Horseracing Museum in Newmarket; but for 2021, an in-person gathering was not possible and instead, the lectures are available online. For 2021, the charity chose the theme of orthopaedic problems, which are such a common challenge in young Thoroughbreds.

Angular Limb Deformities: Evaluation and treatment in foals and yearlings

Recognising, diagnosing and understanding angular limb deviations in young Thoroughbreds are critical skills for horsemen and an important part of both stud management and veterinary care. Angular limb deformities (ALD) refer to deviation of the limb in its frontal plane, or side to side when evaluating the individual from the front or back. A varus deformity is a medial deviation of the limb below the location of the problem (e.g., toeing in), whereas a valgus deformity is a lateral deviation of the limb below the location of the deformity (e.g., toeing out). Angular limb deformities must be distinguished from a flexural limb deformity, which is in the sagittal plane, i.e., from front to back when evaluating the individual from the side.

Examples of Valgus (left) and Varus (right) ALDs: A Valgus deformity is a lateral deviation of the limb below the location of the deformity (e.g. Toeing out) whereas a Varus deformity is a medial deviation of the limb below the location of the problem (e.g. Toeing in).

How do ALD occur?

ALD can be both congenital and acquired. Congenital means the condition has been present from birth and causes include incomplete ossification or immaturity of the small cuboidal bones, which make up the hocks and knees as well as weakness of the ligaments supporting the joints and periarticular laxity. These issues tend to result in valgus knees and hocks. We also know that ALD can be inherited and that as a breed, Thoroughbreds tend to be varus (toe in). 

Acquired ALD develop after birth and come about through overloading of the physis (growth plate), which is usually caused either from hard ground, an over-conditioned foal or a combination of the two. The biomechanics of equine limb lead horses to bear more weight through the inside of the leg; therefore, the inside of the growth plate, which is inhibited more than the outside and when there is overloading the net effect is that the foal will toe in.

How do ALD impact a foal’s future career?

Carpal and fetlock injuries in racing Thoroughbreds account for a large majority of the reasons racehorses spend time out of training. Intervening while foals are growing and developing to help them achieve a protective conformation gives them the best chance of maximising their potential and enjoying their racing career. 

Diagnosis of ALD

Evaluating young stock is certainly best achieved using a team approach involving owners/managers, farriers and veterinarians. Regular evaluation from a young age is key, as is examination of the foal while static and while walking. Severe deviations should also be evaluated radiographically.

Treatment of ALD

Conservative treatment options can include exercise restriction, corrective farriery and nutritional management. Hoof correction and toe extensions can be extremely helpful in managing foals and yearlings with minor deviations; and farriery can often correct such issues without needing to resort to surgical treatment options.

The surgical treatment of choice for correcting ALD is the transphyseal screw. In general, it achieves the most effective and cosmetic outcome of the surgical options. The procedure involves placing a screw across the growth plate on the side of the leg that is growing too fast. For example, for a foal that is toeing in, the screw is placed on the outside of the leg. This allows the inside of the growth plate to grow faster and so correct the deviation. The screws are placed under a short general anesthetic. The screw does need to be removed to avoid over-correction, but often they can be removed with the horse standing using a mild sedative once the desired correction is achieved.

Radiograph of a foal’s fetlock post surgery; a transphyseal screw was placed on the outside of a front fetlock to correct a varus (teoing in) deviation.

Osteochondrosis – recent advances and diagnosis

Osteochondrosis is one of the most important developmental diseases in young athletic horses. It occurs in young, large-breed horses, including Thoroughbreds, and can cause a variety of clinical signs. The age at which the disease starts to cause clinical signs varies from a young foal to horses over 10 years old. This is because lesions can remain silent and only cause clinical signs later on in life. But even in the absence of any clinical signs, the pathological lesions will have been present since the horses reached skeletal maturity.

How does osteochondrosis affect athletes?

Osteochondrosis often starts to cause problems when the horse is put into training—when they are athletically challenged. This age will differ for different populations, starting earlier in Thoroughbred racehorses than in Warmbloods destined for sports horse disciplines. Often the horse will be sound, or can experience different degrees of lameness and may present with joint effusion. This disease affects more than one joint in an individual in over 50% of cases, and it usually occurs in the same joint on the contralateral limb; but it can also affect multiple different joints. 

How does osteochondrosis develop?

In foals, areas of growth cartilage within the joints will continue to ossify (become bone) after birth. When this process is complete and the animal is skeletally mature, a thin layer of normal articular cartilage will remain supported by subchondral bone. Osteochondrosis is caused by a “failure of endochondral ossification,” which simply means the growth cartilage fails to become healthy bone. A defect, with or without a fragment, is then created in the articular surface of the bone. This dynamically changing area is susceptible to trauma or high biomechanical loads. Recent advances in research, carried out in Norway by Dr. Olstad, suggest that failure of endochondral ossification is likely caused by loss of blood supply to these areas of growth cartilage, which prevents it from ossifying. This has been linked to a heritable predisposition, among other factors such as rapid growth, dietary imbalance, exercise, environment and prior joint sepsis.

Diagnosis of osteochondrosis

Thorough clinical examination and radiography remain at the forefront of osteochondrosis diagnosis. This disease occurs at joint-specific predilection sites as a result of site-specific biomechanical forces and differences in the age at which that site becomes skeletally mature. For example, in the femoropatellar joint (pictured), the most common site of osteochondrosis is the lateral trochlear ridge of the femur. This is predilected by the thick cartilage surface, later age of maturation/ossification, and by the shear forces the patella exerts on the ridge as the stifle flexes and extends. Ultrasonography can also be very sensitive in detecting osteochondrosis in the stifle. Research performed by Dr. Martel in Canada suggests early detection of subclinical lesions in the stifle have been found in foals aged 27-166 days old.  

The photograph on the left shows femoropatellar joint effusion of the left stifle. The radiograph on the right shows a large osteochondrosis lesion of the lateral trochlear ridge of the femur within the femoropatellar joint.

Management of osteochondrosis

Lesions can spontaneously resolve, and the majority will have done so by 12 months old. Otherwise, management recommendations to limit lesion development include keeping horses exclusively at pasture up to 1 year old, not using rough terrain, in large group sizes (>3 brood mares) or in a large pasture size (large pasture size > 1 hectare before 2 weeks old and > 6 hectare before 2 months old). Strict box rest is discouraged, and a convalescence paddock of 33ft x 56ft (10m x 17m) for 60-90 days may help stabilise lesions. 

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