“Tying Up”

‘Tying up’, also known as Azoturia, Monday Mornings Disease or Recurrent Exertional Rhabdomyolysis (RER) is the most common muscle disorder in horses, frequently limiting performance in sport horses of varying breeds. Tying-up is basically muscle cramps, the largest muscles in the horse (back and hindquarters) are most often affected by a combination of different (it is not fully understood) mechanisms, leading to a buildup of lack of muscle oxygenation, lactic acid and muscle cell death.

‘Tying-up’ usually affects horses in a high level of work that are rested for 1 or more days and still fed a high carbohydrate:low fat diet. It most often occurs after 20-30 mins of work during the first exercise following a period of rest. However, it may also occur as a result of increasing intensity of work or unfit horses undergoing prolonged periods of exercise. Any breed of horse can be affected. It most often occurs amongst younger horses and affects mares more than males. Some horses experience only one or two isolated cases, whilst others suffer repeat episodes which subsequently limits their athletic potential.

Stress, excessive sweating, lack of drinking before and after work or not travelling well will cause electrolyte imbalances or disturbances which predispose a horse to ‘tying-up’. As can a diet high in cereals (as these contain a high potassium:sodium ratio) or deficient in certain minerals and vitamins. Some blood lines are also prone to producing horses that regularly ‘tie-up’ so there is a suspected genetic component too.

Depending on the severity of the episode, horses will demonstrate varying clinical signs from a mild discomfort and stiff gait to a very stiff gait and refusal to move or even in severe cases recumbency due to the pain. Most horses will have firm painful muscles in the gluteal, hamstring and back area, some horses will develop muscle swelling. Tying up is very painful and horses may become distressed and anxious, they may increase their respiratory rate, sweat or even show colic like behaviour.

If you are out riding away from your horse’s stable and your horse ‘ties-up’, phone for help. The horse should be transported by lorry or trailer to limit any further muscle damage. Once the horse is in a stable, keep them warm with plenty of rugs and offer water.

Diagnosis is made based on clinical signs and a blood test measuring muscle enzymes and kidney parameters. The enzymes are released from inside muscle cells when they are damaged. Myoglobin is a product also released by damaged muscle cells. This can discolour the urine brown or orange, potentially causing kidney damage if severe enough.

Immediate treatment depends on the severity of the episode but the aim is to provide pain relief, reduce further muscle damage and protect the kidneys. If mild; encourage the horse to drink (restoring electrolyte balance) and if the horse is comfortable you can walk them around to stop them stiffening up further, but do this with caution! If the horse is very painful, reluctant to move or recumbent, do not try to move the horse! This may lead to further muscle damage. Call your vet and allow them to provide pain relief and anti-inflammatories. The vet may also give acepromazine (ACP), a drug that calms the horse down and causes the blood vessels to dilate, increasing blood supply to the muscles. If the horse is dehydrated there is a risk of kidney damage so the horse may require rehydration by oral fluids or intravenous (IV) fluids. Other drugs are available to help stabilise the muscles and protect from further damage.

Prevention is better than cure and so if you have a horse prone to tying up it is important to provide a high-fat (bran and oils), low-carbohydrate (grains) diet, ensure your horse is properly warmed up and cooled down before and after work and exercise the horse every day, as one or more days of inactivity seems to preclude ERE episodes.

Vitamin E and selenium supplements can also be of benefit, as can antioxidants and other drugs and herbal supplements which your vet can inform you about.

Some horses suffer from chronic ER, these horses require further investigations to define why they continue to ‘tie-up’, this can involve repeat blood tests, exercise tolerance tests, and muscle biopsies.

Chris Baldwin, BVetMed, MRCVS

Sacroiliac Joint

Sacroiliac pain in horses is a performance limiting condition that can be challenging to diagnose and manage. To understand why horses develop this problem we first need to understand the anatomy involved.

The pelvis is a ring of bones formed of three fused bones; Ilium, ischium and pubis. The lower part of the horses back, the sacrum, is formed of 5 fused vertebrae. The sacroiliac joint (SI) is the joint where the sacrum passes underneath the top of the pelvis (tubera sacrale). The SI joint is strengthened by the ligaments; dorsal, ventral and interosseous sacroiliac ligaments. SI pain is either in-flammation of the joint or ligaments surrounding the joint. The SI joint functions to transfer propulsion from the hindlimbs to the spine, supporting the horses back and driving the horse forward from its hindquarters when in motion.

SI pain typically affects heavier, taller horses usually between the ages of 5 and 15 years old. There is no documented association between a horse’s confirmation and developing SI problems. Warmbloods, Thoroughbreds and Thoroughbred crosses are over represented, as are horses used for show jumping and dressage, which may be due to athletic demands placed on these horses during their work.

The signs that a horse maybe suffering from SI pain are subtle and insidious in onset and progression. Typically the signs are exacerbated when the horse is ridden under-saddle and can be easier to appreciate by the rider than to be seen by an observer. There may be no overt lameness to be seen. Table 1 lists the common signs of SI pain.

 

Common complaints related to SI pain

 

* Poor performance / unwillingness to work / holding back

 

* Lack of impulsion or animation 

 

* Intermittent lameness

 

* Reluctance to be shod or have the leg held in a flexed position for a prolonged period of time

 

* Poor or stilted canter, becoming disunited, taking the wrong lead leg

 

* Stiff through the back, refusing jumps

 

* Poor lateral work

 

* Change in behaviour or performance when worked on the bit

 

Diagnosis is challenging due to the mass of muscles surrounding the SI joint. A thorough physical exam by a veterinarian is required to rule out other conditions. SI pain is a consequence of a change in the mechanics of the horse’s back and hindlimbs. Therefore conditions such as suspensory ligament desmitis or kissing spines (impinging spinous processes) can be a precursor or sequel to SI pain.

Xray and ultrasound of the SI region is limited due to the anatomy. The most sensitive form of diagnosis is a bone scan (nuclear scintigraphy). The SI joint can also be anaesthetised (blocked) and if there is pain at this site an improvement maybe seen or felt.

Treatment of SI pain requires a combination of medication, physiotherapy and a rehabilitation programme. The SI region can be injected with steroids to reduced inflammation of the joint and ligaments. This will be performed by your veterinarian when required and usually requires more than one treatment. Physiotherapy and rehabilitation are important in making sure the horse works to build up strong muscles around its hind quarters so the SI region is protected and used correctly. Each horse with a diagnosed SI condition will have a tailored rehabilitation program outlining the details of exercises and time period. In feed, anti-inflammatories or joint supplements may be beneficial in reducing in-flammation and promoting healthy joints. Other treatments such as acupuncture or magnetic rugs/boots, may be of benefit however there is little published evidence supporting this.

In summary, the SI is the connection point between the horse and its hindlimbs. The condition mainly affects larger horses undertaking dressage and Show jumping. the signs of SI pain are very subtle. Diagnosis is challenging and treatment involves a combination of medication and rehabilitation.

Chris Baldwin, BVetMed, MRCVS

Atypical Myopathy

Atypical Myopathy was first recognised back in 1984 but has largely come to prominence over the last few years with outbreaks in the UK and Europe. It occurs in individuals or groups of horses at pasture and is likely caused by ingestion of seeds known as ‘helicopters’ (and possibly to a lesser extent leaves) of the sycamore tree (Acer Pseudoplatanus) that contain a specific toxin. This toxin has been identified as hypoglycin A. The amount of toxin within seeds is variable and it is not understood why some seeds have more toxin than others nor is it understood how many seeds have to be eaten for a horse to become sick. It is likely that some horses will be more susceptible than others with younger horses appearing particularly susceptible, particularly those in poor bodily condition, on relatively poor quality pasture. As older horses are less likely to become affected it may be that they develop some tolerance to the toxin.

Incidences tend to occur in the autumn and in the spring following large autumnal outbreaks and are often following a sudden adverse change in weather conditions, such as a frost or heavy rain. 

It can cause a variety of clinical signs which can present as dullness or lethargy or as a sudden onset of muscle stiffness or weakness that can progress rapidly to recumbency. Other reported signs also include reluctance to work, choke, whinnying, head tossing or an abnormally low head carriage. It can affect the diaphragm resulting in difficult or laboured breathing and some cases may show some colic like symptoms such as paddling or stretching the limbs. Due to the breakdown of the muscle urine often appears dark red and brown. If it affects the heart muscle it can result in a fast or irregular heart beat and in the worst case some horses may present as a sudden death. The mortality rates vary from 40-100% and vary from year to year.

DIAGNOSIS

Diagnosis is based on clinical signs alongside an increase in serum muscle enzymes (AST/CK) and the presence of red/brown urine.

TREATMENT

Prompt diagnosis and treatment is essential if horses are to have any chance of survival. There is no specific treatment only supportive care which involves hospitalisation, intensive intravenous fluid therapy and nursing. Fluids are required to provide cardiovascular support as horses can become very dehydrated and to support the kidneys as the product of muscle breakdown (myoglobin) can affect their function and can cause renal failure. If there is concern over the kidney function then they may also be given a diuretic to help the kidneys maintain a good urine output. This condition can be extremely painful and so a variety of powerful painkillers and anti-inflammatories may be required. When horses become recumbent then they require frequent turning to encourage them to stand and to prevent sores. If they are inappetant then they are provided with an alternative source of nutrition usually by stomach tube in order to provide their energy requirements. Supplementary vitamins and minerals have also been shown to be useful in some cases.

Prognostic factors for survival are normal mucosae, no respiratory distress signs, a standing position most of the time, no temperature, and normal abdominal transit.
Factors unfavourable to a recovery include recumbency, abundant sedation, anorexia, tachycardia (a high heart rate), tachypnoea (high respiratory rate), respiratory difficulties and severe acid-base disturbances. Euthanasia may have to be considered when horses appear to have reached the stage where they are no longer likely to respond to supportive treatment.

In horses that do recover, recovery is initially slow, but most go on to make a complete recovery and return to work with no long-term effects of the disease.

PREVENTION

Given the high mortality rate prevention is better than cure. If sycamore seeds are present in your fields then the following is advised

- Avoid letting horses graze pasture that are contaminated with the sycamore seeds. 
- Move horses out of the field to as distant a point as is practical, or stable the horses during the risk period. 
- If you are unable to remove horses from pastures then fence off areas where the seeds and leaves have fallen and offer supplementary hay but do not leave it on the ground to get wet and feed extra concentrate.
- Rake up or hoover and remove the seeds, dead leaves and saplings where possible.
- Reducing the stocking density can help to ensure there is good grazing for every horse.
- If you are suspicious that your horse may have ingested some of these seeds then call your vet out to check the muscle enzyme levels (AST/CK) to identify subclinical and pre-clinical cases.

If you suspect that your horse is showing any signs of atypical myopathy then contact your vet IMMEDIATELY. If you have any other concerns then please do not hesitate to contact your vet practice for further advice.

Images of Sycamore trees and seeds.

VWH – 15th July

Tuesday 15th July

After we finished lecturing in Helsinki it was back to the port and onto another overnight ferry to Stockholm. We were crammed into windowless cabins (four of us per cabin) in the bottom of the boat next to the engine rooms and it was a relief to reach Stockholm. The approach to Stockholm by water is beautiful with hundreds of small islands each with the Swedes' summer houses and yachts moored outside. The Swedish police were on fearsome top form and breathalysed every driver coming off the ferry with a 'welcome to Sweden' message for each of us! A long ride to the lecture venue in the middle of Sweden with 35 Swedish equine vets in attendance to hear the full 5 hour programme of talks. There was a lot of discussion about back problems and how best to treat these, in addition to practical questions abut how to manage outbreaks of infectious diseases like flu and strangles. The local organiser did an amazing job and there was a supper for the speakers and delegates at the end of the evening's lectures. Tomorrow we are back on the bikes and off to Norway for an evening of lectures at Sandefjord.

VWH 2014 Tour

Andy Crawford, one of the surgeons from The Arundel Equine Hospital is currently making his way around North Europe with Vets With Horsepower.

Vets with Horsepower is a charity, orginally set up by Professor Derek Knottenbelt from Liverpool University, in which a group of equine specialists partake in long distance tours on motorbikes giving talks to other vets and members of the public on veterinary topics. The fees raised by these talks are all donated to two charities:-

'Gambia Horse and Donkey Trust' www.gambiahorseanddonkey.org.uk

'The Smile Train' www.smiletrain.org.uk

Andy's first blog....

Monday
I left Arundel on Friday afternoon on the bike and before I had got to Horsham I had to stop to put on wet weather gear! Great, only 2700 miles to go! I met up with Professors Roger Smith and Josh Slater at Folkestone and we rode the three bikes in the rain to Antwerp on Friday night. The next day took us 400 miles through industrial Holland beyond Eindhoven where we finally got into green countryside with small farms and yards with lots of very smart Warmbloods and a big selection of other breeds including ponies and a few heavy horses. It was a relief to see a gentle landscape with trees, grass paddocks and horses after so many miles of industry. The rest of the day was a high speed blast up the German autobahns past the industrial centers of Essen and Dortmund, across the Rhine and the Ruhr and then a turn northwards through more horse country to Munster and then onto Bremen and finally Hamburg.

We had a 30 hour ferry journey to Helsinki which gave us time to work on our talks for the lecture tour this week and, of course, experience our first Scandinavian sauna. We discovered two things: first the Finns are passionate about saunas, and everyone goes for at least one sauna a day, second, the Finns do everything naked - not for the fainthearted! (and certainly not for us).

We arrived in Helsinki the next morning and met up with the main bike group to give our first lectures of the Scandinavian leg. The lectures covered flu vaccination, tendon injuries, back problems, sedation and I spoke on advanced diagnostic imaging in the horse including scintigraphy, MRI, and CT. We had 55 delegates which was great and an unexpectedly large turnout because this is normally a holiday in Finland. We are back on the ferry this evening for a night crossing to Stockholm and tomorrow morning's lectures. Not sure whether we will be brave enough to try the sauna again......

COPD

Chronic obstructive pulmonary disease (COPD) also known as recurrent airway obstruction (RAO) or “broken wind” is a chronic condition of horses involving an allergic bronchitis characterised by wheezing, laboured breathing, coughing (usually associated with exercise or eating) and nasal discharge (especially when the head is lowered or after exercise).

The condition was known as ‘heaves’ because horses with COPD have very inflamed narrow airways and as such breathing both in and out is difficult and requires recruitment of other chest and abdominal muscles to aid with respiration, these muscles become enlarged and hence the horse develops “heave” lines.

COPD is an allergic reaction to certain otherwise innocuous substances - allergens. These allergens are typically dust, mould and fungal spores (e.g. Aspergillus). It is therefore most common in horses fed hay and bedded on straw. It is similar to asthma and farmer’s lung in humans.

Allergens enter the horse’s lungs and the horse’s hypersensitive immune system over-reacts to the “normal” pollens. The lungs become inflamed and swollen, causing the airways to become narrowed and mucus production to increase, which then leads to the signs we see in our horses.

Diagnosis is usually based on the results of a clinical exam and auscultation of the horse’s lungs. However sometimes further diagnostics are required, in which instance an endoscopic exam of your horses trachea and bronchioles can be performed and samples can be taken.

Acute flare ups can present dramatically, your horse maybe distressed with markedly elevated respiratory rate and effort, flared nostrils and sweating. If a horse is severely dyspnoeic (really struggling to breathe), the most important measure to take is to REMOVE IT FROM THE STABLE OR BARN into FRESH AIR. Keep the horse (and yourself) CALM and CALL YOUR VET IMMEDIATELY.

Treatment is all about management and minimising exposure to the allergens. When removed from the allergens the symptoms will usually subside, although they will recur if the horse is exposed to the allergens again, even short periods of re-exposure can induce acute episodes.

If it is not practical to stop stabling all together then the following changes will be of benefit:

• Minimise dust and maximise air quality in the stable.
• Soak hay or feed a low dust alternative such as haylage or bagged grass. If you are going to feed hay it should be soaked hay, you only need to soak the hay for an hour to remove the majority of pollens and allergens 60 minutes. Soaking hay for longer will reduce the carbohydrate load of the forage, good for horses and ponies that suffer from laminitis or are looking to lose weight but not necessary in managing COPD.
• Feeding from the ground allows any mucous to drain out of the lungs. Horses are designed to graze for approximately 20 hours a day, during which time the horse has its head down to the ground where mucus within the horses trachea and bronchioles can be expelled, because of this design the horse is very poor at clearing mucus from its lungs without the aid of gravity, by feeding on the floor you encourage the horse natural mucus clearing function.
• Bed on a dust free bedding. Those horses that must be stabled should be bedded on rubber matting and paper, or low-dust wood shavings. Straw contains dust, moulds and fungal spores and so is least advisable. In severe cases horse may be intolerant of any bedding in which case the mats can be washed daily. The matting has a fairly high initial cost but there is a considerable saving in bedding (and veterinary costs if your horse has RAO).
• Make sure the stable is well ventilated.
• Don't muck out or brush up while your horse is in the stable to minimise the dust in the air.

All the stables in the vicinity need to be similarly maintained or the environment will remain high risk for the horse and aim to stable your horse away from the muck heap.

Despite management changes, medication is often required, these break down into 3 broad categories:

• Bronchodilators, theses dilate (open) the bronchioles and smaller airways allowing the horse to breath more freely.
• Corticosteroids: these reduce the inflammation in the airways and damped down the immune hypersensitivity reaction.
• Anti Histamines: these damped down the immune hypersensitivity reaction that leads to the inflammation in the lungs.
• Mucolytics: these make the horse’s mucus less viscose and so easier to clear form the airways.

Care should be taken with all these drugs in competition horses, as many of them are forbidden substances under racing and FEI rules.

If the condition occurs in the summer when the horse is at pasture then it is known as summer pasture associated obstructive pulmonary disease (SPAOPD) In this case, the allergens are derived from the pasture. This is more common is summer, and management is reversed: horses should be stabled in well ventilated areas. Some horses can suffer from RAO and SPARAO which can be very difficult to manage.

RAO often limits the horses' ability to work, and it may find strenuous activity difficult. However, with prompt diagnosis and treatment the condition can be managed successfully.

Ragwort

Ragwort (also known as Senecio Jacobaea) toxicity is one of the most common causes of poisoning to horses in the UK. A recent survey by the British Horse Society showed that 20% of respondents knew of a horse that had been affected. Toxicity is caused by substances in the plant called Pyrrolizidine alkaloids. The effect is cumulative and symptoms may not be seen for up to a year after exposure. The poison effects 3 main body systems - the liver, the central nervous system (brain, spine and its associated nerves) and the skin. Symptoms include weight loss, loss of appetite, depression, diarrhoea, jaundice (yellowing of the whites if the eyes and gums) and constipation. Neurological problems can be seen as wobbling and dizziness, pressing the head against the wall and the appearance of walking aimlessly. Toxic compounds can also enter the skin causing it to become particularly sensitive to sunlight resulting in crusting on white areas that looks like sun burn. This process is called Photosensitisation.

If you’re concerned your horse may have been affected please contact your vet. Blood tests can be used to confirm liver damage but cannot test specifically for the poisoning. A sample of tissue taken directly from the liver may be able to confirm the damage is caused by Ragwort. Horses diagnosed with poisoning rarely recover. Treatment is mostly supportive with nutrition to maintain condition and medications to control the symptoms.

Control of ragwort is crucial in avoiding illness. The first step is the identification of plants. For the first year of life the plant is a small dark green rosette. In subsequent years it becomes the characteristic bright yellow flowers between June and October. Ragwort cannot be entirely eliminated from the UK as it forms an important part of the ecosystem. However, the Weeds Act 1959 made ragwort control a legal obligation for owners and occupiers of grazing land. Those who keep their horses in livery and are unsure of their responsibility in ragwort control should check their contract.

Cutting of ragwort plants is only suitable in emergency short term control to prevent seeding. Cutting the stem stimulates growth and will cause the plant to re flower later in the season. If removing plants by hand, they should be pulled up or levered out by the roots. Ensure the entire root is removed as any left behind will re-grow. Ragwort is best pulled early in the summer before flower heads mature and when the ground is wet. As well as removing adult plants it is important to identify first year rosettes to prevent them seeding the next year. Ragwort is toxic to all species including humans so gloves and long sleeves should be worn. Any skin exposed to the plant should be thoroughly washed in warm soapy water. Once pulled the plants are still toxic and may still seed, in fact wilted plants are more palatable to horses. It is essential all plants are collected and placed in sealed boxes or bags. Disposal can be by incineration, rotting or removal by a waste-management company. The plants should never be composted, placed on the muck heap or transported without being properly sealed in bags.

It is possible to use herbicides as part of a ragwort control strategy although it must be considered that one application does not guarantee total removal. Most products require application in the spring to the growing rosettes and a calm dry day. When choosing a product thought must be given to the environmental implications and proximity to water sources which may become polluted. If spraying you will need a suitably trained person and the means to correctly dispose of unused chemicals. Horses must be moved off the pasture for application and for a period of time afterwards. The manufacturers of pesticides will make recommendations on when it is safe to use the pasture but it is the keeper's responsibility to ensure all dead ragwort is fully wilted before exposing to horses. For a list of approved pesticides please see pesticides.gov.uk.

Ragwort thrives in areas of poorly kept grassland so plant numbers can be reduced by improving pasture management. This includes not over-gazing, adequate manure removal and removing uneaten stale hay. Poaching the ground should be avoided wherever possible as bare patches are ideal for ragwort growth. Co-gazing with sheep can be beneficial as they are far less susceptible to ragwort poisoning than horses and will eat the young first year rosette plants.

For any advice on ragwort control or if you think your horse may be affected by poisoning contact The Arundel Equine Hospital on 01903883050.

Written by Rebecca Dobinson, BVSc, MRCVS

Cushings & EMS

Cushings (Pars Pituitary Intermedius Disorder ((PPID)) and Equine Metabolic Syndrome (EMS) are the two most common metabolic/hormone disorders of the horse and pony. In general, Cushings affects older horses, whereas EMS first develops in young and middle-aged animals. Although they are two separate conditions, they can overlap. All breeds are susceptible but ponies are most at risk.

Cushings

This is due to a dysfunction in a small area of the horse’s brain and it disrupts the normal balance of hormones, mainly affecting ACTH and cortisol (stress hormones). The most common sign are your horse developing a long, thick, curly coat or not losing his/her winter coat. Other early signs of Cushings are vague but include; reduced performance, lethargy and regional fat deposits (bulging supraorbital fat pads, shoulder fat pads, “cresty neck” and fat accumulation around their tail base). The more advanced signs of the disease include; muscle wasting, a pendulous abdomen, sway back, increased sweating (linked to not shedding their coat), blindness, recurrent infections (including parasites, skin infections and synovitis), reduced fertility in mares and increase drinking and urination.

The most import aspect of this disease is laminitis; this can feature early on in the disease process and is usually the condition, which leads to diagnosis of Cushing’s. Laminitis is an inflammation and breakdown of the lamellae. The lamellae suspends and supports the pedal bone within the hoof capsule. When these lamellae are disrupted, the pedal bone sinks and rotates which then causes lameness. Cushings causes a break down in the lamellae proteins and reduces lamellae blood flow. This is why horses with Cushings are predisposed to laminitis.

Diagnosis is usually made on history and clinical exam; however, to be sure a blood test is usually conducted. The blood test measures the hormone ACTH as horses and ponies with Cushings have significantly higher levels of ACTH. It is not 100% diagnostic and may miss early cases but will confirm most and gives you the ability to measure the success of treatment. The hormone ACTH usually peaks in the autumn naturally and so this is the best time of year to test horses suspected of having Cushings. When determining baseline ACTH concentrations it is important to consider that stress may increase ACTH levels so the horse must first recover any bouts of stress or laminitis. Other tests are available if the result of this test does not match with the clinical picture of the horse.

Cushings is a condition mainly of older horses and so management is vital, including; feeding high-quality foods, regular dental care, deworming, and farrier care. Management and treatment depends on severity of condition, if the horse has a hairy coat then you can manage them simply with regular clipping. However, if the horse or pony is suffering from laminitis then management and pharmacological intervention will be required.

Pergolide ‘Pracend’ is the first-line treatment of horses and ponies with Cushings, it is a lifelong treatment that needs to be coupled with management changes. Once a treatment has been started, if there are no signs of improvement after 4 to 6 weeks, the dose should be increased gradually every 3 to 4 weeks. Treatment should be monitored by assessing both improvement of clinical signs and repeat blood tests to check for normalisation of ACTH concentrations. Most horses show improvement within 6 to 8 weeks of treatment. Within a month you can expect to see an improved attitude and reduced lethargy, however improvements in coat, muscle mass and laminitis may take up to a year. This is a lifelong management that needs to include laminitis management as well.

EMS

This occurs because fat tissue is active and produces its own hormones. These hormones reduce your horse’s response to insulin, making your horse insulin resistant (IR) this leads to a high concentration of both insulin and glucose in your horse’s blood stream (it also increases the level of cortisol, like in Cushings). This condition in very basic terms can be considered “Horse Diabetes” with a bit of Cushings. These horses are usually obese or “good doers” however, some horses can be lean but still have EMS.

EMS is characterised by obesity or regional adiposity, insulin resistance (IR), and subclinical or clinical laminitis. Laminitis is the most important component of EMS; this condition is most difficult to manage. IR predisposes a horse to laminitis by; altering blood flow and reducing nutrient delivery to the hoof tissues and generating inflammatory or oxidative damage. EMS horses therefore cannot tolerate normal laminitis triggers such as; grass rich in sugars and starches, grazing on abundant and rapidly growing grass, grazing after a frost or in periods of cold night and warm days (this changes the sugars within the grass and they become more readily available).

Diagnosis is made on clinical examination and history but there are blood tests that can confirm the diagnosis and again it is good to have a base line from which to judge the success of treatment. To diagnose EMS in horses, insulin and glucose concentrations can be measured in a blood test. Horses are starved for 6 hours over night and a blood test taken in the morning. Stress raises insulin concentrations in horses so it is important not to take a blood sample whilst the horse is suffering from laminitis. Another test available is an Oral Glucose Test, the horse is starved overnight for 6 hours then a blood sample is taken in the morning before giving a high glucose feed (1g/kg) in a very small feed. After this, blood samples are collected 2 and 4 hours later.

Management of IR/EMS involves mainly weight loss and laminitis management. This can be achieved by reducing sugar and starch intake, soaking hay, removing fat supplements, restricting turnout and regular daily light exercise. Exercise when the horse is sound is essential as it can decreases IR. Leaner horses with EMS are challenging to manage from a dietary standpoint because more calories must be provided without exacerbating IR. Most horses or ponies with EMS can be effectively managed by controlling the diet and reducing body fat, however, it takes time for these management changes to take effect, so drugs such as Metformin can aid the process and accelerate the improvement if the patient suffers from recurrent laminitis.

For both these conditions, the horse needs to be treated as an individual so close work with your vet and farrier is essential in successful management. If you have any concerns, your horse or pony may be suffering from Cushings or EMS then contact your vet for a consultation.

Navicular Bursar

Once a diagnosis of a problem with the navicular bone, the deep digital flexor tendon or one of the other soft tissue structures associated with the navicular bone is made, one of the treatment options is to inject the navicular bursar with cortisone as an anti-inflammatory. The navicular bursar is the fluid filled pouch between the navicular bone and the deep digital flexor tendon.

The procedure involves injecting with a long needle between the heel bulbs, through the deep digital flexor tendon and into the navicular bursar. This is best carried out under x-ray guidance. First of all a radiograph is taken of the foot with a marker that shows up on the image, to identify the exact location of the navicular bone within the hoof, a mark is made on the hoof wall with a marker pen to be used as an aiming marker for the needle advancement. Often a nerve block will be placed at the palmar digital site to totally desensitise the heel region of the foot, sometimes just the location of the injection site is desensitised with local anaesthetic.

Once the injection site is desensitised the heel region is meticulous cleaned and then aseptically prepped. A 10cm spinal needle with a stylet is placed through the skin between the heel bulbs and advanced towards the navicular bone, roughly parallel with the ground, using the marker on the hoof wall as a guide to the angle of approach. As the needle is advanced it is possible to gently feel it contact the back of the navicular bone. At this point a second radiograph is taken to make sure the needle placement is correct. If the needle is in the right place behind the navicular bone and through the deep digital flexor tendon, then the stylet is removed from the needle and the cortisone is injected into the bursar. Mixed in with the cortisone is a radiopaque substance which shows up on x-rays, a third x-ray is taken to demonstrate filling of the drug within the pouch at the back of the navicular bone and therefore the drug within the navicular bursar, after the needle has been removed.

Following injection the heel region is bandaged to keep it clean for 24 hours. The patient is kept box rested also for the first day after the injection, then hand walked for a further 2 days, followed by an ascending exercise program dependent on what the actual diagnosis was.

It is important that this procedure is carried out as aseptically as possible as to avoid the introduction of infection into the navicular bursar. It is also important to be as accurate as possible with the needle placement, if we know from the series of images obtained that the needle was correctly positioned and that the cortisone was injected into the navicular bursar, then we know if the horse does not become sound it was not due to inaccurate drug placement and that a different treatment option is required.

Navicular bursar medication is only one treatment option available to us for the treatment of navicular disease syndrome. This technique should be used in conjunction with other medications such as Tildren (Equidronate), aspirin, isoxoprine, etc. Probably the most important aspect of treatment is the farriery and obtaining a correct and appropriate foot balance.

Dr. E.A.Lyall, BVetMed, CertEM (StudMed), MRCVS