The old saying “No Foot, No Horse” could not be truer. With hundreds of cases reported each year it is no wonder that the word laminitis is synonymous with fear and heartache for horse owners the world over. The words laminitis, meaning inflammation of the hoof lamellae and founder can be used interchangeably to describe the condition. The word founder is an old nautical term used to describe a sinking ship and its use with horses is apt when one considers the sinking of the pedal bone within the hoof.
The death of one of racings all time superstars, Secretariat in 1989 through a severe laminitis episode only serves to emphasize that this condition has no class or breed prejudice and can potentially strike any horse at any time. Laminitis can mean months, years, or even a lifetime of pain for horses, depending on the severity and specifics of the attack. Once a horse has suffered laminitis, they will always be susceptible and will need careful management to prevent further damage.
Though much research time and finance has been devoted to the study of laminitis, there are still relatively few answers as to the exact mechanism by which the lamellae are affected so catastrophically.
Thankfully, there are now a few basic understandings that can help horse owners to be mindful of the dangers and take steps toward recognizing and preventing those situations where horses are at risk. In the majority of cases, horse owners are now so aware of laminitis that cases are usually picked up early, and with correct treatment and management, many horses can make a good recovery.
Anatomy of the Equine Foot
The equine foot is an amazing feat of engineering, designed to withstand the immense concussive forces of locomotion over rough terrain (see Fig 1). The internal structures are highly organized to ‘buffer’ concussive forces from the hoof wall, sole and frog, through the lamellae so that by the time it gets to the pedal bone (also known as the coffin bone, distal phalanx, 3rd phalanx) the force is reduced by up to 90%. This comparatively tiny structure is critically organized in such a way to support the limbs and subsequent mass of the horse. By domesticating the horse and subjecting the body to a diet that is far removed from that of his wild cousins, and the hooves to greater concussive stresses through ridden work, we invite a number of problems that would be devastating in the wild situation. Laminitis is one such problem.
The equine foot is surrounded by a tough, fibrous cortex: the hoof wall. The wall is incredibly strong and forms a protective waterproof barrier between the sensitive inner organs and the outside world. The tissue of the wall is highly keratinized and like hair and nail, contains no living cells. It takes around 6-8 months for new hoof wall tissue to grow from the coronet band down to the ground, and this process continues throughout the horse’s life.
The hoof wall is connected to the internal structures by numerous lamellae, a series of delicate folds of tissue that extend around the entire inner surface of the hoof wall. There are two categories of lamellae. The outer horny lamellae extend from the hoof wall and are folded into an accordion-like structure, with each fold bearing many smaller, secondary lamellae. Each of these folds interfold with the inner, sensitive lamellae like interlocking fingers. The inner, sensitive lamellae are in turn connected to the pedal bone and as the hoof hits the ground, the tissues of the foot are compressed and expanded to allow absorption of concussive forces and to assist in the pumping of blood from the extremities back to the heart.
The main function of the lamellae is to hold the pedal bone in place within the hoof capsule. The folded structure of the lamellae dramatically increases the surface area of attachment, forming an incredibly strong bond between the hoof wall and the underlying structures including the pedal bone. The stability of the thin membrane between the outer and inner lamellar layers is imperative to the overall stability of the internal structure of the hoof. It is thought to be the failure of this bond which leads to the intense pain and physiological changes within the foot that are known as laminitis or founder.
Pathophysiology of Laminitis
Put simply, laminitis results from the failure of the attachment between the pedal bone and the inner hoof wall i.e. the tearing apart of the inner and outer lamellar folds. It is thought that the tearing is a result of the failure of the thin basement membrane that binds the two layers, though as always with laminitis, more research is required before this can be concluded categorically.
Until recently, our knowledge of the factors that trigger this failure was limited. Australian researchers have recently elucidated a key theory as to how the breakdown is triggered. This theory implicates MMP enzymes which are naturally present in healthy hoof and are designed to break down the cells of the membrane in small areas in response to hoof wall growth, minor hoof damage and the normal stresses and strains of everyday life. The activity of the enzymes is tightly controlled by opposing inhibitors that prevent over-release and allow only tiny breakages and reattachments to happen at one time.
Careful research in this area by Dr. Chris Pollitt of the University of Queensland has led to the theory that laminitis results from a catastrophic imbalance of these enzymes and their inhibitors, leading to a partial or total breakdown of the basement membrane that separates the lamellae. When the membrane fails, the lamellar layers are torn apart, somewhat like tearing apart a Velcro™ strip. In the resulting gap, fluids build up; the lamellae become inflamed and the capillaries supplying the lamellar region become squeezed closed by the resulting pressure, thus depriving the lamellae of the nutrients and oxygen normally delivered in the blood. The loss of these capillaries results in an increased blood pressure due to the diversion of blood to the larger vessels of the foot. This increased pressure is responsible for the bounding digital pulse associated with laminitis. The extra pressure leads to dilation of the larger vessels, and is responsible for the hot feet typical of a laminitis sufferer. The pain of laminitis increases as the horse enters the acute stage of the condition. If the damage is severe, the pedal bone separates from the inner hoof wall leading to sinking or founder. The pedal bone, with its lamellar connections damaged and under the pulling influence of the digital flexor tendon rotates downwards or, where laminar damage extends around the whole circumference of the hoof, simply begins to sink within the hoof capsule – the worst possible scenario. As it descends, further tearing occurs and the underlying hoof tissues are crushed. In some cases, the pedal bone descends so far that it actually perforates the sole of the foot. Rotation or sinking can continue for days or weeks, depending on the severity of the episode, so the horse must be reevaluated often during the first month or so following the attack.
In days not so long gone, pedal rotation would mean only one outcome for the horse, euthanasia. Fortunately, with improvement of our understanding of the mechanics of laminitis, many horses are now able to make at least a partial recovery from this situation, and hope is not entirely lost, even when x-ray evaluation reveals a ‘sinker’. It is important to remember that not every case of laminitis leads to founder. It is believed that many racehorses suffer from sub clinical laminitis caused by both concussion, and a grain rich diet and this may impact on performance, but has no overt symptoms.
It has been found that circulation within the foot is extremely erratic in the first 12 hours of an attack, going both below and above normal circulatory levels within periods of the time frame. Neither situation is desirable: i.e. reduced blood flow will starve the lamellae and possibly lead to further tearing, whilst increased blood flow theoretically delivers more laminitis trigger factors to the feet and thus increases tearing. One thing is agreed, prior to symptoms being seen in the acute stage, a prolonged period of reduced blood supply occurs, and when blood supply is restored, symptoms become evident. In order to elucidate possible treatment indications, we must first understand the significance of the peaks and troughs in circulation that occur during the developmental and acute stages of laminitis. Current work in this area by Dr. Steve Adaire from the University of Tennessee is concentrating on the microvascular blood flow within the feet of induced laminitis cases. Using established models such as administration of black walnut or the classic grain overload model, Dr. Adaire hopes to establish the pattern of circulatory imbalance in the developmental stages of laminitis, and eventually be able to describe a treatment regime to control these circulatory changes. It remains to be seen whether these models accurately reflect the activities within the feet of real laminitis cases in the field, but undoubtedly his work will lead to a better understanding of the cause and effect of circulatory disturbances.
In addition to the enzyme theory of laminitis, there is a theory regarding the inhibition of glucose uptake. Glucose metabolism is regulated by a number of hormones including insulin. In-vitro models of laminitis where glucose is restricted leads to rapid breakdown of the basement membrane and allows easy tearing of the lamellar layers. It could be that there is a hormonal influence on glucose metabolism following carbohydrate overload which is responsible for triggering MMP-3 production.
An even more recent theory questions the basement membrane failure theory altogether. Dr David Hood and his staff at the Hoof Diagnostic and Rehabilitation Clinic at Texas A&M Universtiy have been working on an innovative new hoof biopsy technique to get a close up picture of what is going on at the cellular level when laminitis strikes. Preliminary findings suggest that lesions begin on the outer surface of the hoof to bone laminar attachment and progress inwards. It is not yet clear whether the membrane itself is merely affected, damaged or completely destroyed. Samples taken during the developmental stages of the disease showed damage to the lamellae even though the basement membrane of the secondary lamellae was still intact, so challenging the idea that laminitis begins at the basement membrane. Hood intends to conduct further trials in an effort to discover what is causing the lamellar lesions in the very first stages of laminitis.
What Causes Laminitis?
Though we have ample experience of how laminitis affects the horse during the acute stage, we know less about what causes things to go wrong in such a catastrophic fashion. We know that laminitis occurs following a number of distinct occurrences in areas of the horses body often completely separate from the hooves:
Following ingestion of large quantities of grain or fresh green pasture (carbohydrate overload)
Following localized or systemic infection (e.g. retained placenta, respiratory infections)
Following musculoskeletal problems (e.g. Rhabdomyolysis or ‘tying up’)
Following periods of extended concussion (e.g. working on hard dry ground for long distances without rest)
Severe, painful injury to one limb causes laminitis in the opposite supporting limb
In response to an hormonal imbalance (e.g. Obesity, Equine Cushing’s Disease)
Following prolonged antibiotic treatment (disrupting hind gut microflora)
Following administration of excessive levels of corticosteroids
Disturbingly, there are a number of cases each year for which there is no obvious cause, sometimes, laminitis seems to just ‘happen’ with no preceding occurrence or apparent risk factor to blame. For the non mechanical causes above, we assume that the triggering factor or factors are carried in the blood from wherever they originate and when they arrive at the hooves, begin their path of destruction. What we don’t know is what those triggering factors are, whether they are different depending on the initializing event and how they ultimately lead to the breakdown of the basement membrane.
It’s likely that there is more than just one trigger factor involved, but singling out these substances will be the subject of research studies for some time to come.
This type of laminitis is the most common, is one of the most studied, and so is the type of laminitis that we know the most about. Recent research has suggested a couple of pathways. Current understanding outlines that after a large meal containing excessive levels of starch and sugar (i.e. a large grain meal), carbohydrates that are not fully digested in the small intestine pass back to the hindgut where they are rapidly fermented by certain sugar loving microbes. These microbes produce lactic acid as a by product, which in turn destroys many of the pH sensitive microbes. As the balance is disturbed and the microbes continue to die, they release endotoxins which Dr. Chris Pollitt believes may alter the permeability of the hind gut mucosa. It is thought that the results of this massive shift allows the release of one or more of the laminitis trigger factors into the bloodstream where they travel rapidly to the hooves and begin the process of lamellar devastation. It had been previously thought that the endotoxins themselves might be responsible for the chain reaction of events leading to laminitis, but to date, experimental administration of these endotoxins to normal individuals has failed to result in a positive case of laminitis.
One of the sugar loving bacteria has been identified as a possible trigger factor for laminitis. During carbohydrate overload, using the grain overload model, Streptococcus bovis is the principal bacteria responsible for the rapid fermentation of carbohydrate to lactic acid. The numbers of S. bovis literally explode when sufficient carbohydrate is introduced to the hind gut. In vitro models of laminitis have shown that S. bovis readily activates the MMP enzyme imbalance and experimentally causes lamellar separation. If it can be shown that S.bovis manages to escape the confines of the equine hind gut and reach the internal structures of the foot, this may answer one of the questions regarding trigger factors, at least for laminitis caused by grain overload.
The modus operandi of grass founder is thought to be slightly different to grain founder, and presents slightly differently, though usually leading to the same end result. In grass founder, research has concentrated on the presence of certain carbohydrates in grasses. In 1998 researchers Annette Longland and Andrew Cairns from the institute of Grassland and Environmental Research in Aberystwyth, Wales described the mechanism by which grasses store and use sugars as their energy source. Most plants store carbohydrate as starches (chains of the simple sugar glucose), but grasses store carbohydrate as fructan (chains of the simple sugar fructose).
Grasses contain varying proportions of carbohydrates such as sucrose, glucose, fructose and fructans stored from the process of photosynthesis (the plants mechanism of making food for the energy to grow). Depending on climate and conditions, levels of sucrose and fructans fluctuate in grasses, and the researchers explained that variations in exposure to sunlight, day length, temperature and soil fertility etc. would drastically affect the levels of these carbohydrates in grass. They went on to explain that sugars are only produced during the day whilst there is light to power photosynthesis, and at night the plant uses the stores accumulated during the day. This means that the lowest levels of fructan would be present at first light, and the highest levels would be present in the evening. Some hays cut late in the afternoon in cool but sunny weather can contain high levels of fructan and the temperate grasses of southern regions are deemed to be more dangerous than the tropical species found further north.
Fructans are stored in the lower part of the plant, so when grasses have been cropped close to the ground, the re-growth contains fructans as the primary storage unit. The more stressed the plant is, the slower it will grow, and the higher the concentration of fructans will become as the plant continues to photosynthesize and store its carbohydrate. For example, grasses that are exposed to stressful conditions such as frost will still photosynthesize and produce fructan, but growth will be limited, so the fructan will accumulate in the short grass. In Australia, where severe droughts are commonplace, the re-growth following drought breaking rain can contain dangerous levels of fructan. In these conditions, a horse could be eating a diet that is very high in fructan – but what does this mean?
Grass laminitis is a seasonal problem in most cases, brought on by the fresh growth of spring grass that is high in total carbohydrate (and presumably fructan). But laminitis has also been seen in horses that are restricted to ‘starvation paddocks’, where the short grass is stressed but still rich in fructans. Rapid consumption of these sugar rich grasses is thought to overwhelm the hind gut with fructan and other carbohydrates that escape digestion in the small intestine, similar to grain overload. But there, it is thought that the similarity ends. It has always been difficult to explain why the developmental stage of laminitis is not seen in grass foundered horses as it is in grain overload, with the horse or pony being discovered in severe pain in the acute stage, with no preceding signs. Perhaps differences in the progression of the condition are a result of a difference in the way that fructans are fermented in the hind gut, and the way in which the trigger factor is released. Perhaps in the case of grass founder, the trigger factor is altogether different to that of grain overload, as yet, we just don’t know. This is the area of laminitis research currently being studied by Dr. Chris Pollitt who has recently described a new laminitis induction method involving administration of oligofructose, a commercially available form of fructan. This new method is more reliable and is kinder to the horses than the traditional grain overload model in that it has a lower level of morbidity and mortalitly and seemingly a higher success rate.
New research in this area could lead to the development of an analysis kit to assess the risk of certain pasture types and to indications about the best time of day for turnout in susceptible horses. It has already been accepted as common practice to limit turnout in susceptible horses during the day in the growing season, to beware of grazing stressed pastures and that feeding lucerne hay may be a good alternative as lucerne is relatively low in carbohydrates and fructan. We may in the future see special ‘laminitis proof’ pasture’s being developed with cultivars of grasses designed to have a low fructan content, but for now, we must observe the suggestions based on the facts that we have so far.
Though the feet of our equine friends are strong, they were never designed to take the kind of forces that we regularly thrust upon them. During the long hot summers, when the ground becomes extremely compacted, there is an increased risk of concussion laminitis. Pounding away on hard ground day after day affects the blood flow to the foot and may cause changes in the lamellar membrane. This in turn may lead to the mechanical tearing of the lamellar membrane leading to the partial or total breakdown of attachment to the pedal bone as previously described. This type of laminitis may affect only a portion of the lamellar surface, and so may not lead to a complete breakdown of the membrane, but can nevertheless be devastating for the horse involved.
Symptoms of Laminitis
The most disturbing thing about laminitis is that the initial developmental stages usually go undetected. It is only once the horse has begun to feel the pain of lamellar separation in the acute stage that the owner recognizes that something is amiss. Of course, by the time the pain is evident, much of the damage has already occurred, and the onus is then on damage control. Some of the symptoms currently recognized easily by the owner include:
In the early stages, restlessness, warmth in the feet, shifting of weight from one foot to the other – if you notice these signs after a high risk incident, or your horse has had laminitis previously, it is wise to seek veterinary help immediately.
Once the condition has become acute:
Sore feet, usually in the front, but can also be apparent in the rear, especially in donkeys. The toe region is especially sensitive when tested with hoof testers.
Characteristic ‘rocking horse’ stance with the hind legs tucked well under the body and the forelegs stretched out to allow weight transfer to the heel region.
Bruising on the sole as a result of pedal rotation or sinking crushing the underlying capillaries, and bruising of the white line area
In chronic laminitis cases:
Rings and ridges in the hoof wall
Bruised soles or stone bruises
Seedy toe (widening of the white line)
As we begin to learn more about laminitis, it is hoped that we will be able to pick up on some other early warning systems that can be recognized by the horse owner and used to begin treatment more rapidly.
The first thing that you should do if you suspect laminitis is to call your equine veterinarian. Laminitis should be treated as a medical emergency, and prompt attention can improve the eventual outcome. The severity of clinical signs is directly correlated to the severity of the condition and your vet will do a thorough physical examination to determine exactly how severely the horse is affected.
The vet will want to take x-rays to make a conclusive diagnosis and to measure the severity of any movement of the pedal bone. A series of measurements will be taken from the X-rays, and the conclusions of these observations will guide the veterinarian as to the best course of action. Each case of laminitis is specific and the treatment options are wide depending on the particulars of each case. Rotation can continue to occur for weeks after the initial attack. It is recommended by veterinarians specializing in equine podiatry that new x-rays be taken every 5-10 days following an attack until the full extent of the damage is played out to ensure that treatment takes into account the picture inside the hoof during recovery rather than relying on a ‘snapshot’ taken at the onset.
A relatively new technique, used extensively in the US by Dr. Ric Redden, is the venogram. Dr. Redden is founder of the International Equine Podiatry Centre in Versailles, Kentucky and a respected researcher and gatherer of knowledge in the field of laminitis and foot care. The venogram involves injecting a contrast media into the digital palmar vein that shows up on X-rays. This liquid quickly fills the delicate veins and capillaries of the foot, and when X-rays are taken, highlights the areas where circulation is compressed or dilated and allows the veterinarian to more accurately pinpoint the sites of major damage. This technique may also have some therapeutic benefits, as Redden has noted that following the procedure, there is a marked improvement and reduced pain.
Current Advice on Treating Laminitis
With so many theories concerning the cause of laminitis, it is inevitable that there are a number of theories concerning the correct treatment. We have not yet found a definitive cure for laminitis, to do so would be to preempt the attack. At present we are dealing with the after effects of a catastrophic chain of events that we seemingly have little control over, and no means of detecting until it is too late.
The predisposing condition that has led to the laminitis is usually treated as the primary concern, with the danger of laminitis only realized once foot pain is evident. For each individual case, there will likely be an individual treatment plan, and this can be very dependant on the experience and knowledge of your vet and farrier. Veterinarians and farriers must work very closely together in order to effect the best treatment and pain relief for the horse.
There are a number of possible steps that may be taken depending on the specifics of the case and any pre existing foot or limb conformation abnormalities.
Obviously the first thing to do with a laminitis case is remove the cause of the problem. In the case of grain overload or grass founder, you will need to make changes to the diet. Move the horse or pony to a paddock with very little feed (but avoid over stressed pastures which may be high in fructan), remove grain from the diet and feed only hay and water as an immediate step. Lucerne is ok to feed, having relatively low carbohydrate content and low fructan levels, but do not over-feed any kind of hay in the initial stages. A grassy lucerne/ clover is best, providing quality protein to help rebuild weakened hoof horn. A good quality meadow or grass hay is good, or a cereal hay (oaten, barley) as long as it doesn’t have too much grain attached. Due to the risk of some hays having high fructan levels (up to 30% in some cases) it is wise to soak the hay to reduce the level of water soluble fructan, and feed only small amounts at frequent intervals, perhaps from a double haynet to slow consumption rate as the horse picks the hay through the holes. If a hard feed is required to maintain condition, then concentrating on ingredients that are high in fat and digestible fiber is recommended. Seek assistance from an equine nutritionist if you have any doubts about what to feed. For the longer term, you may be able to reintroduce limited pasture and should concentrate on providing a balanced diet to meet all requirements for protein, energy and minerals with limited carbohydrate intake.
In those cases caused factors other than diet, the aim is to treat the initial condition first, but if laminitis is recognized as a risk, the above steps of changing diet in anticipation will be beneficial. Further preventative measures such as virginiamycin and medications designed to block the absorption of toxins may be beneficial if used early enough.
As an immediate pain killer, Phenylbutazone (Bute) is the primary analgesic recommended by the majority of laminitis specialists. Of course, pain killers will do little to treat the condition, and by alleviating the symptoms may encourage the horse to move more than it should, thus causing further damage. Pain control must be carefully administered whilst the horse is restrained in a well bedded stall to prevent excessive activity. NSAID’s such as bute also serve to help alleviate the pressure and inflammation in the foot. When using bute for extended periods, be aware of the negative effects on gastric health and the possible threat of gastric ulcers. Administering an equine antacid supplement such as Neigh-Lox concurrently with NSAID medication may help to protect the mucosal lining of the stomach whilst the analgesics are being used.
Moderating Circulatory Changes
There is a certain degree of controversy regarding the way that we should be treating the foot in the developmental stages of laminitis. Whilst some researchers focus on trying to increase circulation in the foot, others believe that reducing circulation is the best way to manage and control the damage.
Cold application – Vasoconstricting
There is strong evidence to suggest that the foot circulation during the developmental stage of laminitis is vasodilated. Current thinking by Dr. Chris Pollitt indicates the immediate application of cold (iced) water to the feet to stimulate vasoconstriction and reduce the delivery of the blood borne triggering factors to the foot. This method also serves to relieve some of the immediate pain. In preliminary tests performed in horses that had been induced with laminitis, Pollitt found that application of an ice slurry to one of the front limbs dramatically affected the circulatory system in the foot. Capillaries and veins were successfully vasoconstricted, with no apparent discomfort to the horse. No horse that had cyotherapy applied to its distal limb developed clinical laminitis in that foot, whilst the opposing limb had varying degrees of clinically significant changes. Pollitt and his research partner Dr Andrew van Eps have now successfully shown that cold application during the developmental stage prevents laminitis by reducing the delivery of the blood borne trigger factors to inner hoof wall lamellae (vasoconstriction) and by limiting enzymatic degradation of the lamellar basement membrane (hyometabolism). The problem for horse owners in the real world lies in recognizing the horse in the developmental stages of laminitis, as there are usually few outward signs until the majority of the damage has been done.
Drugs – Vasodilating
In contrast to Pollitt’s theory, many respected experts on the subject still believe that lamellar tearing and founder is the result of reduced circulation in the lamellar region, caused by the build up of fluid and pressure as the basement membrane is damaged. The pressure of extra fluid in the foot closes the capillaries which supply the lamellae, thus starving them of nutrients and oxygen, and resulting in severe pain and further cellular damage to the basement membrane. If this is case, the theory states that further reducing circulation in a vasoconstricted foot may have dire consequences. For proponents of this belief, stimulating vasodilation and increasing blood flow is the recommended course of action. To that end, certain vasodilating drugs are used including: Acepromazine, isoxuprine, pentophyline and nitroglycerin.
The Dilemma – Constrict or Dilate?
The initial results of Adaire’s work on circulation patterns in the feet of induced laminitis cases show that circulation is erratic during the developmental stages of laminitis Early results of studies using the black walnut model of laminitis show an immediate decrease, followed by an increase in circulation that plateaus at around 4-6 hours and lasts until the 10-12th hour, before decreasing again just as clinical signs are noticed.
Recommended treatment options may incorporate elements of both constriction and dilation of circulatory pathways at certain ‘windows’ following the laminitis trigger event Certainly it appears that in the developmental stages, the current research strongly supports the cryotherapy approach, but then at what stage would it be beneficial to introduce vasodilating methods if at all?
It is likely that once we know more about circulatory changes as a result of different types of laminitis, we will establish a rough guide to the windows of opportunity in which to apply cold to vasoconstrict, or apply drugs to vasodilate the foot. It could well be that the windows in which we should be trying to manipulate circulation occupy different time periods following laminitis caused by grain overload or pasture, and different again for laminitis caused by other systemic disturbances. Results of ongoing research can only help us to understand the way in which we should be treating the feet of horses suffering this painful condition in order to limit or prevent further damage.
Exercise Vs Stall Rest
Again, controversy abounds in the argument for exercising horses with laminitis. In the acute stages, most owners will box the horse with deep soft bedding to help relieve the pressure on the pedal bone, help the horse find a comfortable position and prevent further damage that may be caused by walking around. Light hand walking exercise has been previously recommended for horses following the acute painful stages of the condition, to assist in stimulating circulation. As previously described, it is not yet known whether stimulating circulation is desirable, or exactly when we should try to stimulate. One thing is for sure, walking too much and especially forcing movement during the developmental and acute stages of the condition may adversely affect laminar separation and pedal rotation. Do not force a horse to walk if it is clearly in pain and reluctant to move.
As previously mentioned, a venogram is commonly performed in the US to assist with diagnosis, but practitioners have noted that the horse seems to be in less pain following the procedure, indicating that it may have therapeutic applications. These benefits are thought to lie in the fact that the procedure seems to open up blood vessels and improve circulation to constricted sites, reducing the pain associated with the crushing of these vessels.
Expert farriery can mean the difference between a horse making a full recovery or being unable to return to his previous level of work. The assistance of a good farrier preferably with experience in dealing with laminitis cases will be invaluable to horse owners who find themselves dealing with the condition. Mechanical assistance is almost always recommended, but the degree and type of assistance depends on the individual case, its severity and the conformation of the limbs and feet to begin with.
Many farriers feel that supporting the frog is of immediate concern as soon as symptoms are noticed. Support can be given by padding up around the frog with gauze bandages or a commercially available ‘lily pad’ which can be fitted whilst a horse is still wearing shoes.
Immediate pain relief can be offered by using a wedge to raise the heel, thus relieving pressure from the toe area. Raising the heel alters the mechanics of the digital flexor attachment and reduces the pull on the rear of the pedal bone and may help to minimize further lamellar tearing. Remedial shoeing is not recommended until the horse is comfortable, and the acute stage is over (i.e. usually after the first 48 hours). Holding up the feet for extended periods of time in a horse that is still undergoing changes, may exacerbate the condition and cause undue discomfort. For this reason, whilst the acute stage plays out, it is often best to keep the horse in the condition that it was before the attack, i.e. if it was wearing shoes, leave them on, if it was barefoot, leave it barefoot in a well bedded stall.
Once the pedal bone has become stable and is no longer moving according to radiographic evidence, the true road to recovery can begin. In mild cases, simply trimming the hooves to lower the heels and rasping the toe to improve breakover and to realign the pedal bone in a straight line with the pastern bone may be all that is required.
If your farrier and vet decide on remedial shoeing, there are a number of choices depending on the particular horse. All are designed to support the heels, relieve pressure at the toe and support the sole. Designs currently used include the egg-bar, the heart bar and the adjustable heart-bar. Some farriers prefer aluminium shoes which are light weight and need only small nails to hold them on, others advocate glue-on shoes to remove the need to pound on the feet at all. Many will use shoes with a rolled toe, or will cut back the toe in an effort to improve break-over. Most of these shoes will incorporate some kind of padding to support the frog and or sole. This is thought to help relieve pressure on the hoof wall and directly supports the pedal bone. Only the back half of the sole should be supported, as pressure directly beneath the descending tip of the pedal bone will only worsen the situation.
The act of raising or lowering the heels is one of considerable debate, but most farriers agree that shoes with rolled toes – to bring the point of break-over as far back as possible (close to the tip of the pedal bone) is of benefit.
To reduce load on the digital flexor in severe cases of founder, and in cases where flexor pull has a major influence on pedal rotation a tenotomy may be suggested. Cutting the deep digital flexor tendon offers immediate relief in those cases where the pedal bone has rotated downward in response to the strong pull of the tendon. The act of cutting the deep digital flexor tendon is not a decision to be taken lightly, and would usually only be considered in those cases where euthanasia is the only other option available. Trials evaluating this treatment method have shown a better quality of life for serious chronic cases. The procedure may extend the life of these horses, though the cost and effort involved in aftercare should be taken into account. The procedure itself is done under local anesthetic and so is relatively inexpensive, but aftercare involving regular corrective trimming can drive the cost up. The tendon heals with scar tissue forming within two to four months, and the area becomes thickened accordingly. Most horses assume at least pasture soundness following the procedure, with some able to perform light work within eight months to a year of treatment. Some horse have reportedly retuned to full competitive work following tonotomy.
With the work of Dr. Chris Pollitt on laminitis trigger factors and the current evidence supporting the MMP enzyme theory of basement membrane failure, attention is directed towards halting the cascade of devastation at the cellular level. Various substances have been show experimentally to inhibit the activity of the MMP enzymes. Current research is focusing on the possibility of using manufactured inhibitors to block further MMP degradation of the basement membrane within the foot of an affected horse during the developmental and acute stages of the condition.
Assisting in The Road to Recovery
If you have been lucky enough to catch the condition early, and judicious treatment by vet and farrier have paid off, you may be well on your way to a full or at least partial recovery within just a few months.
As the hooves start to recover from the ordeal of laminitis, you will notice some irregularities in the hoof wall re-growth. After an attack, hoof wall can grow sporadically, sometimes growing very fast, and then very slowly, forming ridges and lines as the lamellae beneath become reorganized. To help grow out healthy hoof, you can include a hoof supplement in the diet. A supplement containing Biotin, zinc and methionine such as Equivit Bio-Bloom will ensure good quality horn in the re-growth and may help to grow out the irregular horn more quickly.
Of course, whilst the horse is recovering, and even after everything possible has been done to assist with a return to previous work levels, you must take care to prevent a recurrence. Once a horse has suffered laminitis, it is more likely to suffer a recurrence. If there has been pedal bone rotation, then you will be especially eager to prevent further damage that could permanently incapacitate the horse.
Prevention is always better than cure. Designing a diet to prevent laminitis reoccurring is similar to designing a diet that you would feed during recovery, but with just a little more leeway. The key is to anticipate and be aware of the danger signs.
Don’t allow unrestricted access to lush pasture, use a muzzle or temporary fencing to strip graze and restrict access with some stall or dry yard time each day.
Beware of grazing stressed short grass and do not turn out onto frosted pastures or drought recovering pastures because of the danger of high fructan levels. It may be sensible to graze pastures only after dark and in the early morning when fructan levels are lower.
Do not feed a diet that is high in starch (i.e. grain). Instead, try to formulate a balanced diet that is high in fat and fibre, with minimal reliance on grain and carbohydrate rich pasture for weight maintenance.
Avoid letting your horse or pony get too overweight, this can increase the risk of laminitis. Laminitis is more common in certain breeds, but this is usually related to those breeds being particularly prone to being overweight.
Use a quality vitamin and mineral supplement to balance the deficiencies of hay. If you need assistance in formulating a safe ration, contact one of the nutritionists at KER to help you.
If you have a mare in foal, beware of the dangers of retained placenta, and if your horse gets severely sick for any reason think laminitis, and call your vet’s attention to the fact that your horse is a previous sufferer.
Minimise stress. Stress causes the release of corticosteroids, which have been implicated as a cause of laminitis.
Beware of hard ground in the dry months, and take it easy on your horses feet.
You may want to continue feeding a hoof supplement such as Equivit Bio-Bloom to ensure that your horses feet are as structurally sound as they can be.
Products containing virginiamycin, a bacterial product of Streptomyces virginiae, can reputedly prevent the population explosion of gram-positive bacteria including Streptococcus bovis and Lactobacillus spp. following the ingestion of a large carbohydrate rich meal (lush grass or grain). Though it is no substitute for good management practices, these supplements may help in allowing a susceptible horse live a next to normal life and may help particularly sensitive animals enjoy at least limited access to pasture. Virginiamycin is not recommended for mares in foal or stallions at stud. The sale of virginiamycin containing products in Australia is currently under review by the Australian Pesticides & Veterinary Medicine Association (APVMA) due to concerns about antibiotic resistance through its prolonged use.
Preventing laminitis is about preempting its development. Once you have been unfortunate enough to experience it, you become much more aware of your horses attitude and watch for signs constantly, especially in the high risk periods. The moment you notice that something is amiss, call the vet and get prepared, you may be worrying over nothing, but with laminitis, it’s best to be safe than sorry.
10 A Publication of Kentucky Equine Research Australasia Pty Ltd 1800 772 198 firstname.lastname@example.org www.ker.com