Thoroughbreds For Sale


All appointments or veterinary enquiries: Ph 5852 2000

Contact Us


Horseshoe Sales



Symptoms and Treatment


The Mardi-Chi Dingo Foundation

Find out more...


Delinquent Dog School

(03) 5852 2000

Opening Hours

Mon-Fri: 8am – 6pm

Sat: 8am – 1pm

After Hours Emergency: call (03) 5852 2000 and LISTEN carefully to the entire message, then press 1 when asked, or you may be diverted to mobile.


You are welcome to wear a mask, we are happy to provide one at your request.

In the clinic,  a minimum number of people.

We are happy to consult outside.

With your help we can REDUCE the spread of CORONAVIRUS.

Please remember to continue practising social distancing.

Find us here on the map.


384034_513011598744654_1910755328_nMy goal as a Farrier and Veterinarian is to make the principles of farriery available to all horse people in an easy to understand and accessible form. By doing this I intend to improve the overall standards of farriery for the benefit of horses, horse-owners, farriers and vets.

Thank you for visiting,

 Dr. Judith L. Mulholland BSc. BVMS, Dip WCF



I was foaled in 1962 in Victoria and left school to work in the horse industry. I performed a wide variety of equine work including mustering, droving, clipping racehorses, yearling preparation, stud work and held an owner/trainer’s license before settling into farriery in my late 20’s. I finished my apprenticeship at 33. Then, in my mid 30’s, I decided to return to school and complete year 12 and then put everything into becoming a Veterinarian. I graduated 5 years later. Throughout this time I supported myself solely by farriery, and since graduation the mix of farriery and veterinary has been very rewarding. The wide range of horses I have handled, the many jobs I’ve had and the countries I have visited has enhanced my basic foundation of horse knowledge.

“The more I know, the more I know I don’t know”. I am learning every day.

My goal is to pass what I am learning on to you for the benefit of your horses. I am currently working in my own mixed  practice in Victoria, Australia and maintain a small number of farriery clients. I travel widely to teach or assist horse owners with farriery issues whenever I can. I hope that information within this site will be of help to you.


After The Firestorm – Part One

After The Firestorm – Part Two




Something has to happen within the body, or to the body, to trigger a Laminitic episode. Therefore, in the majority of cases, Lamintis is preventable.


Laminitis has been known of for as long as recorded history, and is the second most common cause of death of horses after colic.

Horses, foals, ponies, weanlings, yearlings, stallions, broodmares, draught horses, race horses, donkeys, cattle and other hooved animals can be affected.

Severely affected animals do not die directly from the disease, but will ultimately be euthanased for humane reasons due to chronic lameness. This may occur weeks or many years after the first laminitic event.

* Please note – the terms ‘horse’ and ‘pony’ may be used interchangeably throughout this section.

‘Laminar’ – made up of layers. ‘Itis’ – inflammation of.

There are two types of laminae in the horse’s foot. The sensitive laminae attached to the pedal bone, and the insensitive laminae attached to the inner hoof wall. The function of the laminae is to bind to each other and to keep the pedal bone suspended within the hoof capsule, and to allow for normal hoof wall growth over the stationary bone.

Laminitis is inflammation of the sensitive laminae of the hooves. However, many horses experience inflammation of these structures without developing the acute disease and chronic changes we all recognise as laminitis.

Founder and laminitis are exactly the same disease process. Founder means to send to the bottom; to sink (like a ship). This accurately describes the phenomenon of the pedal bone sinking lower in the hoof capsule due to the horse’s own body weight tearing the weakened laminae. A comparison is walking through the sole of a pair of shoes or wearing through your socks. The outer hoof capsule can no longer suspend the rest of the foot within it. Therefore, laminitis the disease would be better described as “acute laminar degeneration” which is due to a complicated, interrelated sequence of events including enzymatic breaking of the bonds between the sensitive and insensitive laminae. This leads to partial or complete separation of the laminitic bond.

Detachment of the laminae (laminitis) allows a variable amount of movement of the hoof capsule around the pedal bone. The weight of the horse and the forces of locomotion drive the pedal bone down into the weakly attached hoof capsule. Shearing forces damage the arteries and veins, and the corium of the sole is crushed as the bony column of the limb descends deeper into the foot and the hoof capsule slides up over the pedal bone.

Laminitis causes unrelenting pain and a characteristic, often severe lameness, usually worse in the front feet.



With severe laminitis it is clear that something is wrong because your horse will be obviously uncomfortable, even if you do not realise at first what the problem is. With very mild laminitis a change in normal behavior may be all that is noticed, and it can take some time before anyone realises you are dealing with a laminitic horse. Some owners notice the horse is shuffling its feet; this is a classic laminitic sign and should always be investigated. The horse lifts one foot then another unable to get comfort on any foot for very long. Usually, as the pain in the feet increases, an active horse stops moving about, stays in the one place in the paddock, or is observed lying down at an unusual time of the day. The horse or pony tries to transfer body weight on to the heels and hind legs, by standing with the forelegs well out in front of the body, and the hind feet up under itself with an arched back. This is most noticeable if the horse tries to turn around. There will be a strong or bounding digital pulse, and the hooves feel warm, indicating increased blood flow. Trembling, sweating and anxiety are sometimes observed. The front feet are usually most severely affected, but 1 or all 4 may be variously affected. Temperature increases beyond the normal range of 37.5 – 38.5 degrees Celsius up to 40°C in some cases, and heart rate increases from the usual 30 – 40 beats per minute up to 100 or more. A bloated horse with foul smelling manure with grain in it, a temperature of 39°C, a heart rate over 60, swollen legs, hot feet and strong digital pulses is a classic set of symptoms for carbohydrate overload laminitis. 

Grading of lameness associated with laminitis – the higher the grade, the greater the risk of permanent damage to the laminae of the feet. For example, if laminitis is not recognised until the horse reaches grade 3, then significant laminar degeneration may have already occurred, and the treatment and recovery phases will be longer than for grade 2 with a poorer overall prognosis for return to 100% soundness.

Grade 1: The horse seems uncomfortable, shuffling or lifting its feet repeatedly. It walks and picks up its feet willingly.

Grade 2: The horse moves willingly at a walk but the gait is characteristic of laminitis (landing heel first and wide). The horse does not resist lifting a foreleg.

Grade 3: The horse moves reluctantly and vigorously resists attempts to lift a forefoot because of pain in the opposite foot.

Grade 4: The horse must be forced to move and may be recumbent much of the time (lays down).

Mild laminitis grade 1 – 2 will have moderately increased digital pulses and warmth in the feet. The horse may shift its weight from foot to foot, there is mild lameness and the toe area of the hoof wall and sole may be sensitive to pressure. The symptoms often resolve without permanent laminar damage.

Severe laminitis grade 3 – 4 when all four feet are affected the horse will often lay down for long periods and when it does stand it has the hind feet up under the body to carry more of its weight. The hooves feel warmer and have bounding digital pulses. Anxiety, muscle tremors and increased respiratory and heart rates may be observed. The horse is very lame.
Sinking of the distal phalanx is more likely to occur if the horse is systemically ill. Cavitation or depression along the coronary band may be the first clinical sign. Over time, blood or serum may ooze from the coronary band and the sole will appear flatter. Laminar damage and chronic effects are likely.

Treatment should commence immediately. Sensitivity to hoof testers around the wall and sole varies. The horse may appear lame, but not necessarily sick. It may not show any of the classical symptoms or observe the rules of laminitis. Usually, the horse becomes progressively worse over a period of hours or days, with obvious distress if forced to walk. The coronary band at the toe and area just above it feels soft and swollen. A depression felt behind the coronary band at the toe indicates sinking of the pedal bone lower into the hoof capsule due to loss of laminitic bond. The further back towards the heels this is felt, the more severe the loss of laminitic bond. Discharge or rupture of the coronary band is seen only in the most damaged cases.

Many mild cases of laminitis are confused with loss of form in the horse’s usual activity, shoeing problems or bad temperament as the horse becomes disgruntled and miserable. When the laminitis is treated correctly, movement and personality both improve. The acute stage can last from hours to weeks, depending upon the severity of laminitis and speed of treatment.

Over a period of 2 – 6 weeks, the first chronic signs start to show as an inward ring just below the coronary band, growing down with the wall. Bruising in the sole and white line grow down to the ground surface and can be seen when the hoof is trimmed. In mild cases this confirms the diagnosis.


During the onset (FIRST), or developmental phase, lamellar separation is triggered and occurs before the symptoms of pain. This phase may last from 30 – 40 hours, depending upon the triggering factors. In some cases no developmental phase is recognised. Therefore, early symptoms may go unnoticed and the horse does not receive early treatment.

During the developmental phase, the horse may be suffering from some form of gastrointestinal, respiratory, reproductive, renal, endocrine or other organ system disease, and it is that disease process which leads to laminitis as a secondary condition. Treatment of the primary problem e.g., retained placenta, pneumonia, colic, grain overload, acidosis must be prompt and effective. Unfortunately, the feet may not be considered until laminitic symptoms appear. To wait and see if foot pain is the sequel to a metabolic crisis is to miss the most important opportunity to prevent or reduce laminitis.

During the developmental phase of laminitis, a period of vasodilation, characterised by increased hoof temperature, is strongly implicated. This can be treated by cooling the feet, which inhibits enzyme activity and decreases vasodilation. If you think that your horse or pony is developing laminitis, and the feet are warm with strong digital pulses, bath the feet in ice and water now. Keep ice floating in the water at all times and continue this as often as practical e.g. 15 – 30 minutes every few hours for several days.

The laminitis, (SECOND), or acute phase is considered to be the first 48 hours after the symptoms of hoof pain are noticed. This phase lasts from onset of lameness, to downward displacement of the distal phalanx within the hoof. Not all horses go on to develop chronic changes in the hoof, and effective treatment and management of the primary cause and the laminitis itself at this stage can decrease the ongoing damage and long term effects.

laminitisThe founder, (THIRD), or chronic stage, is when physical changes have occurred in the feet. The distal phalanx has sunk lower in the hoof capsule, caused by loss of the laminitic bond. The chronic phase can last indefinitely, with clinical signs ranging from persistent, mild lameness, severe foot pain, further degeneration of the lamellar attachments, hoof wall deformation, to extreme lameness, and in the most severe cases, penetration by prolapse of the distal phalanx through the sole or sloughing of the hooves leaving the distal phalanx exposed. This is a justification for euthanasia, however horses can survive this, (refer to sinker laminitis).

As the chronic phase progresses there is formation of the laminitic wedge, comprised of keratinised laminar/wall material, which further separates the sensitive and insensitive laminae. The distal phalanx is no longer able to align with the hoof wall normally and is described as rotated, or as I prefer to say “the pliable hoof capsule has been counter rotated away from the pedal bone by the formation of a laminitic wedge’.

The horse’s own body weight forces a degree of movement of the wall upwards over the pedal bone. This is described as sinking, but it is to be expected that if a tonne of horse is relying on the bonded laminae to suspend the sensitive hoof within the hoof capsule, and if most of these bonds were weakened or broken, the wall would simply slide up over the bone like a stone would sink in a glass of  water. It is an effect of gravity. This is why when this occurs to any degree, but especially when it occurs severely, the horse is described as a sinker.


Endotoxin-induced microthrombosis (mini clots) in the vessels of the laminar corium are implicated as part of the laminitic process. These thrombi inhibit blood flow through the capillaries, leading to starvation of the tissues for nutrients and oxygen and accumulation of  toxins and waste products, so that inflammation, oedema, and cell death may result.

Therefore, it is now thought that the decreased perfusion of the tissues was based on studies performed while clinical laminitis was underway, and the effects observed were likely a result of the lamellar injury, rather than the cause of it. The horse tranquilliser acepromazine dilates blood vessels and appears to prevent laminitis in some cases. This effect was attributed to its inhibition of vasoconstriction or vasodilatory effects which prevents ischaemia. This drug has other metabolic effects including increasing insulin secretion, and the production of glucose by the liver, which could lead to increased use of glucose by the tissues within the hoof, which would protect them from hypoglycaemia (glucose starvation). Therefore, a new hypothesis has been put forward based on hoof glucose metabolism which combines all these factors.

Researchers at the University of Queensland, led by Professor C. Pollitt, studied blood flow to the feet of normal horses in the cold and learned that there were periods of normal blood flow, interrupted by long periods of very low flow. The hoof appeared capable of withstanding these long periods of minimal blood flow without developing laminitis. A study by the same team, using 14 horses during developmental and acute laminitis, has shown that blood flow increased prior to the development of laminitic foot pain and that those which had a raised foot temperature, indicative of vasodilatation, became laminitis positive, despite all horses in the study being equally systemically ill. The researchers found that if vasoconstriction is achieved during this phase, laminitis does not occur. It was assumed that the increased blood flow leads to a higher concentration and greater exposure to blood born trigger factors  e.g., acids and toxins. Therefore, evidence strongly suggests that laminitis is not a result of inadequate blood flow, and that this is a result of the tissue injury rather than the cause.

The hoof wall is connected to the pedal bone by connective tissue containing a row of lamellar epidermal cells. These cells are bonded to the keratinised hoof tissue on one side, and to a thin layer of specialised connective tissue, called the basement membrane, on the other. Attachment of these cells to the basement membrane is made by adhesion molecules, which act like “press studs”, keeping the tissue together. These adhesion sites are called hemidesmosomes ,and are formed by several proteins and numerous submicroscopic anchoring filaments e.g., laminin-5, which are unique to hemidesmosomes.

The researchers at Queensland University led by Professor Pollitt demonstrated that if either the anchoring filaments or the hemidesmosomes are damaged and disappear, then the basement membrane separates from the basal cell. These anchoring proteins and connective filaments are substrates of connective tissue enzymes (chemical catalysts) matrix metalloproteinases (MMPs). It is thought that the greater the blood flow, the more exposure of the basal cells and hemidesmosome bonding sites to circulating blood born trigger factors which activate the MMP enzymes. This appears to be the first part of the process in the development of laminitis. The MMPs digest the bonds, and the force on the hoof due to weight-bearing then causes separation of the hoof wall from the underlying tissue, which is characteristic of laminitis. Separation of the laminae during laminitis is the specific undoing of the attachment, and not simply a tearing apart of the tissues. Therefore, separation was caused by the release of MMPs from the tissues that digested the attachment apparatus.

The researchers then blocked the activity of these enzymes, thus preventing separation of the hoof tissue. What activates the MMPs? Using small sections of hoof tissue kept alive in a special culture, they learned that inhibiting the ability of the hoof tissue to metabolise glucose caused an increase in MMP activity, and separation of the hoof. Many of the conditions which will induce laminitis involve changes in the way an animal utilises glucose. It is possible that the inciting event (acute disease, toxins, surgery, etc.) causes sudden glucose starvation in the hoof tissues (hypoglycaemia) and activates the MMPs, thus weakening the attachment of the hoof to the underlying connective tissue. The force of the weight of the horse on the foot then tears the hoof attachment and tissue bleeding and cell death results. Therefore, what now seems most likely is that laminitis is mediated by the uncontrolled release of excess activated MMPs. There is also now some evidence to indicate that MMP activation is inhibited in low temperatures. Therefore, inhibiting enzyme activity by keeping the feet cold during the developmental stages of laminitis (before hoof pain occurs) shows potential as a first aid and preventive measure.

It is important to recognise that the wider veterinary knowledge of laminitis is constantly changing and that research into the biochemical pathways of the disease process and the activity of new and known chemicals and drugs in relation to laminitis may lead to new drugs or treatments which may prevent or minimise the damage done to the hoof, and shorten the recovery time if the disease is recognised and treated early. Ongoing research may lead to preventative treatments for horses at risk as well as better treatments for horses with the disease.

  • Treat the primary problem e.g., colic, colitis, retained placenta, pneumonia etc.
  • You do not need to wait for clinical signs to justify preventative treatment. The process leading to destruction of the bonding apparatus begins before foot pain or the first signs of laminitis are noticed.
  • Discuss the risks or signs with your vet and take on board their recommendations.
  • Be proactive. Get the horse on to soft bedding, keep it cool, take care with what you feed etc.

Place the feet in buckets of water with ice floating in it at all times from the moment signs are noticed e.g., increased warmth or pulse. Keep icing or hosing the feet as often as possible until the horse has shown prolonged steady improvement for its primary problem or for 24 – 48 hours.



The horse has evolved to eat a large volume of low quality roughage which is passed through the digestive tract at a faster rate than most other herbivores. Horses prefer a different part of the plants than other grazers, this is a way of encountering less competition for food. Ruminants (cattle, sheep, goats etc.) have a large fore stomach, which is populated by bacteria and protozoa which allows them to digest cellulose (the fibrous part of plants), and they are 30% more efficient than equines at digesting it. However, once the rumen is full, they must stop eating and ruminate (re-chew) the feed. The poorer the quality of the feed the longer it takes to digest. This limits how much a ruminant can eat. When horses encounter poor quality feed their survival strategy is to eat more. They digest cellulose in their caecum (hind gut), which is also populated by bacteria. Therefore, they cannot, and do not need to re-chew their food. By eating a lot more of what is available, horses will survive where cattle will not because, they eat constantly and digest quickly.

This evolutionary fact is why domesticated horses encounter so many problems when we try to feed them on high carbohydrate diets. The carbohydrate (starches, sugars etc.) which are not digested in the small intestine reach the caecum, where the bacteria which are there to digest the fibre cause energy rich feed to ferment, and this is the first step towards acidosis and feed induced laminitis.

Equines are also subjected to feed grown on poor quality soils which are low in essential minerals and elements. They graze many toxic plants, and different types of grasses to those which they evolved to eat.

Sugar and starch levels in growing grass vary by the hour, depending on the time of day and amount of sunshine. Fructan is a soluble sugar which occurs in high concentrations in the stem of grass. Mammals do not make the enzyme required to digest fructans, and they go through the small intestines undigested to the hind gut, where the microorganisms can ferment and digest it. The Streptococci bacteria, which favour its digestion, undergo a population explosion which precedes acidosis (refer below). Therefore a warm, sunny afternoon in late spring is more likely to cause D-lactic acidosis and laminitis than a cool morning in autumn because the pasture plants have been photosynthesising all day and accumulating fructan. Ponies can get laminitis in hours, or overnight.

  • The horse eats a lot of grain, or a different type of grain, or spring grass rich in carbohydrate (starch and/or sugars).
  • Some digestion of sugars and starches occurs in the small intestine, but much of the grain or grass and all of the fructan will get to the large intestine. This is where all cellulose (the fibrous part of plants) is digested. Bacteria in the large caecum (hind gut) secrete the enzymes which digest the fibre but, when there is a lot of carbohydrate present as well, this is fermented via Lactobacillus species and Streptococcus equinus and bovis bacteria to the D and L isoforms of lactic acid. The host can use the L form but the D form persists in the hind gut and leads to D-lactic acidosis.
  • A venous blood test can confirm the presence of D-lactic acid.
  • The increasing acidity causes the pH to drop from normal 6.8 – 7.0 down to 4.0-5.0 which kills most of the normal bacterial flora of the caecum, including gram negative enterobacteriaceae species which release the lipopolysacharide component of their cell wall as an endotoxin.
  • The endotoxins are absorbed during the developmental phase of laminitis leading to endotoxaemia. This may lead to watery diarrhoea and fever. However, giving endotoxin alone in experimental models has not been able to cause laminitis.
  • By 24 hours after carbohydrate overload the epithelial cells which line the caecum begin to degenerate, and the damaged large bowel becomes leaky. By 49-72 hours, the cells have sloughed off, which allows the lactic acid and endotoxin to be absorbed straight into the blood stream where they act as laminitis trigger factors. About 10 – 15% of horses can die from accidental ingestion of large amounts of grain, leading to cardiovascular shock. These horses appear severely ill, with a high heart and respiration rate, fever, colic, diarrhoea etc.
  • When these severe cases begin to respond and recover from the primary digestive insult, they have reached the time frame for the clinical signs of the second stage of laminitis to appear.
  • The rate of fermentation in the hind gut depends upon the type of grain and starch content. High risk grains are wheat, sorghum, corn, barley and bread. Oats are considered low risk.
  • A few species of bacteria prefer the low pH, and these acid loving bacteria proliferate rapidly and go on to produce more acid as they ferment the carbohydrate and further lower the pH. The result is the whole population of micro flora in the caecum has been changed in a matter of hours.
  • Streptococcus bovis is a bacteria which proliferates during fermentation and acid production. It is suspected that not only does it like an acidic environment and produces acid itself, it also releases an exotoxin that is implicated in the activation of the MMP enzymes which dissolve the basement membrane leading to laminitis.
  • The horse has now absorbed the toxins from the bacteria, the acid from fermentation and the caecum and the large intestines have become inflamed.
  • Inflammation and the low pH attracts water so that fluid is lost into the large intestines from the body. The effect of this is an acidic and dehydrated animal. Dehydration leads to decreased perfusion of tissues. Local tissue effects begin to occur to counteract this which can eventually lead to vasoconstriction. This short term attempt at raising blood pressure leaves the peripheral tissues depleted of blood flow and cellular waste products being to increase in a low oxygen environment so that eventually the vasoconstrictive effects are overcome and this is followed by vasodilation and systemic shock.
  • Laminitis results from the effect of the toxins and acidity which lead to inflammation of the tissues, localised circulatory changes, and derangement of the normal activities of the enzymes which regulate the chemical bonds which adhere the basement membrane and laminae to each other within the hoof.
  • The basement membranes of organs and tissues throughout the body are being affected. In the hoof this is marked by the dissolving of the normal chemical bonds which keep the sensitive and insensitive laminae tightly bound to each other.
  • The laminae separate and the laminitis progresses.


  • Remove at risk ponies from paddocks before the warm spring days and do not return them to the paddock to live until the feed has dried off. Return them to a little free grazing and increase the length daily over several weeks until, if they are low risk cases, they can stay out all the time.
  • Provide supplements in the form of mineral licks or in the feed (make your own to suit your pasture and soil type).
  • Make small, progressive changes in the diet. Never take horses which have been on grain and dry feed and then put them straight into lush grass without a changeover period of at least 3 weeks. Longer is better! When taking horses from poor feed to grain do the same, decrease the roughage and increase the grain slowly to allow the gut flora to adjust so that the new diet is digested and not fermented.
  • Avoid feeding bread and sugar, limit molasses, etc.
  • Monitor green grass and grain intake vs. roughage intake.
  • Reduce grain intake during periods of illness or stress. Grain increases the inflammatory response.
  • Reduce grass and grain intake in comparison to energy outlay. Only replace what is used.
  • Never try to fatten a horse quickly, the main reason horses fail to do well when first brought in from the paddock is because they cannot digest the diet. Make changes slowly and you will get better value from the feed.
  • Include an organic form of the mineral sulfur in the diet which aids enzyme activity in the gut.
  • Balance the diet so that magnesium, calcium, phosphorous and all essential mineral levels are adequate.
  • Balance the diet to compensate for unhealthy pasture, toxic plants and acidic soils (low pH) e.g., on pastures dominated by weeds or plants containing oxalates (African runner grasses such as kikuyu), feed dolomite.
  • After treatment with antibiotics/worming products, restore normal gut flora by feeding probiotics (live, beneficial bacteria).
  • Virginiamycin is an antibiotic which is not absorbed into the blood stream of horses and only exerts its effects on bacteria in the digestive tract. It has been used in the past to control grain induced acidosis in feed lot cattle. Founderguard for horses at the dose rate of 5g/kg body weight has been shown to inhibit those bacteria which lead to high concentrations of D-lactic acid. The antibiotic must be present in the digestive tract for 4 days prior to exposure to the carbohydrate to prevent laminitis and is therefore not a treatment but is a preventive measure if used prophylacticaly. However, in my experience this should not be used as an excuse not to rectify all the risk factors associated with grass and grain and I occasionally hear of cases where laminitis has occurred while feeding this product.


In my experience, certain breeds, families and body types (phenotype) are much more predisposed than others to developing laminitis on certain farms at certain times. I can almost predict the ponies or horses that will have a problem.

A couple of little studies of my own revealed a high risk to females in comparison to males, and that some ponies are innately resistant to the disease. Then I read an article in Equus magazine by Dr. David Kronfeld of the Middleburg Agricultural Research and Extension Center in the USA. A study of 160 related ponies into risk factors for laminitis indicates that metabolic changes in the body associated with obesity and pregnancy, combined with genetics and pasture changes resulting in insulin resistance, contribute to laminitis. Blood tests taken when all the ponies were healthy revealed that those who had previously developed laminitis showed elevated levels of  triglycerides (fats) and increased insulin and insulin compensation. Of this group 11/13 later developed laminitis. Genetically a link was also present with a dominant mode of inheritance that was partially suppressed in males. This genetic predisposition may have given a survival advantage in very harsh conditions in which ponies evolved, but creates disaster when overloaded with rich feed. During the time of the study (spring), pasture testing revealed a two fold increase in starches and sugars known to increase the risk of laminitis. Plasma cortisol was also studied, and this stress hormone has been previously linked to hyperlipemic laminitic syndrome.

Pre Laminitic Metabolic Syndrome (PLMS) is a set of risk factors that can be identified in healthy ponies. Fat tissue plays a role by producing hormones that hamper the action of insulin which is trying to get glucose from the blood into cells for energy production. In other cases, insulin resistance causes the animal to get fat. This process is yet to be fully understood. The body fat of insulin resistant horses forms in patterns e.g., hard, thick, cresty neck, spongy fat on the shoulders, tail base, over the eyes, and in the sheath of males. In my experience, these animals are at risk of developing laminitis with any slight increase in energy in the ration. I can now see the pattern of elevated insulin, cortisol and triglycerides in hypercortisolaemia (Cushing’s-like syndrome), hyperlipemia and laminitis. These three diseases are all fatal in severe form.

Relevant conclusions from Dr. Kronfeld’s study were:

  • A genetic connection and dominant mode of inheritance for pasture laminitis with partial suppression in males.
  • A phenotype e.g., refined head, cresty neck, rounded body (the show pony type) with a distinctive metabolic profile.
  • Characterisation of a pre-laminitic metabolic syndrome in apparently healthy ponies, and exaggerated compensated then decompensated insulin resistance during laminitis.
  • Evidence of association between the onset of laminitis and increased pasture starch content due to rapid growth of clover (the trigger factor for at risk ponies or horses).

The researchers offered the following advice:

  • Blood test ponies and horses at risk of  Pre-Laminitic Metabolic Syndrome.
  • Test for elevations of triglycerides and insulin. This is most relevant to overweight animals related to those with laminitis.
  • I suggest that cortisol or ACTH should also be included if you are blood testing.
  • If your animal is healthy but shows signs of PLMS, it is time to act to change the metabolic profile and improve insulin sensitivity.
  • Begin daily exercise, a controlled weight reduction program, eliminate large grain or molasses based feeds, and begin administering antioxidants and omega 3 and 6 fatty acids.
  • Sample your pasture grasses and test your ponies when nutrient levels are high. Feed seedless grass hay and consult your veterinarian for further advice.

Suggested reading:
Kronfeld. D., PASTURE LAMINITIS BREAKTHROUGH, EQUUS 342, April 2006, pp. 47 – 63.
THE ROLE OF GLUCOSE IN LAMINITIS, Medical Front, EQUUS 341. Equus Magazine

Normal reference ranges for insulin and glucose:
(variation between laboratories):
normal reference range for equine insulin 4.0 – 7.1 mu/L  or
normal reference range for equine insulin 10 – 30 uU/ml
normal reference range for equine glucose 3.4 – 7.7 mmol/L
normal reference range for equine cortisol 83 – 360 nmol/L
normal reference range for equine triglycerides 0.1 – 0.9 mmol/L


Many people believe that certain breeds do not founder. All breeds, including thoroughbreds, founder, and I have seen racehorses in paddocks, yearlings being prepared for the sales, and racehorses in full work develop laminitis (founder).

I believed for some time that obesity did not cause laminitis. I now understand that laminitis can be caused by metabolic (hormonal) changes due to obesity, that make ponies and horses much more sensitive to changes in diet due to insulin resistance. This is the most important issue related to obesity and laminitis because it is an unseen cause of the disease coming from within the animal, not its direct environment, and helps to explain so many cases of laminitis of formerly unknown cause.

Toxins in the body are usually removed by the liver – whatever their source. When an animal is obese, much of the liver tissue is occupied by fat deposits, reducing liver function, prolonging the toxic effects e.g., from grass/grain overload. Overweight ponies have a greater load on the feet and are more likely to live in the environment (e.g., a paddock), where they are at risk of laminitis. However, other factors are always involved. Therefore, when someone tells you to starve your animal or it will get laminitis, obesity is one of the risk factors, but hyperlipemia from negative energy balance (not enough energy in the diet) is another, and therefore sensible weight loss may help to reduce the effects if the other risk factors in the animals environment are also rectified.

When founder/laminitis is finally diagnosed in cases where the horse has been happily grazing in the paddock for months without any problem, people often say, “I had wondered if he was okay? The horse has become stiff and less active lately”. What they were noticing was the slow onset of laminitis, usually after a period of wet weather, followed by warm days and grass growth. It can take weeks before the horse is lame enough to be checked by a Vet.

Some ponies founder if let out onto grass for even half an hour, winter or summer, indicating other health problems. These include metabolic and hormonal problems such as Cushings disease, diabetes, insulin resistance or thyroid gland problems. Obesity effects metabolism and regulation of blood glucose e.g., insulin resistance problems. Mineral deficiency affects the whole system and may be subtle to the untrained eye, and imbalanced gut flora may have no obvious symptoms but predisposes to digestive upset. In many cases, tolerance for grass and grain improves significantly when the underlying problems are treated. This also involves treatment of an unhealthy paddock, not just the horse.

Laminitis, to some degree, can happen “every day”. The only true preventive is to lock the animal away from the cause until the underlying problems are identified and treated. This may mean an almost permanent removal from grazing for severely affected animals. When the horse is progressing well after one bout of laminitis, it often succumbs to a second or even third because the owners reintroduce grazing. This is killing with kindness! Every laminitic episode shortens the horses life by increasing the rate at which the animal will be permanently lame. Some horses and ponies are very sensitive to the carbohydrate (starch) in grain, or rapidly growing grass (soluble sugars). Very small increases will trigger a laminitic episode – Refer to Genetics, Body Type and Laminitis above. The same effect can be produced in other horses by giving large amounts of grain or grass to animals that are not used to it. Obese equines are at greater risk.

  • Beware of rapidly dieting very fat or pregnant equines, as they may develop hyperlipidemia which may be more serious than the original laminitis. Weight loss or gain should be steady. Do not starve a laminitic animal. Feed low carbohydrate, fibrous (seedless hay), and nutritionally balanced food. Refer to The Laminitis Diet for more information.


Equine athletes have lower immunity caused by the demands of training and stress. There is often a lot of grain, protein and sugar in the diet. Confinement for up to 23 hours per day reduces normal circulation in the limbs. Manure from some race horses is loose, sour smelling, and fermented. Stress, racing, respiratory diseases, transportation and bad shoeing all contribute to mild laminitis, which is put down to chronic “race horseitis“.

The feet have a stronger than average pulse, with bruising and widening of the white line at the toe – soreness increases after a race. When spelled, the feet develop severe rings caused by radical changes of diet, exercise and environment, creating distorted hoof angles and shoeing problems later on. A race horse may not have severe laminitis; it could be in a state of chronic laminitic crisis – teetering on the edge. Some horses have allergies to certain grains e.g., barley lumps. Therefore, change feeds carefully.



In Dry areas, laminitis often follows the autumn break, when the new grass is coming up. This grass is very low in essential minerals. During a drought, nitrification bacteria accumulate large quantities in the soil and the first new growth may then have toxic levels. Lush new grass is low in magnesium (Mg) and in cold, overcast weather has higher levels of nitrates accumulate (toxins). Nitrogenous fertilisers also add to the problem. Nitrate is reduced to nitrite in the hind gut of horses and rumen of cattle and can contribute to nitrite poisoning. Refer below to nitrate/nitrite for more information. In areas where the feed dries off completely in summer, the flora of the digestive tract adapt to this and then the microflora cannot change rapidly enough to deal with the sudden change from low energy dry feed to very low mineral content, high nitrate green feed. This can occur even when horses are still fed their normal meals and supplements.

Be careful after rain.

Winter laminitis often occurs when the pony that is normally fed daily and looked after, is put in someone else’s paddock while the owners go away on holiday. The owners think that the pony is safe because laminitis only occurs in spring. Wrong!! The factors causing laminitis are diet and digestive change, combined with the quality of the pasture (as above). For example, going away on holiday is risky if you have a laminitic pony that you rely on someone else to feed and care for unless you thoroughly explain why it is not safe to let the pony graze in the garden, or feed the pony lots of molasses, etc. It can be hard to explain that it leads to fermentation and acidosis. The common scenarios include: show horses that are being fattened for a special event, the pony that is usually fed hay and then goes to pony camp and gets lupins and barley, the pony that comes from a dry paddock and is put into an area hardly big enough to trot in but it is up to its knees in irrigated grass, the horse that lives on irrigation year in year out and is always chronically foot sore but not lame, and the owner who wants the horse to have more energy coming up to an event. The more grain they feed, often the worse the horse feels and behaves. If an animal’s digestive system is barely coping with the high carbohydrate diet it is on and there is already a lot of acid being produced by fermentation, this is absorbed into the body and makes the horse feel unwell. Adding more grain to the feed to pep the horse up may have the opposite effect and lead to laminitis.

Always make gradual increases in energy and look at other factors for why a horse is not gaining weight. It may have other underlying physical causes or be lacking essential minerals or elements e.g., Calcium, Magnesium, Copper, Sulphur, Zinc, Selenium, Potassium, Boron, Cobalt, Iodine etc. Without the correct nutrients in the right ratios the horse cannot make substances essential to life but will still store excess energy as fat which is secondary to other functions in importance. Horses and ponies will also develop laminitis when the brand of feed is changed e.g., from corn and oat based feed to rice based or visa versa. Rice is very high in carbohydrate. Make dietary changes slowly.

Superphosphate and other fertilisers are becoming increasingly associated with laminitis.  New pasture species are also implicated as they contain increased concentrations of water soluble carbohydrates and less effective fibre. These plant species have been developed to increase productivity for farmers as the pasture is more palatable (plant sugars), highly digestible and energy rich. This leads to lowering of rumen pH (more acidic) in cattle and the lowering of large intestinal pH in horses and has led to increased levels of laminitis in cattle and horses. Research has begun into these issues for production animals as chronic laminitis in dairy cattle significantly reduces production. Buying hay and chaff can now be a risky business for the owner of chronically laminitic animals due to dietary causes because you will often not know how the feed was grown or its energy content. Therefore, if you grow your own hay and chaff always begin with a soil analysis from a company that sells nothing but soil analysis and not one that sells fertiliser. Based upon the results of that analysis, top dress to correct for soil pH (acid/base), usually this means lime or dolomite is required. Other elements may correct themselves when the pH has been raised and you can add other minerals as stock-licks, or in feed. Re-test in 12 months and use fertilisers sparingly where horses are concerned. A clue to the health of the soil is also the colour of the grass, bright green or dark green? Darker is healthier. Are the trees struggling to survive? If so, the soil under them is probably not healthy and using superphosphate and other fertilisers without resolving soil pH issues may be the cause. If you cannot afford to spread lime or dolomite on the whole paddock, treat under the trees to save them. Are the horses eating the trees, stripping the bark etc.? If so, they are looking for minerals, particularly copper which is found in the cambium layer of the tree under the bark. Protect the trees by covering with chicken wire and supplement the minerals lacking in the soil. Does the paddock grow nothing but Capeweed, Patterson’s curse, Flat weed or some other weed which can be toxic? This is another sign that the soil is not healthy and is promoting the types of plants which prefer an acidic soil. Grasses grow better in soils which are closer to neutral pH.

In many cases the only ponies or horses on a farm to get laminitis are those in the paddock which has just been “supered”. I have heard this story a few times, “the pony lived in the paddock for years and nothing else changed until it was supered”. The evidence is anecdotal but the warning bells ring when I go to a farm and more than 1 or 2 animals are affected with laminitis and diet changes don’t seem to be the cause. On some properties every equine has laminitis to some degree. This is the best reason I can give you for getting a soil analysis done by companies which sell nothing but analysis. The analysis should direct you to the importance of soil pH and the best way to correct it e.g., lime, dolomite, gypsum and then to the trace elements required. Refer to the list of suppliers at the back of this book.

There are no rules with horses and ponies but this is a good guide, trust your instincts! Be objective about what you hear and read. Make decisions for your animals welfare based on more than what “so and so” told you. I have had many people report that they did this or that which led to the horse developing laminitis because “so and so” who they respect because they win at the shows told them to do it and they must know because they have had horses for a long time. The truth is, there are thousands of professional horse people who do not understand laminitis or the basics of the horses foot. They ride, show, train etc., but most of their knowledge about laminitis and feet is based on hearsay and their own experiences and has not been gained from reliable sources. The advice given to the novice will often be something like “you will never, ever founder that mare”, it needs to put on more weight. I have fed it for 3 years and it hasn’t foundered yet. The horse was already in Royal Show condition and it did founder. Or, the pony needs to keep its energy up this week, it was also in show condition and went from a basic diet to lupins and barley while at a week long pony camp. It did not get through the week sound. The race horse trainer who told me the horse had sore heels but when I went to see it said, “no I think I cooked it with too much hot tucker”. The jockey said it was ready to win so I thought I better feed it up a bit and I bought barley, lupins and corn and now both my horses seem sore”. Or, it is safe to put the pony in the paddock, it is winter. You can feed as much grain as you like or whatever you like as long as you feed this stuff (additive) as well. No you can’t. Every horse, pony, donkey, cow etc., can get laminitis. This is a fact.. Why? because they all have laminae.


In Dry areas laminitis often follows the autumn break, when the new grass is coming up. High intakes of nitrate and nitrite occur in animals fed lush herbage that has been heavily fertilized with ammonium or potassium nitrate (nitrogenous fertilizers). High intake also follows a drought during which time nitrification bacteria accumulate large quantities in the soil and the first new growth may then have toxic levels. Lush new grass is low in magnesium (Mg) and in cold, overcast weather has higher levels of accumulated nitrates (toxins). Nitrate is reduced to nitrite in the hind gut of horses and the rumen of cattle and can contribute to nitrite poisoning. High levels of  nitrate can be found in drinking water but the most important source available to animals is found in crop plants such as oats and barley, also lucerne, kikuyu and capeweed. Nitrate is converted to nitrite in the plant or in the digestive tract of the animal. In a plant nitrate is a precursor of ammonia which is used for amino acid production. Amino acids are the building blocks of proteins and proteins are essential for life. This conversion is performed by an enzyme called nitrate reductase which contains molybdenum and is sensitive to many factors. Nitrite from plants is rapidly absorbed into the bloodstream where it affects vascular smooth muscle leading to vasodilation and pulmonary (lung) hypertension and decreased cardiac (heart) output. Refer to the 3rd theory of the causes of laminitis. Nitrites react with haemoglobin which is the oxygen transport molecule within red blood cells. The oxidisation of haemoglobin forms met-haemoglobin which cannot carry oxygen to the tissues and the animal develops difficulty breathing (dypsnea) coffee coloured mucous membranes and blood (brown blood). Abortion in cattle is also associated. Therefore, clinical signs of toxicity include respiratory distress, discoloured brown or blue gums, rapid, weak pulse and trembling, collapse, coma and terminal clonic convulsions. The signs are exacerbated by exercise. However, it is rare for the disease to be this severe. Horse-owners in cold, wintery, weather see their horse with laminitis and usually cannot understand why.

Many plants including common grasses and weeds are able to absorb nitrate from the soil and accumulate dangerous quantities within their tissues. The rate of accumulation is affected by a wide range of factors including;

  • Crops are particularly dangerous when over treated with nitrogen/nitrate fertilisers and are in a lush stage of growth.
  • Adequate water during early growth stages (a good Autumn break), as the plant grows and matures the concentration is lowered. Young grass is also very low in minerals (Ca & Mg) and nutrients.
  • If a drought occurs before the plant matures, nitrates remain high in the standing feed or hay made from it.
  • When grown in acid soils.
  • When grown in sulphur or molybdenum-deficient soils.
  • Low temperature leads to decreased utilisation of nitrate by the plant but without decreased absorption from the soil.
  • Nitrate reductase is not active at night and in cool, overcast weather. Therefore plants accumulate nitrate at night and use it the next day. Shade, cold, lack of sun and short day length decreases nitrate reductase activity and accumulation of nitrates in the plant increases.
  • Wilting conditions decrease nitrate reductase activity during the day but nitrates continue to accumulate overnight.
  • Treatment with herbicides e.g., 2,4-D which kills N-reductase.
  • Diseased plants accumulate more nitrates than healthy plants.

How do you prevent nitrite/nitrate toxicity in cold wet weather? Provide other sources of feed, especially good pasture hay which is digested in the caecum (hind gut). Breaking down and digesting cellulose into simple sugars breaks the chemical bonds within the fiber and releases the energy held in these bonds as heat. This heat keeps the horse warm and provides the digestive environment suited to neutral pH and normal flora of the hind gut. In many cases I strongly suspect that nitrite/nitrate toxicity plays a role in the development of laminitis in winter and cool overcast weather when horses are out in the paddock.


High levels of Nitrogen in pastures are also thought to play a part in lowered levels of magnesium e.g., young rapidly growing pasture has up to 33% nitrogen and this can lower plant Mg levels by up to half. Sodium (Na) facilitates Magnesium (Mg) absorption from the gut; therefore, when sodium is low, such as occurs in young, fast growing pasture, magnesium absorption is impaired. For example “in Victoria the major cause of death of beef cows over 6 years of age is hypomagnesaemia or grass tetany during autumn calving. In some years substantial losses can occur in poorly managed herds” (Taylor, E., 2002, V437 Production Animal Health and Management, Murdoch University.)  Calcium and magnesium absorption are also linked and therefore the easiest way to ensure that both are present at the same time is to feed dolomite or a commercial calcium and magnesium supplement. Calcium and magnesium are needed for normal muscle and nerve function including the smooth muscles of the digestive tract and blood vessel walls.


Toxaemic – any systemic disease with a septic or toxic focus – pneumonia, pleurisy, diarrhoea, colic or endometriosis. Inflammation of organs remote from the feet, can cause laminitis – colic, colitis, metritis (retained placenta). Bacteria and/or their byproducts which leak into the blood stream. Effective treatment of the cause must be accomplished before improvement in the laminitis can be expected. These forms of laminitis are severe, requiring “immediate” veterinary attention. An organic treatment of viral and toxic infection is Vitamin C. Ask your veterinarian if this may be used in combination with other veterinary treatment. Toxic infection leads to the most serious forms of laminitis. Treat the cause early and effectively.

HYPERLIPIDEMIA / HYPERLIPEMIA is most likely to affect ponies and donkeys and can be triggered by a negative energy balance (starvation) or a stressful event and can lead to laminitis or laminitis can lead to hyperlipidemia. There is an enormous mobilisation of fat from the tissues to the liver. The liver is completely overcome by the overload, fills with fat and fails, often resulting in death. The fat is mobilised during times of  change in glucose metabolism and the laminitis may be due to vasoconstriction as a result of the altered fat metabolism or may be due to starvation of the lamellar tissues due to the lack of glucose (hypoglycaemia) which leads to activation of MMPs and laminitis. When a horse or pony gets mild laminitis, owners often unintentionally add to the misery by starving it. Anyone who tells you to starve a fat horse or pony is giving you very poor advice. People do this because they think it will be helpful as the pony foundered because it was fat. Laminitis is compounded by fat but not directly caused by fat. Refer to the metabolic profile of a laminitic pony in genetics and laminitis above.  Therefore, when an animal is stressed and “starved” the body must respond to the challenge to fuel itself or it will run out of glucose. The brain and blood cells must have glucose to survive.  Below a critical level low glucose can lead to death. Therefore, fat is released for conversion to glucose or ketones (toxic in high concentrations) which at physiologically beneficial levels are used to fuel non glucose dependent cells such as muscle. The liver performs this transformation (gluconeogensis) and also makes the proteins which attach to fats and transport them in the blood. Hyperlipidemia can occur if obese equines fail to eat due to any form of stress, such as colic, surgery, travel, etc. A fat equine with laminitis should be kept as happy as possible, it should be dieted carefully over a long period. All equines especially sick ones need energy to provide the fuel and nutrients for a quick recovery. (Refer to the laminitis diet for more information.)


There is no denying the anecdotal link between obesity and laminitis. However, in most cases the wrong link has been formed as to the cause of laminitis. The fat pony is usually also the pony in the paddock at risk of laminitis from feed induced causes which is discussed above. Obesity is not the primary cause of laminitis but as a contributing secondary factor it may make laminitis much worse. When the liver is already very fatty it is at greater risk of hyperlipidemia, it is less able to detoxify the blood and has impaired ability to perform gluconeogenesis (production of glucose from fats) in times of stress and low blood sugar (hypoglycaemia). This is significant as low glucose levels in hoof tissues and acids and toxins from the digestive tract contribute to the development of laminitis. An overweight animal is also insulin resistant and a metabolic and genetic profile of ponies shows many are at very high risk at all times and that weight loss and exercise can reduce this risk. A fat animal also has a greater pounds per square inch pressure over the bonded laminae surface area. The bigger the horse the greater the load on the laminae. However, starving horses plays no role in treatment of laminitis. The only time a laminitic horse should not be given food is if feeding it will contribute to a septic, toxic or inflammatory condition of the digestive tract, in which case the animal should be under veterinary supervision, receiving balanced intravenous fluids including glucose. Ponies should be started on IV glucose ASAP in these circumstances to prevent hyperlipidemia.


After treatment for the primary cause of laminitis

  • Never starve the overweight animal, not even for half a day.
  • Confine the horse or pony away from grazing and feed roughage at this time.
  • To prevent ulcers, a minimum of 3-4 roughage feeds per day is essential if there is no access to grazing.
  • Use low quality roughage (grass hay) and high quality supplements. It is the energy in the diet which needs to be reduced, not the nutrients as these are essential for life. Minerals, vitamins etc., contain no kilojoules and do not cause obesity! In-fact, supplying balanced nutrition is an essential part of every human weight loss program. All animals must have their nutritional needs met along with their requirement for energy. Mix the supplements (refer to the laminitis diet) with bran and chaff.
  • Only allow access to grazing when the feed has totally dried off and even then make sure the paddock has been grazed by cattle or other stock first so that the grass is not like a crop of hay.
  • Limit grazing severely when feed is lush and give roughage/grass hay instead.
  • Feed roughage just before giving access to grazing as this will fill the stomach helping to  decrease the volume of grass consumed.
  • Set a time limit e.g., half an hour morning and night in a dry paddock. Imagine how much grass your horse actually eats while it is picking constantly. It is much more than you probably think.
  • Give dolomite and bicarbonate with each small meal and before and after access to grazing to decrease acidity in the digestive tract from fermentation of green grass.
  • Increase exercise steadily.
  • Some horses must be allowed only very limited access to grazing if at all. Hand held and allowed to pick for 15 minutes is enough to cause an obesity or laminitis problem in some cases. You must judge how much grazing can be allowed so that a balance between hay and grazing will provide sufficient roughage.
  • Do not kill the horse with kindness. This is a common mistake that many people make feeling that confining the horse is cruel. Chronic laminitis is deadly chronic boredom is boring. You can improve your horse or ponies quality of life in many ways such as more exercise, going to events, more time spent grooming, scratching, picking out feet, invent some interesting tricks to teach your horse. Giving the horse small amounts of feed often is good management and also provides a reason for your horse to be pleased to see you.


Corticosteroids vary in their ability to induce laminitis e.g., (Prednisolone < Dexamethasone < Triamolone) and the effect may be dose related. Traimcinalone is used for intra-articular injections of fetlock joints and in much of the medical literature the advised dose for the number of joints should not exceed 18mg/horse. These drugs vary in their effect between horses, the sicker the horse, the more likely laminitis is to occur. However, it is often the acutely ill animal that requires corticosteroids. Therefore, it is a combination of health status, dose and potency which combine to cause the effects leading to laminitis.

Corticosteroids and NSAIDs all act synergistically (together), and the effect of combining them can be to increase the degree of side effects dramatically compared to the increase in drug dose. Therefore these drugs should NOT be used in combination with one another.

Equine Cushing’s Disease or Equine Pituitary Gland Hyperplasia (EPGH)

Refer to this section of the website.


A 20-year-old gelding taken to a show jumping day in very hot weather was reluctant to go out for the second round of jumping. The rider forced him on, and after completion retired the horse for the day; he was foot sore. The ground was described as “like rock”. That night the horse appeared lame. The next morning it was lying in the stable with acute laminitis, unwilling to get up, shivering and miserable. The contributing factors were hard ground, age, heat, travel, stress, being unfit for the exercise and the lack of early treatment when the lameness was first noticed.

A horse escaped from the paddock and went galloping up and down the bitumen road until its feet were so worn that they were bleeding. When the excitement was over the horse was so footsore and the laminae so traumatised that road founder was diagnosed.

Some endurance horses will work so hard and fast that each competitive ride traumatises the coronary band and causes a break in the wall which grows down with the feet.

Concussion, lack of fitness, riding too fast or too far, combined with poor shoeing, can cause road founder, “MAN MADE” laminitis.


Severe lameness in a front or hind hoof may lead to unilateral weight bearing for a long period of time. The front feet are carrying more of the body weight, and are at greater risk of supporting limb laminitis.

For example a limb bone fracture or infected distal joint may lead to this. After only 24 hours, the loaded foot has decreased tissue perfusion to a marked extent. The ischaemia of the tissues leads to laminitis. Prevention may be achieved in these cases by wrapping the loaded leg in a firm, evenly applied elastic support bandage, the hoof should be balanced and shod well for maximum support if possible, and the horse stabled on sand or soft bedding. Lying down and taking the weight off this leg is the best therapy as it will aid blood flow through the tissues.

It is a good prognostic sign when the horse is getting up and down unassisted e.g., with an olecranon fracture that has not been plated and is left for conservative healing with the horse confined in a stable for up to 2 months. Horses who have not been given the right size stable, suitable bedding, and just the right amount of pain relief may stand for days – weeks, and if they do get down, may have trouble getting up and risk further injury. Some horses seem to avoid lying down because it is too hard to get back up. It is as “if they lay down they may never get back up”.

In all cases, create the right environment and treat the injured limb ‘if possible’ ASAP, so that it can begin to take a share of the load. Surgeons & specialists go to a lot of trouble to get the horse to take at least part of the load on the injured limb as soon as practical.

The bigger the horse, the greater the risk when laminitis does occur as there is increased pounds per square inch of pressure on the weight bearing laminitic surface. Therefore, for this reason alone, size and weight are factors in the severity of the disease and the prognosis.

Horses which have been put into a cast e.g., tendon injuries, fractures etc., which have had the heel lifted with some form of wedge as part of the cast, may need to have a dense polystyrene foam wedge placed under the heels of the normal leg so that the limbs are level in length and angle. This may increase the load able to be taken by the damaged limb immediately.

Monitor the digital pulses, heat and swelling of the weight bearing limb and take steps to prevent laminitis at the early stages. Low doses of non-steroidal antiinflammatory drugs (NSAIDs) may be required on a daily basis throughout the recovery process.


An animal with sinker has suffered near or total destruction of the inter-laminar bond at the toe and the pedal bone is loose within the hoof. The further you raise the sole from the ground, the further the bony column can sink (founder). The hoof is mobile because it is no longer attached, and sinker could also be described as walking through the bottom of the sole of your shoe or, if you could imagine pulling a sock on and going straight through the toe. The horse’s leg has not changed only the attachment to the hoof has changed. Therefore, the bony column is usually still aligned normally and is not always rotated despite this description usually being used. In fact the mobile hoof capsule is counter rotating as the bone is forced through the sole by the weight of the horse. This is important to understand because the word rotation is used so often in association with laminitis and all descriptions are of the bones rotating. If we concentrate on the only freely mobile part of the foot during laminitis “the hoof” this condition is much easier to understand.

Sinker is life threatening! Depending upon the type of treatment and individual case, it may take hours, days or weeks to occur. In the worst cases, the horse sloughs the hoof wall from one or more hooves leaving the sensitive structures completely exposed, or the pedal bone prolapses through the sole (as above). Horses can survive this extreme form of laminitis if given constant nursing. During this time the feet are at risk from injury and infection. If a hoof is cast, the pedal bone penetrates the sole, or the coronary bands have ruptured, the Veterinarian may suggest euthanasia as the kindest option. This may be a decision determined by the degree of suffering, expense of treatment, as well as emotions. Despite the best of efforts not all horses with acute laminitis can be saved, it would be cruel to try. A soft, inflamed coronary band with a dip felt behind its edge and low distal phalanx position on x-ray, indicate severe loss of laminitic attachment. The further back the ridge behind the coronary band can be felt towards the heels, the greater the loss of laminitic bond. These cases should be carefully monitored for the first 60 – 90 days after which the risks reduce as new attachment forms and grows down from the coronary band.

Nothing nailed to the hoof or pressing on the sole or frog will prevent “sinker” laminitis if the damage is already done. A sinker hoof is not obvious; the horse may not adopt a classic laminitic stance or may be misdiagnosed as having azoturia (tied up) or even hypocalcaemia. In all severe cases of laminitis, Veterinary treatment for anti-inflammatory and pain relief is needed until the horse shows prolonged steady improvement. If not correctly managed, pain and inflammation can lead to further bouts of laminitis.

Horses which have sloughed the whole hoof have been nursed through the crisis on very thick, soft bedding. They cannot stand to defecate or urinate. This problem must be addressed so that the environment for the horse is hygienic. They need to be turned every 4 hours so that they do not develop pressure sores, ischaemia and muscle necrosis. They benefit from physiotherapy and massage. The feet must be dressed and bandaged to prevent further damage and infection. Over a period of 3 – 5 months a new hoof will begin to grow down. The heels will reach the ground surface first (approx 3 months) and the hoof which grows may be perfectly normal as it does not have to overcome the effects of a laminitic wedge. Hooves that prolapse through the sole will also recover but may have long term damage to the pedal bone due to necrosis of the bone. It is a dedicated owner, constant nursing, and attention to detail that restores quality of life. There are many horses who are living proof that the most severe form of laminitis “sinker” can be survived. However, the chance of restoring the horse to 100% soundness is low.

When sustained long-term pain relief is required there are many pharmaceutical and organic anti-inflammatory/pain relieving preparations available (DMSO, MSM, devils claw (herb), arnica etc.) which have minimal side effects. This is important as gastrointestinal tract ulceration and haemorrhage can result as a side effect of the use of NSAID’s to relieve pain. Therefore,  you must manage the pain so that the animal is eating which will help protect the digestive tract from these side effects while keeping the dose as low as possible. You are damned if you do and damned if you don’t.  How can you keep the use of pain relievers down?  Keep the feet cool by using ice baths. Get them onto a soft surface, apply the correct farriery principles and try some other products, MSM, Arnica, Devils Claw,  etc. Ask your veterinarian about integrating natural therapies and/or using commercial preparations with the least side effects when sustained long-term treatment is required.

Farriery is very important at this stage and the heel should form the primary weight bearing area of the hoof. The posterior surface area can be increased to relieve pressure at the toe by fitting bar shoes. The surface the horse is kept on, feeding and management are critical. If the hooves are shod and the heels raised, wedged, or the sole is filled with silicone etc., and the horse is no better then it may have been better to do less. If the horse is not worse then wait and see. However, if the horse is immediately worse after shoeing the effort was in vain. In these cases the farriery should be reassessed and the horse returned to a more comfortable state. When you place pads and wedged pads over the sole you can no longer see what is happening and they often contribute to sole pressure. I have seen many laminitic equines worse after shoeing, and then made to suffer through this for several days before the shoes are removed or changed. Therefore, I prefer to be conservative and manage the horse with trimming or basic shoeing, on a sandy or soft surface so the horse can make itself comfortable. In severe cases, bar shoes and/or hospital plates may be required. My favourite shoe for ponies and smaller breeds is an open toe bar shoe (reverse shoe), it provides posterior support and the open toe relieves all pressure under the damaged laminae which can be resected if necessary. The ponies thrive in them, they are cost effective for the client and easy to fit on very small feet.


Harsh chemicals can burn of exposed sensitive tissue and kill essential horn secreting cells, causing long-term complications to the hoof. Avoid strong iodine, formalin, and other harsh treatments. Use sugardine or Betadine (buffered iodine). Sugardine soaked swabs can be used to help prevent infection of exposed sensitive tissues. Made from 1 part Betadine to 3 – 4 parts sugar, store in an airtight container. Sugar has a strong poulticing effect and draws inflammation to it. Betadine has an antifungal, antibacterial effect gently sterilising the tissues and promotes healing. The medi-honey products are also suitable.


Pain is severe so it must be your goal to make the acute phase as short as possible. Your veterinarian is the first person you should call.

While you are anxiously waiting:

  • If possible identify the cause of the problem and do something about it e.g., don’t leave the horse in the paddock eating grass if you think that is the cause. If the horse is too sore to move stay with it in the paddock.
  • Prevent the horse eating anything else which you suspect has caused the laminitis e.g., take the new feed you have just started using three days ago away and don’t give it any more.
  • Hose the legs and feet with cold water. Or better yet, place the feet in an ice water bath. This is when cold therapy may decrease further damage and is the time when the feet should remain in the cold for as long as possible. Ice should always be floating in the water.
  • Rule: Never use ice directly onto skin, it will freeze and kill the cells.
  • Where possible, place in a sand yard or on a soft, friable surface while you wait for the vet – move the horse as little as possible to achieve the above listed goals.
  • In warm weather, keep the horse cool and provide water and shade. In winter also keep the horse comfortably cool.
  • If possible, clean and pick out the feet if packed up with mud or dirt causing sole pressure.
  • If you have experience with laminitis and are not calling the Vet, DMSO in a roll-on form can be bought from most saddleries. This is a powerful anti-inflammatory/antioxidant. It can be used as first aid if applied sparingly to the coronary band and distal limb. Wear gloveswhile handling this product and whenever touching this area after treatment and warn others to do the same. Do not use on damp skinas this causes a heating (exothermic) reaction which may blister the skin. Dry the skin first.
  • Reduce environmental stress. Do not separate the horse from its mates, bring the horse’s friend up to the stables with you and keep it nearby.


  • It is most important to try and identifying the cause to speed treatment and prevent a recurrence.
  • Keep the horse standing in the ice bath during treatment.
  • Drenching (stomach tubing) to speed the transit of ingested material and reduce absorption of toxic byproducts which enter the blood stream from the gut (grass or grain induced).
  • Alkaline buffers to decrease acidity e.g. magnesium hydroxide (1st choice) or sodium bicarbonate (baking powder) administered by drenching tube or in feed.
  • Dolomite, which is a form of finely ground calcium and magnesium carbonate lime mineral and can also be administered by stomach tube or in feed.
  • IV fluids, if the animal has concurrent colic, acidosis or other problem, fluid therapy may be indicated to maintain normal hydration and metabolism.
  • Administering anti-inflammatory/pain relieving drugs. Too little pain relief prolongs the acute phase; too much allows the horse to walk around in a masked state of pain, aggravating the damaged laminae. This treatment must be monitored for the maximum benefit to the animal, with minimal side effects.
  • Low dose anti-endotoxic doses of the NSAID Flunixin if Gram negative bacteria are implicated due to grass/grain induced laminitis or infection.
  • DMSO topically for anti-inflammatory, anti-endotoxic and antioxidant effects.
  • Antihistamines T1 have been used in combination with anti-inflammatory drugs for the treatment of laminitis in cattle. This is to decrease the inflammatory effects of absorbed bacterial endotoxins. This is worth discussing with your Vet as another option during the acute phase of the disease.
  • Antibiotics, if there is evidence or risk of systemic infection. Remember that all drugs can also lead to laminitis.
  • Anti-ulcer treatments may be beneficial if it is likely that the patient isn’t eating because of stomach or foot pain, has a poor appetite, or if there is a risk of gastric ulceration as a side effect of NSAID use. Ask your Vet about the best choices and side effects of withdrawal from these medications.
  • The most important mineral at this stage is magnesium, which may be administered by nasogastric tube as an epsom salt solution. The most important vitamins are B1 and vitamin C which can both be given as an injection by your Vet.
  • Protecting the feet from sole pressure/trauma with soft foam padding and bandaging.
  • Radiographs (X-rays) may show inflammatory fluid (transudate), infection or gas between the distal phalanx and wall, and can indicate if drainage is necessary. They also help assess the loss of laminitic bond and position of the pedal bone in relation to the coronary band and sole. Treatment of the disease process which has caused the laminitis should always be the first priority.
  • Drainage at the toe may relieve pressure over the sensitive laminae and minimise damage to these structures if there is evidence of fluid, gas or separation on x-ray. à Refer to farrier/shoeing for more information of how, when and why to resect).
  • The Veterinarian will require the assistance of a farrier to remove the shoes and to trim and balance the feet for accurate x-rays; or to fit shoes for treatment.

Treatment summary
This information is presented for horse owners and Veterinarians as a guide only, and is not a suggested or definitive treatment protocol. I hope that it may give you ideas about other drugs or homeopathic remedies other than those you are familiar with. The supply or use of some of these drugs to a horse owner is illegal except under the supervision of a veterinarian.


  • No forced exercise – in the short term (acute). Do not exercise a horse which is showing any signs of pain.
  • Allow free exercise – have the horse in a large area at least 20’x20’ with a soft surface and shade. Make access to feed and water easy. Provide company close by.
  • Yes hand walking – carefully, in the longer term (chronic). Only if the horse is free of pain.
  • Preferably, allow only self exercise in the first 30 days.

During the acute stage of laminitis, exercise was once thought to be beneficial; however, there is already a great increase in blood flow to the foot during the acute stage, and the tissues which are bonding the insensitive and sensitive laminae are very fragile and easily weakened. Exercise causes further tearing of the remaining laminae and increases the damage.

Ideally, the horse should be in an area big enough for it to move around if it wants to. A normal stable is too small, as standing stock still is also not ideal.

Inflammation is part of the repair process, and although it is necessary to minimise the pain and inflammation in the short term, once the acute stage has passed it is possible to minimise or eliminate anti-inflammatory drugs from the horses treatment, and reintroduce some controlled exercise such as walking in hand. Exercise increases blood flow and metabolism by the cells so that healing progresses.

Balanced trimming and shoeing are very important factors in increasing the horse’s comfort and returning blood flow to the affected parts of the foot through movement.

Depending upon the severity of the laminitis, a horse may return to normal activities in 30 days in very mild cases, and several months to one year or more in the most severe cases. Some never return to being 100% sound. The time is entirely dependant upon the individual case and response to treatment.


The ideal bedding surface is soft and loose, without packing into the feet; e.g., sand (must be shaded), rice hulls or wood shavings. These surfaces encourage the horse to lie down and rest, to “Take a load off the feet”.

If the horse is progressing well in a sand yard, leave it there. When sand is slightly damp it conforms to the sole of the foot, this may increase frog pressure which is known to enhance circulation to the toe via anastimoses between blood vessel and delivers it via an alternate blood supply to the affected areas. Damp sand is cooling and this is important during the acute stage. If sand is heated it will exacerbate the problem.

On soft surfaces, a sore horse will position its feet for comfort, angle and pressure over the frog and sole. If sand is not available, many horses respond to padding and protection of the sole (if not excessive). Too much packing causes sole pressure. Compressible, dense foam is ideal.

Laminitis causes varying degrees of sinking of the pedal bone lower into the hoof capsule and dropped/convex sole. Avoid walking the horse over, or standing the horse on, surfaces which will cause sole pressure. Make a mound in the centre and let the horse sort its own hoof angles out.


Shoes are a positive option, not a necessity in all cases. They combine well with sand as bedding. Most horses which have failed to improve begin to if the feet are protected or shod with supportive bar shoes.

  • Since writing this section I avoid packing feet entirely. I get the best surface for the horse I can. I will cover the feet, protect the sole, Use compressible packing to medicate exposed sensitive sole and fit shoes etc., but I avoid any form of packing leading to sole pressure that the horse cannot get relief from and that includes commercial sole packs of any kind.
  • A large sheet of H-grade polystyrene is really handy for standing the horse on while you are working.
  • If the horse is able to be shod and will benefit from it, protect the sole of the weight-bearing foot during shoeing. Stand the horse on dense foam, which helps prevent sinking and tearing of the laminae at the toe and crushing of the circumflex artery (during the acute stage).
  • Open-toe bar shoes, egg bar shoes and English bar shoes, and commercially made therapeutic bar shoes specific for laminitis are available. One advantage of the open-toe bar shoe, when correctly fitted, is that no pressure is applied to the wall at the toe. This means no pressure is transferred to the laminae, and none to the coronary band. For chronic cases and ponies I have found that this shoe gives an increased weight bearing surface area behind the widest part of the foot and relieves all pressure from the toe allowing for resection of the laminitic wedge.
  • For acute cases, my first choice is a bar shoe that can form the basis of a hospital plate, so that the sole can be supported without excess pressure of any kind, frog pressure can be accurately increased and the soles are protected. Filling the whole sole with very soft foam soaked in Betadine is often enough. I do not like any form of firm setting hoof reconstruction products, not even the flexible ones. In my experience they lead to too much pressure.
  • If the wall is very soft and weakened, the feet may collapse onto the shoe and the wall will distort. I have found that one of the best ways to deal with this is removing the shoes and making adjustments to maximise contact with the outer edge of any hardened laminae and solid wall, and to let the feet harden as much as possible. Often by this stage it is leading into Summer, and therefore I use the dry weather to my advantage and encourage the owners to keep the horses feet away from moisture. The harder and dryer they are, the better the weak laminae are at transferring force to the limb without collapsing.
  • In chronic cases where the hoof has become distorted or if the sole is convex (normal is concave) there may be a lot of sole pressure and pain. Relieve this by removing excess built-up sole, and use foam to stand on, so the horse has less pain or is pain free before spending a lot of time working on one foot. The horse will be a lot easier to work with if you take the time to do this.
  • Make sure the hind feet are comfortable as these are now the primary weight bearers.
  • The sole is extremely sensitive to pressure from mud, stones and badly fitted shoes.
  • Seating out the inner border of the shoe to prevent sole pressure is essential.
  • Most cases require only front shoes if the horse is on a soft surface.
  • The shoe must offer maximum posterior support (shoe length). Egg bar, straight bar, English bar shoes and set-under toe bar shoes or reverse shoes are all suitable. In effect, the shoe is modified to suit the individual. Freedom from sole pressure, ease of break-over (the toe is set under or bevelled or both) and posterior support are the key features.
  • The hoof/pastern angle must be normal, not broken forward or broken back. A suitable surface will allow the horse to choose an adjusted angle if raising the heel increases comfort.
  • The frog can help support body weight. Frog pressure can be achieved with padding, bar shoes, or padding combined with hospital plates, hoof construction materials etc. This method allows for easy adjustment if the horse shows signs of discomfort and immediate removal of pressure when no longer required.
  • Frog pressure has some benefits on circulation to the toe. It activates the pathway (anastimose) from the dorsal digital artery to the circumflex digital artery near the heel, bringing blood around to the toe by an alternative route. This is very beneficial in keeping damaged tissues at the solar border supplied with fresh blood. However, excess pressure can be worse than none at all. Judge the response to alterations and decrease or remove the pressure if a negative response is produced. This is a key reason I prefer hospital plates which allow for as much adjustment as needed.
  • Cover exposed sensitive tissues with sugardine swabs, treat as an open wound, combine with a hospital plate or bandaging and change regularly. House the horse in a clean, dry area.
  • Fill space between sole and plates or pads with sugardine or some other form of soft, antiseptic dressing and foam.
  • If there are signs of sub-solar fluid build up or infection in the wall on X-ray, or laminitis is severe, drainage should be established at the toe. Remove an inverted V-shape section of anterior wall (toe) to the level of the sensitive sole. In severe cases, the wall and sole will drain a large amount of serum immediately, giving relief. Treat as an open wound; use sugardine swabs and bandage.
  • Do not remove sole during the first 30 – 40 days other than to relieve sole pressure. Exposed sensitive sole will form granulation tissue, requiring treatment to discourage it.
  • The wall can be thinned across the toe (anterior wall) to just outside the insensitive laminae. This may relieve pressure over the laminae and distal phalanx. This is not a severe resection, does not bleed, and none of the sensitive structures are exposed. It is thought to allow more flexibility of the wall and allows for some swelling.
  • Resection of the laminitic wedge can be performed when the horse’s condition has stabilised (6 weeks or longer). This does not expose the sensitive laminae or remove the wall at the coronary band over the toe and will still offer good regrowth without the risks associated with resection up to the coronary band.
  • Should you raise the heels? I think the only way to answer that is to place a wedge under the heel of the dressed hoof and see what the animal does. If you do it to one foot and it begins to take more load on it, then go ahead. However, if you raise the heels and wedge the foot and fill the sole with filler and the horse is not better. You have made it worse. Raise the heel < 15° only when you can demonstrate a benefit. I have seen a few horses much worse after this has been done. I don’t do it. I encourage a mound and a soft surface and let the horse sort it out itself.
  • If the horse is not better with farriery changes in less than 24 hours, reassess them carefully and make adjustments if necessary, small details matter at this stage.
  • A 30 day shoeing schedule will make it easier to reduce distortion and keep the hooves in balance. Never go more than 6 weeks between farrier visits.
  • Remove nails individually with nail pullers – this reduces pressure and damage to the hoof.
  • If the horse was recovering well and the shoeing was successful, then a week or 2 later the client rings and says the horse/pony has gone lame again and they suspect a problem with the shoeing, be diligent in checking every detail of your work. The space for sole pressure may have filled with dirt causing pressure, the wall may be collapsing onto the shoe, un-shod patients may have worn all the wall away because they were running about and feeling good – then they get sole pressure and go foot sore. Some have gut pain and inappetance from the drug therapy used to treat the pain, which is then a cause of more laminitis or confused with foot pain. This is the time when horses may experience their next bout of laminitis because e.g., ‘the horse was going really good so we put her out in the paddock for a while’ or, ‘I didn’t think a few days without the supplements would make any difference’, or ‘I started to put her back on her old feed because she has lost so much weight’, or ‘I let my child ride it yesterday’, etc. You need to discuss the whole lifestyle, because laminitis relapses due to these types of issues are common.


In severe cases the reaction may be extreme, so veterinary assistance with nerve blocks and sedatives may be required. However older, well-educated horses usually allow you to shoe them the first time without much trouble.

Constantly picking up sore feet makes the horse resentful. If a horse is comfortable and recovering in its living area, leave it alone, you can still check the hoof temperature, pulse and coronary band etc., without picking up feet.

The opposite applies if there is a risk of sole pressure due to the bedding packing into the feet. In these cases, cleaning the sole out 2 – 3 times per day is the minimum.

At the second shoeing, the horse may expect it to hurt and therefore misbehave. Tapping vibration causes pain. As the laminitis improves, so should behaviour.

Use smaller, thinner nails. Avoid the toe area, and drive the minimum number of nails (4 – 6). Tap gently, with rhythm, and don’t try and tighten them right down. When nailed with care, many acutely laminitic horses do not react badly. Glue on shoes and hoof reconstruction compounds are options.


The laminitic equine is fragile. Therefore, these are “the rules”.

  • Within the first 48 hours the horse or pony will still benefit from cold and ice water therapy. Use ice baths as much as possible (ice should never be used directly on the skin). After 48 hours they may begin to resist and I take this as a sign that it is no longer beneficial.
  • The surface must be sand or very soft (e.g., shavings) so that it can easily dig its toes into it. If you can’t make a hole by shuffling your own toes it is too hard.
  • The pony or horse must have shade and the feet and whole animal should be kept cool in warm weather over 18°C. The hotter the patient the longer the recovery! Only rug at night or in cool weather. If necessary create shade where the horse wants to be. In very cold weather keep the patient comfortably warm with 1 – 2 rugs – never hot.
  • Feeding oaten hay and small mixed feeds is important, and the more often it is done the better, therefore 4 small feeds + supplements + hay per day are the minimum (see below).
  • Feeding the suggested supplements e.g., antacids to a laminitic animal that does not like them and will not eat them defeats their purpose. Therefore, mix them into a paste and squirt this into the mouth or add a little molasses to the mix or delete them completely until the patient is eating. Don’t wait more than an hour or two to see if the patient will eat it. If no – start again. Therefore, no matter how much I believe in the benefits of these ingredients in the diet it is more important to have roughage in their gut at all times. Get the laminitic patient to eat fibre.
  • Stick to the no grain diet, use other tasty treats to get it to eat e.g., a few grated carrots.
  • A pony that is not eating is likely to have pain. If there are signs of pain ask the vet to check the horse for colic or worsening of the laminitis. Colic may cause laminitis, may follow laminitis, may be due to the treatments for laminitis or is concurrent with laminitis because the horse isn’t eating. The horse’s foot pain may have decreased the appetite and it is important to break the cycle by managing the pain effectively.
  • Therefore, Try ice bathing the feet and then offer some food and monitor the dose of NSAIDs carefully.
  • While you having any further conversation with your vet ask about treatment for prevention of ulcers and gastritis and how best to minimise the dose of NSAIDs and pain management.
  • If the patient is not receiving antibiotics, probiotics can be given to help repopulate the caecum and colon with beneficial bacteria species.
  • Take the feed and water to the pony.
  • Place the feed at knee height, this takes some of the weight bearing off the front legs. Feed time is a good time to ice bath as well.
  • Don’t put anything in the water that tastes funny! Keep it close and keep it clean.
  • Ice bath the feet for as long as there is any signs of pain and heat. During the first few days I suggest every 2 – 3 hours during the day. Continue while are acute signs, heat, pain, swelling etc.
  • DMSO roll on can be applied very sparingly every day while the acute symptoms persist. It is absorbed immediately and will get into the system despite the water baths.
  • Check with your vet before combining NSAIDs such as Phenylbutazone, DMSO, Flunixin,  etc. These drugs work synergistically and the side effects from their combined actions are worse than that of any single drug.
  • Do not change anything if the laminitic patient is getting better. If it’s not broken, “don’t fix it”.
  • Do not separate the patient from its mates. Provide company, this is a good incentive to eat and be happy.
  • What else can you do to make the patient comfortable?
  • When everything is stabilised and the patient is free of pain. Wait another 30 days before moving the horse off sand. Maintain the diet indefinitely.
  • Like all medical situations, good nursing leads to rapid recovery.

Advice to the owner from the Vet and Farrier – If we do not hear from you we often assume that all is well. If there is no improvement, please tell your vet and farrier “not everyone else”.

If the horse has pain, please “call the vet”. Ask lots of questions, research widely, and seek second opinions only from those who are qualified to give them. I encourage you to get as much information as you can. We must all learn from each experience and every laminitic horse is unique.

Please keep us informed. If you get a second opinion that is beneficial to the situation, convey the advice, even if you have to write a letter so that your vet and farrier may learn from it as well. Then they may go on to offer better service to other people in the future.


Infection is harder to prevent and treat in areas of poor blood supply and dead tissue. It can be an ongoing  problem in cases of laminitis, acute and chronic, leading to recurring abscesses and occasionally infection of the pedal bone (infective osteitis/osteomyelitis). Bone infection can eventually lead to the horse being euthanased unless it is treated aggressively as early as possible, even then, the prognosis is guarded.

Preventing infections and seedy toe in the chronic foot requires regular trimming and good hygiene.


An area of dead tissue, bruised and damaged sensitive and insensitive laminae, forming rapidly after the acute phase of laminitis. Cells in the damaged area die off, while cells on the edges of the afflicted area are inflamed and produce a wound secretion. This is combined with an over production of weakly keratinised cells growing off the sensitive laminae to form the wedge. Mechanical tearing, caused by a long toe and movement increases the problem. Depending upon the severity of the laminitic episode, the affected wall may grow down with minimal long-term effect, or stay as a wide fibrous white line (laminitic wedge) which distorts the hoof angles.

Thick wall/laminitic wedge at the toe must be rasped back at each shoeing to restore a normal hoof/pastern angle. A severe laminitic wedge can cause pressure on the distal phalanx, leading to devitalisation and re absorption of bone. The wedge is the ideal place for bacteria to breed, leading to infections and seedy toe.

Seedy toe is the most common secondary effect of neglected laminitic feet. It can underrun more than a third of the wall, and decreases the attached surface area even further. It needs to be resected, and in some cases, the hoof may require a partial or complete reconstruction to restore function. In the long term, wall resection may help normalise hoof growth, function and appearance. It is easier to prevent seedy toe with regular farriery than it is to treat the consequences. Infections and seedy-toe are both worse in neglected feet, wet weather and dirty conditions.

When there are signs of consistent improvement and the horse can be shod. Only remove 30% of the wall, straight across the toe. The resection needs to be trimmed back every three weeks as it continues to keratinise, forming a hard outer layer. If not regularly removed, the keratinised layer forces the new wall over it, making the resection unsuccessful.


X-rays are a valuable diagnostic tool. They tell us whether or not the distal phalanx is sinking lower into the hoof capsule, they show the positions of the wall and pedal bone, the thickness of sole, and indicate whether there is fluid, infection or gas forming in the soft tissue space.

Many people describe the pedal bone as ‘rotated’. X-rays during the acute phase often show the pedal bone against the angles created by a flared and distorted hoof capsule. This can be misleading when assessing for rotation or sinking. The term ‘rotation’ creates panic and scares many owners unnecessarily. They expect the pedal bone to drop through the sole at any moment.

Rotation is defined as a state of being pivoted around an axis. The axis in this case is the distal interphalangeal (coffin joint). The phalanx bones are normally all at the same angle. When the heel is raised or the toe is shortened this angle is broken forward at the coffin joint and the pedal bone appears to have rotated around its pivot point at the center of the joint. I have described true cases of rotation in the section on club feet, as this is what a rotated pedal bone is. Therefore rotation is incorrectly described if the pastern bones are in normal alignment, or the hoof is distorted with a laminitic wedge or if the heel is long or toe is short and these imbalances have not been corrected for with farriery before the radiograph is taken.

When x-rays are taken, the hoof/pastern angle should be normal, and the hoof in a normal weight-bearing position; i.e., trim the foot if necessary, as laminitis does not always strike a neatly balanced foot. If the wall at the toe  is chronically flared, the top 1/4 is still usually in a normal alignment and forms a guide to trim the rest off from the front. The excess heel is judged with experience. Then an accurate x-ray of the pedal bone and the hoof capsule is achieved.

If an x-ray is taken of a chronic laminitic foot while it is non weight bearing and the hoof is untrimmed, and then another x-ray is taken after addressing these problems, the difference is dramatic. In these cases, I doubt that any rotation truly exists other than that created by a lack of good farrier.

Long term changes to the distal phalanx associated with long term neglected laminitis include a curling upward of the pedal bone around its edges (pixie toe), pedal osteitis, remodelling of the distal phalanx e.g., the solar surface flattens. Even these feet, with a correctly trimmed hoof capsule, will appear dramatically better when re-radiographed.

Occasionally very flat feet with a long toe/low heel laminitic feet are allowed to develop a severely broken-back hoof/pastern angle. This increases the tearing forces on the damaged laminae at the toe. This is prevented by good, regular farriery. Normal hoof angles at all stages of the treatment of laminitis essential.

After the acute stage, the rapidly forming laminitic wedge exaggerates the forces affecting the wall at the toe, forcing it away from the pedal bone, which is now repositioned within the capsule that has moved around it. The deep digital flexor tendon plays only a small part in this effect, and most rotated x-rays are produced from chronic feet with excess heel or short toe, or a flared toe and wide laminitic wedge. In other words, the hoof capsule is distorted more than the bone structure. This could be described as counter rotation of the pliable hoof capsule, while the phalanx bones are in normal alignment. True rotation does occur, but cannot be accurately assessed by using the distorted hoof capsule as a guide. The first step is always to normalise the hoof as much as possible.

The hoof is still held in place all the way around the back, in most cases, by the laminitic attachment of the lateral cartilages and bars, and the pedal bone within the hoof is attached to the deep digital flexor tendon at the back and extensor tendons at the front.

Consider the relative heights of the coronary band and extensor process on x-ray and the alignment of the phalanx bones, rather than using a distorted hoof capsule as a guide. This has more diagnostic relevance than “rotation” when the hoof capsule is distorted.


Several severe laminitic episodes, months or years apart, can lead to chronic degeneration of the distal phalanx, circumflex artery and the cells producing the wall, white line and sole. Tension on the deep digital flexor tendon due to muscle spasm as a cause or effect of pain can lead to a broken forward hoof pastern angle and chronic rotation of the pedal bone. Severing the tendon (desmotomy) gives short term relief, but research has shown that most do not progress well for more than a year or so. Therefore, why not investigate alternative therapies including nutrition, acupuncture, massage, trigger point therapy, physiotherapy and stretching combined with farriery.

Management of the feet becomes a complex problem involving many environmental factors. It can be difficult to maintain quality of life. Some horses never return to a totally pain-free existence. Many cope with this, functioning as valuable stud animals. Others never respond sufficiently to therapy and should be euthanased on humanitarian grounds.

The principles are the same, no matter how chronic or severe distortion of the feet has become. Trim for normal hoof/pastern angles and heel length within the capabilities of the damaged or contracted structures; shoe for maximum posterior support and avoid sole pressure. Hoof reconstruction may aid your ability to shoe the hoof as required to normalise it.

Use the diet as fuel to promote health and grow healthy hoof without letting the patient gain excess weight. Do everything possible to restore normal hoof growth and function. The feed bin motivates most horses who have survived this long. They eat everything and have a great desire to live.

Successful treatment of laminitis requires long-term treatment of the whole horse, not just the feet. It is a long, slow process. Vets or Farriers who are unsure of what to do next, or have a patient which is failing to improve, should seek a second or third opinion. Sharing information with the owner or carers is important. Well informed people make better decisions.


The symptoms of laminitis may be mild and last for less than 1 – 2 days, and often the horse will return to normal activity in weeks with few if any chronic effects. If the symptoms are initially severe and decrease steadily over 2 – 4 days or even a week or more, then a return to normal soundness may take months. Acutely painful feet for more than a week can lead to a very long recovery.

The aim is steady improvement in soundness and no setbacks. There are no two horses with laminitis which are exactly the same. Horses with mild symptoms may surprise you with the severity of the hoof changes. Therefore, the best advice I can give you on likely outcomes is that the longer and more severe the clinical signs are, the slower the recovery and the less likely the horse is to be sound in the short term. After 2 or 3 annual episodes of laminitis some horses are never 100% sound.

I recommend that while you have an acute case in your care that you think in months not weeks, so that you do not get disappointed. It will take 8 – 12 months to regrow the hoof completely so that the crisis line (the groove in the hoof where the laminitis occurred) should serve as a time guide. When this line is more than a third of the way down the wall there should be significant improvement, and therapeutic farriery should restore normal hoof shape and angles.

Steady improvement is a good sign. Intermittent or ongoing lameness is a bad sign and should prompt you to talk to your farrier and vet. At this time, reassess all factors, including daily management, feeding etc. For most owners laminitis is a big learning curve and a few setbacks may occur.

Laminitis should be viewed as a preventable disease, and not just “bad luck’.


* WALK EASY – available from D & M Stockfeeds.
‘Prime Horse Walk Easy Treatment & Maintain’ are designed to assist in the treatment and management
of overeating, founder, and laminitis in pleasure horses and ponies.

Please visit the D & M Stockfeeds site here for more information re this feed, and for contact details.

(Also good for arthritis)
The reason this diet has been described in volumes and proportions instead of by weight, is because not many horse people use scales. Every horse is an individual and the amount of feed required by two horses of the same weight may vary dramatically. With this diet you may vary the volume of feed for energy and roughage while the minerals and supplements remain constant, as suggested.

This diet is a guide to feeding generally, it is also used for feeding severe cases (no grain) and for feeding race horses showing laminitic symptoms or arthritis. The roughage is made up by volume per feed – most horses require to eat 1.5 – 2.0 % of body weight as roughage e.g., 20 – 40 liters (2 large buckets) per day plus hay. The greatest risk factor for ulcers is to confine a horse and only feed it twice a day. These feeds could be divided to make 4 – 6 smaller feeds which is a better way to feed horses and reduces the risk of ulcers. A recovering horse has a better attitude and greater desire to get well if it is fed little and often because while it is eating, the body produces many “happy hormones”. Only dampen each small feed as it is fed. Many horses fed this diet start putting on weight. This is a good sign and shows that you can reduce the energy with lower quality roughage (hay) or by soaking hay, while retaining the additives, to stabilise body weight. This is low protein, low carbohydrate, highly nutritious feed to maximise hoof growth and repair and increase well-being. For larger horses this diet would supply a minimum of 60 grams of dolomite a day. For some  warmblood and draught horses > 650 kg  this could be increased to 90 grams. For ponies divide the supplement volumes by half or a third or make one feed and divide this into multiple smaller feeds for the day. To make sure that a laminitic equine gets enough magnesium have some dolomite available in a dish so that it can lick if it wants to. The same can be done with kelp and salt in a separate container.

Race horses – after 2 – 4 weeks with low or no grain, it is slowly reintroduced into a race horse’s diet and the volume of grain replaces part of the volume of bran. Exercise is continued gently when possible.

Some laminitic equines are really miserable at being taken off what they are used to eating, even if it was killing them. Pain is a primary cause of laminitic equines not eating many sick animals are fussy and it is more important to eat something than nothing! You must prevent hypoglycaemia and hyperlipidemia in ponies. Treating any nutritional deficiency that is exacerbating the condition is vitally important. You and your vet can discuss minerals, magnesium, vitamins C and B etc. However, if the patient does not like the taste of the supplements but will eat the feed without them give a small feed with nothing in it. Do not wait hours to make this decision, the horse will eat it or it won’t. Find something the patient likes. It is better to feed a litre or less of mixed feed each hour or two as long as it contains a thimble full of the supplements as well. Than to give the whole lot and have the horse eat nothing. Use very small amounts of honey and water to damp the feed or add a little more of the lucerne chaff if it likes that. Small amounts of feed through the system regularly decrease the risk of ulcers and other digestive problems associated with microflora imbalances, anorexia and anti-inflammatory drugs.

Pain-relieving anti-inflammatories should be prescribed by a veterinarian and the dose varied from day to day, usually decreasing the dose steadily. Too little prolongs the acute phase; too much allows the patient to move around in a state of masked pain, aggravating the damaged laminae. Gastrointestinal side effects can be severe if overdosed repeatedly.


  • Feed roughage (bulk) to keep the patient happy, lower gastric and hind gut pH and for  healthy gut flora. For most laminitic ponies hay (sometimes chaff too) should be soaked in warm water for 1 hour to release sugars from the plant matter prior to feeding. The water is discarded and the hay can be spread out to dry or fed immediately. Oaten hay, oaten chaff, grass hay even lucerne can all be soaked. Shake the seed heads and grain out of grass/oaten hay. These extra steps can make a great difference in chronic cases.
  • Include essential vitamins and minerals.
  • Grain should be avoided and only reintroduced in small amounts, when the acute stage is over. Not in high risk cases such as ponies.
  • Avoid all legumes (peas, beans, or excessive amounts of lucerne, clover etc.) which are high in protein which requires metabolism by the liver which is already under great stress and legumes depress iodine uptake. Some ponies should avoid lucerne altogether as many are very sensitive to even small amounts such as 1 handful in a feed. Horses are less sensitive but in some cases where the horse fails to improve eliminate it from the diet for 2 weeks as part of a diet trial and feed soaked hay (as above) only.
  • Lucerne is a legume and should be kept to less than a quarter of the roughage in the diet of laminitic horses or 1/3 of the roughage of normal horse and avoided for most ponies. Use seedless grass hay or oaten hay, chaff and bran for the other three quarters of the roughage in the diet.
  • VITAMIN C: (30 grams daily for horses) helps eliminate free radicals as it is an important antioxidant and supports the body’s immune system. Vitamin C is necessary for connective tissue (collagen) and cartilage formation in joints and assists with detoxification and strengthening of small blood vessels.
  • CIDER VINEGAR: (1/4 cup daily) is a source of potassium and an organic anti-inflammatory, it is good for arthritis, however this should not be included while the patient has an acidic pH in the caecum and large intestine. In most cases horses prefer it mixed in with bran and water to make a mash (not too wet, not too dry). Some ponies are sensitive to this small amount of very weak acid and therefore, it may be better left out for the first week or two or altogether if an adverse response continues to occur.
  • SULFUR: Required for healthy keratin (skin, hooves, hair etc.). Sulfur is necessary for absorption of selenium and a deficiency can lead to anorexia, weight loss and poor digestion.
  • SEAWEED MEAL/LIQUID (Kelp): is an economical source of minerals e.g., natural selenium which is an essential antioxidant mineral and iodine which is essential for metabolism and is now being used as potassium iodide in the treatment of some infectious and inflammatory conditions, amino acids (precursors of proteins) and other elements. If feeding powdered kelp free choice access is ideal as equines will help themselves to what they require, consuming large amounts or leaving it alone as they choose. It is no longer advised to give it in feed unless for the short term, giving only a dessertspoon full to an average sized horse every other day for 2 – 4 weeks. Liquid kelp can be fed according to the manufacturer’s recommendations. Kelp will increase appetite, promote detoxification, increase metabolism and well-being.
  • DOLOMITE: The most important supplement. Make sure your horse gets this as a source of magnesium and calcium carbonate and small amounts of other minerals. A ratio of Ca 60%:Mg 40% is ideal. Quality dolomite is very fine to aid digestion and the carbonate acts as an antacid in the digestive tract which is beneficial during lactic acidosis and feed induced laminitis. All equines can be fed dolomite in the long-term as an alternative to calcium carbonate. Quality varies shop for the best. Giving free choice as for kelp may be the answer.
  • EPSOM SALTS: Magnesium sulphate is mixed with bran and fed to a laminitic horse as a mash or can be mixed with water and administered by stomach tube by your veterinarian. In acute cases this will help to move the offending feed through the gut quicker by the osmotic effect of the salts drawing water into the gut during feed induced laminitis (0.5 – 1.0 g/kg). Therefore, make sure plenty of water is available. It also supplies magnesium to the system as it is depleted during illness and stress (all cases of laminitis). Epsom salts can affect the kidneys and should only be fed during the short term, less than 10 days.
  • BICARBONATE: an antacid and buffer found in blood, it may be beneficial in feed induced cases to help neutralise acid in the hind gut. Give 30 – 60g daily during the acute phase.
  • THIAMIN (vitamin B1): Essential for normal glucose metabolism and the oxidation of amino acids and fatty acids to produce energy. Thiamin as thiamin triphosphate has a direct role in nervous tissue function. Growing horses require 3 mg/kg of thiamin per day. Adult horses receive their thiamin as a product of digestion of the hard hull of whole grains, bran etc., by the microbial population of the caecum. High grain diets and fermentation lead to low pH in the caecum which favours proliferation of bacteria which contain type II thiaminases which break down thiamin. Therefore, during laminitis horse may benefit from B group supplementation, especially B1. Thiamin is high in brewers yeast, rice bran, wheat bran and is low in dehulled grains. Deficiency signs include anorexia (not eating) and incoordination.
  • SELENIUM: This element is constantly excreted from the body and must be supplied in trace amounts every day. It is used in the pathway which protects cells from free radical damage and is therefore an essential antioxidant nutrient along with vitamin E, C, copper and sulphur which is required for its assimilation. Selenium is also required for fertility in both sexes. It is found in a bio-available form in kelp. In some high rainfall and coastal areas deficiency in soils is so profound that other supplementation is also required. Supplementary vitamin E may help to treat a mild deficiency. Some commercial products contain enough to treat a deficiency. Many horses with stiff muscles and chronic soreness respond to selenium supplementation and boron. A response to Vitamin E indicates that supplementation would be beneficial. Therefore, feed the whole diet to get best value from your supplements.
  • VITAMIN E: is incorporated into cell membranes and functions as an antioxidant protecting them from free radical attack. It is directly linked in the antioxidant pathway with Vitamin C and the selenium and copper containing enzyme glutathione which removes free radicals via the liver. A lack of any of these elements can lead to muscle and nerve damage and a weaker immune system. Vitamin E is found in green grass and is renowned for its healing properties. many commercial supplements are available. Refer to manufacturer’s feeding instructions.
  • BORON: A trace mineral required for the correct utilisation of calcium, magnesium and the absorption of selenium. It may be used in the dietary treatment of arthritis and  laminitis. Boron is often referred to in gardening programs for the health of soil and plant growth. Deficiency is common in Australia. A small amount is fed 1 – 2 x per week.
  • COPPER SULPHATE: Always in the same feed as dolomite to decrease any risk of toxicity. Horses have a higher copper requirement than much of the literature states. Many sources quote 6 – 10 parts per million (ppm), horses actually require 25ppm. Check your feed and pasture as you may need to supplement this essential mineral. Deficiency signs include rough, yellow coat with hair that curls back at the ends, OCD in young horses and arthritis in all ages. Abnormal intestinal parasite burdens and diarrhoea are symptoms of deficiency. Leave copper sulphate out of the feed if the patient is anorexic (not eating). Small amounts of copper e.g., 6.5ppm are found in kelp and this can supply some copper safely. Do not give if there is risk of liver disease, hyperlipaemia or a history of toxic plants such as Patterson’s Curse or lupinosis as copper is stored in the liver and in these cases the organ is chronically diseased. In these cases offer kelp. Over supply of copper is toxic. Therefore, it should be fed at all times with dolomite which helps to neutralise any excess.
  • HERBAL PREPARATIONS: For relief of pain and inflammation e.g., Devil’s claw. Consult any promotional literature and follow feeding instructions accurately.
  • COD-LIVER OIL: Supplies vitamins A, D, E and omega 3 fatty acids. Cod liver oil can be mixed 50:50 with linseed oil or another omega 3 and 6 supplement. This can be administered separately to the feed if the horse does not like the smell or taste. Try mixing it with a little honey if your horse won’t eat it.
  • LINSEED OIL: One of the richest sources of omega-3 fatty acids which play a role in decreasing inflammation but, it does not replace the fat soluble vitamins found in Cod Liver Oil (CLO).
  • CORN OIL: Has high energy (4 x the energy of grain per gram) for a low volume and is digested from the small intestine without the risk of carbohydrate overload in the large intestine. Feed small amounts and build up over 3 weeks to larger volumes of 1 cup per 100 kg body weight per day for horses in training that require high energy such as race horses that are prone to exercise induced myositis / tying up syndrome, laminitis etc., on a grain based diet. You must feed enough roughage with the large volume of oil.
  • HONEY (natural): is a preferred sweetener and molasses should be avoided.
  • SALT: Sodium chloride (sea salt). Feed ad-lib rock salt, loose sea salt in a container, or as a salt block. Do not mix in the feed. Horses will seek salt when they want it.
  • PROBIOTICS: Live beneficial bacteria which help to restore the normal bacterial flora of the caecum and colon (hind gut). Not useful while on antibiotics and should be fed immediately after. à Refer to the manufacturer’s instructions for dose rates.
  • VAM paste (originally for injection) is an ideal way to give vitamins, mineral and aminoacids. Available from NATUREVET.

30 grams (g) is approximately equivalent to one rounded dessertspoon (dsp) or one level tablespoon or one ounce (28.4 grams). 10 grams is equivalent to 0.35 ounces 1/3z (oz) or a small rounded teaspoon (tsp.). 3.5 grams is equivalent to ½ a level teaspoon.

WATER: clean water ad lib at all times.

  • GRASS HAY/OATEN HAY: Ad lib grass hay or large amounts of moderate quality. Do not feed a lot of top quality hay or lucerne as it defeats the purpose of a low energy, low protein diet. Grass hay can contain very high amounts of fructans so choose the quality carefully. If in doubt feed oaten hay. The aim is to get low energy roughage and fibre into the hind gut where it will promote a healthy gut flora to re-establish after digestive upset. Lucerne should not exceed 1/3 of the total roughage of the diet. Some horses and ponies are very sensitive to lucerne and any adverse effect should be noted and avoid lucerne  completely in these cases.

ROUGHAGE: By volume 1/4 lucerne chaff, 2/4 wheaten chaff or oaten chaff, 1/4 bran.

150 – 250 KG
250 – 400 KG
15 – 16 HH
400 – 500 KG
16 – 17 hh +
> 500 – 650 KG
Twice per day or in every feed. It is better to slightly over-dose than under-dose.
1 level teaspoon or 10 grams twice daily. 1 rounded teaspoon or 15 grams twice daily. 1 level dessertspoon or 20 grams twice daily. 1 level tablespoon or 30 grams twice daily. 1 rounded tablespoon or 50 grams
twice daily.
Free choice from a feed bin. If adding to feed, give every other day and stop after 2 – 4 weeks.
Ad-lib access or 1 level teaspoon or 10 grams. Ad-lib access or 1 rounded teaspoon or 15 grams. Ad-lib access or 1 rounded dessertspoon or 20 grams. Ad-lib access or 1 level tablespoon or 30 grams. Ad-lib access or 1 rounded tablespoon or 50 grams.
For short term use only (1 – 3 days). Bicarb can be mixed into paste and squirted into mouth 1/2 an hour before feeding if the laminitis was feed induced or if the patient is acidotic.
1 – 2 rounded teaspoons or 20 grams twice per day. 2 – 4 rounded teaspoons or 30 grams twice per day. 1 – 2 rounded dessertspoons or 40 grams twice daily. 1 – 2 level tablespoons or 60 grams twice daily. 1 – 2 rounded tablespoons or 100 grams twice daily.
1 level teaspoon or 10 grams once daily. 1 rounded teaspoon or 15 grams once daily. 1 level dessertspoon or 20 grams once daily. 1 level tablespoon or 30 grams once daily. 1 rounded tablespoon or 50 grams.
Minimise the risk of toxicity by always mixing into the same feed as Dolomite. Can offer ad lib (free choice) with the Dolomite.
1/4 teaspoon or 0.8 gram once per day. 1/3 teaspoon or 1 gram once per day. 1/3 teaspoon or 1 – 1.5 grams once per day. 1/2 teaspoon or 2- 2.5 grams once per day. 1/2 – 3/4 of a  level teaspoon or 2.5 – 3 grams once per day. Blacks and chestnuts may require the higher dose rate.
As sodium borate or boron sulphate. Borax is available from the supermarket cleaning aisle.
1/4  teaspoon or 0.85 grams once daily for one week then ¼  tsp. once only per week. 1/4 teaspoon or 0.85 grams once daily for one week then ¼  tsp. once only per week. 1/2 level teaspoon or 3.5 grams once daily for one week then ½ tsp. once only per week. 1/2 level teaspoon or 3.5 grams once daily for one week then ½ tsp. once only per week. 1/2 slightly rounded teaspoon or 4 – 5 grams once daily for one week then ½ tsp. once only per week.
Supplementation is dependant upon local deficiency. Refer to Laminitis Diet notes above.
Ad-lib kelp powder. If severe deficiency occurs in your area research additives carefully. Ad-lib kelp powder. If severe deficiency occurs in your area research additives carefully. Ad-lib kelp & vitamin E. If severe deficiency occurs in your area research additives carefully. Ad-lib kelp powder & vitamin E. If severe deficiency occurs in your area research additives carefully. Ad-lib kelp powder & vitamin E. If severe deficiency occurs in your area research additives carefully.
1 ounce = 30 ml = 1 tablespoon. 60 ml = 1/4 of a cup.
20 ml per day.
Mix with bran, honey and water until just damp, use to carry the other minerals.
30 ml per day 50 ml per day 60  – 70 ml  per day 80 ml per day
Vitamins A, D, E & fatty acids.
5-10 ml once per day for 7 days then 1-2 times per week. 10-15 ml once per day for 7 days then 1-2 times per week. 20 ml once per day for 7 days then 1-2 times per week. 30 ml once per day for 7 days then 1-2 times per week. 40 ml once per day for 7 days then  1- 2 times per week.
Omega 3 fatty acids. Can be mixed with CLO (as above) 50:50
5-10 ml daily. Reduce to every other day after 2 weeks. 10-15 ml daily. Reduce to every other day after 2 weeks. 20 ml daily. Reduce to every other day after 2 weeks. 30ml daily. Reduce to every other day after 2 weeks. 40 ml daily. Reduce to every other day after 2 weeks.
Sodium ascorbate powder. Decrease dose over several weeks, or can be a part of on-going diet.
5-10 grams or 1 – 3 level teaspoons per day. 10-15 grams or 3 – 5 level teaspoons. per day. 20-30 grams or 1 – 2 level dessertspoons per day. 30-40  grams or 1 – 2 rounded dessertspoons per day. 40-50 grams or 1 – 2 level tablespoons per day.
Sodium Chloride. Unless in hard training, salt should be by free choice, separate to the mixed feed. Horses will select how much they need.
Free choice from a dish or as a block of rock salt. Free choice from a dish or as a block of rock salt. Free choice or as rock salt. Horses in heavy training may require 1 rounded tsp. in feed after strenuous exercise. Free choice or as rock salt. Horses in training may require 1 rounded tsp. in feed after strenuous exercise. Free choice or as rock salt. Horses in training may require 1 – 2 rounded tsp.s, in feed after strenuous exercise.


Using a standard cup. All measures are level.


error: Content is protected !!