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LAMINITIS

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SOMETHING HAS TO HAPPEN WITHIN THE BODY OR TO THE BODY TO TRIGGER A LAMINITIC EPISODE. THEREFORE, IN THE MAJORITY OF CASES LAMINITIS IS PREVENTABLE.

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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 laminitic event.

Please note; the terms horse and pony may be used interchangeably throughout this section.

Day 1 - Chronic Laminitic	12 Months Later - Recovered	2 Years Later - Back to Start

WHAT IS LAMINITIS?
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.

After 2 years of neglect.		Same day after trimming.

SYMPTOMS

With severe laminitis it is clear that something is wrong even if you do not realise at first what the problem is because your horse will be obviously uncomfortable. 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 horses 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 varyingly 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 damage is. 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.

THE THREE STAGES OF LAMINITIS

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 is 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.

1. 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.

The 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, then 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 that the horse is described as a sinker.

30 days after an acute laminitic episode the old sole has sloughed and a new sole is forming.

 

THE LAMINITIC EPISODE - THEORIES ABOUT THE CAUSE

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 where 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 has 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 (hgypoglycaemia) 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.

1. Treat the primary problem e.g., colic, colitis, retained placenta, pneumonia etc.
2. 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.
3. Discuss the risks or signs with your vet and take on board their recommendations.
4. 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  HEAVIER  THE HORSE, THE GREATER THE LOAD ON THE  LAMINAE.  A DRAUGHT HORSE HAS LESS CHANCE OF SURVIVAL THAN A SHETLAND PONY.

FEED INDUCED (grass or grain) LAMINITIS:
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 are 30% more efficient than equines at digesting it. However, once the rumen is full they must stop eating and ruminate (rechew) 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 rechew 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 is 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.

PREVENTION OF GRASS AND GRAIN INDUCED LAMINITIS

• 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. Founderguardâ 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.

GENETICS, BODY TYPE  AND LAMINITIS

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 certain areas 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 and in the sheath of males and over the eyes and in my experience these animals are at risk of developing laminitis with any slight increase in energy in the ration. Relevant conclusions from this 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.
• Characterization 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.
• 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.
www.EquusMagazine.com

YOU CAN'T FATTEN A THOROUGHBRED - OH YES YOU CAN!
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 and 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 à 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. à Refer to the laminitis diet for more information.

 

RACE HORSE CRISIS, VERSUS LAMINITIS
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, smelling sour 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.

PADDOCKS, PASTURES AND DIETARY CAUSES OF LAMINITIS

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. à 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 horse that is 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 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. 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 animals 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, Cobolt, 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 time, "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. à 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.

NITRITE/NITRATE
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, 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. à 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.

MAGNESIUM
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.

TOXIC INFECTION: 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.)

OBESITY

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. 

Tips for losing weight
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.

Equine Cushing’s Disease or Equine Pituitary Gland Hyperplasia (EPGH)
Refer to this sectin of the web-site

ROAD FOUNDER

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.

SUPPORTING LIMB 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 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 it “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.

SLOUGHING THE HOOF/SINKER

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
and 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.

SUGARDINE

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 medihoney products are also suitable. In a crisis honey from the supermarket will do.

TREATMENT OF ACUTE LAMINITIS
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 gloves while handling this product and whenever touching this area after treatment and warn others to do the same. Do not use on damp skin as 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.

VETERINARY TREATMENT MAY INCLUDE:

• 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.

Continued - click here.