Look out for Laminitis


with Sonja Vandermark (KER)
by Karen McDonald

New research is paving the way to unlocking the mysteries of laminitis, giving horse owners fresh strategies for identifying, preventing and managing this potentially devastating condition.

Anyone who has owned a ‘good doer’ - meaning the type of horse that seems to put on weight merely by looking at feed - that begins to develop a hard, cresty neck and ample proportions reminiscent of a Thelwell character at the first sign of spring grass, is likely to be familiar with the advice ‘lock him up and starve him or he’ll founder’. Aside from recognising that founder is also known as laminitis and ‘causes sore feet’, many of us admit, somewhat guiltily, to having little idea on how to identify and manage this serious condition in its early stages.
Much of the research information available is directed at the scientific community rather than to the average horse owner, and in some cases is difficult to understand and apply. Subsequently, this well-intentioned reading material is often consigned to the ‘too hard basket’!

In their natural environment, horses are not faced with the same conditions their domesticated cousins are in terms of an overly rich diet, confinement to a small area, under-exercise,
drug administration, exposure to disease and subjection to unnaturally high concussive stresses through ridden work. In short, since most forms of laminitis occur as direct consequences of human intervention, we really owe it to our horses to ensure they have the lowest possible chance of developing this condition by being fully aware of the risk factors and using sound day-to-day management practices. Although often mistakenly believed to be confined to childrens’ chubby ponies, laminitis shows no class or breed prejudice when it strikes. In fact, the death of one of Thoroughbred racing’s all time superstars - Secretariat - in 1989 was as a consequence of a severe episode of founder.

A diagnosis of laminitis needn’t necessarily spell the end to a horse’s performance career or be considered a life sentence of pain and disability. The good news is that, across the world, funds are continuing to be poured into research aiming at discovering exactly what triggers laminitis and governs the catastrophic chain of events in the equine body that lead to the inner mechanisms of the hoof being so drastically affected. Although we are far from knowing all the answers, there is ‘light at the end of the tunnel’ as a result of what has been learned in recent years.

Given the enormity of the subject of laminitis, it would be impossible to cover all aspects in one article therefore, Part One focusses on how and why the condition develops and outlines short term ‘damage control’ procedures. Part Two will deal with specific strategies for managing the laminitic horse including advice on feeding regimes and the corrective shoeing techniques thought to be most effective during the various stages of an attack of founder.

Inside The Hoof
An acutely painful and disabling condition, laminitis occurs where the lamellae (a series of delicate folds of tissue inside the hoof wall) become inflamed and eventually tear apart. The result is partial or total destruction of the strong, supportive bond that usually holds the inner wall of the hoof to the pedal bone (the furthest extent of the leg).

To understand why this process leads to such intense pain and disability, think of the normal hoof as being a very efficient type of shock absorber. When it strikes the ground, the resulting force is ‘filtered’ through the outer wall, sole and frog then through the blood-filled (and therefore cushioning) lamellae. This process actually helps to squeeze blood out of the foot, pushing it back towards the heart. By the time it reaches the pedal bone, the ‘buffering’ influence of the areas this force has passed through have reduced its intensity by up to 90%. This is a marvellous piece of engineering on the part of Mother Nature but, at first glance, it is hard to comprehend how and why tiny structures like the pedal bones play such a significant role in a horse’s weightbearing and ease of movement. Yet, the bones are critically important and, as long as their attachment to the hoof wall via the lamellae remains strong, each pedal bone (also known as the coffin bone, distal phalanx or third phalanx) is remarkably effective in supporting its own limb and, collectively, carrying the entire mass of the horse.

Imagine then, the chaos created in this delicately balanced system by a ‘squeezing’ effect being introduced, which is exactly what happens when the lamellae become inflamed, swell up and the pressure starts to push outward in all directions - causing some of the tiny blood vessels the lamellae depend on for nutrients and oxygen to be ‘squeezed’ closed. As this process continues, the shock-absorbing qualities of the inner hoof become severely compromised, as much of the blood supply to the lamellae is diverted away into larger vessels as the ‘pressure-cooker’ effect builds up. Weakened and damaged, the lamellae begin to separate and the pedal bone loses its attachment to the inner hoof wall.

Now free of its support, the unstable pedal bone is pulled from its usual position by strong tendons in the leg. Rotating downwards or, in the worst case scenario, simply ‘sinking’ within the hoof capsule, the pedal bone then falls towards the sole. The amount and area of lamellar damage governing the extent of the rotation or ‘sinking’ and the ultimate severity of the condition. Further tearing of the lamellae and crushing of the underlying tissue of the hoof results as the pedal bone pulls and pushes at the tissue surrounding it. In some severe cases, the pedal bone descends so far that it actually perforates the sole of the foot.

The Cause
Although consumption of large quantities of grain or fresh green pasture is, in many cases, rightly accused for the onset of a bout of laminitis, it can also result from occurences elsewhere in the body - often completely separate from the feet. Some of the long list of possible underlying causes include a localised or systemic infection (e.g. a retained placenta or respiratory ailment), a musculoskeletal problem such as ‘tying up’, working on hard, dry ground for long distances without sufficient rest, a hormonal imbalance arising from conditions such as Cushings Disease, prolonged antibiotic treatment and excessive intake of cortico-steroids. In addition, a severe, painful injury to one limb sometimes leads to laminitis developing in the opposite supporting limb. Somewhat disturbingly, there are also a number of cases reported of laminitis each year for which there is no obvious cause; it just seems to ‘happen’ with none of the usual risk factors to blame.

Grain Overload
The most common and one of the most studied forms of laminitis is that arising after a horse has eaten a large grain meal or series of meals - resulting in a ‘carbohydrate overload’ the digestive system is unable to cope with. The typical story of the horse breaking into the feed room and going through a full bag of grain is one such example. Under normal circumstances, grain is digested in the small intestine but, in the case of a large intake containing high levels of carbohydrates, the small intestine becomes overwhelmed and some of the grain passes back undigested to the hindgut - where it is rapidly fermented by ‘sugar-loving’ microbes. This, in turn, disturbs the delicate balance in pH (acidity) levels in the hind gut and, ultimately, is thought to lead to the release of laminitic ‘trigger factors’ into the bloodstream - sending them on their journey to the hooves to begin their destruction of the lamellae.

Grass Laminitis
Also considered to be a form of ‘carbohydrate overload’, in that it seems to stem from the hind gut being overwhelmed with grass sugars that escape the digestive process in the small intestine. This situation is usually a seasonal problem, brought on by the consumption of carbohydrate-rich, fresh growth of spring grass but, interestingly, has also been seen in horses that are restricted to ‘starvation paddocks’. The short grass in these paddocks may seem innocent enough but can still be rich in the particular type of sugars that have been linked with laminitis.

Developmental signs of laminitis are not as readily seen in grass-foundered horses as they are in those suffering from ‘grain overload’ - with the former usually being discovered in severe pain in the acute stage, with very few or no warning signs. Some researchers believe there may be variations in the way the fermentation process takes place in the hindgut, possibly leading to a difference in how the ‘trigger factor’ is released into the bloodstream. The trigger substance may even be totally different for grain-based founder than for the grass-based condition. These questions continuing to be the subject of ongoing research around the world.

Concussion Laminitis
Although the hooves are incredibly strong, they were never designed to take the kind of forces thrust upon them during ridden forms of exercise therefore, pounding away on hard ground day after day is literally ‘asking for trouble’. The high concussion generated by working on compacted, dry surfaces - predominantly in summer - affects the blood flow to the feet, which in turn can lead to changes in the lamellae and tearing of its attachment to the pedal bone as in other forms of laminitis. Despite the fact that only a portion of the lamellae may be affected, rather than the whole structure as seen in feed-related founder, concussion laminitis still has the same consequences in terms of pain, lameness and the need for careful ongoing management.

Danger Detection
One of the most frustrating aspects of laminitis is that very few signs of an impending attack are apparent in the initial developmental stages, therefore it is usually only once the horse has begun to feel the pain associated with separation of the lamellae that the owner recognises something is amiss. Unfortunately, by the time pain behaviours are evident, much of the damage has already occurred. Even once ‘damage control’ measures have been implemented, rotation or ‘sinking’ of the pedal bone can continue for days or weeks, depending on the severity of the episode.

The main sign to watch for if laminitis is suspected is a general restlessness, often characterised by the horse continuously shifting weight from one foot to another when standing still - especially if this is happening with the front feet. The hooves may also feel warmer than usual, which is a response to the extra pressure building up inside as the large blood vessels expand and the inflammatory response brings more blood to the area for healing the smaller ones in the lamellae. The same process is also responsible for an increase in blood pressure, which can be detected by feeling or sometimes even by merely looking at what is known as the digital pulse. This is located in the fist- sized hollow between the fetlock and the bulbs of the heel, to the inside of the leg where the vein crosses the bone. Feeling or seeing a ‘throbbing’ or ‘bounding’ quality rather than a steady, even beat in the digital pulse is a well-recognised indication of the acute stage of founder.

As the condition progresses, the degree of soreness in the feet becomes steadily worse - with the toe region especially sensitive if hoof testers are applied. Over the course of a few days, the sole of the hoof may take on a bruised appearance either just in front of the frog or in the white line area. This is an indication of the damage being done to the small blood vessels as the lamellae tear apart and the pedal bone crushes the underlying tissues in its descent. Often, a characteristic ‘rocking horse’ stance is seen, with the hind legs tucked well under the body and the forelegs stretched forward to allow weight transfer to the less painful heel region. Although usually reluctant to move, if the horse is forced to walk, its strides commonly appear short and ‘choppy’, with lameness generally apparent in one or more limbs - especially when turning circles. If observed lying down, which many do in order to ease their discomfort, the laminitic horse will tend to lie flat on one side with all four limbs extended straight out and may have difficulty regaining their feet.

X-rays for diagnosis
Laminitis should be treated as a medical emergency, with a thorough veterinary examination required at the earliest opportunity to determine exactly how severely the horse has been affected and why. It is impossible to tell if there has been pedal bone rotation just by looking at the hoof from the outside, unless there is obvious bruising so, in most cases, X-rays of the lower limbs are taken in order to make a conclusive diagnosis, measure the severity of any movement of the pedal bone and assist in deciding the best course of action. Every case is different but it is often beneficial if new x-rays can be taken every 5-10 days until the full extent of the damage inside the hoof is clear - rather than merely relying on an initial ‘snapshot’ to guide the treatment regime.

Recent advances in the technology used to assess laminitis have seen the development of a procedure known as a venogram - injecting a liquid that shows up on X-rays - which allows the veterinarian to more accurately pinpoint the sites of major damage within the hoof capsule. Quickly filling the delicate veins and capillaries of the foot, the liquid highlights the areas where circulation is restricted or increased and may even have some therapeutic benefits in terms of reducing pain.

Damage Control
In the short term, there are several ‘damage control’ measures most experts on laminitis agree should be implemented as soon as the condition is suspected. The most obvious is to remove any potential causes, which in the case of ‘carbohydrate overload’, ideally means relocating the horse to a sand yard or deeply bedded stall and immediately eliminating grain from the diet. The next step is to provide some form of pain relief, usually in the form of phenylbutazone (bute), which does little to actually treat the condition but will assist in relieving the inflammation and pressure in the affected feet. Pain relief, however, must be carefully administered as, if the horse’s discomfort is completely alleviated, this may encourage more movement than is advisable - causing further damage. It may be wise to consider using an equine antacid supplement to provide some protection to the lining of the stomach and reduce the risk of gastric ulcers while analgesics are being administered.

Once a horse has suffered laminitis, it will always be susceptible and requires careful management. This involves the horse owner becoming vigilant; not only watching for signs and symptoms and becoming practiced at detecting subtle changes that can indicate the early developmental stages of an attack but also identifying situations and conditions that may trigger an episode. If ‘caught’ before the acute stage, there are some options for treatment that can be tried such as cryotherapy (applying ice to the feet) and/or a category of drugs known as vasodilators (acepromazine, isoxuprine, pentophyline and nitroglycerin) but both rely on early detection of an impending bout of laminitis to be effective.

The Equine Foot
An amazing feat of natural engineering, the internal structure of the equine foot is designed to ‘buffer’ the concussive forces generated by travelling over rough ground - thus reducing their effect on the rest of the horse’s body.

The outer tough, fibrous layer of the hoof, known as the wall, forms a protective, waterproof barrier between its sensitive inner organs and the environment. Containing no living cells and with similar properties to hair and teeth, the tissue of the hoof wall takes between six to eight months to grow from the coronet band down to the ground - this process continually taking place throughout the horse’s life.

Connecting the wall to the internal structures of the hoof are numerous, delicate folds of tissue known as lamellae (see image on page 13), which extend around the entire inner surface. The first of two types, the outer horny lamellae, extend from the hoof wall in accordion-like folds - each of these bearing many smaller, secondary lamellae. These secondary folds then interface with another type - the inner, sensitive lamellae - which, in turn, connect to and provide a means of support to the pedal bone.

Central to the inner stability of the hoof is a thin yet incredibly strong membrane that lies between the inner and outer layers of the lamellae. Although this is still to be proven beyond doubt by further research, the failure of this membrane is thought to be a key factor in the tearing apart of the attachment between the inner hoof wall and the pedal bone - as happens when a horse is suffering from laminitis.

Reader's Story - Laminitis Lament
The dreaded ‘L’ word, laminitis, strikes fear into the most staunch horseperson or, if it doesn’t, it should. For Maria McCahill, her experience of the devastating consequences of this condition began in September 2003 when her twenty year old Quarter Horse gelding, Pride, came to his morning feed with ‘a wobble’ instead of his usual purposeful gait. Concerned, Maria contacted her veterinarian; “After some preliminary blood tests, my vet told me Pride had laminitis and so began our road to recovery or so I thought. I asked a lot of questions like what, why, how, when, prognosis, is it life threatening, what can I do? Treatment began very aggressively with anti-inflammatory drugs by drench, antibiotic injections, saline drips and x-rays to find out the level of pedal bone rotation Pride had experienced. I was also advised to get heart bar shoes onto him as soon as my farrier could come out.

Confined to a small corner of the paddock on knee deep straw, Pride stopped eating by himself altogether. He would only drink water if I held it and would eat grass in the same manner. He had been my horse for nineteen years, we’d grown up together, I’d broken him in myself when I was a ‘bullet proof’ twelve year old, and I couldn’t help wondering what I had done wrong.

After a month of treatment, Pride’s condition worsened and he began to go septic, with his gums and eyes turning a bright shade of purple as his body also started to retain enormous amounts of water. Although there was only a 30% chance of him surviving, I gave my old friend around the clock care to help him through the routine of drips and injections, massaging him daily in the hope this would provide some relief. Suddenly, one morning, he seemed to turn a corner in that he was out looking for his own grass, picking a little and drinking from the tub on his own. But, just as suddenly, he suffered a massive heart attack and died.

Pride had under 5% rotation of the pedal bones, which meant that if he had recovered he would have had most of his mobility back. So what happened? I was told that the septicemia associated with the laminitis had most likely caused damage to his heart and that had lead to the attack. Later, I was told that he actually had colitis as well and the treatments for the laminitis had caused a rupture in his bowel or intestines and that was what killed him. Nonetheless, I was devastated to lose such a beloved part of my family and vowed to find out every last bit of information regarding laminitis that I could.

After his death I read everything I could lay my hands on and found out about the research done by Australians such as Professor Chris Pollitt and at various overseas institutes. I never want to go through a similar experience again but, more importantly, I have realised that knowledge is much more powerful than ignorance. I have learnt to ask questions - not just the easy ones, but the hard ones too. Buying hay is no longer a case of simply taking what is offered but finding out when it was cut and exactly what it has in it. Feeding has become a process of carefully reading the analysis on the bag and being strict about giving amounts that are in relation to weight, age, type and activity. I have also learned not to be afraid to ask for help from the many offering services out there that can work with you to determine a feeding regime designed around a horse’s work, their paddock and your budget.

Finally, in the case of laminitis, I don’t think you can under-state the value of a good equine vet who can work on your horse with you - one you can talk to and he or she will talk back in language you can understand.”

Hoofbeats thanks Sonja Vandermark (nee Gardner) BSc. (Hons) from Kentucky Equine Research for her assistance in preparing this article. KER can be contacted on 1800 772 198

Part Two will cover treatment, ongoing management issues of the laminitic horse including shoeing , considerations for returning to the paddock (in relation to grass sugar content at different times of day and in different seasons), exercise, feeding and natural remedies to assist recovery.