Laminitis – A serious matter
It is undoubtedly one of the most dreaded conditions affecting horses: laminitis! It strikes suddenly and without warning, and is always associated with severe pain. And it is by no means only overweight ponies that are affected. Although it has long been known, is widespread and has been fairly well researched, it does not always seem clear exactly what triggered or contributed to the laminitis episode. Furthermore, the uncertain prognoses are a cause for concern for us horse owners.
But what exactly is laminitis? What are the triggers, causes and symptoms?
And what do prevention and feeding management involve?
What is laminitis?
Laminitis is an inflammation of the hoof corium. The hoof corium connects the bony hoof bone to the hoof capsule, which forms the externally visible hoof. The hoof corium has a lamellar structure and contains very fine blood vessels (capillaries). Inflammation leads to swelling and impaired blood flow within the hoof corium. The swelling causes pressure, which in turn causes the horse immense pain.

The inflammation can cause the navicular bone to become detached from the hoof corium and to sink towards the sole. In cases of advanced navicular bone sinking, it may be possible to see, on the underside of the hoof, the curve of the tip of the navicular bone pressing against the sole; in severe cases, this may even pierce through the sole. In addition to the sinking of the navicular bone, rotation of the navicular bone may also occur. The deep flexor tendon attaches to the back of the pastern bone. The constant pull of the flexor tendon causes the pastern bone to rotate backwards, which in turn is associated with severe pain. In the worst-case scenario, this can lead to the complete detachment of the hoof capsule (hoof slippage).
Inflammation is often triggered by endotoxins which are released, for example, in the gut or in the uterus of mares – that is, from a completely different part of the body – and enter the bloodstream, where they can then cause local inflammation of the hoof corium.
A basic distinction is made between acute and chronic laminitis, with the acute form always constituting a medical emergency.



Causes and symptoms
Laminitis can have various causes. Depending on the cause, a distinction is made between medication-induced laminitis, exercise-induced laminitis, starvation-induced laminitis, birth-related laminitis and feeding-related laminitis. Excessive or improper administration of medication (e.g. cortisone) can cause Drug-induced laminitis trigger. In the event of a Exercise-induced soreness Often only one hoof is affected, for example when the healthy hoof becomes overloaded because the other hoof has been rested for several days. In such cases, circulatory problems are the cause of the inflammation. Stress laminitis can also be caused by incorrect hoof trimming by the farrier or by running on ground that is too hard. This can lead to Labour pains It occurs when (parts of) the afterbirth remain in the uterus. This may be due to retained afterbirth or the afterbirth becoming detached. The part of the afterbirth remaining in the uterus begins to decompose, leading to the release of endotoxins, which in turn enter the bloodstream and can trigger inflammation of the hoof corium. A Starvation laminitis is caused by acidosis resulting from a lack of food and thus follows the same principle as feeding-induced laminitis. The Feeding-induced diarrhoea is likely to be the most significant factor in terms of quantity. Feeding-induced laminitis is usually triggered by an excess of readily available carbohydrates – namely starch and sugar. The horse has only a limited capacity for starch- and sugar-breaking enzymes in the small intestine. Whatever the small intestine enzymes cannot digest passes into the caecum and large intestine. There, the lactic acid-producing lactobacilli thrive in particular; they multiply rapidly due to the flood of starch and lower the pH level by producing lactic acid. This drop in pH value leads to the death of other intestinal bacteria that cannot cope with the acidic environment. As these dead microorganisms break down, they release endotoxins, which pass through the intestinal wall into the bloodstream and can trigger laminitis. Improper grazing practices can also lead to laminitis due to excessive intake of fructans from pasture grass. Certain pre-existing conditions or metabolic problems, such as Equine Metabolic Syndrome (EMS), PPID (Cushing’s syndrome), insulin resistance or simply being overweight, and their adverse effects are contributing factors and are usually associated with an increased risk of laminitis.
The symptoms of acute laminitis are extremely clear; unfortunately, however, it is difficult to recognise the early signs of laminitis. Early warning signs may include resistance when the farrier is working, increased lifting and lowering of the hooves, leaning back when the hoof is lifted, or an irregular gait. As these can occur for no apparent reason, they are not definitive warning signs. Acute laminitis then becomes apparent through the following symptoms:
- Obvious lameness or refusal to move
- Increased load on the feet, reduced load on the toes → shift of the centre of gravity backwards
- You may need to lie down to relieve pressure on your hooves
- Hot Hooves
- Increased pulsation in the arteries of the foot
Chronic laminitis is generally diagnosed approximately two to three days after the acute episode. X-rays may reveal sinking and/or rotation of the coffin bone. Lameness and apathy are observed. The hooves may feel cold, which is indicative of the typical circulatory disturbances. As the condition progresses, changes to the hoof capsule may occur:
- Horizontal grooves/ridges
- Concave hoof capsule shape
- Tuber formation
- Widening of the white line
Acute laminitis is always a medical emergency! The vet will treat the horse with anti-inflammatories, painkillers and blood thinners. It is important and advisable to cool the hooves as well. During an acute episode of laminitis, the horse should be fed nothing but hay (washed if necessary to reduce the sugar content) and a little straw: no concentrated feed, no pasture grass (no grazing!) and no treats to comfort the horse. This is where the horse owner’s responsible behaviour is required and essential. To relieve the pressure on the painful hooves, the horse should stand on a soft surface (a thick layer of bedding) and, where possible, should not be made to walk on hard ground. Exercise should not be forced.
In cases of chronic laminitis, the main aim is to relieve pressure on the painful toe. Special shoes fitted by the farrier shift the weight onto the heels and the ball of the hoof, thereby relieving pressure on the toe.
Otherwise, the therapeutic approach involves addressing the underlying causes, e.g. avoiding being overweight, using more effective contraception, etc., because Prevention is the best treatment.
Feed management
Feeding during an acute episode of laminitis is particularly restrictive, as described above. As the condition progresses, the treatment follows the same principles as those for prevention in horses at increased risk of laminitis. Starch and sugar should be kept to a minimum – i.e. a low-glycaemic diet. Hay and pasture grass can sometimes contain significant amounts of sugar, and in the case of pasture grass, climate-dependent fructan levels must also be taken into account. Overweight should be avoided, and overall, the energy content of the ration should be appropriate to the horse’s performance requirements.
Please note: a restricted diet for horses with laminitis or at risk of laminitis relates to high-energy feedstuffs, but not to micronutrient intake, which is just as important for horses with laminitis and may in some cases even be associated with an increased requirement. This means that a high-quality supply of minerals and vitamins should be a given. The trace element chromium, for example, is said to increase the insulin sensitivity of the relevant cell receptors and is therefore an important factor in cases of insulin resistance.
To minimise the risk of laminitis, we recommend:
Our low-glycaemic products (for horses with a sensitive appetite):
Our low-glycaemic products (for horses with normal to difficult appetites)
Click here for the scientific Study About Equigard & Glucogard
References:
Coenen, M. & Vervuert, I. (2020). Horse Nutrition. 6th, updated edition. Georg Thieme Verlag, Stuttgart.
Dyer, J., Merediz, E. F. C., Salmon, K. S. H., Proudman, C. J., Edwards, G. B., & Shirazi-Beechey, S. P. (2002). Molecular characterisation of carbohydrate digestion and absorption in the equine small intestine. Equine Veterinary Journal, 34(4), 349–358.
Frank, N. (2007). Diagnosis and management of insulin resistance and Equine Metabolic Syndrome (EMS) in horses. In: Applied equine nutrition and training. Arno Lindner (ed.), Wageningen Academic Publishers, pp. 107–125.
Gäbel, G. & Loeffler, K. (2018). Anatomy and Physiology of Domestic Animals. Ulmer Verlag. Stuttgart.
Lithersson et al. (2017). Laminitis: Risk Factors and Outcome in a Group of Danish Horses. Journal of Equine Veterinary Science 53, pp. 68–73.
Treiber, K. H., Kronfeld, D. S., & Geor, R. J. (2006). Insulin resistance in equids: a possible role in laminitis. The Journal of Nutrition, 136(7), 2094S–2098.
Wylie et al. (2012). Risk factors for equine laminitis: A systematic review of published evidence with quality assessment. The Veterinary Journal 193, pp. 58–66.
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