Quick summary:

Laminitis is an inflammatory condition of the tissues (laminae) that bond the hoof wall to the pedal (coffin) bone in the horses hoof. Although it was traditionally considered a disease of fat ponies, new research illustrates that laminitis can be triggered by a variety of metabolic or physical causes – it can affect any horse, of any age or sex, at any time of the year. Once there is weakening of the supporting lamina within the hoof, there can be painful tearing of the support structure suspending the pedal bone within the hoof. Without prompt treatment, the pedal bone can drop or rotate downwards.

Anatomical Insight

In the healthy horse the pedal bone (PI or coffin bone or distal phalanx) is held securely in position within the hoof capsule by laminae. Some 600 insensitive laminae project from the inner surface of the hoof wall and interlock with a corresponding number of sensitive laminae on the surface of the pedal bone. Each lamina consists of 100 – 200 secondary microscopic laminae which further increase the surface area for attachment. Laminitis is the inflammation of these sensitive laminae, and can lead to disruption of the bond between the sensitive and insensitive laminae.

Unless action is taken to halt the progress of the condition, the combined effects of the horse’s weight pushing down and the upward pull of the deep digital flexor tendon on PI exacerbated by the horse’s movement will cause the sensitive and insensitive laminae to separate. This in turn will lead to PI rotating and/or sinking within the hoof capsule, and, indeed, may lead to PI breaking out of the sole itself (“founder”). This process is extremely painful and, unless arrested early, is catastrophic, leading to euthanasia on humane grounds. It should be remembered that once the horse is showing signs of pain and lameness, damage within the hoof capsule has already occurred and immediate action should be taken to minimise further progress of the condition.

Causes (Pathogenesis)

The inflammation of the sensitive laminae of the hoof is a severely painful condition affecting all ungulates (hooved animals) and is notorious in the horse. Despite extensive research, the cause is unknown. THere are three theories:

  1. Inflammatory – cytokines cause matrix metalloprotease overproduction leading to tissue damage
  2. Vascular – capillary bypass shunts lead to tissue ischaemia and damage.
  3. Metabolic – overproduction of insulin leads to tissue damage

It is reasonable to assume that all of these mechanisms have a role to play. They can be triggered mechanically, e.g. by excessive work on hard surfaces or by overproduction of endotoxins in the gut. Endotoxins are toxic by-products from the cell walls of dead gut bacteria which leak into the bloodstream. So, an excessive release of endotoxins can trigger the above mechanisms in the hoof. Increased breakdown of gut bacteria (the horse is a large intestine fermenting herbivore) results from eating too much readily digestible carbohydrate. This may be in cereal-based hardfeed, rich grass or stressed grass (e.g. after recent frost). Alternatively, gut stasis, e.g. from colic, may lead to more endotoxin release. Endotoxins in the blood are usually controlled by the horse’s immune system. This can be suppressed by increased blood cortisol and related metabolic imbalances. Equine Metabolic Syndrome and Cushing’s Disease pre-dispose horses to develop laminitis. High levels of blood insulin is an important pre-disposing factor.

If the triggers for the laminitis can be removed, e.g. stop grazing frosted/new grass, reduce movement and treat Cushing’s disease, the rotation and sinking may stop and the horse can be saved. 


  1. Breed type  Laminitis afflicts native ponies, and certain family lines within each breed. Native ponies have evolved on poor grazing, gaining weight and building up fat deposits during the summer so that they can survive long winters with snow-covered ground and sparse forage. The use of paddocks, hard feed, forage and rugs have prevented the over-winter natural weight loss occurring.
  1. Metabolic Syndrome and disease Fat deposits, e.g. on the mane crest and around the kidneys are indicators that the horse/pony may be insulin resistant. High blood insulin triggers the mechanism for laminitis either directly or indirectly. The best control for this is diet and exercise. Long term “insulin resistance” can lead to Cushing’s disease, where pituitary gland overproduction of adrenocorticotrophic hormone (ACTH) causes increased cortisol production by the adrenal glands. Insulin resistance and pre-deliction to Cushings Disease increases with age. Some breeds such as New Forest, Connemara, Welsh, and certain Arab family lines are predisposed to the condition, so watching the diet and exercise of these breeds and detecting/treating metabolic conditions is the best way to prevent laminitis.
  1. Controlling grazing and diet Overfeeding of cereal-based hardfeed and eating new grass can cause laminitis. It is essential to avoid spring grass, summer grass on a sun/rain cycle and the “autumn flush” in native ponies and predisposed animals. Restricted grazing, using electric fencing, starvation paddocks and grazing muzzles should be used.
  1. Foot care Regular hoof trimming to keep the heels down and the toe pulled back is important. This reduces the impact of the concussive forces of movement and the pull from the DDFT. Assessing the hoof quality and angle at the time of trimming in laminitically disposed animals is essential – inflamed laminae cause growth rings/grooves to grow down the hoof and, along with angle changes, may be indicative of sub-clinical laminitis. NB a hoof takes nine months to grow from the coronary band to the ground.


Laminitis should be considered as an potential diagnosis for any lameness. Although the front feet are the most commonly affected, it is not unusual to see early laminitis in a single back foot and it may take several days before the diagnosis is clear. Typical symptoms include rocking back on the heels, shifting weight, lying down, hot feet with throbbing blood vessels (digital pulses) and even sweating and a temperature (due to the pain).


Early recognition increases the chances of a full recovery. In acute cases “icing” the foot may be effective in the first 24 hours. Similarly the use of peripheral vasodilators including acepromazine or isoxuprine may help early on. Later, acepromazine may help keeping normally active horses quiet in the box. Removal of shoes, taping on foot pads, and/or deep, spongy bedding to the door all help with symptomatic relief. Reduce the energy in the diet, e.g. stop hardfeed and use soaked hay at less than half the usual poundage; soaking should be for more than 2 hours (preferably 12) as this leaches the sugars from the hay. Purgitives may be useful in hardfeed-induced laminitis. Non-steroidal anti-inflammatories (NSAIDs), intravenously then oral are important to control the inflammation and pain.

X-rays and remedial farriery

X-rays should be taken once controlling measures have been in place for a suitable period, e.g. between one and three weeks after onset, at the discretion of the vet. This may well be subject to economic constraint. It should be noted that rotation and sinking may continue for several weeks before “stabilisation”. The angle of rotation of the pedal bone in relation to the dorsal hoof wall (they should be parallel) and the “sinking distance” of PI below the coronet are important prognostic indicators. Gas shadows may be visible on x-ray. X-rays help with the trimming of the hoof with respect to cutting back the dorsal hoof wall and lowering the heels.

Remedial shoes may include a reverse “normal shoe”, square-toed shoes with plastic frog supports and cushioning material, plastic “Imprint” shoes, or more traditional heart bar shoes. The shoe choice must result from discussion between the vet, farrier, owner and/or yard manager. Once the horse is walking sound and off painkillers, it may be walked and gradually re-exposed to limited turnout.


It may be several months before a laminitic pony or horse can be ridden again. Once the laminae are damaged, the bond between the hoof and pedal bone remains weakened. Avoidance of repeat episodes and continued vigilance by the owner, keeper, farrier and vet is essential

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