Laminitis is a crippling disorder of the feet, resulting from damage to the sensitive soft tissues known as ‘laminae' which connect the skeletal pedal bone to the inside of the hoof wall. There are about 600 interlocking laminae in each hoof and they provide the support for the weight of the horse.
Founder is the physical change that occurs within the hoof as a result of laminitis. When the laminae are damaged their supporting function is weakened. This may allow the pedal bone within the hoof to 'sink' downwards and ‘rotate' backwards due to the weight of the horse pushing downwards on the bone and the upward pull of the flexor tendon which attaches to the base of the bone. Damage to the laminae can lead to abnormal hoof growth with obvious ‘growth rings‘, long toes, flat soles and separation of the sole from the hoof wall at the white line (often followed by ‘seedy toe').
One of the more common causes of laminitis is overeating of feeds rich in ‘soluble carbohydrates’ also referred to as non-structural carbohydrates or NSC (mainly found in cereal grains and lush/stressed pasture).
Laminitis can also result from endocrine disorders such as equine Cushing’s disease or equine metabolic syndrome. Gastrointestinal problems such as colic, diarrhoea, retained placenta after foaling, metritis, pneumonia, peritonitis, enteritis etc. can also result in laminitis. Laminitis can also be caused by certain drugs and management factors such as standing for long periods in trucks or floats and by excessive work on hard surfaces for example hoof concussion from galloping or jumping on hard surfaces.
Feeds rich in starch and sugar/fructan can cause a digestive upset in the large intestine. Mammals have no enzyme to digest fructan so this passes undigested directly into the hindgut (caecum and colon). An excess of grain consumption will also ultimately overflow into the hindgut.
ln the hindgut, excess starch or fructan undergoes rapid fermentation to lactic acid, with many normal bacteria, unable to survive the acid or low pH conditions- As the acid builds up, it damages the gut lining and toxic substances including bacterial endotoxins and other toxins are released and enter the bloodstream. Once in the bloodstream, the toxins appear to either directly or indirectly stimulate increased production and activity of certain enzymes called matrix metalloproteinases (MMPs). The over activity of these enzymes destroys the laminae, resulting in the onset of laminitis.
High heart rate, rapid breathing, increased digital pulses, fever, sweating, colic, diarrhoea and depression are signs of horses battling grain overload.[i]
No - All horses can develop laminitis and founder. Although pasture-associated laminitis is more common in ponies- Certain breeds are known to have a higher risk of developing laminitis. Obese horses and ponies are more likely to experience pedal bone rotation and permanent hoof damage due to the extra weight their feet have to support even in a relatively mild case of laminitis.
Surveys have shown that valuable show and equestrian horses are also at risk of developing laminitis even when fed on hard feeds containing relatively small amounts of grain- It is also now known that many racehorses have low-grade laminitis, which may only cause mild sore footedness. A scratchy gait and separation at the ’white line‘. Studies have shown that low grade laminitis can significantly affect racing performance.[ii]
Yes. Once a horse has foundered it is likely to suffer from continued repeated attacks. These horses can become very sensitive to the carbohydrates in feed, which may trigger a founder episode with only small amounts of grain or lush pasture. Symptoms of laminitis can also occur if the horse’s hooves are not kept correctly trimmed or the animal is worked on hard surfaces.
Of all the common lameness problems that affect horses and ponies, laminitis and founder are most feared by horse owners. Horses that have suffered from laminitis remain susceptible to the disease.
The first step is to understand what components of the horse’s diet create the risk of laminitis. What do grains and lush pastures have in common? Cereal grains contain abundant amounts of starch – a form of carbohydrate that is broken down to simple sugars such as glucose in the digestive tract. Lush green grass can have high levels of sugars/fructans that are directly available in the digestive tract.
Therefore careful management is called for – especially after rain. The new grass growing in the cooler times of late winter and spring contains far higher levels of the danger molecule ‘fructan’ than grass growing at warmer, drier times of the year. Growing grasses are highly palatable to grazing horses due to the high levels of carbohydrates contained within the leaves. This carbohydrate or ‘fructan’ is the causative factor in the development of pasture-associated laminitis and. when ingested in significant amounts, will cause a severe bout of laminitis. The re-growth following drought-breaking rain can also contain dangerous levels of fructan, even in what seems to be a small amount of grass.
Therefore, even on starvation paddocks, the amount of fructan ingested by a horse can be enough to cause laminitis.
Restricting horses’ intake of lush green grass and grain can reduce the rate or’ lactic acid production.
Even if you have never experienced laminitis in your horse before, now is the time to make preventative changes in order to minimise your horse's chances of succumbing to this potentially fatal disease.
Metabolic disorders such as EMS (Equine Metabolic Syndrome] and Cushing‘s Disease (pituitary pars intermedia dysfunction - PPID) are associated with increased risk of laminitis. In the case of EMS, the underlying issue is a result of hormonal imbalance related to insulin metabolism. Insulin resistance appears to be one of the criteria defining EMS, with clinical signs including obesity-associated laminitis and abnormal fatty deposits or regional adiposity.
PPID on the other hand, is fairly common in older horses (generally over 15 years) and is a disease of the pituitary gland. Clinical signs include laminitis, shaggy coat, undue sweating, lethargy, loss of topline, increased thirst and urination.
Lack of proper management factors such as stress brought on by prolonged transport, poor hoof care and shoeing, sheer neglect and riding horses on hard surfaces may also lead to laminitis.
Common gastrointestinal factors that often precede laminitis are severe colic, retained placenta in post-foaling mares, metritis, septicaemia conditions, pleuritis/pneumonia (lung inflections), enteritis etc.
Laminitis most commonly affects the forefeet of the horse. This is because approximately 65% of the horse's weight is carried through the forequarters. However, laminitis can also occur in the hind feet. Usually both front feet are affected, but laminitis may also occur only in one hoof or in all four feet simultaneously.
The common clinical signs of laminitis are listed below. It is important to note that affected horses may show all of these signs or only some of them.
[i] Watts, K., & Pollitt, C. (2010). Equine Laminitis: Managing Pasture to Reduce Risk. Rural Industries Research and Development Corporation (RIRDC) publication no: 10/063, Australia.
[ii] Linford, R., O'Brien, T., & Trout, D. (1993). Qualitative and morphometric radiographic findings in the distal phalanx and digital soft tissues of sound thoroughbred racehorses. American journal of veterinary research, 54(1), 38-51.