This week we continue to look at laminitis and discuss the different factors implicated in the disease process. To read about what laminitis is and what it looks like please click here.
Causes of Laminitis
Basically, there are 3 causes of laminitis which can be classed as:
- Limb overloading (including concussive forces)
It is now recognised that 90% of laminitis cases have an underlying endocrinopathic (hormonal) cause with laminitis being a secondary consequence of the horse/pony having equine metabolic syndrome (EMS) and/or Cushing’s disease (pars pituitary intermedia dysfunction, PPID). The remaining 10% of cases are the result of either sepsis (an excessive response of the immune system to infection) or excessive loading e.g. supporting limb laminitis when a horse is non-weight bearing on one limb or sustained work on very hard ground. The mechanism by which grain overload causes laminitis is inflammatory as the presence of large quantities of starch in the large intestine causes massive shifts in gut flora and absorption of endotoxin into the bloodstream which overstimulates the immune system. Other than excessive loading laminitis from, which can occur in just one overloaded limb, laminitis looks the same regardless of cause.
It has now been shown that normal treatment doses of corticosteroids do not cause with laminitis in adult horses unless there is underlying hormonal or severe inflammatory disease.
Equine Metabolic Syndrome
EMS is characterised by obesity, abnormal regulation of insulin concentrations (insulin dysregulation) and laminitis. This includes hyperinsulinaemia (too much insulin in the blood) and insulin resistance (when the body becomes less responsive to insulin). Increased levels of insulin in the blood and reduced insulin sensitivity of cells to insulin predispose the horse to laminitis. The exact mechanism by which insulin dysregulation predisposes to laminitis is still not clear but laminitis can be induced experimentally within several days by very high blood levels of insulin. Chronically high levels of insulin in the blood results in the blood vessels in the foot constricting which reduces blood flow to the foot so the delicate laminae become starved of oxygen and nutrients. This starvation causes local inflammation and eventually cell death. If sufficient laminae die, the pedal bone tears away from the hoof capsule allowing rotation and sinking towards the sole of the foot.
Native British breeds have a genetic predisposition for EMS as they possess a ‘thrift’ gene which gave them the evolutionary advantage to gain sufficient weight whilst forage was plentiful in the summer to survive a harsh winter with little pasture. Most native breeds are no longer managed extensively on poor pasture which therefore effectively leads to their chronic overnutrition and obesity. Non-native breeds are more tolerant to these improved pastures, high plains of nutrition and obesity without developing laminitis because they do not have this ‘thrift’ gene.
As a horse puts on excessive amounts of weight, the adipose tissue (fat) becomes overwhelmed so fat is then stored in other organs such as in the muscle and liver. The liver and muscle cells play an essential role in the control of blood sugar levels by removing sugar from the bloodstream for storage in response to increased insulin levels post-feeding. If these liver and muscle cells become full of fat, the normal response to insulin is disrupted and they become unable to respond to insulin. This is what we term ‘insulin resistance’. As a result, blood sugar stays high and the pancreas produces even more insulin (hyperinsulinaemia) to try and remove excess sugar from the blood stream.
Clinical signs of EMS include excess weight, which is often seen deposited in regional fat pads such as the neck crest area (Fig. 1). EMS horses/ponies are very good do-ers and are usually middle-aged horses (normally 5 to 15 years old). Obesity is the precursor to EMS but not every horse which is fat has EMS. EMS can be diagnosed by measuring blood insulin concentration and an oral sugar challenge to investigate if insulin dysregulation affects how sugar is processed in the body.
Cushing’s Disease (PPID)
Cushing’s disease is caused by an overgrowth and dysfunction of part of the pituitary gland within a horse’s brain. This overgrowth is caused by loss of nerves, and therefore neurochemicals, that regulate the gland due to oxidative damage associated with aging. This creates an imbalance of hormones which have multiple effects within the body including altering concentrations of insulin and cortisol.
Clinical signs of Cushing’s disease include a long curly coat, excessive drinking and urination, abnormal fat stores, weight and muscle loss, and increased predisposition to infections in an older horse. The long, curly hair coat (Fig. 2) that many people associate with Cushing’s disease is usually a very late sign of the disease and many horses have Cushing’s disease without obvious external clinical signs. Studies have shown that 20% of horses over 16 years old have evidence of Cushing’s disease on blood tests. It is therefore paramount that any older horse/pony presenting with laminitis is investigated for Cushing’s disease.
Horses can develop laminitis due to severely overloading one limb from a non-weightbearing lameness of the opposite limb e.g. fracture. In these situations, it is important to give appropriate support to the limb bearing additional weight using support bandages and providing sufficient analgesia to encourage weightbearing of the injured leg. The most famous case of this was the American racehorse Barbaro who sustained a fracture of one hindlimb, which was successfully repaired, but developed severe laminitis in the other hindleg which necessitated euthanasia.
Excessive concussion in the feet from repeated riding on very hard ground can also cause overload laminitis.
Severe inflammation within the body can lead to laminitis. One form of this is starch overload when horses eat large quantities of starch-rich grain in one go. This leads to the presence of non-digested starch in the hind gut where rapid fermentation causes massive changes in the gut, ultimately resulting in gut damage, absorption of toxins and severe diarrhoea and laminitis. Other causes include difficult colics and colitis (diarrhoea) where the gut is severely damaged allowing absorption of toxins. Septic conditions like pleuropneumonia and retained placenta (afterbirth) causing massive stimulation of the immune response can also lead to inflammatory laminitis. Common to all of these is severe systemic illness and absorption of toxins into the blood which have wide-reaching effects in the lamellae of the hoof.
Next week: Treatment of laminitis.