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Welcome to the Equestrian Outreach Laminitis or Founder Page
Laminitis or Founder Overview
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Laminitis (Commonly called Founder, from the nautical term "to sink") is a disease of the digital laminae of the hoof (term for the foot of a horse). It is a debilitating disease and is most well known in horses and cattle.
Description: The coffin bone is suspended within the hoof capsule by means of two types (Dermal and Epidermal) of tendon like structures know as the digital lamina. The digital Laminae are responsible for suspension of the axial skeleton of the animal within the hoof and dissipate concussive forces during locomotion. There are about 600 pairs of interleaved Laminae: the epidermal Laminae attached to the hoof wall and the dermal Laminae attached to the coffin bone.
Laminitis results from a compromise of this interaction, the mechanism of which remains unclear and is currently the subject of much research. Laminitis literally means inflammation of the Laminae, and while it remains controversial whether this is the primary mechanism of disease, evidence of inflammation occurs very early in some instances of the disease. Once the Laminae are compromised the coffin bone 'sinks' into hoof capsule. this is an intensely painful process which in later stages causes the coffin bone to rotate, crippling the animal.
Cause: There are a large number of processes which attack the Laminae (see partial list below) The one that is most important in this article is the relationship between man made fertilizers which contain large amounts of nitrogen and the effect of certain types of potentially-toxic non-protein nitrogen (NPN) compounds have on the digestive system and lead to diseases such as Laminitis.
Diagnosis: Early diagnosis is essential to effective treatment. However, early outward signs may be fairly non-specific. Careful physical examination typically is diagnostic, but radiographs are also very useful.
- Increased temperature of the wall, sole and/or coronary band of the foot.
- A pounding pulse in the digital palmar artery. (The pulse is very faint or undetectable in a cold horse, readily evident after hard exercise.)
- Visible trembling
- Increased vital signs and body temperature
- Flared Nostrils
- Walking very tenderly, as if walking on egg shells
- Repeated "easing" of affected feet
- The horse standing in a "founder stance" (the horse will attempt to decrease the load on the affected feet). If it has laminitis in the front hooves, it will bring its hindlegs underneath its body and put its forelegs out in front called "pointing"
- Tendency to lie down, whenever possible or, if extreme, to remain lying down.
Cause List (Partial):
- Carbohydrate Overload: One of the more common causes. Current theory states that if a horse is given grain in excess or eats grass that is under stress and has accumulated excess non-structural carbohydrates (NSC, i.e. sugars, starch or fructan), it may be unable to digest all of the carbohydrate in the foregut. The excess then moves on to the hindgut and ferments in the cecum. The presence of this fermenting carbohydrate in the cecum causes proliferation of lactic acid bacteria and an increase in acidity. This process kills beneficial bacteria, which ferment fiber. The endotoxins and exotoxins may then be absorbed into the bloodstream, due to increased gut permeability, caused by irritation of the gut lining by increased acidity. The endotoxaemia results in impaired circulation, particularly in the feet. This results in laminitis.
- Nitrogen Compound Overload: Herbivores are equipped to deal with a normal level of potentially-toxic non-protein nitrogen (NPN) compounds in their forage. If, for any reason, there is rapid upward fluctuation in levels of these compounds, for instance in lush spring growth on artificially fertilized lowland pasture, the natural metabolic processes can become overloaded, resulting in liver disturbance and toxic imbalance. For this reason, many avoid using artificial nitrogen fertilizer on horse pasture. If clover (or any legume) is allowed to dominate the pasture, this may also allow excess nitrogen to accumulate in forage, under stressful conditions such as frost or drought. Many weeds eaten by horses are nitrate accumulators. Direct ingestion of nitrate fertilizer material can also trigger laminitis, via a similar mechanism.
- Colic: Laminitis can sometimes develop after a serious case of colic, due to the release of endotoxins into the blood stream. Refer to Carbohydrate Overload.
- Lush Pastures: When releasing horses back into a pasture, after being kept inside (typically during the transition from winter stabling to spring outdoor keeping), it is important to re-introduce them gradually. Feed horses before turning them out and limit the amount of time outside (45 minutes to an hour at first, gradually increasing the amount of time) and decrease the amount fed to them beforehand, as the season progresses. If a horse consumes too much lush pasture, after a diet of dry hay, the excess carbohydrate of grass can be a shock to its digestive system. If the horse is fed beforehand, it will not eat as much fresh grass when turned out and will be less likely to founder. It is also true that ponies are much more susceptible to this form of laminitis than are larger horses.
- Frosted Grass: Some cases of laminitis have occurred after ingestion of frosted grass. The exact mechanism for this has not been explained but sudden imbalance of the normal bowel flora can be surmised, leading to endotoxin production.
- Untreated Infections: Systemic infections, particularly where caused by bacteria, can cause release of endotoxins into the blood stream. A retained placenta in a mare (see below) is a notorious cause of laminitis and founder.
- Insulin Resistance: Laminitis can also be caused by insulin resistance in the horse (See also Equine Metabolic Syndrome, below. Insulin resistant horses tend to become obese very easily and, even when starved down, may have abnormal fat deposits in the neck, shoulders, loin, above the eyes and around the tail head, even when the rest of the body appears to be in normal condition. The mechanism by which laminitis associated with insulin resistance occurs is not understood but may be triggered by sugar and starch in the diet of susceptible individuals. Ponies and breeds that evolved in relatively harsh environments, with only sparse grass, tend to be more insulin resistant, possibly as a survival mechanism. Insulin resistant animals may become laminitic from only very small amounts of grain or "high sugar" grass. Slow adaptation to pasture is not effective, as it is with laminitis caused by microbial population upsets. Insulin resistant horses with laminitis should be removed from all green grass and be fed only hay that is tested for Non Structural Carbohydrates (sugar, starch and fructan) and found to be below 11% NSC on a dry matter basis. Soaking hay underwater may remove excess carbohydrates and should be part of a first-aid treatment for any horse with laminitis associated with obesity or abnormal fat deposits. This can have the effect of depleting the hay of soluble minerals and vitamins, however, so care with dietary balance is important.
- Vasoactive Amines: The inflammatory molecule histamine has also been hypothesized as a causative agent of laminitis. However, contradictory evidence has demonstrated that the role of histamine in laminitis has not been conclusively established.
- Mechanical Separation: Commonly known as road founder, this occurs when horses with long toes are worked extensively on hard ground. The long toes and hard ground together contribute to delayed break over and hence mechanical separation of the Laminae at the toe. Historically this was seen in carriage horses. These horses were bred for heavy bodies and long slim legs with relatively small hooves; their hooves were trimmed for long toes (to make them lift their feet higher, enhancing their stylish "action"); and they were worked at speed on hard roads. Road founder is also seen in overweight animals, particularly when hooves are allowed to grow long: classic examples are ponies on pasture board in spring, and pregnant mares.
- Poor Blood Circulation: Normal blood circulation in the lower limbs of a horse depends in part on the horse moving about. Lack of sufficient movement, alone or in combination with other factors, can cause stagnant anoxia, which in turn can cause laminitis.
- Static Laminitis: A horse favoring an injured leg will both severely limit its movement and place greater weight on the other legs. This sometimes leads to static laminitis, particularly if the animal is confined in a stall.
- Transport Laminitis: sometimes occurs in horses confined in a trailer or other transportation for long periods of time. Historically, the most extreme instances were of horses shipped overseas on sailing ships. However, there is some evidence that the continual shifting of weight required to balance in a moving vehicle enhances blood circulation. For this reason, some horsemen recommend trailering as an initial step in rehabilitation of a horse after long confinement.
- Cold Weather: Laminitis has been observed following an equine standing in extreme conditions of cold, especially if there is a depth of snow.
- Hot Conditions: Laminitis has also followed prolonged heating such as may be experienced from prolonged contact with extremely hot soil or from incorrectly-applied hot-shoeing.
- Pituitary Pars Intermedia Dysfunction (PPID): is common in older horses and ponies and causes an increased predisposition to laminitis.
- Peripheral Cushing's Disease: Peripheral Cushing's disease (or more properly, Equine Metabolic Syndrome) is an area of much new research and is increasingly believed to have a major role in laminitis. It involves many factors such as cortisol metabolism and insulin resistance. It has some similarities to type II diabetes in humans (see also insulin resistance, described above). In this syndrome, peripheral adipocytes (fat cells) synthesise adipokines which are analogous to cortisol, resulting in Cushings-like symptoms.
- Retained Placenta in Mares: It is common practice, in horse-breeding establishments, to check by careful inspection that the entire placenta has been passed, after the birth of a foal. It is known that mares that retain the afterbirth can founder, whether through toxicity or bacterial fever or both.
- Drug Reactions: Anecdotally there have been reports of laminitis following the administration of drugs, especially in the case of corticosteroids. The reaction however may be an expression of idiosyncrasy in a particular patient as many horses receive high dose glucocorticoid into their joints without showing any evidence of clinical laminitis.
- No evidence exists to show the mechanism by which glucocorticoids may trigger laminitis in the horse nor is there any research definitely proving a causal link between the two.
- Exposure to Agrichemicals: Even horses not considered to be susceptible to laminitis can become laminitic when exposed to certain agrichemicals. The most commonly-experienced examples are herbicide and synthesized nitrate fertilizer.