Laminitis In The Equine

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Written By Dr. Kris Hiney

Earlier we posted an article on the typical causes of laminitis and some feeding strategies that may help in preventing laminitis (Feeding Horses for the Prevention and Management of Laminitis).  We also discussed how we might approach feeding a horse which has already experienced  laminitis.  This month we will begin to delve deeper into the causative factors of laminitis and how to prevent its development.

Remember that laminitis is actually a systemic disease, with just the symptoms being visualized within the hoof.  Some insult to the horse’s system creates an alteration in circulation, ultimately leading to tissue damage of the sensitive laminae.   This period of time, referred to as the development phase or prodromal phase, includes the actual insult prior to the development of symptoms.    It is thought to be due to some change within the vasculature, that leads to ischemia, or lack of blood flow to the digit.  Whether it is a lack of nutrients or oxygen due to the decreased blood flow, tissue damage or death results.  This initial insult is then followed by the acute phase of laminitis.

In the acute phase, blood flow returns to the foot, typically at an increased rate, as this is the body’s normal response to tissue injury.  Even this reperfusion response can cause tissue damage.  This is when the owner now recognizes the development of symptoms. The horse will appear very stiff and reluctant to move, and may even lie down.  A particular stance may be assumed by the horse as he appears to rock back on the hindquarters and place the forefeet forwards in order to limit weight bearing.  Due to the pain and anxiety the horse is experiencing, his heart rate and respiration rate may both be elevated.  Finally, the owner may even be able to detect an increase in temperature of the hoof wall and a bounding or throbbing digital pulse.

If permanent changes to the architecture of the foot occur, whether in PIII displacement, permanent changes to the normal lamellar architecture of hyperkeritization of the hoof wall, the horse has entered into the chronic phase. These horses are typically more susceptible to recurrent episodes of laminitis. Diet restrictions and specialized hoof care are typically required to allow the horse to lead a comfortable life (Feeding Horses for the Prevention and Management of Laminitis).
Obviously laminitis can be a devastating disease for the owner, and most would strive to prevent the disease, rather than address a symptomatic horse. If we look more closely at the causative factors in these alterations to circulation of the horse’s digit, we may be able to do a better job at identifying horses at risk.
We will begin with a review of pasture associated laminitis, which has been addressed in previous articles (Feeding Horses for the Prevention and Management of Laminitis and Carbohydrates III: Metabolic Syndrome). Remember that pastures grow more rapidly at certain times of the year, and may store their energy as different types of polysaccharides depending on the species of the plant. Frequently fructans are noted as the culprit in causing laminitis. Fructans are found in greater quantities in cool season grasses, as well as during periods where photosynthesis is favored over plant growth. As fructans contain beta bonds, which are not digested enzymatically by the equine small intestine, they pass through the tract and arrive at the large intestine where they then undergo bacterial fermentation. Other types of carbohydrates may act similarly, including sugars and starches which escape the small intestine undigested (the classic carbohydrate overload model of the horse in the grain bin), as well as other types of carbohydrates that may be rapidly fermented (pectins, resistant starches etc). (For more information on carbohydrates, please revisit Carbohydrates: Definitions and Relationship to Equine Diseases.)

In this first model of carbohydrate/rapidly fermentable fiber overload, too much of this rapidly fermentable material reaches the hindgut of the horse. These feedstuffs favor the proliferation of a particular bacterial population. These bacteria produce more lactate as their excretory waste. Excess lactate production lowers the pH of the hindgut which allows the mucosal cell wall to become permeable. In addition, too low of a pH stresses the bacteria causing them to either die or release endotoxins. Furthermore, altering the bacteria’s environment also changes their metabolism, releasing vasoactive amines into the hindgut. As the gut wall becomes more permeable, these toxins and amines are able to cross the mucosal wall and enter the bloodstream of the horse, where they then can exert their effects at the level of the hoof.

Horses which need to be restricted from pasture typically include ponies, as they are highly susceptible to laminitis.  In addition, any horse that has a history of laminitis, or has been diagnosed with PPID (pituitary pars intermedia disfunction)(Carbohydrates III: Metabolic Syndrome) should be grazed with care.  Horses with elevated insulin levels, or insulin resistant horses, also have a greater sensitivity to pasture associated laminitis, due to the influence of insulin on the vasculature of the horse.  Hyperinslulinemia increases the production of endothelin-1, and down regulates the production of nitric oxide.  A decrease in nitric oxide production has been linked to an elevation of homocysteine.  Incidentally, elevations in blood homocysteine are also linked to heart disease in humans. There has even been a suggestion, although with no scientific data to support this theory, that excessive supplementation of sulfur amino acids to horses with insulin resistance is unwarranted.  Typically sulfur amino acids (ie methionine) are included in hoof supplements, and homocysteine originates from methionine metabolism.   To further confuse the issue, it does appear that individuals are more susceptible to this disease, even if they are the same age, sex, breed and are managed the same as non-effected individuals.

Obviously preventative measures aimed at reducing carbohydrate related laminitis issues center on diet management. Certainly it is not practical or even advisable to state that all horses must be kept away from pastures. However, knowledge of which horses are susceptible to pasture associated laminitis is key. Once these individuals are identified, they should be placed on a principally harvested forage diet. The forage chosen should have very little rapidly fermentable material. However, horse’s which do not have these susceptibilities can continue to be managed with relative ease.
Next month we will continue to discuss laminitis at a more detailed tissue level, and address further strategies to limit your horse’s chances of acquiring this disease.

Feeding Horses for the Prevention and Management of Laminitis

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Written By Dr. Kris Hiney

Nothing is more devastating to the horse owner than to have a treasured partner be afflicted by the painful, crippling disease of laminitis. Laminitis can be a debilitating disease that may ultimately result in the death of the horse or humane euthanization. Unfortunately there are so many factors that can manifest in development of this syndrome that it can be difficult to sort through.
To understand the development of laminitis one should really understand the physiology of the equine foot. Essentially the hard keratinized tissue which forms the hoof wall is held to the soft tissue by the interdigitation between the sensitive and insensitive laminae. The insensitive laminae (seen here in Figure 1) is formed in vertical sheets on the inside of the hoof wall. 
Figure 1. An interior view of a horse’s hoof with the soft tissues removed. 1b. A schematic of the vertical lines of insensitive laminae lining the interior of the horse’s foot.
Connecting to the insensitive laminae is the sensitive laminae, which is living tissue requiring an adequate blood supply of oxygen and nutrients to survive. When an alteration of blood flow or a vascular insult occurs inflammation or even death of the sensitive laminae can occur. The sensitive laminae ultimately stabilize the internal structures of the horse’s hoof, including the third phalanx (or coffin bone). When this stable connection is lost, the pull of the deep digital flexor tendon on the base of PIII rotates it out of place. This condition is referred to as chronic laminitis or founder.
Figure 2. The sensitive laminae which connect the hoof wall to the horse’s foot.

Figure 3. A foundered hoof where PIII has rotated out of place due to the pull of the deep digital flexor tendon.
 
There are many reasons why blood flow can be disrupted to the equine digit. Laminits is often a systemic disease which is only visualized in the foot. While digestive issues lead the list of causes of laminitis there are other physical insults which can occur as well. When procuring wood shavings from a reputable dealer, care should be taken never to include those of the black walnut tree. These shavings contain the chemical juglone, actually a toxin which can kill other plants in the black walnut environment. Other physical causes are concussive trauma, from being ridden on hard surfaces resulting in decreased blood flow to the foot, and excessive loading (i.e., one limb is severely lame resulting in extra loading to the sound limb). Endotoxemia, such as what might be seen in a mare with a retained placenta, may also result in the development of laminitis.
 Nutritionally, a whole series of gastric insults can alter blood flow to the foot.  These include a carbohydrate overload (the classic example of the horse breaking into the feed bin) which leads to an alteration of fermentation in the hindgut.  In order to prevent starch from escaping enzymatic digestion in the small intestine and escaping to the hind gut, it is recommended to avoid a starch intake of more than 2-4 g/kg of body weight per meal. Therefore, a 500 kg horse should receive no more than 1-2 kg of starch per meal.  Pasture grasses have also long been known to precipitate bouts of founder, but typically only in susceptible populations. Ponies, and horses with thrifty genotypes are the most likely to suffer from pasture-associated laminitis. It is believed to be caused by a high level of fructans, although the quantity of fructans required to cause laminitis is unknown. Fructan content is known to vary with the time of year, with a higher content seen in the spring, when most pasture-associated laminitis occurs. Horses which are susceptible to pasture-associated laminitis should also limit their intake of pasture grass in the afternoon, when photosynthesis throughout the day has resulted in a higher level of fructans in the plant. The levels of water soluble carbohydrate gradually decline through the night, making grazing in the morning relatively safer. As the majority of horses which develop laminitis due so on pasture, rather than through the owner feeding excessive concentrates, at least some thought or caution should be used when grazing horses. Ideally horses should be introduced gradually to consuming fresh grass, and susceptible horses’ grazing should be limited to when fructan concentrations are at their minimum.
If a horse does develop chronic laminitis, unfortunately there is little the owner may do nutritionally to manage the horse. Obviously exposure to pasture grasses at peak times of fructan concentration should be avoided. Also, the horse should be managed to lower body weight to decrease the mechanical load on the laminae. Low energy forage should be the primary feed for the foundered horse. However, because low energy forages will typically be deficient in protein, minerals and vitamins, it is important to ensure that the horse is supplemented with a low energy concentrate to make up for dietary insufficiencies. As these horses are often in a great deal of pain, NSAID administration may often be needed, but can also contribute to gastrointestinal upsets. Alternatives to NSAIDS, such as Omega-3 fatty acid supplementation, may help to alleviate some discomfort, without the negative side effects.
Overall, close attention to the diet of the horse, avoiding GI disturbances or causing fluctuations within the hind gut, and limiting grass intake during periods of time where fructan concentrations can be high, will hopefully prevent the horse from ever experiencing this deadly disease.