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.