Laminitis, also known as Founder, is defined as inflammation of the sensitive laminae of the hoof. Laminitis is now thought to be a transient ischemia (loss of blood supply and therefore oxygen) associated with blood coagulation (clotting) and inflammation. The alteration of blood flow leads to the breakdown and degeneration of the union between the horny and sensitive laminae of the hoof. When blood supply to the foot is severely diminished, the resulting laminitis may cause the hoof capsule to slough. Rotation of the pedal bone is a common complication that may eventually perforate the sole. The condition may be subacute, acute or chronic.

Causes of Laminitis include complications of severe lameness or orthopedic disease in the contralateral limb due to excessive weight distribution, the ingestion of excessive amounts of carbohydrates (grain overload), grazing of lush pastures (pasture or grass founder), ingestion of large amounts of cold water (Water Founder) and excessive exercise and concussion in an unfit horse. Additional causes of laminitis include postparturient metritis, endotoxemia, colic, enteritis or the administration of an excess amount of corticosteroid or other medication. Excessive weight bearing on any leg following lameness or fracture may result in Support-Limb Laminitis. Grain overload and excessive concussion in an unfit horse are the most common causes of laminitis in horses and pasture founder is the most common type of laminitis seen in ponies.

In acute laminitis, the horse is depressed, anorectic (will not eat), and stands reluctantly. The animal will attempt to shift weight from the affected feet. The forelegs are most commonly affected but the condition usually involves all feet over the course of the disease.

Typically heat will be apparent in the whole hoof, especially near the coronary band. The digital artery will have an exaggerated and bounding pulse. Clinical signs of pain including muscular trembling and a fairly uniform tenderness that can be detected when pressure is applied to the feet. The horse exhibits a short-striding gait. Each hoof, after being lifted, is set down as quickly as possible. The pedal bone may rotate during or after the acute stage, in as little as 72 hours.

In chronic laminitis classical clinical signs will be present, but to a lesser degree than with acute laminitis. A characteristic sign of chronic disease is the visualization of irregular bands of horn growth in the hoof, known as laminitic rings.

Several factors appear to come together resulting in laminitis. According to some researchers, laminar inflammation appears to play a larger role than decreased blood flow in the early stages of laminitis. Septic (infectious) systemic inflammation and an intense inflammatory response appear to alter blood flow to the hoof. The veins in the equine foot respond differently than the arteries. The arteries appear to work normally but the veins don’t contract as well as normal, causing the blood to stagnate. Deoxygenated (blood with little or no oxygen) blood will then predominate within the laminae of the hoof. The laminar endothelium will activate area neutrophils due to the poor environmental conditions. These neutrophils are responsible for the production of inflammatory cytokine and COX-2 expression. This intense inflammatory response is present long before the horse exhibits any clinical signs of laminitis. The resulting inflammation is believed to cause the failure of the bond between the hoof wall and the coffin bone. The vascular problem may actually be a secondary reaction to the inflammation in most cases of laminitis.

In the case of support-limb laminitis, changes in weight-bearing appear to directly alter the blood flow within the laminae, suggesting a primary vascular role. Research conducted at Louisiana State University suggests that as limb-loading (weight bearing) increases, laminar circulation decreased concurrently. In support-limb laminitis, clinical signs of disease tend to appear six weeks after the resulting injury and surgery. Laminitis characteristically occurs in the contralateral limb but will often progress, finally affecting all four legs.

Two important genes may be directly involved in the inflammatory process, ADAMTS4 and FOS. These genes may have important roles in determining why disease occurs in advance of clinical signs, and why some horses are more susceptible to laminitis.

An additional factor involved in laminitis may be overactivation of the MMP-9 enzyme. The MMP-9 enzyme degrades the attachment of the sensitive and insensitive lamina. Significant changes in this one enzyme were found within eight hours of ingestion of a ration that led to clinical laminitis. Insulin Resistance (IR) may also be expected to reduce the supply of glucose and blood flow to the hoof. University of Tennessee researchers have found that many obese horses with laminitis suffer from IR. A University of Tennessee graduate student has also found a correlation between endotoxemia (toxic substances in the blood produced by gram-negative bacteria) and the alteration of glucose metabolism and the induction of IR.

Treatment for laminitis must be aggressively started at the time of initial insult and is a medical emergency! In spite of therapy, permanent changes to the hooves may occur rapidly. In the case of grain overload, mineral oil should be given as a laxative. The mineral oil prevents the adsorption of toxic materials and excessive carbohydrates. Pain must be treated early and aggressively. Higher doses of non-steroidal anti-inflammatory drugs or NSAID’s will help block the inflammatory response. The most commonly used NSAID’s include phenylbutazone and flunixin meglumine or Banamine®. Early treatment with systemic lidocaine has been shown to decrease leukocyte and endothelium activation of neutrophils. Acepromazine shows some efficacy in increasing blood flow to the hoof.

The age-old treatment of icing the hooves beside a cold stream has been updated and is now known as cryotherapy. Vasoconstriction of the blood vessels to the feet results in fewer mediators of inflammation being delivered to the laminar area. The feet may be placed in ice or a commercially available product called Game Ready Equine® which is a compressive cold therapy system that may be used. Present research indicates that temperatures below 35°F should be maintained to the foot. The length of time the icing should be maintained is usually considered to be 72 hours. The use of leeches to remove stagnant, deoxygenated blood in the veins has been suggested but has not fully been researched at this time.

In an effort to prevent contralateral limb laminitis in horses recuperating from severe lameness and fractures, a Kentucky Veterinarian and a blacksmith have teamed together to develop an Ambulatory Sling. The specialized sling allows the horse to apply some weight to the legs but prevents the horse from overloading weight to any one leg. Since the Sling apparatus is on wheels, it allows a horse to move around. The mobility in turn improves their attitude and may allow them to graze. The sling prevents the development of weak and atrophied muscles and tendons since some weight bearing may occur. The horse must have a congenial behavior to tolerate the apparatus. Initial results obtained when the sling has been used have been quite favorable. A patent has been applied for and the device will be available on a custom-built basis.

In general the prognosis with laminitis is guarded at best. Therapeutic shoes may provide increased comfort and cushioning. Corrective trimming and shoeing may restore normal phalangeal alignment and balance. Once a horse undergoes an episode of laminitis, repeat attacks are more common. Treatment may extend serviceable soundness but the condition is never cured.


References:
King, Marcia. Veterinary Practice News. Volume 19, Number 4 “The Quest of the Laminitis Killers” pp. 42 and 47.

Steffanus, Denise. Veterinary Practice News. Volume 19, Number 4, “Ambulatory Sling May Help Avert Laminitis” pg. 44.

Heflin, Marissa; “The Race They Couldn’t Win”, Veterinary Practice News. Volume 19, Number 3 March 2007 pp 1 and 6.

Adams, O.R. Lameness in Horses. Third edition 1974. pp 247-253.

Kahn, Cynthia, Editor. Merck Veterinary Manual. p 906.