EQUINE LAMINITIS: CAUSE, TREATMENT AND PREVENTION
Exert from the MHU Horse Nutrition Course
Laminitis, a metabolic disorder commonly referred to as founder, can affect all four feet, but is most common in the front feet. Laminitis causes the sensitive and insensitive lamina of the hoof wall to become inflamed, leading to separation (Figure 1). The lamina provides support to the coffin bone. When separation occurs, typically the coffin bone rotates downward. As the coffin bone rotates downward, it presses the sole of the hoof, causing severe lameness. In severe cases, the tip of the coffin bone can penetrate the sole of the hoof. A less common occurrence is total separation of the lamina supporting the coffin bone and the entire coffin bone will sink within the hoof capsule.
There are four phases to the progression of laminitis:
Developmental: Period of time that is initiated by a cause or insult and ends with the first appearance of lameness.
Acute: Follows the developmental phase where either no radiographic changes to the hoof occur or movement of the coffin bone occurs.
Subacute: If there is no physical or radiographic collapse of the coffin bone, the next 8 –12 weeks are considered the recovery or repair stage.
Chronic: If there is physical or radiographic movement of the coffin bone, the horse has chronic laminitis or founder. The length of this phase is dependent on the degree of rotation in the coffin bone and the success of treatment. For horses with chronic laminitis, the degree of recovery may not be determined for months or even years.
Laminitis can be categorized into rotating and sinking laminitis.
Sinking Laminitis: The coffin bone and hoof wall separate and the coffin bone sinks downward. It is possible for the coffin bone to penetrate the sole of the hoof. Sinking laminitis is often more life-threatening than rotating laminitis. In an extreme case a horse could possibly "walk out" of the hoof capsule.
Rotating Laminitis: The coffin bone and hoof wall separate, and the coffin bone rotates within the foot.
Laminitis can be caused by many factors, including overeating (obesity), working on a hard surface (commonly referred to as road founder), running high fevers, exposure to black walnut shavings, and stress. Ponies are extremely susceptible to laminitis, especially when fed rich, lush forage. Geldings are more prone than mares, and laminitis is more common in adult horses than younger horses. In addition, horses with Equine Metabolic Syndrome and Equine Cushing’s Syndrome are predisposed to laminitis.
There is no relationship between the amount of protein in the diet and laminitis: however, the incidence of laminitis does appear to increase with excessive or sudden carbohydrate intake. Rapid fermentation of soluble carbohydrates (starch, sugars and fructans) reaching the large intestine results in lactic acid buildup, and a horse’s hindgut has not evolved to handle much lactic acid. One possible reason for laminitis is that the lactic acid causes an excessive decrease in pH in the hindgut, which in turn causes the lysis (bursting) of certain bacteria and a release of endotoxins. If the lining of the hindgut is damaged by the lactic acid or irritated by diarrhea, it absorbs these endotoxins. These endotoxins may alter circulation in the foot leading to the development of laminitis.
Signs of laminitis include lameness (more commonly in the two front feet), stiffness and settling on the back feet to take pressure off of the front feet. If a horse is not showing laminitic signs, radiograghs can reveal rotation of the coffin bone or changes in the distal aspect of the coffin bone which is suggestive of chronic laminitis. Cases range from mild to severe. If all four feet are affected, a horse may lie down to relieve the pain. Once the laminae begin to separate from the pedal bone, a favorable prognosis for an athletic horse decreases. In the most severe case, laminitis will result in the horse being euthanized. If treated at early onset, however, the horse may have a partial to complete recovery.
Treatment and Prevention
Treatment of laminitis is much more successful when started early. It is absolutely necessary for an equine veterinarian to prescribe an early treatment course. Once the horse is past the acute phase, the attending veterinarian, farrier and owner will work together in developing management strategies and a corrective trimming/shoeing program to rehabilitate the horse. Acute (sudden onset) laminitis, if caught early enough, may be resolved; and with the proper preventive measures, the disease can be kept from becoming chronic. Medication and a change in diet are the most common treatments. Long-term treatment will include frequent corrective hoof care and dietary changes involving reducing dietary starch, optimizing forage and feeding dietary fat, if needed, to balance for energy demands.
Research continues on laminitis, but for now, here are some pointers for treatment and prevention.
Avoid overfeeding or irregular feeding of concentrate (grain).
Use caution when introducing horses to early spring pastures and reduce the consumption of sugars (especially fructans) from lush forage. Acclimate horses from hay to pasture slowly by:
Increasing turnout time gradually in 30-minute increments over several weeks
Using grazing muzzles on equine that are prone to get fat or founder on pasture (Figure 4)
Using similar precautions during the late summer and early fall when heavy rains may simulate spring growth-type conditions.
If feeding concentrates, limit concentrate feeding and starch intake to a maximum of .2% - 0.4% of body weight or 2 to 4 g starch/kg body weight/meal (assuming two to three meals are fed per day).
Increase digestion and absorption of starch in the small intestine to reduce starch reaching the hindgut by feeding at least two small meals per day rather than one large meal of concentrates.
Optimize the forage component of the diet but maintain adequate nutrients for hoof repair and growth (protein, amino acids, and various micronutrients).
References and recommended reading: