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Laminitis is one of the most serious hoof conditions affecting horses. It can strike adult horses of all breeds and can be severely debilitating, resulting in excruciating pain, loss of usefulness, and in some cases necessitating euthanasia. Due to the complex nature of the disease, prevention and treatment of laminitis have often been causes of confusion and controversy. However, as research increases the understanding of the pathophysiology of the disease, more effective preventive and therapeutic strategies have also been developed.
A simple definition of laminitis is inflammation of the sensitive laminae and structural damage of the insensitive laminae of the foot, though this is perhaps an over simplification of a complicated condition (Stashak 2002). The laminae are folded connective tissues that serve to attach the distal phalanx or coffin bone to the inner hoof wall. When the attachment fails, a horse is considered to have laminitis (for a review of hoof anatomy visit this site). There are three phases of laminitis: developmental, acute, and chronic. The developmental phase begins with the initiation of subclinical pathological changes in the laminae and ends with the emergence of clinical signs of laminitis. There are generally no signs of laminitis present during the developmental phase. The acute phase is considered the time between the onset of lameness and the failure of digital support by the laminae. In the acute phase of laminitis, the laminae fail at the basal cell layer; this “basement membrane zone” appears to be the weak link in the anatomy of the laminae (Dyson and Ross 2003). Loss of interdigitation may result in rotation and/or displacement, and in some cases sinkage of the coffin bone (Stashak 2002). Without the laminae to secure it, the coffin bone is driven into the hoof capsule by the weight of the horse, forces of locomotion and the pulling force of the deep digital flexor tendon. In the chronic phase of laminitis, there has been displacement of the coffin bone with or without intermittent recurrent active inflammation of the laminae, depending on the severity of the disease and whether or not the foot has been stabilized and the initiating condition adequately treated.
The acute phase of laminitis involves onset of variable lameness in one or more feet. Usually both front feet are affected, but unilateral lameness as well as hind foot lameness may occur. Horses with laminitis will be extremely reluctant to move and if forced to do so will move with a short gait in which the hind limbs are placed unusually far underneath the body. Lameness is worse when the ground is hard. The digital pulse of a horse with acute laminitis is described as “bounding” due to increased systolic and decreased diastolic pressures, resulting in a pulse that is much easier to feel than it would be in a normal horse. The pulse rate (number of beats per minute) will also be increased in response to pain. Pressure applied to the feet might cause pain, but the response to hoof testers is variable. The sole of the foot may be flat or convex (bulging downward) instead of the normal concave shape and in the most severe cases, the tip of the coffin bone and associated soft tissues can penetrate the sole. Palpation of the coronary band may reveal swelling, serum seepage, and/or an unusual depression associated with sinking (Dyson and Ross 2003). When standing, the hind feet are tucked underneath the body in an attempt to take weight off of the front feet (Higgins and Synder 2006). The horse may lie down more frequently or for extended periods, which can eventually lead to decubital ulcers (“bed sores”). Some horses are anxious, have muscle tremors, increased respiration, and an elevation in rectal temperature (Stashak 2002).
The risk factors for the development of laminitis vary widely and include inflammatory conditions of the gastrointestinal tract, grain overload, grazing on rich and/or frosted pasture, retained placenta, pleuropneumonia, endotoxemia or sepsis, Cushing’s disease, obesity and associated Metabolic Syndrome, prolonged weight bearing on one limb, exposure to black walnut wood shavings, exercising on hard surfaces and the administration of large doses of corticosteroids. No association between age, breed, or sex has been established for the development of acute laminitis although generally older horses are affected by chronic laminitis (Stashak 2002). However, a correlation between obesity, hyperinsulinemia, and laminitis has been established and breeds that are more prone to obesity, such as pony breeds, Morgans, and others, are considered to be at greater risk of developing laminitis (Treiber et al., 2006).
Despite substantial research in the last few decades, laminitis and its complex physiologic cascade are still not completely understood and are likely to differ depending on cause. Laminitis frequently develops secondary to a disease occurring elsewhere in the body and it is therefore vital that the primary disease is treated (Stashak 2002). Researchers at the University of Queensland have shown that during the developmental phase of laminitis, cryotherapy, or therapeutic cooling of the tissue, may be useful to induce digital vasoconstriction and to reduce the activity of the enzymes that degrade the basement membrane that attaches the insensitive laminae to the sensitive laminae (van Eps et al., 2004). In the study, continuous cryotherapy during the developmental phase was successful in markedly reducing the severity of acute laminitis in horses known to be at high risk for developing the condition.
The metabolic related form of laminitis can occur as a result of insulin resistance (IR) and hyperinsulinemia in horses and ponies. Obesity also has been associated with an increased risk for laminitis, likely as a result of insulin resistance. In these horses, dietary factors, particularly the amount of nonstructural carbohydrates (NSC) in the diet, should be considered. High levels of NSC can increase the risk of developing laminitis because they can trigger insulin resistance or gastrointestinal disturbances in the hind gut that induce laminitis. Specific dietary management strategies to lessen the risk for laminitis include caloric restriction to promote weight loss and improve insulin sensitivity in obese animals, and strict control of NSC in the diet. Grains and sweet feeds should be removed from the diet and obese horses or those with insulin resistance should have their access to rich pastures that may be high in NSC restricted (Geor and Harris 2009). Daily aerobic exercise for obese horses or those with insulin resistance is also important and when combined with changes in diet can play a significant role in improvement of body condition and in insulin sensitivity (Orsini et al 2009).
The diagnosis of laminitis is made largely on clinical signs (Stashak 2002). If the onset of acute laminitis cannot be prevented through cryotherapy, diet or other therapeutic strategies, non-steroidal anti-inflammatory drugs can be used to reduce inflammation and pain. Acute laminitis should always be considered a medical emergency. Horses with acute laminitis should be confined and placed in a stall with soft bedding. Frog pads or Styrofoam pads can be used to relieve pressure on the hoof wall by placing more pressure on the frog and heels. Radiographic examination is necessary for establishing both prognosis and treatment protocol. Radiographic abnormalities include rotation or sinking of the coffin bone. Horses with a rotated coffin bone should have their feet trimmed to realign the hoof capsule with the coffin bone. Therapeutic shoeing is important in the treatment of laminitis as different types of shoes can serve to support the frog and coffin bone and decrease the pull of the deep digital flexor tendon. However, shoeing in the acute phase (first 24-48 hours) should be avoided so that there is no further injury to the laminae (Dyson and Ross 2003). Making a prognosis for horses with acute laminitis is difficult, though the degree of rotation, lameness severity, and response to treatment can be used as predictors. The lamellar damage is never completely reversed and horses that have developed laminitis are at increased risk of developing it in the future (Stashak 2002). In cases with severe rotation, sinking or extensive infection, humane euthanasia may be necessary (Higgins and Synder 2006). Preventative measures are vital due to the devastating nature of the disease.
While there is still much that remains unknown about laminitis, researchers continue to investigate the causes and are working to develop improved treatment and prevention strategies. For further information regarding laminitis, please speak with your veterinarian. The references listed in this fact sheet are provided as additional sources of information related to laminitis in horses.
Date: September 12, 2011
Equine Health Fact Sheet
Carissa Wickens, PhD, Assistant Professor, Delaware Equine Extension Specialist
Stephanie Fraze, Extension Scholars Intern
ToriAnne Davies, Extension Scholars Intern
Hannah Galantino-Homer, VMD, PhD, Senior Research Investigator
Laminitis Research Initiative
Department of Clinical Studies, New Bolton Center
School of Veterinary Medicine, University of Pennsylvania
Dyson, S. J., M. W. Ross. 2003. Diagnosis and Management of Lameness in the Horse. Saunders, Philadelphia, PA.
Geor, R. J., P. Harris. 2009. Dietary Management of Obesity and Insulin Resistance: Countering Risk for Laminitis. Vet. Clin. North Am. Equine Pract. 25: 51-65.
Higgins, J. A., J. R. Snyder. 2006. The Equine Manual. 2nd Edition. Saunders, Philadelphia, PA.
Orsini, J., H. Galantino-Homer, C. C. Pollitt. 2009. Laminitis in Horses: Through the Lens of Systems Theory. J. Equine Vet. Sci. 29: 105-114.
Staschak, T. S. 2002. Adam's Lameness in Horses. 5th edition. Lippincott Williams & Wilkins, Baltimore, MD.
Treiber, K. H., Kronfeld, D. S., and Geor, R. J. (2006) Insulin Resistance in Equids: Possible Role in Laminitis. J Nutr 136 (Suppl): 2094S-2098S.
Van Eps, A. W., L. J. Walters, G. I. Baldwin, M. McGarry, and C. C. Pollitt. 2004. Distal limb cryotherapy for the prevention of acute laminitis. Clin. Tech. Equine Pract. 3 (Suppl. 1): 64-70.
See theHorse.com, Free Reports, Factsheets, Laminitis.
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