Winter appears to be on the backstretch (finally!) and so it seems appropriate to broach some issues associated with spring. Spring and summer are notorious months for the development of laminitis in the Boulder area, with the highest incidence occurring in May and June. You are plenty familiar with my words of caution about not allowing horses to eat too much or get too fat. Over the years, I have been struck by several things when faced with treating laminitis: The pain and suffering experienced by affected horses, and the heartache shared by an owner, and myself. At the American Association of Equine Practitioners (AAEP) annual meeting this past winter, extensive information was presented about the equine hoof. One topic that was examined in detail was the latest research about laminitis.
The most up-dated information is an interesting and complex story explained to us by Dr. Chris Pollitt, a veterinarian from Australia who has made it his life's work to figure out what goes on in the foot during a laminitis episode. Below is my attempt to present a synopsis of his findings for your understanding, hopefully so we can head off laminitis cases related to grass pasture or to over-feeding of carbohydrates. As you read, you might find a new perspective about the practice of turning horses out onto green grass for unlimited periods of time, and you might rethink the routine feeding of grain supplements. After "digesting" this information, I trust that more concerted efforts will be made to either restrict pasture and/or invest in a grazing muzzle, for the sake of your horses. And, hopefully, the amount of grain and concentrate fed will be cut to a bare minimum. I realize that it is a chore to read even a paragraph or two about cellular anatomy, but your perseverance will be rewarded by a deeper understanding of hoof health. Your horse comes out a winner for your efforts. Best regards, Nancy
Laminitis is a crippling disease of the equine hoof, that is fraught with pain and suffering by the horse, and heartache by the horse's owner. An understanding of what laminitis is provides us with the tools to prevent its occurrence. First off, think of the hoof wall as a modified extension of the skin. Much in the same way fingernails grow out from the cuticles, a horse's hoof continuously grows down from the coronary band. Cells arising from the coronary band (or coronary corium) push older cells downwards to achieve growth of the hoof wall. Successive layers of cells layer themselves within the inner surface of the hoof wall, folding into extensive leaves of tissue, called lamellae, or laminae. (These "leaves" are woven together like interlaced pages of two books. It is difficult to pull two books apart when each leaf is so interlocked.) The vast surface area provided by the layers of lamellae not only brings in an extensive blood supply, but it also stabilizes the attachment of the coffin bone inside the hoof capsule. Now, here is where it gets a little tricky to visualize the anatomical architecture within the hoof: What holds the coffin bone in suspension within the hoof capsule is a structure called the basement membrane. The basement membrane is a tough, connective tissue that attaches the lamellae of the hoof capsule to the surface of the coffin bone. At contact points between the cells of the lamellae and the basement membrane are "spot-welds" called hemidesmosomes. Anchoring filaments further bridge the attachments of hemidesmosomes to the basement membrane to increase stability. The short version: Laminitis is caused by failure of the basement membrane and its anchoring points.
Remodeling of the Hoof in Growth and in Response to Stress and Injury
Hoof growth occurs in a highly controlled fashion: In order for new cells to migrate and proliferate downwards to form new hoof wall, some attachments to the basement membrane must be loosened. As a normal consequence of hoof growth and replacement, or when there is minor injury to the hoof wall, this process occurs with careful, localized cellular organization. The normal process of hoof growth relies on activity of enzymes called matrix metalloproteinases, or MMPs to loosen some attachment points to the basement membrane. The basement membrane then forms a template over which new cells migrate to reconstruct fresh lamellae. Localized MMP activity facilitates:
Maintenance of lamellar orientation as the hoof grows down
Repair of local areas of injury
MMP activity is orchestrated by opposing activity of other enzymes known as MMP inhibitors that keep this process in check to retain structural stability of the foot while a small area either grows or repairs. Cellular detachment from the basement membrane only occurs in small portions at a time so the coffin bone remains suspended safely within the hoof capsule. This process can be likened to the pulling apart of a small portion of Velcro with the rest of the Velcro holding everything together while a small, separated piece of Velcro is "repaired."
What is Laminitis?
Laminitis describes an inflammatory condition of the sensitive laminae, or lamellae, of the hoof. The process of laminitis can be viewed as a a variation on a natural physiologic process that has gone amuck. When activity of the metalloproteinase (MMP) enzymes proceeds unchecked without normal inhibition of its effects, devastating destruction is done to the lamellae. (In fact, excess MMP activity has been identified in many medical disorders from osteoarthritis to cancer.) Lamellar tissue affected by laminitis loses contact with the basement membrane, resulting in tissue separation and lamellar disorganization. On-going disintegration within the hoof leads to irreversible anatomical defects. To envision what might be occurring, think of what happens when a knit sweater starts to unravel -- One strand (the basement membrane) begins to pull apart, and all the attaching knitted fibers (anchoring filaments and hemidesmosomes) pull loose from the large strand. The lamellar leaves of a laminitic hoof disintegrate into incongruous parts much in the same way that an unraveled sweater shreds into a disarray of fibers that no longer connect to one another.
Laminitis results from failure of the lamellar attachments. But, before clinical signs are noted, a developmental phase lasting about 40 hours occurs with progressive separation of the lamella. It is at this point, before a horse becomes appreciably painful, that aggressive treatment measures may head off a crisis before it becomes irreversible. In many cases, an owner is unaware of the occurrence of this developmental phase. However, in instances of known carbohydrate overload from rich pasture or feed, or when a horse has accidentally gotten into the grain bin, strategies may be implemented to arrest the developmental phase. (This is described below.) Typically, laminitis develops from metabolic disturbances related to a rich diet, obesity, or hormonal imbalances such as occur with Cushing's disease or Equine Metabolic Syndrome. Gastrointestinal disturbances related to colic, diarrhea, or colitis also encourage microbial overgrowth in the bowel. In distance sport horses, laminitis may develop secondary to the effects of dehydration, electrolyte imbalances, colic, and/or exhaustion syndrome. In some cases, laminitis may occur as a mechanical consequence of excessive foot concussion, particularly on a thin-soled horse.
Characteristics of Laminitis
An affected horse appears "stiff" in the front end, or shifts its weight from foot to foot. The horse is often reluctant to move, and places both hind legs well under its body to shift weight from the painful front feet to the rear. This weight shift is amplified as the horse is asked to turn. An affected horse is said to appear as if "walking on eggs." Sensitive owners may be able to appreciate warmth of the hooves. Bounding pulses may be felt in the digital arteries just behind the fetlock. Rapping on the front face of the hoof wall often causes an affected horse to flinch and pick up its painful foot. Some horses react to hoof pain by sweating, acting anxious or colicky. Others spend a lot of time lying down. The degree to which a horse exhibits pain correlates well with the extent of microscopic lamellar damage.
In most cases, laminitis occurs only in the front limbs. Laminitis is a true emergency condition; immediate damage must be attended promptly and an underlying problem corrected. It is critical to provide sole support to minimize the risk of rotational or vertical displacement of the coffin bone within the hoof capsule. Radiographic (x-ray) examination of the coffin bone and its position relative to the hoof capsule yields information as to the consequences of this disease to a horse's athletic future. The hoof wall will later record an inflammatory event by forming ripples, ridges, or dishing on the front face.
Rich Pasture Consumption
Current research by Dr. Chris Pollitt has identified a plausible explanation of what occurs in the hoof tissues when a horse is afflicted with laminitis. Using a model of carbohydrate overload, he has explored the role of dietary starch in stimulating a laminitic attack. His research model mimics what happens to a horse that consumes too much rich pasture grass, a source of a complex sugar known as fructan, or oligofructose. Fructan is present in abundant concentration in grass stems in spring and fall when ground temperatures are low. Fast growing, short grasses contain the highest concentrations of fructan sugars so a pasture need not be full and lush to pose a risk of developing laminitis. This does not eliminate lush pasture as a laminitis risk because of an abundance of carbohydrate content. In certain conditions, dependent on sunlight, temperature, moisture availability, and the species of grass, a horse grazing on fructan-rich pastures is able to consume 5 kg of fructan in a single day - This is twice the amount of starch that is known to induce laminitis. A British study noted that fructan concentrations vary at different times of the day, with more fructan present in the morning and early afternoon than in the later afternoon and evening. This finding should not be used as a specific rule of thumb for implementing a grazing strategy in Boulder, Colorado. Not only does fructan concentration vary throughout the seasons, but it has daily and geographical variations; every individual environment must be evaluated based on its unique set of conditions. Some pastures may never be suitable for grazing, particularly of easy keepers.
Horses (and other mammals) do not possess digestive enzymes to metabolize fructan so it passes into the cecum (a portion of the large colon) in a relatively undigested form. The extent of metabolic insult is dependent on the amount of fructan ingested. In the cecum, rapid fermentation of fructan by bacterial microbes promotes proliferation of bacteria, namely Streptococcus bovis, a Gram-positive organism. In addition, a change in the pH related to fructan fermentation results in acidification of the cecal contents, and this damages the intestinal lining. The overgrowth of Gram-positive bacteria are absorbed through the fragile bowel lining into the systemic circulation. Release of related laminitis trigger factors (endotoxin and other inflammatory mediators) add to the overall metabolic insult on the horse's body. A horse may spike a fever, have an elevated heart rate and/or respiratory rate, and break with diarrhea in response to the systemic assault. As pertains to the feet, circulation of Strep spp. organisms and laminitis trigger factors elicit activation of specific enzymes, notably matrix metalloproteinases, or MMPs, which cause separation of the basement membrane of the laminae.
When the internal process goes amuck, and enzyme activity of MMPs proceeds unchecked without normal inhibition of the activity of this enzyme, excess damage is done to the lamellae and basement membrane. Lamellar tissue that is affected by laminitis loses contact with the basement membrane, leading to irreversible anatomical defects. Anchoring filaments and hemidesmosomes are lost during basement membrane disintegration.
Insulin Resistance and Its Effects on the Hoof
In addition to unchecked MMP activity, another event occurs following over-consumption of fructan (or of daily amounts of carbohydrate-rich supplements): Insulin resistance. Excess circulating glucose from abundant dietary sources alters the uptake and storage of glucose in glucose-dependent tissues, such as hoof tissue. Normally, the pancreas secretes insulin in response to the presence of glucose obtained from food ingestion. Insulin enhances uptake of glucose by skeletal muscle, fat cells, and the liver. Factors, like fructan ingestion, obesity, or Equine Metabolic Syndrome interfere with the normal action of insulin so blood glucose levels continue to increase; ironically, insulin increases in response. Yet, despite the presence of abundant glucose in the circulation, there is insufficient glucose delivery to target cells dependent upon glucose, such as structures in the hoof. At the same time, other tissues that do not depend upon glucose for metabolism, such as red blood cells, are presented with levels of glucose that are toxic to red blood cells. This results in oxidative stress in the circulation of many tissues, including the hoof, further compounding the problem.
Glucose "deprivation," as a side effect of insulin resistance, triggers laminitis. This occurs because of damage to the linking attachment points (hemidesmosomes) that adhere the lamellae to the basement membrane. The combination of insulin resistance and overgrowth of Strep spp. bacteria in the gut and over-activation of MMP enzymes leads to disintegration of these anchoring points within the hoof tissues, followed by pain and lameness. As the basement membrane separates from the lamellae, there is nothing to counteract the weight of the horse and the pull of the deep digital flexor tendon that attaches to the back of the coffin bone. The toe creates a lever effect, further amplifying pull from the tendon. The coffin bone may detach from the hoof wall, in part or in whole. Without its supportive laminar attachments, the coffin bone can rotate or sink to the bottom of the sole. It is possible to see rotation as soon as three hours after the laminae begin their cycle of damage and swelling. In a very severe case, the bone may perforate the bottom of the foot. Immediate action must be taken to halt the progression of damage.
Equine Metabolic Syndrome (EMS, also referred to as Obesity-Associated Laminitis) is known to stimulate insulin resistance. Horses suffering from EMS are those easy keepers with the cresty necks and fat pads over the shoulders, back, and rump. Affected male horses often develop thickening (or fat) within the prepuce. Over-feeding, coupled with relative inactivity, is usually the cause of such obesity. High levels of circulating corticosteroids originate from enzyme activity in local intestinal sources. These sources include liver or the fat cells within the abdomen, including the omentum that covers the bowel. Fat cells are responsive to endocrine signals; the more fat cells present in the abdomen as occurs with obesity, the greater the risk of hormonal irregularities. Many fat horses are erroneously diagnosed as being hypothyroid. Although there may be some degree of diminished thyroid hormone levels, the problem is not within the thyroid gland itself but rather is due to irregular hormonal feedback as a result of high circulating levels of corticosteroids, also referred to as "steroids." Insulin resistance also may be a consequence of gastrointestinal disease, uterine infection, or any profound stress or systemic disease that triggers increased cortisol production. Horses with Cushing's disease experience insulin resistance due to high levels of circulating corticosteroids associated with over-activity of the pituitary gland. Insulin resistance also develops in obese horses subsequent to an inflammatory response that requires direction of glucose towards immune and inflammatory cells related to wounding or infection. Persistence of insulin resistance in these situations may lead to muscle wasting, and potentially laminitis. Pain from laminitis is a stressor in itself, acting as a trigger for insulin resistance, making it difficult to resolve metabolic problems that are self-perpetuating.
Prevention of Laminitis Using Cryotherapy
Dr. Pollitt's research further elaborated suggestions about first aid measures that may be taken in a horse with a known carbohydrate or fructan overload. His thinking advocates the use of cryotherapy BEFORE the presence of clinical signs. (Please take note -- Once clinical signs appear, cryotherapy cannot undo the damage and other therapeutic measures must be implemented.) But prior to or during the developmental phase, immersion of a horse's front limbs into a slurry of crushed ice to the level of the knees elicits vasoconstriction of hoof circulation. Dr. Pollitt believes this is beneficial for several reasons:
Tissue metabolism within the hoof is reduced
Reduced circulation minimizes delivery of laminitis trigger factors that would otherwise activate MMP enzymes.
Enzymatic activity of MMPs is reduced by 50 percent for every 10 degree Celsius decrease in temperature.
Under normal circumstances, every few hours a horse's hooves vacillate between periods of vasoconstriction and vasodilation. In his study, all horses that were left untreated to experience vasodilation cycles of the hooves did develop laminitis. Enzymatic separation of the basement membrane from the lamellae occurs 36 - 48 hours prior to the appearance of clinical signs, during the "developmental phase." In contrast, when a horse's limbs are immersed in a slurry of ice and water at 41 degrees Fahrenheit for 48 hours, only minor cellular changes were noted. Unlike humans, horses do not appear to have receptors to cold in their hooves so are not bothered by the application of cold for a prolonged period. (Think about how unfazed horses are living outside in the dead of winter, their feet immersed in snow or treading on frozen ground.)
Previous theories incriminated poor circulation to the hooves as the event that precipitates laminitis. If the theory of poor blood circulation and reduced oxygen delivery to the hoof tissues is to have validity, then it would seem that vasoconstriction with ice therapy would cause more harm than good. In Dr. Pollitt's research, this was not the case. Favorable results achieved with cryotherapy lend credence to the proposed theory that matrix metalloproteinases (MMPs) and insulin resistance elicit profound lamellar damage at the cellular level.
Management Strategies to Prevent Laminitis
The best therapy for laminitis is one of prevention. The objective is to maintain your horse in good body condition, and not allow him to become "pleasingly plump" or fat. Refrain from the temptation to offer a horse grain and supplements that he most likely doesn't need in the first place. In most cases, less is better. Horses thrive best on a high fiber diet that includes hay and non-irrigated pasture. Limit or restrict a horse's intake of fructan-rich pasture, and just as importantly, give him plenty of exercise to keep him in trim condition.