Laminitis is a disease most horsemen know. But, despite its familiarity, laminitis is a mystery in many ways; there are many causes and different scenarios under which it occurs. The term laminitis simply means inflammation of the laminae–the tiny interlocking, finger-like tissues that attach the coffin bone to the insensitive outer wall in the horse’s foot.

There are three phases to laminitis: the developmental stage, the acute phase and the chronic phase. A common progression from laminitis is breakdown of the portion of the inner hoof wall that normally holds the coffin bone suspended, and then the weight of the horse forces the bone downward.

There are numerous causes of laminitis, and many cases develop secondarily to an illness or injury such as colic, severe diarrhea, a uterine infection or exposure to black walnut shavings. Other cases develop after excessive carbohydrate ingestion, such as a grain overload or after a horse or pony gorges on spring pasture.

Scott Morrison DVM, of Rood and Riddle Equine Hospital in Lexington, Ky., said there are several theories regarding how laminitis occurs. One, the blood flow hypo-thesis, is that decreased blood flow to the laminae may factor in, causing the damage. Some studies have contradicted this belief, however, stating that increased blood flow is the problem. And researchers are still examining and measuring blood flow as a cause.

There’s also a theory that activation of certain enzymes within the laminae destroys the bond between the hoof wall and the coffin bone (see sidebar). Another theory is that there’s an abnormality in which glucose can’t be utilized by the basal cells of the laminae. This affects some of the bonds that are dependent upon glucose. It seems these cells are unable to utilize glucose for some reason, as in horses with Cushings syndrome or diabetes-type syndrome (horses that are prone to founder).

 “There are also some mechanical causes, such as road founder, in which the laminae are overstressed. There are many theories about laminitis. It’s probably a combination of several of these things that cause it. Each case is different,” Morrison noted. A horse that has laminitis from over-eating grass may have different factors than a horse with Cushing’s disease or a horse that develops road founder.

“The blood flow research is difficult to analyze and is very confusing because of the different research projects and the contradictions. It makes a difference in how the researchers induced laminitis, as well. Most of the studies, however, point to decreased blood flow,” said Morrison.

Once It Happens

In the developmental stage of laminitis there’s rarely a sign. When a horse enters the acute phase, he has swelling and pain in the foot, heat is emitted and there’s a palpable digital pulse. The challenge at this stage is to keep the condition from becoming chronic, which is when damage in the foot becomes significant enough that the laminar bond fails, and the coffin bone displaces or rotates.

When a horse with laminitis is presented to the veterinarian or farrier, usually all that can be done is to assess the damage and work on a medical and mechanical plan to repair it and prevent it from happening again. There are several shoeing mechanics (see sidebar) and surgeries used in chronic cases to gradually realign the coffin bone.

Stephen E. O’Grady BVSc, a veterinarian and farrier who has worked with equine feet for 30 years, operates a practice in Virginia devoted exclusively to foot care. “The ability to rehabilitate a horse with laminitis is inversely proportional to the amount of damage that’s taken place in the laminae. It depends on the balance between the forces applied to the laminae [the weight of the horse] and the damage to the integrity of the laminae–the amount of surface area of laminae that is left,” he said. “What works for one case may not work for another,” he added.

“All too often if someone discovers a method that works well for one horse, we tend to think that method will work on every horse. If someone puts a heart bar shoe on a horse and it works, then every case of laminitis that comes along will get a heart bar shoe. Other methods can work as well or better for dealing with laminitis, yet heart bar shoes are still considered the method of choice.” O’Grady said having clinical experience is critical in working with laminitis cases because it’s hard to predict how a foot will be affected and how much of the laminae will be destroyed.

“If you administer a big dose of phenyl-butazone as soon as the horse comes down with laminitis, some of these horses will be better the next day. Others are so severe that you can’t reverse the condition, and they must be put down. The damage, in the majority of horses we’re unable to turn around with medical treatment, has taken place in the laminae before the horse ever shows pain,” he said.

O’Grady said the timeframe from the cause of laminitis to clinical symptoms is anywhere from 12 to 36 hours. This period, called the developmental stage, is when the damage takes place within the foot. “Once the horse is showing pain, he’s reached the acute stage, and most of the damage has already been done. There’s a very small window of time in which to treat a horse and prevent further damage. If you don’t turn it around within the first 24 to 48 hours, you’re getting into a serious problem,” he said.

From the acute stage, the horse either goes into recovery or to the chronic condition. A chronic diagnosis means there’s displacement of the bone within the hoof capsule. The bone has changed its position, usually in the form of rotation, sinking, or both. If the damage to the laminae is so extensive that it goes all the way around the hoof, you get what’s called distal displacement and the entire bone drops. A horse with distal displacement usually doesn’t recover.

The weight of the horse pushes the bone downward, the hoof capsule goes upward–creating a trough around the coronary band–and the coffin bone penetrates through the sole. Morrison said that the bone may sink straight down, but a few may sink on the outside or the inside. “Most cases, however, [about 90 percent] rotate down in front. So we treat them all in the acute phase to prevent this rotation, if possible,” he said.

When a horse has weakened laminae, the veterinarians try to prevent the bone from rotating. “We try to decrease the tension on the deep digital flexor tendon, such as using wedge pads in the early stages of laminitis,” said Morrison. “This lifts up the heel and takes the tension off the tendon, so there’s less pull at the back of the coffin bone. We also use sole supports to load the sole, frog and bars and take the weight off the hoof wall and laminar interface, to help protect the laminal bond.”

The horse has more blood circulation at the rear of the foot than at the toe. So,the rear part of the coffin bone may not tear loose because damage in that area is less acute. “The horse has a dual blood supply to the heel area,” explained O’Grady. “The front of the foot, by contrast, has poor circulation to the dorsal laminae. Half of it comes up from the circumflex artery at the perimeter of the coffin bone, going upward against gravity. The other part of the dorsal laminae [has] blood vessels coming down from the coronary band.”

Treating The Horse

Since laminitis often follows another problem–and the window for treating it to prevent further damage is so short–O’Grady suggests protecting the foot as well as treating the primary disease condition. Veterinarians have had success using anti-endotoxin serum to prevent the onset of laminitis in experiments where horses were given carbohydrate overload. Banamine? is also frequently used, along with medications to help increase the blood flow to the secondary laminae, such as aspirin.

If weight can be spread over the whole hoof, rather than concentrated on the walls, there will also be less stress on the laminae. Providing deep bedding, such as sawdust on sand, or filling the space inside the shoe with a rubber dental impression material, can also prevent the laminae from tearing. “During the developmental stage of laminitis, the only sign you might see is a slightly elevated pulse. You should obviously aggressively treat the primary cause of a problem–the colic, the diarrhea, the retained placenta–but the possibility of laminitis should also be considered,” said O’Grady.

Because a small percentage of horses in the acute stage are teetering on the brink, you have a very short time in which you can reverse it. O’Grady uses phenylbutazone and DMSO at the onset. “DMSO works as an anti-inflammatory and a diuretic, and is what we call an oxygen radical scavenger, which may also help decrease inflammation in the tissues. The DMSO is administered orally, by stomach tube. In earlier years DMSO was given intravenously, but veterinarians found that it’s absorbed just as quickly into the body systems when given orally.

O’Grady uses DMSO once or twice a day for up to three days, since that’s the time it’s most effective. While the horse is still in the acute stage, any foot support should be attached with temporary devices. “There are several devices on the market, such as wedged, cuffed shoes that can be taped on the foot,” said Morrison. “Everything you use should be put on as non-traumatically as possible. The hoof at this point is so unstable that often you may need to change what you’ve put on it. “You don’t want to be pulling nails out,” he added. “The last thing you want to do is stress the horse during the acute phase; you need to keep him in a stall and not walk him around to a farrier. You want the farrier or the vet to come to the horse.”

What They’ve Found Down Under

For more than 40 years, researchers in Australia have been trying to discover the agent in the bloodstream that triggers laminitis. According to Christopher Pollitt BVSc, Ph.D., of the Australian Equine Laminitis Research Unit at the University of Queensland, they’re closer than ever.

Pollitt discovered a substance produced by certain bacteria (Streptococcus bovis, one of the microbes in the equine large intestine that helps digest feed) that activates lamellar enzymes. He said S. bovis might be the missing link connecting events in the horse’s large intestine with development of laminitis in the hoof–at least in the cases where digestive tract problems result in laminitis.

Pollitt said the separation of laminar tissues precedes the onset of foot pain by many hours–as short as eight to 12 hours when horses are exposed to toxins in black walnut shavings or as long as 30 to 40 hours when they eat too much grain. He said that certain trigger factors in the bloodstream activate enzymes in the laminae that disintegrate attachments between the coffin bone and the hoof wall. The normal enzymatic remodeling of the laminae–which is necessary for the ever-growing hoof wall to stay in proper relationship with the stationary coffin bone–is suddenly altered.

Enzymes capable of destroying key components of the lamellar attachments are found in increased quantities in tissues affected by laminitis, explained Pollitt. The crucial enzymes (MMP-2 and MMP-9) are found in many tissues that continually remodel (bones, joints and even the inner membranes of the uterus). They’re needed to dissolve the hoof’s attachments as required, in order to maintain the correct shape and orientation of the hoof laminae. And sometimes an injury to the underlying tissues requires its disintegration and reconstruction.

The controlled release of specific MMP inhibitors keeps this remodeling process in equilibrium so the hoof laminae and the hoof itself can slowly migrate past the stationary base cells that are firmly attached to underlying membrane and connective tissues. When laminitis occurs, however, the lamellar tissues increase MMP production, cells in the laminae lose their normal shape and become elongated, sliding over one another. Sheets of the underlying surface peel away.

Pollitt’s research confirmed that lamellar disintegration is due to uncontrolled release of excess activated MMP, and he sought to identify what was activating it. He developed a model for equine laminitis, using small pieces of tissue from the inner hoof wall of normal horses after they were killed at a slaughterhouse. After testing a possible trigger factor, the piece of tissue was subjected to tension, recording the force required to separate the lamellar tissues.

The lamellar tissues were resistant to virtually all known cytokines, tissue factors, prostaglandins, gram-negative bacterial endotoxins and anaerobic cultures–with one notable exception. A factor present in the overlying liquid from cultures of S. bovis (isolated from the equine cecum) activated the hoof MMP-2 and caused lamellar separation.

Pollitt said that during grain overload, S. bovis is the principal microorganism responsible for the rapid fermentation of carbohydrate to lactic acid in the equine large intestine. If it crosses the mucosal barrier of the large intestine–as can happen when the lining is compromised–and enters the circulation, it may be a cause of laminitis.

Trials to test whether MMP inhibitors can prevent or relieve field cases of laminitis are now being done. Ongoing Australian research will hopefully lead to better ways to deal with this devastating disease.

The Next Step Could Be Glue-On Shoes

After a horse has laminitis, the veterinarian and farrier work to remove the forces on the compromised laminae, aid breakover by moving the breakover point back farther, and decrease tension on the deep digital flexor tendon. The horse’s shoes are usually removed and X-rays are taken. “I’m against shoeing a horse during the acute stage,” said Stephen O’Grady BVSc.

“If you have a horse with shoes on, the weight is concentrated on the hoof wall and the laminae. If I take the shoe off and use a different way to support the foot–letting the horse stand in sand, using Styrofoam or impression material in the bottom of the foot or any combination of those–the whole solar surface is taking weight.”

To help the hoof breakover more quickly, O’Grady suggests beveling the horse’s toe. “If the owner wants the horse shod, my criteria is first that the horse must be past the acute stage and relatively comfortable,” said O’Grady. “He also needs to be off [or on minimal] medication. Third, he needs to have no further radiographic changes for at least 10 days to two weeks. And the laminae have [settled] and damage doesn’t seem to be getting any worse. At that point the horse is in the chronic stage that we can deal with mechanically by trying to correct the rotation of the coffin bone.”

The advent of glue-on shoes has been a help to many horses. A farrier can also place the shoe wherever it’s needed on the hoof to attain the most area for weight bearing. (see article, p. 32) Glue-on shoes are ideal for realigning the coffin bone, especially if the foot doesn’t have enough hoof wall or sole to accomplish this by traditional trimming and shoeing methods.

A radiograph of the foot will show the farrier and veterinarian how much the coffin bone has rotated, how to trim the foot and apply the glue-on shoe at proper angle to place the coffin bone in a better relationship with the ground surface. O’Grady said that attaching rails to the shoe also helps. “When we lower the heels and apply a glue-on shoe and put the bone more parallel to the ground [which raises the toe] it creates stress again on the deep flexor tendon,” he said. “So we put the horse up higher on rails [raising the heels] to alleviate that stress.”

O’Grady said the final step is to support the solar surface. “Instead of having a shoe with rails and a big open place in the center of the shoe, the opening is filled in so it all helps carry the load,” he explained. This type of shoe helps reduce the pain, often limits further damage to the laminae, and may facilitate better circulation–which in turn will help produce better sole and horn growth. O’Grady said after the shoes are applied, the horse should be confined to a stall for the first three weeks and can be hand walked, gradually increasing his exercise.

Non-steroidal anti-inflammatory drugs are given as needed. The shoes are reset every four to five weeks, with the rails lowered at each reset as the hoof wall grows out and the coffin bone gradually returns to normal position. Usually the rail shoes are only needed for the first few shoeings, but the glue-on shoes are used until the hoof wall has grown enough to maintain the alignment with trimming and conventional shoeing.

O’Grady kept records on 42 horses with chronic laminitis in which this technique was used. At the first reset (five weeks after the glue-on shoes were applied), lameness was decreased and the horses showed no pain with hoof testers. There was increased sole thickness and notable hoof wall growth at the toe in all 42 horses. By the third reset, the hoof wall and sole growth kept the coffin bone in proper alignment and could be accomplished simply by trimming, and conventional shoeing.

O’Grady said few horses with chronic laminitis ever return to a former level of athletic use, but all the horses he’s treated with glue-on shoes have become comfortable enough to return to some level of use or be pasture sound with minimal pain medication.

Dealing With Digestion

If a horse’s laminitis was caused by a digestive tract problem such as grass or grain overload (also referred to as founder), you’ll need to monitor the horse’s food intake in the future. If he’s an easy keeper, he shouldn’t have access to spring grass or lush grass. Any fresh and tender grass, or stressed (such as after a frost) grass, may have a high sugar content. Some grass hay can also be high in carbohydrates.

“There can be differences, depending on species of grass, the time of year or stage of maturity it was cut, [or] growing conditions,” said Scott Morrison DVM, of Rood and Riddle Equine Hospital in Lexington, Ky. “Recent studies have shown that you can decrease carbohydrate levels in some hays just by soaking them in water because the sugar is soluble in water. If you have a horse that has a problem with sugars, this can help.” A horse that’s prone to founder should be fed little or no grain, yet you need to ensure he receives all the vitamins and minerals he needs. “Sometimes we recommend feeding a vitamin-mineral mix along with a hay ration, to make up for what a horse is missing in grain,” said Morrison. “Some feed companies have specially formulated feeds for these horses–that are low in carbohydrates.

This can be an option for a horse that has a hard time maintaining body weight. “If a horse is a hard keeper, a feed that has more calories in the form of fats or oils may be helpful,” he noted. “Feeding fat supplements can be an option for horses at risk for laminitis, providing calories in a safer form. It’s the soluble carbohydrates in the grain or lush grass that are really dangerous.”