Your horse walks stiffly?when he’s willing to walk at all. Standing, he shifts weight from one front foot to the other or keeps both “parked out” in front. His front feet are warm, and when you put your fingers behind and just below the fetlock, you feel a throbbing pulse.

A horse with laminitis often presents with an odd stance. If his front feet are involved, he may stand with his feet “parked out” in front and his hind legs farther under his body than normal.

These are classic signs of laminitis in horses, a potentially devastating disease that can end your horse’s career or lead to ?euthanasia. Laminitis has frustrated ?veterinarians for decades. How does it develop? How should it be treated?

Thanks to advances in molecular ?biology, researchers are closing in on some answers. In this article, you’ll learn what happens in laminitis, as it’s understood so far, what you should to do if it strikes your horse and what factors shape his future outlook.

How Laminitis Develops
A quick review of how your horse’s hoof is constructed makes it easier to understand why laminitis is such a dreaded diagnosis. Delicate, leaflike structures?the laminae?secure the hoof wall to the coffin bone (also known as the third phalanx, distal phalanx or P3). The inner (dermal, or sensitive) laminae are extensions of connective tissue adhered tightly to the coffin bone. They mesh like interlocking fingers with the outer (epidermal, or ?insensitive) laminae, which line the ?inside of the hoof wall. The inner laminae are rich in nerves and blood vessels that supply oxygen and nutrients to the outer laminae. A thin basement membrane, interwoven with the tissue of the inner laminae, attaches to the epithelial cells on the surface of the outer laminae.

There are typically about 600 primary laminae in each foot, and each one is feathered with tiny extensions called secondary laminae. That feathering increases the total surface area and allows the two sides to grip like Velcro?. The bond between the basement membrane and the epithelial cells is so strong that it can hold the horse’s entire weight, catching the load carried down through the leg to the coffin bone and transferring it out to the hoof wall. The bond is also dynamic; as the hoof wall grows, epithelial cells periodically release their grip and migrate down, replaced by new cells generated in the coronary band?while maintaining enough hold to support the horse’s weight.

When laminitis develops, this well-orchestrated system breaks down. The laminae lose their grip on each other, and the coffin bone begins to pull away from the hoof wall. The separation usually occurs first at the toe. Then the bone, which normally is positioned parallel to the front of the hoof wall, is free to ?rotate vertically. The tug of the deep digital flexor (DDF) tendon, which runs down the back of the leg and ?anchors to the back of the coffin bone, encourages the rotation. Even a small degree of rotation is excruciatingly painful. The tip of the bone presses down, crushing soft tissues below it and sometimes even pushing through the sole just in front of the frog. In severe cases, the laminae may give way all around the foot, and the entire coffin bone sinks in the hoof capsule. Often both sinking and rotation occur. In such cases, the horse’s outlook is not good.

Laminitis (and founder, the term often used to describe displacement of the coffin bone) usually strike adult horses. All four feet can be affected, but front feet (usually both) are hit more often, largely because they support about 60 percent of the horse’s weight. According to a 2000 US Department of Agriculture survey, this ?disease is second only to colic as ?reason for a horse to get veterinary treatment and it leads to death or ?euthanasia in about 5 percent of cases overall. The death rate is much higher among severe cases.

Why Laminitis Develops
Any horse can get laminitis, but certain conditions greatly increase the risk. Among them:

• Carbohydrate overload. The horse gets too much rich spring grass or breaks into the grain bin and stuffs himself with sweet feed.
• Metabolic problems. Some horses (including many overweight individuals and those with Cushing’s syndrome) have metabolic disorders that put them at especially high risk.
• Severe gastrointestinal disease, including Potomac Horse Fever and other infections that cause ?severe ?diarrhea, or colic that compromises the intestine.
• Pleuropneumonia?infection and ?inflammation in the lungs and the pleura (the membranes covering the lungs).
• Acute uterine infection, from a ?retained placenta after foaling, for example.
• Black walnut shavings in bedding (if the horse ingests them) and certain other toxic substances.
• Mechanical stress?carrying excessive weight on one leg (because of severe lameness in the opposing leg), or repetitive hard work on hard ground.

Many of these conditions have a common thread: They provoke a whole-body inflammatory response similar to human sepsis. In severe sepsis, the body overreacts to an infection, setting off a cascade of events that leads to overwhelming inflammation. In people it can lead to multiple organ failure. In horses it can lead to failure of the laminae?or, laminitis.

Research hasn’t yet found a “silver bullet” that will stop laminitis in its tracks. It’s likely instead that a combination of approaches, blocking different pathologic events, will bring better ?results. But perhaps the most important thing learned so far is that early, aggressive treatment can save a horse’s life. There’s typically a lag of 24 to 72 hours between a triggering event?a septic ?reaction to infection or grain overload, say?and the first external signs of laminitis. But the damaging inflammatory response begins almost immediately. The horse still moves normally and there’s no increased pulse or heat in the foot?but the bomb has already gone off. And the time to prevent serious damage is before the outward signs show up.

Act Fast

If you know your horse broke into the feed room and stuffed himself with grain, call your veterinarian at once and begin treatment as she ?directs. If your horse develops one of the infections often linked to laminitis, it’s smart to add preventive treatment for laminitis to his treatment for that disease. There’s a huge range in the way that individual horses react to various triggers, but early treatment (more on this below) can stop the chain of events before the coffin bone sinks or rotates. If you can do that, there’s a good chance your horse will return to full work.

In the X-ray of this laminitic hoof, the dark “gas line” behind the front edge of the hooof wall indicates laminar separation. Both rotation and “sinking” (distal displacement) of the coffin bone have occurred within the hoof, and the tip of the coffin bone is close to perforating the sole.

Preventive treatment ?isn’t always possible, of course. Laminitis sometimes seems to appear out of the blue. Here are the symptoms to watch for:

• A strong, or “bounding,” digital pulse. A strong pulse in one foot could be a sign of a fracture or abscess, but a bounding pulse in both front legs is often the first sign of laminitis.
• Heat in the foot, especially at the front.
• Lameness, ranging from a stiff, hopping gait (especially when your horse makes a sharp turn or tight circle) to complete unwillingness to move.
• An odd stance. When his front feet are involved, your horse often stands with front feet “parked out” in front and hind feet placed much farther under his body than normal. He’s trying to take weight off his forelimbs. When all four feet are involved, the stance may seem more normal or “camped out” (forelimbs farther forward and hind limbs farther back)?but the lameness is usually more severe.

Fast action can still minimize the ?destruction, so don’t wait for these symptoms to get better on their own. Call your vet and, while you’re waiting, keep your horse quiet. Standing him in ice water will do no harm and may help (more on this below).

Your vet may use a short-acting lidocaine nerve block in both front feet to find out if his back feet are involved and to allow your horse to stand for ?radiographs (X-rays). Most horses who are affected both front and back turn out to be “sinkers”?cases in which the coffin bones sink, rather than rotate. ?Radiographs will show if the coffin bone is displaced.

The X-rays are essential?they’ll serve as a baseline for tracking changes in the weeks ahead?but unfortunately they don’t show everything. Researchers at Ohio State recently studied MRI views of the feet of horses who were euthanized in acute stages of laminitis at several clinics. The views showed that even when radiographs appeared normal, the laminae could be totally separated. In time, the coffin bone would have displaced.

Your vet also will want to know your horse’s history?whether he’s had a recent illness, injury or sudden change of feed. That will help identify what set off the episode.

Fight Back
Recognizing and treating the cause is the first step in fighting an acute attack of laminitis. ?Beyond that, treatment focuses on stopping the cycle of in?flammation and protecting the feet as much as possible from its effects.

Block Inflammation

• Nonsteroidal anti-inflammatory drugs (NSAIDs) are the one class of medications that have stood the test of time in fighting laminitis. In the early stages, NSAIDs are most effective at high doses. High con?centrations of these drugs ?appear to block multiple inflammatory pathways. At Ohio State, Dr. Belknap may give a 1,000-pound horse 10 cc of ?Banamine three times a day for the first two to three days, as long as the horse isn’t dehydrated and has no kidney or gastrointestinal problems. (Horses at risk for those problems may do better on a different drug, such as ketoprofen.)
• Cryotherapy?standing the horse in ice water?is a tried-and-true defense. It’s thought that cold may slow the actions of destructive enzymes and even decrease inflammation. This may be most helpful before symptoms appear. Researchers were able to prevent laminitis by keeping horses in ice water to the knees (or hocks) for 72 hours. That’s not practical in most settings, but icing as much as possible in the early stages may still help. Once ?full-blown laminitis develops, the benefits are less clear.
• Analgesic drugs interrupt the cycle of inflammation as well as reduce pain. NSAIDs have an analgesic effect, but more powerful painkillers are also ?sometimes used. One experimental early treatment is intravenous lidocaine, which may decrease some of the specific changes leading to laminar ?failure.
• Drugs are sometimes given to increase blood flow to the foot, on the theory that restricted blood flow damages the laminae, but the majority of these drugs may be of limited use. ?Acepromazine given intravenously is the only one that is scientifically proven to get more blood to the foot.

Keep medications up for a couple of days past the point where severe symptoms (pulse, pain, heat) ease. Then, depending on how your horse is doing, your vet can adjust the program. Meanwhile,

Protect the Feet
The goal is to take as much strain as possible off the laminae.

• Remove your horse’s shoes, which put most of his weight on the hoof wall.
• Cushion his feet by taping on ?Styrofoam pads (cut from 2-inch foam insulation board, for example) or commercial supports that protect the entire sole or at least the caudal aspect (from the tip of the frog back). The foam pads compress to about 3?4-inch thick over a day or so, and then a second set can be taped over them.
• Put your horse in a stall to limit ?movement. If the laminae are hanging by threads, any exercise could be too much.
• Bed the stall deeply or provide soft but supportive footing (such as sand or tanbark) for cushion and to encourage him to lie down.

If radiographs show coffin-bone rotation, some horses respond well to raising the heels, to lessen the pull of the DDF tendon on the coffin bone. That’s done with pads or by taping on specialized shoes, such as the Redden Ultimate shoe, in combination with a resilient putty to support the caudal sole.

Other steps may be called for. A foot that is rapidly ?deteriorating may stabilize in a cast. In a clinic, a sling can help take weight off a horse’s feet?but some horses won’t tolerate this.

Watch Closely
The first two to three weeks are a critical period. Call your vet if:

• Symptoms such as heat in the feet or a bounding digital pulse return.
• Your horse seems more uncomfortable. Don’t walk him up and down. Just watch him in his stall. If he lies down to rest but gets up during the day and moves around comfortably, he’s probably not in so much pain. Each horse is different; but if your horse becomes less willing to move, that’s not a good sign.
• You see cracking at the coronary band, or cracking or a bulge on the sole (usually directly in front of the frog). These signs indicate severe, sudden changes inside the foot?the coffin bone is displacing?and you need your vet quickly.

Your vet will take follow-up radiographs (every couple of days, in a ?severe case) to see what’s happening in the foot. If you can keep the coffin bone from displacing further in the first weeks, the foot usually stabilizes. Then you can begin the long process of ?reversing the damage.

Long-Term Hoof Care
The laminae won’t be firmly attached until a healthy new hoof grows in. At an average growth rate of 1?4 to 3?8 inch per month, that can take a year. Your horse may need corrective shoeing for that time or longer. The laminar bond will be strongest when the coffin bone aligns as closely as possible to its normal position. Even with corrective shoeing, that can be hard to achieve in cases with severe coffin bone displacement (sinking or ?rotation of 15 degrees or more)?and the odds of a return to full work may be poor in these cases. Still, if they don’t ?return to full work, it’s often possible to get these horses pasture-sound. The ?outlook is better for cases with little or no rotation.

Involve your vet and an experienced farrier as a team to manage your horse’s recovery and develop a long-range plan tailored to his case. The goal is to help the hoof grow out with the position of the bone aligned as closely as possible to normal.

Your vet will take follow-up radiographs to guide the work. Typically the farrier will come monthly to shorten long toes, trim excessive heel length, and fit corrective shoes as indicated?but there’s no one-size-fits-all program. Take the lead, if necessary, to keep the team in communication and get follow-up exams and shoeing changes done on schedule.

What shoes? You’ll hear people insist that certain shoes, or no shoes, are the only way to go. The fact is that each case is different, and no approach works every time. However, most horses seem to do better with shoes of some type?as long as the shoes fit the case and provide support for the sole, not just the wall. Innovative shoeing systems are producing good results. Among them are these:

• the Equine Digit Support System uses a wide-web, square-toe, bevel-front aluminum shoe that’s set back at the toe, to relieve the stress of breakover on the laminae. It’s paired with support ?material over the sole and various ?attachments, including wedges (rails) to raise the heels varying degrees.
• the Four-Point Rail Shoe is a glue-on aluminum shoe built on similar principles, with a raised heel and beveled toe; the heel height is not adjustable.
• full rocker designs, like the Steward Clog, allow easy breakover in any ?direction and can be particularly helpful for “sinkers.”

A skilled farrier can also get good ?results by customizing heart-bar, egg bar or other traditional shoes and using various pads. Reverse shoes are not used as often as they were a decade ago. They provide heel support and move the breakover point back, ?relieving stress, but they leave the toe unprotected?and the toe can be a site of soreness.

Overall Management
If all goes well over the following months, normal wall will slowly grow down from all around the coronary band. You may notice a “fever ring,” a slight deformity, marking the point where new growth begins. Meanwhile, your horse needs careful management and a watchful eye, to be sure symptoms don’t return.

Nutrition: A number of supplements and herbal products are marketed as aids for horses with laminitis. Clinical studies have yet to show that any of them are helpful. But horses with metabolic problems need special low-carbohydrate, high-fiber diets and, often, medication. If there’s a chance that your horse is in this group, your vet can run blood tests and send away a sample of your hay for analysis to help you figure out a program for him.

Exercise: Stall or turnout? You may hear people say that exercise promotes recovery. Researchers are investigating this, especially in horses with metabolic syndrome. Doing too much too soon definitely has risks, though. When your horse is past the acute stage and moving comfortably in his shoes, ask your vet if you can hand-walk or turn him out in a small paddock with level, soft footing.
The timing for this is highly variable, so follow the program set by your vet. A horse with severe displacement and massive damage to the laminae will need to be stalled longer than a mild case. Overweight horses who founder for metabolic reasons may benefit from getting out a little sooner?inactivity contributes to obesity, and fat plays a part in the inflammatory process. These cases also tend to have more laminar stability than horses who founder from septic causes. You don’t want them running around, but even limited activity helps burn calories?and it’s been shown to reduce systemic ?inflammation in people with metabolic syndrome.

Return to work: This may be the biggest variable of all. A horse with a mild case and no displacement might start back into light work in three or four months. With extensive separation of the laminae, you simply have to wait until enough healthy hoof has grown in to support the horse’s weight, which could be up to a year. Some horses never come back.? ?Recovery from laminitis takes time and commitment, and??despite all the progress that’s been made?it is ?unpredictable.? PH

At Ohio State University Veterinary ?Teaching Hospital, James Belknap, DVM, MS, PhD, DACVS directs a laboratory ?exploring the pathophysiology of laminitis and focuses on new treatment and prevention strategies. He also works ?clinically on laminitis cases with a team of farriers and clinicians. Dr. Rustin Moore, a ?well-known laminitis researcher, leads the equine group at OSU as their department head. Dr. Belknap is an associate professor in the ?Depart?ment of Veterinary Clinical Sciences at the OSU College of Veterinary Medicine.

This article originally appeared in the February 2008 issue of Practical Horseman magazine.