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.
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.