Head Into The Horror Of Laminitis Well-Armed

Laminitis is a devastating affliction. In its most severe form, the pain probably feels like crushing your fingertip in a car door and then having the fingernail torn off with pliers. And even after the horse weathers the acute episode, he faces a prolonged recovery period, from several months to a year.

Just like us, overweight horses are more prone to health problems, including laminitis. Read supplement labels: Glucosamine can contribute to insulin resistance.

If severe displacement or “rotation” of the coffin bone occurs (actual founder), the horse may never be normal again. To minimize the chances of your animal experiencing laminitis, and to know how to treat it in the acute phases, you must understand its causes.

Laminitis means an inflammation of the laminae, a network of fine connective tissue bands in the hoof that secure the coffin bone in place. How the laminae become inflamed, weakened or destroyed is debatable, but altered circulation to the feet sets the stage for most, if not all, cases. That said, it’s likely more than one mechanism is in operation in any case of laminitis, probably with several initiating causes.

Elaborate research by the Australian Equine Laminitis Research Unit, under the direction of Dr. Chris Pollitt, has greatly advanced the understanding of what happens in laminitis. The horse’s foot contains many arteriovenous shunts, or “short cuts,” for arterial blood to bypass the capillary beds, where nutrients are extracted and waste materials picked up and jump directly over from the arteries to the veins.

These shunts protect the foot during exposure to extreme cold. The “hot” arterial blood rushing in from deeper body areas mixes directly with the more superficial venous blood in the foot that has been cooled by the environment, preventing the foot from freezing. It’s been hypothesized that over-activation of this shunting may be a part of the vascular changes that induce laminitis.

Research at the University of Minnesota and at the University of Tennessee shows that in the early stages, before clinical signs of lameness develop, the foot goes through a period of vasoconstriction or blood-supply loss. A University of Georgia study revealed increased resistance to blood flow on the venous side, causing back pressure that makes the capillaries more “leaky.” What all this proves is what we said in the beginning: Blood flow to the foot is definitely compromised in laminitis.

When the blood supply decreases, the cells go into oxygen starvation, which means they enter an anaerobic mode in an attempt to survive. This, in turn, generates free radicals and other toxic end products, but eventually the cells die or become damaged anyway.

If blood supply to a heart or a leg is severely decreased, the damage is obvious. However, the most damage actually occurs when the blood flow gets restored to the damaged area. This is because the injured tissues trigger a huge inflammatory influx of white cells, which then release cytokines and enzymes that begin cleaning up the damaged cells and, quite often, do damage of their own in the process. This is called “reperfusion injury,” and research in laminitis appears to indicate this is the most damaging phase as well.

With experimental models of laminitis in horses, there’s been noted to be an initial prodromal, or symptom-less, phase that lasts 12 to 16 hours during which circulation to the foot drastically decreases (called vasoconstriction). This blood-vessel constriction can be triggered by a number of factors, including endotoxins, inflammatory body substances and elevated hormone levels (cortisol and insulin).

What follows is the stage we’re all most familiar with — the hot feet with pounding pulses and extreme lameness. This occurs when the blood flow is restored, which occurs due to a drop in the level of the offending vasoconstrictive substances and local mechanisms that increase pressure in the foot and “blow open” the constricted vessels.

This is similar to what happens in people with a migraine headache. During the vasoconstrictive phase when visual disturbances may occur, there’s no pounding pulse or headache. But when the blood rushes back in, the pain starts.

The combination of all these factors — high blood pressures in the foot, tissue damage from the blood-constriction phase and energy-metabolism alterations, plus a further release of inflammatory substances in the area when the blood flow is restored — combine to further damage the delicate laminae, which are supposed to hold the coffin bone in place. And, when the coffin bone moves out of place — or rotates — you’re moving from laminitis into actual founder and a long, shaky road to recovery.

We realize these scientific studies can be rather complicated, but they’re necessary to make sense of how different things can cause laminitis and what to do about it. While it’s simple to say that laminitis is caused by a retained placenta, too much grain or spring grass, black-walnut exposure or any number of other things, this won’t help you understand what’s actually going on in your horse’s body — and that’s what you need to understand to devise the right emergency treatment.

Retained placenta in mares is a classic example of endotoxin production, the effects of which are more than likely enhanced further by all the hormonal upheavals at that time.

Black-walnut poisoning and corticosteroid-induced laminitis seem to share a common cause as both make the vessels more sensitive to the constricting effects of circulating catecholamines.

Laminitis due to grain/spring grass overload, Cushing’s and obesity is complex but, apparently, all these causes share a common pathway: ingesting too much easily digestible carbohydrates, simple starches and sugars. How much is “too much” depends in some cases on the level of insulin resistance, a condition similar to adult-onset diabetes in people.

For seriously insulin-resistant animals, even a few mouthfuls of a carbohydrate-rich grass or a cupful of grain or sweet feed can be more than their systems can manage. Insulin resistance is a common metabolic consequence of pituitary tumor and/or Cushing’s disease in horses, and these horses may also have high circulating levels of the cortisol hormone in their blood, or possibly a higher-than-normal ratio of cortisol to its inactive metabolites.

It takes a lot more than this to overwhelm the system of a normal horse — something along the lines of getting into the grain bin for a few hours of unsupervised “pigging out.” The diabetic-like state that results can produce vasoconstriction, and resistance to relaxation has also been demonstrated in carbohydrate-loaded horses. It’s also been hypothesized that an impaired ability to utilize glucose in the connective-tissue-producing cells of the foot is part of the problem.

A second component to carbohydrate-induced laminitis may be related to what happens in the hind gut/large intestine when part of this huge load of sugars and starches escapes digestion in the small intestine and gets dumped in with the rich microbial populations of the large intestine.

Most of these organisms normally have to work hard for their glucose by breaking down intricate plant starches and fiber. When presented with a load of simple sugars and starches, the microflora capable of using them quickly metabolize s the unusual abundance of fuel and, in the process, generates a huge amount of lactic acid. This, in turn, acidifies the fluid in the bowel, effectively killing off the microflora that rely on more-complex carbohydrates, leaving those that generate the lactic acid to flourish.

Before the information regarding insulin resistance and parallels with circulatory problems in human diabetics was known, it was assumed that this shift in the intestinal microflora encouraged the growth of endotoxin-producing species and that the acidity was somehow responsible for laminitis.

Studies since then have pretty much discounted this theory, although the release of other substances destructive to the laminae by the proliferating bacteria is possible. What role, if any, “acidity” plays is unclear, but since lactic acid is readily converted into glucose by the liver it would add to the already high glucose load.

The reason understanding the mechanics and causes of laminitis is so important is so you can determine the best treatment options for an acutely foundered horse. We’ve gathered in our chart (see end of story) common laminitis first-aid measures and treatments and explain when they are indicated — or not indicated. Of course, proper diet and hoof care, are always required treatments.

A horse with laminitis should receive a diet of high-quality, late-cutting, high-fiber hay, water and any needed supplements only. No grain. Even if the laminitis wasn’t carbohydrate-induced, the last thing the horse needs is the addition of any factor, like a high-carbohydrate diet (including rich, early cuttings of hay), that could worsen the problem. In grain or grass laminitis, laminitis in obese animals and in horses with Cushing’s, the diet should be followed rigidly and permanently.

Cutting out grain might not be enough. Glucosamine should also be avoided, since it can contribute to insulin resistance with chronic use. This isn’t a problem for a normal horse, but it could be important in a metabolically compromised one. Grazing also needs to be either strictly limited or cut out entirely and even the type of hay you feed can have an effect (see sidebar at end of story).

When you call your veterinarian to come see your acutely laminitic horse, make sure he or she understands you want X-rays. And as soon as you hang up the phone from that call, get right back on the horn to your farrier.

Proper emergency care of laminitic feet not only increases the horse’s comfort immensely but also can influence whether or not coffin-bone rotation occurs — and you want to avoid that as this is what puts horses out on permanent disability.

Shoes should be pulled gently, one nail at a time, and heels adjusted to stabilize the coffin bone in a ground parallel position. If the foot has already started to rotate, the farrier and veterinarian should confer to decide how much heel to remove to eliminate the pull that the coffin bone is putting on the laminae. This is where those X-rays you had done will come in handy.

If there’s not enough foot to work with to stabilize the coffin bone, a short-term fix can be obtained by wedging the toe up using a degree pad turned around so that it’s higher in front than at the heels.

With sore and rotated horses, or when farrier care isn’t available on an emergency basis, a rubber door stop/wedge can be used instead.

Horses that are too sore to stand also often obtain considerable relief by cutting a piece of inch-thick styrofoam to match the outline of the bottom of the foot and securing the styrofoam in place with duct tape.

Care of a laminitic horse can be considered a specialty. If your farrier is not familiar with this area, regardless of how wonderful a job he or she does otherwise, locate an expert farrier to either do the foot care or a veterinarian or farrier who can advise your farrier on how to proceed with your horse.

Bottom Line
As the understanding of laminitis grows, so does our ability to decide on treatments that are rational and effective. Time-honored, common-sense treatments such as cooling hot feet, keeping the horse on a soft, deep surface and not forcing a lame horse to walk still apply.

Knowledge of the timing and nature of the vascular changes we described in the foot makes the choice of drug therapies easier and explains how some folk remedies, like magnesium, might work. In addition, the realization that grain- and grass-related founder is linked to problems with handling glucose certainly makes more sense than just that these feeds might be “too rich” and also opens many new avenues for prevention and treatment. Note: We currently have a field test in process with medications and supplements for specific types of acute and chronic laminitis.

See also: “Cresty And Laminitic’ Give ’Em Magnesium,” January 2001; “Herbal Offers Hope For Cushing’s Syndrome,” December 2000; “Pony Problems: Grain,” April 2000.

Also With This Article
Click here to view “Laminitis Emergency Procedures.”
Click here to view “Common Laminitis Treatment Indications.”
Click here to view “Could A Low-Carb Hay Be On Its Way'”
Click here to view “No Corticosteroids For Laminitis.”
Click here to view “Magnesium For Acute Cases Of Laminitis In Horses.”