Mechanical Treatment of Laminitis and Founder
Tom Stovall, CJF © copyright 1997

If anyone ever figures out what exactly triggers the mechanism of the pathology we call "founder"; or, better yet, figures out how to halt the process, they will be assured of wealth and fame.

Actually, the terms "founder" is often used incorrectly to describe an inflammation of the laminae. More properly, an inflammation of the laminae is called, "laminitis" and the term "founder" used to describe the partial detachment of the coffin bone from the hoof wall at the laminar interface.

The main attachment to the hoof capsule of the column of bones that comprise a horses lower leg is at the interface of dermal and epidermal laminae. Dermal laminae originate from the dermal corium on the dorsal surface (front) of the coffin bone. Epidermal laminae are found on the stratum internum, the most proximal (innermost) portion of the three layers which make up the hoof wall, and arise from the coronary corium.

The attachment of the laminae arising from different structures is anatomically analogous to a hook and eye attachment with one very notable exception: once laminae are separated, they will not reattach. They will not grow back together.

The coffin bone exists in precarious balance within the hoof capsule. On its dorsal side, the convoluted folds of the laminae serve to attach it to the hoof wall; simultaneously, the deep digital flexor tendon, which inserts at the semi-lunar crest ("wings") of the coffin bone, exerts constant tension on the bone and pulls the bone downward each time the foot is turned over ("flexed").

Any inflammation of the laminae, from whatever origin, is called "laminitis". As long as the laminae are well supplied with oxygenated blood, the balance between laminae and tendon is largely undisturbed; however, laminitis can disrupt the capillarial blood flow which supplies the laminae and can result in separation of the laminae at the junction of dermal and epidermal laminae (between the inner hoof wall and the top of the coffin bone). This phenomenon can have serious consequences.

Laminitis has many causes: among them, overwork, overfeeding, infections, organic toxins, shock and probably a change in the weather. All of the causes are unknown, but once laminitis occurs, the changes within the foot are fairly well-documented. Inflammation of the laminae causes blood circulation to be compromised to the middle third of the foot; with nowhere to go, this blood is immediately shunted back up the leg through the venous plexuses. Unfortunately, most of the relevant laminae are located in the middle third of the foot.

The most obvious symptoms of laminitis are distress, lying down with an unwillingness to get up, a "camped out" attitude, a reluctance to move, a pain response to hoof testers at the toe, and a pronounced digital pulse. There's a lot going on within a laminetic horse's foot and most of it's painful.

Separation at the laminar interface reduces the strength of the coffin bone's attachment to the hoof wall and laminar separation often causes bleeding within the hoof capsule.

This combination of laminar destruction and hydraulic pressure within the dorsal portion of the hoof capsule when coupled with the constant downward pull of the deep digital flexor tendon can be strong enough to pull the coffin bone downward.

Why downward? The top (proximal) portion of the coffin bone pivots at the coffin (distal interphalangeal) joint. The deep digital flexor tendon, using the navicular bone as a fulcrum, flexes that joint each time foot flexes (turns over). If the attachment of the coffin bone to the wall is compromised, when the flexor muscles pull on the tendon, instead of the foot turning over, the coffin bone is pulled away from the hoof wall. The subsequent rotation of the coffin bone is called "founder".

After coffin bone rotation has been initiated, other factors occur which can cause the phenomenon to worsen, the most important of which has to do with the incompressibility of fluids. As the laminae are torn, bleeding occurs within the hoof capsule: because the dorsal hoof wall is the least flexible portion of the wall and the coffin bone is inflexible, the hydraulic pressure exerted by this blood flow often causes more tearing, more bleeding and more coffin bone rotation. When this occurs, instead of attachment loss at the laminar interface and the pull of the deep flexor being responsible for rotation, the bone is also pushed downward by the relevant hydraulics - in severe cases, through the sole.

Laminitis and founder can be of systemic origin (as previously discussed) as well as mechanical origin. The most common mechanical origins of laminitis and founder are pawing, poor husbandry and poor farriery. Mechanical founder can sometimes occur without laminitis in the case of catastrophic insult or loss of hoof wall to disease.

These maladies most often occur in the front feet - occasionally in all four - of large equines, with all four feet being affected more often in ponies, small mules and asses. Occasionally, only one front foot is affected, but the cause of unilateral founder is always mechanical.

The third phalanx (P3) cannot rotate downward if it is stable. Once destabilized by laminitis, hydraulics, disease or injury, it will rotate downward until stability is achieved.

"Stability" is that delicate balance in which the dermal and epidermal laminae manage to maintain a hold on the hoof wall, themselves and the coffin bone while the deep digital flexor tendon (DDFT), using the navicular bone as a fulcrum, causes the articulation of the coffin (distal interphalangeal) joint. Another way of saying this is to say that if the laminae don't tear, the hoof will be turned over by those muscles high in the leg called "flexors" which transmit their energy to the foot through the associated flexor tendons. Since the foot turns over each time the horse takes a step, it follows that successful treatments for founder involve stability, support and enhanced turnover.

As an aside, medication and mechanical treatment get a lot of the credit for stabilizing horses that rightfully belongs to Nature. A great many horses destabilize, founder, then restabilize and nobody is the wiser until some farrier notices the thickened white line and asks, "When'd this horse founder?"

From a  mechanical standpoint, stability of P3 is achieved by the application of some kind of mechanical pressure to the frog. (The frog lies directly below P3 and is a weight bearing structure.) But, what kind of mechanical pressure? Mechanical pressure can take many forms, including pulling the shoes and turning the horse out on sand, the application of frog pressure pads (e.g., Lily Pads), soft packing, or the forging and application of shoes that apply pressure to the frog, which includes heart bars, g-bars, t-bars, and variations thereof.

Obviously, there's a thin line between stabilization and support. Mechanical support means that some mechanical device, pressure pad, pressure packing, or pressure bar, is placing constant, direct pressure on the frog; environmental support means that the ground surface of the frog (foot shod or unshod) is in contact with the ground any time the foot is on the ground.

Assuming that the horse, for whatever reason and by whatever means, has stabilized, the most important factor becomes enhanced turnover.

Turnover is the fourth phase of motion. At any gait, at any speed, in order to move forward, the foot must be turned over; therefore, anything that enhances turnover will lessen the inherent stress at the interface of dermal and epidermal laminae at turnover and serve to ease the pressure of the DDFT on both the navicular bone and at its insertion on P3.

How is turnover enhanced? In the main, in two ways: by increasing phalangeal angulation and/or by decreasing the effective length of the phalangeal lever. Additionally, turnover can be facilitated to a lesser degree by the farrier's choice of shoe configuration and by various forging methods.

All other things being equal, the most important factor influencing turnover is the placement of the shoe on the foot because the length of the phalangeal lever is determined by the distance from the coronary band to to the breakpoint of the shoe, not by the distance from the coronary band to the end of the hoof capsule. For this reason, the wall is not considered, other than as a limiting factor, in the placement of the shoe on the foot.

In my experience, the most effective means of mechanical treatment of founder consists of a pressure bar, set under. The problem with pressure bars is that their application must be absolutely correct; if not, they will do more harm than good. For this reason, many veterinarians are reluctant to prescribe their use and instead prescribe methods that are not as effective, but do not have the potential for damage - and litigation.

One of those stop-gap methods is the application of several wedge pads - a method that certainly increases phalangeal angulation but does not necessarily stabilize P3 angulation, with or without frog pressure. Increased angulation may negate the pull of the DDFT, but it does not necessarily stabilize P3 because other factors, especially hydraulics, can contribute to the rotation of P3.

The reader should be aware that there is no single, "best" method of mechanically treating founder. Hot (acute) founders are treated differently than chronic founders; systemic founders are treated differently than mechanical founders; however, if I were limited to only one mechanical means of treating founder, it would be a set of pressure bars, set under as far as they'd go.

Applied without drains to a stable horse; or, applied to a hot founder with pressure relief, properly applied pressure bars are unquestionably the most successful method of treating founder when mechanical treatment is indicated.