Laminitis, a known debilitating disease of the foot, has been noted back to early history from Greek writings that cautioned
against feeding horses too much barley, and Romans noted the condition following overuse of horses on stone roads. It continues
to plague horses to this day.
This cut section of an equine foot depicts evidence of rotation and penetration of the tip of P3 through the sole.
Regardless of the origin of the initial insult, including gastrointestinal (GI), carbohydrate or grain overload, excessive
early-spring grass intake, toxins from black walnut shavings, colitis, metritis, placental retention, at-risk Cushing's horse
or from pounding the pavement, the end result is acute disease.
At one point, you have a normal healthy foot, then a trigger from a variety of origins, then laminitis and eventual lameness.
In its most severe form, laminitis results in breakdown of the laminar attachment, separation and movement of the coffin bone
as it rotates and descends within the hoof capsule, which can lead to a chronic or fatal prognosis. The disease begins with
the initiation point and proceeds through a developmental stage prior to the acute phase of excessive laminar inflammation.
Total destruction of the hoof structure can occur depending on the degree of inflammation and the extent of laminar tissue
Laminitis cases by perceived cause
The two theoretical initial pathways are: The foot is affected by toxins or metabolites via its blood supply that damages
the cells of the laminar tissue, or by what is thought to be a vascular origin promulgated by sustained decrease in blood
flow through the laminar interface to a point where oxygen delivery to the foot falls below the level needed for normal metabolic
function. Various mechanisms have been hypothesized to cause reduction of blood flow through the foot.
The final common pathway is thought to be one of mediation of extreme inflammation within the hoof capsule that eventually
severely damages the laminar tissue leading to detachment of the coffin bone. But whether inflammation or possibly ischemia,
the final common pathway is still unidentified at this time, according to David Hood, DVM, PhD, Texas A&M University. It would
be of interest to know how the triggers promote the inflammatory mediators and how the disease can be prevented.
Why? Theoretical response
Countless ponies, pleasure horses and other performances horses have been affected by laminitis. Why do some get it? Why do
some survive? The complete picture isn't clear.
"You're limited in what you can do to treat the initial cause because we don't have a clue of what triggers this thing," says
Ric Redden, DVM, farrier, International Equine Podiatry Center in Versailles, Ky. "We have a lot things that are primary that
will precipitate the syndrome, but we don't know the linkage of how they do it."
Presently, the best tactic is to try to recognize the disease as early as possible and prevent it from advancing, says James
Orsini, DVM, University of Pennsylvania.
"We know during the developmental phase of the disease we can prevent the progression to the acute phase by using an old technique
of icing the feet; standing the horse in a cold stream," Orsini says. "The other important goal is to identify risk factors.
We can then identify the at-risk patient and spend more time monitoring for the disease or even better, prophylactically icing
the feet and more aggressively using anti-inflammatories to prevent the disease from progressing to the acute stage and then
the chronic phase."
The chronic stage is the most devastating because once rotation begins, the foot is unstable, and a more difficult clinical
situation arises relative to day-to-day care and expense, frequently ending in humane destruction.