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Managing and preventing laminitis (“founder”) in your horse
Preventing Laminitis (“Founder”) in Your Horse
Department of Veterinary Clinical Sciences
Laminitis is one of the most devastating diseases confronting equine owners and trainers
due to its crippling nature. Laminitis results in a structural failure of the laminar tissue which supports the entire horse‟s musculoskeletal system by suspending the coffin bone (also called the third phalanx, analogous to the last bone in your middle finger) within the hoof wall (discussed further below). Founder, a term commonly used interchangeably with laminitis, is more appropriately used to describe the condition after downward displacement/rotation of the coffin bone has occurred. There are four main causes of laminitis: and 1) laminitis secondary to the same type of systemic diseases that can lead to organ failure in human sepsis cases (sepsis is generally defined as an infection that results in the presence of bacteria or their toxins in the blood [septicemia] or in other tissue of the body), 2) supporting limb laminitis (the type Barbaro developed) occurring when horses must place the majority of their weight on one limb due to any type of condition on the opposite limb (i.e. a fracture) which does not allow the animal to put weight on that limb, 3) pasture-associated laminitis seen in ponies and horses which are usually overweight, and 4) Equine Cushings Syndrome seen in older horses due to the development of a benign tumor in their pituitary gland which results in high levels of circulating steroids. The last two types of laminitis are commonly lumped into the term “endocriopathic laminitis”.
In this article, we are going to concentrate on sepsis-related laminitis, the cause of
laminitis that has been most extensively studied. The types of diseases commonly seen in the horse that lead to this type of laminitis include diarrhea (enterocolitis), grain overload, pneumonia, retained fetal membranes (placenta), and any type of colic which leads to compromise of the intestinal wall and absorption of bacterial toxins. These diseases lead to horses becoming very „toxic‟ (similar to human sepsis patients, due to absorbed bacterial toxins, commonly termed “endotoxemia” in the horse) in the initial phase of these different disease processes. The signs these “endotoxemic” horses will commonly exhibit include lethargy/depression, dark red mucous membranes (gums), and possibly a fever. Interestingly, after the horse suffers a „toxic‟ episode from one of the disease processes described above, signs of lameness due to laminitis will not appear until for approximately 20-40 hours. Therefore, you can not rest easy that a horse will not get laminitis when a horse has developed one of these diseases for approximately 2 days after resolution of the disease and all associated signs, and should therefore work with your veterinarian to treat that animal aggressively in the meantime.
To understand the disease, we need to first understand the anatomy of the laminae of the
equine digit. The digital laminae (also termed lamellae) are specialized structures in which 500-600 „leaves‟ of tissue attached to the hoof wall consisting mainly of epithelial cells (epidermal laminae) interweave with the same number of leaves of tissue consisting mainly fibrous connective tissue attached to the coffin bone (dermal laminae). The critical interface between the two sets of laminae that fails in laminitis is the attachment of epidermal epithelial cells (similar to your skin cells) to the underlying connective tissue called the dermis. This interface is dynamic because the epithelial cells must play two simultaneous but highly orchestrated roles
where, at any one time, some are unattached from the dermal connective tissue (to allow the hoof wall to grow down) while a critical number of others are still attached to allow for suspension of the coffin bone (and therefore the entire weight of the horse) by the hoof wall. Support of the entire weight of the horse is dependent on this highly orchestrated process. In laminitis, there is a disruption of this process leading to separation of the epithelial cells of the epidermal laminae away from the underlying connective tissue and, importantly, loss of laminar support of the coffin bone. The downward displacement of the coffin bone can take place either 1) by rotating, where the laminae on the dorsal (front) aspect of the foot separate and the coffin bone pulls away from the dorsal hoof wall and the toe rotates downward, or 2) by “sinking” (also termed distal displacement), where all laminar attachments of the foot (not only the toe but quarters also) give way at once and the entire foot “sinks” straight down. Rotation occurs most commonly, and more commonly affects the front feet (although they will look like their back feet are also affected because they place them well underneath themselves to take more weight off the forelimbs). “Sinkers” are commonly affected in all four limbs. In some horses, both sinking and rotation will take place.
A combination of the most recent research findings with those from studies performed
in the past suggests the most likely scenario occurring in the horse’s digit in the early stages of
the disease being a severe inflammatory injury (similar to that reported in organ failure in
human sepsis) and, to a lesser extent until late in the disease process, a disruption of the
normal blood flow to the foot.
Both of these events are likely to disrupt the highly orchestrated
regulation of the laminar epithelial cells resulting in a general detachment of the cells, and
therefore the epidermal laminae, from the underlying connective tissue of the dermal laminae.
So, if you have a horse with one of the disease processes listed above, what can you
expect to happen when? The take home message from the new information discussed above is
that this first 1-2 days when the horse is exhibiting signs of “endotoxemia” is the critical time
to treat these horses aggressively well before they show signs of laminitis. If we wait to treat
once signs of laminitis to be observed, we will be far “behind the eight ball”.
If we can block
the disease process at this point (before signs of laminitis) and do not reach the point of the third
phalanx displacing by either rotating or “sinking”, we have a good chance of having these horses
return to full athletic activity. First, we should treat aggressively with anti-inflammatory drugs
(i.e. NSAIDs such as banamine/flunixin). What can we do besides giving NSAID drugs? There
is strong evidence at this point that “icing the feet” (placing the feet in bags of ice water)
decreases the laminar injury, by decreasing inflammation and generally slowing the metabolism
in a foot where injurious enzymes are likely being released. This typically requires long-term
icing (possibly up to 72 hours) and should be coordinated/overseen by a veterinarian. We can
also protect the laminae as much as possible, by first removing the shoes (gently!), because a
standard horse shoe places all forces on the hoof wall and laminae and no support where it is
needed on the sole (the other choice is to leave the shoe on and fill the sole with a resilient
We can then either tape a soft but supportive substance to the bottom of the feet
(e.g. 2 inch commercial Styrofoam insulation for houses, or, better, closed cell foam as used for
wrestling/gymnastic mat material), or just place the animals on a soft supportive substance such
as sand or thick sawdust which will contour to the concave shape of the bottom of the foot and
support the coffin bone through the sole. The author feels that some type of padding supporting
the sole is still useful in most situations. Finally, we should not walk the horse, and should
encourage it to lay down as much as possible (by deep straw bedding, etc. over the sand or
sawdust) to reduce the weight and resulting biomechanical forces on the laminae. Researchers
and clinicians have used multiple drugs to try to increase blood flow to the foot; almost all of
these drugs have been found to be ineffective (including nitroglycerin, isoxsuprine, and
pentoxifylline), mainly because they do not cause vasodilation in the horse. The only drug that
has been shown to cause an increase in digital blood flow is acepromazine, a commonly used
tranquilizer in horses.
This drug has the added value that it is a sedative and may decrease the
stress level of the horse.
Not every horse with one of the diseases described above is going to get laminitis.
However, due to the crippling nature of the disease once coffin bone displacement occurs,
laminitis or those diseases or conditions that predispose horses to developing laminitis should
be considered emergency situations.
You should contact your veterinarian immediately if your
horse is suffering from one of these septic events (i.e. accidental grain overload in any horse or
pony, retained placenta in a broodmare) so that the appropriate preventive or therapeutic
treatments can be instituted in a timely manner, which will increase the likelihood of getting the
horse through the episode without career-eneding and/or life-threatening consequences.
Please keep in mind that we are now realizing that laminitis caused by entitities besides
sepsis do not appear to have the same pathophysiology; this is exemplified by our recent
discovery that there appears to be minimal inflammation in the laminae in an experimental
model of pasture-associated laminitis. In regards to supporting limb laminitis, recent research
supports that decreased blood flow in the weight bearing foot may be the central event in laminar
injury in that model. Thus, as we learn more about the different types of laminitis, we are likely
to be able to design distinct effective therapeutic strategies to treat animals at risk of or suffering
from this devastating disease process. Dr. Belknap is a board-certified equine surgeon at Ohio State University who specializes in
soft tissue surgery, lameness, and podiatry (foot diseases such as navicular disease and
laminitis) when on clinical rotations. He works with Journeyman farriers Todd Adams
and Trey Green on Wednesdays on podiatry cases. Dr. Belknap also has an internationally
recognized research program studying equine laminitis. He has published numerous
articles and book chapters on laminitis, and has speaks nationally and internationally on
the topic. He has given two international awards for his laminitis work.
UNIVERSIDAD NACIONAL AUTÓNOMA DE NICARAGUA UNAN-MANAGUA VICE RECTORÍA ACADÉMICA “ AÑO DE LA TRANSFORMACIÓN CURRICULAR ” CALENDARIO ACADÉMICO 2011 CURSOS REGULARES CURSOS SABATINOS (PROFESIONALIZACIÓNY POR ENCUENTROS) PRIMER INGRESO 2011 CURSOS DE VERANO 2011 ACTIVIDADES ESPECIALES VACACIONES DEL PERSONAL FERIADOS NACIONALES Y LOCALES
REVISTA PACEÑA DE MEDICINA FAMILIAR ACTUALIZACIONES TRICOMONIASIS UROGENITAL * Medicos Familiares Pol. Central GENERALIDADES: presentar cuatro flagelos dispuestos de dos en dos en la parte anterior, y un flagelo recurrente Es la presencia de protozoos flagelados, que forma la membrana ondulante, que no llega a pertenecientes a la Familia Tricomonadidae y al la parte poster