If you’ve felt soaking feet in cold water could play role in laminitis treatment, researchers are starting to agree

EXCITING NEW IDEAS for understanding and treating laminitis, including use of cold water therapy, were revealed during December’s American Association of Equine Practitioners annual meeting.

Some 4,711 attendees, including a sizable number of farriers who attended a special half-day podiatry session, were on hand for this meeting in Albuquerque, N.M.

Critical Lamellar Changes

Dr. Chris Pollitt, a world-renowned hoof researcher from the University of Queensland in Queensland, Australia, shared valuable updates on the causes behind the three phases of laminitis.

He believes lamellar changes with laminitis are caused by a disturbance of a normally tightly controlled process or structure in the horse’s body. The result is that the horse produces a specific class of enzymes known as matrix metalloproteinases (MMP) in response to the stresses and strains of normal equine life as well as ongoing body growth.

“When called for, enough MMP is produced to maintain the correct shape and orientation of whatever structure is in need—bone, joint, or in this case, the lamellae,” says Pollitt. “It is possible that repair of the lamellae, necessary for the hoof wall to grow past the stationary coffin bone, is the target of the laminitis disease process.”

When MMP enzymes are not inhibited, Pollitt says they dislodge cells that produce new lamellae from the basement membrane (a delicate tissue layer that serves as the protective barrier between the epidermis and dermis) which then peels away from the hoof in sheets. Because the basement membrane is the key structure between the lamellae and the coffin bone, it leads to the failure of that attachment between the inner hoof wall and the coffin bone.

Circulatory Changes

Pollitt told farriers and equine vets that additional components of lamellar anatomy are affected by overproduction of MMP in the lamellar capillaries. As the basement membrane disappears, the loss of these capillaries may explain why resistance to blood flow can be increased by as much as 3 1/2 times in horses during early laminitis. This is also why blood bypasses the capillary bed, flowing instead through the larger arteries and veins.

“These two changes in circulation produce the ‘bounding digital pulses’ felt in the acute phase of laminitis that are believed to occur as a result of excess MMP,” he says.

Pollitt says the concept of MMP triggering has led to a challenge of alternative views that laminitis develops because of circulation changes in the foot. Current theories conclude that the constricting of veins with high fluid pressure blocks the flow of blood through the capillaries of the lamellae, eventually causing the lamellae to die.

“However, our research has not provided any evidence that vein construction and high fluid pressure occur,” says Pollitt. “What appears certain in the light of our research is that the disintegration of lamellae is caused by the uncontrolled release of excess MMP.”

Test Tube Laminitis

Pollitt and other Australian researchers have developed a unique in vitro laboratory model for equine laminitis that relies on a small tissue sample taken from the inner hoof wall of normal deceased horses. Each piece of tissue includes the stratum medium, lamellar layer and sublamellar connective tissue. The tissue is incubated for 48 hours and subjected to tension and a determination of the amount of force needed to separate epidermal from dermal lamellae. As this separation occurs, he says the tissue develops into what is described as normal in vitro laminitis. Pollitt says a factor found in cultures obtained from the gut of the horse activates MMP and causes lamellar separation in the laboratory. These cultures contain Streptococcus bovis, the principal bacteria responsible for fermentation of sugars in the stomach during grain overload.

“We are investigating the role of this bacteria MMP activator in natural cases of equine laminitis,” says Pollitt. “If it is able to cross the barrier of the gut and enter the circulation, it may be a new cause of laminitis.”

In addition, Pollitt says there’s now strong evidence from three independent sources that foot circulation during the developmental phase of laminitis is vasodilated. Australian studies indicate laminitis does not occur during this phase of laminitis when the foot is in a state of vasoconstriction. This suggests the trigger factors will only cause laminitis if they reach the lamellar tissues through dilated blood vessels at a high concentration and over a long enough time.

Pollitt has found laminitis does not occur if these blood vessels are constricted, suggesting the critical trigger factors will only cause laminitis if:

⇒They reach the lamellae when the blood vessels are dilated.

⇒They are at a high enough concentration.

⇒They occur over a long enough period of time.

Keep Feet Cool

Since the hoof’s blood vessels constrict as temperature decreases, Pollitt says keeping feet that are in danger of developing laminitis as cool (vasoconstricted) as possible seems logical. Trials to determine the effect of a slurry of iced water applied to the feet are under way. Preliminary results show horses do not regard extremely cold feet as uncomfortable and can tolerate having their feet iced for up to 48 hours without any adverse effects.

Pollitt maintains the factors which cause laminitis are at work in the developmental stage long before foot pain is apparent.

“Because these factors cannot enter the foot and cause damage unless the foot’s blood vessels are dilated, cold water should be beneficial in the prevention of laminitis.” says Pollitt. “In addition, research has shown that one of the tissue MMPs blocks the activity of the laminitis MMPs in vitro and has the potential to be a useful tool in the prevention and management of acute laminitis. Trials to test if these MMP inhibitors can indeed prevent or improve laminitis are under way.”

Lameness Vs. Solar Pain

A team of researchers from Auburn University and Great Britain’s University of London’s Royal Veterinary College set out to cause lameness in a half-dozen horses with no signs of forelimb lameness. They did it with shoes to which a 3/8-16 nut was welded to the inside of each branch dorsal to the frog.

Researcher Michael Schramme says lameness due to solar pain in the distal interphalangeal joint (DIPJ) was created by forcing setscrews with pointed tips through the nuts into the sole of the toe.

The horses were videotaped when walked or trotted on a hard surface both before and after application of the set-screws. The DIPJ was then injected with 10 milliliters of saline or 2 percent mepivacine hydrochloride. After 10 minutes, the gaits were videotaped again.

As you would guess, applying pressure with the set-screws caused a significant increase in lameness scores of the affected limb. Lameness in the limb was compared with the contralateral limb and with the same limb prior to the set-screw application.

The induced lameness was significantly reduced by the mepivacine hydrochloride injection, but not by the saline injection.

“When lameness was localized to the heel by analgesia of the palmar digital nerves, injection of the DIPJ with a local anesthetic has been recommended in the past to distinguish lameness caused by navicular syndrome from lameness caused by pain originating from other structures in the heel,” says Schramme.

“Based on results of our investigation, we question the value of anesthesia of the DIPJ to localize pain to the joint or the navicular bursa bone and ligaments.

“Erroneous perceptions as to what structures are desensitized by analgesia of the DIPJ may lead to misinterpretation of the result of diagnostic analgesia during clinical examination of a lame horse.

“Pain arising from the sole should be considered as a cause of lameness when lameness is abolished by diagnostic analgesia of the DIPJ.”

Changing Locomotion Concepts

In an equine locomotion study recently done in France, J.M. Denoix found interphalangeal joints undergo combined movements in the sagittal, frontal and transverse planes. The professor at the Clinique Equine, Ecole Veterinaire d’Alfort in Maisons-Alfort Cedex, France, found this to be particularly true with horses exercised on uneven surfaces or during turns.

“Each movement induces specific stresses on the articular surfaces and ligaments,” he says. “Asymmetric elevation of one quarter induces collateromotion and sliding on the same side and rotation in the opposite direction.

“With this knowledge, the biomechanical causes of every injury of the interphalangeal joint structures can be determined and a rational shoeing procedure can be established.”

Results indicate the DIPJ can move in the sagittal plane (flexion and extension movements), frontal plane (lateromedial movements) and transverse plane (rotation and sliding).

During limb weight bearing, the passive movement of flexion is limited by the tension of the deep digital flexor tendon (DDFT) palmarly, the dorsal digital extensor tendon (DDET) dorsally, and the dorsal part of the collateral ligament on each side. Each is important in maintaining joint stability.

During the stance phase as propulsive forces are exerted on P2 (distal condyle of the middle phalanx) and oriented palmarodistally and the DDFT remains taut, the propulsion phase will likely be accompanied by high pressure on the distal sesamoid bone.

With the frontal and transverse planes, movements occur mainly during the stance phase and are totally passive since no muscles exist to induce them. Instead, they are spontaneously associated due to the oblique orientation of the articular surfaces of P3 and P2.

With the frontal plane, asymmetric foot placement (quarters at different levels) induces lateral or medial displacement (a combination of rotation and sliding) of P3 relative to P2 and P2 relative to P1.

“These movements are usually called ‘lateroflexion’ or ‘abduction/adduction’ movement, but the movement can be displayed medially,” says Denoix. “These movements do not correspond to a flexion, as there is no abductor or adductor muscles inducing them and they are symmetric relative to the sagittal plane.”

As a result, Denoix has introduced the concept of collateromotion to describe these passive movements in the frontal plane. With this concept, a lateromotion represents displacement of P3 in a lateral direction relative to P2. A mediomotion is a displacement of P3 in a medial direction. Collateromotion of the digital joints is a passive movement induced by asymmetric foot orientation.

In the transverse plane, Denoix says rotation and sliding are totally passive and can occur during the stance phase with asymmetric placement of the hoof. When the lateral quarter is elevated, the lateral distal condyle of P2 slides palmarly on the oblique articular surface of P3, which corresponds to a medial rotation of P3.

The opposite occurs when the medial side is elevated. As a result, rotation is automatically associated with collateromotion. It is also accompanied by a sliding of P3 relative to P2 toward the side of elevation.

Denoix says the main structure that limits collateromotion and rotation is the collateral ligament opposite the elevated quarter.

He maintains the precise nature of the interphalangeal joint improvement must be considered for corrective shoeing of both sound and lame horses. “All the anatomical structures of the DIPJ are highly stressed during weight bearing and especially during the stance phase on uneven ground or asymmetric foot placement,” he says.

“An adequate trimming and shoeing program requires a precise diagnosis of each injured structure, mainly based on radiography and ultrasonography.”