Bob Childs - ESA/AHA/PHCP Certified Hoof Specialist
News
Article by: Nancy S. Loving, DVM March 18 2009, Article # 13802
At the 2008 AAEP Convention, which was held Dec. 6-10 in San Diego,
Calif., Bill Moyer, DVM, professor of sports medicine and head of the
Department of Large Animal Clinical Sciences at the Texas A&M
College of Veterinary Medicine and Biomedical Sciences, presented a
variety of considerations on the state of medical treatment for
laminitis. He stressed that once clinical signs are evident, damage has
already been done: Pain and lameness are preceded by vascular and
structural damage within the hoof laminae (lamellae).
So, he posed the question to the audience, "Is any specific medical
treatment for acute laminitis efficacious in altering the outcome after a
horse has developed clinical signs?"
Is any specific medical treatment for acute laminitis efficacious in
altering the outcome after a horse has developed clinical signs?
The current consensus on effective therapy revolves around addressing
and resolving the initiating cause(s) of laminitis. Other strategies
attempt to alter blood flow in the foot, decrease inflammation, and
avert endotoxemia. Moyer addressed these in his talk.
He explained that evidence is lacking about blood flow-altering agents
having any effect on increasing laminar circulation. While use of
digital nerve blocks might improve blood flow by inhibiting constriction
of blood vessels, numbing the pain stops the horse from protecting his
feet. Increased weight bearing exacerbates laminitis.
Acepromazine increases digital blood flow by direct action on vascular
smooth muscle, but studies have not shown improvement in lamellar blood
flow.
Isoxsuprene has vasodilating properties, while pentoxyfylline requires
weeks of administration to decrease blood viscosity. It does this by
acting on platelets to increase red blood cell flexibility. Both these
medications are absorbed poorly when administered orally.
Nitroglycerin placed over digital blood vessels might increase blood
flow, but it has not been shown to increase lamellar blood flow after
the onset of clinical signs. Coupling this ineffectiveness with
potential risks to the person handling the drug makes nitroglycerin a
poor therapeutic choice.
Heparin removes red blood cells from the system to decrease blood
viscosity and thereby improve blood flow, but researchers have not
examined its use in acute cases.
Inflammation is not always a component of laminitis, but when it is,
non-steroidal anti-inflammatory drugs (NSAIDs) have been used. Moyer
said there is humane justification for judicious use of NSAIDs, but one
should be aware of downsides. Pain relief might increase mobility that
exacerbates tearing of the lamellae.
Phenylbutazone (Bute) might reduce inflammation and pain, and it is
affordable, but it does not prevent laminitis if given during the
developmental stage and has not been shown to alter the course of acute
cases.
Flunixin meglumine (Banamine) provides both anti-inflammatory and
anti-endotoxin effects. However, if flunixin and phenylbutazone are
given together, there is an increased risk of loss of serum protein,
gastric ulcer disease, and/or colitis.
There is anecdotal support for use of dimethyl sulfoxide (DMSO) for its
anti-inflammatory properties and ability to scavenge oxygen-derived free
radicals, which form during hypoxia (deprivation of an adequate supply
of oxygen) and reperfusion (restoration of blood flow to tissues
following an incident or hypoxia). Damage can occur when blood flow is
restored to tissues following an incident of reduced blood and oxygen
supply. However, Moyer noted there is no evidence of hypoxia or
reperfusion in this disease.
Anti-endotoxin drugs (flunixin meglumine, ketoprofen, and polymyxin B)
might be warranted as there is an association between endotoxemia and
the development of laminitis. Endotoxin causes insulin resistance with
decreased use of glucose by the lamellar tissue. While they might not
necessarily be effective in treatment of laminitis, anti-endotoxic drugs
might be life-saving.
Moyer said caretakers and veterinarians should address environment and
ground surface, housing, causes of obesity, and management of the foot
itself. He recommends explaining to clients that the pathogenic
mechanisms of laminitis are not well-understood and that a horse's
clinical appearance might correlate with the outcome, but it is not
always an accurate predictor due to potential for complications.
In general, controlled studies do not exist regarding the efficacy of various treatments for laminitis, and some therapies have additional risks beyond their failure to improve the situation.
Endotoxemia and the roll of ET-1 in acute Laminitis
"Although administration of a low-dose of endotoxin to horses causes a
significant decrease in laminar perfusion and digital blood flow, there
have been no repeatable models of endotoxemia that consistently induces
acute laminitis. However, diseases that are often complicated by
laminitis are accompanied by endotoxemia (intestinal strangulating
obstruction, anterior enteritis, enterocolitis, pleuropneumonia, and
metritis). In a study in our laboratory, we demonstrated a significant
decrease in digital arterial blood flow from 30 min to 2 h after
administration of a low dose (35 ng/kg over 30 min) of endotoxin to
conscious horses. There was a concomitant decrease in digital arterial
blood pressure from 30 min to 1.5 h after endotoxin infusion. These
digital hemodynamic effects were accompanied by a significant increase
in cephalic venous plasma ET-1 concentrations. These findings suggest
that perhaps endotoxin does play a role in initiation of the early
hemodynamic alterations in laminitis, and that this may be at least
partly mediated through increased synthesis and release of ET-1."
Authors: Susan C. Eades, DVM, PhD; Ashley M. S. Holm, DVM; and Rustin M. Moore, DVM, PhD
Kathryn Watts
says: "As with humans, diet and exercise are the only way that insulin
resistance, which causes high levels of circulating insulin, can be
managed."
Read the article: Laminitis: New Study on Sugar and Starch as a Cause
Article by: Philip J. Johnson, BVSc, MS, MRCVS, DACVIM
Affected horses tend to be aged between 6-to-20 years and there does not
appear to be a sex predilection. The problem is reported more commonly
in some pony breeds, domesticated Spanish mustangs, Peruvian Pasos, Paso
Finos, European Warmbloods, American Saddlebreds, and Morgan horses.
Affected horses are commonly obese and develop excessive adiposity at
specific locations, especially in the crest of the neck, at the
shoulders, above the gluteal muscles, and in the sheath (geldings).
Female horses are notoriously difficult to breed and exhibit abnormal
ovarian cycling behavior. Horse owners refer to many of these horses as
"easy keepers" and vigorously contend that all efforts to reduce the
horse's obesity by dietary restriction are futile. Ample intra-abdominal
(omental) adiposity is evident during ultrasonographic examination of
the abdomen or at necropsy of affected horses.
Many of these horses are presented to veterinarians for diagnosis of lameness attributable to laminitis. There is a very strong association between the development of obesity, metabolic syndrome and the risk for developing laminitis. Commonly, at initial veterinary examination, there already exists both physical and radiographic evidence for long-standing laminitis in these horses although reputable and credible owners and managers report that there have been no prior signs of laminitis or any obvious explanation. Metabolic syndrome is often recognized incidentally when horses are presented for other reasons, such as routine health care or other medical problems. In these horses, visible changes in the hoof that are commonly attributable to laminitis (including prominent growth lines, palmar divergence of growth lines, and a convex sole) may be evident in the absence of laminitic pain or any history of laminitis or lameness. There are minimal hematological changes in horses affected with metabolic syndrome (unless laminitic pain is prominent). Abnormal results of routine serum biochemical profiling might include a slight-to-moderate elevation in the glucose and triglyceride concentrations.
Interesting comments on laminitis and obesity by Donald M. Walsh, DVM
"Based on my experience observing laminitic horses over the past 36
years in veterinary practice, I believe that obesity leads to the
development of weakened laminae and other supporting structures of the
foot and to changes in the growth pattern of the feet. 2 Radiographs
reveal that the appearance of the laminae begins to change in horses
that are becoming obese, even before any signs of lameness from
laminitis are observed.
Perhaps, when a horse becomes obese, there is a messenger substance that
promotes or allows for the skin's basement membrane to stretch so the
skin can "enlarge itself" in order to accommodate for the increased
layer of fat under the skin. If this is so, perhaps this same messenger
substance is also recognized by the epithelial laminar basement membrane
in the foot, which would cause the basement membrane to stretch, which
could result in the weakening of the laminae of the foot in the obese
horse. These weakened feet are much more susceptible to grass laminitis
and other predisposing insults known to cause laminitis.
Obese horses need a major change in lifestyle in order to become healthy. Accomplishing this can be a challenging task for the owner because weight reduction in these horses requires a low caloric diet together with a considerable amount of exercise. Many of the horses experiencing laminitis are so sore-footed that much exercise is not possible. Many live lives of constant pain associated with ongoing bouts of laminitis, which finally results in so much damage to the feet that recovery is impossible. These (heavy-type) horses are the most common group associated with the ingestion of grass as a cause of laminitis."