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Hoof tester used to evaluate hoof pain.
Try these websites for lameness info:
http://www.horseshoes.com/anatomy/anatomy.htm
http://www.equisearch.com/horses_care/health/lameness/
Polysaccharide Storage Myopathy (PSSM):
http://www.cvm.umn.edu/umec/lab/PSSM.html#acute
Testing equine feed
Equi-analytical Lab at Cornell University will test feed. Site includes phone numbers, information, and instructions on how to take a sample.
http://www.equi-analytical.com
Insulin Resistance and Equine Metabolic Syndrome
This is an excellent article concerning a problem that is more common than previously recognized. Proper feeding and exercise is critical. Evaluate your horse's condition, whether he really needs grain and supplements, your hay quality, and his history of medical problems such as laminitis.
Insulin Resistance in Horses
Nicholas Frank, DVM, PhD, Diplomate ACVIM Dept of Large An Clinical Sciences, University of Tn .2006 AAEP
1. Introduction
Insulin resistance (IR) is important to the equine
practitioner because of its association with laminitis.
Older horses with pituitary pars intermedia
dysfunction (PPID) are pre-disposed to both IR and
laminitis, and it is likely that these conditions are
related.1,2 Horses or ponies that exhibit delayed
shedding of the haircoat or hirsutism, loss of skeletal
muscle mass, or polyuria/polydipsia should,
therefore, be tested for PPID and IR and managed
accordingly. There is also a second condition associated
with IR in horses, and this syndrome is more
challenging to define. Affected horses are described
by owners as “easy keepers,” because body
weight is maintained on a relatively low caloric intake
compared with other horses. In our experience,
this condition is most common in ponies,
Morgans, Paso Finos, and Norwegian Fjords, but it
also occurs in Arabians, Quarter Horses, American
Saddlebreds, and Tennessee Walking Horses.
Horses with this condition can often be recognized
by their appearance. Some exhibit generalized
obesity; others are thinner throughout the mid region
of the body but suffer from regional adiposity in
the form of a cresty neck or enlarged fat pads next to
the tailhead. These horses were previously assumed
to suffer from hypothyroidism because of perceived
similarities between this condition and
canine hypothyroidism and the detection of low or
low-normal resting serum total triiodothyronine
(tT3) and total thyroxine (tT4) concentrations.
However, it is now accepted that lower circulating
tT3 and tT4 concentrations are a consequence rather
than a cause of the horse’s metabolic state, and
these concentrations can be attributed to secondary
hypothyroidism (decreased thyroid-stimulating hormone
release from the pituitary gland) or interference
from drugs such as phenylbutazone.3 Therefore,
alternative terms have been adopted to describe this
condition in horses and ponies, including peripheral
Cushing’s disease,4 equine metabolic syndrome
(EMS),4 and pre-laminitic metabolic syndrome
(PLMS).5 For the purpose of this discussion, we
will use the term EMS to signify this condition, but
we will require that all three of the following criteria
be met before the term is applied: (1) insulin resistance,
(2) history of laminitis or pre-disposition to
the disease (presence of abnormal growth rings on
the hooves), and (3) regional adiposity in the form of
a cresty neck or enlarged fat pads.
2. What Is IR?
Physiology Review
Insulin is a hormone secreted by the pancreas that
stimulates the uptake of glucose by tissues when
sugar is abundant (i.e., after feeding). Skeletal
muscle and adipose tissues are the major sites of
insulin-mediated glucose uptake, but the liver also
AAEP PROCEEDINGS Vol. 52 2006 51
IN-DEPTH: ENDOCRINOLOGY
NOTES
responds to insulin by increasing the uptake of glucose
from the blood. Insulin binds to receptors on
the surface of plasma membranes. It triggers a
series of internal events that results in the movement
of glucose-transporter proteins (GLUT4) to the
cell surface, which facilitates rapid glucose uptake.
Insulin plays an important role in the storage of
energy by moving glucose into cells where it can be
stored as glycogen or converted into fat.
IR
This condition is defined as the failure of tissues to
respond appropriately to insulin. There are numerous
mechanisms responsible for IR including reduction
in the density of insulin receptors on the cell
surface, malfunction of insulin receptors, defects in
internal signaling pathways, and interference with
the translocation or function of GLUT4 proteins.
3. IR and Laminitis
All of the pieces of the puzzle must be assembled
before we can fully understand the association between
IR and pasture-associated laminitis in horses
and ponies. There are two broad mechanisms by
which IR could pre-dispose horses to laminitis:
(1) insulin resistance might impair glucose delivery
to hoof keratinocytes, or (2) insulin resistance could
alter blood flow to the foot. The first theory is supported
by results of a study performed by Pass et al.6
in which it was shown that hoof tissue explants kept
in culture separate at the dermal-epidermal junction
when deprived of glucose. Furthermore,
Mobasheri et al.7 determined that GLUT4 proteins
are found in equine keratinocytes, which suggests
that insulin-stimulated glucose uptake occurs in the
hoof. Studies examining the relationship between
IR and blood flow have not been performed to date in
horses; however, insulin is known to act as a slow
vasodilator in humans, and IR has been associated
with a decrease in peripheral vasodilation.8
If IR is a determinant of susceptibility to pastureassociated
laminitis, then what triggers the laminitis
episode itself? It seems that non-structural
carbohydrates (NSC) within pasture grasses play an
important role in this process. Most NSC measurements
include simple sugars, starch, and fructans
(polymers of fructose), and levels of these components
vary considerably within grass according to
geographical location, soil type, weather conditions,
and time of day.9 NSC are likely to affect the susceptible
horse in two ways. First, excessive sugar
consumption could exacerbate IR like it does in diabetic
humans. Second, consumption of large
quantities of NSC might alter the bacterial flora
found within the large intestine. These alterations
in bacterial flora are thought to increase the production
of as yet unidentified triggering factors for laminitis
that may include exotoxins, endotoxins, or
vasoactive amines.10 Alterations in large intestinal
bacterial flora have been induced by orally administering
oligofructose (a fructan) to horses.11
4. How Do You Test for IR in Horses?
Ideally, a test that provides a specific measure of
insulin sensitivity would be used to assess affected
horses, and the frequently sampled IV glucose-tolerance
test (FSIGT) or euglycemic hyperinsulinemic
clamp (EHC) procedure are available for this purpose.
12 Unfortunately, these tests are technically
challenging and require a large number of samples.
Practitioners are advised to use two simple but indirect
methods of assessing insulin sensitivity:
Combined Glucose–Insulin Test
The procedure for the combined glucose–insulin test
(CGIT) involves collection of a baseline blood sample,
infusion of 150 mg/kg body weight (bwt) 50%
dextrose solution, and infusion of 0.10 units/kg bwt
regular insulin immediately after the first infusion.
13 Blood samples are collected at 1, 5, 25, 35,
45, 60, 75, 90, 105, 120, 135, and 150 min postinfusion.
When this test is used, IR is defined as
maintenance of blood glucose concentrations (measured
with a hand-held glucometer) above the resting
(baseline) value for 45 min. The test can be
abbreviated to 60 min when used in the field, but it
is advisable to complete the measurements so that
the time taken for the blood concentration to return
to baseline can be recorded for future reference.
This allows assessment of the response to diet, exercise,
or medication. There is a small risk of hypoglycemia
when performing this test. Therefore,
two 60-ml syringes containing 50% dextrose should
be kept on hand and administered if muscle fasciculations
or profound weakness are observed or if the
blood glucose concentration drops to 40 mg/dl.
Note that stress is an important cause of transient
IR that can significantly impact CGIT results. In
one of our studies, we detected IR in healthy, nonobese
horses when CGITs were performed immediately
after endoscopic examinations.13 Therefore,
horses must be kept calm before and during the
procedure to avoid false positive results. An IV
catheter should be used to reduce the stress associated
with blood collections, and ideally, this catheter
is placed the night before the CGIT. Because pain
affects results, horses suffering from acute laminitis
must be given time to recover before testing. Feed
deprivation also causes stress, so horses should be
permitted to eat grass hay during the testing
procedure.
Measurement of Resting Serum-Insulin Concentration
This is the easiest measurement to perform, and it is
a useful screening test, because compensatory hyperinsulinemia
is a common feature of IR in horses.
There are, however, two situations where this test
will not be helpful. In the first situation, the horse
has mild or early IR, and hyperinsulinemia has not
developed yet or the rise in serum insulin concentration
is too small to exceed the reference range.
This problem is magnified by the wide reference
ranges currently available for horses and differences
52 2006 Vol. 52 AAEP PROCEEDINGS
IN-DEPTH: ENDOCRINOLOGY
between laboratories. For instance, hyperinsulinemia
is defined as a serum insulin concentration
above 30 units/ml at the University of Tennessee,
whereas the Diagnostic Center for Population and
Animal Health at Michigan State University uses a
300 pmol/l (43 units/ml; conversion factor approximately
equal to 7.0) cut-off value. In the second
situation, a horse with pancreatic insufficiency as a
consequence of prolonged disease would escape detection
if serum insulin concentrations had returned
to within the reference range.
Practitioners are advised to screen horses for IR
by measuring resting serum-insulin concentrations.
The CGIT should also be used to further investigate
the normoinsulinemic horse that has a physical appearance
consistent with EMS or PPID. Horses
should be fasted or fed only grass hay overnight, and
stress should be avoided when collecting blood samples.
If hyperinsulinemia is detected, this finding
is usually sufficient to arrive at the diagnosis of IR;
however, horses with serum insulin concentrations
that fall within the reference range should be assessed
with the CGIT. When measuring insulin
concentrations, samples should be sent to a laboratory
that is accustomed to handling equine blood
and has established reference ranges for horses.
Establishment of a reference range for a particular
farm is also recommended when serial measurements
are to be performed.
5. Management of IR in Horses
The two principal strategies for addressing IR in
horses are diet and exercise, but affected horses can
be divided into three groups: (1) obese horses with
IR, (2) non-obese horses with regional adiposity
(cresty neck) and IR (many horses with PPID fall
into this category), and (3) severely affected horses
from either group that are currently suffering from
laminitis.
1. Obese horses with IR should be placed on a
diet containing fewer calories and an exercise
program to lower body weight and increase
fitness. Feeds that contain readily
available sugar, such as sweet feed, should
be completely eliminated from the diet. If
the horse does not suffer from laminitis, it
can be allowed to graze on pasture. Clients
should be warned that horses with EMS can
often maintain their body weight even when
grazing is limited, and pasture-associated
laminitis remains a risk if the horse is left
out on pasture. Strategies to limit the
amount of grass consumed include limiting
grazing time (1–2 h/day), enclosing the horse
in a smaller area using a round pen or electric
fence, or using a grazing muzzle.
Hay should be the principal component of
the diet along with protein and trace mineral
supplements as needed. Analysis of hay is
strongly recommended to ensure that the
NSC content of the hay is low. Samples can
be sent to the Dairy One Forage Laboratory,
and the cost of analysis is $25/sample.
Hay with a NSC level 12% should ideally
be selected for affected horses. If only hay
containing a higher level of NSC is available,
soaking the hay for 30 min in cold water will
reduce the sugar content. Be aware that
this process can also leach out other nutrients
from the hay. Horses should be exercised
as consistently as possible (every day is
ideal), and clients should be encouraged to
exercise the horse on a lunge line or in hand
even if it is lame (excluding those with acute
laminitis).
2. Non-obese horses with IR should be placed
on a similar diet and exercise program to
improve insulin sensitivity but with more
calories provided, particularly when the
horse is being strenuously exercised. Many
horses with PPID fit this description. High
glycemic feeds such as sweet feed should be
removed from the diet and replaced with fat
and fiber. Up to 20% of calories can be provided
by fat in the form of vegetable oil or rice
bran. Low-starch or low-NSC commercial
feeds are also available.
3. Severely affected horses with laminitis
should be taken off pasture altogether.
Grass hay with a low NSC content should be
fed along with concentrates that primarily
contain fat and fiber until laminitis has subsided.
After the acute phase has passed,
obese horses should be placed on a weightreduction
diet composed primarily of grass
hay with a low NSC content. Hay should be
weighed out to avoid overfeeding. Weight
loss can be accelerated in these horses by
limiting their caloric intake and administering
levothyroxinea at a dosage of 4 teaspoons
(48 mg) once daily orally for an average-sized
horse. Levothyroxine reduces body-fat mass
and improves insulin sensitivity in horses
that are kept off pasture and maintained on
a controlled diet.14 Treated horses should
be weaned off the drug after the ideal body
weight has been attained by reducing the
dosage to 2 teaspoons (24 mg) once daily
orally for 2 wk and then 1 teaspoon (12 mg)
once daily orally for 2 wk. Some horses that
suffer from chronic laminitis in association
with EMS must be kept off pasture
indefinitely.
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Medical Information
LAMENESS EVALUATION
Lameness evaluation is a common procedure in our practice. Because of the wide range of horse breeds and uses in this practice we see a variety of different lameness problems.
Evaluation of the lame horse begins with a complete history of the animal and its particular problem. The age, sex and breed of the animal is determined and the onset, progression and duration of the lameness is described by the client. Because certain lamenesses are more common in certain breeds or ages or in their onset or progression, this information is extremely valuable in determining the definitive cause of the problem. Only by making an accurate diagnosis of the problem can we institute a rational plan for treatment.
In general, the lameness evaluation itself begins with a determination of which leg is lame. In the forelegs this is determined by the “head nod” (the head and neck nodding down on the sound leg and then up as the lame leg strikes the ground) while in the hind end the “hip hike” (the pelvis raising up as the lame leg hits the ground while the pelvis sinks with the weight of the sound limb as it hits the ground) is observed. This is best observed on a flat, firm area. If the lameness is subtle or difficult to observe then observing the horse on the longe line, on harder ground or under saddle may be necessary. It is important to note that the large majority of lameness problems occur in the forelegs because more of the horse’s weight is borne here (60%) and the large majority of these lamenesses originate from the foot.
Once the affected leg is determined, then the next step is palpation or feeling of the leg. Because the majority of lameness problems involve the foot the hoof tester examination is an invaluable part of any lameness exam. The hoof tester is an instrument that allows us to put pressure on different parts of the foot and thereby determine any sore or painful areas. The rest of the leg is then carefully felt again to determine any sore, painful, hot or reddened areas indicative of inflammation. Manipulative procedures such as “flexion tests” may also be performed to compare the degree of lameness before and after the test.
Local nerve blocks are also an integral part of the lameness exam. In this procedure a small amount of local anaesthesia is injected around the nerves that supply a given portion of the leg thereby removing feeling from this part. If the horse is sound following this “block” then we know that this is the area from which the lameness is coming. If the horse is still off then we move further up the limb with these blocks until we have caused the lameness to disappear. Using these local nerve blocks allows us to definitively determine at least the anatomic area of the problem.
When the particular area of lameness is determined then we have several diagnostic options available to us to further identify the problem. Most commonly we use radiographs (x-rays) to evaluate the particular region. We carry a portable x-ray machine in the vehicle and have an automatic processor in our home so that results are available promptly. Some cases require the use of the diagnostic ultrasound machine, especially if the lameness involves tendons or soft tissues as opposed to the bone. More advanced imaging techiniques are available on a referral basis. These include nuclear scintigraphy (bone scans), MRI, thermography, etc.
Following determination of the precise cause of the lameness it becomes necessary to formulate a treatment plan for the horse and owner. This plan may involve rest, drugs, physical therapy, complementary therapies (chiropractic, acupuncture), trimming and shoeing changes or any combination of these. We feel that working with local farriers is an important part of the equine health care team especially when it comes to soundness issues.
In general, all lameness evaluations follow this overall approach. This allows us to put our years of experience to work in a consistent, reproducible manner to clarify the sometimes confusing and frustrating group of equine lameness problems.
Misc. topics of interest
Forefoot Lameness-the most common source of lameness: Whether shod or unshod, the condition of the hoof should be monitored frequently for chips, cracks, evidence of thrush, white line disease, and any abnormal growth patterns that will require expert farrier care. Your farrier and veterinarian will assist in evaluating the hoof for a variety of conditions that can occur but your daily observation is essential !!! Take a good look at the hooves of all your horses. If you intend to buy a horse, your knowledge of what constitutes a good hoof may help you avoid a disappointing purchase.
Talk to your farrier about your horse's pastern-hoof axis and evaluate the hoof for the presence of rings, abnormal wall shape (ie: dish) cracks, frog problems, deep fissures, a convex sole, underrun heels, contracted heels, and hoof balance.
White line disease is a condition that may start with a fungus (and bacteria) that moves into the inner hoof wall via an injury or due to poor hoof condition (widened white line). White line disease can also be caused by chronic laminitis or underlying diseases such as Cushings disease and other autoimmune problems. The white line is the junction between the hoof wall and the sole. In cases of chronic laminitis, the laminae can be enlarged and quite visible which then becomes a natural route of infection. This condition needs to be carefully monitored and aggressively treated by your farrier and veterinarian since it can become a frustrating problem if left untreated.
NAVICULAR SYNDROME / CAUDAL HEEL PAIN
One of the most common causes of chronic forelimb lameness, navicular syndrome, is a constellation of diseases, problems, or injuries of the posterior (back) aspect of the hoof. The cause of the syndrome is not fully understood but is thought to have multiple origins involving the navicular bone, the navicular bursa, the coffin joint, the surrounding ligaments, the region's blood supply, and the deep digital flexor tendon. This syndrome is most frequently a bilateral problem. Quarterhorses appear to be at greatest risk, but any horse with a particularly upright conformation involved in concussive activities may be affected.
Horses with small feet, inappropriate hoof angles, poor conformation, and other hoof imbalances are known to be prone to navicular problems. There may also be a genetic predisposition to this condition either directly or through inherited conformational defects. Clinical signs are varied and numerous: generally bilateral foreleg lameness, worse on hard ground and on turns, landing on the toe, short, choppy forelimb movement and often stumbling. The horse may stand with the involved leg pointed forward and the toe may be chipped or worn.
Diagnostic tests include: observation of the lameness including watching the horse on hard ground and on a longe line, a painful response to hoof tester pressure across the frog (the navicular bone lies deep to the central third of the frog), and the alleviation of the lameness by injecting local anaesthetic into the nerves that innervate this area.
Radiographs taken following the clinical diagnostic work-up may reveal remodeling or degeneration of the navicular bone.These radiographic changes must be viewed in conjunction with the clinical signs of the horse. Radiographic changes by themselves may not be significant. Similarly, normal radiographs do not rule out all causes of caudal heel pain/navicular syndrome
Treatments for navicular syndrome may include: corrective trimming and shoeing, anti-inflammatories and other medications given both systemically and possibly into the coffin joints, oral supplements and in the worse cases, surgery (nerving ). Persistence in trying to find the appropriate treatment may be called for in difficult cases. Dedication by the veterinarian, farrier and owner is essential.
This condition used to be termed navicular disease but the newer terminology is navicular syndrome / caudal heel pain. This is because we now know that a number of structures within this anatomic area may be causing the pain responsible for the above described signs. The navicular bone, the navicular bursa, the impar ligaments, the coffin joint, the articular cartilages of the navicular, coffin and short pastern bones and the deep flexor tendons may all be involved.
WEBSITE OF INTEREST:
http://www.equipodiatry.com Dr. Steve O’Grady’s excellent site.
Cross section of an equine hoof.
A. short pastern bone (P2)
B. coffin bone (P3)
C. navicular bone
D. deep digital flexor tendon
E. navicular bursa
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