Everybody meet Rosie,
She's 22 years old and is a thoroughbred cross (although we're not sure what she's crossed with!) She's suffered from laminitis for the past few years so is on restricted grazing and has to wear a muzzle. She has a soft canvas one. A lot of people think they look cruel but honestly it is for her own good because if she eats too much grass it causes her to become lame and she has to be on box rest, which she definitely doesn't like and box walks profusely in protest.
She has recently been diagnosed with Cushing's disease after she lost quite a lot of weight in a short space of time. As Cushing's disease doesn't have a cure she is now on medication that keeps her condition under control (Prascend) She is currently on a small dose as she is a git with tablets, we have to hide the tablet in the middle of an apple! God help us if she finds it! But for now it seems to be working. I went to visit her the weekend just gone and she appears to have put weight on since I last saw her, which is a fantastic sign!
This is a photo taken on Sunday (20th October 2013) And she's definitely put on weight! You can't see her ribs anymore :)
I'm going to track her progress and I'll try let you all know of any updates!
Here's an article I put together during first year with a little bit of information on Laminitis, I hope it's useful!
Laminitis
in horses: the cause and effect
Chloe Dix
In the recent National Equine
Health survey instigated by the animal welfare charity, The Blue Cross, the
occurrence of Laminitis was recorded at 4.9%. This is a slight decrease than
the usual estimates that are published in Veterinary publications which suggest
the figures are nearer 7%.(
Slater, 2012) The figures for equine obesity show that 8.6% of
the samples were overweight. Following this, World Horse Welfare, stressed the
fact that horses are getting fatter and that obesity is classed as one of the
biggest welfare issues among the UK equine population.(
Butcher, 2009) With this in mind and that obesity is recognised
as a trigger factor for laminitis, this could potentially mean that the cases
of laminitis will increase.
What is Laminitis?
 |
| Figure 1. Characteristic stance of laminitis |
Laminitis is a main cause of death in equines and normally affects those that are overweight. Defined as the inflammation of the sensitive laminae of the horses foot. (Pilliner
and Davis, 2004a), it causes lameness and the
characteristic stance of leaning backwards to relieve the forefeet of weight
(Figure 1).
Laminitis
can be categorised into two types: acute and chronic. The symptoms of acute
laminitis can surface quite often suddenly and can be quite severe. Symptoms of
acute laminitis include: inability or reluctance to move, lying down and
unwillingness to stand again, visibly lame when moving in a circle, a raised
digital pulse and of course, the characteristic stance. With chronic laminitis,
symptoms are on-going and usually stem from previous attacks. Symptoms are as
follows: the appearance of growth rings around the wall of the hoof, the heel
will grow faster than the toe and the white line in the hoof will have widened.
Inflammation of the hoof can be shown by five characteristics, heat, pain,
swelling, redness and loss of function. (Constable, 2010) Heat in the hoof is
displayed by an increase in temperature of the front hoof wall, a change in
gait is a sign of pain. The swelling is
not normally seen but occurs underneath the hoof wall. Like the swelling, the redness is not
normally seen however when the feet have been trimmed, a red horn of the foot
can indicate previous inflammation. Loss of function as previously mentioned
can be indicated by the characteristic leaning back and foot structure itself
can be altered. (Constable, 2010) Further details of
these symptoms will be provided later.
The
Structure of the Hoof
The
old English proverb “No hoof, no horse” highlights just how important the hoof
in the mechanical functioning of the horse. They are able to withstand large
amounts of force whilst still resisting wear and supporting the horses body
weight. Without this ability, the horse would be rendered immobile, with the
inability to travel to find lush areas for grazing, mate and escape predators.
The hoof can be split into two distinct parts: the external hoof and the
internal hoof. The external hoof can be divided further into the wall, sole and
frog. The wall
is produced by the coronary band and grows down and is made of dense horn.
There are two sets of lines that are visible: vertical and rings of alternating
ridges and depressions.(
Pilliner and Davis,
2004b). The vertical lines run down in the direction of hoof growth
which indicates the direction of tubules from the papillae of the coronary
band. In opposition to these, the rings
of alternating ridges and depressions run parallell to the coronary band and
these indicate the growth rate of the hoof. It is also possible to distinguish if
the growth rate has been abnormal from these rings which can suggest laminitis.(
Pilliner and Davis,
2004b)
The hoof wall itself
consists of three different layers, the first being the periople and stratum
tectorium. The periople originates from a rim of soft grey horn at the coronary
band, the perioplic cushion and extends roughly three- fourths of an inch below
the coronet apart from at the heels. The coronet circles the top of the hoof
and identifies where the skin ends and the hoof wall starts and the stratum
tectorium, likened to a human fingernail, extends down towards the bottom of
the foot. The stratum tectorium is a thin layer of hardened cells that make the
periople to appear hard and glossy.(
Snellow, 2006). The middle layer is the densest and contains the majority
of the wall. The third layer of the wall is the one that is effected during
laminitis, the Laminar layer.(Figure 2) This consists of two types of laminae,
insensitive and sensitive and these dovetail(
Pilliner and Davis,
2004b) to create a strong bond between each other and this connection
is made visible by the white line on the underside of the foot. The insensitive
laminae comprise of around 600 primary laminae, each with around 100 secondary
laminae in it’s surface and this structure bears much of the horses weight.
How is the
hoof affected during Laminitis?
Laminitis
is caused by undernourishment of the cells of the laminae from the lack of
nutrients in the blood supply. With the reason unknown, blood is actually
shunted away from the hoof which explains the bounding pulse of horses
suffering from laminitis. This undernourishment leads to inflammation and
eventually cell death which weakens the laminae. (Bishop, et al., 2012) With the laminae
weakened, this means it is no longer able to maintain the position of the pedal
bone and in severe cases, the pedal bone tips down towards the sole of the
hoof. Once the weakening and breakdown of the structures begins, the horse
begins to experience pain that can be career ending. (Bishop, et al., 2012)
What can increase a horse’s susceptibility
to laminitis?
Equine Metabolic Syndrome
Equine Metabolic Syndrome
is a fairly new concept (Johnson, 2002) and it is suggested
that obesity, insulin and resistance are all constituents of a clinical
syndrome identified in horses and ponies. (N.Frank, et al., 2010) Obesity can arise
from the overeating of carbohydrates in feeds or the overgrazing of lush spring
pasture without a sufficient amount of exercise to burn off the excess energy.
In obese horses or ponies there is an increase of fat in specific locations
(regional adiposity) and characteristic of this is a cresty neck, the
development of fat pads close to the top of the tail and the accrual of fat
behind the shoulder (N.Frank, et al., 2010) However, horses and
ponies with EMS seem to have a heightened metabolic efficiency in conjunction
with the use of dietary energy. (N.Frank, et
al., 2010)
With this in mind, it has been suggested that horses and ponies evolved to
adapt to survival in environments that are nutritionally sparse. For example,
when food was scarce in winter, horses would begin to build up their fat stores
during the previous summer which would enable them to survive even the harshest
of winters. (Davis, 2009) Now with the modern
management conditions under which horses are kept, a plentiful supply of food
is availlable all year round meaning that the horses will tend to continue to
feed on the nutritional feed and build up fat stores throughout the year.
Insulin resistance
Insulin
resistance is the inability of tissues to respond to insulin appropriately by
the reduction in the number of insulin receptors on the cell surface, the
failure of insulin receptors themselves and defects in the internal signalling
pathways. (Nicholas Frank, 2006) Insulin is a hormone
that is secreted by the pancreas when blood glucose levels rise above the set
point to stimulate the absorbtion of glucose by tissues. (Wasserman, 2008) The major sites of
glucose uptake via the influence of insulin are skeletal muscles, adipose (fat)
tissues and the liver. There are two types of insulin resitance that can occur.
The first being the most common in the majority of horses and ponies suffering
from Equine Metabolic Syndrome. This is where the pancreas secretes more
insulin to compensate for raised blood sugar levels and this helps to move
glucose into the tissues (Davis, 2009) however, far too
much glucose is taken in to the tissues causing hypoglycaemia. The other type
of Insulin Resistance is where the pancreas no longer meets the required demand
for insulin so therefore the blood glucose levels remain high thus causing
hyperglycaemia. Symptoms of which include glucosuria, where glucose is present
in the urine and polyuria which is an increase in the volume of urine produced.
(Davis, 2009) It is proposed that
insulin resistance increases the susceptibility to laminitis in a couple of
ways: (1) it might prevent glucose delivery to hoof keratinocytes, or (2) it
could alter the blood flow to the foot. (Nicholas Frank, 2006) In an experiment
involving hoof tissue explants deprived of glucose (Pass, et al., 1998), it can be derived
that insulin stimulated glucose uptake occurs in the hoof because the hoof
tissue explants separated at the dermal-epidermal junction providing evidence
for the first theory. (Nicholas Frank, 2006) In horses. There
have been no studies to date to confirm the effect of insulin resistance and
blood flow in horses, however insulin is known to act as a slow vasodilator in
humans so therefore, iinsulin resistance has been linked to a decrease in
peripheral vasodilation (Yki-Jarvinen &
Westerbacka, 2000)
thus affecting blood flow to the hoof.
The Trigger
factors
Carbohydrate
overload and excessive fructan intake
This normally occurs through
the overeating of lush grass rich in fructans or grain high in starch.(
MRVCS,
2012) Fructans consist of chains of
fructose molecules and these are present in the lower parts of grass so
therefore highly grazed paddocks are higher in fructans. The levels of fructans
and sucrose can fluctuate daily due to environmental elements such as sunlight
intensity, temperature, water availability, and soil fertility. The occurrence
of frost overnight during the winter can also increase the levels of fructans
in the grass as growth of the grass slows.
(Davis, 2009)
After the horse has ingested the grass containing fructans, they pass to the
foregut of the horse where they are unable to be digested it then follows that
they pass to the hindgut undigested and rapidly ferment which alters the
microbial populations living in the gut due to the production of lactic
acidosis which destroys the environment within the hindgut causing the death of
the micro-organisms.(
Ltd, 2000-2011) This disruption to the
environment of the gut causes an increase in acidity which then leads to the
permeability of the intestinal wall resulting in endotoxaemia as a result of
endotoxins, exotoxins and vasoactive amines flooding the horse’s system and it
has been suggested that this prompts an inflammatory response.
(Davis, 2009)
Toxaemia
Laminitis can
occur due to the onset of toxaemia from a number of causes. Causes include: the
retention of the placenta after the birth of a foal, the delay in treatment of
a mastitis with antibiotics, poisoning, for example ingestion of acorns as this
causes impaction an may cause bowel toxaemia as there is a delay in ingesta
transport time (Duncanson, 2010), colic and
diarrhoea. The cause of the retention of the placenta is currently unknown but
the condition is usually related to abortion, infection, shortened or
lengthened gestation periods and uterine atony. (Robert
O.Gilbert, 2011)
Whilst endotoxaemia hasn’t been proven to be a direct cause of laminitis, for
example administration of endotoxins during experiments have failed to induce
the disease (Tadros, et al., 2012), endotoxaemia may
expose the laminar tissue to damage by other mediators during an inflammatory
response. (Tadros, et al., 2012)
Roadwork and excessive concussion to the feet
Concussion
laminitis is commonly recognised as a mechanical or traumatic laminitis. (Hamilton-Fletcher, 2004) Excessive concussion
to the feet can be caused by large amounts of trotting , cantering or galloping
on hard or uneven surfaces such as during hot summer days when fields have
dried out in the sun. Possible effects of excessive concussion are: tearing of
the laminae which then contributes to constricted capillaries within the feet
of the horse leading to reduced perfusion, inflammation of the foot and
eventually, structural collapse. (Hamilton-Fletcher, 2004)
Corticosteroids as a trigger for laminitis
Corticosteroids
are mainly used as anti-inflammatory drugs and can be split into two types of
steroid hormones; mineralocorticoids and glucocorticoids. (Leland Thompson, 2011) Mineralocorticoids
are mainly involved in regulating the levels of electrolytes and the regulation
of water balance by their effect on ion transport within the epithelial cells
of the intestines which leads to the maintenance of sodium ions and the loss of
potassium ions. (Company, 2004) Another type,
glucocorticoids, allows the release of amino acids from muscles, enables
skeletal muscles to maintain contractions and prevent fatigue and allows fatty
acids to be transferred from fat stores. (Mosby, 2009) The mechanism in
which corticosteroids induce laminitis is so far still unknown (Constable,
2010)
so more research is needed to determine to exact mechanism.
Clinical signs of Laminitis
Apart from the characteristic
leaning stance of laminitis, one of the clinical signs is an increased digital
pulse which allows you to feel pulsing of the arteries that run down the leg.
The digital pulse can be located just above the fetlock and on either side of
the back pastern. This increase in pulsation occurs due to a decrease in
diastolic pressure which can transpire from inflamed blood vessels as they
dilate so more blood leaves the arteries of the feet. Also arterio-venous
shunts divert blood straight from the artery to the vein so blood therefore
avoids the capillary bed of the foot. As a result of these shunts, blood is
moved quickly from the arteries supplying the hoof, thus lowering diastolic
pressure. (Constable, 2010) An increase in hoof
temperature should perhaps be taken with a pinch of salt on its own, as it
could be a result of increased blood flow to the hoof however, it has been
suggested that horses have an intermittent blood supply to their legs, so blood
isn’t flowing all the time, it happens in bursts. (Constable,
2010)
If you happen to feel the hoof during one of these ‘bursts’ the foot may feel
slightly warmer than normal.
Lameness
is also an obvious characteristic of laminitis and levels of severity can be
identified by the Obel Grading. (Constable, 2010) Grade 0 is where the horse is sound in
walk and trot on a straight line on a hard surface, Grade 1, at rest the horse
shifts its weight from foot to foot but is sound in walk and at trot the gait
is stilted. At grade 2 the horse walks stiffly and the gait is stilted in trot
on a hard surface and the horse will find it hard to turn and at grade 3 the
horse is reluctant to move on any surface and it is hard to pick up its foot.
Grade 4 is the most severe and the horse won’t move of its own accord and if
forced is very unwilling to move from a soft ground to a hard ground and it is
almost impossible to pick up the foot. (Ltd, 2012)
The clinical
signs of chronic laminitis are often less reliable and are more often
accompanied by signs of acute laminitis (as mentioned previously) and include
alterations in hoof growth, external indicators of sinkage, widened white line
and variability in lameness, as distinguished by the Obel Grading system. (Constable,
2010)
Treatment of Laminitis
When treating
any type of laminitis (chronic or acute) the owner should endeavour to remove
any suspected cause of the case for example, removing the horse from the grass
if it is suspected to have been caused by carbohydrate overload or excessive
fructan intake. (Practice, 2009) When treating acute
laminitis a number of areas should be addressed. Movement of the horse or pony
should be restricted, this can be achieved by box rest as it allows the
prevention of any unnecessary movement that would be otherwise painful to the
equine. (Constable, 2010) Along with box rest,
a deep, thick bed should be offered to reduce concussion to the feet but also,
if the animal decides to lie down, will reduce any damage to other parts of its
body such as the hocks. A many cases of laminitis are induced due to weight
problems and over load of carbohydrates, the horse or pony should be fed a low
calorie diet to control the weight but also, a horse on box rest requires less
energy. Soaking of hay is often used to reduce the number of water soluble
carbohydrates present in the hay (K. Martinson, et al., 2012) which reduces the
intake of carbohydrates by the horse.
To prevent pedal
bone rotation by reducing the tension in the deep digital flexor tendon (DDFT)
and reduce pressure on the sole frog support is often useful and can be in the
form of bandages, Styrofoam pads and hoof putty. (Constable,
2010)
Anti-inflammatory drugs are often prescribed by a veterinarian however these
are non-steroidal and their role is to reduce inflammation and control pain.
There are two types that are used: phenylbutazone (commonly known as bute) and
flunixin. Flunixin is used to protect against the cardiovascular results of
endotoxaemia by preventing blood vessel dilation (Constable, 2010) but is also known to be used for the
treatment of toxic shock. (Foster & Smith, 2010) To improve blood
flow to the hoof, vasodilators can be administered to widen the blood vessels.
The most commonly used is ACP and its sedative qualities are useful in reducing
movement and increasing the blood flow to the hoof however, blood flow to the
laminae remains unaltered. (Rendle, 2006)
When treating
chronic laminitis what works for one horse may not necessarily work for
another. (Constable, 2010) The diagnosis of
chronic laminitis is normally done by x-rays to reveal the position of the
pedal bone and treatment is carried out by corrective farriery.
Prognosis and Management
It is often difficult
to make a prognosis as Laminitis is an unpredictable condition however careful
management can prevent it. Prevention is mainly driven by monitoring feeding
such as restricted pasture, by strip grazing or a grazing muzzle, limited turn
out time and daily exercise of obese equines. (Practice,
2009).
Once diagnosed, Laminitis is a lifelong condition that cannot be cured only
managed carefully for the rest of the horses life.
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