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.

References

Bishop, C., Pagan, J.D., Crandell, K., Lawrence L., Huntington P. & Gardner S., 2012. The Latest on Laminitis. [Online]
Available at: http://www.ker.com/library/equinews/v6n2/v6n214.pdf
[Accessed 10 10 2012].

Butcher, A., 2009. Horse and Hound - News. [Online]
Available at: http://www.horseandhound.co.uk/news/397/291718.html
[Accessed 6 10 2012].

Clinic, M. E., 2012. My Equine Clinic – Equine Laminitis. [Online] Available at: http://www.myequineclinic.com/equine-laminitis/ [Accessed 12 11 2012]

Company, H. M., 2004. The American Heritage Medical dictionary. s.l.:Houghton Mifflin company.

Constable, S., 2010. Simon Constable's Veterinary Practice - Equine Vets in the North West. [Online]
Available at: http://www.equine-vets.com/fact-sheets/legs-and-lameness/laminitis
[Accessed 2 11 2012].

Davis, Z., 2009. Introduction to Horse Nutrition. Chichester, U.K. ; Ames, Iowa: Wiley-Blackwell.

Duncanson, G. R., 2010. Hoof conditions and problems. In: Veterinary treatment for working equines. s.l.:CABI Publishing, pp. 92-104.

Foster & Smith, 2010. Doctors Foster and Smith's Pharmacy. [Online]
Available at: http://www.drsfostersmith.com/Rx_Info_Sheets/rx_eq_flunixin.pdf
[Accessed 5 11 2012].

Frank N, D. A., 2006. Insulin Resistance in Horses. AAEP Proceedings, Volume 52, pp. 51-54.

Frank N., Geor, R., Bailey, S. & Johnson, A. D. a. P., 2010. Equine Metabolic Syndrome, Tennessee: Americna College of Veterinary Internal Medicine (ACVIM).

Hamilton-Fletcher, R., 2004. Veterinary advice on Laminitis in Horses. s.l.:Ringpress Books Ltd.

Johnson, P. J., 2002. The Equine Metabolic Syndrome peripheral Cushing’s Syndrome. The Veterinary Clinics of North America. Equine Practice, Volume 18(2), pp.271-293. Europe Pubmed Central [Online] Available at: www.europepme.org/abstract/MED/15635908 [Accessed 7 11 2012]

K. Martinson, P., Hathaway, M., H. Jung, P. & C. Sheaffer, P., 2012. Hay Soaking: All washed up or a good management option?. [Online]
Available at: http://www1.extension.umn.edu/agriculture/horse/nutrition/hay-soaking/
[Accessed 5 11 2012].

Leland Thompson, B. D., 2011. The Merck Veterinary Manual - Anti-inflammatory agents - Corticosteroids. [Online]
Available at: http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/191604.htm
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Ltd, W. E. C., 2012. Whitebarn Equine Clinic Ltd - Laminitis. [Online]
Available at: http://whitebarnequineclinic.webs.com/handoutslaminitis.htm
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Mosby, 2009. Mosby's Medical Dictionary. 8th ed. s.l.:Elsevier.

Pass, M., Pollitt, S. & Pollitt, C., 1998. Decreased glucose metabolism causes spearation of hoof lamellae in vitro: a trigger for laminitis?. Equine Veterinary Journal (supplement), Volume 6, pp. 133-138. Wiley Online Library [Online] Available at: http://www.onlinelibrary.wiley.com/doi/10.1111/j.2042-3306.1998.tb05132.x/full [Accessed 7 11 2012]

Pilliner, S. & Davis, Z., 2004. Equine Science. In: Equine Science. s.l.:Oxford:Blackwell pub.; Ames, Iowa: Iowa State Press, p. 278.

Pilliner, S. & Davis, Z., 2004. Equine Science. In: Equine Science. Oxford; Ames,Iowa; Carlton,Victoria: Blackwell Publishing, pp. 61-66.

Practice, S. C. E., 2009. Stable Close Equine Practice - Laminitis. [Online]
Available at: http://www.horsevet.co.uk/laminitis.php
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Rendle, D., 2006. Equine Laminitis. 1. Management in the acute stage. In Practice, Volume 28, pp. 434-443. In Practice [Online] Available at: http://www.inpractice.bmj.com/content/28/8/434.fullpdf [Accessed 7 11 2012]

Robert O.Gilbert, B. M. D. A. M., 2011. The Merck Veterinary Manual - retained foetal membranes in large animals. [Online]
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[Accessed 29 10 2012].

Slater, P. J., 2012. ACPAT - Association of Chartered Physiotherapists in Animal Therapy - National Equine Heath Survey. [Online]
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Tadros, E. M., Frank, N., Newkirk, K. M., Donnell, R. L., Horohov, D. W., 2012. Research paper: effects of a 'two hit' model of organ damage on the systematic inflammatory response and development of laminitis in horses. Veterinary immunology and immunopathology, Volume 150, pp. 90-100. Science Direct [Online] Available at: http://www.sciencedirect.com/science/article/pii/50165242712003182 [Accessed 7 11 2012]

Wasserman, S. A., 2008. Hormones and the endocrine system. In: Biology. San Francisco: Pearson Education Ltd., pp. 982-983.

West, C., 2010. Guided Tour Horse Hoof Anatomy [Online] Available at: http://www.thinklikeahorse.org/images/h%20hoof%20step-by-step.pdf [Accessed 12 11 2012]

Yki-Jarvinen, H. & Westerbacka, J., 2000. Vascular actions of insulin in obesity. International journal of obesity, Volume 24, pp. 25-28. Europe Pubmed Central [Online] Available at: http://www.europepmc.org/abstract/MED/10997603/reload=0;jsessionid=0m85FyYPkVGdMpCwIphA.4 [Accessed 7 11 2012]

Lumped State	Initial Encoding	Description
AL	Standing	Standing up on hind legs
	Looking (L-R)	Movement of head looking left and right
	Looking (U-D)	Movement of head looking up and down
	Cocking of head	Tilting of head to the left and right
	Sitting	Sitting down on hind legs and tail (legs not extended)
LOCO	Run	Running
	Hop	Pulls self-forwards with front legs and hind legs collect together
	Investigate	Move as a pack to check where a possible previous threat/object of interest was
FOR	Eat	Eating food straight from the floor
	Sniff	Sniffing of the ground
	Digging	Using front paws to move dirt
SOC	Play	Mock aggression, bearing of teeth, jumping on each other
	Chasing	Running after each other
	Parental reprimand	Parent reprimands child by putting paw on top of the child’s head and pushes down
HIDE	Retreat	Move into indoor enclosure/burrows
CLEAN	Genital	Cleaning of anogenital area
	Ear	Cleaning of ear with hindfoot/front paws
NOISE	Growling	Low frequency rumble, associated with play
	Warning Squeak	High frequency yip, associated with retreat when threatened

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Wednesday, 13 November 2013

Green Gym #2

Wednesday, 6 November 2013

A tribute

Meerkat Ethogram

Wednesday, 30 October 2013

Cotwold Wildlife Park

Monday, 21 October 2013

Laminitis