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Equine Metabolic Syndrome

2021-02-12T11:40:30Z

Catrionag98: Created page with "{{OpenPagesTop}} Also known as: ''''' EMS, Peripheral Cushing's syndrome, Pre-laminitis syndrome, Pre-laminitic metabolic syndrome''''' == Introduction == Equine Metabolic S..."

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Also known as: ''''' EMS, Peripheral Cushing's syndrome, Pre-laminitis syndrome, Pre-laminitic metabolic syndrome'''''

== Introduction ==

Equine Metabolic Syndrome (EMS) describes a collection of risk factors that predispose horses to the development of endocrinopathic [[laminitis]]. The main feature of the condition is insulin dysregulation, although there are a number of metabolic processes that contribute.

== Aetiology ==

EMS is a hormone disorder which causes insulin resistance. The official definition of EMS is ‘a collection of historical, clinical and laboratory risk factors for endocrinopathic laminitis’ however insulin dysregulation is the most important feature of the disease. The pathophysiology is extremely complex and is not yet fully understood. Like many endocrine conditions, EMS has an insidious onset.

Increasingly the endocrine function of adipose tissue is being recognised, and this is thought to play a major role in pathgenesis of EMS. EMS is most common in overweight animals, although not all animals are obese.

The exact pathogenesis of endocrinopathic laminitis in horses with EMS is unclear, but high resting blood glucose concentrations, inflammatory mediator release from fat, alterations in steroid hormone metabolism by adipose tissue and direct functions of insulin are all thought to play a role.

== Epidemiology==

There are a number of intrinsic and environmental factors which are involved in the development of EMS:

* Genetic predisposition: EMS is more common in ponies, particularly native breeds
* Age: older horses are less sensitive to insulin
* Obesity: excess intake of calories with respect to exercise/ metabolic requirements (over a prolonged period)
* Epigenetic factors: excessive or undernutrition in utero can alter metabolism later in life
* Dietary factors: high CHO diets
* Influence of the GI microbiome

The most common presentation of EMS is recurrent laminitis in 5-15yo ponies with a high BCS.

== Pathogenesis ==

Adipocytes have an important (but often overlooked) endocrine function within the body. They produce hormones (adipokines) which act systemically in a number of processes.

Animals with EMS have increased concentrations of adipokines which antagonise the effect of insulin and cause hyperglycaemia. The body responds to this by increasing insulin production and the ultimate effect of this is hyperinsulinaemia. If this continues for a prolonged period of time, some animals may develop beta cell exhaustion, where the pancreas can no longer produce insulin (i.e. Type 2 diabetes).

It is unclear what role this hyperinsulinaemia plays in the pathogenesis of laminitis, but it has been suggested that stimulation of IGF-1 receptors may cause endothelial dysfunction.

Insulin resistance results in high blood glucose concentrations, which can damage blood vessels and alter blood flow to the hoof- contributing to laminitis.

Fat plays an additional role in steroid hormone metabolism, which also antagonise insulin. Steroid-like hormones can be primarily produced by fat cells, but adipocytes also have the ability to convert inactive cortisone into the active molecule cortisol.

Many cases of EMS go undiagnosed, despite high levels of obesity, laminitis and hyperinsulinaemia in the equine population. There are a number of owner and veterinarian directed campaigns highlighting the effects of equine obesity and EMS.

https://www.beva.org.uk/Home/Guidance-and-Resources/Routine-Healthcare/Equine-Obesity

https://www.liverpool.ac.uk/equine/common-conditions/weight/

https://www.worldhorsewelfare.org/advice/management/right-weight

== Clinical Signs ==
• Obesity: BCS >3/5; abnormal fat accumulation along the crest, shoulders, tailhead and rump
• Laminitis (chronic): dropped sole, divergent growth lines on hoof wall, widened white line
• Laminitis (acute): FL lameness (shifting weight, pottery gait, reluctance to move), pain (increased HR, RR, behavioural changes), increased digital pulses, heat around foot

== Diagnosis ==

Diagnosis should be suspected based on '''clinical signs and patient history'''.
Blood testing can help confirm a diagnosis (and is often used to rule out [[PPID]] which is the main differential diagnosis).

Resting insulin levels (interpreted alongside glucose) can give a good indication of insulin resistance. Glucose levels are rarely above the reference range but tend to lie towards the upper end. High glucose levels are often a sign of severe insulin resistance. Glucose values can also be affected by stress, so care when interpreting high values. In some cases insulin levels may be low, where beta cell exhaustion has occurred.

Dynamic tests are more accurate for diagnosis, and there a number of different techniques available:

'''Oral Glucose Tolerance Test (OGTT) ''': 1g/kg glucose is administered as a 20% solution and blood glucose and insulin levels are tested prior to administration and at 30, 60, 90, 120, 150, 180, 240 min.
Blood glucose should double within 2 h and normalise within 6 h. Glucose (>11.1mmol/l) or delay to normal levels indicates insulin resistance.
Using the insulin levels as well as glucose gives more information and the I:G ratio can be a useful measure. >0.3-0.5 indicates relative insulin resistance. Total insulin secretion is also raised with insulin resistance.
Horses with type 2 DM (rare) may have low/normal insulin and high resting glucose or glucose responses (as the beta cells are no longer producing adequate amounts of insulin).
Beware of other conditions which could affect this test e.g. gastrointestinal function.

'''Intravenous Glucose Tolerance Test (IVGTT) ''' 0.5g/kg dextrose is given IV as a 50% solution following 12 h fast. Samples for glucose and insulin are collected at 0, 0.25, 0.5, 1,2,(3,4,5,6) h.
Normal is >300% increase in glucose @ 15 min followed by rapid decrease alongside more than 600- 700% increase in insulin @ 15 and 30 min, followed by a decrease. Glucose and insulin concentrations should return to baseline within 1 h.

'''Insulin Tolerance Test (ITT) ''' 0.05IU/kg insulin is given IV. Blood samples for glucose and insulin are taken at 0, 30, 60, 90, 120, 180, 240, 300 min.
Normal response is 30-50% decrease in insulin at 15 min, 60% at 30 min. Normal levels should be reached by 2 h.
CARE not to induce hypoglycaemia with this test.

'''Combined Intravenous Glucose and Insulin Tolerance Test (CGIT) ''' Collect baseline blood sample for glucose and insulin. Infuse 50% dextrose (0.15 g/kg), immediately followed by 0.10 units/kg regular insulin. Further samples are collected for glucose at 1,5,25,35,45,60,75,90,105,120,135, and 150 min; and for insulin at 45 min.
Impaired glucose tolerance is shown by the maintenance of blood glucose above baseline for >45 min. Insulin levels should decline to < 100 IU/ml by 45 min; anything longer is suggestive of IR.

For all of these tests horses may have small amounts of forage and water without affecting test results, but concentrates should be withheld for at least 12 hours.

== Differential Diagnosis ==

The other main cause of endocrinopathic laminitis is [[PPID (Equine Cushing’s disease)]]. Resting ACTH levels may help exclude this disease, but raised levels combined with clinical suspicion may indicate that dynamic tests are required (e.g. TRH response test).

== Treatment ==

The key to controlling EMS is dietary control and exercise. If cases are recognised early, then strictly implemented management strategies to reduce weight and control diet may prevent the development of laminitis.
Care should be taken when devising a weight loss plan because severe caloric restriction can lead to [[hyperlipidaemia]]. Furthermore, severe calorie restriction promotes metabolic processes designed for survival in poor conditions, where insulin resistance is increased and energy is conserved which prevents weight loss.
Overweight horses should not be given access to rich grazing, and ideally owners should have the sugar content of their hay analysed. Hay should be soaked for at least 12 hours to remove some of the soluble carbohydrate. Having horses out at pasture can help promote natural exercise, however grass muzzles may need to be used to prevent overgrazing on rich grass. An alternative solution is to graze these animals at night when the sugar content of grass is lowest. If additional feeding is required then foods with a low glycaemic index should be used. Unmollassed sugar beet or alfalfa chaff are good examples of low GI foods, or there are some commercial feeds designed for laminitics. In some situations it may be helpful to consult a nutritionist (who will often help analyse hay samples with minimal expense).
Ideally dietary modification should be combined with increased energy expenditure through exercise, but in some individuals it is difficult to increase exercise due to laminitis and associated pain. In these cases dietary management is the main component of the weight loss plan.
Historically thyroid hormone supplementation has been used in overweight ponies under the belief that they are hypothyroid. This is unlikely in most animals, and treatment with thyroxine is not indicated. In some cases it may be used in the short term to aid weight loss but ideally simple management changes should be attempted first.

== Prevention ==

Owner education is key in the prevention of EMS. Animals predisposed to obesity and EMS should be managed carefully to prevent excessive weight gain, and as with many things prevention is better than cure. Often conveying this to owners requires highly skilled communication, as they feel that they are being kind to their horse by feeding them things that they enjoy or rugging them unnecessarily.

There are a number of resources circulated in the veterinary and equestrian press which can be helpful. Some examples are included above.

==References==
Vetstream Vetlexicon Equis: Equine Metabolic Syndrome
https://www.worldhorsewelfare.org/advice/management/right-weight
RDSVS staff (2019) ''PPID, EMS and weight loss in horses''' BVM&S Intergrated Clinical Course: Equine, ''Royal Dick School of Veterinary Studies''

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[[Category:Musculoskeletal Diseases - Horse]]

Laminitis - Horse

2021-02-10T12:35:51Z

Catrionag98: /* Epidemiology */

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Also known as: '''''Founder'''''

== Introduction ==

Laminits is a common and debilitating condition of horses caused by '''separation of the laminae of the [[Hoof - Anatomy & Physiology|hoof]]'''. It can be acute or chronic and can result in the horse being put down.

== Aetiology ==

Laminitis is an '''acute degeneration''' of the '''sensitive primary and secondary laminae'''. The cause for this is unknown.

== Epidemiology==

Although the cause for laminitis is not fully understood, several risk factors have been recognised:

* Obesity
* Access to lush pastures - particularly in the Spring or Autumn, on cold bright days, and during daylight hours when levels of fructans are highest
* [[Grain Overload - Horse|Grain overload]] (ingestion of large quantities of soluble carbohydrates)
* Retained placenta, [[Colic|colic]], diarrhoea and any other systemic illness causing endotoxaemia
* Animals having little exercise
* Pituitary Pars Intermedia Dysfunction / Equine Cushing's
* [[Equine Metabolic Syndrome]]
* Trauma/excessive work on hard surfaces
* Increased weight bearing on one limb - normally caused by lameness in the contralateral limb.
* Pony breeds

== Pathogenesis ==
[[File:Founder_severe_rotation.JPG|right|thumb|200px|Severe pedal bone rotation with penetration into the hoof sole (Wikimedia Commons)]]
The separation of the sensitive laminae (originated from the third phalanx/pedal bone) from the laminae lining the inside surface of the hoof is followed by the pedal bone '''rotating''' within the '''hoof capsule''' and coming to '''rest on the sole'''. This causes the sole to be pushed downwards and the pedal bone may penetrate the sole at the toe. Rotation occurs due to '''torque''' from the '''deep digital flexor tendon'''. Another possibility is that he pedal bone ''sinks''' (displaces ventrally) due to the weight of the animal. The bone may rotate, sink or both. Serum accumulates in the space between the laminae and can breakdown the white line.

=== Mechanism of Separation of the Laminae ===

The mechanism is unknown but theories are:

(1) '''Ischaemia and necrosis'''. Ischaemia may be caused by vasoconsriction, arterio-venous shunts, interstitial oedema or a mixture of all three mechanisms.

(2) '''Inflammation''' and then '''degeneration''' of the sensitive laminae

(3) '''Enzymatic digestion''' of laminae by Matrix Metalloproteins (MMPs)

(4) '''Abnormalities in the hoof metabolism or corticosteriods''' (endogenous cortisol or iatrogenic) which results in increased glucocorticoid activity.

Subsequent to separation of the laminae a '''pain-hypertension-vasoconstiction''' cycle will occur in acute cases. '''Pain''' causes the release of '''vasoconstictors''' such as catecholamines, [[Renin Angiotensin Aldosterone System|angiotensin II]], and [[Pituitary Gland - Anatomy & Physiology#Antidiuretic Hormone|vasopressin]]. This vasoconstriction then causes a '''reduced blood flow to the foot''' and [[Systemic Hypertension|systemic hypertension]].

== Clinical Signs ==

=== Acute Disease ===

Acute disease develops rapidly and most commonly occurs in the '''front feet'''. In the early stages of disease or if the case is mild the horse presents as '''reluctant to move''', with frequently '''shifting of weight between the affected feet''' and a characteristic '''stilted gait'''.

In more severe cases the horse normally presents with a characteristic '''posture''' in which the horse appears to be '''leaning back on its heels'''. In this posture the feet are placed normally but the '''head is low''' and the '''back arched''' as the horse attempts to '''relieve the pressure on the toe''', particularly in the fore-feet. The horse may also be '''unwilling to move''' or pick up its feet and can potentially collapse if it is forced to do so. Signs of pain such as '''anxiety''', '''sweating''', '''increased heart and respiration rate''' are frequently seen.
In the most severe cases there may be '''serum like exudate''' at the '''coronary band''' and the '''hoof''' may become '''detached and shed'''. Although this does indicate a bleak prognosis, with good and dedicated owners, vets and farriers who are prepared for the time and cost of treatment the horse can survive sloughing of the hoof and go back to normal work.

=== Chronic Disease ===

In chronic cases '''separation of the laminae''' and '''sinking and/or rotation of the pedal bone''' will have occurred. The sole drops and the hoof wall spreads which results in '''marked transverse ridges on the hoof'''. Also the angle of the hoof as viewed laterally decreases. Degeneration of the white line may allow for infection to enter, potentially resulting in sepsis of the pedal bone. It is common for the animal to become '''lame with exercise''' and have repeated bouts of '''mild laminitis'''. Often there is a recognised '''underlying cause''' such as Cushing's disease in chronic laminitis cases.

== Diagnosis ==

Diagnosis should be based on '''clinical signs and patient history'''. '''Pain''' and '''heat''' may be present on palpation around the coronet and the horse may display a marked withdrawal in response to '''hoof testers'''. The height and strength of '''pulse''' in the '''palmer digital artery''' is normally '''increased'''. If the pedal bone has sunk a concavity may be palpable at the junction of the coronet, and in very severe cases the pedal bone may be visible through the sole of the hoof. Definitive diagnosis is achieved using '''radiography.'''

=== Radiography ===
[[File:Laminitic.jpg|right|thumb|200px|Radiograph of the laminitic foot (Wikimedia Commons)]]
Radiographs should be taken of front feet or all feet if all legs are affected. A '''metal strip''' should be placed on the '''dorsal wall''' of the hoof and the '''sole''' should be marked with a similar metal strip or a pin can be used. They allow for the angle of the pedal bone in relation to the hoof to be analysed. There may be no radiographic changes if the case is acute or mild. However, in more severe cases radiographs may show:
* '''Rotation''' of the pedal bone as a tilting of the distal aspect towards the sole
* '''Sinking''' of the pedal bone (which is the main indicator of prognosis).
*'''Serum''' build up may be evident as a '''radiolucent line''' between the dorsal hoof wall and the pedal bone.
*In chronic cases the pedal bone may even develop the appearance of a '''Turkish slipper''', as a result of the pressure placed on tip of the rotated P3.

You should measure:
* Distance between the top of the hoof wall and the top of the extensor process of pedal bone to assess sinking of P3. This is called the ''''Founder distance''''
* Distance between the dorsal hoof wall and the dorsal cortex of pedal bone to calculate the ''''Rotation angle'''' of P3

The radiograph should be shown to the '''farrier''' who is working with you on the case. Radiographs are essential for prognosis.

== Differential Diagnosis ==

Symptoms of the following diseases can be similar but there is no pain in the feet:
* Equine Rhabdomyolysis Syndrome
* [[Clostridium tetani|Tetanus]]
* [[:Category:Colic in Horses|Colic]]
* Spinal Ataxia

== Treatment ==

Acute laminitis is an '''emergency''' requiring immediate treatment.

Aims:
* Removing inciting cause
* Relieve pain and reduce inflammation
* Prevent rotation or sinking of the pedal bone
* Promote hoof growth

Additional aims (controversial):
* Dilate blood vessels in the foot
* Prevent microthrombi formation

'''Analgesics''', mainly [[NSAIDs]] (Phenylbutazone) and '''box rest''' are the standard treatments. Other available NSAIDs are Flunixin Meglumine, Ketoprofen and Dimethyl Sulfoxide.
As the pathogenesis of laminitis is not fully understood there is some controversy surrounding the use of some drugs and the theories behind their use - such as vasodilators and anticoagulants. Therefore it is up the individual clinician to decide whether these drugs are indicated. However it is unanimously agreed that box rest and anti-inflammatory drugs are the mainstays of treatment.

'''Mechanical support''' is important and may provide some '''pain relief''' and help '''prevent rotation or sinking of the pedal bone'''. It can be done with '''polystyrene''' or other '''packing materials''' or by keeping the animal on '''soft, deep bedding'''. Elevating the '''heel''' with a '''wedge''' or wedge shoe may be useful to take off some of the strain on the deep digital flexor tendon and help to reduce rotation. '''Remedial farriery''' can be used to minimise the detrimental effects of disease by; stabilising the pedal bone, decreasing the forces placed on the dorsal laminae, removing infection, and improving blood supply and growth. Techniques include the use of trimming and egg bar, heart bar and plastic shoes. Numerous trimmings will be required.

Horses should be fed on a '''very low energy diet of soaked hay'''. Low carbohydrate, high fibre concentrates such as 'Happy Hoof' may be added in small quantities if appropriate. Supplements such as Biotin may also be given to improve hoof growth.

The response to treatment should be monitored physically and radiographically.

It should be stressed that '''management''' plays a huge role in both the treatment of an active case of laminitis and in preventing its recurrence in the future. Recovery from laminitis may be prolonged especially in severe cases, and return to work should always be gradual. In the cases where an underlying cause (e.g. Cushing's Disease) is suspected, this should be identified and treated appropriately.

In very severe cases the only option may be '''euthanasia'''.

== Prevention ==

Identification and management of any '''predisposing factors''' is extremely important in preventing the recurrence of laminitis.

Overweight and unfit animals should be managed appropriately with diet and exercise changes. Horses with a history of laminitis should not be allowed to graze lush pasture, especially in Spring and Autumn and early in the morning. Following injury or lameness to one limb, the other limbs should be monitored closely for signs of laminitis (increased heat and digital pulses) and the animal placed on a deep bed to help prevent it occurring. In horses where endotoxaemia may develop, anti-endotoxic drugs such as NSAIDS should be given as they may prevent the development of laminitis. As mentioned, in the cases where an underlying disease is suspected, this should be identified and treated appropriately.

== Prognosis ==

Several factors effect the prognosis in laminitis cases. The pursuit of treatment and the likelihood of its success is very dependant of financial and emotional commitment of the owners.
'''Larger''' and '''heavier''' animals carry a '''poorer''' prognosis, as do animals with a '''greater number of affected feet'''. '''Clinical signs''' help guide prognosis but there are big differences between the signs displayed by stoical and relatively wimpy horses, and it is considered better to use response to treatment in the individual horse as a guide. The '''Obel grading system''' was developed (in 1948) to help grade prognosis, with lower grade horses having a better prognosis:

'''GRADE 0'''. There is no lameness at walk or straight trot on a hard surface

'''GRADE 1.''' At rest, the horse alternately lifts its feet, but no lameness is observable at walk. There is a short stilted gait at straight trot on a hard surface and when turned at walk

'''GRADE 2.''' The horse does not move freely at walk and has a ‘stiff’ gait. At trot on a hard surface, the animal has a short stilted gait, and it turns with great difficulty. A foot can be lifted off the ground without great difficulty

'''GRADE 3.''' The horse is reluctant to move at walk on any surface. It is difficult to lift a limb and the animal might be virtually non-weightbearing on the affected limb

'''GRADE 4.''' The horse will not move without coercion. It is particularly reluctant to move from a soft to a hard surface and it is almost impossible to lift a limb

'''GRADE 5.''' The horse is mostly recumbent and will not stand for more than a few minutes

'''Radiography''' is the main tool required for prognostics. It is generally recognised that the worse the '''rotation''' of the pedal bone the less chance of returning to athletic function. However there should not be too much emphasis placed on pedal bone rotation when considering the prognosis. A '''fast rate of rotation''' is suggestive of further structure collapse - repeat radiographs are useful when assessing this. The '''acute''' appearance of '''radiolucent lines''' parallel to the dorsal hoof wall suggests structural collapse and a poor prognosis. However, the level of '''sinking''' of the pedal bone is the main prognostic indicator, with '''distal movement of the pedal bone suggesting a very poor prognosis'''.

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|flashcards = [[Equine Orthopaedics and Rheumatology Q&A 01]]
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==References==
Rendle, D (2006) '''Equine laminitis 1. Management in the acute stage''' ''In Practice 2006 28: 434-44''

Rendle, D (2006) '''Equine laminitis 2. Management and Prognosis in the Chronic Stage''' ''In Practice 2006 28: 526-536''

Obel, N. (1948) '''Studies on the histopathology of acute laminitis''' ''Almquisst and Wiksells Boktryckeri ab Uppsala''

Merck & Co (2009) '''The Merck Veterinary Manual''' (Ninth Edition), ''Merial''

May, SA & McIlwraith, CW (1998) '''Equine Orthopaedics and Rheumatology Self-Assessment Colour Review''' ''Manson Publishing Ltd''

RVC staff (2009) '''Locomotor System''' RVC Intergrated BVetMed Course, ''Royal Veterinary College''

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[[Category:Musculoskeletal Diseases - Horse]]
[[Category:Dermatological Diseases - Horse]]
[[Category:Expert Review - Horse]]