Servicio Veterinario en Equinos

13/09/2025

Pacientes

12/09/2025

21/08/2025

Equine Metabolic Syndrome (EMS)
Brian S. Burks, DVM
Diplomate, ABVP
Board Certified Equine Specialist

Equine metabolic syndrome is known for its multiple risk factors for laminitis due to insulin dysregulation (ID), genetic predisposition, and obesity. Internal adipose tissue—visceral and retroperitoneal—appears to experience the strongest pathologic disruptions.

Affected animals typically are obese, with increased condition score overall and increased regional adiposity in the neck and tailhead regions. Laminitis, both chronic and acute, is common. Hyperinsulinemia with normal blood glucose concentrations (insulin resistance) is the primary clinical pathologic finding. Other associated signs include infertility, altered ovarian activity, and increased appetite. Other laboratory findings include hypertriglyceridemia, increased serum concentrations of leptin, and arterial hypertension.

At one time, this cluster of clinical signs was referred to as hypothyroidism, but thyroid responses are normal and thyroidectomized horses do not develop obesity or laminitis. EMS/ID is the result of an inability to properly metabolize carbohydrate, and many horses have exaggerated glucose and insulin responses to oral carbohydrate. Any abnormality in carbohydrate metabolism in horses is called insulin dysregulation.

EMS develops in horses five to 16 years old, in horses, donkeys, and ponies. It is most common in ponies, Saddlebreds, Tennessee Walking Horses, Paso Finos, Morgans, Mustangs, and Quarter horses, but is infrequently diagnosed n Thoroughbreds and Standardbreds.

The underlying reason why some horses develop equine metabolic syndrome and others do not is not known. There appears to be a genetic disposition. Affected horses may possess a “thrifty” gene that enabled their ancestors to survive in harsh environments. This increased efficiency of energy metabolism became maladaptive in modern environments with plentiful, nutrient-dense feedstuffs.

EMS may be a predisposing factor for pituitary pars intermedia dysfunction (PPID; also called equine Cushing’s disease). Both endocrine disorders can occur concurrently in middle-aged and older horses. Horses with EMS should therefore be monitored to detect the onset of PPID.

Affected equids are typically obese, with a body condition score >6/9. There is regional adiposity with a cresty neck (the nuchal ligament is full of fat and can get large enough to ‘fracture’ and fall to one side), fat deposition over the ribs, topline, and tail head. There may be increased fat deposition in the prepuce and mammary glands.

Adipocyte size and hypertrophy occur with excess calorie intake and these characteristics are associated with insulin resistance and dyslipidemia in humans. EMS horses experienced marked adipocyte hypertrophy and subsequent inflammation and circulating cytokines. Marked leptin gene expression also occurs in EMS horses and is related to adipocyte volume.

Acute and chronic laminitis are common. Horses brought in for evaluation with no previous history of laminitis often show evidence of prior episodes, such as abnormal hoof growth rings and radiographic evidence of third phalanx rotation or pedal osteitis. Laminitis may occur secondary to ingestion of feeds high in soluble carbohydrates, either in the form of lush pasture or high-carbohydrate hays and supplements. This can result in bouts of laminitis developing in the spring, when new pasture growth appears, and in the fall, when night temperatures are below freezing.

The common denominators behind many of the signs associated with EMS appear to be increased adiposity, insulin resistance, and hyperinsulinemia. When obesity develops, adipose tissues elaborate leptin and other adipokines as well as tumor necrosis factor and other inflammatory mediators. Increased fat stores in the liver may also predispose to insulin resistance due to down-regulation of insulin receptors.

Hyperinsulinemia leads to laminitis in horses and ponies. Insulin has vasoregulatory actions. Insulin resistance can decrease nitric oxide production and promote vasoconstriction. Altered glucose and insulin levels may also lead to altered epidermal cell function and glucose uptake by epidermal laminar cells. These effects predispose horses with EMS to develop laminitis.

Affected horses often do not lose weight without extreme food restriction, and obesity is exacerbated by laminitis, which limits exercise. Horses have increased appetites and will eat continually.

The development of obesity leads to increased glucocorticoid production by omental adipocytes, contributing to insulin resistance. This may be a survival mechanism as wild horses and ponies are able to gain weight during the summer months when forage is plentiful but lose weight over the winter during harsh periods when forage does not grow. This response maintains blood glucose for the CNS, and this may confer an advantage over others during times of food deprivation. Horses and ponies are commonly fed energy-rich rations that exceed requirements for exercise and survival. These diets also have potential complications of colic, typhlocolitis, osteochondrosis, and laminitis. Mares that suffer malnutrition for even short periods may cause damage to fetal cells, leading to the development of equine metabolic disease as an adult.

Diagnosis requires documenting insulin resistance and excluding PPID. Clinical signs alone are not enough to make a diagnosis. Even without a history of laminitis, the feet should be carefully examined and radiographed.

Many conditions can affect blood glucose and insulin levels, including diet, pain, and stress. Testing should be delayed in horses with laminitis until the animal is relatively pain free and should be performed in a controlled manner with minimal stress.

Blood glucose concentrations are within reference range or slightly increased with EMS. Persistent hyperglycemia should lead to PPID testing. Insulin measurement should follow a 6-8 hour fast, leaving only one flake of hay overnight. A blood insulin concentration >20 μU/mL is suggestive of insulin resistance.

Documentation of insulin dysregulation requires an oral sugar test; some horses are normal in all respects except for the ability to handle an oral carbohydrate load. The OST is performed by fasting the horse for 3-12 hours and then giving an oral dose of corn syrup at 0.15-0.45 mL/kg. Blood should be collected at 60 or 90 minutes after administration of the corn syrup for insulin determination. An insulin concentration >60 mU/L is abnormal.

To determine whether insulin can stimulate normal glucose uptake by peripheral tissues, an insulin tolerance test can be performed. This is accomplished by collecting a baseline blood sample for glucose concentration, giving regular human recombinant insulin, and then collecting a second blood sample for glucose concentration 30 minutes later. A second blood glucose concentration that does not decrease to 50% or less of the baseline value indicates insulin resistance.

Tests for PPID such as measuring endogenous ACTH concentration or thyroid releasing hormone response test are normal in horses with EMS. Positive results indicate that the horse is concurrently affected by EMS and PPID, which can occur in older horses. Detection of PPID is important, because it is thought that PPID exacerbates insulin resistance in horses affected by EMS.

Treatment for equine metabolic syndrome involves dietary management and, if diet and exercise is not sufficient to treat the condition, medical therapy. Correction of the diet may be all that is needed to return the horse to normal body weight. Total caloric intake should be reduced.

Forced activity is helpful, but despite this, weight can be difficult to lose. When diet and exercise are not sufficient, thyroxine or metformin may be used to improve insulin sensitivity. Thyroxine will also accelerate weight loss. The latter does not work well in horses, as it is poorly absorbed in horses. The longterm efficacy and safety of metformin has not been established in horses. If it is used, blood glucose should be carefully monitored. Use of metformin should be discontinued if hypoglycemia is documented.

The nonstructural carbohydrate (NSC) content of forage should be determined by feed analysis. This can be calculated by adding starch and water-soluble carbohydrate percentages. Ideally, NSC should comprise < 10% of the hay dry matter, and it should never exceed 16%. Soaking hay in water for 60 minutes has been recommended to lower water-soluble carbohydrate concentrations, but the actual amount reduced is extremely variable; hence, this is not a reliable method to produce a low-NSC forage.

Because there is insulin resistance, removing carbohydrates from the diet is essential. This means that all sweet feed products, including many complete feeds, should not be fed. Typical sweet feeds contain 80-90% simple sugars. Oats are approximately 60-80% simple sugar. Reducing the nonstructural carbohydrates to less than 15% is extremely helpful in improving the clinical signs of affected horses. Often grain is only fed because of the owner’s perception that it is a necessary part of the diet; however, simply removing grain and maintaining the horse on good quality grass hay often helps tremendously. In some cases, grass hay with

15/08/2025

Anatomy of the Equine Foot
Brian S. Burks, DVM
Diplomate, ABVP
Board Certified in Equine Practice

Horses have evolved over the last 55 million years. The first horse was the size of a cat- only 10 inches tall, and walked on padded feet, much like a dog. This was when the world was quite tropical, and before the Ice Age when horses had to adapt to a different environment. The pad of the third digit eventually became the frog of the modern horse’s foot. The modern horse (Equus caballus) first appeared about 5 million years ago.

Horses were first domesticated about five thousand years ago in what is today southern Russia. Their domestication influenced human history, mainly due to their extensive use in warfare.

The hoof, or hoof wall, is the three layered outer surface of the foot. The foot includes the hoof, bones, blood vessels, ligaments, tendons, and nerves. The horse stands on what is the human middle finger and the middle bone in the hand is the cannon bone. The wrist is the human carpus, corresponding to the ‘knee’ of the horse.

The hoof plays a very large role in weight-bearing in the horse, and protects the structures within the hoof capsule. For the foot to work properly, it must be healthy, and the equine owner plays a role here. Horses have been removed from their natural environment and the natural selection process has been disturbed. Horses with poor feet in the wild do not survive, but domesticated horse receives special care and may be bred, passing along undesired traits.

The external surface at the front of the foot is its dorsal surface, and the surface facing the ground is the solar surface. On the front leg, the caudal (rear) aspect of the foot is its palmar surface. In the rear leg this is referred to as the plantar surface. Medial (inside) is the term for the portion of the foot nearest the foot on the opposite side. Lateral (outside) is the term for the portion of the foot farthest away.

The hoof is composed of several layers. The outermost layer is the periople (stratum externum) which is cuticle on the human finger. As it advances down the hoof wall, it is called the stratum tectorium, but most of this is abraded by dirt and sand and is lost.

The middle layer, the stratum medium is the thickest layer. It is composed of many hollow tubules of keratin which are embedded in a matrix of keratin. This latter structure gives the foot its strength, being less likely to fracture than the tubules. There is a gradient within this layer. The outer tubules are smaller, but greater in number. As they progress inward, the tubules enlarge and are less numerous. This allows the foot to keep the outside of the hoof dry (if they are not standing in water- the hoof will imbibe water within 24 hours) and the inside more moist, adding flexibility to the hoof capsule, which is a dynamic structure, constantly growing downward toward the ground.

Inside is the stratum internum, which is made of epidermal laminae- leaf-like structures that run the length of the hoof wall, parallel to the stratum medium. There are 600 laminae in the hoof; each lamina has 150 -200 secondary laminae.

The hoof grows down from the coronary band (corona; crown) from papillae that fit into the tubules. Keratinocytes are made in this region, and are continually being pushed down the wall. They eventually lose their nucleus and become officially dead cells. The coronet has a massive blood supply to feed the hoof. Injury to the coronary band can have a serious negative effect on hoof growth and development. If the injury to the coronary band is serious, it can result in permanent disfigurement of the hoof and, in some cases, disrupt proper hoof growth to the point where the horse is no longer usable.

The corium is similar to the dermis of the skin elsewhere in the body. In the case of the foot, there are epidermal laminae and dermal laminae. The outer portion of skin is epidermis, while the deeper layer is the dermis, filled with blood vessels and nerves. There are several parts to the corium of the foot: perioplic, coronary, laminar, solar and frog corium. The first two form the coronary band.

The sole is similar in construction to the hoof wall, with vertical tubules fed by the solar corium. These tubules curve near the ground, limiting growth and allowing shedding of the sole. The sole is designed to carry internal weight, not weight from the ground. The sole is the area inside the white line, excluding the bars and frog.

The white line is the junction between the wall and the sole and is clearly visible around the front three-fourths of the circumference of the sole in a freshly trimmed foot. The white line is yellowish and during the 1800s was commonly called the golden line. It joins the sole to the inner wall of the hoof and seals the border of the third phalanx to protect it from bacterial infiltration. It creates a shallow crease at the bottom of the hoof which fills with dirt, aiding with traction.

The inner hoof wall is white due to a lack of pigment. It has a high moisture content making it more pliable than the outer wall. This allows for stretching of the inner wall to protect the internal hoof structures from shock. It also allows the third phalanx and outer wall to move in different directions, while preserving strength of attachment.

The outer hoof wall is pigmented and much stronger than the inner wall. It bears the horse’s weight, protects internal structures from damage, and stores and releases energy like a spring, helping to propel the horse during movement. A healthy outer hoof wall is slightly thicker at the toe and has no growth rings or cracks. It is nearly impermeable to water, dirt, and mud, but a damaged wall can allow pe*******on of external substances, allowing infection of the white line or subsolar abscesses to occur.

The frog is a wedge shaped rubbery tissue between the bars of the sole. It should be wide and substantial, and while keratinized, the frog is about 50% water, making the frog soft. The apex points forward and the base, at the heel, has a shallow central sulcus. It acts as a shock absorber from the ground and redirects force from the bony column through the lateral cartilages of the hoof. It also pumps blood through the foot every time the hoof lands on the ground. An unhealthy frog can cause significant loss of structure in the caudal portion of the internal hoof, leading to lameness.

The frog works with the coronet, bars, and sole to provide resistance to distortion of the hoof capsule. Frog pressure influences the digital cushion above. The frog stay (triangular area cut out of the sole that in which the frog sits) allows independent movement at the heels as the horse lands on uneven ground. The frog also plays a part in protecting the sensitive structures beneath, providing traction, assisting circulation and absorbing shock. It also contains many nerves which enable the horse to feel what it is standing upon and to know where its feet are in relation to the rest of the body (proprioception).

In the center of the frog, towards the back of the foot is the central sulcus. A healthy sulcus is wide and shallow, but if the frog is weak and narrow it can become a deep crease which is a haven for bacteria and fungus. This deep crease is common, but abnormal.

The collateral groove runs along either side of the frog. The outer wall of the groove is made up of the wall of the bar and sole and the wall on the other side comprises the wall of the frog.

The angle of the bar is commonly known as the heel, although this can be misleading. This area is designed to receive the initial impact of the horse’s stride and a healthy angle of the bar comprises mainly of pliable inner wall, enabling it to dissipate excess shock. This area plays a major role in supporting the weight of the horse and it is important that it remains correctly balanced.

The heel bulbs are at the back of the foot. The heels make an abrupt turn toward the toe to form the bars, which are supported by the internal digital cushion.

The Skeletal System

The bones of the foot provide a frame and facilitate locomotion. They are light, yet strong enough for the rigors of weight bearing and concussion during trotting and galloping.

Third phalanx (P3)--It is also called the distal phalanx, os pedis, pedal bone, and coffin bone. It is the most distal (farthest out from the body) of the four bones comprising the digit (equivalent to man's finger or toe) and is completely enclosed by the hoof. Interaction between this bone and the surrounding hoof structures serves as a shock absorber for the horse in motion. It does not have a medulla (bone marrow) and has an unusually high density of tiny blood vessels. Surrounding the bone are the laminae (leaves) which hold the wall to the bone. Underneath, the bone is covered in solar corium which produces the sole. Caudally, the bone attaches to the cartilage of the digital cushion. Tendons and ligaments are attached to this bone and a dense network of blood vessels run around and through the distal phalanx.

Second phalanx (P2)--This bone is also called the middle phalanx, os phalanx, and the short pastern bone. It rests on the third phalanx and articulates with it and the first phalanx, which is above P2.
Distal sesamoid--This structure is often called the navicular bone or shuttle bone and is located on the back surface of both the second and third phalanx. This bone is shaped like a boat. The deep digital flexor tendon passes over the bone on its way to attach to the distal phalanx. It is an integral part of the shock absorbing mechanism, along with its ligamentous attachments.
First phalanx (P1)--This bone is also called the os compendale, os saffragenous, and long pastern bone. The first phalanx is the longest bone of the digit. It rests on the second phalanx and also articulates with the third metacarpal (in the foreleg) or metatarsal (in the hind leg), also called the cannon bone. It is closely attached to the paired proximal sesamoids by strong ligaments.

Soft Tissue Structures of the Foot

Tendon of the common digital extensor muscle--It is considered in this discussion, the authors say, because of its insertion onto a process (protrusion) of the third phalanx and on the anterior (front) surfaces of the second and third phalanges. Its action is to extend the digit.
Deep flexor tendon--This is an extension of the muscle lying on the back part of the leg and which inserts on the posterior aspect of the third phalanx. It flexes the digit.

Superficial flexor tendon--This structure runs parallel to the deep flexor tendon and splits below the fetlock to insert on both the first and second phalanges. It also flexes the digit, but not the coffin joint (between P2 and P3).

The navicular bursa lies between the deep digital flexor tendon and the navicular bone, changing the direction of the bone and protecting it from damage. This synovial sack is similar to a joint and may communicate with the distal interphalangeal (coffin) joint.

The digital cushion is a wedge-shaped structure with a fibro-fatty composition that sits directly behind the third phalanx and above the sensitive frog. It is very elastic and has very few blood vessels or nerves. When the digital cushion is compressed by the pastern bones and frog with weight bearing, it absorbs shock, cushions the bones, and is divided by the frog's exterior spine so that it is forced outward and obliquely upward against the lateral cartilages. Flat footed horses often have a severely atrophied digital cushion.

The lateral cartilages are part fibrous tissue and part hyaline cartilage. They slope upward and backward from the wings of the coffin bone and reach above the margin of the coronary band.

The blood supply of the foot is extensive. The blood is pumped into the foot by arteries, with valves to prevent retrograde flow during weight bearing. Blood is returned to the heart by extensive venous plexi and veins. The venous plexi are multidirectional and contain no valves, allowing blood to follow the path of least resistance during weight bearing. The veins above the coronet have valves to prevent retrograde flow. Approximately 80-90% of fluid is picked up by the venous return system, leaving the remainder to be drained by the lymphatic system, which requires pumping to move fluids as it lacks this capability. Horses that ‘stock up’ have fluid stasis during stall time from not moving enough to remove the fluid.

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