EquineSite.com

Ella Pittman, DVM  www.newenglandequine.com

Abstract

Laminitis, commonly called founder (founder is when actual rotation occurs due to the inflammation), is inflammation of the lamina. But to understand what that definition means for you and your horse, it’s important to appreciate hoof anatomy. The wedge-shaped bone that sits within the hoof, called the coffin bone, is suspended from the hoof wall by finger-like projections known as the laminae. Inflammation and disruption of blood flow to the hooves damage the laminae, causing the bonds between the finger-like projections to break down. As a result, the coffin bones loses its attachment to the hoof wall, enabling the bone and the wall to separate. In chronic cases, this separation allows the coffin bone to “sink” or “rotate” therefore affecting the structures within the foot.

Clinical Signs

Laminitis can affect all four feet but most commonly is seen in the forelimbs. Laminitic horses may stand in a sawhorse posture to alleviate pressure on their feet or lie down more frequently to avoid bearing any weight. They most often are lame on tight circles, walk with a stilted gait or be reluctant to lift up their feet when asked. Often, the hooves are warm and bounding digital pulses are present. Digital pulses are the pulses that can be felt along the sides of the sesamoid bones on palpation.

Diagnosis

Diagnosis is usually based on x-rays where measurements are taken to determine whether the coffin bone has rotated or sunk within the foot. You can also determine if there is increased gas opacity along the laminar line indicating active inflammation present. Unfortunately, changes on x-rays lag behind what is actually going on in the foot and damage can occur without evidence of rotation or sinking. Therefore, treatment is usually initiated as soon as laminitis is suspected.

Etiology

Often, the inflammation and disruption of blood flow to the feet result from a problem elsewhere in the horse’s body. Several causes of laminitis include excess grain or lush green grass, severe fever or illness such as colic or Potomac Horse Fever, retained placenta after foaling, endocrine conditions such as Cushing’s or Equine Metabolic Syndrome, or excessive weight-bearing on one limb (contralateral limb laminitis). The exact link between these conditions and laminar damage is still unknown. It is generally agreed upon that the laminar damage results from decreased blood flow to the feet. But how does a disease in one part of the body cause decreased blood flow in another?
One thought is called the circulation theory. This states that inflammation in another part of the body causes constriction of the blood vessels in the foot, decreasing blood flow in the smallest blood vessels in the lamina. As a result, the cells making up the lamina die. The finger-like projections disintegrate as the cells die and nothing is left to suspend the coffin bone. In addition, because the smallest vessels are constricted, blood is rerouted through the larger vessels, which produces the bounding digital pulses seen in acute laminitis. Another theory focuses on primary destruction of the lamina. One of the ways the body repairs itself is by producing enzymes called matrix metalloproteinases (MMPs). MMPs are involved in breaking down tissue at the molecular level to promote the growth of new tissue. In the normal environment, tissue repair is a delicate balance between breakdown by MMPs and restoration by other enzymes and cells. In this theory, severe systemic inflammation causes excessive release of MMPs, which in turn destroy cellular components of the lamina and enables the coffin bone to shift.

Treatment

Despite disagreement about the exact mechanism of laminitis, treatment is generally the same regardless of cause. If laminitis is a consequence of a systemic disease, first and foremost is to treat the disease. Restriction of grains and lush hay, corrective shoeing, anti-inflammatory medications such as phenylbutazone (Bute), banamine or equioxx, soft bedding, and keeping the feet cool with ice baths or ice boots are mainstays of treatment. More debated therapies include the use of vasodilators such as acepromazine or isoxsuprine and rheological agents such as pentoxyfylline to improve blood flow to the feet. Rheological agents cause the membrane of red blood cells to be more flexible, reportedly enabling them to better sneak through the constricted capillaries.

Prognosis

Prognosis depends on cause, whether the laminitis is acute or chronic, severity of rotation or sinking of the coffin bone, and how quickly steps are taken to reduce the continued destruction of the lamina. Managing a laminitic horse will require good communication between you, your veterinarian, and your farrier. If you suspect your horse is developing laminitis, it is important to contact your veterinarian as soon as possible.

References
Parks, A. H. (2016). Horse Health. Retrieved from American Association of Equine Practioners : https://aaep.org/horsehealth/laminitis
Pollitt, C. C. (2018). Horse Health . Retrieved from American Association of Equine Practitioners: https://aaep.org/horsehealth/equine-laminitis-update-its-causes#
Reed, S. M., Bayly, W. M., & Sellon, D. C. (2010). Equine Internal Medicine . Saunders Elsevier .

Equine odontoclastic tooth resorption and hypercementosis, or “EOTRH”, is a painful disease of the incisor teeth most often seen in older horses. The disease begins by the body resorbing the bone and soft tissue around the roots of the incisors (and sometimes the canines). This resorption leads to spacing between the gum line and tooth, allowing food and debris to become trapped which leads to infection within the gum pockets. Infections here can destroy parts of the tooth root and soft tissue structures, which hold the teeth in place. This underlying infection and increased inflammation of the gum leads to the proliferation of the tooth cementum (or enamel) along the gum line in attempts to stabilize the tooth. Unfortunately, once this process has started it only progresses, leading to the teeth falling out or fracturing, and continues to be painful for the horse. 

This disease is typically seen in older horses over the age of 15 years old. EOTRH is believed to have some risk factors such as horses that chew less often (not able to have constant grazing access) and horses that concurrently suffer from Endocrine diseases such as Equine Metabolic Syndrome or Cushing’s disease. This is due to a decreased immune system and higher concentration of circulating Insulin and ACTH. 

Clinic signs of this disease are often hard to detect in the early stages due to the low-grade level of pain compared to when the disease is advanced. Some early signs of incisor discomfort are the unwillingness to grab hard treats with their front teeth. These horses may also try to use their lips for grasping food or grazing to help avoid contact with the incisors. A “smiling” face (when a horse lifts if upper lip at work and rest) can be a common sign in EOTRH as well to try and help alleviate pressure on the teeth. In more advanced disease, head shaking, unwillingness to take a bit and weight loss due to decreased eating can be seen due to the level of pain these horses are experiencing. 

The inflamed gums and the hypercemetosis along the gum line can be seen surrounding the infected incisors as EOTRH progresses. These teeth may also become loose and sensitive to oral examination. These signs along with a complete dental exam and possible dental radiographs are the definitive way to diagnose EOTRH. Unfortunately, this disease is not reversible and once there is radiographic evidence or changes to the integrity of the teeth, there is not much that can be done to slow the process. 

The recommendation for advanced EOTRH is to have the affected incisors removed. Removing the diseased incisors allows for pain relief and it may also help prevent the disease from affecting the neighboring teeth if removed soon enough. These horses that lack incisors can cope extremely well with only a diet change to help manage them after surgery. After surgery, soaked grain meals followed by either hay stretcher pellets or a complete pelleted feed are recommended to ensure a rationed diet is available. Most of these horses learn to use their lips and tongue to help grasp grass and hay while grazing. Some even, can also go back to being ridden though their tongue often sticks out through their gums. It has shown however, that horses with advanced  EOTRH who have their incisors removed live a happier good quality life. 

A good way to help identify the clinical signs early in EOTRH is by having your horse receive regular, yearly dental examinations by your veterinarian. Regular dental maintenance can help not only keep your horses mouth comfortable but also help monitor for any signs of disease presence progression.

Equine Dental Pathology: Dixon, Toit, Dacre

Getting to Know EOTRH: Norton            

Dr. Taylor Mahren
New England Equine Medical and Surgical Center
15 members way
Dover NH 03820
603-749-9111

OSTEOCHONDROSIS:

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Osteochondrosis (OC) is a developmental disorder that leads to failure of bone and cartilage formation (endochondral ossification). Failure of normal bone and cartilage formation results in irregularities in the thickness of cartilage at joint surfaces. This creates areas of weakness and affects the nutrition of the deeper layers of  cartilage and bone and can lead to necrosis (decay). Biomechanical influences, mainly shearing forces, lead to the formation of fissures (tiny fractures) and produce cartilage flaps, or detachment of cartilage or fragments of cartilage and bone. 

DIAGNOSIS:

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The typical OC patient is a yearling with effusion (swelling) of the upper hock joint or stifle joint.  The horse is typically not lame, and radiographs reveal a fragment on part of the tibia called the distal intermediate ridge of the tibia or irregularities of the femur at what is called the lateral trochlear ridge. However, there are many variations on this scenario and age, lameness, effusion, and the joint affected can vary. Most OC patients are juvenile with the most severe cases being seen in foals as young as 6 months of age. OC can also only manifest itself when the horse is put into training and the joint becomes challenged by activity which varies with discipline. Radiography is the gold standard for diagnosing OC but it is not capable of detecting subtle lesions. 

DISTRIBUTION OF LESIONS:

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OC is most commonly diagnosed in the tarsus (hock), femoropatellar joint (stifle), and the fetlock, but it has been described in almost every synovial joint.     

CAUSE OF THE DISORDER (PATHOGENESIS):

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OC is a complex disease and multiple factors are involved in the progression and development of the disorder. Biomechanical influences, exercise, failure of vascularization, nutrition imbalances, and genetics have all been linked to the disease. 

TREATMENT:

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Treatment of lesions depends on size, clinical signs, location, and severity. Small OC lesions in very young horses where there is still good capacity for regeneration or in very mild OC cases,  nonsurgical management consisting of  rest, controlled exercise, systemic anti-inflammatories, and intra-articular (within the joint) medications can be successful. Surgical management is the treatment of choice in most cases.  This involves removal and debridement of the fragments from the joint via a small incision and use of an arthroscope (surgical instrument with camera). 

PROGNOSIS:

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The prognosis after surgical intervention varies among joints and the severity of the lesion. However, prognosis for return to athletic activity is fair to good for the majority of joints involved. 

TAKE HOME:

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Things to consider when trying to prevent osteochondrosis would be to avoid feeding high energy feeds to growing animals which can lead to excessive rapid growth and secondary osteochondrosis development. Breeders should monitor sires and mares suspect of yielding offspring with osteochondrosis. Any young horse with persistent joint effusion should be evaluated with radiography. Horses with OCD that are identified and treated early may be athletic; however , if left unrecognized osteoarthritis (degenerative joint changes) and lameness can develop. 

SUBCHONDRAL BONE CYSTS:

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Subchondral bone cysts, also known as subchondral cystic lesions (SCLs), are a serious cause of lameness and difficult to treat. They are characterized by radiolucent (darker than normal) areas of bone often accompanied by sclerosis (boney remodeling) at a joint surface. In the past, they were considered to be part of the osteochondrosis complex, however, the location of OC lesions differs from SCLs. SCLs are found underneath the cartilage in a weight-bearing area of the joint. 

CAUSE OF THE DISORDER (PATHOGENESIS):

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Many mechanisms have been proposed for the development of SCLs. However, only two hypotheses have been supported experimentally. The first hypothesis is based on the hydraulic theory in which there is primary cartilage damage followed by secondary intrusion of synovial fluid. The fluid is thought to place mechanical pressure on the subchondral bone through its hydraulic action during weight bearing, resulting in necrosis of the subchondral bone plate. The second hypothesis is the inflammatory theory in which various inflammatory mediators become upregulated (increased) leading to the development of cysts. 

DISTRIBUTION OF LESIONS:

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SCLs occur mainly in the stifle (medial femoral condyle) and the phalanges (fetlock, pastern, coffin bone, and navicular bone) and less commonly in the carpus (knee), cannon bones,  tibia, radius, talus (hock), proximal sesamoid bones, humerus, patella, scapula, and mandible. 62 % of lesions occur in males and Thoroughbreds represent the majority of affected animals. 

CLINICAL SIGNS:

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Horses often present with lameness in the affected limb with or without joint effusion (swelling). SCLs occur mostly in young horses between the ages of 1 and three years and lameness commonly occurs at the onset of training. 

DIAGNOSIS:

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Diagnosis is made via lameness examinations and radiographs. In rare cases, computed tomography, CT, has been of great value when SCLs cannot be visualized radiographically. 

MANAGEMENT:

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Nonsurgical management of SCLs involves rest and the use of non-steroidal anti-inflammatory drugs; however, success rate is variable. Intralesional corticosteroid injections do have better success rates but this is generally performed under arthroscopic guidance under general anesthesia. Surgical management is the treatment of choice and involves debridement of the cyst and a combination of intralesional corticosteroid injection, bone grafts, and other modalities. 

PROGNOSIS:

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The healing of treated SCL normally is slow and can take several months to years if just surgical debridement is used, but the use of bone replacements and growth factors to enhance bone healing shortens the healing time considerably. Younger horses have a better prognosis for complete recovery compared to older horses. If the SCLs are associated with osteoarthritis in older patients a cautious prognosis is given. 

REFERENCES:

1.) Auer and Stick. Equine Surgery, 4th edition. Chapters 88 and 89. 

Katy Raynor, DVM

www.newenglandequine.com

Equine injuries can be just as common whether your horse is stalled or turned out to pasture. The best way to treat any injury, however, is to be prepared with a well-stocked, easily accessible first aid kit. In fact, keeping even a few of the below first aid essentials could help save a severely injured horse's life while you wait for your veterinarian to arrive. 

Vital first aid supplies

Every horse owner needs a few basic first aid essentials. These items will help you dress wounds, reduce swelling and inflammation until your veterinarian arrives. Depending on your preference, pre-made first aid kits are available at our clinic. Or, you can make your own kit with the following items: 

• Bandages - protect wounds, support muscles, and hold ice packs with horse leg wraps or self-adhesive bandages.
• Blunt-Tipped Scissors - safely cut away and remove bandages and wraps.
• Buckets - soak hooves and more with a few buckets kept specifically for first aid use.
• Flashlight/Head lamp - view wounds and injuries in darkness or poor light conditions.
• Hoof Pick
• Ice Packs - prevent and reduce swelling.
• Rubbing Alcohol - used as a disinfectant as well as good for cooling horses rapidly if febrile.
• Sheet or Roll Cotton - help apply pressure bandages or offer support to injured muscles or bones.
• Sterile Gauze - clean and cover minor cuts and wounds with sterile gauze or Telfa (non-stick) pads of various sizes. Use gauze rolls to hold dressings and pressure wraps in place.
• Exam Gloves- keep your hands clean and help prevent wound contamination.
• Thermometer - measure your horse's temperature (normal range is 99.0°F to 101.5°F) whenever you have a concern before you call the vet. EVERY FARM SHOULD HAVE ATLEAST 1 WORKING THERMOMETER!
• Stethoscope- Know how to take your horses heart rate! Great information to help your vet!
• Wound Antiseptic
• Wound Cleaner

Easy access to your veterinarian's and farrier's contact information is also vital. In addition, a complete record of all your horse's medications, vaccinations, and wormers is essential - especially in an emergency. 

Helpful first aid extras

The best first aid kit holds a range of products to deal with a wide variety of injuries or accidents. In addition to the basics, however, having the following products accessible will help you further prepare for almost any mishap: 

• Electrolytes
• Probiotics- (good quality)
• Eye Cleanser/Saline
• Hoof Boot
• nSAIDS (phenylbutazone, banamine, Equioxx) - Only used after consulting a veterinarian Always take temperature before administration.
• Poultice
• Trailering and Barn additional tip!

Always have a fire extinguisher available in your barn and trailer/truck at all times!

by Dr. Kathy Samley

New England Equine Medical & Surgical Center

What is Equine Cushing’s Disease?

Have you ever noticed a horse with a long curly hair that does not shed out in spring? This may be an early sign of Equine Cushing’s Disease. Pituitary pars intermedia dysfunction, often referred to as Equine Cushing’s Disease, is a common disorder in older horses and ponies. Research shows that it can occur in up to 25% of aged horses. The typical age of a horse diagnosed with PPID is 18-23 years. Early diagnosis is often difficult, but can lead to a better prognosis for treatment. The most common, and often earliest, clinical sign is an abnormal haircoat that does not shed out in the spring. 

What causes Equine Cushing's Disease?

This endocrine disease begins with a deficiency of dopamine within the brain. This deficiency is caused by degenertion of dopamine-producing neurons in the brain and is similar to the disease process that occurs in human Parkinson’s disease. In normal horses, dopamine acts to inhibit the pars intermedia of the pituitary gland. Without dopaminine's inhibitory effect, the pituitary gland englarges and begins producing an overabundance of hormones. These hormones affect many different body systems, including causing the adrenal gland to overproduce its own hormone: cortisol. PPID is slowly progressive, and may occur in up to 25% of aged horses. 

Common clinical signs

Besides an abnormal haircoat, other common clinical signs of PPID include weight loss and/or muscle wasting, abnormal distribution of body fat, lethargy and hyperhidrosis (excessive sweating). The excessive production of cortisol can often lead to chronic laminitis. Depending on the progression of the disease, the laminitis can become severe and life-threatening. Chronic laminitis often appears externally as divergent rings in the hoof capsule. Since cortisol is immunosuppressive, horses with PPID are more prone to chronic or recurrent infections. If you notice any of these clinical signs, you may consider getting your horse tested for PPID. 

Testing

There are several different tests that can be performed to diagnose PPID. All of these tests involve drawing at least one blood sample from the horse and measuring the levels of various hormones in the bloodstream. The two most commonly used tests are baseline ACTH and the TRH stimulation test. All horses with suspected Cushing’s disease should have their insulin levels evaluated as well because insulin resistance is commonly associated with PPID.  

Treatment

The drug pergolide (Prascend) is the treatment of choice for PPID. This drug works by mimicking the action of dopamine in the brain, which inhibits the pituitary gland and prevents the overproduction of pituitary hormones. In addition to pergolide treatment, proper management and nutrition is important for treating horses with PPID. Since PPID horses are at risk for developing insulin resistance, they should be fed a diet that is low in soluble carbohydrates. This can include a complete feed, such as a senior feed, that is high in fiber but low in starch. Grazing should be limited due to the high carbohydrate content of lush pasture. PPID horses should have dentals performed twice a year, and should have regular fecal floats performed in order to develop an appropriate deworming program. Proper trimming/shoeing is vital for managing horses with chronic laminitis due to PPID.  

Prognosis

With pergolide treatment and proper management, horses with PPID can live many years with a good quality of life. Pergolide is a life-long treatment for affected horses, and often the dose will need to be increased in order to continue controlling the signs of the disease. Early diagnosis and treatment can improve the prognosis. Good management practices are equally as important as pergolide in maintaining a good quality of life for horses with PPID.