Our internal medicine department is headed by Dr. Rodney Belgrave, a board certified internal medicine specialist. Under Dr. Belgrave's direction, we offer an extensive range of state-of-the-art diagnostic technology to ensure a complete, thorough work up of your horse's condition. Such diagnostics include digital radiography, myelography, upper and lower respiratory tract endoscopy, lower urinary tract endoscopy and gastroscopy and ultrasonography. We specialize in the diagnosis and treatment of a wide variety of conditions, including disorders of the upper respiratory tract, ophthalmological, gastrointestinal, cardiovascular, central nervous and urinary system.
Our facility has a dedicated isolation unit with four stalls that are self-contained with separate ventilation units. Horses are cared for using strict isolation protocols in this separate facility. Thorough surveillance and voluntary quarantine protocols are utilized to minimize the risk of exposure of infectious diseases to other patients.
Your horse's neurologic examination is performed by your veterinarian to determine whether he or she is exhibiting clinical signs consistent with neurologic disease and to determine the origin or location of the lesion accounting for the signs seen. Neurologic abnormalities may be associated with brain involvement, spinal cord involvement, or both. In horses with subtle gait abnormalities, it can be difficult to discern whether the problem is stemming from a neurologic or lameness issue. You need an experienced clinician with the ability to perform a thorough systematic examination to make an accurate diagnosis.
Your horse may be neurologic if it has one or more of the following signs:
- It trips or stumbles intermittently at the walk, trot or while being ridden.
- It stands with its legs abnormally placed. Either its feet too wide apart or too close together.
- It has abnormal toe wear. Its toes may be rounded off from intermittent dragging of the toes.
- It has an exaggerated forelimb gait when walked with its head elevated.
- It has an uneven, spastic gait at the walk or trot.
- It knuckles over in the hind fetlocks when stopped suddenly.
What to Expect
Comprehensive Physical Examination:
- A thorough history will be obtained, including duration of clinical signs, whether there is a history of trauma, and your horse's vaccination history for certain diseases.
- Observation of your horse in its stall. This gives the veterinarian the ability to assess your horse's demeanor. If your horse appears dull and lethargic, it may be an indication of brain involvement. If the neurologic abnormalities are confined to the fore and hind limbs and your horse is bright and alert otherwise, then there may only be spinal cord involvement. The examination may also reveal whether there is abnormal wear of your horse's toes caused by toe-dragging, which is seen with certain neurologic diseases.
- Close evaluation of your horse's body muscling for any muscle wasting or atrophy.
- Assessment of your horse's tail and anal tone will also be assessed to determine if the tail portion of the spinal cord is affected.
- Observation of your horse during urination and defecation.
Evaluation of the cranial nerves: These are 12 nerves that originate from the brain and govern various functions of the head and face, such as the ability to prehend and swallow, the ability to move the facial muscles (blink response, muzzle, ear movement), and the response of the pupils to light. Identification of any cranial nerve abnormalities may aid in localizing which part of the brain is involved. The examination involves close examination of the entire head, including the eyes. Your veterinarian will also assess various reflexes - the most important ones are the menace, palpebral, and pupillary light reflexes.
- To perform the menace reflex, the examiner abruptly moves a hand toward the horse's eye. The appropriate response is to blink the eye, and perhaps move the head away. This helps determine if your horse can see.
- To perform the palpebral reflex, the examiner lightly touches the eyelid, and the horse should close his eye. This helps to determine if the horse has skin sensation, and if he has control of the muscles of the face.
- To perform the pupillary light reflex, the examiner brings the horse into dim lighting, and shines a penlight first into one eye, then the other. The pupils of the eye should constrict. This helps to assess pathways in the brain that control eye function.
Evaluation of the neck: The neck is then examined for any muscle wasting and any signs of neck pain. Neck pain may be evidenced by a pain response upon deep palpation of the vertebrae in the neck. A reluctance or inability of the horse to move its head/neck towards either flank, or to the ground or up in the air may indicate a component of neck pain. An inability to perform these maneuvers may indicate arthritis of the vertebrae of the neck, Wobblers syndrome or neck trauma.
Analysis of gait: The next portion of the exam involves analysis of your horse's gait. The entails observing your horse at the walk and trot, walking up and down an incline, backing up and turning in tight circles. When walking or trotting in a straight line your horse is observed for any stumbling, dragging of its toes (sign of weakness), inconsistent placement of its feet, and outswinging of its legs during the anterior phase of its stride (circumduction). When being circled tightly, your horse is observed for any excessive outswinging of the outer hind limb (circumduction), any pivoting on any of its feet, or any interference of any of its feet. While being circled the tail is also pulled to ascertain any weakness of the hind limbs. To maintain an intact normal gait, the nerve impulses must be able to get from the brain, to the spinal cord, and to the nerves that govern the muscles. If the circuit is interrupted at any point along this line, your horse will likely exhibit gait abnormalities. Abnormal placement of your horse's feet by your veterinarian to determine if your horse will properly replace them should also be performed to determine if your horse has the ability to know where its feet are (proprioception).
Diagnostic Tests: Based upon the clinical exam findings certain tests may be recommended. If compression of the spinal cord in the neck is suspected (cervical vertebral malformation or wobblers) then X-rays of your horse's neck are warranted to look for any fractures, abnormalities with respect to alignment of the vertebrae or evidence of degenerative joint disease or arthritis of the joints (articular facets) of the neck. These X-rays do not allow for visualization of the spinal cord, so if spinal cord compression is suspected then a myelogram will need to be performed to confirm the site of compression.
If a disease such as Equine Protozoal Myeloencephalitis (EPM) is suspected, a standing lumbosacral spinal tap is warranted to obtain spinal fluid for testing. This procedure is performed with your horse standing while mildly sedated. Spinal fluid can then be submitted for testing for EPM. Cytological analysis of the fluid should be performed to evaluate the cell population and protein concentration. The spinal fluid may be grossly abnormal with diseases such as Equine Herpesvirus Myeloencephalopathy.
If fevers accompany the neurologic signs, then bloodwork should also be performed. Fevers may accompany viral diseases such as Eastern Equine Encephalitis (EEE) and West Nile Virus (WNV). Blood can be submitted for determination of viral titers. Blood work is also useful in determining if the neurologic signs are associated with concurrent liver or kidney disease.
Cervical Vertebral Malformation
Cervical Vertebral Malformation (CVM) is a malformation of the vertebrae of the neck region resulting in compression of the spinal cord and stumbling and incoordination. It is also known as Cervical Stenotic Myelopathy (CSM) or Cervical Compressive Myelopathy or "Wobblers" syndrome.
There are two recognized forms:
- Dynamic stenosis: Defined as deformation of the vertebral column with compression of the spinal cord with the neck in flexion or extension. Affected animals are typically younger (6-18 months)
- Static stenosis: Bony and soft tissue impingement into the vertebral canal resulting from degenerative joint disease of the articular facets. Affected animals are typically older (greater than 18 months-3 years).
There has been no clear evidence that CVM is hereditary, however wobbler to wobbler matings have resulted in animals with a propensity for rapid growth. Dietary factors such as high protein and caloric intake may play a role in the development of the disease, by giving rise to osteochondrosis (OCD) of the articular facets and vertebral physes (growth plates). This OCD results in multiple vertebral abnormalities, one of which is a disparity in longitudinal growth of the vertebral body and dorsal lamina. This abnormality allows for subluxation of the vertebra upon flexion and subsequent compression of the spinal cord.
The condition is seen mostly in Thoroughbreds, Standardbreds and Quarter Horses. Males are most commonly affected, and usually are well grown. They may have a previous history of developmental orthopedic disease, such as OCD of other joints and physitis. Many horses may have subtle neurologic disease that goes unnoticed until the horse experiences a traumatic incident such as a fall, which worsens its neurologic status.
Clinical Signs: Common signs include ataxia or incoordination, tripping or stumbling while walking, and weakness characterized by toe dragging, most often in the hind limbs. The forelimbs are usually less severely affected (1 grade less). The horse may adopt a base wide or base narrow stance in an effort to support itself. Reluctance to flex the neck laterally is a common finding. These findings are often seen upon neurologic examination.
Diagnosis: A presumptive diagnosis can sometimes be made by cervical (neck) radiographs or x-rays if narrowing of the vertebral canal is observed. Vertebral canal to body ratios can be measured to support a diagnosis of vertebral canal narrowing. A ratio of less than 52% from the 2nd cervical vertebrae to the 6th cervical vertebrae predicts spinal cord compression with a 95% sensitivity and specificity. Other supportive findings include malformation, degenerative joint disease or OCD of the articular facet joints. A confirmatory diagnosis can be obtained by performing a contrast myelographic study. Confirmation of the affected sites is necessary if surgical decompression is being considered.
Medical Treatment: Younger horses under 1 year of age can be given a restricted diet, referred to as the "Paced Diet." It reduces energy and protein intake and increases trace mineral intake. If still suckling, the foal should be weaned. Free choice grass hay plus an appropriate quantity (according to body weight) of a high nutrient/low caloric supplement should be fed.
Surgical Treatment: Surgical decompression of the cervical spinal cord and fusion of the involved vertebral bodies is performed. A stainless steel basket is implanted with cortical bone to promote fusion of the vertebrae. This realignment and fusion of the affected vertebrae results in relief of the dynamic compression or stenosis. Static stenosis may improve over months as atrophy of the degenerate intervertebral joints occurs. Improvement in neurologic status may be seen in 44-90% of horses with dynamic compression. 12-62% of horses may return to previous athletic function. Generally there is a 60% chance that the affected horse will improve at least 1 neurologic grade. That being said, the neurologic grade at presentation should be taken into consideration when formulating a prognosis for return to athletic function.
To determine whether your horse may need a neurologic examination and what it entails click here.
To learn more about a myelogram and what it entails click here.
EHV 1 Fact Sheet
In recent years there has been an increasing incidence of outbreaks throughout North America of Equine Herpes Myelitis (EHM) caused by Equine Herpesvirus 1(EHV 1). Why are we seeing this disease with increased frequency, we don't really know. What we do know is that it's a virus that been around for decades. The effects of EHV-1 on the equine population are 3 fold. It has the ability to cause mild respiratory disease and fever, abortion, typically in the 3rd trimester, neonatal foal death, and outbreaks of neurologic disease or EHM.
EHV's 1&4 are what we refer to as alpha herpesviruses. One of the key features of these alpha herpesviruses is latency and reactivation. Once infected the virus has the ability to reside in the lymphoreticular system and trigeminal nerve, and in times of stress the dormant virus can become re-activated (stress of transport, weaning, handling, experimental induction with corticosteroids) leading to virus shedding and transmission. The frequency of reactivation is generally unknown, but what we do know is that these horses are general asymptomatic.
With respect to latency, this is actually established during the first weeks to months of life. It is thought that viral reactivation in in latently infected mares leads to the foal becoming infected at this stage. The prevalence of latency in the equine population ranges from 60-88% based on necropsy studies where testing for the virus has been performed in bronchial and retropharyngeal lymph nodes. So it's safe to assume that the majority of horses are latently affected with EHV 1. Given the high prevalence of latency, and the size of the equine population outbreaks of EHM are still considered rare.
The best analogy is to compare EHV 1 with the Human Herpes Simplex 1 virus, where 67% of people around the world under the age of 50 are affected with the virus. Like EHV 1 this virus also establishes itself during childhood and the infection is life long. Stressors in life may also precipitate the development of disease.
Back to EHV 1. There are two strains of the virus, the D 752 strain referred to as the neurolologic or neuropathic strain. This strain is more commonly isolated from horse with EHM (85%) than the N752 strain or non neuropathic strain. Now the nomenclature can be somewhat confusing, since the non neurologic strain can account for a minority of neurologic outbreaks (15-25%). The Non neurologic starin is however responsible for 95% of the abortion outbreaks. With respect to latency, the good news is that approximately only 5-20% of the equine population is latently affected with this strain. So latency likely plays a significant role in these outbreaks, with the source being either a latently infected horse with the D variant becoming re-activated or spontaneous mutation from the N variant to the D variant.
Risk / protective Factors
- The presence of an infected/shedding horse in the herd along with other susceptible horses in the herd. Data suggests that older horses >5yrs are at an increased risk of developing EHM. May be related to the immunological status of older horses.
- Season: The majority of EHM outbreaks occur in late autumn, winter and spring.
- Introduction of horses into a herd is a commonly reported before the development of EHM outbreaks.
- Breed and sex: In one epidemiological survey, ponies and smaller breeds were les likely affected and females more commonly affected.
- Stressors: Weaning, Commingling, transportation and concurrent infections
Treatment with anti-viral drugs may decrease the chance of developing EHM in horses with a high risk of exposure. IV acyclovir or gangciclovir are preferable, followed by oral acyclovir.
Immunity: Past exposure produces a limited period of immunity which may last only 3-6 months.
Vaccination: EHM has been observed in horse vaccinated against EHV 1 at 3-4 month intervals. No evidence that the vaccines that are currently available have the ability to prevent naturally occurring cases of EHM. The current goal with vaccination against EHV 1 is to stimulate the immune response with the hope of reducing or eliminating the viremia that develops with infection.
Incubation period: 2-8 days. Once a fever occurs, neurologic signs may develop within the next week.
Shedding: Shedding in horses with EHM may occur for as long as 28 days. The virus does not survive outside of the host for very long in the environment. Dies within hours on a smooth dry surface and if exposed to sunlight. Same goes for clothing and dry hands. Can be easily killed by washing hands and using hand sanitizer.
Transmission: Direct contact or fomites most common mode. Coughing is not a common feature of EHM, so aerosol transmission is not a common feature of the disease.
Mules, donkeys and zebras can be infected with EHV1 and can shed the virus, as well as develop neurologic disease.
Recurrence of disease: There have been no confirmed cases of recurrence of disease in horses that have been previously affected with EHM
Infectious Respiratory Disease (IURD)
This clinical syndrome refers to infectious diseases that affect the upper respiratory tract of the horse. The upper respiratory tract encompasses from the nasal passages to the larynx. This syndrome occurs worldwide, is generally contagious and can be caused by several viruses and bacteria, such as equine influenza virus, equine herpesviruses, equine adenovirus virus, equine rhinitis viruses and the bacteria Streptococcus equi subspecies equi.
Horses with IURD generally develop a fever, cough, and nasal discharge. They also may demonstrate lethargy, reduced feed intake, and enlarged lymph nodes of the head and neck.
Strangles is a specific type of IURD caused by the bacterium Streptococcus equi subspecies equi. It is the most common infectious disease affecting the upper respiratory tract, and is characterized most often by purulent nasal discharge, and swelling of the lymph nodes of the head and neck. These lymph nodes may rupture and drain pus. Infected horses also may develop other signs such as fever and breathing and eating difficulties.
Infectious Lower Respiratory Tract Disease
This refers to infectious diseases that affect the lungs and thoracic cavity. Horses with this syndrome are referred to as having pneumonia, and typically exhibit fever, cough, nasal discharge and an increased respiratory rate. Their respiratory effort may be increased and characterized by nostril flare and increased abdominal effort. The primary cause of pneumonia is bacterial, however pneumonia can also be caused by viral and fungal infections of the lower respiratory tract. At the Mid-Atlantic Equine Medical Center a large number of horses are treated for pneumonia annually.
Pleuropneumonia is a severe form of pneumonia most often seen in racehorses. Upper respiratory tract viral infections, as well as stressful events such as long distance transportation and racing may all contribute to development of disease. General anesthesia, immunosuppressive therapy, and poor nutritional status may also lead to compromise of the respiratory defense mechanisms. These stressful events may alter your horse's respiratory defense mechanisms. Bacterial pleuropneumonia as a result of esophageal obstruction from the aspiration of feed material is also seen in other breeds.
Clinical signs vary with the stage of the disease. Symptoms include a cough or nasal discharge, exercise intolerance, and some degree of respiratory effort as evidenced by nostril flaring or an abdominal component to expiration. Acutely, most horses are febrile, anorectic, and or lethargic. Your horse may exhibit a reluctance to move, abducted elbows or stiff forelimb gait, and may be mistaken for laminitis or exertional rhabomyolysis. Rapid weight loss may occur in chronically affected horses. The development of sternal and distal limb edema may be present in advanced cases.
Diagnosis of the condition is based upon historical information gathered, in addition to clinical and diagnostic findings. Our veterinarians perform the following:
- Thoracic auscultation
- Blood work
- Thoracic ultrasound
- Endoscopic examination
- Cytological analysis
- Aerobic and anaerobic bacterial culture
Treatment for bacterial pleuropneumonia includes broad-spectrum intravenous and oral antibiotic therapy; drainage of fluid from the lungs to allow for re-expansion; and bronchial irrigation. For chronically affected patients, we also recommend thoracotomy and rib resection surgery.
Non-Infectious Respiratory Disease
This refers to diseases of the lung that are inflammatory in nature. Horses with this condition typically exhibit an increased respiratory rate and effort. A cough or nasal discharge may also be observed. Inflammatory conditions typically do not elicit a fever, so the presence of a fever is a reliable way to distinguish between a condition that is infectious as opposed to inflammatory. An individual may have an inflammatory disease without an infectious component, however most infectious diseases are usually accompanied by an inflammatory component.
Heaves, formerly referred to as COPD, is the most common inflammatory disease that affects the lower respiratory tract of horses. It is precipitated by exposure to dusts and allergens in the horse's environment, which in turn cause inflammation of the lower or small airways. Inflammation may then lead to mucus production and/or constriction of the small airways leading to respiratory compromise. Of the many respiratory ailments that horses present to the Mid Atlantic Equine Medical Center for evaluation of, heaves is the most frequently diagnosed disorder.
Infectious Gastrointestinal Disease
This syndrome can be caused by a variety of infectious agents that typically inflict damage to the large intestine (colon and cecum). Infection and inflammation of the large intestine is referred to as colitis, and may be associated with infectious agents such as Salmonella, Clostridium difficile, Clostridium perfringens, Neorickettsia risticii (Potomac Horse Fever) and Coronavirus. The infection and inflammation may cause diarrhea, fever and inappetance. The endotoxins that are released from dying gram negative bacteria in the affected colon, put these patients at an increased risk of developing laminitis.
Non-Infectious Gastrointestinal Disease
These conditions are inflammatory in nature and may give rise to diarrhea, weight loss and inappetance. There may be an accompanying fever. These inflammatory bowel diseases may be associated with inflammation with no specific cause or cancer of the intestinal tract such as lymphoma or adenocarcinoma.
Liver stones, also known as choleliths or hepatoliths, occur infrequently in horses. The stones are composed of calcium and bilirubin, which is a breakdown product of hemoglobin derived from red blood cells. Middle-aged horses are most commonly affected, and clinical signs often include icterus or jaundice, abdominal pain, weight loss and poor appetite. The presence of theses stones can give rise to secondary bacterial infections of the liver, leading to fevers in some cases. Advanced cases may lead to liver failure and neurologic signs, as the levels of ammonia in the blood accumulate.
Diagnosis is confirmed by ultrasonographic imaging of the liver in conjunction with clinical signs and changes on the bloodwork consistent with liver disease. Liver biopsies may also aid in diagnosis of the condition.
Due to the difficulty in removing these stones via surgery, the prognosis for severe cases involving obstruction of the common bile duct is unfortunately poor. Less severe cases may respond to fluid, and long-term antibiotic and anti-inflammatory therapy.
Gastric ulceration refers to defects in the mucosal (inner) lining of the stomach that extend into your horse's underlying muscular layer. In contrast, gastric erosions do not extend into the muscular layer. Ulceration occurs when there is an imbalance of digestive factors such as hydrochloric acid and protective factors such as mucus, protective prostaglandins and blood flow to the mucosal lining.
Studies show up to 70-90% of sport horses will have some degree of gastric ulceration when evaluated endoscopically. However it is important to note that not all of these horses will demonstrate signs consistent with gastric ulceration.
Few specific causes of gastric ulceration in horses have been clearly identified. There has been an association with stressors and ulceration in foals, intense training, and low volume roughage feeding. There has been no definitive link between bacterial infection with H. pylori and gastric ulceration as is the case with people. Horses, unlike people, are continuous secretors of gastric acid. This is in line with their natural lifestyle as continuous grazers. If there is not a constant volume of roughage in the stomach to buffer the continuously secreted acid, ulceration will develop. Administration of certain drugs such as phenylbutazone and banamine has been shown to induce gastric ulceration in horses. They do so by inhibiting the production of protective factors such as prostaglandin E2.
Anatomy of Your Horse's Stomach
Horses have small stomachs relative to their body size. The average horse's stomach can only hold approximately 4 gallons. This is in line with their eating habits in the wild - consuming frequent small meals, so their stomachs are never stretched to full capacity. The inner lining of your horse's stomach is made up of two parts separated by the margo plicatus. The primary difference between these two parts is the types of cells lining them: the squamous mucosal epithelium and the glandular mucosal epithelium.
The glandular epithelium contains many glands that produce gastric secretions. There, feed material is mixed with hydrochloric acid and pepsin to begin the digestive process. This glandular portion of the stomach also secretes a mucus-bicarbonate layer that helps protect its lining.
The squamous epithelium contains no glands, and merely serves to contain food, without aiding in any chemical digestion. However, the secretions that protect the glandular epithelium lining have no protective effect on the squamous epithelium lining, putting it at greater risk from increased acid production.
When should I suspect that my horse has ulcers?
Symptoms associated with gastric ulceration in adult horses may include recurrent or acute low-grade colic especially after eating. A decreased appetite for grain is also common. Greater amounts of acid are released when a horse eats grain. As a result, horses with gastric ulceration may learn to associate the consumption of grain with the pain associated with release of acid onto an ulcerated stomach. Decreased manure production, poor body condition, poor haircoat, poor performance and a change in the horse's normal attitude may also be seen.
How is a Diagnosis of Gastric Ulceration made?
The only way to definitively diagnose gastric ulceration is to have a gastroscopic examination performed. The exam is performed under sedation and takes approximately 15-20 minutes. Your horse will need to fast for 10-12 hours prior to the procedure. Gastroscopic examination in the hands of an experienced clinician will allow for a thorough evaluation of the entire stomach, including both the squamous non-glandular layer and glandular layers. The exit portal of the stomach, called the pylorus, should also be evaluated for any abnormalities of function or structure. Finally, the stomach should be exited, and the portion of small intestine, the duodenum, coming off the stomach evaluated for ulceration. Duodenal ulceration is seen most often in foals and weanlings.
Treatment of Gastric Ulceration
Treatment of gastric ulceration generally involves the use of medications that suppress gastric acid production. Gastrogard® or Ulcergard® are proton pump inhibitors, while drugs such as ranitidine (Zantac®) and cimetidine (Tagamet®) are histamine receptor antagonists. Both classes of drug work well to treat existing ulcers. Choice often comes down to practicality, as Gastrogard is administered once daily while ranitidine and cimetidine require three times a day administration. A 30-day course of treatment with either class of drug is recommended.
Sucralfate (Carafate) is a different class of drug used in the treatment of gastric ulceration. It is most effective in treating ulcers of the glandular mucosa. Sucralfate acts locally in an acidic environment (pH < 4), reacting with stomach acid to form a thick paste-like material capable of acting as an acid buffer as long as 6 to 8 hours. It also attaches to proteins on the surface of ulcers to form complexes that serve as protective barriers at the ulcer surface, preventing further damage from acids and bile. It has been shown that sucralfate also stimulates the increase of gastroprotective factors such as prostaglandin E2, epidermal growth factors (EGF), and gastric mucus. A 30 day course of treatment with sucralfate is also recommended for glandular ulcers.
A repeat gastroscopic exam should be performed towards the end of the treatment to determine if the ulcers have fully healed or whether treatment should be continued. Some horses may need to be maintained on preventative ulcer therapy once the active ulcers are fully healed.
Prevention of Gastric Ulceration
Administration of either proton pump inhibitors or histamine receptor antagonists can be used for the prevention of ulceration, once any ulceration has been effectively treated. Diets rich in calcium such as alfalfa hay have been shown to be effective in the prevention of gastric ulceration. Environmental management is also critical. Frequent small meals, free access to unlimited amounts of roughage, and ample turn-out time are also critical to the well-being of the horse's stomach.
The effects of different cardiovascular diseases on the athletic performance of horses are difficult to quantify. Valvular heart disease is the most common cardiac disorder seen in horses admitted to the Mid-Atlantic Equine Medical Center, however these conditions do not impact athletic performance as was once generally thought. Heart arrhythmias more commonly affect performance, however may not be detected without the aid of 24 hour heart monitoring or exercise ECGs (electrocardiogram). Echocardiography or ultrasonography of the heart allows an accurate estimate of the significance of valvular disease in horses. Many of these horses present with a history of poor performance or exercise intolerance.
Evaluation of Urinary System
The urinary system is comprised of the upper (kidneys and ureters) and lower urinary tracts (bladder and urethra). The kidneys' most important function is to filter waste from the blood. When this does not happen properly, waste products can build to dangerous levels in the blood, giving rise to azotemia. Evaluation of horses with kidney disease is performed via ultrasonography of these organs.
Evaluation of the bladder and urethra for the presence of stones (uroliths) or calculi is performed via endoscopic examination (cystoscopy). Uroliths are formed when minerals that naturally occur in urine clump together to form tiny crystals. These stones can develop anywhere in the urinary tract, including the kidneys, ureters, bladder, or urethra. The formation of uroliths is seen most frequently in adults. There is no one breed that is more prone to urolithiasis than another; however, it is seen more frequently in males than females.
Ocular disorders are particularly common in horses. What may appear to be a slightly swollen eye can quickly become a serious problem. The Mid-Atlantic Equine Medical Center offers extensive services to care for your horse's eyes and treat vision-related problems.
For simple conditions, such as superficial corneal ulcers, we thoroughly examine the eye on an outpatient basis. More serious conditions, such as deep ulcers or uveitis, may require hospitalization for treatments, or placement of a sub-palpebral lavage system for more aggressive therapies.
Complex conditions are evaluated by our board-certified specialist in veterinary ophthalmology who conducts clinics at the hospital twice a month.