White Line Disease and Laminitis in a Horse!

Figure 1

 The radiograph in Figure 1 is that of a middle-aged gelding that presented for intermittent foot pain. One year prior, the gelding had developed a high fever of unknown origin (presumed viral). During the weeks that followed the high fever, the gelding was slow to walk in small circle and on concrete surfaces. Over several months, the gelding's lameness improved however he was consistently tender immediately after being trimmed by the farrier.  There are 2 disease processes identifiable in Figure 1. The first is chronic laminitis or founder.

Figure 2

 In Figure 2, the yellow lines correspond to the dorsal hoof wall and the dorsal aspect of the coffin bone. Normally, these lines are parallel to each other such that a horizontal line drawn across them would yield equal angles (angle A and angle B). However, when the coffin bone has "rotated" from its axis then the angles will differ as they do in Figure 2. Hence, the radiographic finding is consistent with laminitis (founder) and subsequent coffin bone rotation. This condition appears to be chronic, evidenced by the "flaring" of the tip of the coffin bone seen in the blue circle in Figure 3. This flaring often corresponds to small fractures of the tip of the coffin bone secondary to increase concussive forces over the toe region of the foot. The red arrow highlights the extremely thin sole which measured less than 5 mm!  Ideally, the sole depth at the tip of the coffin bone should measure between 10-15 mm in thickness.

Figure 3

 The second disease process noted in these radiographs is White Line Disease. This is evidence by the gas lucency traveling up the dorsal hoof wall (yellow arrows in Figure 4). The lateral radiograph is only 2 dimensional hence it is impossible to predict if this gas lucency is right down the middle of the hoof or if it wraps around the medial and lateral aspect of the hoof. Regardless, the gas lucency corresponds to separation of the hoof wall from the underlying tissue. White line disease may be the primary problem or secondary. In this case, it is likely secondary to the chronic founder/laminits however in primary cases, it can cause coffin bone rotation and result in laminitis. This condition results from the accumulation of dead/decaying material that slowly works its way from the sole surface up the hoof wall. The offending organism is believed to be in part anaerobic bacteria that thrive in a low-oxygen environment and produce gas that can be seen on a radiograph. Excessive gas accumulation may result in hoof wall separation from the coffin bone and coffin bone rotation.  Treatment involves aggressive removal (hoof wall resection) of ALL dead and decaying hoof wall to expose the offending organisms. Hoof wall resection along is very effective in treating this condition but it is typically paired with soaking the foot after resection in a variety of solutions to kill off the offending organisms.

Figure 4

Often, the early signs of white line disease can be detected at the time of hoof trimming and appear as a shallow crack at the toe region. The opposite foot of this horse had the very beginnings of white line disease evidenced by a small amount of gas lucency noted at the very tip of the hoof (Figure 5). When identified at this early stage, the condition is easily managed with regular balanced 4-pt trimmings by the farrier. Successful  management of white line disease is best accomplished through a farrier-veterinarian team effort. The farrier is the most important part of the team since they will be doing 99% of the work. The veterinarian will provide the radiographic studies to verify that adequate exposure of the diseased foot is accomplished.

Figure 5

EPM in a Horse

A middle-aged Quarterhorse gelding presented for a history of strange gait and apparent pelvic limb weakness. The clinical signs developed suddenly over 24 hours. The gelding was current on vaccination for West Nile virus, Eastern Equine Encephalitis, and rabies. Neurologic exam noted a gelding in good body condition, alert, responsive yet quite "wobbly" in the hind limbs. Closer examination of all 4 limbs revealed severe weakness in both hind limbs. The degree of weakness was significant enough that the horse was having difficulty remaining standing. Importantly, the hind limb weakness was NOT symmetrical but was more severe in the left hind limb compared to the right hind limb. In the video below, the gelding is bearing most of his weight on the forelimbs and the result is a tendency to spin on the hind limbs due to the severe weakness of the pelvic limbs. 

Based on the neurologic exam, the most likely disease processes affecting this horse include Equine Protozoal Myeloencephalitis (EPM), spinal cord trauma, Eastern Equine Encephalitis (EEE), and West Nile Encephalitis. The sudden or acute onset of clinical signs is most consistent with spinal cord trauma however there was no history of a traumatic event and there were no external signs of such. Equine Protozoal Myeloencephalitis typically does not develop such severe signs over night however such clinical history is possible. The likelihood of either EEE or West Nile virus encephalitis is low in a well vaccinated horse yet not impossible! Diagnosis of encephalitis is dependent on serum testing and confirmation of EPM is dependent on testing of cerebral spinal fluid (CSF). Cerebral spinal fluid can be collected from two location including the atlanto-occipital (AO) joint space and the lumbo-sacral (LS) joint space. It was determined to collect CSF from the LS region. This option was chosen since it would be performed in the standing horse with moderate sedation. Collecting CSF from the AO site typically requires short term anesthesia and the ability of this horse to rise from recumbency was questioned. CSF fluid was collected and submitted for testing. The sample was positive and EPM was confirmed as the disease process in this horse. He is currently being treated with a variety of medications/supplements and the client is committed to treating for 4-6 months.

Read more about EPM @

http://www.aaep.org/health_articles_view.php?id=248

Stifle OCD!!

A yearling thoroughbred presented for sudden lameness and swelling around the stifle joint. The filly had been purchased several months prior from a select thoroughbred sale and repository radiographs were performed at the time of purchase. At the time of purchase, the filly was sound, there was no effusion of the stifle joint and there were no obvious radiographic changes noted in either stifle joint. When the filly presented for lameness, the stifle radiographs were repeated. Close inspection of the lateral trochlear ridge suggested irregular contours (yellow arrows inside blue box, Figure 2) of the trochlear ridge along the mid body region (Figure 1 and 2, blue box). Based on the radiographs alone, the filly was treated with intra-articular Hylartin and forced stall rest for 30 days.

Figure 1

Figure 2

Unfortunately, the filly remained lame after 30 days of stall rest and a follow-up exam included an ultrasound evaluation of the stifle joint. The ultrasound exam revealed significant changes along the lateral trochlear ridge which were not fully appreciated on the radiographic exam. In Figure 3, the lateral and medial trochlear ridge are displayed. The bony surfaces of the trochlear ridges appear as a bright white lines and the cartilage as  thin black lines that follow the contour of the bony surface. Any disruption of the bony surface/cartilage will appear as a mix of disrupted white lines and black pockets. In Figure 3, the image on the left is of the lateral trochlear ridge and there is clearly disrupted bone and cartilage along the bony surface.

Figure 3

In Figure 4, the lateral trochlear ridge is imaged in a longitudinal plane to assess the length of the defect. Irregular bone/cartilage appears to extend for several centimeters along the length of the trochlear ridge (yellow lines). The filly was referred for arthroscopic exam and a large bone/cartilage defect was identified on the lateral trochlear ridge consistent with a osteochondritis dissecans or OCD lesion.

Figure 4

Osteochondritis dissecans is defined as a disorder that results in cracks in the articular cartilage and underlying subchondral bone. The "cracks" and cartilage separation result due to lack of blood flow to the region resulting in avascular necrosis of the tissues involved.  This condition is considered in part a hereditary disorder AND nutritional.  Unfortunately OCD lesions are common in young horses that were bred for sport such as racing thoroughbreds, performance quarter horses, and warm blood breeds.  Some cases of OCD can be managed with surgical intervention however the OCD lesion in this filly's stifle was so large that there was no hope for soundness. This case is a good example of the benefit of multiple imaging modalities in diagnosing the source of lameness in the equine stifle.

Resolved Aspiration Pneumonia

Approximately 2 months ago a young warm blood gelding presented for a 4-6 month history of chronic coughing, bilateral nasal discharge, poly-synovitis, and failure to thrive. At presentation, the gelding was in poor body condition and there was a moderate amount of nasal discharge which consisted of mucus mixed with feed/hay. Auscultation of the thorax noted abnormal lung sounds, bilaterally.  As I reported previously, endoscopic exam revealed feed material within the larynx and trachea (Figure 1 and 2). The feed material was noted through out the entire trachea and a trans-tracheal wash revealed the presence of feed material and bacteria in the cranial ventral lung lobes! The gelding was diagnosed with dysphagia and aspiration pneumonia.

Figure 1

Figure 2

Based on the trans-tracheal culture results the gelding was treated with oral antibiotics for 30 days. In addition, he was treated with systemic anti-inflammatory medication and systemic anti-arthritic medication. Once the antibiotic treatment was started, the coughing episodes subsided but were not completely abolished. The gelding began to gain weight and for the first time was seen laying down to sleep and roll in the pasture! A follow-up endoscopy performed at the end of 30 days of antibiotics revealed feed material within the larynx (Figure 3) and an intermittent dorsal displacement of the soft palate (Figure 4). Mild to moderate ulcerations were noted along the caudal edge of the soft palate when displaced. At this point, we were not sure what was going to happen once we stopped treating with antibiotics however based on the continued presence of feed material in the pharynx, it was assumed that a recurrence of aspiration pneumonia was soon to follow.

Figure 3

After discussing the limited options with the owner, it was decided to pursue acupuncture as a potential source of treatment. Dr. Marilyn Maler was asked to examine the gelding and provide her expert opinion and treatment options. She immediately instituted an acupuncture regiment that was directed at treating the horse's difficulty with swallowing among other points of interest. According to the owner, the gelding's cough improved significantly and in a short period of time was completely absent! The gelding continued to gain weight and has been eating "normally" for over 4 weeks. A follow-up exam was performed 2 days ago and the gelding's condition has improved so dramatically that I did not even recognize the horse!  Endoscopic exam noted NO feed material in the pharynx and normal lung sounds!! The gelding has a long way to go but our conversation has shifted from when might it be time to "do the humane thing" to when might it be time to ride him!!  This case is a strong reminder of the benefits of acupuncture for treating chronic diseases and I wish to extend a special thanks to Dr. Maler for all her help!!

Figure 4

Final note: On the day of the most recent exam, the gelding was feeling so good that he played hard to get. So, he was enticed with several hand fulls of feed just prior to the endoscopic exam. This happens to be a crude method of detecting dysphagia in horses and the gelding passed with flying colors!!

Figure 5