High Ring Bone!!

The radiographic image below is of the right hind pastern of a 4 year old mare that presented for a prepurchase exam. The mare had only been under saddle for 6 months. During the active exam, the mare cross-cantered when lunged to the left. In addition, the pastern area was "thicker" when compared to the opposite hind limb and the mare was moderately positive to flexion of the limb in question. Due to the suspicion of a significant problem, the right hind pastern was radiographed. The yellow arrows highlight new bone growth along the edges of the pastern joint. The bone growth or osteophytes are large and proliferative. These findings are indicative of advanced osteo-arthritis of the pastern joint otherwise known as "high ring bone". 

Figure 1

In Figure 2, the same osteophytes are noted as the course around the front of the pastern joint. The yellow arrows point to the osteophytes or irregular "white" structures along the edge of the pastern joint. 

Figure 2

Figure 3 and 4 are radiographs of a normal pastern joint. There are no osteophytes noted along the margins of the pastern joint. Notice in Figure 4 the smooth, curved border of the normal pastern joint. Interestingly, the pastern imaged in Figures 3 and 4 was radiographed because it palpated "thicker" than the opposite limb. Fortunately, there was no evidence of pastern arthritis. 

Figure 3

Figure 4

 In Figure 5 there is significant new bone growth or osteophyte development along the margins of the coffin joint. This is known as "low ring bone". Generally speaking, "high" or "low" ring bone is a significant finding during a prepurchase exam. Low ring bone is more common in draft breed horses. In addition, varying degrees of coffin joint arthritis, in active sport horses, is more common than pastern arthritis.

Figure 5

 High ring bone or pastern arthritis should be a concerning finding in any horse that is expected to carry a rider. Medical management of pastern osteoarthritis is limited to intra-articular treatment with cortisone or regenerative therapies. Unfortunately, the degeneration of the joint progresses rapidly and commonly results in chronic lameness. Surgical management involves fusion of the joint either with hardware or chemicals.

Pythiosis!

The endoscopic images below are of the pharynx of a horse with a 30 day history of a bloody nose. The nasal discharge consisted of bright red blood mixed with some purulent debris. The middle-aged gelding lives in a pasture that includes multiple low-lying areas that have been flooded with stagnant water. In addition, the gelding has suffered from failure to thrive most likely due to a poor appetite.

Figure 1

The endoscopic exam revealed bleeding tissue that surrounded the pharynx but was most severe along the dorsal wall of the pharynx. There was purulent debris mixed with the bleeding tissue and multiple small, white granuoles were noted within the bleeding tissue (Figure 2) .  Possible disease processes for this condition include fungal granuloma, cancer, bacterial abscess, and pythiosis.  Pythiosis is caused by the invasion of tissues by the pathogen pythiosis insidiosum and may affect external and internal tissues. The pathogen typically gains access to the horse via exposure to stagnant water that contains p. insidiosum.  As such the lower limbs (pasterns, coronary bands, and fetlocks) are most commonly affected. Once infected, the wound becomes increasingly inflamed with persistent bloody discharge. In addition, the lesions are very puritic resulting in additional inflammation via the horse biting and scratching at the wounds. Within the large areas of inflammation are firm, yellow granuoles also known as "kunkers".  This condition can be very deadly and requires aggressive treatment. For external cases, surgical removal and topical treatment are common. In addition a vaccine is available that has proven effective for cases of equine pythiosis.

Figure 2

However, pythiosis of the pharynx is not treatable with surgical resection or the common topical medications. Fortunately, systemic antifungals have proven effective if treated early and for the appropriate amount of time. The endoscopic images below are from the same horse approximately 4 weeks into the systemic anti-fungal treatment protocol. I recommend a specific protocol that involves  6 weeks of a tapering dose and a follow up endoscopic exam. In the past 8 years I have treated nearly a dozen cases of pharyngeal pythiosis. In every case there was a body of stagnant water available to the horses and all but 1 case responded to the systemic anti-fungal medication. For more information regarding the condition and the vaccine check out the following link: http://pythium.pavlab.com/subpage5.html

Figure 3

Figure 4

Phenylbutazone Toxicity!!

The yearling pictured below was being treated with Phenylbutazone for a severe lameness. The yearling weighed approximately 750 lbs and was being treated with 2 grams of Phenylbutazone twice per day for 2 weeks! Although the lameness improved, the yearling stopped eating and developed mild colic symptoms, severe oral ulceration (Figure 1) and eventually generalized edema. 

Figure 1

The serum levels of total protein and albumin were well below normal values and an abdominal ultrasound revealed severe edema of the right dorsal colon (Figure 2) . These findings were consistent with an advanced case of right dorsal colitis secondary to excessive phenylbutazone administration. Most often, when we discuss "ulcers" in horses we are referring to gastric or stomach ulcers. These types of ulcers may be caused by drugs such as banamine and phenylbutazone or are often a result of poor nutritional management. However, colonic ulcers may also be caused by such drugs, especially phenylbutazone. These types of ulcers are poorly understood and often difficult to diagnose in a standing horse. A typical history is that of a horse that presents for mild, recurrent colic, mild to severe diarrhea, ill-thrift, and a history of recent phenylbutazone treatment. Although the dose of phenylbutazone in this case was excessive, some horses appear to be super sensitive to the drug and may develop right dorsal colitis on an accepted dose of phenylbutazone. 

Figure 2

 Sadly, the yearling described could not be saved and was euthanized. A necropsy was performed and severe ulceration of the right dorsal colon (Figure 3 and 4) was discovered along with the marked edema of the colon wall (Figure 5). These large button-like ulcers cannot be detected via an ultrasound exam and would require surgical exploration of the colon to diagnose. The edema of the right dorsal colon wall can be diagnosed via trans-abdominal ultrasound and is secondary to the significant loss of serum protein. The protein is lost through the GI tract due to the inflamed colonic surface.

Figure 3

Figure 4

Figure 5

 Phenylbutazone toxicity can range from mild to severe. Mild cases are rather common and may present as only mild colic symptoms following administration of the drug. As such, careful observation should be made at all times when treating with these types of drugs and a reduction in dose and frequency of administration should be considered sooner than later! Horses suffering from colonic ulcers do NOT respond to gastric ulcer medication such as ranitidine and omeprazole. There is no specific medication for this condition. Treatment includes termination of phenylbutazone treatment, de-bulking the diet (more pellets and less hay), and time. Prognosis is guarded for advanced cases and good for mild cases.

Club foot!!

The radiograph below is from a weanling colt with a severe case of a "club foot". Figure 1 is the affected foot and figure 2 is the normal foot. X-ray vision was not necessary in this case to confirm the diagnosis due to the classic distortion of the hoof capsule. Club feet in foals develop from tendon contracture or secondary to accelerated skeleton growth. As the leg bones grow in length the soft tissue structures (tendons and ligaments) cannot keep up with the rate of growth resulting in contracture of the joint spaces. In the case of a "club foot" it is the coffin joint or DIP joint that is contracted and results in abnormal hoof growth.

Figure 1

Figure 2

The yellow line below corresponds to the alignment of the short pastern bone and the coffin bone. In Figure 3, the alignment is normal. However in Figure 4 the dorsal surface of the coffin bone is not aligned with the short pastern bone. The letter "A" in figure 4 corresponds to the angle of contracture. The contracture occurs in part due to the strong pull of the deep digital flexor tendon that attaches to the bottom of the coffin bone. As the leg bones lengthen and the flexor tendons do not keep up with the growth rate, the coffin bone is pulled resulting in contracture of the joint.

Figure 3

Figure 4

Treatment of this condition in young horses varies and includes early weaning, reduced caloric intake,  repeated injections of oxytetracycline to relax the tendons, corrective trimming/shoeing, and surgical transection of the distal check ligament. In my clinical experience, many foals with mild contracture respond well to the oxytetracycline and corrective trimming protocol. However, more advanced cases such as this colt require surgical intervention. The distal check ligament attaches to the deep digital flexor tendon and essentially keeps it in "check". By cutting the ligament, there is some release of the pull by the deep digital flexor tendon on the coffin bone. This surgical procedure can be performed in a stall-side setting, in a standing patient. Once it is determined that surgery is indicated, the sooner the better!  The colt in this case was treated with oxytetracycline and corrective trimming for 2 months with minimal improvement. When he was 6 months old, the distal check ligament of the affected limb was transected. Figure 5 is the "club foot" 45 days post surgery, note the corrected alignment of the pastern and coffin bones. The colt's lameness resolved.  This case highlights the importance of early documentation with radiographs and early intervention to correct the "club foot".

Figure 5