History
A 6-year-old Friesian gelding was referred to the Veterinary Medical Teaching Hospital of the University of Wisconsin for further evaluation of severe, progressive bilateral hind limb lameness of 10 days' duration. A diagnosis of bilateral intermittent upward fixation of the patella had been made 5 months previously. Following a lack of response to conservative management, splitting of the medial patellar ligament (MPL) was performed in both stifle joints 2 weeks prior to evaluation at the veterinary medical teaching hospital. In the immediate postoperative period, no adverse effects of the surgery were observed; however, 3 to 4 days following the surgery, the gelding began to have signs of persistent, worsening bilateral hind limb lameness that culminated in long periods of recumbency.
The gelding was recumbent on arrival at the veterinary medical teaching hospital. Findings on a general physical examination and CBC were unremarkable; however, a serum biochemical profile revealed high creatine kinase and aminotransferase activities, consistent with muscle damage due to recumbency. Examination of the hind limbs revealed soft tissue swelling over the cranial aspect of each stifle joint. The patellar ligaments could not be appreciated on deep palpation of the area, and there appeared to be proximal displacement of the patellae bilaterally. With the horse sedated and positioned in lateral recumbency, radiographs of the right stifle joint were obtained; radio-graphic images were obtained with the stifle joint in extension and also in flexion (Figure 1).
Lateromedial (A) and a flexed lateromedial (B) radiographic views of the right stifle joint of a laterally recumbent 6-year-old Friesian gelding evaluated because of severe, progressive bilateral hind limb lameness of 10 days' duration that culminated in long periods of recumbency.
Citation: Journal of the American Veterinary Medical Association 239, 6; 10.2460/javma.239.6.749
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Radiographic Imaging Findings and Interpretation
On the lateromedial radiographic projection of the right stifle joint (Figure 2), proximal and slightly caudal displacement of the patella is evident. Despite flexion of the right stifle joint, the degree of proximal displacement of the patella persists. With flexion, the patella does not move distally onto the femoral trochlea, failing to follow the distal motion of the tibial tuberosity. Similar radiographic findings were present for the left stifle joint.
Same radiographic images as in Figure 1 (A and B) and a flexed lateromedial radiographic view (C) of the right stifle joint of an unaffected clinically normal horse. For the horse of Figure 1, notice that the patella is displaced proximally and slightly caudally with the stifle joint in extension (A); in the affected horse, proximal displacement of the patella persists despite flexion of the stifle joint (B). By comparison, notice the typical relationship maintained by the patella with the trochlea of the femur as well as the tibial tuberosity in the clinically normal horse (C).
Citation: Journal of the American Veterinary Medical Association 239, 6; 10.2460/javma.239.6.749
Clinical and radiographic evaluation of the horse of this report suggested disruption of the patellar ligaments of the right and left stifle joints. Ultrasonographic examination of the patellar ligaments confirmed bilateral disruption of the MPLs and intermediate patellar ligaments (IPLs); the lateral patellar ligaments (LPLs) appeared intact.
Comments
In the horse of this report, bilateral rupture of the MPLs and IPLs disrupted the hind limb passive stay apparatus, preventing the horse from stabilizing the stifle joints in extension. This resulted in disruption of the reciprocal apparatus, which links the movements of the stifle joint with the tarsus.1 When the passive stay apparatus of the upper portion of the hind limb is completely disrupted, affected horses are unable to bear weight on that hind limb. As this horse was affected bilaterally, it was unable to stand.
The LPLs, IPLs, and MPLs serve as the functional insertions of the quadriceps femoris and biceps femoris muscles to the tibial tuberosity, with the patella acting as a sesamoid bone.2 In a clinically normal horse, the distance from the tibial tuberosity to the patella is fixed, with flexion of the stifle joint resulting in the femoral trochlea moving proximally, relative to the patella. In the horse of this report, proximal displacement of the patella persisted during flexion of the stifle joint, suggesting that the patellar ligaments were disrupted. Because of the grave prognosis for recovery, the horse was euthanatized and a full necropsy was performed.
Necropsy confirmed complete disruption of the MPL and IPL of both the right and left stifle joints. Histologic examination of the affected tissues revealed abundant active fibroplasia and granulation tissue formation. Underlying pathological changes that may have affected the patellar ligaments prior to splitting of the MPLs 2 weeks previously or an infectious process following the surgery were not detected. The LPLs were not affected, and results of histologic examination of other ligaments, remote from the regions of interest, were considered within normal limits.
We speculate that during flexion of the stifle joint in a clinically normal horse, most of the tension in the patellar ligaments is transmitted through the MPLs and IPLs, with a small component carried by the LPL. During flexion, the increase in distance from the proximal aspect of the femoral trochlea to the tibial tuberosity occurs cranially with a minimal change in distance occurring on the lateral aspect. In the horse of this report, disruption of the MPL and IPL and the typically small lateral trochlear ridge of the femur permitted complete lateral displacement of the LPL during flexion; therefore, movement of the patella in a distal direction did not occur. For this horse, genetic test results were negative for polysaccharide storage myopathy and malignant hyperthermia.
Intermittent upward fixation of the patella and its treatment and associated surgical complications have been documented.3,4 However, reported complications do not include rupture of the IPLs. We speculate that following the surgical procedure in which the MPLs were split, the IPLs and traumatized MPLs were unable to withstand the biomechanical forces during extension and weight bearing, resulting in their complete rupture. Alternatively, the IPLs may also have been weakened if inadvertently traumatized at the time of surgery.
- 1.↑
Durham M, Dyson SJ. Applied anatomy of the musculoskeletal system. In: Ross MW, Dyson SJ, eds. Diagnosis and management of lameness in the horse. Philadelphia: WB Saunders Co, 2003, 80–93.
- 2.↑
Budras KD, Sack WO, Rock, S. Passive stay apparatus of the hindlimb. In: Anatomy of the horse. 5th ed. Hanover, Germany: Schlütersche Verlagsgesellshaft mbH & Co KG, 2003, 22–23.
- 3.
Walmsley JP. The stifle. In: Ross MW, Dyson SJ, eds. Diagnosis and management of lameness in the horse. Philadelphia: WB Saunders Co, 2003, 455–470.
- 4.
Tnibar MA. Medial patellar ligament splitting for the treatment of upward fixation of the patella in 7 equids. Vet Surg 2002; 31: 462–467.