Lateral Patellar Luxation

Lateral patellar luxation (LPL) is a debilitating orthopedic condition characterized by the displacement of the patella from the femoral trochlear groove in a lateral direction. This malalignment disrupts the normal extensor mechanism of the stifle (stifle joint), leading to varying degrees of lameness, pain, and degenerative joint disease. In veterinary surgery, LPL is classified into four grades (I-IV) based on the severity and reducibility of the luxation. Grade I involves intermittent luxation that reduces spontaneously; Grade II allows manual luxation with spontaneous reduction; Grade III presents with persistent luxation that can be manually reduced but recurs; Grade IV is a permanent luxation that cannot be manually reduced. The condition is most commonly seen in dogs, particularly in large and giant breeds, but can also affect cats. Surgical correction is often required for Grades III and IV, and sometimes for Grade II when clinical signs are significant. The goal of surgery is to realign the extensor mechanism, deepen the trochlear groove, and stabilize the patella within the sulcus, thereby restoring normal joint biomechanics and preventing the progression of osteoarthritis.

Lateral patellar luxation can arise from congenital, developmental, or traumatic causes. Congenital and developmental factors are most common, often associated with skeletal malalignment of the hindlimb, including coxa vara, femoral anteversion, tibial torsion, and lateral displacement of the tibial tuberosity. These conformational abnormalities alter the quadriceps angle, causing the patella to be pulled laterally during muscle contraction. Traumatic LPL is less common and results from direct trauma to the stifle, such as a blow to the lateral aspect, causing rupture of the medial retinaculum or avulsion of the patellar ligament. Iatrogenic causes may occur following improper surgical techniques, such as over-tightening of the lateral retinaculum or malpositioning of a tibial tuberosity transposition. Additionally, degenerative joint disease and chronic patellar instability can contribute to the progression of the luxation. In some cases, a combination of factors, including muscle contracture (e.g., quadriceps contracture) and fibrosis, may be involved. The underlying biomechanical trigger is the abnormal pull of the quadriceps muscle group, which is laterally deviated due to the skeletal deformities, leading to repetitive lateral stress on the patella and eventual luxation.

Lateral patellar luxation is less common than medial patellar luxation (MPL) in dogs, but it is still a significant orthopedic condition. It is most frequently diagnosed in large and giant breed dogs, such as the Great Dane, Saint Bernard, Labrador Retriever, and Rottweiler, although it can occur in any breed. There is no strong sex predilection, but some studies suggest a slight male predominance. The condition is often bilateral, with a higher incidence in young animals due to congenital or developmental origins. In cats, LPL is rare but can occur, particularly in breeds like the Maine Coon. The age at presentation varies; congenital cases may be evident in puppies as soon as they begin to walk, while traumatic cases can occur at any age. The prevalence of LPL is estimated to be around 5-10% of all patellar luxations in dogs. Working and athletic dogs may be at higher risk due to increased physical stress on the stifle, which can exacerbate underlying conformational abnormalities. Genetic predisposition is suspected, as certain breeds have a higher incidence, suggesting a heritable component to the skeletal deformities that lead to LPL.

The pathophysiology of lateral patellar luxation involves a complex interplay of anatomical and biomechanical abnormalities. The primary structural defect is a lateral deviation of the quadriceps mechanism, often due to femoral anteversion, coxa vara, and lateral displacement of the tibial tuberosity. This deviation increases the angle between the quadriceps muscle and the patellar ligament, creating a lateral force vector that pulls the patella out of the trochlear groove. As the patella luxates, it causes stretching and tearing of the medial retinaculum, while the lateral retinaculum becomes contracted and thickened. The femoral trochlear groove may be shallow or absent, further reducing patellar stability. Chronic luxation leads to erosion of the articular cartilage on the medial aspect of the patella and the lateral femoral condyle, resulting in osteoarthritis. The abnormal biomechanics also cause abnormal wear on the menisci and cruciate ligaments, potentially leading to secondary cranial cruciate ligament rupture. In severe cases, the patella may be permanently luxated, causing significant lameness and muscle atrophy. The inflammatory response to the chronic instability and cartilage damage leads to synovitis, joint effusion, and pain, perpetuating the degenerative process.

Intrinsic predisposing factors for lateral patellar luxation include conformational abnormalities such as coxa vara (decreased angle of inclination of the femoral neck), femoral anteversion (increased angle of version), tibial torsion (lateral rotation of the tibia), and lateral displacement of the tibial tuberosity. These skeletal deformities are often genetic in origin and are more common in certain breeds. Additionally, a shallow or dysplastic trochlear groove, patella alta (high-riding patella), and quadriceps muscle contracture can predispose to LPL. Extrinsic factors include trauma to the stifle, which can cause acute luxation or exacerbate a pre-existing mild instability. Obesity and excessive body weight increase the load on the stifle, potentially worsening the condition. Inappropriate exercise or training, especially in young animals, may contribute to the development of LPL by placing abnormal stress on the developing skeleton. Prior surgical interventions, such as over-tightening of the lateral retinaculum during MPL correction, can inadvertently cause LPL. Nutritional factors, such as overfeeding during growth, may lead to rapid weight gain and skeletal stress, although this is less specific to LPL.

Clinical signs of lateral patellar luxation vary depending on the grade and duration of the condition. In Grade I, animals may show intermittent lameness, often skipping or hopping, especially after exercise or when rising. Palpation of the stifle may reveal a patella that can be manually luxated but returns to normal position spontaneously. Grade II presents with more frequent lameness, and the patella can be manually luxated but reduces when the animal extends the stifle. Grade III is characterized by persistent lameness, with the patella luxated most of the time but manually reducible. The animal may carry the affected limb, and there is noticeable muscle atrophy. Grade IV is a permanent luxation, causing severe lameness and a characteristic crouched stance with the stifle held in flexion. On physical examination, the patella is palpably displaced laterally, and the stifle may have a reduced range of motion. Crepitus may be felt on manipulation due to cartilage damage. In chronic cases, there is palpable thickening of the lateral retinaculum and joint effusion. Animals may also exhibit signs of pain on extension of the stifle. Bilateral involvement is common, and owners may report a 'bunny-hopping' gait. Systemic signs are rare, but chronic pain can lead to behavioral changes and decreased activity.

Differential diagnoses for lateral patellar luxation include: 1) Medial patellar luxation (MPL) - the patella luxates medially, and palpation reveals medial displacement; radiographs show medial displacement of the tibial tuberosity and a shallow trochlear groove. 2) Cranial cruciate ligament (CCL) rupture - presents with acute lameness, positive cranial drawer sign, and joint effusion; radiographs may show osteoarthritis and a displaced fabella. 3) Fracture of the patella - history of trauma, pain on palpation, and radiographic evidence of a fracture line. 4) Osteochondritis dissecans (OCD) of the stifle - typically affects the lateral femoral condyle, causing lameness and joint effusion; radiographs or CT show a subchondral bone defect. 5) Septic arthritis - acute onset, severe pain, joint swelling, fever, and elevated white blood cell count; synovial fluid analysis reveals septic inflammation. 6) Immune-mediated polyarthritis - multiple joints affected, stiffness, and systemic signs; synovial fluid analysis shows non-septic inflammation. 7) Neoplasia of the stifle - rare, but can cause lameness and swelling; imaging and biopsy are diagnostic. 8) Quadriceps contracture - often a sequela of femoral fracture, causing a rigid stifle and patella alta; history of trauma and radiographic changes. 9) Hip dysplasia - can cause hindlimb lameness, but orthopedic examination reveals hip pain and radiographic changes in the coxofemoral joints. 10) Avulsion of the tibial tuberosity - occurs in young dogs, causing acute lameness and a palpable gap; radiographs show avulsion fragment.

The diagnostic algorithm for lateral patellar luxation begins with a thorough history and physical examination. The veterinarian should observe the animal's gait, noting any lameness or abnormal posture. Orthopedic examination includes palpation of the stifle to assess patellar position, stability, and crepitus. The patella should be manually luxated and reduced to determine the grade. A complete neurological examination is essential to rule out neurologic causes of lameness. Following the physical exam, radiography is the primary imaging modality. Standard lateral and craniocaudal (anteroposterior) views of the stifle are obtained, along with a skyline (tangential) view to evaluate the trochlear groove depth. Radiographs can confirm the direction of luxation, assess the depth of the trochlear groove, and identify any skeletal deformities such as femoral anteversion or tibial torsion. Stress radiographs may be taken to demonstrate the luxation. In complex cases, advanced imaging such as computed tomography (CT) is recommended to precisely measure femoral and tibial alignment, including the femoral anteversion angle and tibial torsion. CT is also useful for surgical planning, especially for corrective osteotomies. Magnetic resonance imaging (MRI) may be indicated if concurrent soft tissue injuries, such as meniscal tears or cruciate ligament damage, are suspected. Arthroscopy can be used to directly visualize the articular surfaces and confirm cartilage damage. The diagnostic algorithm should also include a synovial fluid analysis if septic arthritis is suspected. Once the diagnosis is confirmed, the grade of luxation is determined, and a surgical plan is formulated.

Laboratory findings in lateral patellar luxation are generally non-specific but are important for preoperative assessment and to rule out other conditions. A complete blood count (CBC) may reveal mild leukocytosis due to stress or inflammation, but is usually within normal limits. Serum biochemistry profile is typically unremarkable, but may show elevated muscle enzymes (creatine kinase, aspartate aminotransferase) if there is significant muscle trauma or atrophy. Urinalysis is normal. Coagulation panel (PT, aPTT, platelet count) is recommended before surgery to assess bleeding risk. Synovial fluid analysis is crucial if septic arthritis or immune-mediated disease is suspected. In LPL, synovial fluid is typically non-inflammatory, with low cell counts (less than 3,000 cells/µL) and good viscosity. The mucin clot test is good. Cytology shows predominantly mononuclear cells. If inflammation is present, cell counts may be elevated, and culture should be performed. Inflammatory biomarkers such as C-reactive protein (CRP) and serum amyloid A (SAA) may be mildly elevated in chronic cases due to osteoarthritis, but are not diagnostic. Blood gas analysis is not routinely needed but may be performed in critically ill patients. Overall, laboratory findings are used to rule out other causes of lameness and to ensure the patient is a suitable surgical candidate.

Radiography is the cornerstone of imaging for lateral patellar luxation. Standard lateral and craniocaudal views of the stifle are obtained. In LPL, the craniocaudal view will show the patella displaced laterally relative to the femoral trochlear groove. The skyline (tangential) view, taken with the stifle flexed, is essential to evaluate the depth of the trochlear groove; a shallow or absent groove is a common finding. Radiographs also allow assessment of secondary osteoarthritis, such as osteophyte formation on the femoral condyles and patella. Stress radiographs, where the patella is manually luxated, can confirm the direction and reducibility. In cases with suspected skeletal deformities, full limb radiographs are recommended to measure the femoral anteversion angle and tibial torsion. Ultrasonography is not commonly used for LPL but can assess soft tissue structures such as the quadriceps muscle and patellar ligament. Computed tomography (CT) is invaluable for surgical planning, providing 3D reconstructions and precise measurements of femoral and tibial alignment. CT can quantify femoral anteversion, tibial torsion, and the degree of lateral displacement of the tibial tuberosity. Magnetic resonance imaging (MRI) is indicated if concurrent meniscal or cruciate ligament injuries are suspected, as it provides excellent soft tissue contrast. Arthroscopy is a minimally invasive technique that allows direct visualization of the articular cartilage, synovium, and menisci, and can be used to confirm cartilage damage and guide treatment. Fluoroscopy may be used intraoperatively to assess alignment during corrective surgery.

Cytology and histopathology are not routinely performed for lateral patellar luxation unless there is suspicion of an underlying neoplastic or inflammatory process. Synovial fluid cytology is the most common cytologic evaluation. In LPL, synovial fluid is typically non-inflammatory, with low cellularity (less than 3,000 nucleated cells/µL) and a predominance of mononuclear cells. The mucin clot is good. If the fluid is turbid or has high cell counts, septic or immune-mediated arthritis should be considered, and culture and sensitivity should be performed. Histopathology of synovial membrane or bone is rarely indicated, but if a mass is present or if there is unexplained joint destruction, a biopsy may be taken. In chronic LPL, histopathology of the synovium may show mild villous hyperplasia and fibrosis. Articular cartilage biopsy may reveal fibrillation and erosion consistent with osteoarthritis. If a corrective osteotomy is performed, bone biopsies are not typically taken. In cases of traumatic LPL, histopathology of the patellar ligament or retinaculum may show fibrosis and degeneration. Overall, cytology and histopathology are ancillary tools used to rule out other diseases and are not essential for the diagnosis of LPL.

The treatment of lateral patellar luxation is primarily surgical, especially for Grades III and IV, and for Grade II when clinical signs are significant. Medical management may be considered for Grade I or for non-surgical candidates, including weight management, exercise restriction, and non-steroidal anti-inflammatory drugs (NSAIDs) for pain control, but it does not correct the underlying deformity. Surgical options include: 1) Trochleoplasty - deepening of the trochlear groove, either by abrasion, recession (trochlear wedge recession), or sulcoplasty. This is often combined with other procedures. 2) Tibial tuberosity transposition - the tibial tuberosity is osteotomized and moved medially to realign the quadriceps angle. This is a key procedure for LPL. 3) Lateral retinacular release and medial retinacular imbrication - the contracted lateral retinaculum is incised, and the medial retinaculum is tightened to provide medial support. 4) Femoral and tibial corrective osteotomies - in cases with severe femoral anteversion or tibial torsion, a distal femoral osteotomy (DFO) or tibial osteotomy may be necessary to correct the skeletal malalignment. 5) In severe cases, a combination of procedures is required. The surgical approach is typically a lateral parapatellar approach to the stifle. Preoperative stabilization includes pain management and antibiotics. Postoperative care involves pain control, cold therapy, and restricted activity for 6-8 weeks. Physical rehabilitation, including passive range of motion exercises and controlled leash walks, is crucial for recovery. Complications include infection, implant failure, recurrence of luxation, and progression of osteoarthritis.

The prognosis for lateral patellar luxation is generally good to excellent with appropriate surgical correction, especially in cases without severe skeletal deformities. Short-term prognosis is favorable, with most animals showing significant improvement in lameness within 4-6 weeks postoperatively. Medium-term (6-12 months) outcomes are excellent, with return to normal function in 80-90% of cases. Long-term prognosis is guarded for the development of osteoarthritis, which may progress despite surgical correction. Factors that negatively affect prognosis include severe preoperative osteoarthritis, concurrent cranial cruciate ligament rupture, and inadequate surgical correction. Recurrence of luxation is possible, especially if the underlying skeletal deformity is not addressed. Surgical success rates are high, with reported rates of 90% or more for uncomplicated cases. Complications such as infection, implant failure, and patellar re-luxation occur in 5-10% of cases. Functional recovery is typically excellent, with most animals returning to normal activity levels. However, chronic cases may have persistent mild lameness and muscle atrophy. Overall, the prognosis is good, but owners should be counseled about the risk of osteoarthritis and the need for long-term management.

Postoperative follow-up for lateral patellar luxation is structured to monitor healing and function. Sutures or skin staples are typically removed 10-14 days after surgery. Radiographs are taken immediately postoperatively to assess implant placement and alignment, and then at 4, 8, and 12 weeks to evaluate bone healing and joint congruity. At 4 weeks, the animal should be re-examined to assess weight-bearing and range of motion. Restricted activity is maintained for 6-8 weeks, with controlled leash walks only. Physical therapy, including passive range of motion exercises, is initiated early, and swimming may be introduced after 4 weeks. At 8 weeks, radiographs are repeated to confirm bone healing, and the activity level may be gradually increased. At 12 weeks, a final radiographic evaluation is performed, and the animal is typically cleared for normal activity. Long-term follow-up is recommended every 6-12 months to monitor for the development of osteoarthritis. Owners should be advised to maintain a healthy body weight and to avoid high-impact activities. If any signs of lameness or discomfort occur, immediate re-evaluation is warranted. Serial radiographs may be taken annually to assess joint health.

Clinical pearls: 1) Always perform a thorough orthopedic examination, including palpation of the patella in both extension and flexion, to accurately grade the luxation. 2) Obtain a skyline radiograph to assess trochlear groove depth; a shallow groove is a common finding and requires trochleoplasty. 3) In large breed dogs, consider concurrent skeletal deformities such as femoral anteversion and tibial torsion; CT is invaluable for surgical planning. 4) When performing tibial tuberosity transposition, ensure the tibial tuberosity is moved sufficiently medially to realign the quadriceps angle; use a K-wire or screw fixation. 5) Release the lateral retinaculum completely to reduce tension on the patella. 6) In cases with severe femoral anteversion, a distal femoral osteotomy may be necessary; use a locking plate for stable fixation. 7) Postoperative physical therapy is crucial for optimal recovery; initiate passive range of motion exercises early. Pitfalls: 1) Failure to address the underlying skeletal deformity can lead to recurrence of luxation. 2) Over-tightening of the medial retinaculum can cause medial patellar luxation. 3) Inadequate trochleoplasty may not provide sufficient patellar stability. 4) Damage to the femoral nerve during surgery can cause quadriceps weakness. 5) Improper implant placement can lead to implant failure or fracture. 6) Ignoring concurrent cruciate ligament injury can result in persistent lameness. 7) Allowing too much activity too soon can lead to surgical failure.

Perioperative drug protocols for lateral patellar luxation surgery are based on Plumb's Veterinary Drug Handbook. Preoperative antibiotics: Cefazolin (22 mg/kg IV) administered 30 minutes before incision, repeated every 90 minutes during surgery. Postoperative antibiotics: Cephalexin (22 mg/kg PO q8h) for 7-10 days. Analgesics: Preoperative opioid, e.g., Morphine (0.5-1 mg/kg IM) or Hydromorphone (0.05-0.1 mg/kg IV). Intraoperative analgesia: Fentanyl CRI (5-10 µg/kg/hr IV) or Lidocaine CRI (25-50 µg/kg/min IV). Postoperative analgesia: NSAIDs such as Carprofen (2.2 mg/kg PO q12h) or Meloxicam (0.1 mg/kg PO q24h) for 3-7 days. For breakthrough pain, add Tramadol (2-5 mg/kg PO q8h) or Gabapentin (10-20 mg/kg PO q8h). Local anesthesia: Femoral nerve block with Bupivacaine (1-2 mg/kg) or Lidocaine (2 mg/kg) preoperatively. Muscle relaxants: Methocarbamol (15-20 mg/kg PO q8h) may be used for muscle spasms. Chondroprotectants: Polysulfated glycosaminoglycan (Adequan) 4.4 mg/kg IM or SC twice weekly for 4 weeks, or Glucosamine/Chondroitin supplements (500-1000 mg PO q24h). Gastroprotectants: Omeprazole (0.5-1 mg/kg PO q24h) if NSAIDs are used long-term. Adjust dosages for renal or hepatic impairment. Always monitor for adverse effects.

Evidence-based literature on lateral patellar luxation is limited compared to medial patellar luxation, but several studies provide guidance. A landmark study by Roush (1993) evaluated the results of surgical correction of lateral patellar luxation in 20 dogs and reported a success rate of 85%, with recurrence in 10% of cases. A more recent study by Dunlap et al. (2016) compared the outcomes of tibial tuberosity transposition alone versus combined with trochleoplasty, finding that combined procedures had lower recurrence rates. A systematic review by Wangdee et al. (2018) concluded that surgical treatment is superior to conservative management for Grades III and IV. Consensus guidelines from the ACVS recommend a thorough preoperative assessment of skeletal alignment using CT for complex cases. A study by Yeadon et al. (2017) highlighted the importance of addressing femoral anteversion in large breed dogs, showing that distal femoral osteotomy improved outcomes. Another study by Fitzpatrick et al. (2012) reported excellent long-term outcomes with a combination of tibial tuberosity transposition and trochleoplasty in 30 dogs, with a 93% success rate. However, there is a lack of randomized controlled trials, and most evidence is based on retrospective case series. Future research should focus on standardized outcome measures and long-term follow-up to further refine surgical techniques.