Quadriceps Tendon Rupture
- Article Author:
- Jacob Pope
- Article Author:
- Youssef El Bitar
- Article Editor:
- Mark Plexousakis
- Updated:
- 9/14/2020 9:28:04 PM
- For CME on this topic:
- Quadriceps Tendon Rupture CME
- PubMed Link:
- Quadriceps Tendon Rupture
Introduction
The quadriceps tendon is derived from the muscular junction of the rectus femoris, vastus lateralis, vastus medialis, and vastus intermedius muscles at the anterior superior pole of the patella. The quadriceps tendon in combination with patellar tendon and the patella bone make up the extensor mechanism of the lower leg. These muscles derive their neurovascular innervation from the femoral nerve and artery. Specifically, the rectus femoris, vastus intermedius, and vastus lateralis gain their arterial supply from the lateral femoral circumflex artery. The vastus medialis gains its arterial supply from the femoral artery, superior medial genicular branch of the popliteal artery, and the profunda femoris artery. The vastus lateralis, vastus medialis, and the vastus intermedius act both as knee extenders as well as assist with patellar tracking. The vastus lateralis is the largest of the quadriceps muscles. It helps pull the patella laterally. This action must be counterbalanced by the vastus medialis, which is the smallest of the quadriceps muscles and acts to pull the patella medially. The vastus intermedius acts to help stabilize midline tracking of the patella. The combined contraction of this group of anterior thigh muscles causes extension of the lower leg. The rectus femoris also plays a role in hip flexion. A rupture of this central tendon drastically hinders knee extension and directly effects functionality. The degree that a quadriceps tendon rupture limits lower leg extension is based on the severity of tendon damage. Minor tendon tears may have minimal impact on extensor function, while complete tendon tears may totally impede lower leg extension.[1][2][3][4][5]
Etiology
Quadriceps tendon ruptures have a positive correlation with age and multiple medical comorbidities. This injury historically is more prevalent in males, with susceptibility increasing proportionally with age after 40 years. This is in contrast to patellar tendon ruptures, which commonly occur before age 40, and are often related to sports injuries. Medications and medical comorbidities associated with quadriceps tendon ruptures include fluoroquinolones, corticosteroids, anabolic steroids, hyperparathyroidism, gout, diabetes mellitus, obesity, chronic kidney disease, hypercholesterolemia, hyperuricemia, rheumatoid arthritis, systemic lupus erythematosus, and osteogenesis imperfecta.[1][2][3][4][5]
Epidemiology
Lower leg extensor mechanism ruptures as a whole are very rare, but are reported to have high morbidity and are often debilitating.[6] Quadriceps tendon ruptures are reported to have an incidence of 1.37/100,000, compared to 0.68/100,000 for patellar tendon ruptures. Extensor mechanism ruptures are most commonly unilateral. However, there are several case reports of this injury occurring bilaterally, from one precipitating event.
Pathophysiology
Quadriceps tendon ruptures in athletes are the direct result of a sudden and strong contraction of the quadriceps muscle from a jump and land mechanism, or sudden change in direction while running. Quadriceps tendon ruptures in non-athletes are usually the direct result of a fall or other trauma in individuals with predefined medical comorbidities which are thought to cause pathologic tendon degeneration. One proposed biomechanical mechanism involves knee flexion with simultaneous quadriceps contraction. Another proposed mechanism involves extensive rotation as well as hyperflexion of the lower leg. The majority of quadriceps tendon ruptures occur at the myotendinous junction with patellar tendon ruptures occurring most commonly within the tendon itself. End-stage renal disease patients on dialysis have the highest association with tendon degeneration resulting in ruptures. The pathophysiologic mechanism involved in chronic kidney disease is theorized to involve uremic toxins, renal osteodystrophy, and hyperparathyroidism.[7] As renal function declines, there is often a homeostatic imbalance of calcium, phosphorus, vitamin D, and parathyroid hormone. Elevated parathyroid hormone results in increased bone turnover. Over time, this is thought to weaken myotendinous junctions, resulting in increased potential for tendon rupture with minimal tensile stress. In patients receiving dialysis with insufficiently permeable filters, there has been higher reported serum beta-2 microglobulin. Beta-2-microglobulin collects in bones, joints, and tendons. This phenomenon is known as dialysis-related amyloidosis. Beta-2 microglobulin accumulation results in functional impairment in tissue elasticity and therefore a higher potential for tendon rupture with minimal trauma. The proposed mechanism involved in diabetes mellitus involves the accumulation of advanced glycation end products. Advanced glycation end products form covalent bonds with collagen fibers. This results in the release of inflammatory cytokines which cause progressive tendon damage. As one ages there is also decreased arterial capillaries per unit surface area. This results in a decreased healing potential after repeated microtrauma.
History and Physical
Patients presenting with potential quadriceps tendon ruptures usually report hearing an audible pop or experiencing a tearing sensation. This is immediately followed by a decreased ability to bear weight and is commonly accompanied by swelling and effusion. A palpable defect can usually be felt at the superior pole of the patella. Patients with complete tears have an impaired ability to perform a straight leg raise. With partial tears, there is impaired knee extension. With complete tears, knee extension is usually absent. There is usually no impaired range of motion at the hip or ankle.
Evaluation
History and physical exam are usually sufficient to diagnose quadriceps tendon ruptures, and imaging is usually not necessary. However, ultrasound may have some clinical utility. Ultrasound can be used to detect a tendon defect, and to assess the degree of tendon gap with knee flexion.[8][9] Ultrasound has also been used serially to assess healing and to determine the presence of associated hematomas, effusions, or calcifications. Plain radiographs are usually not helpful in making this diagnosis but may have some clinical utility in ruling out other associated injuries or conditions. Plain radiography may be helpful in determining patella position. A superior patella may be indicative of a patellar tendon rupture, while an inferior patella may be suggestive of a quadriceps tendon rupture. Plain radiography may also rule in or out associated patella avulsions or other associated patellar fractures. MRI may be used preoperatively but is usually not necessary. Due to the low prevalence of quadriceps tendon ruptures, there is limited data comparing ultrasound with MRI in diagnostic superiority. Both imaging modalities have a high sensitivity for patellar and quadriceps tendon injuries. However, ultrasound may be slightly more specific for patellar tendon ruptures, while MRI may have slightly higher specificity for quadriceps tendon ruptures. This difference is likely not clinically significant.
Treatment / Management
Like most musculoskeletal injuries, initial management of suspected quadriceps tendon ruptures includes rest, ice, compression, and elevation. Partial quadriceps tendon ruptures may be managed non-operatively. However, the majority of complete quadriceps tendon ruptures require early diagnosis and surgical treatment to limit long-term morbidity and disability. The timing of surgical repair has been attributed to optimal recovery and functionality rather than the specific surgical approach.[10][11]
Limited data directs the optimal surgical technique. Historically, surgical repair has been based on anecdotal evidence and surgeon experience. However, there is a trend toward the application of transosseous patellar drill holes if the tendon rupture is located near the patellar poles. More recently, suture anchors have replaced traditional patellar drill holes. Suture anchors require smaller skin incisions and result in shorter operative times. The effectiveness of this trend is unknown. Intratendinous ruptures have been repaired classically by way of an end to end sutures. Despite the specific surgical approach, a delayed recognition or operative intervention results in tendon retraction and reduced tissue quality. These factors both impair surgical success and hinder recovery. Operative repair is advised within the first 48 to 72 hours after complete tendon ruptures. If there is a delay in treatment, tendon retraction makes surgical repair more technically challenging, and may limit functional recovery. If there is significant tendon retraction resulting in a large tendon gap, allograft reconstruction may be necessary.
Few studies have evaluated optimal postoperative management. Historically, the knee was immobilized at full extension for 6 weeks postoperatively to allow complete tendon healing before stressing the extensor mechanism. There has been a trend toward early post-operative joint mobilization to reduce joint stiffness and quadriceps atrophy. In more recent literature, early mobilization has been shown to result in more adverse outcomes and additional operative interventions when compared to 6 weeks of full knee extension. However, due to the low incidence of this injury, there is limited statistically significant evidence to direct gold standard operative interventions or post-operative management.
Despite the surgical approach or postoperative course, the most common complications involve pain and quadriceps weakness. Patients report pain and weakness most commonly associated with prolonged standing, squatting, or ascending and descending stairs. However, few patients who receive timely medical intervention report significant functional impairment.
Differential Diagnosis
Differential diagnoses include:
- Patellar tendon rupture
- Patellar stress fracture
- Femoral shaft stress fracture
- Bone or soft tissue tumor
- Compartment syndrome
- Referred lumbar spine pain
- Meralgia paresthetica
- Femoral nerve injury or entrapment
Enhancing Healthcare Team Outcomes
The diagnosis and management of quadriceps tendon rupture is best managed by an interprofessional team that includes an emergency department physician, physical therapist, nurse practitioner, radiologist, sports physician, and an orthopedic surgeon.
Like most musculoskeletal injuries, initial management of suspected quadriceps tendon ruptures includes rest, ice, compression, and elevation. Partial quadriceps tendon ruptures may be managed non-operatively. However, the majority of complete quadriceps tendon ruptures require early diagnosis and surgical treatment to limit long-term morbidity and disability. The timing of surgical repair has been attributed to optimal recovery and functionality rather than the specific surgical approach.[10][11]
The outcomes for most patients are good but the recovery is often prolonged. Without physical therapy, recurrences are known to occur.