Continuing Education Activity
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 the patellar tendon and the patella bone, makes up the extensor mechanism of the lower leg. A rupture of this central tendon drastically hinders knee extension and directly affects 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. This activity reviews the etiology, presentation, evaluation, and management of quadriceps tendon rupture and reviews the role of the inter-professional team in evaluating, diagnosing, and managing this condition.
Objectives:
- Describe risk factors and at-risk populations associated with quadriceps tendon rupture.
- Outline the typical presentation of a patient with a quadriceps tendon rupture, including differentiating it from a patellar tendon rupture.
- Review the treatment and management options for patients with quadriceps tendon ruptures.
- Summarize inter-professional team strategies for improving care coordination and communication for evaluating, treating, and rehabilitating quadriceps tendon tears.
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 the patellar tendon and the patella bone, makes up the extensor mechanism of the lower leg. Structurally and biomechanically, the quadriceps tendon can withstand very high loads without rupture. The quadriceps muscle derives its neurovascular innervation from the femoral nerve and artery.[1][2]
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, the superior medial genicular branch of the popliteal artery, and the profunda femoris artery. The vastus lateralis, vastus medialis, and 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 affects 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.[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 a male-to-female ratio of 8:1.The susceptibility increases 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. Quadriceps tendon rupture after total knee replacement is a special etiological case that predominantly affects men between 50 and 65 years of age.
Certain medical conditions pose a higher risk for quadriceps tendon ruptures, such as diabetes mellitus, hyperparathyroidism, gout, chronic kidney disease, obesity, and hypercholesterolemia, in addition to multiple connective tissue disorders, rheumatoid arthritis, systemic lupus erythematosus, and osteogenesis imperfect. Other risk factors involve medications such as anabolic steroids, corticosteroids, and fluoroquinolones.[1][2][3][4][5] Intra-articular injections carry a 20 to 33% risk of quadriceps tendon rupture.
Epidemiology
Lower leg extensor mechanism ruptures are very rare but are reported to have high morbidity and are often debilitating.[6] Quadriceps tendon ruptures are more common than patellar tendon ruptures. Quadriceps tendon rupture is 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 rupture can be a result of direct or indirect trauma. There have been reports of spontaneous ruptures, even sometimes bilaterally, when certain medical conditions preexist, as mentioned in the etiology.[7] Or in healthy personnel during sports participation.[8]
Quadriceps tendon ruptures are due to violent eccentric loading of the knee extensor mechanism as a direct result of a sudden and strong contraction of the quadriceps muscle from a jump and land mechanism or a sudden change in direction while running, or attempting to regain balance to avoid a fall.[9] 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. Most 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.[10] 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 in diabetes mellitus involves accumulating 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 person ages, there are also decreased arterial capillaries per unit of surface area. This results in a decreased healing potential after repeated microtrauma.
The quadriceps tendon has been subdivided into three zones based on the distance from the superior pole of the patella.[11] With zone 2 being the most commonly involved.[12]
- Zone 1 : 0 to 1 cm.
- Zone 2 : 1 to 2 cm.
- Zone 3: is located >2 cm from the superior pole of the patella
Zone 2 has been reported to be a hypovascular zone and correlates with the spontaneous ruptures of the quadriceps tendon reported in the literature.[11]
Histopathology
Tendon Tissue Response to Load
Upon loading, the tendon responds in three phases. Initially, in the "toe" phase, which is up to 2% of the load. Flattening of the crimp pattern of collagen fibers happens during this phase. Following this and up to 4 % of the load, "elastic" tendon deformation occurs, where the tendon still has the capacity to return to its original length once the load is removed. This elasticity is due to the intramolecular sliding of collagen triple helices by which the fibers align parallel with each other.[13] During the last phase, where the strain is beyond 4% and up to 8 to 10%, "plastic" deformation may occur. This is where microscopic tissue failure happens. Then a macroscopic failure happens once the strain exceeds 10%.[14]
Tendon deformation shows viscoelastic properties such as creep and stress relaxation and is time-dependent. During a fall, while attempting to maintain balance, a sudden and eccentric quadriceps contraction can exceed the plastic deformity and results in complete or incomplete rupture. But less commonly, slowly applied higher loads can exceed the tendon capacity and cause macroscopic failure.[9]
The degree of retraction following rupture depends on the viscoelastic properties of muscular and tendon tissue. Therefore, during repair, the original length should be restored. Otherwise, the retracted quadriceps is too short to function properly, which is why inadequate muscle function is expected in neglected cases.[15][16]
History and Physical
The clinical diagnostic triad includes acute pain, loss of active straight leg raising, and a palpable suprapatellar defect.[17] 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. In the case of tendinopathy, patients will usually experience a preceding pain. A palpable defect or a gap 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 examination are usually sufficient to diagnose quadriceps tendon ruptures, and imaging is generally not necessary.
Ultrasound is the diagnostic modality of choice. It can be used to detect a tendon defect and to assess the degree of tendon gap with knee flexion.[18][19] 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 help determine patellar position. A patella Alta (high-riding patella) may indicate a patellar tendon rupture, while a patella Baja (an inferior riding patella) may suggest a quadriceps tendon rupture. Plain radiography may also rule in or out associated patella avulsions or other associated patellar fractures.
MRI has high sensitivity and specificity to detect quadriceps tendon rupture.[20] 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
Non-operative Treatment
Like most musculoskeletal injuries, initial management of suspected quadriceps tendon ruptures includes rest, ice, compression, and elevation. Partial quadriceps tendon ruptures with intact extensor mechanism can be managed non-operatively with a knee immobilizer and physiotherapy. However, most 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.[21][22]
Operative Treatment
Acute rupture can be primarily repaired. Multiple repair techniques have been reported in the literature. End-to-end direct sutures were described for mid-substance tears.[17][23][24] Patellar drill holes were more commonly reported and used for rupture near or at the level of the osseous tendinous junction.[25][26][27] Suture anchors are an alternative technique to drilling holes. Anchors are advantageous because of the smaller incision and reduced operative time.[28][29] Clinically and biomechanically, no difference was reported between both patellar drill holes and suture anchors.
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 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. Allograft reconstruction may be necessary if significant tendon retraction results in a large tendon gap.
Technique: Approaching the knee through a midline incision. The repair technique involves drilling longitudinal tunnels in the patella and using nonabsorbable sutures in the tendon end (Kesseler or Krakow) in a locking fashion with free ends to be passed through the patella and tied at the inferior pole. The suture anchors technique has been shown to result in better biomechanical performance with increased ultimate loads to failure, as they have less gap formation. In either method, the retinaculum is repaired with heavy absorbable sutures. Testing the repair intraoperatively, ideally, the knee should be able to flex to 90 degrees. Immediate postoperative care involves immobilization in full extension for a short period, followed by a progressive range of motion and strengthening exercises.
Chronic ruptures can still be primarily repaired. However, usually, the tendon retracts proximally up to 5 cm in ruptures older than two weeks. Similar techniques as in acute rupture can be adopted, bearing in mind that a tendon lengthening procedure may be required, e.g., the Codivilla procedure (V-Y lengthening).[30] Auto, allograft tissue, or synthetic tape may be needed to secure the quadriceps tendon to the patella.
Additionally, multiple augmentation (reinforcement) techniques have been proposed in scenarios where tendon tissue quality is poor or in case of delayed surgery. These techniques include wire augmentation, Merisilen tape, and fascia lata reinforcement.[23][31]
Few studies have evaluated optimal postoperative management. Historically, the knee was immobilized at full extension for six weeks postoperatively to allow complete tendon healing before stressing the extensor mechanism. There has been a trend toward early postoperative 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 postoperative management.
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
Prognosis
Slightly over half of people will experience thigh weakness and soreness at the site of injury. Surgical cases will have a better prognosis if the surgery is performed immediately following the initial injury. Most patients can return to their previous occupations and activities following recovery from a quadriceps tendon tear.
The surgeon must thoroughly assess the affected limb in competitive athletes before permitting a return to sport. The goal is for the injured limb to be at least 85 to 90% as strong as the uninjured leg. In addition to leg strength, the patient's balance must be assessed, and if there is any residual swelling.
Complications
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.
- Weakness: 33% to 50% of patients may experience a strength deficit.
- Stiffness
- Functional impairment: 50% of patients will be unable to return to their prior level of activity or sports.
- Painful sensations around the patella or hypersensitive scar.[24]
Postoperative and Rehabilitation Care
Immobilization: patients should be immobilized; the recommended period varies from 3 to 10 weeks.[23][17] However, many studies recommend six weeks of immobilization as the preferred duration to protect the repair, whether it is primary or delayed.[24][32][33][26][34]
Weightbearing status: Patients can be allowed partial weight bearing while immobilized.[32][33] Or they can start early passive motion at 0 to 55 or 0 to 60 degrees along with partial or full weight bearing.[35][25]
Outcome measures: In assessing the functional outcome of the repair, several scoring systems can be used. Some scoring systems are tailored specifically by surgeons, as in Siwek and Rao and Rougraff et al., who introduced their own functional assessment.[17][23] Other commonly used scores include:
Deterrence and Patient Education
The clinician and physical therapist must customize a rehabilitation plan for each patient. How long therapy will be needed and which exercises your treatment team prescribes will be based on the type of tear, the surgical repair, the patient's overall medical condition, and specific post-surgical needs. Patients must understand the role they must play in their recovery.
Complete recovery generally takes at least four months., with most repairs nearly healed in 6 months. Many patients report that it took 12 months to reach their recovery goals.
Enhancing Healthcare Team Outcomes
The diagnosis and management of quadriceps tendon rupture are best managed by an interprofessional healthcare team that includes an emergency department clinician, physical therapist, radiologist, sports clinician, orthopedic surgeon, and specialty orthopedic nurse, and all members of the team must utilize open communication regarding patient progress and recovery, whether or not the case requires surgery. Interprofessional case management will yield improved patient outcomes. [Level 5]
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, most 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.[21][22]
The outcomes for most patients are good, but the recovery is often prolonged. Without physical therapy, recurrences are known to occur.