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Patellar Tendon Rupture

The patellar tendon functions as the distal aspect of the knee extensor mechanism and inserts at the tibial tuberosity. It assists in a person's capacity to perform and maintain full knee extension. When the patellar tendon ruptures, the patella loses support from the tibia and moves proximally upon contraction of the quadriceps, subsequently making tasks involving knee extension, such as standing up and ascending stairs, difficult.1 Surgical intervention is of paramount importance after acute rupture of the patellar tendon. It allows the tendon to be corrected for length as well as tension; failure to intervene results in loss of range of motion and power of the knee joint.

To date, no studies have adequately documented the true incidence of patellar tendon rupture. However, the general consensus is that this injury is relatively uncommon and generally occurs in patients younger than 40. It is the third most common injury involving the knee extensor mechanism, following patellar fracture and rupture of the quadriceps tendon.2

Patellar tendon rupture can occur unilaterally or bilaterally. Unilateral rupture is often due to traumatic athletic injury and bilateral rupture is often the result of a chronic inflammatory process. Traumatic injury results from sudden eccentric contraction of the quadriceps, usually with the foot planted and the knee flexed.1 Chronic inflammation causes microtrauma to the tendons, which compromises their collagen vascular integrity and makes them far more susceptible to rupture. These two etiologies of rupture can be further differentiated according to the site of injury. The osseo-tendinous junction is more often involved with traumatic rupture; in contrast, the patellar tendon tends to tear in the mid-substance when it is the result of a chronic inflammatory disease.1

This article highlights a unique case in which a 52-year-old white man with chronic tophaceous gout suffered a patellar tendon rupture during a jump from a shallow height.

Case Presentation

The patient, "C.J.," presented to the emergency department with severe pain in the right knee and reported that his knee buckled while jumping. C.J. described playing with his grandson, who had jumped to the ground from the second-to-last stair, a height of about 15 inches. In an attempt to "prove his youth," the patient attempted to mimic the maneuver in front of his grandson. According to the patient, his knee buckled and he ended up lying in excruciating pain at the bottom of the staircase.

Upon arrival in the emergency trauma department, the physical examination showed a high-riding patella in the knee with active flexion, eliciting exquisite tenderness and complete loss of active leg extension. A palpable defect could not be felt with certainty, secondary to knee effusion.

With a high index of suspicion for a patellar tendon rupture, plain radiographs of both lower extremities were obtained (anteroposterior and lateral). Review of the patient's medical records determined that CJ had experienced chronic tophaceous gout for the past two decades, which likely contributed to the compromise in patellar tendon integrity.

The patient was taken to the operating room for surgical reconstruction/repair by the orthopedic consultant. Upon exposure of the patella tendon, the structure was observed to present with marked tophaceous infiltration and partial rupture of the tendon (see photo). After debriding of the tendon to a viable bed, the surgeon repaired the remaining tendinous structure. Copious irrigation and knee closure were performed in the usual manner. A cylinder cast was applied to prevent any stress on the repair; the patient was instructed not to perform any straight leg raises postoperatively.


Rupture of the patellar tendon is a relatively infrequent yet disabling injury. It tends to occur during athletic activities when a violent contraction of the quadriceps muscle group is resisted by the flexed knee. Rupture usually represents the final stage of a degenerative tendinopathy that results from repetitive microtrauma to the patellar tendon.

Unilateral patellar tendon rupture is often attributed to trauma. The greatest forces put on the patellar tendon are at 60 degrees of knee flexion.3 A flexed knee puts greater force on the patellar tendon as opposed to the quadriceps tendon.1 Furthermore, the sites of insertion often succumb to a higher tensile load than does the mid-substance.1

Forces propagated through the patellar tendon are 3.2 times the body weight when a person is climbing a set of standard 7.5-inch steps.3 A force 17.5 times body weight is an estimated requirement to disrupt the extensor mechanism of the knee.1

Rupture in the setting of systemic inflammatory disease often occurs in the setting of diabetes mellitus, chronic renal failure, systemic lupus erythematosus or chronic steroid injections at the inferior pole of the patella for treatment of patellar tendonitis.4 Chronic multiple steroidal injections can induce atrophy of collagen organization, making the tendon brittle and vulnerable to spontaneous rupture under stress.1 A series by Kelly et al showed that among patients who sustained patellar tendon ruptures, 60% had received an average of two to three steroid injections around the patellar tendon before its rupture.5

A history of patellar tendonitis should be considered a predisposing factor to patellar tendon rupture in the first place. Histopathologically, chronic tendinous inflammation and degeneration due to repetitive microtrauma appears to be the common endpoint among the various causes of tendon rupture in the setting of systemic inflammatory disease.6

Rarely, gouty infiltration of monosodium urate crystals has been reported to cause tendinous rupture. Gout is believed to cause fibrinoid necrosis and chronic inflammation.7 Plain radiography is often the initial imaging modality used to assess patellar tendon rupture presumed to be of traumatic etiology. However, in patients with monosodium urate deposits in tendons, plain radiographs may not identify deposits of tophaceous gout.8 One study suggested that CT should be the imaging modality of choice, secondary to its ability to visualize dense linear opacities within the patellar tendon and within its tibial insertion, a finding standard radiographs can fail to identify.8 It has been speculated that the physical presence of monosodium urate tophi deposition within the tendon may be responsible for a drastic reduction in tensile strength, making rupture more likely.

Summary and Conclusion

We have presented a typical case of patellar tendon rupture from an atypical etiology in a 52-year-old white man. The rupture took place after the patient jumped from a height of approximately 15 inches. Patellar tendon rupture often occurs unilaterally in the setting of eccentric contraction of the quadriceps, usually with the foot planted and the knee flexed or bilaterally in the setting of a systemic inflammatory disease. The patient in this case had components of both etiologies.

Rarely, infiltration of the tendons with monosodium urate crystals in the setting of longstanding gout can cause fibrinoid necrosis and chronic inflammation leading to tendon rupture. Chronic inflammation causes microtrauma and degeneration of the tendons, which compromise their integrity and make them more susceptible to injury.

We would like to emphasize that tenosynovitis and tendon rupture can occur in the setting of longstanding gout and should be incorporated into the differential diagnosis of tendon rupture with minimal force in a patient with gout.

This is an original case report of particular interest to orthopedic surgery. We were able to find only limited articles in the literature discussing occurrences of tendon rupture in the setting of longstanding chronic tophaceous gout.

Neil Anand is a volunteer research fellow in the Emergency Trauma Department at Hackensack University Medical Center in Hackensack, N.J. Chinwe Ogedegbe is the director of research in the department, and Gordon Huie is a research coordinator in the department. Joseph Feldman is chairman of the Emergency Trauma Department at the medical center.


1. Annunziata C. Patellar Tendon Rupture. eMedicine.

2. Ramseier LE, et al. Quadriceps and patellar tendon rupture. Injury. 2006;37(6):516-519.

3. Koval KJ, Zuckerman JD. Patella and extensor mechanism injuries. Handbook of Fractures. Philadelphia: Lippincott Williams & Wilkins: 2006: 391-396.

4. Taylor BC, et al. Bilateral patellar tendon rupture at different sites without predisposing systemic disease or steroid use. Iowa Orthop J. 2009;29:100-104.

5. Kelly DW, et al. Patellar and quadriceps tendon ruptures -jumper's knee. Am J Sport Med. 1984;12(5):375-380.

6. Kannus P, Jozsa L. Histopathological changes preceding spontaneous rupture of a tendon. A controlled study of 891 patients. J Bone J Surg. 1991;73(10):1507-1525.

7. Levy M, et al. Bilateral spontaneous and simultaneous rupture of the quadriceps tendons in gout. J Bone Joint Surg Br. 1971;53(3):510-513.

8. Gerster JC, et al. Enthesopathy and tendinopathy in gout: computed tomographic assessment. Ann Rheum Dis. 1996;55(12):921-923.



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