Practice Essentials
The patellar tendon serves as the distal extent of the quadriceps insertion. Rupture of the patellar tendon usually occurs at the osseotendinous junction and causes complete derangement of the knee extensor mechanism. This is a disabling injury in an active person, resulting in an inability to actively obtain and maintain full knee extension.
The patellar tendon ruptures relatively infrequently. However, the complications of an untreated rupture to the extensor mechanism can be extremely disabling. If the tendon does not heal properly and at the correct length and tension, knee range of motion (ROM) and strength can be altered significantly, leading to early fatigue, patellofemoral pain, and, possibly, instability, which can thereby prevent return to preinjury status. [1, 2]
Immediate surgical repair is recommended for optimal return of knee function and power. Surgical intervention allows excellent recovery of motion and strength, provided that the injury is diagnosed in a timely fashion and repaired immediately.
In the past, the surgical technique for acute rupture of the patellar tendon was primary suture repair. Augmentation of the repair was believed to be necessary and was achieved by using a cerclage of wire, suture, or autogenous graft (eg, semitendinosus) in order to reinforce the repair. [3] Routinely, the knee was kept locked in extension for up to 6 weeks to prevent undue stress on the repair.
Earlier and more aggressive rehabilitation techniques are now available. Krackow introduced a novel interlocking stitch technique, [4] and Marder and Timmerman demonstrated that repair alone is equally durable without augmentation. [5]
The focus of this article is acute patellar tendon ruptures, especially those associated with acute sports-related injuries. Patellar tendon ruptures also can occur as a complication of total knee arthroplasty, [6] anterior cruciate ligament (ACL) reconstruction using the patellar tendon as an autograft, [7] or excision of chronic tendinosis. However, the etiology and treatment in these circumstances are beyond the scope of this article.
Anatomy
The patellar tendon is actually a ligament connecting two bones, the tibia and the patella. The extensor mechanism of the knee starts proximally as the quadriceps femoris muscle group. Anteriorly, the fibers of the rectus femoris tendon traverse the patella and condense inferior to the patella to insert on the tibial tubercle as the patellar tendon.
The fibers of the vastus lateralis expand to the superolateral border of the patella and proximal tibia to form the lateral retinaculum. Similarly, the tendons of the vastus medialis insert into the superomedial border of the patella and tibia to form the medial retinaculum. The retinacula converge into the patellar tendon. Injuries to the tendon usually involve the adjacent retinacula as well, causing dysfunction of the entire extensor hood.
Pathophysiology
Unilateral traumatic ruptures of the patellar tendon tend to occur when a violent contraction of the quadriceps is resisted by the flexed knee (eg, during landing after a jump). The estimated force required to disrupt the extensor mechanism has been reported to be as high as 17.5 times body weight.
In the flexed knee position, the patellar tendon sustains greater stress than the quadriceps tendon, and the tensile load is much higher at the insertion sites than in the midsubstance of the tendon. Therefore, the patellar tendon most commonly ruptures near its proximal end, off the inferior pole of the patella.
Given that considerable force is needed to rupture a healthy tendon, it is likely that ruptures occur in areas of preexisting disease.
Etiology
Patellar tendon rupture often occurs in the setting of long-standing patellar tendon irritation. The rupture is the final result of chronic tendon degeneration due to repetitive microtrauma. Histopathologically, ruptured tendons studied by Kannus et al demonstrated changes consistent with chronic inflammation and degeneration. [8]
Ruptures also may occur after local injection of corticosteroid near the inferior pole of the patella as treatment for patellar tendinitis (ie, jumper's knee). This complication, first reported in 1969 by Ismail et al [9] and later elucidated by Kennedy et al, [10] is probably a result of steroid-induced breakdown of collagen organization and strength. In a series by Kelly et al, nearly 60% of patients who sustained patellar tendon ruptures had received an average of two or three steroid injections around the patellar tendon before rupture. [11, 6]
Patellar tendon rupture is usually unilateral and is the result of a traumatic athletic injury. The typical mechanism is a sudden eccentric contraction of the quadriceps, usually with the foot planted and the knee flexed as the person falls. However, in the setting of systemic inflammatory disease, diabetes mellitus, or chronic renal failure, bilateral ruptures can occur with lower-energy stress. [12, 13, 14, 15] Additionally, patellar tendon ruptures can result from a posterior knee dislocation. [16]
Systemic disorders are related to an increased incidence of tendon ruptures. Pritchard et al found that tendon ruptures in systemic lupus erythematosus (SLE) appear to be associated with extended disease duration, long-term corticosteroid therapy, evidence of steroid-induced musculoskeletal complications, minimal disease activity at the time of rupture, and deforming hand arthropathy. [17]
Inflammatory changes have been noted at the site of rupture in patients with SLE, [18] amyloid deposition has been noted at the site in patients with chronic renal failure undergoing dialysis, [19] and elastosis has been noted in patients with chronic acidosis. [20]
Anatomically, the patellar tendon tends to tear in the midsubstance in patients with systemic disease, rather than at the osseotendinous junction, as typically occurs in acute traumatic injury. After a tear of the midsubstance, tendon repair and rehabilitation can be especially difficult, and the difficulty is exacerbated by the preexisting comorbid condition.
Patellar tendon ruptures also can occur after surgery for total knee arthroplasty, procedures using the central third of the patellar tendon as an autograft, or excision of patellar tendinosis.
Epidemiology
The true incidence of patellar tendon rupture is not known, but this injury is observed less frequently than rupture of the quadriceps tendon and usually occurs in those younger than 40 years. It has been quite rare in children, but its frequency has been growing in this population as a consequence of increased participation in sports and high-energy recreational activities during childhood. [21] Overall, patellar tendon rupture is the third most common injury to the extensor mechanism of the knee, following patellar fracture and quadriceps tendon rupture. [22, 23]
Prognosis
Immediate surgical repair of the ruptured patella tendon is recommended for optimal return of function. Outcome after repair is closely related to the length of time between injury and repair. If the tendon is repaired immediately, most patients experience nearly full return of knee motion, quadriceps strength, and preinjury activity levels. [24, 25, 26, 27] Persistent quadriceps atrophy is common but is not considered a complication, in that the atrophy does not prevent the return of strength.
Reasonable function can be obtained in most individuals, especially in those with an acute tendon rupture that is repaired immediately. Multiple authors have attributed an earlier return to preinjury activity to a more aggressive rehabilitation program with an emphasis on earlier ROM. [28, 29, 30, 31]
Because of the relative infrequency of patellar tendon rupture, the sample sizes in all the studies are rather small, and a meta-analysis has yet to be performed to further delineate the statistical significance of an aggressive rehabilitative protocol. Nonetheless, there appears to be a definite trend toward aggressive postoperative rehabilitation for earlier return to preinjury activity, much like that observed with the repaired Achilles tendon.
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Patellar tendon rupture. This image depicts the defect within the patellar tendon at the inferior pole of the patella.
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Patellar tendon rupture. A lateral radiograph of the right knee from a patient with an acute patellar tendon rupture. Note the superior patellar migration as well as the calcification below the inferior pole of the patella. This represents preexisting calcification within the patellar tendon, which likely contributed to the rupture.
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Patellar tendon rupture. This intraoperative picture depicts a rupture of the patellar tendon from the inferior pole of the patella with associated medial and lateral retinacular tears.
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Patellar tendon rupture. Two Krackow stitches with number 5 nonabsorbable sutures are sewn through the patellar tendon.
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Patellar tendon rupture. The inferior pole of the patella is debrided of soft tissue, then decorticated.
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Patellar tendon rupture. An anterior cruciate ligament tibial tunnel guide is positioned along the anterior half of inferior pole and angled such that the drill exits along the superior pole of the patella. A total of 3 parallel tunnels are created. Note the contralateral knee within the operative field, which later serves as the guide in recreating normal patellar height.
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Patellar tendon rupture. The Beath pin replaces the drill bit. The suture is then placed through the eyelet.
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Patellar tendon rupture. All of the suture ends are now along the superior pole of the patella. The inner limbs of the stitches are within the central tunnel while the outer limbs are within the corresponding outer tunnels.
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Patellar tendon rupture. A cerclage stitch was passed along the superior pole of the patella and through a tunnel within the tibial tubercle. This is now being tensioned to maintain normal patellar height so that the repair sutures can now be tied.
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Patellar tendon rupture. The repair is now complete with recreation of normal patellar height. The retinacular tears were repaired with absorbable suture with the knee positioned in 30° of flexion.
Tables
Time After Surgery |
Weightbearing |
Immobilization |
Therapy |
0-3 d |
None, with use of crutches |
Hinged knee brace locked in extension |
1. Motion - None 2. Modalities and/or exercises - None |
4-13 d |
Toe touch with crutches |
Hinged knee brace locked in extension |
1. Motion - Active flexion to 45° and passive extension to 0° (no active extension) 3 times a day 2. Modalities and/or exercises - Swelling control with ice, gentle medial and lateral patellar mobilization, gentle isometric hamstring exercises, contralateral isometric quadriceps exercises 3 times a day |
2-4 wk |
Partial (25-50%) with crutches |
Hinged knee brace locked in extension |
1. Motion - Active flexion to progress to 90° and passive extension to 0° (no active extension) 3 times a day 2. Modalities and/or exercises - Swelling control with ice, gentle medial and lateral patellar mobilization, gentle (~25%) isometric quadriceps exercises (sets, no straight leg raises), continue with ipsilateral hamstring exercises and contralateral quadriceps exercises 3 times a day |
4-6 wk |
Progress to weightbearing as tolerated, crutches discontinued when good quadriceps control is obtained |
Hinged knee brace locked in extension |
1. Motion - Active flexion to progress as tolerated and passive extension to 0° (no active extension) 3 times a day 2. Modalities and/or exercises - Swelling control with ice, gentle medial and lateral patellar mobilization, gentle (~25%) isometric quadriceps exercises (sets, no straight leg raises), continue with ipsilateral hamstring exercises and contralateral quadriceps exercises 3 times a day |
6-12 wk |
Weightbearing as tolerated |
Hinged knee brace locked in extension until good active quadriceps control and normal gait are obtained |
1. Motion - Progress to full 3 times a day 2. Modalities and/or exercises - Swelling control with ice, more aggressive medial and lateral patellar mobilization, begin straight leg raises without resistance, continue with ipsilateral hamstring exercises and contralateral quadriceps exercises 3 times a day; start stationary cycling at 8 weeks |
12-16 wk |
Complete weightbearing |
No immobilization |
Progress with quadriceps strengthening (isokinetic) exercises and start neuromuscular retraining |
16-24 wk |
Complete weightbearing |
No immobilization |
May start running and sport-specific training |
>6 mo |
Complete weightbearing |
No immobilization |
May return to jumping and contact sports when obtain 85-90% of strength of contralateral extremity on isokinetic strength testing |
